A
                                TREATISE
                                   ON
                                POISONS
                             IN RELATION TO
     MEDICAL JURISPRUDENCE, PHYSIOLOGY, AND THE PRACTICE OF PHYSIC.


                                    BY

                    ROBERT CHRISTISON, M.D., F.R.S.E.,


  Professor of Materia Medica in the University of Edinburgh, Fellow of
       the Royal College of Physicians, &c., Member of the American
 Philosophical Society,—of the Royal Acad. of Med. of Paris,—of the Imp.
    Soc. of Physicians of Vienna,—of the Imp. Med. Chir. Acad. of St.
  Petersburg,—of the Med. Chir. Soc. of Berlin,—of the Med. Chir. Assoc,
     of Hamburg,—of the Soc. of Nat. and Phys. of Heidelberg,—of the
                       Philadelphia Coll. of Pharm.


            FIRST AMERICAN, FROM THE FOURTH EDINBURGH EDITION.


                              PHILADELPHIA:
                    ED. BARRINGTON & GEO. D. HASWELL.
                                  1845.




                                PREFACE
                         TO THE FOURTH EDITION.


[Illustration]

The author regrets that circumstances beyond his control have delayed
the re-appearance of the present work beyond the period at which it was
called for by the favourable reception of the last edition. He has
endeavoured to take advantage of the numerous investigations which have
been carried on during the interval into the several departments of
Toxicology in the leading countries of Europe; and has in consequence
been led to enlarge the work materially.

He trusts it may be allowed him to express his satisfaction at finding,
that the rapid progress made by Toxicological science during the last
eight years, while it has been productive of many important additions to
our knowledge, has nevertheless not rendered any important alterations
necessary either in the general principles formerly laid down in this
work, or in what had been there stated as well ascertained general
facts.

 EDINBURGH COLLEGE,
   _November, 1844_.




                               CONTENTS.


                    PART FIRST.—OF GENERAL POISONING.

                                                                    PAGE

 CHAP. I.         Of the Physiological Action of Poisons               9

       SECTION 1. Of their Mode of Action                              9

                  Of the Discovery of Poisons in the Blood            21

       SECTION 2. Of the Causes which modify their Action             27

                  Application of the preceding observations to the
                    Treatment of Poisoning                            36

 CHAP. II.        Of the Evidence of General Poisoning                39

       SECTION 1. Of the Evidence from Symptoms                       42

                  Characters of the Symptoms of Poisoning             42

                  Characters of the Symptoms of Natural Disease       46

       SECTION 2. Of the Evidence from Morbid Appearances             51

       SECTION 3. Of the Evidence from Chemical Analysis              54

                  Causes which remove Poisons beyond the reach of
                    analysis                                          55

                  Chemical Evidence not always indispensable to the
                    proof of Poisoning                                59

       SECTION 4. Evidence from Experiments on Animals                62

                  With suspected articles of food or drink            63

                  With vomited matter or contents of the stomach      67

                  With the flesh of poisoned animals                  69

       SECTION 5. Moral Evidence                                      71

                  Suspicious conduct of prisoner, 73 and 78.—Proof
                    of administration of poison, 73.—Proof of
                    intent, 78.—Proof from simultaneous illness of
                    several people, 80.—Proof from death-bed
                    declaration                                       83

 CHAP. III.       Of Imaginary, Pretended, and Imputed Poisoning      85


                     PART II.—OF INDIVIDUAL POISONS.

 CHAP. I.         Classification of Poisons                           90

 CHAP. II.        CLASS FIRST. Of Irritant Poisons generally          92

       SECTION 1. Of the Symptoms of Irritant Poisons compared with
                    those of Natural Disease                          93

       SECTION 2. Of the Morbid Appearances of Irritant Poisoning
                    compared with those of natural disease           110

 CHAP. III.       Mineral Acids                                      121

       SECTION 1. Sulphuric Acid                                     123

                  Tests, 123, Action, 128, Morbid Appearances, 135,
                    Treatment,                                       140

       SECTION 2. Nitric Acid                                        142

       SECTION 3. Hydrochloric Acid                                  146

 CHAP. IV.        Phosphorus. Sulphur. Chlorine. Iodine. Iodide of
                    Potassium. Bromine                               149

 CHAP. V.         Acetic Acid                                        164

 CHAP. VI.        Oxalic Acid                                        167

       SECTION 1. Tests                                              168

       SECTION 2. Action and Symptoms in Man                         173

       SECTION 3. Morbid Appearances                                 177

       SECTION 4. Treatment                                          178

                  Tartaric and Citric Acid                           180

 CHAP. VII.       Fixed Alkalis                                      180

 CHAP. VIII.      Nitre                                              187

 CHAP. IX.        Alkaline and Earthy Chlorides                      191

 CHAP. X.         Lime                                               192

 CHAP. XI.        Ammonia and its salts                              193

 CHAP. XII.       Alkaline Sulphurets                                196

 CHAP. XIII.      Arsenic                                            197

       SECTION 1. Tests for its compounds                            198

                  Fly-powder                                         199

                  Oxide of Arsenic                                   200

                  Tests in its solid state                           203

                  —— a pure solution                                 206

                  —— when in organic mixtures                        215

                  Arsenite of Copper                                 223

                  —— of Potass                                       223

                  Arseniate of Potass                                224

                  Sulphurets of Arsenic                              224

                  Arseniuretted-hydrogen                             227

       SECTION 2. Action and Symptoms in Man                         227

                  Mode of Action                                     227

                  Symptoms in ordinary cases                         234

                  —— very short cases                                241

                  —— tedious cases                                   244

                  Effects through other channels besides the
                    Stomach                                          251

                  Force of the evidence from Symptoms                259

       SECTION 3. Morbid Appearances                                 262

       SECTION 4. Treatment                                          283

 CHAP. XIV.       Mercury                                            289

       SECTION 1. Tests for its preparations                         289

                  Red Precipitate                                    290

                  Cinnabar                                           290

                  Turbith Mineral                                    290

                  Calomel                                            291

                  Corrosive Sublimate                                291

                  —— Tests in the solid state                        292

                  —— solution                                        292

                  —— organic mixtures                                296

                  Bicyanide of Mercury                               303

                  Nitrates of Mercury                                303

       SECTION 2. Mode of Action and Symptoms                        303

                  Mode of Action                                     303

                  Symptoms of Corrosive Poisoning                    310

                  Symptoms of Irritation and Erethysm combined       314

                  Symptoms of Erethysm and Mercurial Tremor          316

       SECTION 2. Action on different Tissues and in different
                    Chemical forms                                   327

                  Force of evidence from Symptoms                    336

       SECTION 3. Morbid Appearances                                 337

       SECTION 4. Treatment                                          342

 CHAP. XV.        Copper                                             345

       SECTION 1. Tests for its Compounds                            346

       SECTION 2. Action and Symptoms                                358

       SECTION 3. Morbid Appearances                                 364

       SECTION 4. Treatment                                          365

 CHAP. XVI.       Antimony                                           367

       SECTION 1. Tests for its Compounds                            367

       SECTION 2. Action and Symptoms                                371

       SECTION 3. Morbid Appearances                                 376

       SECTION 4. Treatment                                          377

 CHAP. XVII.      Tin, 379—Silver, 380—Gold, 383—Bismuth,
                    383—Chrome, 385—Zinc, 386—Iron, 391—Other rarer
                    metals, 395                                      378

 CHAP. XVIII.     Lead                                               396

       SECTION 1. Chemical History, and Tests for its Compounds      396

                  Action of Water on Lead                            399

                  Action of Acidulous Fluids on Lead                 416

                  Process for Lead in Organic Fluids                 423

       SECTION 2. Action and Symptoms in Man                         424

                  Tradesmen who are apt to suffer from Lead          436

       SECTION 3. Morbid Appearances                                 439

       SECTION 4. Treatment, and Precautions for Workmen             441

 CHAP. XIX.       Baryta                                             446

 CHAP. XX.        Vegetable Acrids, Euphorbia, Castor-oil seed,
                    Physic-nut, Bitter Cassava, Manchineel, Croton,
                    Bryony, Colocynth, Elaterium, Ranunculus,
                    Anemone, Caltha, Clematis, Trollius, Mezereon,
                    Cuckoo-pint, Gamboge, Daffodil, Jalap, Savin     451

 CHAP. XXI.       Cantharides                                        470

 CHAP. XXII.      Poisonous Fish                                     477

 CHAP. XXIII.     Venomous Serpents and Insects                      484

 CHAP. XXIV.      Diseased and Decayed Animal Matter                 487

 CHAP. XXV.       Mechanical Irritants                               501

                  Substances, irritant, in large doses,—Pepper,
                    Epsom Salt, Alum, Cream of Tartar, Sulphate of
                    Potass, Common Salt, &c.                         506

 CHAP. XXVI.      CLASS II. Of Narcotic Poisons, 510—of Narcotic
                    Poisoning generally, and the distinction
                    between it and natural disease, 511              510

 CHAP. XXVII.     Opium                                              530

       SECTION 1. Chemical History and Tests                         530

       SECTION 2. Action and Symptoms                                539

                  Action of Morphia and Narcotine                    557

       SECTION 3. Morbid Appearances                                 562

       SECTION 4. Treatment                                          566

 CHAP. XXVIII.    Hyoscyamus, Lactuca, and Solanum                   571

 CHAP. XXIX.      Hydrocyanic Acid                                   577

       SECTION 1. Tests                                              578

       SECTION 2. Action and Symptoms                                582

       SECTION 3. Morbid Appearances                                 593

       SECTION 4. Treatment                                          596

                  Of the Vegetable Substances which contain
                    Hydrocyanic Acid, 600—Bitter Almond,
                    601—Cherry-laurel, 605—Peach,
                    608—Cluster-cherry, 608—Mountain-ash,            608

 CHAP. XXX.       Carbazotic Acid                                    610

 CHAP. XXXI.      Poisonous Gases                                    611

                  What Gases are Poisonous                           612

                  Effects on Man of Nitric Oxide Gas, 615—Chlorine,
                    616—Ammonia, 617—Hydrochloric Acid,
                    617—Hydrosulphuric Acid, 617—Carburetted
                    hydrogen, 622—Carbonic Acid, 624—Carbonic
                    Oxide, 634—Nitrous Oxide, 635—Cyanogen,
                    636—Oxygen,                                      636

 CHAP. XXXII.     CLASS III. Narcotico-Acrid Poisons                 637

 CHAP. XXXIII.    Nightshade, 639—Thorn-Apple, 644—Tobacco, 647      639

 CHAP. XXXIV.     Hemlock, 653—Water-hemlock, 657—Hemlock Dropwort,
                    658—Fool’s Parsley, 661                          653

 CHAP. XXXV.      Monkshood, 662—Black Hellebore, 670                662

 CHAP. XXXVI.     Squill, 671—White Hellebore and Cevadilla,
                    672—Meadow-Saffron, 674—Foxglove, 678—Rue,
                    681—Ipecacuan, 682                               671

 CHAP. XXXVII.    Strychnia, 683—Nux Vomica, 686—St. Ignatius’
                    Bean, 691—False Angustura, 692                   682

 CHAP. XXXVIII.   Camphor, 694—Cocculus Indicus, 696—Upas Antiar,
                    698—Coriaria myrtifolia, 698—Yew, 699            694

 CHAP. XXXIX.     Poisonous Fungi, 700—wholesome and poisonous
                    kinds, 701—qualities how modified,
                    701—poisonous principles of, 704—effects on
                    man, 704—Poisonous Mosses, 710                   700

 CHAP. XL.        Poisonous Grain, 710—Spurred rye, 711—Spurred
                    maize, 718—rust of wheat, 719—unripe grain,
                    719—Darnel-grass, 721—Leguminous seeds, 722      710

 CHAP. XLI.       Alcohol, 725—symptoms in man, 725—morbid
                    appearances, 731—treatment, 735—ether,
                    736—Empyreumatic Oils, 736                       725

 CHAP. XLII.      Compound Poisoning                                 740

 INDEX                                                               745

 Description of Plate                                               755,
                                                                     756




                              PART FIRST.
                         OF GENERAL POISONING.


[Illustration]




                               CHAPTER I.
                ON THE PHYSIOLOGICAL ACTION OF POISONS.


I shall discuss this subject by considering first the mode in which
poisons act, and secondly, the causes by which their action is liable to
be modified.


             SECTION I.—_On the Mode of Action of Poisons._

On attending to the effects which follow the application of a poison to
the body, we perceive that they are sometimes confined to the part where
it is applied, and at other times extend to distant organs. Hence the
action of poisons may be naturally considered as _local_ and _remote_.

The local effects of poisons are of three kinds. Some decompose
chemically or corrode the part to which they are applied. Others,
without immediately injuring its organization, inflame or irritate it.
Others neither corrode nor irritate, but make a peculiar impression on
the sentient extremities of the nerves, unaccompanied by any visible
change of structure.

We have examples of local _corrosion_ or chemical decomposition in the
effects of the concentrated mineral acids or alkalis on the skin, and in
the effects of strong oxalic acid, lunar caustic, or corrosive sublimate
on the stomach. In all of these instances the part to which the poison
is applied undergoes chemical changes, and the poison itself sometimes
undergoes chemical changes also. Thus oxalic acid dissolves the gelatin
of the animal textures; and in the instance of corrosive sublimate, the
elements of the poison unite with the albumen, fibrin, and other
principles of the tissues.

Of local _irritation_ and its various consequences we have many
examples, from redness, its slightest, to ulceration and gangrene, its
most severe effect. Thus externally, alcohol reddens the skin;
cantharides irritates the surface of the true skin and causes
vesication; tartar-emetic causes deep-seated inflammation of the true
skin and a pustular eruption; the juice of manchineel[1] spreading
inflammation of the subcutaneous cellular tissue; arsenic inflammation
of all these textures, and also death of the part and subsequent
sloughing. Internally, alcohol reddens the stomach, as it does the
skin,—but more permanently; while other substances, such as the diluted
mineral acids, arsenic, cantharides, euphorbium, and the like, may cause
all the phenomena of inflammation in the stomach and intestines, namely,
extravasation of blood, effusion of lymph, ulcers, gangrene. Many of
these irritants, such as arsenic, are in common speech called
corrosives; but they have not any power of causing chemical
decomposition: if they produce a breach in the texture of an organ, it
is merely through the medium of inflammation and its effects.

Of _nervous impressions_, without any visible organic change, few well
authenticated and unequivocal instances are known. A good example has
been mentioned by Sir B. Brodie in the effect of monkshood on the lips
when chewed,[2] an effect which I have also often experienced: it causes
a sense of numbness and tingling in the lips and tongue, lasting for
some hours, and quite unconnected with any affection of the general
nervous system. Another instance, first mentioned to me by M. Robiquet,
and which I have verified, occurs in the effects of the strong
hydrocyanic acid: when this acid is confined in a glass tube with a
finger on its open end, the point of the finger becomes benumbed,
exactly as from the local action of great cold. These are undoubted
instances of a purely nervous local impression on the external surface
of the body. The most unequivocal instance I know of a similar
impression on internal parts is a fact related by Dr. W. Philip with
regard to opium.[3] When this poison was applied to the inner coat of
the intestines of a rabbit during life, the muscular contractions of the
gut were immediately paralyzed, without the general system being for
some time affected. The same effect has been observed by Messrs. Morgan
and Addison to follow the application of ticunas to the intestine:[4] an
instant and complete suspension of the peristaltic movement took place
as soon as it touched the gut. A parallel fact has also been described
by Dr. Monro, _secundus_:[5] when an infusion of opium was injected
between the skin and muscles of the leg of a frog, that leg soon became
palsied, while the animal was able to leap briskly on the other three.
Analogous results have farther been obtained with the prussic acid by M.
Coullon.[6] He remarked, that when one hind-leg of a frog was plunged in
the acid, it became palsied in thirty-five minutes, while the other
hind-leg continued perfectly sensible and irritable. Acetate of lead
probably possesses the same property.

These facts are important, because some physiologists have doubted
whether any local impressions of a purely nervous nature, unconnected
with appreciable organic change, may arise from the action of poisons.
Yet the existence of impressions of the kind is essential to the
stability of the doctrine of the sympathetic operation of poisons,—that
is, of the transmission of their influence from organ to organ along the
nerves. Nay, in the instance of many poisons supposed to act in that
manner, we must still farther believe in the existence of primary
nervous impressions, which are not only unconnected with organic change,
but likewise undistinguishable by any local sign whatsoever.

Of the three varieties in the local effects of poisons—corrosion,
irritation, and nervous impressions,—the first two may take place in any
tissue or organ; for example, they have been observed on the skin, on
the mucous membrane of the stomach, intestines, windpipe, air tubes,
bladder, and vagina, in the cellular tissue, in the serous membranes of
the chest and abdomen, in the muscular fibre. We are not so well
acquainted with the nature of local nervous impressions on different
tissues; but it is probable that in some textures of the body they are
very indistinct.

So much for the local effects of poisons.

On tracing the phenomena which follow more remotely, we observe that the
affected part sometimes recovers without any visible change, sometimes
undergoes the usual processes consequent on inflammation, sometimes
perishes at once and is thrown off; and if the organ is one whose
function is necessary to life, death may gradually ensue, in consequence
of that function being irrecoverably injured. The purest example of the
last train of phenomena is to be seen in the occasional effects of the
mineral acids or alkalis: death may take place simply from starvation,
because the inner surface of the stomach and intestines is so much
injured that a sufficient quantity of nutriment cannot be assimilated.

But death and its antecedents can seldom be accounted for in this way.
For symptoms are often witnessed, which bear no direct relation to the
local injury: death is generally too rapid to have arisen from the
function of the part having been annihilated: and the rapidity of the
poisoning is not proportional in different cases to the local injury
produced. Even the mineral acids and alkalis seldom kill by impeding or
annihilating digestion, because they often prove fatal in a few hours;
and among other poisons there are few which ever cause death simply by
disturbing the function of the part primarily acted on. Death and the
symptoms preceding it arise from an injury of some other organ, to which
they are not and cannot be directly applied. We are thus led to consider
their remote action.

The term _remote_ is here used in preference to the common phrase
_general_ action, because the latter implies an action on the general
system or whole body; whereas it appears that an action of such a kind
is rare, and that most poisons which have an indirect action exert it on
one or more of the important organs only, and not on the general system.

There is not a better instance of the remote action of poisons than
oxalic acid. It has been already mentioned that concentrated oxalic acid
is a corrosive: yet it never kills by destroying the function of the
stomach. Man, as well as the lower animals, will live several days or
weeks without nutriment. Now this poison has been known to kill a man in
ten minutes, and a dog in three minutes only. Neither does it always
induce, when swallowed, symptoms of an injury of the stomach; for death
is often preceded by tetanus, or apoplexy, or mortal faintness. Nor is
the violence of the poisoning proportional to the extent of the local
injury: in fact, death is most rapid under circumstances in which the
stomach is least injured, namely, when the acid is considerably
diluted.[7]

Let us now proceed to enquire, then, in what way the influence of a
poison is conveyed from one organ to another.

Here it will at once be perceived that the conveyance can be
accomplished in one of two ways only. Either the local impression passes
along the nerves to the organ secondarily affected; or the poison enters
the bibulous vessels, mingles with the blood, and passes through the
medium of the circulation. In the former way poisons are said to act
through _sympathy_, in the latter, through _absorption_.

1. _On the Action of Poisons through Sympathy._ In the infancy of
toxicology all poisons were believed to act through sympathy. Since
Magendie’s discoveries on venous absorption in 1809, the favourite
doctrine has on the other hand been, that most, if not all, act through
the medium of the blood. And a recent theory, combining both views,
represents that, although many poisons do enter the blood, the operation
even of these nevertheless consists of an impression made on the
sentient extremities of the nerves of the blood-vessels and conveyed
thence along their filaments to the brain or other organs.

The nerves certainly possess the power of conveying from one organ to
another various impressions besides those of the external senses. This
is shown by many familiar phenomena; and in reference to the present
subject, is aptly illustrated by the remote or sympathetic effects of
mere mechanical injury and natural disease of the stomach. Acute
inflammation of the stomach generally proves fatal long before death can
arise from digestion being stopped; and it is accompanied with
constitutional symptoms, neither attributable to injury of that
function, nor developed in so marked a degree during inflammation in
other organs. These symptoms and the rapid death which succeeds them are
vaguely imputed to the general system sympathizing with the affected
part; but it is more probable that one organ only is thus, at least in
the first instance, acted on sympathetically, namely, the heart. The
effects of mechanical injuries are still more in point. Wounds of the
stomach may prove fatal before inflammation can begin; rupture from
over-distension may cause instant death; and in either case without
material hemorrhage.

These observations being held in view, it is impossible to doubt, that
some organs sympathize with certain impressions made on others at a
distance; nor can we imagine any other mode of conveyance for these
impressions except along the nerves. The question, then, comes to be
what are the impressions that may be so transmitted?

The statements already made will prepare us to expect a sympathetic
action in the case of poisons that manifestly injure the structure of
the organ to which they are applied. In the instance of the pure
corrosives its existence may be presumed from the identity of the
phenomena of their remote action with those of natural disease or
mechanical injury. It was stated above that the mineral acids when
swallowed often prove fatal in a very short space of time; and here, as
in mere injury from disease or violence, the symptoms are an
imperceptible pulse, fainting, and mortal weakness. Remote organs
therefore must be injured; and from the identity of the phenomena with
those of idiopathic affections of the stomach, even if there were no
other proof, it might be presumed that the primary impression is
conveyed along the nerves. We are not restricted, however, to such an
argument: The presumptive inference is turned to certainty by the effect
of dilution on the activity of these poisons. Dilution materially
lessens or even takes away altogether the remote action of the mineral
acids. Now dilution facilitates, instead of impeding their absorption:
consequently they do not act on remote organs through that channel.
There is no other way left by which we can conceive them to act, except
by conveyance of the local impression along the nerves.—As to the
irritants that are not corrosive, it can hardly be doubted, since they
inflame the stomach, that the usual remote effects of inflammation will
ensue, namely, a sympathetic injury of distant organs.

But it remains to be considered, whether distant organs may sympathize
also with the peculiar local impressions called nervous,—which are not
accompanied by any visible derangement of structure. This variety of
action by sympathy is the one which has chiefly engaged the attention of
toxicologists; and it has been freely resorted to for explaining the
effects of many poisons. Nevertheless its existence is doubtful.

The only important arguments in support of the sympathetic action of
poisons are, that unequivocal instances exist of local nervous
impressions being conveyed to a limited extent along the nerves,—and
that the rapidity of the effects of some poisons is so great as to be
incompatible with any other medium of action except the nervous system.

In the first place it is maintained, that a limited nervous
transmission, that is, the conveyance of a local impression, purely
functional in its nature, to parts at a short distance from the texture
acted on directly, must occur in some instances,—as, for example, in the
action of belladonna in dilating the pupil when applied to the
conjunctiva of the eye, and in the effect of opium in allaying
deep-seated pain when applied to the integuments over the affected part.
It is by no means clear, however, that nervous transmission is in such
circumstances the only possible medium of action; and that the phenomena
may not as well be owing to the agent being conveyed in substance, by
imbibition or absorption, to the parts ultimately acted on. It is not
unworthy of remark too, that in the case of hydrocyanic acid,—a poison,
which, more perhaps than any other, has been held to act by sympathy,
and which produces on the integuments a direct local impression of a
peculiar and unequivocal kind,—there is positive evidence of the direct
impression not being conveyed along the nerves, even to the most limited
distance; for I have not been able to observe the slightest effect
beyond the abrupt line on the skin which defines the spot with which the
acid had been in contact.

Secondly, it is thought that certain poisons, such as hydrocyanic acid,
strychnia, alcohol, conia, and some others, produce their remote effects
with a velocity, which is incompatible with any conceivable mode of
action except the transmission of a primary local impulse along the
nerves, and more especially incompatible with the poison having followed
the circuitous route of the circulation to the organs which are affected
by it remotely. Thus in regard to the hydrocyanic acid, Sir B. Brodie
has stated,[8] that a drop of the essential oil of bitter almonds, which
owes its power to this acid, caused convulsions instantly when applied
to the tongue of a cat; and that happening once to taste it himself, he
had scarcely applied it to his tongue, when he felt a sudden momentary
feebleness of his limbs, so that he could scarcely stand. Magendie,[9]
speaking of the pure hydrocyanic acid, compares it in point of swiftness
of action to the cannon ball or thunderbolt. In the course of certain
experiments made not long ago with the diluted acid by Dr. Freer, Mr.
Macaulay and others,[10] to decide the true rapidity of this poison,
several dogs were brought under its influence in ten, eight, five, and
even three seconds; during an experimental inquiry I afterwards
undertook for the same purpose,[11] I remarked on one occasion that a
rabbit was killed outright in four seconds; and Mr. Taylor has more
recently stated, that he has seen the effects induced so quickly in
cats, that there was no sensible interval of time between the
application of the poison to the tongue and the first signs of
poisoning.[12] Strychnia, the active principle of nux-vomica, acts
sometimes with a speed little inferior to that of hydrocyanic acid; for
Pelletier and Caventou have seen its effects begin in fifteen
seconds.[13] Alcohol, according to Sir B. Brodie,[14] also acts on
animals with equal celerity; for when he introduced it into the stomach
of a rabbit, its effects began when the injection was hardly completed.
Conia, the active principle of hemlock, is not less prompt in its
operation: when it was injected in the form of muriate into the femoral
vein of a dog, I was unable, with my watch in my hand, to observe an
appreciable interval between the moment it was injected and that in
which the animal died;[15] certainly the interval did not exceed three
or at most four seconds.

Facts such as these have been long held adequate to prove that some
poisons must act on remote organs by sympathy or transmission of a local
impulse along the nerves; and in the last edition of this work they were
acknowledged to warrant such a conclusion. It was thought difficult to
account for the phenomena on the supposition that the poison was
conveyed in substance with the blood to the organ remotely affected by
it; for it appeared impossible that, in so short a space of time as
elapsed in some of the instances now referred to, the poison could enter
the veins of the texture to which it was applied, pass into the right
side of the heart, follow the circle of the pulmonary circulation into
the left side of the heart, and thence be transmitted by the arterial
system to the capillaries of the organ ultimately affected. But the
progress of physiological discovery has lately brought the soundness of
these views into question. Some years ago Dr. Hering of Stuttgardt
showed that the round of the circulation may be accomplished by the
blood much more speedily than had been conceived before; for the
ferro-cyanide of potassium, injected into the jugular vein of a horse,
was discovered by him throughout the venous system at large in the short
space of twenty or thirty seconds, and consequently must have passed in
that period throughout the whole double circle of the pulmonary and
systemic circulation.[16] This discovery at once shook the validity of
many, though not all, of the facts which had been previously referred to
the agency of nervous transmission on the ground of the celerity with
which the effects of poisons are manifested. More recently an attempt
has been made by Mr. Blake to prove, that the circulation is so rapid as
to admit even of the swiftest cases of poisoning being referred to the
agency of absorption. Mr. Blake, who is altogether opposed to the
occurrence of nervous transmission in the instance of any poison, has
found that ammonia, injected into the jugular vein of a dog, was
indicated in its breath in four seconds; and that chloride of barium or
nitrate of baryta, introduced into the same vessel, could be detected in
the blood of the carotid artery in about sixteen seconds in the horse,
in less than seven seconds in the dog, in six seconds in the fowl, and
in four seconds in the rabbit.[17] These interesting discoveries,
however, will not absolutely destroy the conclusiveness of all the facts
quoted above in support of the existence of a sympathetic action. For
example they do not shake the validity of those observations, in which
it appeared that an interval inappreciable, or barely appreciable,
elapsed between the application and action of hydrocyanic acid and of
conia. Mr. Blake indeed denies the accuracy of these observations,
insisting that, in those he made himself with the most potent poisons,
he never failed to witness, before the poison began to act, an interval
considerably longer than what had been observed by others, and longer
also than what he had found sufficient for the blood to complete the
round of the circulation; that, for example, the wourali poison injected
into the femoral or jugular vein did not begin to act for twenty
seconds, conia and tobacco for fifteen seconds, and extract of nux
vomica for twelve seconds; and that hydrocyanic acid dropped on the
tongue did not act for eleven seconds if the animal was allowed to
inhale its vapour, and not for sixteen seconds, if direct access to the
lungs was prevented by making the animal breathe through a tube in the
windpipe. But Mr. Blake cannot rid himself thus summarily of the
positive facts which stand in his way. Duly weighed, the balance of
testimony is in favour of those whose accuracy he impugns. For in the
first place, they had not, like him, a theory to build up with their
results, but were observing, most of them at least, the simple fact of
the celerity of action. Then, their result is an affirmation or positive
statement, and his merely a negative one: They may perfectly well have
observed what he was not so fortunate as to witness. And lastly, it is
not unreasonable to claim for Sir B. Brodie, Dr. Freer, Mr. Macaulay,
and Mr. Taylor, all of them practitioners of experience, the faculty of
noting time as accurately as Mr. Blake himself. As for my own
observations, I feel confident they could not have been made more
carefully, and that I had at the moment no preconceived views which the
results upheld, but, if anything, rather the reverse.

It is impossible therefore to concede, that Mr. Blake’s inquiries,
merely because they are at variance with prior results, apparently not
less precise and exact than his own, put an end to the argument which
has been drawn, in favour of the existence of a sympathetic action, from
the extreme swiftness of the operation of some poisons. At the same
time, on a dispassionate view of the whole investigation, it must be
granted to be doubtful, whether this argument can be now appealed to in
its present shape with the confidence which is desirable. And on the
whole, the velocity of the circulation on the one hand, and the celerity
of the action of certain poisons on the other, are both of them so very
great, and the comparative observation of the time occupied by the two
phenomena respectively becomes in consequence so difficult and
precarious, that it seems unsafe to found upon such an inquiry a
confident deduction on either side of so important a physiological
question as the existence or non-existence of an action of poisons by
sympathy.

In concluding these statements it is necessary to notice certain
positive arguments which have been brought against the doctrine of
nervous transmission.

It is alleged to be contrary to nature’s rule to adopt two ways of
attaining the same end; and therefore, that, since many poisons
undoubtedly act through absorption, it is unphilosophical to hold that
others act by sympathy. There seems no sound reason, however, for thus
imposing arbitrary limits on the functional powers conferred by nature
on the organs of the animal body. And besides, the presumption thus
derived is counterbalanced by the equally plausible supposition,
that,—since nature has clearly established an action on remote organs
through the medium of the nerves in the case of poisons which cause
destruction or inflammation of the tissues to which they are
applied,—the same medium of action may also exist in the instance of
poisons which produce merely a peculiar nervous impression where they
are applied.

But it is farther alleged, that poisons of the most energetic action
have no effect, when they are applied to a part, the connection of which
with the general system is maintained by nerves only. It is true that
poisons seem to have no effect whatever when the circulation of the part
to which they are applied has been arrested, or when every connecting
tissue has been severed except the nerves. Thus Emmert found that the
wourali poison does not act on an animal when introduced into a limb
connected with the body by nerves alone.[18] And I have ascertained that
in the same circumstances no effect is produced on the dog by pure
hydrocyanic acid dropped into the cellular tissue of the paw. But it
cannot be inferred absolutely from these facts, that the wourali poison
and hydrocyanic acid do not act through sympathy; because it has been
urged that the integrity of the functions of the sentient extremities of
the nerves, more especially their capability of receiving those nervous
impressions which are held to be communicated backwards along their
course, may be interrupted by arresting the circulation of the part.
Still, as the function of sensation is maintained for some time in a
severed limb connected with the trunk by nerves only, there is a
probability, that all other functions of the nerves must be retained for
a time also. And the presumption thus arising is strengthened by an
imperfect experiment performed by Mr. Blake, which tends to show,
although it does not absolutely prove, that a poison, introduced into
the severed limb whose nervous connection with the trunk is entire, will
not act, even if the blood be allowed to enter the limb by its artery
and to escape from a wound in its vein, so that local circulation is in
some measure maintained, without the blood returning to the trunk and
general system.[19]

On considering impartially all the facts that have been adduced in this
inquiry, an impression must be felt that the doctrine of the sympathetic
action of those poisons which produce merely a nervous local impression
is insecurely founded. But an _experimentum crucis_ is still wanted to
decide the question.

2. _Of the Action of Poisons through Absorption._—If doubts may be
entertained whether poisons ever act by the transmission of local
impulses, from the part to which they are applied, along the nerves to
the organ upon which they act, no reasonable doubt can be entertained
that many poisons act through the medium of absorption into the blood.

Poisons are believed to act through the blood for the following reasons.
First, they disappear during life from the shut cavities or other
situations into which they have been introduced; that is, they are
absorbed. Several clear examples to this effect have been related by Dr.
Coindet and myself in our paper on oxalic acid. In one experiment four
ounces of a solution of oxalic acid were injected into the peritoneal
sac of a cat, and killed it in fourteen minutes; yet, on opening the
animal, although none of the fluid had escaped by the wound, we found
scarcely a drachm remaining.[20] In recent times Professor Orfila has
proved that various poisons, such as arsenic, tartar-emetic, and acetate
of lead, disappear in part or wholly from wounds into which they had
been introduced.[21] Next, many poisons act with unimpaired rapidity,
when the nerves supplying the part to which they are applied have been
previously divided, or even when the part is attached to the body by
arteries and veins only. Dr. Monro, _secundus_, proved this in regard to
opium;[22] and the same fact has been since extended by Sir B. Brodie
and Professor Emmert to wourali,[23] by Magendie to nux vomica,[24] by
Coullon to hydrocyanic acid,[25] by Charret to opium,[26] and by Dr.
Coindet and myself to diluted oxalic acid.[27] Magendie’s experiment was
the most precise of all: for, besides the communication with the
poisoned part being kept up by a vein and an artery only, these vessels
were also severed and reconnected by two quills. Farther, many poisons
will not act when they are applied to a part of which the circulation
has been arrested, even although all its other connections with the body
have been left entire. This has been shown distinctly by Emmert in
regard to the hydrocyanic acid; which, when introduced into the hind-leg
of an animal after the abdominal aorta has been tied, produces no effect
till the ligature be removed, but then acts with rapidity.[28] An
experiment of a similar nature performed by Mr. Blake with the wourali
poison yielded the same result.[29] Again, many poisons act with a force
proportional to the absorbing power of the texture with which they are
placed in contact. This is the criterion which has been commonly
resorted to for discovering whether a poison acts through the medium of
the blood. It is applicable, however, only when the poison acts sensibly
in small doses; for those which act but in large doses cannot be applied
in the same space of time over equal surfaces of different textures. The
difference in the absorbing power of the different tissues has been well
ascertained in respect to a few of them only. The most rapid channel of
absorption is by a wound, or by immediate injection into a vein; the
surface of the serous membranes is a less rapid medium, and the mucous
membrane of the alimentary canal is still less rapid. Now it is proved
of many poisons that, when applied in similar circumstances to these
several parts or tissues, their activity is proportional to the order
now laid down. Lastly, it has been proved of nux-vomica, that if the
extract be thrust into the paw of an animal after a ligature has been
tightened round the leg so as to stop the venous, but not the arterial
circulation of the limb, blood drawn from an orifice in a vein between
the wound and the ligature, and transfused into the vein of another
animal, will excite in the latter the usual effects of the poison, so as
even to cause death; while, on the contrary, the animal from which the
blood has been taken will not be affected at all, if a sufficient
quantity be withdrawn before the removal of the ligature. These
interesting facts, which are capable of important practical
applications, were ascertained by M. Vernière.[30]

On weighing attentively the arguments here brought forward, it seems
impossible to doubt, that some poisons are absorbed into the blood
before they act, and that their entrance into the blood is not a mere
fortuitous antecedent, but a condition essential to their action.

But it is farther held that poisons which act through absorption, do so
by being conveyed in substance along with the blood to the part where
their action is developed,—that their action eventually depends on the
organ, whose functions are thrown into disorder, becoming impregnated
with poisoned blood. Now, the arguments detailed above do not absolutely
prove this conveyance and impregnation. They show that poisons enter the
blood, and act somehow in consequence of entering it; but they do not
prove in what manner the action subsequently takes place.

It was at one time indeed supposed that the same facts, which prove
their admission into the blood, proved also their transmission in
substance to the organs acted on by them. But Dr. Addison and Mr. Morgan
have shown that this is not a legitimate conclusion, and that a
different theoretical view may be taken of the facts,—namely, that the
action may really take place by the poison producing on the sentient
extremities of the nerves of the inner membrane of the blood-vessels a
peculiar impression which is conveyed through the nerves to the part
ultimately affected.[31] They have endeavoured to found this theory upon
evidence, that the poison is not carried beyond the venous system; or
that, if conveyed farther, it is carried incidentally, and not for the
purpose of impregnating the textures of the organ which suffers. The
evidence they have brought forward on this head is chiefly the
following. 1. Poisons which act on a particular organ at a distance do
not act more quickly when introduced into the artery which supplies it,
than when introduced into its vein, or even into the principal artery of
a distant part of the body.[32] 2. If a poison be introduced into a
great vein with a provision for preventing its passage towards the
heart, it will act with as great rapidity, as if no obstacle of the kind
existed. Thus, if the jugular vein, secured by two temporary ligatures,
be divided between them and reconnected by a tube containing wourali,
the animal will not be affected more quickly on the removal of both
ligatures, than on removing only the ligature farthest from the
heart.[33] 3. The arterial blood of a poisoned animal is incapable of
affecting another animal. Thus, if the carotid artery and jugular vein
of one dog be divided, and both ends of each reciprocally connected by
tubes with the divided ends of the corresponding vessels of another dog,
and extract of nux-vomica be introduced into a wound in the face of one
of them,—the animal directly poisoned alone perishes, and the other
remains unharmed to the last.[34]

These are at first view strong arguments against the transmission of
poisons with the blood to the organs remotely acted on; and the facts on
which they are founded are on the other hand easily explained under the
new theory advanced by the authors, that the medium of action is the
nerves which supply the inner membrane of the blood-vessels. But their
inquiries, however ingenious and plausible, have not stood the test of
physiological scrutiny. Their first experimental fact has been
contradicted by Mr. Blake; who has found that the wourali poison, which
does not begin to act for twenty seconds when injected into a vein, will
produce obvious effects in seven seconds only if injected into the aorta
through the axillary artery.[35] The second experiment, showing that
poison confined in a vein will act although prevented by a ligature from
reaching the heart, is held by the opponents of Dr. Addison and Mr.
Morgan to be fallacious, in as much as the blood behind the ligature may
be carried backwards till it meets with an anastomosing vein and is so
carried by a collateral vessel to the heart. To the third experiment it
may be objected, that there was, in the mode in which they conducted it,
no satisfactory evidence that the reciprocal circulation was kept up by
the carotid artery and jugular vein. And this will appear an important
objection to every one practically acquainted with experiments of
transfusion. For on the one hand it is exceedingly difficult, in such
complicated experiments, to prevent coagulation of the blood in one
vessel or another, before the connection of all the arteries and veins
is established; and on the other, it may be urged, as Mr. Blake has
done, that the pressure of the blood in the distal end of the carotid
artery in the animal not directly poisoned may be equal, or even
superior, to the pressure in the proximal end of the same vessel in the
other animal,—so that the blood may not pass from the latter into the
former, although it should continue fluid.

In opposition to the theory of Dr. Addison and Mr. Morgan, and in
support of the doctrine, that poisons act by being carried in substance
with the blood into the tissues of the remote organs on which they act,
a variety of important experimental evidence has been brought forward
since the publications of the Essay of these gentlemen. In the first
place, the concurrent testimony of a great number of recent chemical
inquirers establishes undeniably, that poisons absorbed into the veins
of the part to which they are applied are to be detected throughout many
of the tissues of distant organs. This fact will be enlarged on and
illustrated presently. Secondly, on the authority of Mr. Blake, and in
contradiction of the experiments of Dr. Addison and Mr. Morgan, it
appears that, as already stated, poisons act more quickly when injected
into the aorta than into the venous system; a fact which is easily
understood, on considering that when injected into the aorta they reach
their destination directly, whereas, if injected into a vein they must
first arrive at the right side of the heart, and then be transmitted
through the circle of the pulmonary circulation before reaching even the
aorta. Thirdly, the relative rapidity with which poisons act on
different animals follows the ratio of the velocity of the circulation
in each. Thus, Mr. Blake found, that in the horse nitrate of baryta is
conveyed by the circulation from the jugular vein to the carotid artery
in sixteen seconds, and that strychnia injected into the jugular vein
begins to act on the nervous system after exactly the same interval:
That in the dog chloride of barium passes from the vein to the artery in
seven seconds, and extract of nux-vomica begins to act as a poison in
twelve seconds: That in the fowl the passage of the blood seems to take
place in six seconds, and the nitrate of strychnia to act in six seconds
and a half: And that in the rabbit the passage of the blood is effected
in four seconds only, and the first signs of the action of strychnia
occur in four seconds and a half.[36]

On the whole, then, it may be considered as well established, that
probably all, but certainly some, poisons,—of the kind whose topical
action does not consist in causing destruction or inflammation of the
textures to which they are applied,—produce their remote effects solely
by entering the blood, and through its means impregnating the organs
which are acted on at a distance. And farther, if this doctrine be
admitted as established, it may also be allowed, that many poisons which
do cause topically destruction or inflammation, and remotely the usual
sympathetic effects of these changes of structure, also possess the
power of affecting distant organs through the medium of the blood.

_Of the discovery of Poisons in the Blood._—Such being the case, it
becomes an object of paramount interest, with reference both to the
practice of medical jurisprudence, to inquire whether poisons can be
detected in the circulating fluids, or generally in parts of the body
remote from the place where they are introduced.

A variety of circumstances long rendered it impossible to determine
satisfactorily the question, whether poisons could be detected in the
blood, the secretions, and the soft textures of the body. In the first
place, we now know that the quantity of the more active poisons, which
is required to occasion death, is so small, that, considering the
crude methods of analysis formerly trusted to, and the obstacles
opposed to the successful application of them by the presence of
organic matter, there can be no wonder that chemists, even but a few
years ago, could not satisfy themselves whether the objects they were
in search of had been detected or not. Then, it was partly known
before, and is now fully established, that various poisons are removed
beyond the reach of analysis before death, in consequence of passing
off with the secretions, particularly the urine. Farther, it seems
probable that, of the poisons which act through absorption, several do
not remain or at least do not accumulate, in the blood; and that they
are not distributed with it throughout the textures indifferently, but
are deposited, as absorption goes on, in particular organs, such as
the liver,—which it was not much the practice to examine in former
investigations. And lastly, some poisons are speedily decomposed on
entering the blood: They either cause obvious changes in the
constitution of the blood, and themselves undergo alteration likewise;
or without the blood becoming appreciably different in its properties
from the healthy state, the poison undergoes a rapid change in the
molecular affinities of its elements, and so disappears. Of the former
course of things distinct illustrations are furnished by nitric oxide
gas and sulphuretted-hydrogen gas when injected into a vein in a
living animal: of the latter an equally unequivocal example occurs in
oxalic acid, which Dr. Coindet and I found to be undiscoverable in the
blood of the vena cava of a dog killed in thirty seconds by the
injection of eight grains and a half of it into the femoral vein.

But the improvements that have been lately made in the methods of
analysis for the detection of poisons in a state of complex mixture with
organic substances have done away with a great part of the obstacles
which prevented a thorough inquiry as to the existence of poisons in the
blood and textures of the body. Some important researches of this kind
were referred to in the last edition of the present work; and since then
many additional facts, of equal variety and precision, have been
communicated by different observers, but especially by Professor Orfila.
Under the head of each poison an account will be given hereafter of the
evidence in support of the discovery of it by chemical analysis in the
blood, textures, and excretions. In the present place it is sufficient
to state in general terms that the evidence is quite satisfactory in the
instances of iodine, sal-ammoniac, oxalic acid, nitre, sulphuret of
potassium, arsenic, mercury, copper, antimony, tin, silver, zinc,
bismuth, lead, hydrocyanic acid, cyanide of potassium, carbazotic acid,
sulphuretted-hydrogen, camphor, and alcohol.

_Of the Organs affected by the remote action of Poisons._—Having now
taken a general view of the mode in which poisons act on distant parts,
I shall next consider what organs are thus brought under their
operation. Poisons have been often, but erroneously, said to affect
remotely the general system. A few of them, such as arsenic and mercury,
do indeed appear to affect very many organs of the body. But by much the
larger proportion seem on the contrary to act on one or more organs
only, not on the general system.

Of the poisons which act remotely through a sympathy of distant parts
with an organic injury of the textures directly acted on, many appear to
act sympathetically on the heart alone. Taking the mineral acids as the
purest examples of poisons that act independently of absorption into the
blood-vessels, it will be seen on inquiry that all the symptoms they
produce, in addition to the direct effects of the local injury, are
those of depressed action of the heart,—great feebleness, fainting,
imperceptible pulse, cold extremities. Even the less prominent of the
secondary symptoms are almost all referrible to a depressed state of the
circulation. In particular, they are not necessarily, and indeed are
seldom actually, blended with any material symptom of disorder in the
brain; which certainly could not be the case if the general or whole
system suffered.

With respect to that more numerous class, which act remotely either
through the medium of the blood or by the transmission along the nerves
of an undiscernible impression made on their sentient extremities, some
certainly possess a very extended influence over the great organs of the
body; but the greater number are much more limited in their sphere of
action. Some act chiefly by enfeebling or paralyzing the heart, others
principally by obstructing the pulmonary capillaries, others by
obstructing the capillaries of the general system, others by stimulating
or depressing the functions of the brain or of the spinal cord, others
by irritating the alimentary canal, others by stimulating one or another
of the glandular organs, such as the salivary glands, the liver, the
kidneys, or the lymphatic glands.

Some poisons of this kind act chiefly, if not solely, on the _heart_.
The best examples are infusion of tobacco, and upas antiar. Sir B.
Brodie observed, that when the infusion of tobacco was injected into any
part of the body, it speedily caused great faintness and sinking of the
pulse; and on examining the body instantly after death, he found the
heart distended and paralyzed, not excitable even by galvanism, and its
aortal cavities filled not with black, but with florid blood, while the
voluntary muscles were as irritable as after other kinds of death.[37]
The upas antiar he found to be similarly circumstanced.[38] Arsenic and
oxalic acid are also of this kind. In an animal killed by arsenic, and
in which the gullet and voluntary muscles continued long contractile,
Dr. Campbell found the heart immediately after death containing arterial
blood in its aortal cavities, and insensible to galvanism.[39] Dr.
Coindet and I frequently witnessed the same facts in animals killed with
oxalic acid: When the heart at the moment of death was completely
palsied and deprived of irritability, we saw the intestines moving, and
the voluntary muscles contracting long and vigorously from the mere
contact of the air.[40]

An interesting series of investigations has been lately made by Mr.
Blake, relative to the influence of poisons on the heart, when they are
directly introduced into the great veins. It does not absolutely follow
that an action on the heart manifested in this way proves the occurrence
of a similar action when the substance is admitted into the body through
more ordinary channels, such as the stomach, intestines or cellular
tissue. For on the one hand, some of the substances used by this
physiologist cannot be admitted into the blood through ordinary channels
in the quantity necessary for developing that action on the heart, which
is excited when they are injected at once into the blood-vessels. And on
the other hand, the results at which he thus arrives are not always in
conformity with what have been obtained by prior observers, who resorted
to the ordinary channels for introducing poisons into the body. It is
possible, therefore, that Mr. Blake’s researches may not have the
extensive bearings, which might at first sight appear, on the physiology
of poisons and remedies. Nevertheless they are in themselves full of
interest. They show that the salts of magnesia, zinc, copper, lime,
strontia, baryta, lead, silver, ammonia, and potash, also oxalic acid,
and digitalis, if injected into the jugular vein, produce a powerful and
permanent depression of the heart’s action; which is evinced by the
hæmadynamometer,[41] indicating diminution of pressure in the great
arteries, by the heart becoming motionless or nearly so before the
breathing ceases, by its muscular structure presenting little or no
irritability when stimulated immediately after death, and by the left
cavities being found full of florid arterial blood.[41]

Other poisons act on the _lungs_; but probably few, perhaps none, act on
them alone. Magendie found that in poisoning with tartar-emetic the
lungs are commonly inflamed and sometimes even hepatized.[42] Mr. Smith
and M. Orfila both remarked similar signs of pulmonary inflammation in
animals poisoned with corrosive sublimate.[43] But these poisons produce
important effects on other organs likewise.

A set of novel and important facts setting forth the frequent operation
of poisons on the lungs when they are admitted directly into the blood,
has been recently brought to light by the researches of Mr. Blake. Many
of the poisons mentioned above as acting powerfully on the heart were
found by him not to exert any influence upon the lungs, such as oxalic
acid and the salts of magnesia, lime, zinc, copper, ammonia, potash, and
strychnia. Others, however, such as the salts of strontia, baryta, lead,
and silver, as well as digitalis, all of which powerfully affect the
heart, and, in addition to these, the salts of soda, which have no
action at all on the heart, and hydrocyanic acid, tobacco, and
euphorbium, which influence it feebly, or even dubiously,—produce, when
injected into the jugular vein, obstruction of the capillaries of the
pulmonary circulation, and consequently asphyxia. This is proved by the
hæmadynamometer introduced into a vein indicating great increase of
pressure in the venous circulation a few seconds after the introduction
of the poison; by this instrument introduced into the femoral artery
indicating great diminution of arterial pressure, although the heart
continues to beat vigorously; by the breathing becoming at the same time
laborious, without the heart suffering; by these symptoms preceding any
signs of action on the nervous system; by the heart pulsating for some
time after death; and in many instances by frothy mucus having
accumulated in the air-passages, and congestion and extravasation having
taken place in the lungs themselves.[44]

A great number of the poisons whose action is remote, operate on the
_brain_. The most decided proof of such an action is the nature of the
symptoms; which are, giddiness, delirium, insensibility, convulsions,
palsy, coma. Some physiologists have also sought for evidence in the
body after death, and have imagined they found it in congestion of the
vessels in the brain, and even extravasation of blood there; but it will
be seen under the head of Narcotic Poisons that such appearances are far
from being essential, and indeed are seldom witnessed. All narcotic
poisons act on the brain, and most narcotico-acrids too; but very
frequently other organs are affected at the same time, and in particular
the spine and heart.

The influence of poisons on the brain seems to be sometimes induced, not
immediately, but indirectly through the intervention of a more direct
influence on the pulmonary circulation. Thus Mr. Blake appears to have
succeeded in proving that the insensibility and tetanic convulsions
which immediately precede death, when certain substances, such as the
salts of soda, are injected into the veins, depend simply on the
obstruction directly produced in the pulmonary circulation causing
increased pressure in the systemic veins, and consequently upon the
brain and nervous centre generally. For when the jugular vein was opened
after the development of tetanic convulsions, and blood was allowed to
flow out, the nervous symptoms ceased, and the animal continued for two
hours sensible and without any return of convulsions, dying eventually
of hemorrhage.[45] But more generally the effect produced on the brain
is direct and specific. Thus opium and its active principle morphia
suspend the functions of external relation, which are peculiarly
dependent on the brain; while for a long time the respiration and
circulation are little affected. Even when the poison is admitted
directly into the veins, the pulmonary capillaries are not obstructed,
and the heart is only somewhat enfeebled in its contractions;[46] and in
ordinary cases of poisoning with these substances the heart continues to
pulsate, and the lungs also discharge their office, long after
sensibility is extinguished and voluntary motion arrested,—until at
length the circulation and respiration become affected consecutively by
the depressed state of the nervous system.

Some poisons act specifically on the _spinal cord_. Those which are best
known to possess such an action are nux-vomica, the other species of
plants which, like it, contain strychnia, and also conia and the wourali
poison. The tribe of poisons of which nux-vomica may be taken as the
type excite violent fits of tetanus, during the intervals of which the
mind and external senses are quite entire; and death takes place during
a paroxysm, apparently from suffocation caused by spasmodic fixing of
the chest. Their action on the spine is quite independent of any action
on the brain; if indeed such action exist at all. For when the spinal
cord is separated from the brain by dividing the medulla oblongata, the
effects on the muscles supplied by the spinal cord are produced as
usual.[47] Conia, the active principle of hemlock, according to my own
researches, produces in the lower animals, howsoever introduced,
gradually increasing paralysis, without insensibility or delirium, and
without the circulation or respiration being for some time affected,
till at length death takes place from stoppage of the breathing by palsy
of the respiratory muscles; and after death the heart continues beating
vigorously, the muscles contract when irritated, and arterialization of
the blood in the lungs may be kept up long by maintaining artificial
respiration. In this instance it would appear, that the first effect is
arrestment of the functions of the spinal cord; that the paralysis does
not depend upon a direct action on the muscles; and that neither the
brain, heart, nor lungs can be influenced, except secondarily through
the consequences of general muscular paralysis.[48] Many poisons which
act on the brain also act on the spinal cord.

Other poisons apparently possess the singular property of impeding or
arresting the _general capillary circulation_, and produce their
tangible effects more or less through the medium of this operation. Such
at least are the inferences which seem to flow from the researches of
Mr. Blake; who found that many substances, soon after they are injected
backwards by the axillary artery into the aorta, produce increased
pressure in the arterial system indicated by the hæmadynamometer during
life, and frequently congestion of the membranous textures as observed
after death. Some substances have no effect of this kind. Others act on
the general capillaries in concurrence with a similar action on the
capillaries of the pulmonary circulation, such as the salts of strontia,
baryta, lead, silver, and soda, euphorbium, tobacco and digitalis. But a
few, such as potash and ammonia, with their salts, seem to influence the
capillaries of the general circulation only.[49] These are important
conclusions, if legitimate; but it cannot be denied, that the facts on
which they are based must be very difficult to isolate and observe with
accuracy and without bias.

The organs not immediately necessary to life may be likewise all acted
on by poisons indirectly. On this subject details are not called for at
present. It may be sufficient to remark that there is hardly a
considerable organ in the body, except perhaps the spleen and pancreas,
which is not acted on by one poison or another. Arsenic inflames the
alimentary mucous membrane, mercury the salivary organs and mouth,
cantharides the urinary organs, chromate of potass the conjunctiva of
the eyes, manganese the liver; iodine acts on the lymphatic glands; lead
on the muscles; and spurred rye causes gangrene of the limbs.

Some poisons, as was already mentioned, may act on one important organ
only, every other being left undisturbed: thus nux-vomica in general
acts only on the spine. But much more commonly they act on several
organs at once; and the action of some of them is complicated in an
extreme degree. I may instance oxalic acid and arsenic. Oxalic acid when
swallowed irritates and inflames the stomach directly, and acts
indirectly on the brain, the spine, and the heart. A large dose causes
sudden death by paralyzing the heart; if the dose is somewhat less, the
leading symptom is violent tetanic spasm, indicating an action on the
spine, and death takes place during a paroxysm, the heart continuing to
contract for some time after; if the dose is still less, the spasms, at
first distinct, become by degrees fainter and fainter, while the
sensibility in the intervals, at first unimpaired, becomes gradually
clouded, till at length pure coma is formed without convulsions,—thus
indicating an action on the brain. As for arsenic, coupling together the
symptoms during life and the appearances in the dead body, it will be
seen afterwards to have the power of acting on the brain, heart, and
lungs,—the throat, gullet, stomach, and intestines,—the lining membrane
of the nostrils and eyelids,—the kidneys, bladder, and vagina; and, what
is remarkable, proofs of an action on all these parts may be witnessed
in the course of a single case. The effects of mercury are hardly less
multifarious.


    SECTION II.—_On the Causes which modify the Actions of Poisons._

By a variety of causes the action of poisons may be modified both in
degree and in kind. The most important of them are—quantity; state of
aggregation; state of chemical combination; mixture; difference in
tissue; difference in organ; habit; idiosyncrasy; and lastly, certain
states of disease.

1. _Quantity_ affects their action materially. Not only do they produce
their effects more rapidly in large doses; it is sometimes even quite
altered in kind. A striking example has just been related in the case of
oxalic acid; which, according to the dose, may corrode the stomach, or
act on the heart, or on the spine, or on the brain. In like manner
arsenic in a small dose may cause gastritis of several days’ duration;
while a large dose may prove fatal in two or three hours by affecting
the action of the heart. White hellebore in small doses excites
inflammation in the stomach and bowels, in larger doses giddiness,
convulsions, coma; and in either way it may prove fatal.

2. _As to state of aggregation_,—poisons act the more energetically the
more minutely they are divided, and hence most energetically when in
solution. Some which are very energetic in the fluid state, hardly act
at all when undissolved. Morphia, the alkaloid of opium, may be given in
powder to a dog without injury in a dose, which, if dissolved in oil or
alcohol, would soon kill several. Previously dissolving poisons favours
their action in two ways,—by diffusing them quickly over a large
surface, and by fitting them for entering the bibulous vessels. Poisons,
before being absorbed, must be dissolved; and hence, those which act
though solid and insoluble in water, must, as a preliminary step, be
dissolved by the animal fluids at the mouths of the vessels. In this way
the poisonous effects of carbonate of baryta and arsenite of copper are
explained; for though insoluble in water, they are soluble in the juices
of the stomach.

Differences in aggregation, like differences in quantity, may affect the
kind as well as the degree of action. Camphor in fragments commonly
causes inflammation of the stomach; dissolved in spirit or olive oil, it
causes delirium or tetanus and coma.

The reduction of certain poisons to the state of vapour serves the same
end as dissolving them. When poisons are to be introduced by the skin,
no previous operation is more effectual than that of converting them
into vapour.

3. The next modifying cause is _chemical combination_. This is sometimes
nothing more than a variety of the last. If a poison, in combining with
another substance, acquire greater solubility, it also generally
acquires greater activity, and _vice versa_: Morphia, itself almost
inert, because insoluble, becomes active by uniting with acids, for they
render it very soluble: Baryta as a very active poison, becomes quite
inert by uniting with sulphuric acid, for the sulphate of baryta is
altogether insoluble.

In regard to the influence of chemical combination two general laws may
be laid down. One is, that _poisons which only act locally, have their
action much impaired or even neutralized, in their chemical
combinations_. Sulphuric acid and muriatic acid on the one hand, and the
two fixed alkalis on the other, possess a violent local action; but if
they are united so as to form sulphates or muriates, although still very
soluble, they become merely gentle laxatives. But the case is altered if
either of the combining poisons also act by entering the blood. For the
second general law is, that _the action of poisons which operate by
entering the blood, although it may be somewhat lessened, cannot be
destroyed or altered in their chemical combinations_. Morphia acts like
opium if dissolved in alcohol or fixed oil; if an acid be substituted as
the solvent, a salt is formed which is endowed with the same properties:
The sulphate, muriate, nitrate, acetate of morphia all act like opium.
Strychnia, arsenic, hydrocyanic acid, oxalic acid, and many more come
under the same denomination: Each produces its peculiar effects, with
whatever substance it is combined, provided it do not become insoluble.

Mr. Blake has recently laid down what may be considered a branch or
corollary of the second of these general propositions, and has confirmed
it by many appropriate experimental facts,—namely, that _the salts of
the same base produce the same actions, independently of the acids with
which they are combined_.[50] The law, however, is a more general one,
as given above, and was stated in former editions of the present work.
It applies not only to bases, but likewise to acids, such as the
hydrocyanic, oxalic, arsenious, and arsenic acids, and also to neutral
organic principles which act through the blood, such as picrotoxin,
colocynthin, elaterin, and narcotin.

The same author considers it to be also a probable conclusion from a
variety of experiments on the salts of various bases, that _those salts
which are isomorphous, or possess the same crystalline form, are closely
allied in action_.[51]

4. The effect of _mixture_ depends partly on the poisons being diluted.
Dilution, by prolonging the time necessary for their being absorbed,
commonly lessens their activity; yet not always; for if a poison which
acts through the blood is also a powerful irritant, moderate dilution
will enable it to enter the vessels more easily: a small dose of
concentrated oxalic acid acts feebly as an irritant or corrosive;
moderately diluted, it quickly enters the blood and causes speedy
death.[52] The effect of mixture may depend also in part on the mere
mechanical impediment interposed between the poison and the animal
membranes. This is particularly obvious when the mass containing the
poison is solid or pulpy; for then the first portions of the poison that
touch the membrane may cause an effort of the organ to discharge the
rest beyond the sphere of action,—if, for example, it is the stomach,—by
vomiting. The effect of mixture in interposing a mechanical impediment
is also well illustrated where the substance mixed with the poison is a
fine, insoluble powder, capable of enveloping its several particles.
Thus it is that small, yet poisonous doses of arsenic may be swallowed
and retained with impunity, if mixed with finely powdered charcoal,
magnesia, and probably cinchona-bark, or the like. Besides diluting and
mechanically obstructing their application, the admixture of other
substances may alter the chemical nature of poisons, and so change their
action.

It is important to keep in view, that the influence of mixture may be
exerted in consequence of the cavity into which a poison is introduced
being at the time filled with contents. Some of the most powerful and
unerring poisons may in such circumstances altogether fail to produce
their usual effect, if speedily vomited. Thus Wibmer notices the case of
a man, who swallowed an ounce and a half of arsenic after a very hearty
meal, had merely a severe attack of vomiting with subsequent colic, and
got quite well in four days.[53] And a still more pointed instance has
been briefly mentioned by Dr. Booth of Birmingham, where an ounce of
corrosive sublimate was swallowed after a full meal without any material
ill consequence, vomiting having been speedily induced.[54]

5. _Difference of tissue_ is an interesting modifying power in a
physiological point of view, but does not bear so directly on
medico-legal practice as the rest, and may therefore be passed over
cursorily.

On the corrosives and irritants a difference of tissue acts but
indirectly: their effects vary not so much with the tissue as with the
organ of which it forms part. But as to poisons which act through the
blood, their energy must evidently depend on the activity of absorption
in each texture.

The cutaneous absorption is slow, on account of the obstacle presented
by the cuticle, and by the intricate capillaries of the true skin.
Accordingly many active poisons are quite inert when applied to the
unbroken skin, or even to the skin deprived of the cuticle. Hydrocyanic
acid, perhaps the most subtle of all poisons, was found by Coullon to
have no effect when dropped on the skin of a dog.[55] Some authors have
even gone so far as to deny that poisons can be absorbed at all through
the skin, unless they are pressed by friction through the cuticle. But
this is an error; most gaseous poisons, such as carbonic acid and
sulphuretted hydrogen, and some solid poisons when volatilized, such as
the vapours of cinnabar, will act though simply placed in contact with
the skin; and there is distinct evidence that corrosive sublimate will
bring on mercurial action in the form of a warm bath, or when used as a
liniment.

On the mucous membrane of the stomach and intestines, poisons act much
more energetically than on the skin; which clearly depends in a great
measure on the superior rapidity of absorption there,—or, according to
some, on the facility with which poisons come in contact with the
sentient extremities of nerves.

The serous membranes possess an activity of absorption which hardly any
other unbroken texture can equal. Accordingly many poisons act much more
rapidly through the peritonæum than through the stomach. When oxalic
acid is introduced under the same collateral circumstances into the
stomach of one dog and the peritonæum of another, the dose may be so
apportioned, that the same quantity, which does not prove fatal to the
former, kills the latter in fourteen minutes.[56]

While the preceding modes in which poisons enter the blood are indirect,
they may be introduced directly by a wound in the vein. There is no way
in which poisons, that act through the blood, prove more rapidly fatal.
Some which act very slowly through the stomach cause instant death when
injected into a vein. A peculiar variety of this mode of introducing
poisons deserves to be distinguished, namely, the application of them to
a wound. If the surface bleeds freely, they may not act at all, because
they are washed away. But if they adhere, they soon enter the divided
veins. Hence, if they act in small doses, this mode of applying them is
hardly less direct than if they were at once injected into a vein.

So far the effect of difference in tissue has been determined. Poisons
that act through the blood act least energetically on the skin, more
actively on the alimentary mucous membrane, still more so on serous
membranes, and most powerfully of all when introduced directly into a
vessel. There are other textures, however, which merit notice, although
their place in the scale of activity has not been exactly settled.

On the mucous membrane of the pulmonary air-cells and tubes, poisons act
with a rapidity which is scarcely surpassed by their direct introduction
into a vein. This is plainly owing to the exceeding delicacy and wide
surface of the membrane. Hence three or four inspirations of carbonic
oxide gas will cause instant coma. A single inspiration of the noxious
gas of privies has caused instant extinction of sense and motion. Nay,
liquid poisons have been known to act through the same channel with
almost equal swiftness. For M. Ségalas found that a solution of extract
of nux-vomica caused death in a few seconds when injected in sufficient
quantity into the windpipe; and that half a grain will thus kill a dog
in two minutes, while two grains will rarely prove fatal when injected
into the stomach, peritonæum, or chest.[57]

As to the nervous tissue, it is a fact worthy of mention, that the
poisons which appear to act on the sentient extremities of the nerves,
do not act at all on the cut surface of the brain and nerves, or upon
any part of the course of the latter. This has been proved with respect
to most active narcotics.

The power of the cellular tissue as a medium of absorption, has not
been, and cannot easily be, ascertained. On the one hand it is difficult
to apply poisons to it, without also applying them to the mouths of
divided vessels; and, on the other hand, it is difficult to make a set
of experiments for comparison with others on the stomach, pleura, or
peritonæum, as the cellular tissue does not form an expanded cavity, and
consequently, the extent of surface to which a poison is applied cannot
be made the same in each experiment of a series. It is a ready medium,
however, for admitting poisons into the blood, especially if an
artificial cavity be made where the tissue is loose, as, for example, by
separating the skin from the muscles of the back with the finger
introduced through a small incision in the integuments.

The variations caused by difference of tissue in the activity of poisons
have been viewed in the previous remarks as depending chiefly on the
relative quickness with which absorption goes on. But in this way it is
impossible to explain the whole amount of the differences sometimes
observed. Some poisons cause death when applied to a wound in the
minutest quantity, but are quite harmless when swallowed in large doses:
Others are diminished a little in activity, but still remain powerful
and fatal poisons. There is not much difference in the power of arsenic
when it is applied to different textures, the skin excepted. But oxalic
acid injected into the peritonæum will act eight or ten times more
rapidly than when swallowed and the poison of the viper may prove fatal
to a man through a wound in almost invisible doses, while the whole
poison of six vipers may be swallowed by so small a creature as a
blackbird, with complete impunity.[58] Differences in the absorbing
power of the tissues cannot explain these facts.

The only rational way of accounting for them is by supposing that a part
of the poison is decomposed,—the change being greatest where absorption
is slowest and the power of assimilation strongest, namely, in the
stomach,—and least where absorption is quickest and assimilation almost
wanting, namely, in a wound. This explanation derives support from the
different effects of change of tissue on poisons of the different
kingdoms. Mineral poisons are least, and animal poisons are most,
affected in their action by differences of tissue, while vegetable
poisons hold the middle place:—an arrangement which coincides with the
respective difficulty of decomposition among mineral, vegetable, and
animal substances generally, whether under physical or under vital
processes.[59]

6. With respect to differences arising from _difference of organ_, these
will, of course, be partly attributable to differences in tissue, but
not altogether. For example, in the case of the pure corrosives or
irritants, the injury caused will depend for its danger on the
importance of the organ to the general economy of the body: Inflammation
caused by a local poison in the stomach will be more quickly fatal than
that excited in the intestines only; and such a poison may act violently
on the external parts without materially impairing the general health.

7. _Habit and Idiosyncrasy._—The remarks to be made under the present
head are important in a medico-legal point of view: for they show how
one man may be poisoned by a substance generally harmless, and another
not harmed by a substance usually poisonous.

The tendency of _idiosyncrasy_ is generally to increase the activity of
poisons, or even to render some substances deleterious which are
commonly harmless.

The effect of opium in medicinal doses is commonly pleasant and
salutary; but in some individuals it produces disagreeable and even
dangerous effects. Calomel, which in moderate doses is for the most part
a mild laxative or sialagogue, will cause in some people, even in the
dose of a few grains, violent salivation, ulceration of the mouth, nay,
fatal gangrene. On the other hand, a few substances, which to most
people are actively poisonous, have on some individuals comparatively
little effect. There are extremely few poisons, however, in regard to
which this kind of idiosyncrasy is well established and prominent.
Mercury and alcohol are examples. The compounds of mercury, which in
moderate quantity are mildly laxative or sialagogue to most people, but
to some persons dangerously poisonous in very small doses, would, on the
contrary, appear in other constitutions to be extremely inactive; for it
has occasionally been found impossible to bring on the peculiar
constitutional action of mercury by continuing the use of its
preparations for months together. In general children are not easily
affected by calomel as a sialagogue, but easily by its laxative action.
As to alcohol, it is a familiar fact, that independently of the effects
of habit, there are some constitutions which cannot be brought under the
influence of intoxicating liquors without an extraordinary quantity of
them and a long-continued debauch, while others are overpowered in a
short space of time, and by very moderate excess; and there is no reason
to doubt that very great constitutional differences also prevail in
regard to the operation of a single large dose. A rarer idiosyncrasy is
unusual insensibility to the action of opium. I am acquainted with a
gentleman unaccustomed to the use of opium who has taken without injury
nearly an ounce of good laudanum,—a dose which would certainly prove
fatal to most people.

But not only does idiosyncrasy modify the action of poisons: Through its
means, too, some substances are actually poisonous to certain
individuals, which to mankind in general are unhurtful, nay, even
nutritive.

With some people all kinds of red fish, trout, salmon, and even the
richer white fish, herring, mackerel, turbot, or holibut, disagree as it
is called—that is, act after the manner of poisons: They produce
fainting, sickness, pain of the stomach; and if they were not speedily
evacuated by vomiting, dangerous consequences might ensue. The same is
often the case with mushrooms. The esculent mushrooms act on some people
nearly in the same way as the poisonous varieties. Bitter almonds and
other vegetable substances that contain hydrocyanic acid, sometimes
produce stupor or nettle-rash in the small quantities used for seasoning
food. In like manner many flowers, which to most persons are agreeable
and not injurious, cannot be kept in the same room with some people on
account of the severe nervous affections that are developed.

This idiosyncrasy may even be acquired. One of my relations, who was for
many years violently affected by very small quantities of the richer
kinds of fish, used at a previous period to eat them, and can now again
do so, with impunity. Many people have acquired a similar idiosyncrasy
with respect to eggs; instances of the same kind will be afterwards
mentioned in respect to shell-fish, particularly muscles; indeed there
are probably few articles of food in regard to which such idiosyncrasies
may not in a few rare instances be met with, if we except the grains and
common kinds of butcher-meat. I may add, that from facts which have come
under my notice, I have sometimes suspected that a similar idiosyncrasy
may be acquired in a slight degree, and for a short time only, in regard
even to some kinds of butcher-meat, especially the flesh of young
animals and pork. On this subject some illustrations will be found at
the close of the chapter on diseased and decayed animal matter.

It does not appear well ascertained, that the effect of idiosyncrasy is
ever to impair materially the energy of poisons, except in the instances
of mercury, alcohol, and opium.

On the contrary, the tendency of _habit_ when it does affect their
energy, is, with a few exceptions, to lessen it. By the force of habit a
person may take without immediate harm such enormous quantities of some
poisons as would infallibly kill an unpractised person or himself when
he began. There have been opium-eaters in this country who took for days
together ten or even seventeen ounces of laudanum daily.

The influence of habit has been ascertained precisely in the case of a
few common poisons only. On the whole, it would appear that more change
is effected by habit in the action of the organic than in that of the
inorganic poisons; and that of the former, those which act on the brain
and nervous system, and produce _narcotism_, are altered in the most
eminent degree. The best examples of the influence of habit are opium
and vinous spirits. The action of such poisons is not always, however,
entirely thrown away; they still produce some immediate effect; and
farther, by being frequently taken, they may slowly bring on certain
disease, or engender a predisposition to disease. A very singular
exception to this rule prevails in the instance of tobacco; which, under
the influence of habit, may be smoked daily to a considerable amount,
and, so far as yet appears, without any cumulative effect on the
constitution, like that of opium-eating or drinking spirits.

The inorganic poisons are most of them little impaired in activity by
the force of habit. The pure irritants, indeed, do lose a little of
their energy: for it seems that persons have acquired the power of
swallowing with impunity considerable doses of the mineral acids. But as
to inorganic poisons that enter the blood, habit certainly does not
diminish, probably rather increases, their power. There is no
satisfactory evidence, that a person by taking gradually-increasing
doses of arsenic may acquire the power of enduring a considerably larger
dose than when he began: On the contrary, the stomach rather becomes
more tender to the subsequent dose by each repetition. I have little
hesitation in avowing my disbelief of the alleged cases of
arsenic-eaters and corrosive-sublimate-eaters, who could swallow whole
drachms at once with impunity. Some have expressed surprise at this
statement having been made in former editions of the present work, when
there is such authority as Byron, Pouqueville, &c., for the hackneyed
story of Soleyman, the sublimate-eater of Constantinople, who lived to
the age of a hundred, eating a drachm of corrosive sublimate daily. I
must avow, however, that such reporters of a feat so very extraordinary,
and where deception was so highly probable, are to me no authority at
all.

In the relative influence of habit on poisons of the three kingdoms of
nature, a new argument will be discovered for the opinion given above
respecting the partial decomposition of organic poisons in some of the
tissues. In fact this partial decomposition accounts very well for the
effect of habit: The effect of habit is probably nothing more than an
increased power acquired by the stomach of decomposing the poison,—just
as it gradually acquires an increased facility in digesting some
alimentary substances which are at first very indigestible.

8. The last modifying cause to be mentioned comprehends certain
_diseased states of the body_. The effect of disease, like that of
habit, is in general to impair the activity of poisons. But it is only
in the instance of a few diseases that this diminution is so strongly
marked as to be important in relation to medical jurisprudence.—In the
continued fever of this country there is a diminished susceptibility of
the constitutional action of mercury; and this peculiarity is very
strongly marked in the yellow fever, as well as in the bilious fevers
generally of tropical climates. In some varieties of typhoid fever there
is obviously a diminished sensibility to the action of wine and other
spirituous liquors; but this diminution in a great majority of cases is
much inferior to what some physicians have represented.—In severe
dysentery the susceptibility of the narcotic action of opium is so much
impaired, that a person unaccustomed to the use of that drug, may
continue to take daily, for several days together, a quantity which
might prove fatal to him in a state of health. In the severe form which
dysentery occasionally puts on in this country I have known a patient
take from twenty-four to thirty grains of opium daily, and retain it
all, without experiencing more than a mild narcotic action.—In epidemic
cholera the same insensibility has been remarked to the operation of
opium.—It also occurs in the instance of excessive hemorrhagy.—According
to the doctrines and practice of the present dominant school in Italy,
there is an unusual insensibility during inflammatory dropsy to the
irritant action of gamboge, so that sixty or eighty grains may be taken
without harm.—There is no disease, however, in which the power of
mitigating the action of poisons is more remarkably exhibited, than in
tetanus: It is often scarcely possible to bring on the narcotic action
of opium by any doses which can be administered; calomel, too, acts with
much less energy than usual; and even common purgatives must be
administered in doses considerably larger than those required in most
other disorders.—Mania is similarly circumstanced: almost all remedies
must be given in increased doses, narcotic remedies in particular. But
there is good reason for believing that the impaired susceptibility of
the action of poisons remarked in this disorder is far from being always
so great as some have alleged.—Another disease allied to the last, where
the diminution of susceptibility is often great, is delirium tremens. It
has in particular been often found, that to produce sleep in this
disease opium must be given in frequent large doses,—so large indeed,
that they would undoubtedly prove fatal to a person in health. At the
same time it is worthy of remark, that in some cases of delirium
tremens, even violent in degree, the peculiarity now specified, as I
have myself several times witnessed, is far from being strongly
marked.—Hydrophobia always, and hysteria sometimes, impair the activity
of poisons. I have seen cases of hysteria, more particularly those
assuming the form of tetanus, where very large doses of opium were
required to produce a calmative effect and sleep; and in hydrophobia it
is well shown that the narcotic action of opium is not produced even by
large doses often repeated.—The same state occurs in excessive
hemorrhage.

In the operation of this class of modifying agents it is a general law,
to which there are probably few exceptions, that they chiefly affect
poisons of the organic kingdoms, and the narcotics above all. At least
in the instance of most mineral poisons their influence is very
inferior. Their operation may be accounted for in various ways.
Sometimes, as in dysentery and cholera, the poison is carried with
unusual rapidity through the alimentary canal. Sometimes again it
remains comparatively inert, because on account of the impaired activity
of absorption, it is not taken up with the usual quickness by the
absorbent vessels. And sometimes, as in the instance of tetanus, mania,
and rabies, the nervous system is in a state of peculiar excitement, by
which the customary action of the poison is in a great measure, if not
entirely, counteracted.

In a few diseased states of the system there is an increased
susceptibility of the action of poisons: and it is important that the
medical jurist should attend to this circumstance. When a poison has a
tendency to bring on a peculiar pathological state of the system, or of
a particular organ, which state is also produced by a disease existing
at the time or impending, violent and even fatal consequences may ensue
from doses of poisons which in ordinary circumstances are innocuous or
beneficial. Thus in persons affected with apoplexy an ordinary dose of
opium may accelerate death; and in people even with a mere tendency to
apoplexy, if it is strongly marked, or appears from what are called
warning symptoms to be on the point of developing itself, a common dose
of such narcotics as occasion determination to the brain may excite the
apoplectic attack. Thus, too, in cases of inflammatory disorders of the
alimentary canal, irritating substances, in doses not otherwise
injurious, may produce dangerous impressions on the tender membrane with
which they come in contact. But in respect to this last example, it must
be remarked, that the improvements or the caprice of medical practice
have gone directly in face of the rule, by suggesting that some internal
inflammations of the alimentary canal may be successfully treated with
irritating remedies.

I might here perhaps have added among the causes which modify the action
of poisons, sleep, and the administration of other poisons. The latter
subject, however, will be better considered at the end of the Individual
Poisons, under the title of Compound Poisoning. The former agent is of
doubtful effect. Some observations on its influence will be found in the
chapter on the Evidence of General Poisoning, p. 41.

_Application of the preceding remarks to the Treatment of Poisoning._ As
an appendix to what has been said respecting the physiological action of
poisons, and the causes by which it is liable to be modified, I shall
here state shortly certain applications to the treatment of poisoning.

In the instance of internal poisoning, the great object of the physician
is to administer an antidote or counter-poison. Antidotes are of two
kinds. One kind takes away the deleterious qualities of the poison
before it comes within its sphere of action, by altering its chemical
nature. The other controls the poisonous action after it has begun, by
exciting a contrary action in the system. In the early ages of medicine
almost all antidotes were believed to be of the latter description, but
in fact very few antidotes of the kind are known.

Chemical antidotes operate in several ways, according to the mode of
action of the poison for which they are given. If the poison is a pure
corrosive, such as a mineral acid, it will be sufficient that the
antidote destroy its corrosive quality: Thus the addition of an alkali
or earth will neutralize sulphuric acid, and destroy or at least
prodigiously lessen its poisonous properties. In applying this rule care
must be taken to choose an antidote which is either inert in itself, or,
if poisonous, is, like the poison for which it is given, a pure
corrosive or local irritant, and one whose properties are reciprocally
neutralized.

If the poison, on the other hand, besides possessing a local action,
likewise acts remotely through absorption, or by an impression on the
inner coat of the vessels, mere neutralization of its chemical
properties is not sufficient; for we have seen above that such poisons
act throughout all their chemical combinations which are soluble. Here,
therefore, it is necessary that the chemical antidote render the poison
insoluble or nearly so; and insoluble not only in water, but likewise in
the animal fluids, more particularly the juices of the stomach. The same
quality is desirable even in the antidotes for the pure corrosives; for
it often happens that in their soluble combinations these substances
retain some irritating, though not any corrosive power. When we try by
the foregoing criterions many of the antidotes which have been proposed
for various poisons, they will be found defective; and precise
experiments have in recent times actually proved them to be so.

The other kind of antidote operates not by altering the form of the
poison, but by exciting in the system an action contrary to that
established by the poison. On considering attentively, however, the
phenomena of the action of individual poisons, it will be found
exceedingly difficult to say what is the essence of a contrary action,
and still more how that counter-action is to be brought about.
Accordingly, few antidotes of the kind are known. Physiology or
experience has not yet brought to light any mode of inducing an action
counter to that caused by arsenic and most of the irritant class of
poisons. It appears probable that the remote operation of lead may be
sometimes corrected by mercury given to salivation, and that the violent
salivation caused by mercury may be occasionally corrected by nauseating
doses of antimony. But these are the only instances which occur to me at
present of antidotes for irritant poisoning which operate by
counter-action, unless we choose to designate by the name of antidote
the conjunction of remedial means which constitute the antiphlogistic
method of cure. In the class of narcotics we are acquainted with equally
few constitutional antidotes, although the nature of the action of these
poisons seems better to admit of them. Ammonia is to a certain extent an
antidote for hydrocyanic acid, but by no means so powerful as some
persons believe; and I am not sure that in this class of poisons we can
with any propriety mention another antidote of the constitutional kind.

On the whole, then, it is chiefly among the changes induced by chemical
affinities that the practitioner must look for counter-poisons; and the
ingenuity of the toxicologists has thence supplied the materia medica
with many of singular efficacy. When given in time, magnesia or chalk is
an antidote for the mineral acids and oxalic acid, albumen for corrosive
sublimate and verdigris, bark for tartar-emetic, common salt for lunar
caustic, sulphate of soda or magnesia for sugar of lead and muriate of
baryta, chloride of lime or soda for liver of sulphur, vinegar or oil
for the fixed alkalis; and these substances act either by neutralizing
the corrosive power of the poison, or by forming with it an insoluble
compound.

In recent times a new object in the treatment of poisoning has been
pointed out by the discoveries made in its physiology. As it has been
proved that many of the most deadly poisons enter the blood, and in all
probability act by circulating with that fluid, so it has been inferred
that an important object in the treatment is to promote their discharge
by the natural secretions. In support of this reasonable inference it
has been lately rendered probable by Orfila, as will be seen under the
head of the treatment of the effects of arsenic, that it is of great
advantage in some forms of poisoning to increase the discharge of urine.

In the instance of external poisoning the main object of the treatment
is to prevent the poison from entering the blood, or to remove it from
the local vessels which it has entered.

One mode, which has been known to the profession from early times, and
after being long in disuse was lately revived by Sir D. Barry, and
applied with success to man, is the application of cupping-glasses to
the part where the poison has been introduced.[60] This method may act
in various ways. It certainly prevents the farther absorption of the
poison by suspending for a time the absorbing power of the vessels of
the part covered by the cup. It also sucks the blood out of the wound,
and may consequently wash the poison away with it. Possibly it likewise
compresses the nerves around, and prevents the impression made by the
poison on their sentient extremities from being transmitted along their
filaments.

Another mode is by the application of a ligature between the injured
part and the trunk, so as to check the circulation. This is a very
ancient practice in the case of poisoned wounds, and is known even to
savages. But as usually practised it is only a temporary cure: As soon
as the ligature is removed the effects of the poison begin. It may be
employed, however, for many kinds of poisoning through wounds, so as to
effect a radical cure. We have seen that most poisons of the organic
kingdom are in no long time either thrown off by the system or
decomposed in the blood. Hence if the quantity given has not been too
large, recovery will take place. Now, by means of a ligature, which is
removed for a short time at moderately distant intervals, a poison,
which has been introduced into a wound beyond the reach of extraction,
may be gradually admitted into the system in successive quantities, each
too small to cause death or serious mischief, and be thus in the end
entirely removed and destroyed. Such is a practical application which
may be made of some ingenious experiments performed not long ago by M.
Bouillaud with strychnia, the poisonous principle of nux-vomica.[61]

The last mode to be mentioned is by a combination of the ligature with
venesection, deduced by M. Vernière from his experimental researches
formerly noticed (p. 19). Suppose a fatal dose of extract of nux-vomica
has been thrust into the paw of a dog; M. Vernière applies a tight
ligature round the limb, next injects slowly as much warm water into the
jugular vein as the animal can safely bear, and then slackens the
ligature. The state of venous _plethora_ thus induced completely
suspends absorption. The ligature is next tied so as to compress the
veins without compressing the arteries of the limb, and a vein is opened
between the wound and the ligature in such a situation, that the blood
which flows out must previously pass through, or at least near the
poisoned wound. When a moderate quantity has been withdrawn, the
ligature may be removed with safety; and the extraction of the poison
may be farther proved by the blood that has been drawn being injected
into the veins of another animal; for rapid death by tetanus will be the
result.[62] It is not improbable that in this plan the preliminary
production of venous plethora may be dispensed with; and then the
treatment may be easily and safely applied to the human subject.




                              CHAPTER II.
                 ON THE EVIDENCE OF GENERAL POISONING.


This subject is purely medico-legal. It comprehends an account of the
various kinds of evidence by which the medical jurist is enabled to
pronounce whether poisoning in a general sense (that is, without
reference to a particular poison), is impossible, improbable, possible,
probable, or certain. It likewise comprises an appreciation of the
circumstances which usually lead the unprofessional, as well as the
professional, to infer correctly or erroneously a suspicion of such
poisoning.

Under the present head might likewise be included the history of
poisoning, the art of secret poisoning, and some other topics of the
like kind. But the want of proper documents, and the unmeasured
credulity which has prevailed on the subject of poisoning throughout all
ages down to very recent times, has entangled these subjects in so
intricate a maze of fable, that a notice of them, sufficiently detailed
to interest the reader, would be quite misplaced in this work.

On the art of secret poisoning, however, as having been once an
important object of medical jurisprudence, it might be expected that
some comments should here be offered. But really I do not see any good
reason for wading through the mass of credulous conjectures and
questionable facts, which have been collected on the subject, and which
have been copied into one modern work after another, for no other cause
than that they are of classic origin, or feed our appetite for the
mysterious. No one now seriously believes that Henry the Sixth was
killed by a pair of poisoned gloves, or Pope Clement the Seventh by a
poisoned torch carried before him in a procession, or Hercules by a
poisoned robe, or that the operation of poisons can be so predetermined
as to commence or prove fatal on a fixed day, and after the lapse of a
definite and remote interval. With regard to the noted instances of
secret poisoning, which occurred towards the close of the seventeenth
century in Italy and France, it is plain to every modern toxicologist,
from the only certain knowledge handed down to us of these events, that
the actors in them owed their success rather to the ignorance of the
age, than to their own dexterity. And as to the refined secrets believed
to have been possessed by them, it is sufficient here to say, that
although we are now acquainted with ten times as many and ten times as
subtle poisons as were known in those days, yet none exist which are
endowed with the hidden qualities once so universally dreaded.

The crime of poisoning, from its nature, must always be a secret one.
But little apprehension need be entertained of the art of secret
poisoning as understood by Toffana or Brinvilliers,[63] or as it might
be improved by a modern imitator. It seems to have escaped the attention
of those who have written on the subject, that the practice of such an
art requires the knowledge not only of a dexterous toxicologist, but
also of a skilful physician; for success must depend on the exact
imitation of some natural disease. It is only among medical men,
therefore, and among the higher orders of them, that a Saint-Croix can
arise now-a days. How little is to be dreaded on that head is apparent
from the domestic history of the European kingdoms for the last half
century, compared with their history some centuries ago. Few medical men
have even been suspected, and those few only upon visionary grounds, and
under the impulse of violent political feeling.[64] In one late instance
only, so far as I am aware, has it been proved that the physician’s art
was actually prostituted to so fearful a purpose; and the detection of
the crime in that case shows how difficult concealment will always be
wherever justice is administered rigorously, and medico-legal
investigations skilfully conducted.[65]

Two extraordinary incidents which happened lately in Germany may appear
at first sight at variance with these views. I allude to the cases of
Anna Margaretha Zwanziger and Margaretha Gottfried, which justly excited
much interest where they occurred, and are notorious to continental
toxicologists. Zwanziger, while serving as housekeeper in various
families in the territory of Bayreuth in Bavaria during the years 1808
and 1809, contrived to administer poison,—sometimes under the
instigation of mere revenge or spite, sometimes for the purpose of
clearing the way for her schemes of marriage with her masters,—to no
fewer than seventeen individuals in the course of nine months; and of
these three died.[66] Gottfried, a woman in affluent circumstances and
tolerable station in the town of Bremen, was even more successful. For
she pursued her criminal career undiscovered for fifteen years; and when
detected in 1828 had murdered actually fourteen persons, and
administered poison unsuccessfully to several others. Her motive, as in
the case of Zwanziger, was the mere gratification of a malevolent
temper, or the removal of supposed obstacles to her matrimonial dreams.
In neither of these instances, however, did the criminal possess any
particular skill, or observe much measure in her proceedings. The cases
of poisoning were of the common kind,—produced by arsenic,—proving in
general quickly fatal,—and presenting the ordinary phenomena. I cannot
help thinking, therefore, that the events now alluded to prove rather
the ineffectiveness of the police where they happened, than the
adroitness of the actors by whom they were brought about; and that they
constitute no sound objection to the statement, that the art of secret
poisoning is now unknown, and is not likely to be again revived.

It must be granted, indeed, that the late discoveries in chemistry and
toxicology have made poisons known which might be employed in such a way
as to render suspicion unlikely, and to baffle inquiry. But the methods
now alluded to are hitherto very little known; they cannot easily be
attempted on account of the rarity and difficult preparation of the
poisons; they can never be practised except by a person conversant with
the minute phenomena of natural disease; and it is no part of the object
of this work to make them public.

The evidence, by which the medical jurist is enabled to pronounce on the
existence or non-existence of poisoning in general, and to determine the
subordinate questions that relate to it, is derived from five
sources,—1, the symptoms during life; 2, the appearances in the dead
body; 3, the chemical analysis; 4, experiments and observations on
animals; and 5, certain moral circumstances, which are either
inseparably interwoven with the medical proof, or cannot be accurately
appreciated without medical knowledge.


              SECTION I.—_Of the Evidence from Symptoms._

Not many years ago it was the custom to decide questions of poisoning
from the symptoms only. Till the close of last century, indeed, no other
evidence was accounted so infallible: and for the simple reason, that in
reality the other branches of evidence were even more imperfectly
understood. So lately as 1763, and even in Germany, the solemn opinions
of whole colleges were sometimes grounded almost exclusively on the
symptoms.[67] About that time, however, doubts began to be entertained
of the infallibility of such evidence; these doubts have since assumed
gradually a more substantial form; and it is now laid down by every
esteemed author in Medical Jurisprudence, that the symptoms, however
exquisitely developed, can never justify an opinion in favour of more
than high probability.[68] In laying down this doctrine medical jurists
appear to me to have injudiciously confounded together actual symptoms
with their general characteristics. If the doctrine is to be held as
applying to the evidence from symptoms, only so far as they are viewed
in questions of general poisoning,—that is, as applying to the general
characters merely of the symptoms,—it is deduced from accurate
principles. But if it is likewise to be applied, as recent authors have
done, to the actual symptoms produced by particular poisons, and in all
cases whatever of their action, then it is a rule clearly liable to
several important exceptions. These exceptions will be noticed under the
heads of the mineral acids, oxalic acid, arsenic, corrosive sublimate,
nux vomica, &c. At present it is only the general characters of the
symptoms, and the points in which they differ from the general
characters of the symptoms of natural disease, that I propose to
consider.

The chief characteristics usually ascribed to the symptoms of poisoning
considered generally, are, that they commence suddenly and prove rapidly
fatal,—that they increase steadily,—that they are uniform in nature
throughout their course,—that they begin soon after a meal,—and that
they appear while the body is in a state of perfect health.

1. The first characteristic is the _suddenness of their appearance and
the rapidity of their progress_ towards a fatal termination. Some of
them act instantaneously, and the effects of most of them are in general
fully developed within an hour or little more. But this character is by
no means uniform. The most violent may be made to act, so as to bring on
their peculiar symptoms slowly, or even by imperceptible degrees. Thus
arsenic, which usually causes violent symptoms from the very beginning,
may be so administered as to occasion at first nothing more than slight
nausea and general feebleness; and afterwards in slow succession its
more customary effects. In like manner corrosive sublimate may be given
in such a way as to cause at first mild salivation, and finally gangrene
of the mouth. Even many vegetable poisons might be administered in the
same way. The well-known consequences of digitalis in medicinal doses
will serve as a familiar instance. A still better illustration is
supplied by the medicinal effects of the alkaloid of nux-vomica, whose
action in other circumstances is most rapid and violent: Strychnia in a
moderate dose will cause death by violent tetanus in two or three
minutes; but when given in frequent small doses as a remedy in palsy, it
has been known to bring on first starting of the limbs, then stiffness
of the jaw, afterwards pain and rigidity of the neck; and these effects
might be increased so gradually, that the patient would seem to die
under ordinary tetanus. Nevertheless, the foregoing considerations being
kept always in mind, it still remains true, that the effects of poisons
for the most part begin suddenly, when the dose is large. This is an
important circumstance in regard to certain active poisons, such as the
mineral acids, oxalic acid, arsenic, strychnia, &c. For when it is
considered that in criminal cases they are given for the most part in
unnecessarily large doses, it follows that if the effect ascribed to
these poisons in such doses have not begun suddenly, the suspicion is
probably incorrect.

The same remarks may be applied to the sudden termination of the
symptoms. Poison is for the most part given criminally in doses so large
that it proves rapidly fatal. Yet this is not always the case; the
diseased state occasioned by poisons has often been prolonged, as will
be seen hereafter, for several weeks, sometimes for several months; nay,
a person may be carried off by a malady, the seeds of which have been
sown by the operation of poison years before.

The present would be the proper place for noticing the important
question regarding the interval of time, after which, if death
supervenes, it cannot be laid to the charge of the person who
administered the poison. It is unnecessary, however, to say much on the
subject. According to the English law, death must take place within a
year. As to the Scottish law, it may be inferred from what has been said
by the late Baron Hume on the subject of homicide generally, that a
charge of poisoning is relevant although the person should die at a
period indefinitely remote, and that it will infer the pains of law,
provided the operation of the poison can be distinctly traced,
unmodified by extraneous circumstances, from the commencement of the
symptoms to the fatal termination.[69] Of course the influence of these
modifying circumstances in lessening the criminal’s responsibility will
increase with the interval. The question for the medical jurist to
determine in such a case would therefore be, the distance of time to
which death may be delayed in the case of poisoning generally, and in
that of the particular poison. This question cannot be answered even
with an approach to precision, except in the instance of a few common
poisons. Most vegetable and animal poisons prove fatal either in a few
days or not at all; but some mineral poisons may cause death after an
interval of many days. It appears probable that arsenic may cause death
after an interval of several months, and it is well ascertained that the
symptoms of poisoning with the mineral acids have continued
uninterruptedly and without modification for eight months, and then
terminated fatally.

2. The next general characteristic of the symptoms of poisoning is
_regularity in their increase_. It is clear, however, that even this
character cannot be universal. For in all cases of slow poisoning by
repeated small doses there must be remissions and exacerbations, just as
in natural diseases. Besides, as we can seldom watch the symptoms
advancing in their simple form, but must endeavour to remove them by
remedies, remissions may thus be produced and their tendency to increase
steadily counteracted. Farther, some poisons admit of exacerbations and
remissions, even when given in one large dose; and there are others, the
very essence of whose action is to produce violent symptoms in frequent
paroxysms. Of the latter kind are nux vomica, and the other substances
that contain strychnia. Of the former kind is arsenic: in cases of
poisoning with arsenic it often happens, that after the first five or
six hours have been passed in great agony, the symptoms undergo a
striking remission for as many hours, and then return with equal or
increased violence. Still it is true that on the whole the symptoms of
poisoning are steady in their progress; so that this should always be
attended to as one of the general characters. In the case of slow
poisoning, too, when the most remarkable deviations from it are
observed, the very occurrence of exacerbations and remissions, combined
with certain points of moral proof, may furnish the strongest evidence
possible. Thus, on the trial of Miss Blandy at Oxford in 1752, for the
murder of her father, one of the strongest circumstances in proof was,
that repeatedly after she gave the deceased a bowl of gruel, suspected
to be poisoned, his illness was much increased in violence.[70]

As connected with the present subject, a question might here be noticed
that has been discussed on the occasion of various trials, namely,
whether the symptoms of poisoning are susceptible of a complete
intermission. It cannot be answered satisfactorily, however, except with
reference to particular poisons. The property alluded to has been
ascribed to several poisons, even to mercury, arsenic, and opium; but
oftener, I believe, in consequence of an improper desire on the part of
the witness to prove or to perfect their view of the case, than through
legitimate induction from facts.

3. Another characteristic is _uniformity in the nature of the symptoms_
throughout their whole progress. This character is the least invariable
of them all; for many poisons cause very different symptoms towards the
close from those which they cause at the beginning. Arsenic may induce
at first inflammation of the alimentary canal, and afterwards palsy or
epilepsy; nux-vomica may excite at first violent tetanus, and afterwards
inflammation of the stomach and bowels; and corrosive sublimate, after
exciting in the first instance inflammation, may prove eventually fatal
by inducing excessive ptyalism. In truth, certain changes of this kind
in the nature of the symptoms will, in special cases, afford strong
presumption, perhaps absolute proof, not only of general poisoning, but
even also of the particular poison given. The reason for mentioning so
uncertain a character as uniformity in the nature of the symptoms among
their characteristics will appear presently.—[pp. 47 & 50.]

4. The fourth characteristic is, that _the symptoms begin soon after a
meal_, or rather, soon after food, drink, or medicine has been taken.
The occasions on which we eat and drink are so numerous and so near one
another, that unless the poison suspected is one which acts with
rapidity, it may be difficult to attach any weight to this circumstance.
Some poisons rarely produce their effects till a considerable time after
they are swallowed; the poisonous mushrooms, for example, may remain in
the alimentary canal for several hours or even an entire day and more,
before their effects begin; poisonous cheese in like manner may not act
for five or six hours,[71] or even a whole day;[72] and that kind of
cholera, which is caused in some people by putrid, diseased, and
new-killed meat, seldom begins, so far as I have observed, till twelve
hours or more after the noxious meal. With regard to the commoner
poisons, such as arsenic, corrosive sublimate, the mineral acids, oxalic
acid, nux-vomica, and the like, it is a good general rule, that the
symptoms, if violent from the beginning, must have begun soon after
food, drink, or medicine has been taken.

In making inquiries respecting this point, however, care must be taken
not to lose sight of certain circumstances which may cause a deviation
from the general rule.

In the first place, it should be remembered that poisons may be
administered in many other ways besides mixing them with articles of
food or drink, or substituting them for medicines. They may be
introduced into the anus; they have been introduced into the vagina;
they have also been introduced by inhalation in the form of vapour; and
there can be no difficulty in introducing some of them through wounds.

Secondly, another circumstance which may be kept in view is, that, if a
person falls asleep very soon after swallowing a poison, especially one
of the irritants, the commencement of the symptoms may be considerably
retarded, provided it be not one of the powerful corrosives. This
statement is not so fully supported by facts as to admit of its being
laid down with confidence as a general rule. But from various incidents
which have come under my notice it appears not improbable, that sleep
does possess the power of putting off for a while the action of some
poisons. In particular some instances have occurred to me where arsenic
taken at night did not begin to act for several hours, the individual
having in the meantime been asleep.[73] The occurrence of so long an
interval between its administration and the first appearance of the
symptoms is so contrary to what generally happens, that some cause or
another must be in activity; and the insensibility of the system during
sleep to most sources of excitement seems to supply a sufficient
explanation. The slow operation of laxatives during sleep compared with
their effects during one’s waking hours, is an analogical fact.

A third consideration to be attended to is, that poison may be secretly
administered during sleep to a person who lies habitually with his mouth
open. This is fully proved by an interesting case which will be noticed
under the head of the moral evidence of poisoning. In that particular
case the individual immediately awoke, because the poison was
concentrated sulphuric acid; but it may admit of question whether a
sound sleeper might not swallow less irritating poisons without being
awakened. In such circumstances no connexion of course could be traced
between the taking of a suspected article and the first appearance of
the symptoms.

5. Lastly, _the symptoms appear during a state of perfect health_. This
is an important character, yet not universal; for it cannot be expected
to apply to cases of slow poisoning, and poisons may be given while the
person is actually labouring under natural disease. Cases of the last
description are generally very embarrassing; for if, instead of
medicine, a poison be administered, whose symptoms resemble the natural
disease, suspicion may not arise till it is too late to collect
evidence.

It must be apparent from the preceding observations, that the characters
common to the symptoms of general poisoning are by no means universally
applicable. Yet on reviewing them attentively it will also appear, that,
considering the little knowledge possessed by the vulgar of the action
of poisons, and consequently the rude nature of their attempts to commit
murder by poisoning, the exceptions to the general statements made above
will not be numerous.

It now remains to be seen how far these characters distinguish the
symptoms of poisoning from those of natural disease; and

1. As to the _suddenness of their invasion and rapidity of their
progress_, it is almost needless to observe, that many natural diseases
commence with a suddenness and prove fatal with a rapidity, which few or
no poisons can surpass. The plague may prove instantaneously fatal; and
even the continued fever of this country may be fully formed in an hour,
and may terminate fatally, as I have once witnessed, at the beginning of
the second day. Inflammation of the stomach also begins suddenly and
terminates soon. Cholera likewise answers this description: I have known
the characters of ordinary cholera fully developed within an hour after
the first warning symptom, and frequently in hot climates, nay, in some
rare instances even in Britain, it proves fatal in a few hours.
Malignant cholera frequently proves fatal in a few hours. Inflammation
of the intestines, too, may begin, or at least seem to begin, suddenly
and end fatally in a day: One variety of it, now well known to affect
the mucous membrane, may remain quite latent till the gut is perforated
by ulceration, and then the patient is attacked with acute pain,
vomiting, and mortal faintness, and frequently perishes within
twenty-four hours.[74] But in particular many organic diseases of the
heart prove suddenly fatal, without any previous warning; and this is
also true to a certain extent even of apoplexy; for, as will afterwards
be seen, it is an error to suppose that apoplexy is always, or even
generally, preceded by warning symptoms. The first characteristic,
therefore, as applied to the symptoms of poisoning generally, contrasted
with those of general disease, must appear by no means distinctive. But
opportunities will occur afterwards for showing, that it is sometimes a
good diagnostic in the case of particular poisons.[75]

2. As to the uniformity or _uninterrupted increase of the symptoms_, it
is equally the attribute of many common diseases. I am not aware, that
in speedily fatal cases of the internal _phlegmasiæ_ a considerable
remission is often observed. Apoplexy, too, very frequently continues
its course without interruption; and the same may be said of cholera,
and indeed of most acute diseases, when they prove rapidly fatal.

3. It was stated above, that the third character, _uniformity in kind_
throughout their progress, is by no means an invariable circumstance.
Still less is it distinctive; for many diseases are marked by great
uniformity of symptoms. It has been enumerated nevertheless among the
general characters of poisoning, because, although its presence can
hardly ever add any weight to the evidence in favour of death by poison,
its absence may sometimes afford even positive proof in favour of
natural death. That is, changes of a certain kind occurring in the
symptoms during their progress may be incompatible with the known
effects of a particular poison or of all poisons, and capable of being
accounted for only on the supposition of natural disease having been at
least the ultimate cause of death. This statement, which is one of some
importance, is illustrated by a pointed case, that of Charles Munn,
mentioned at the close of the present section.

4. In the next place, it was observed that some reliance may be placed
on the fact, that the symptoms of poisoning _appear very soon after a
meal_. But we also know this to be the most frequent occasion on which
some natural disorders begin. An attack of apoplexy after a hearty meal
is a common occurrence. That kind of cholera which follows the
immoderate use of acid fruit likewise comes on soon after eating.
Sometimes mere excessive distension of the stomach after a meal proves
suddenly or instantaneously fatal. Drinking cold water when the body is
over-heated likewise causes at times immediate death. It appears that
perforation of the stomach, the result of an insidious ulcer of its
coats, and likewise rupture of the stomach from mechanical causes, are
most apt to occur during the digestion, and therefore soon after the
taking of a meal.

These few observations will make it evident that the appearing of
violent symptoms soon after eating may arise from other causes besides
the administration of poison. At the same time, as the diseases which
are apt to commence suddenly at that particular time are few in number,
and none of them by any means frequent, it is always justly reckoned a
very suspicious circumstance; and when combined with certain points of
moral proof, such as that several people, who have eaten together, were
seized about the same time with the same kind of symptoms, the evidence
of general poisoning becomes very strong indeed. Sometimes the evidence
from the date of their commencement after a meal may singly supply
strong evidence, as in the case of the mineral acids and alkalis, or
corrosive sublimate, which begin to act in a few seconds or minutes.

On the other hand, if the symptoms do not begin soon after food, drink,
or medicine has been taken (the circumstances being such as to exclude
the possibility of poison being introduced by a wound, by the lungs, or
by any other channel but the stomach), the presumption on the whole is
against poisoning; and sometimes the evidence to this effect may be
decisive. The principle now propounded may be often a very important one
in the practice of medical jurisprudence; for when united with a little
knowledge of the symptoms antecedent to death, it may be sufficient to
decide the nature of the case. Thus it is sufficient, in my opinion, to
decide the celebrated case of the Crown Prince of Sweden. The prince,
while in the act of reviewing a body of troops on the 28th May, 1810,
was observed suddenly to waver on his horse; and soon afterwards he fell
off while at the gallop, was immediately found insensible by his staff,
and expired in half an hour. As he was much beloved by the whole nation,
a rumour arose that he had been poisoned; and the report took such firm
root in the minds of all ranks, that a party of military, while
escorting the body to Stockholm, were attacked near the city by the
populace, and their commander, Marshal Fersen, murdered; and Dr. Rossi,
the prince’s physician, after narrowly escaping the same fate, was in
the end obliged to quit his native country. Now, no other poison but one
of the most active narcotics could have caused such symptoms, and none
of them could have proved so quickly fatal unless given in a large dose.
It was proved, however, that on the day of his death the prince had not
taken any thing after he breakfasted; and an interval of nearly four
hours elapsed after that till he fell from his horse. This fact alone,
independently of the marks of apoplexy found in the head after death,
and the warning symptoms he repeatedly had, was quite enough to show
that he could not have died of poison, as it was incompatible with the
known action of the only poisons which could cause the symptoms. This is
very properly one of the arguments used by the Medical Faculty of
Stockholm, which was consulted on the occasion.[76]

The same circumstances will often enable us to decide at once a set of
cases of frequent occurrence, particularly in towns,—where the sudden
death of a person in a family, the members of which are on bad terms
with one another, is rashly and ignorantly imputed to poison, without
any particular poison being pointed at; and where, consequently, unless
the morbid appearances clearly indicate the cause of death, a very
troublesome analysis might be necessary. In several cases of this kind,
which have been submitted to me, I have been induced to dispense with an
analysis by resting on the criterion now under consideration. The
following is a good example.

A middle-aged man, who had long enjoyed excellent health, one afternoon
about two o’clock returned home tired, and after having been severely
beaten by his wife went to bed. At a quarter past two one of his workmen
found him gasping, rolling his eyes, and quite insensible; and he died
in a few minutes. As his wife had often maltreated and threatened him, a
suspicion arose that he had died of poison, and the body was in
consequence examined judiciously by Sir W. Newbigging and myself. The
only appearance of disease we could detect was a considerable
tuberculation of the septum cordis and anterior parietes of both
ventricles. This disease might have been the cause of death; for there
is no disease of the heart which may not remain long latent, and prove
fatal suddenly. But, as the man never had a symptom referrible to
disease of the heart, it was impossible to infer, in face of a suspicion
of poisoning, that it must have been the cause of death; since the man
might very well have died of poison, the disease of the heart continuing
latent. Poisoning, however, was out of the question. The man had taken
nothing whatever after breakfasting about nine. Now no poison but one of
the most active narcotics in a large dose could cause death so rapidly
as in this case; and the operation of such a poison in such a dose could
not be suspended so long as from nine till two. An analysis was
therefore unnecessary.

5. Little need be said with regard to _the symptoms beginning, while the
body is in a state of perfect health_; because in truth almost all acute
diseases begin under the same circumstances. Connected with this
subject, however, a point of difference should be noticed which may be
of use for distinguishing poisoning by the irritants from acute diseases
of the inflammatory kind:—the latter rarely begin without some adequate
and obvious natural cause.

On considering all that has now been said regarding the characteristics
of the symptoms of general poisoning, as contrasted with those of
natural disease, no one can hesitate to allow, that from them alone a
medical jurist can never be entitled to pronounce that poisoning is
certain. At the same time he must not on that account neglect them. For,
in the first place, they are of great value as generally giving him the
first hints of the cause of mischief, and so leading him to search in
time for better evidence. Next, they will often enable him to say that
poisoning was possible, probable, or highly probable; which, when the
moral evidence is very strong, may be quite enough to decide the case.
Thirdly, although they can never entitle him to say that poisoning was
certain, they will sometimes enable him to say, on the contrary, that it
was impossible. And to conclude, when the chemical or moral evidence
proves that poison was given, the characters of the symptoms may be
necessary to determine whether it was the cause of death.

As the last statement is one of consequence, and yet has been overlooked
by some authors on medical jurisprudence in this country, it may be
illustrated by one or two comments. It does not follow, because a poison
has been given, that it is the cause of death; and therefore in every
medico-legal inquiry the cause of the first symptoms and the cause of
death should be made two distinct questions. The question, whether a
poison, proved to have been administered, was the cause of death, is to
be answered by attending to the second and third characteristics
mentioned above, and considering whether the symptoms went on
progressively increasing, or altered their nature during the course of
the patient’s illness, and whether the alteration, if any, was such as
may occur in the case of poisoning generally, or of the special poison
given. These remarks are very well exemplified by a case, of which I
have related the particulars elsewhere,[77] that, namely, of Charles
Munn, tried at the Inverary Spring Circuit of 1824 for the double crime
of procuring abortion, and of murder by poisoning. The moral evidence
and symptoms together left no doubt that arsenic had been given, and
that the deceased, a girl with whom the prisoner cohabited, laboured
under the effects of that poison in a very aggravated and complex form
for twelve days. After that she began to recover rapidly, and in the
course of a fortnight more was free of every symptom except weakness and
pains in the hands and feet: In short, all things considered, she was
thought to be out of danger. But she then became affected with headache
and sleeplessness, and died in nineteen days more under symptoms of
obscure general fever, without any local inflammation. Dr. Duncan,
junior, and I, who were consulted by the Crown in this case, were of
opinion,—that granting the girl’s first illness, as appeared from moral
and medical evidence, was owing to arsenic, her death could not be
ascribed to it with any certainty. It is true that in a few instances
the primary irritant symptoms caused by arsenic have been known to pass
into an obscure general fever, which has ended fatally; and that this
mode of termination coincides with the effects ascribed to arsenic as
the chief ingredient in the celebrated _Aqua Toffana_. But the latter
phenomena, at best of doubtful authenticity, are not represented to have
been preceded by the ordinary symptoms of violent irritation, or to have
been developed except under the use of continuous small doses; and as
for the more recent and less ambiguous cases of fever succeeding the
usual primary effects of a large dose, in no instance yet recorded was
there an intermission between the two stages.

So much, then, for the force of the evidence drawn from the characters
of the symptoms of general poisoning. According to the example of
others, I might consider in the present place the force of evidence
derived from the symptoms themselves, which distinguish the three
classes of poisons. But this subject, together with the special natural
diseases which imitate the symptoms of poisoning, will be treated of
more conveniently as an introduction to each of the classes.


         SECTION II.—_Of the Evidence from Morbid Appearances._

The appearances left in the dead body after death by poison used
formerly to be relied on as strongly as the symptoms during life; and
with even less reason. Except in the instance of a very few poisons, the
morbid appearances alone can never distinguish death by poison from the
effects of natural disease, or from some other kinds of violent death.
There is not much room, therefore, for general remarks under the present
head.

It was at one time thought by the profession, and is still very
generally imagined by the vulgar, that unusual blackness or lividity of
the skin, indicates death by poison generally. But every experienced
physician is now well aware, that excessive lividity is by no means
universally produced by poison, and that it is likewise produced by so
many natural diseases as not even to form, in any circumstances
whatever, the slightest ground of suspicion. Neither is there any
difference in kind, as some imagine, between the lividity which succeeds
death by poison, and that which follows natural death. Yet it is right
for the medical jurist to be aware that lividity as a supposed
consequence of poison ought to be strictly attended to by medical
inspectors and law officers while investigating charges of poisoning,
because the vulgar belief on the subject sometimes leads to such conduct
or language on the part of the poisoner as betrays his secret at the
time, and constitutes evidence of his guilt afterwards.

Another appearance equally unimportant is early putrefaction of the
body. Early putrefaction, at one time much insisted on as a criterion of
poisoning,[78] cannot even justify suspicion. It is by no means
invariably, or even generally caused by poisons; nay, sometimes a state
precisely the reverse appears to be induced;[79] and it is seen quite as
frequently after natural death.

Some other appearances, not more conclusive, might also be mentioned
here; but they belong properly to the effects of individual poisons, or
of classes of poisons, not to those of poisoning generally. It may
merely be remarked at present, therefore, that the appearances after
death, which are really morbid, and which may be produced by poisons,
are, in one great class, the signs of inflammation of the alimentary
canal in its progressive stages,—in another class, the signs of
congestion within the head,—and in a third, a combination of the effects
of the two preceding classes; that neither set of appearances is
invariably caused by the poisons which usually cause them; that
congestion within the head is really seldom produced by those which are
currently imagined to produce it; and that most of the appearances of
both kinds are exactly similar to those left by many natural diseases.

But although, on the whole, the appearances after death, when considered
singly, can seldom supply evidence of poisoning even to the amount of
probability, they may nevertheless prove very important under other
points of view. Thus, in connection with the symptoms and the general
evidence, the appearances after death may furnish decisive proof; and
even should the history of the symptoms be unknown, or have been
unskilfully collected, the appearances after death, by pointing out the
nature of the previous illness, may furnish evidence enough to decide
the case, when the moral proof is strong. Again, in cases of alleged
_imputation of poisoning_ they are necessary to determine whether a
poison actually found in the body was introduced during life or after
death. Besides, the very absence of morbid appearances may afford
presumptive proof in some circumstances,—when, for example, the question
is, whether a person has died of apoplexy or of poisoning with
narcotics? Farther, a few poisons, as was formerly stated, occasionally
produce appearances so characteristic, as not to be capable of being
confounded with the effects of any other agent whatsoever: It will be
found hereafter, for example, that the mineral acids have at times left
behind them in the dead body unequivocal evidence of their operation.
And finally, in cases where no doubt can be entertained that poison was
taken, the evidence from morbid appearances may be useful or necessary
for settling whether or not it was the cause of death. Two pointed
examples of this kind will be noticed under the next section.

When signs of the action of poison are not found in the dead body, and
on the contrary marks are found of the operation of natural disease, the
presumption of course is that the person died a natural death. But here
a few words of caution must be added with regard to the drawing of that
inference in cases where the history of the symptoms is not known. It
does not follow merely because certain appearances of natural disease
are found, that their cause was the cause of death. For death may have
arisen from a totally different cause, such as poisoning. This remark is
not, as some may imagine, the offspring of hypothetical refinement, but
a necessary caution, drawn from actual and not unfrequent occurrences.
Thus, for example, the following cases will show, that there may be
found in the dead body diseased appearances, arising from pleurisy,
hydrothorax, or peripneumony, sufficient to cause death, or to account
for death in ordinary circumstances; and that nevertheless the disease
may have been completely latent, and death have arisen from poison. In
Rust’s Magazin is related the case of a German apothecary, who poisoned
himself with prussic acid, and in whose body the lower lobe of the left
lung was found consolidated and partly cartilaginous.[80] In Corvisart’s
Journal an army-surgeon has described the case of a soldier, who died of
a few hours’ illness, and whose right lung was found after death forming
one entire abscess; yet to the very last day of his existence he daily
underwent all the fatigues of a military life; and in fact he died of
poisoning with hemlock.[81] In Pyl’s Memoirs and Observations, there is
a similar account of a woman who enjoyed tolerable health, and died
during a fit of excessive drinking, and in whose body the whole left
lung was found one mass of suppuration.[82] Under the next section will
be mentioned other equally pointed cases of death by poison, where the
apparent cause of death was external violence.

The conclusions to be drawn from these facts are that, at all events,
the medical inspector in a question of poisoning, must take care not to
be hurried away by the first striking appearances of natural disease
which he may observe, and so be induced to conduct the rest of the
inspection superficially; and likewise, that he should not so frame his
opinion on the case, as to exclude the possibility of a different cause
from the apparent one, unless the appearances are such as must
necessarily have been the cause of death. It may be said, that in
requiring this condition for an unqualified opinion, a rigour of
demonstration is exacted, which can rarely be attained in practice. But,
on the one hand, it must not be forgotten, that an unqualified opinion
is not always necessary; and on the other hand, although it were, I
think it might be shown, if the subject did not lead to disproportionate
details, that we may often approach very near the rigour of
demonstration required. At present no more need be said, than that the
inspector should be particularly on his guard in those cases, in which
the appearances, though belonging to the effects of a deadly disease,
are trifling; and still more in those in which the appearances, though
great, belong to the effects of a disease, whose whole course may be
latent. And I may add, that, from what I have observed of medico-legal
opinions, the caution now given is strongly called for.

It may be right to allude here also to another purpose which may be
served by a careful consideration of the morbid appearances. In cases in
which the history of the symptoms is unknown or imperfect the extent and
state of progress of the appearances will sometimes supply strong
presumptive evidence of the duration of the poisoning. This is an
obvious and important application of the knowledge of the pathology of
poisoning; but the simple mention of it is all which can be here
attempted, as special rules can hardly be laid down on the subject.


            SECTION III.—_Evidence from Chemical Analysis._

The chemical evidence in charges of poisoning is generally, and with
justice, considered the most decisive of all the branches of proof. It
is accounted most valid, when it detects the poison in the general
textures of the body, or in the blood, or in the stomach, intestines or
gullet, then in the matter vomited, next in articles of food, drink or
medicine of which the sufferer has partaken, and lastly, in any articles
found in the prisoner’s possession, and for which he cannot account
satisfactorily.

When poison is detected in any of these quarters, more especially in the
stomach or intestines, it is seldom that any farther proof is needed to
establish the fact of poisoning. In two circumstances, however, some
corroboration is necessary.

In the first place, in cases where a defence is attempted by a charge of
imputation of poisoning it may be necessary to determine by an accurate
account of the symptoms, or by the morbid appearances, or by both
together, whether the poison was introduced into the body before or
after death. For it is said, that attempts have been made to impute
crime by introducing poison into the stomach or anus of a dead body; and
although I have not been able to find any authentic instance of so
horrible an act of ingenuity having been perpetrated, it must
nevertheless be allowed to be quite possible.

Secondly, an account of the symptoms and morbid appearances is still
more necessary, when the question at issue is, not so much whether
poison has been given, as whether it was the cause of death, granting it
had been taken. Some remarks have been already made on this question in
the two former sections. In the present place some farther illustrations
will be added from two very striking cases. They are interesting in many
respects, and particularly as showing the importance of strict
medico-legal investigation: I am almost certain that but a few years ago
their real nature would not have been discovered in this country. The
first to be noticed occurred to Dr. Wildberg of Rostock. Wildberg was
required to examine the body of a girl, who died while her father was in
the act of chastising her severely for stealing, and who was believed by
all the bye-standers, and by the father himself, to have died of the
beating. Accordingly, Wildberg found the marks of many stripes on the
arms, shoulders and back, and under some of the marks blood was
extravasated in considerable quantity. But these injuries, though
severe, did not appear to him adequate to account for death. He
therefore proceeded to examine the cavities; and on opening the stomach,
he found it very much inflamed, and lined with a white powder which
proved on analysis to be arsenic. It turned out, that on the theft being
detected the girl had taken arsenic for fear of her father’s anger, that
she vomited during the flogging, and died in slight convulsions.
Consequently, Wildberg very properly imputed death to the arsenic. In
this case the chemical evidence proved that poison had been taken; but
an account of the symptoms and appearances was necessary to prove that
she died of it.[83] The other case occurred to Pyl in 1783. A woman at
Berlin, who lived on bad terms with her husband, went to bed in perfect
health; but soon afterwards her mother found her breathing very hard,
and on inquiring into the cause discovered a wound in the left side of
the breast. A surgeon being immediately sent for, the hemorrhage which
had never been great, was checked without difficulty; but she died
nevertheless towards morning. On opening the chest it appeared that the
wound pierced into it, and penetrated the pericardium, but did not wound
the heart; and although the fifth intercostal artery had been divided,
hardly any blood was effused into the cavity of the chest. Coupling
these circumstances with the trifling hemorrhage during life, and the
fact that she had much vomiting, and some convulsions immediately before
death, Pyl satisfied himself that she had not died of the wound: and
accordingly the signs of corrosion in the mouth and throat, and of
irritation in the stomach, with the subsequent discovery of the remains
of some nitric acid in a glass in her room, proved that she had died of
poison.[84]

_Causes of the disappearance of poison from the body._—Chemical evidence
is not always attainable in cases of poisoning. Various causes may
remove the poison beyond reach. Hence although poison be not detected in
the body,—the experimenter being supposed skilful and the poison of a
kind which is easily discovered,—still it must not be concluded from
that fact alone that poison has not been the cause of death. For that
which was taken into the stomach may have been all discharged by
vomiting and purging, or may have been all absorbed, or decomposed; and
that which has been absorbed into the system may have been all
discharged by the excretions.

1. It may have been discharged by vomiting and purging. Thus on the
trial of George Thom for poisoning the Mitchells, held at Aberdeen at
the Autumn Circuit of 1821, it was clearly proved, that the deceased had
died of poisoning by arsenic; yet by a careful analysis none could be
detected in the stomach or its contents; for the man lived seven days,
and during all that time laboured under frequent vomiting.[85] In a
remarkable case related by Dr. Roget, arsenic could not be found in the
matter vomited twenty-four hours after it had been swallowed;[86] in
another related by Professor Wagner of Berlin, that of an infant who
died in twelve hours under incessant vomiting after receiving a small
quantity of arsenic, none could be detected in the stomach;[87] in
another which I have described in a paper on arsenic, although the
person lived only five hours, the whole arsenic which could be detected
in the tissues and contents of the stomach did not exceed a fifteenth
part of a grain;[88] in an American Journal there is a striking case of
a grocer, who died eight hours after swallowing an ounce of arsenic, and
in whose body none could be found chemically,—at a period however
antecedent to the late improvements in analysis;[89] and in a case
communicated to me not long ago by Mr. Hewson of Lincoln, where arsenic
was given in solution, and death ensued in five hours, none of the
poison could be detected either in the contents or tissues of the
stomach by a careful analysis conducted according to the most modern
principles.

Nevertheless, it is singular how ineffectual vomiting proves in
expelling some poisons from the stomach. Those which are not easily
soluble, and have been taken in a state of minute division, may remain
adhering to the villous coat, notwithstanding repeated and violent
efforts to dislodge them by vomiting. Many instances to this effect have
occurred in the instance of arsenic. Metzger has related a case, where,
after six hours of incessant vomiting, three drachms were found in the
stomach.[90] Mr. Sidey, a surgeon of this city, has mentioned to me an
instance of poisoning with king’s yellow, in which he found the stomach
lined with the poison, although the patient had vomited for thirty
hours. In three cases which I have investigated arsenic was detected,
although the people lived and vomited much for nearly two days;[91] and
Professor Orfila has noticed a similar instance in which that poison was
found in the contents of the stomach, although the person had vomited
incessantly for two entire days.[92]

It is not easy to specify the period after which a poison that has
excited vomiting need not be looked for in the stomach. It must vary
with a variety of circumstances whose combined effect it is almost
impossible to appreciate, such as the solubility and state of division
of the poison, the frequency of vomiting, the substances taken as
remedies, and the like. When the poison is in solution and the patient
vomits much, an analysis may be expected to prove frequently abortive,
even though the individual survives but a few hours, as in Mr. Hewson’s
case already noticed. In other circumstances, however, as various facts
quoted above will show, poisons may frequently be found after two days
incessant vomiting; and on the whole it may be stated, that the recent
improvements in analysis render the period much longer than it has
generally been, and would naturally be imagined. Metzger has related the
case of a woman poisoned with arsenic mixed with currants, in whose
body, after eight days of frequent vomiting, he found ten or twelve
currants, which gave out an odour of garlic when burnt;[93] but here the
dose, if there was really arsenic, must have been repeated recently
before death, for it is not possible to conceive how currants could
remain in the stomach so long, whatever may be thought of the
possibility of arsenic remaining. It is farther proper to add, that
Professor Henke of Erlangen, one of the highest living authorities in
Germany, once found grains of arsenic in the gullet, although he found
none in any other part of the body, of a person who survived the taking
of the poison four days.[94] Allowing to this fact all the weight
derived from the high name of its author, I must nevertheless express
great doubt whether the arsenic was not repeated more recently before
death.

2. The poison may have disappeared, because it has been all absorbed. It
has several times happened that in the bodies of those poisoned with
laudanum, or even with solid opium, none of the drug could be detected
after death. Sometimes indeed it is found, even though the individual
survived the taking of the poison many hours. Thus a case related by
Meyer of Berlin, in which the person lived ten hours after taking the
saffron-tincture of opium; and nevertheless it was detected in the
stomach by a mixed smell of saffron and opium.[95] But more commonly it
all disappears, unless the dose has been very large. In a case of
poisoning with laudanum, which I examined here along with Sir W.
Newbigging in 1823, none could be detected, although strong moral
circumstances left no doubt that laudanum had been swallowed seven or
eight hours before death. An instance of the same kind has been minutely
related by Pyl. It was that of an infant who was poisoned with a mixture
of opium and hyoscyamus, and in whose stomach and intestines none could
be detected by the smell.[96] Similar observations have been often made
on animals; and several additional cases of the same purport, occurring
in man, will be related under the head of opium.

It might be of use to quote some of the numerous errors committed by
medical witnesses, in consequence of having overlooked the effect of
absorption in removing poisons beyond the reach of chemical analysis.
But not to be too prolix, I shall be content with mentioning a single
very distinct case in point, which happened at a Coroner’s Inquest in
London, in 1823. A young man one evening called his fellow-lodger to his
bedside; assured him he had taken laudanum, and should be dead by the
morrow; and desired him to carry his last farewell to his mother and his
mistress. His companion thought he was shamming; but next morning the
unfortunate youth was found in the agonies of death. The moral evidence
was not very satisfactory; but that is of little consequence to my
present object. The point in the case I would particularly refer to is
the declaration of the medical inspector, that laudanum could not have
been taken, because he did not find any by the smell or by chemical
analysis in the contents of the stomach.[97]

3. Poisons may not be found, because the excess has been decomposed.

Vegetable and animal poisons may be altogether destroyed by the process
of digestion. This observation will explain why sometimes no poison
could be found in cases of poisoning with crude opium or other vegetable
solids. A French physician, M. Desruelles, has related the case of a
soldier, who died six hours and a half after swallowing two drachms of
solid opium, and in whose stomach nothing was found but a yellowish
fluid, quite destitute of the smell of the drug.[98]

Some mineral poisons, such as corrosive sublimate, lunar caustic, and
hydrochlorate of tin, are also decomposed in the stomach. But they are
not removed beyond the reach of chemical analysis. The decomposition is
the result of a chemical, not of a vital process; and the basis of the
poison may be found in the solid contents of the stomach under some
other compound form. Other poisons again may be apt to elude detection
by altering their form, by combining with other substances, without
themselves undergoing decomposition. Thus it appears from a case related
by Mertzdorff of Berlin, that, in poisoning with sulphuric acid, after
the greater part of the poison is discharged by vomiting, the remainder
may escape discovery by being neutralized: For, although he could not
find any free acid in the contents of the stomach, he discovered 4½
grains in union with ammonia by precipitation with muriate of
baryta.[99]

It may be also right to mention another kind of decomposition which may
render it impossible to detect a poison that has been really
swallowed—namely, that arising from decay of the body. In several recent
cases bodies have been disinterred and examined for poison months or
even years after death. In these and similar cases it would be
unreasonable to expect always to find the poison, even though it existed
in the stomach immediately after death. Some poisons, such as oxalic
acid, might be dissolved and then exude; others, such as the vegetable
narcotics, will undergo putrefaction; and others, such as prussic acid,
are partly volatilized, partly decomposed, so as to be undistinguishable
in the course of a few days only. The mineral poisons, those at least
which are solid, are not liable to be so dissipated or destroyed. Some
authors, indeed, have said that arsenic may disappear in consequence of
its uniting with hydrogen disengaged during the progress of
putrefaction, and so escaping in the form of arseniuretted-hydrogen gas;
and they have endeavoured to account in this way for the non-discovery
of it in the bodies of the people who had been killed by arsenic, and
disinterred for examination many months afterwards.[100] But the
supposition is by no means probable: at least arsenic has been detected
in the body fourteen months, nay, even seven years, after interment. For
farther details, on this curious topic, the reader may turn to the
article Arsenic.

On the whole, the result of the most recent researches is that the
effect of the spontaneous decay of dead animal matter in involving
poisons in the general decomposition appears to be much less
considerable than might be anticipated. For this most important
medico-legal fact, the toxicologist is indebted to the experimental
inquiries of MM. Orfila and Lesueur.[101] The poisons tried by them
were—sulphuric and nitric acids, arsenic, corrosive sublimate,
tartar-emetic, sugar of lead, protomuriate of tin, blue vitriol,
verdigris, lunar caustic, muriate of gold, acetate of morphia, muriate
of brucia, acetate of strychnia, hydrocyanic acid, opium, and
cantharides. They found that after a time the acids become neutralized
by the ammonia disengaged during the decay of animal matter;—that by the
action of the animal matter the salts of mercury, antimony, copper, tin,
gold, silver, and likewise the salts of the vegetable alkaloids, undergo
chemical decomposition, in consequence of which the bases become less
soluble in water, or altogether insoluble;—that acids may be detected
after several years’ interment, not always, however, in the free
state;—that the bases of the decomposed metallic salts may also be found
after interment for several years;—that arsenic, opium, and cantharides
undergo little change after a long interval of time, and are scarcely
more difficult to discover in decayed, than in recent animal
mixtures;—but that hydrocyanic acid disappears very soon, so as to be
undistinguishable in the course of a few days.

4. Lastly, the poison which has been absorbed into the system, and may
consequently be detected in certain circumstances in the textures of the
body at a distance from the alimentary canal, may also be removed beyond
the reach of analysis, by being gradually discharged along with the
excretions. It has been fully proved in recent times, that in poisoning
with arsenic the poison may be found in ordinary cases, for some days
after being swallowed, in the liver especially, but also in the other
textures, in the blood, and in the urine; but that if a flow of urine be
established and kept up, in nine or ten days, and sometimes much sooner,
it can no longer be discovered anywhere by the nicest analysis.[102]

_Is the discovery of poison in the body or the evacuations essential to
establish a charge of poisoning?_ It was mentioned at the commencement
of the present section, that the chemical evidence is generally, and
correctly, considered the most decisive of all the branches of proof in
cases of poisoning. But some toxicologists have even gone so far as to
maintain that without chemical evidence, or rather, in more general
terms, without the discovery of poison either in the body itself or in
the evacuations,—no charge of poisoning ought to be held as proved.
This, however, is a doctrine to which I cannot assent. In the preceding
observations on the evidence of general poisoning it has been several
times alluded to as unsound; and repeated opportunities of establishing
exceptions will occur in the course of this work, under the head of
individual poisons. At present it may be well to illustrate its
unsoundness in reference to those charges of poisoning, where no
particular poison is pointed at by the medical evidence, but where a
whole class of poisons must be kept more or less in view. Even here I
apprehend there may be sufficient evidence in the symptoms and morbid
appearances, without any chemical facts,—to render poisoning so highly
probable, that in conjunction with strong moral evidence, no sensible
man can entertain any doubt on the subject. Several illustrations might
be here given; and some will be found scattered throughout the work. In
the present place a few instances will be mentioned which cannot be
conveniently arranged any where else, and which are well worthy of
notice, as being striking examples of the decision of questions of
poisoning without chemical evidence.

A man of doubtful character and morals, well acquainted with chemistry
and medical jurisprudence, and of disordered finances, was known to
harbour a design on a friend’s wife, who possessed a considerable
fortune. At last he one morning invited the husband to breakfast with
him at a tavern; and they breakfasted, in a private apartment, on
beef-steaks, fried potatoes, eels, claret, and rum. They had scarcely
commenced the meal when his guest complained of feeling unwell; and soon
afterwards he vomited violently. This symptom continued, along with
excruciating pain in the belly, for a long time before the prisoner sent
for medical aid; indeed he did not procure a physician till the sufferer
had been also attacked with very frequent and involuntary purging. The
physician, who, before seeing his patient, had received the prisoner’s
explanation of the apparent cause of the illness, was led at first to
impute the whole to cholera caught by exposure to cold; but on returning
at seven in the evening, and finding the gentleman had been dead for an
hour, he at once exclaimed that he had been poisoned. On the body being
inspected much external lividity was found, contraction of the fingers,
and great inflammation of the stomach and intestines, presenting an
appearance like that of gangrene.[103] On analyzing some fluid left in
the stomach, no arsenic or other poison could be detected. The attention
of the inspectors was turned specially to arsenic, because the prisoner
was proved to have bought that poison, and to have made a solution of
some white powder in his kitchen not long before the deceased died. The
prisoner in his defence stated, that the deceased had been for some time
much weakened by the use of mercury, and while in this state was seized
with cholera; and he likewise attempted to make it probable that the
man, in despair at his not recovering from a venereal disease, might
have committed suicide. The council of physicians who were required to
give their opinion on the case state on the contrary, that the diseased
was a healthy man, without any apparent disposition to disease; that
there was no pretext whatever for supposing suicide; that the
inflammatory state of the stomach and bowels supplied strong probability
of poisoning with arsenic, but not certain evidence; that acute
gastritis from natural causes is always attended with constipation; that
the deceased presented symptoms of stupor and other signs of derangement
of the nervous system remarked in rapid cases of poisoning with arsenic;
that cholera is very rare at the end of November, the season when this
incident occurred; and that the poison might well be discharged by
vomiting. Although all the prisoner’s statements in defence were
contradicted by satisfactory proof, and the medical evidence of
poisoning was supported by a chain of the strongest general
circumstances, the crime was considered by the court as not fully
proved, because the prisoner could not be induced to confess, and
because poison was not actually detected in the body. But on account of
the very strong probability of his guilt, he was, in conformity with the
strange practice of German courts in the like cases, condemned to
fifteen years’ imprisonment.[104] In this instance—considering the kind
of symptoms, their commencement during a meal, the rapidity of death,
the signs of violent inflammation in the stomach after so short an
illness, and the facility with which the absence of poison in the
contents of the stomach may be accounted for, more especially if it be
supposed that the poison was administered in solution,—I consider the
medical evidence of death by poisoning so very strong, that, the general
evidence being also extremely strong, the prisoner’s guilt was fully
demonstrated.

A case of the same kind, but of still greater interest, is that of Mary
Anne M’Conkey, who was tried at the Monaghan Assizes in 1841 for the
murder of her husband. I am indebted for the particulars to Dr.
Geoghegan, one of the principal Crown witnesses. The prisoner who had
been too intimate with another man, and had been heard to express her
intention of getting rid of her husband, was observed one day before
dinner to separate some greens for him from the plateful intended for
the rest of the family. None of the latter suffered at all. But her
husband was taken violently ill immediately after dinner, and died; and
a neighbour accidentally present, who partook, though sparingly, of the
same dish with him, was also similarly and violently affected but
recovered. The deceased before finishing the greens said they had a
disagreeable sharp taste, and was seized soon after with burning at the
heart, tenderness at the pit of the stomach, vomiting, coldness, a sense
of biting in the tongue and tingling through the whole flesh, excessive
restlessness, occasional incoherence, locked-jaw, clenching of the
hands, and frothing at the mouth; and he expired three hours after the
meal. His neighbour, two minutes after finishing his greens, experienced
a sense of pricking in the mouth and burning in the throat, gullet, and
stomach; then salivation, a feeling of swelling in the face without
actual fulness, general numbness and creeping in the skin; next
excessive restlessness, coldness of the integuments, dimness of sight,
and stupor; about an hour after the meal he became speechless,
repeatedly fainted, frothed at the mouth, and clenched his hands;
vomiting ensued, with considerable relief, and subsequently he had
frequent attacks of it, with purging, tenderness of the epigastrium,
cramps, and tingling in the flesh; and from these symptoms he recovered
so slowly as to be unable to work for five weeks. The only morbid
appearance of any note in the body of the deceased was a number of
irregular brownish-black patches on the inside of the stomach. No poison
could be detected in the contents or tissues of the stomach; none could
be discovered in the house except a corrosive-sublimate solution which
the prisoner used for a gargle; and none could be traced into her
possession. A variety of circumstances of a general nature, which are
passed over here for brevity, as not strictly appertaining to the
present view of the case, threw very great suspicion over the prisoner.
The medical witnesses deposed, that poisoning could alone explain the
medical circumstances; and Dr. Geoghegan was of opinion that death was
owing to some vegetable poison, although he could not specify the
particular substance. He suspected, however, that it was monkshood. In
these views, when consulted by him before the trial, I entirely
concurred. Considering the taste observed by the deceased at the time he
ate the greens, the rapidity with which he was taken ill afterwards, and
the very peculiar symptoms, unlike those of any natural disease with
which physicians are acquainted, and agreeing with those which are
produced by monkshood,—considering also that another individual, who
partook of the same dish with him, was similarly and simultaneously
attacked, and with a severity proportioned to the quantity he took,
while other persons who ate the same food from a different dish, did not
suffer at all,—it appears to me that poisoning was clearly established;
and I also think that the general evidence brought home the charge of
administering the poison to the prisoner. She was condemned and
executed, and confessed before execution, that she did poison her
husband, and that the substance she used was the powdered root of
monkshood, which is well known as a poison to the peasantry of Monaghan
under the name of Blue Rocket.

It is scarcely necessary to add, that great caution must be observed in
applying the general principle here inculcated. But the opposite
doctrine, that no charge of poisoning can be established without the
discovery of poison in the body or in the evacuations, appears to me a
great error, though upheld by no mean authority. Under that doctrine few
criminals would be brought to justice, were they to resort to a variety
of vegetable poisons, which in certain seasons are within the reach of
every one.


          SECTION IV.—_Evidence from Experiments on Animals._

Evidence from experiments on animals with articles supposed to contain
poison is more equivocal than was once imagined. But it may be doubted
whether some medical jurists have not overstepped the proper limits,
when they hold it to constitute little or no proof at all.

Evidence from express experiments should rarely form part of a regular
medical inquiry into a charge of poisoning. For in the first place, to
make sure of performing an experiment well requires more experimental
skill than the generality of practitioners can be expected to possess;
then, as will seen in the sequel, evidence procured from this source can
very rarely be more than presumptive; and lastly, if the quantity of
poison in the suspected substance is great enough to affect one of the
perfect animals, it may generally be recognized to a certainty by its
physical or chemical properties.

For these reasons it is not likely, that, in an inquiry undertaken by a
skilful toxicologist, he will put himself in the way of delivering an
opinion on the force of such evidence. But it is nevertheless necessary
for me to consider it in detail, because he may have to give his opinion
regarding experiments made inconsiderately by others, or accidents
caused by domestic animals eating the remains of substances suspected to
be poisoned.

The matter subjected to trial may be either suspected food, drink, or
medicine; or it may be the stuff vomited during life, or found in the
stomach after death; or it may be the flesh of poisoned animals.

1. The evidence derived from _the effects of suspected food, drink, or
medicine_ is better than that drawn from the effects of the vomited
matter or contents of the stomach. But an important objection has been
made to both, namely, that what is poison to man is not always poison to
the lower animals, and that, on the other hand, some of the lower
animals are poisoned by substances not hurtful to man.

A good deal of obscurity still hangs over the relative effects of
poisons on man and the lower animals. There are two species, however,
whose mode of life in respect to food closely resembles our own, and
which, according to innumerable experiments by Orfila, are affected by
almost all poisons exactly in the same way as ourselves, namely, the cat
and dog, but particularly the latter.

In general poisons act less violently on these animals; thus two drachms
of opium are required to kill a middle-sized dog,[105] while twenty
grains have killed a man, and undoubtedly less would be sufficient. It
appears that one poison, alcohol, acts more powerfully on them than on
man. There are also some poisons, such as opium, which, although
deleterious to them as well as to man, nevertheless produce in general
different symptoms. Yet the differences alluded to are probably not
greater than exist between man and man in regard to the same substances;
and therefore it may be assumed, that, on the whole, the effects of
poisons on man differ little from those produced on the dog and cat.

The present objection is generally and perhaps justly considered a
stronger one, when it is applied to other species of animals. But it
must be confessed after all, that our knowledge of the diversities in
the action of poisons on different animals is exceedingly vague, and
founded on inaccurate research; and there is much reason to suspect,
that, if the subject is studied more deeply, the greater number of the
alleged diversities will prove rather apparent than real. Both reasoning
and experiment, indeed, render it probable, that some orders, even of
the perfect animals, such as the _Ruminantia_, are much less sensible
than man to many poisons, and especially to poisons of the vegetable
kingdom. But so far as maybe inferred from the only accurate inquires on
the subject, their effects differ in degree more than in kind. Some
exceptions will without doubt be found to this statement. For example,
oxalic acid, besides inflaming the stomach, causes violent convulsions
in animals, but in man it for the most part excites merely excessive
prostration; and opium most generally excites in man pure sopor, in
animals convulsions also. Other exceptions, too, exist by reason of
functional peculiarities in certain animals. Thus irritant poisons do
not cause vomiting in rabbits or horses, because these animals cannot
vomit; neither do they appear to cause much pain to rabbits, because
rabbits have not the power of expressing pain with energy. But
exceptions like these, and particularly such as are unconnected with
functional peculiarities, will probably prove fewer in number, and less
striking than is currently imagined. For it is, on the other hand, well
ascertained, that many, indeed most of the active poisons whose effects
have been examined by a connected train of experiments, produce nearly
the same effects on all animals whatever from the highest to the lowest
in the scale of perfection. It has been fully proved, that arsenic,
copper, mercury, the mineral acids, opium, strychnia, conia, white
hellebore, hydrocyanic acid, cyanogen gas, sulphuretted hydrogen, and
many others, produce nearly the same effects on man, quadrupeds, birds,
amphibious animals, and even on fishes and insects.[106]

Accordingly there are cases, in which the evidence from experiments on
animals with suspected articles of food is unequivocal. For example;—a
sexton and his wife, who had got a bad name in their village in
consequence of informing against the bailiff for smuggling, and who were
on that account shunned by all the neighbours, accused the bailiff and
his wife of having tried to poison them by mixing poison with their
bread. Immediately after eating they were attacked, they said, with
sickness, griping, swelling, and dizziness; and they added, that a cat
was seized with convulsions after eating a part of it, had sprung away,
and never returned. A large portion of the loaf was therefore sent to
the Medical Inspector of the district; who reported, that it seemed
exactly similar to another unsuspected loaf;—that, although he was not
able to detect any poison, it might after all contain one,—vegetable
poison particularly;—but that he could hardly believe it did, for he fed
a dog, a cat, and a fowl several days with it, and they not only did not
suffer any harm, but even appeared very fond of it.[107] In this case it
was clear that poisoning was out of the question. On the other hand, the
effects of some poisons on man may be developed so characteristically in
animals as to supply pointed evidence. Thus, in the case of Mary
Bateman, an infamous fortune-teller and charm-worker, who after cheating
a poor family for a series of years, at last tried to avoid detection by
poisoning them, it was justly accounted good evidence, that a portion of
the pudding and the honey, supposed to have been poisoned, caused
violent vomiting in a cat, killed three fowls, and proved fatal to a dog
in four days, under symptoms of irritation of the stomach such as were
observed in the people who died.[108]

It has been farther objected to experiments on animals with suspected
articles of food, drink, or medicine, that it is difficult to administer
poison to them in a state of concentration, and to prevent it from being
discharged by vomiting. This objection, however, may be obviated by
performing the experiment in the way recommended by Professor Orfila. A
small opening is made into the gullet, previously detached from its
surrounding connexions, the liquid part is introduced by a funnel thrust
into the opening, and the solid portion previously made into little
pellets is then squeezed down. Lastly, the gullet is tied under the
aperture. The immediate effect of the operation is merely an appearance
of languor; and no very serious symptom is observable till four or five
days at soonest after the tying of the gullet. Hence if signs of
poisoning commence within twenty-four hours, they are independent of the
injury done by the operation.[109] This process requires some adroitness
to execute it well. It cannot be tried successfully but by a practised
operator, who, for reasons already given, would hardly ever try
experiments of the kind with suspected articles. Mention is here made of
it, therefore, chiefly because it is the best mode of experimenting in
those cases in which it is necessary, as will presently be seen, to
determine disputed points in the physiology of poisons.

I may here shortly notice a method which has been lately proposed for
detecting poisons that enter the blood, and which is founded on their
effects on animals. M. Vernière suggests that advantage may be taken of
the extreme sensibility of the medicinal leech to procure at least
presumptive evidence, when no evidence can be procured in any other
manner. He has related some experiments to prove that the leech, when
placed in the blood of dogs killed by nux-vomica, is affected even when
the quantity of the poison is exceedingly small.[110] It is extremely
doubtful whether any importance can be attached to this criterion, as
every one knows that the leech is apt to suffer from a variety of
obscure causes, and among the rest from some diseased states of the
body.

2. In the case of _the vomited matter_ or _contents of the stomach_
there are other and weightier objections to experiments on animals.—In
the first place, the poison which has caused death may have been either
in part or wholly vomited before-hand, or absorbed, or transmitted into
the intestines, or decomposed by the process of digestion. Secondly,
though abounding in the matter vomited or which remains in the stomach,
it may be so much diluted, as not to have any effect on an animal. And,
thirdly, the animal fluids secreted during disease are believed to act
occasionally as poisons.

The first two objections are so plainly conclusive as scarcely to
require any illustration. It may be well, however, to mention as a
pointed practical lesson, that Professor Orfila once detected a
considerable quantity of arsenic in the contents of the stomach, where a
prior investigation had shown that the same article produced no effect
on two animals, and where the reporters from this and other
circumstances declared, that in their opinion death was not owing to
poison.[111]

The last objection is a very important one; but there is reason for
suspecting that it has been a good deal exaggerated by medical
jurists.—Animal fluids are certainly poisonous when putrid. The repeated
and fatal experience of anatomists, together with the precise
experiments of M. Gaspard and M. Magendie,[112] leave no doubt that
putrid animal fluids, when introduced into an external wound, cause
spreading inflammation of the cellular tissue; and although Magendie
says he has found such fluids harmless when introduced into the stomach
of dogs,[113] it is probable, from their effects on man, that they will
act as irritants on animals not habituated to their use. I believe, too,
that independently of putrefaction, vomited matter or the contents of
the stomach may be apt to make dogs vomit on account of their nauseous
taste; and perhaps we may infer, that they will also cause some of the
other symptoms of poisoning with the irritants, particularly if not
vomited soon after being administered.—As to the influence of disease in
rendering the contents of the stomach deleterious, it is to be observed
that the effects just mentioned are probably owing to the influence of
disease on the secretions, but that beyond this we know very little of
the subject. In authors I have hitherto found only one fact to prove
that disease can render the contents of the stomach decidedly poisonous;
and on the negative side of the question there exists no facts at all.
Morgagni describes the case of a child who died of tertian ague, amidst
convulsions, and in whose stomach a greenish bile was found, which
proved so deleterious, that a little of it given with bread to a cock
caused convulsions and death in a few minutes, and a scalpel stained
with it, when thrust into the flesh of two pigeons, killed them in the
same manner.[114] It is not easy to say what to think of this
experiment; which, if admitted to the full extent of the conclusions
deducible from it, would lead to the admission, that disease may impart
to the secretions the properties of the most active narcotics. Farther
researches are certainly required before this admission can be made
unreservedly.

On the whole, it appears that in the present state of our knowledge,
experiments or accidental observations on the effects of the contents of
the stomach, or of vomited matter, on animals are equivocal in their
import. At the same time it may be observed, as with regard to articles
of food, drink, or medicine, that the effects of some poisons on man may
be developed so characteristically on animals by the contents of the
stomach, as to supply very pointed evidence indeed. Of the force of this
statement the following example is a striking illustration. In the case
of a girl, who was proved to have died of accidental poisoning with
laudanum, the inspector evaporated the contents of the stomach to
dryness, made an alcoholic extract from the residue, and giving this to
several dogs, chickens, and frogs, found that they were all made
lethargic by it, some of them oftener than once, and that a few died
comatose.[115] Facts such as these, agreeing so pointedly with the known
effects of the poison suspected, appear to me to yield evidence almost
unimpeachable.

3. The effects of _the flesh of poisoned animals_, eaten by other
animals, constitute the least conclusive of all the varieties of the
present branch of evidence. For the flesh of animals that have died of
poisoning is not always deleterious; while on the other hand flesh is
sometimes rendered so by natural causes, as will be seen in the Chapter
on Diseased and Decayed Animal Matter.

This subject stands much in need of careful and methodic investigation.
And it is of more practical importance than might be imagined at first
sight. For the question has actually occurred in a legal inquiry in this
country,—Whether poisoning in the human subject may be caused by the
flesh of a poisoned animal?

In regard to some poisons it is well established, that animals killed by
them may be eaten with impunity, such as game killed with the wourali
poison, or fish by cocculis-indicus. This seems the general rule. But it
is not clear that all poisons are similarly circumstanced.

The only systematic researches hitherto undertaken on this question are
some recently made at Lucca by Professor Gianelli; of which however I
have only seen an abstract. He found that the blood, urine, and lungs of
animals poisoned with arsenic acted as a poison on small birds, such as
sparrows, whether the parts were taken from the body while the animal
was alive, or after death; but that alcohol, cherry-laurel water,
corrosive sublimate, sulphate of copper, tartar-emetic, acetate of lead,
nitrate of silver, trisnitrate of bismuth, chloride of tin, sulphate of
zinc, laudanum, acetate of morphia, strychnia, and cantharides, had no
such effect.[116] Orfila has since shown some reason for doubting the
conclusiveness of Gianelli’s investigations; and on repeating them,
obtained such results as render it doubtful whether any reliance can be
put upon experiments made upon small birds.[117] Guérard however has
ascertained, that dogs, fed on the flesh and entrails of sheep which had
taken arsenic, were attacked with vomiting and purging, became reduced
in flesh, and at length would not eat what was put before them; but none
of them perished, or seem to have been seriously ill. Arsenic was
detected in their urine.[118]

The importance of the inquiry, which the preceding experiments are
intended to elucidate, will appear from the following singular case, for
the particulars of which I am indebted to the kindness of Mr. Jamieson
of Aberdeen, who was employed by the authorities to investigate it. An
elderly woman, who kept fowls which occasionally trespassed on a
neighbour’s fields, one morning observed four of them very sickly; and
in the course of the day they became so ill that she killed them. She
cleaned and prepared two of them for cooking, buried another, and gave
away the fourth to a beggar, who was afterwards lost sight of. Next day
soup made with the half of one of the fowls was given to a little girl,
who suffered severely from sickness and vomiting, and also to a cat,
which was similarly affected for the whole evening. On the day
afterwards the woman herself and a female lodger, took broth made with
what remained of the fowls, and also ate the gizzards; but the remainder
was thrown with the offal upon the dunghill. In the course of five or
six hours both women were attacked with severe illness. One had
sickness, vomiting and great coldness; but after encouraging the
vomiting with hot water and then taking some spirits, she got better in
the night-time, and next morning was pretty well. The other, who was the
owner of the fowls, was seized somewhat later than her friend with great
thirst and shivering, and next day with pains in the stomach, severe
sickness, and fruitless efforts to vomit. On the sixth day, when a
medical man first saw her, she had great pain throughout the abdomen,
much thirst, difficult breathing, a red, dry tongue, and a very
frequent, small pulse. Next day the pain and difficult breathing became
worse; and in the evening, after an attack of sneezing, she became
gradually insensible and motionless, in which state she remained till
the tenth day, when she expired. The stomach and intestines did not
present any distinct morbid appearance; but the vessels of the brain
were turgid, there were about two ounces of serosity in the lateral
ventricles, both corpora striata were softened anteriorly, and a clot of
blood as big as an almond was contained in the right anterior lobe of
the brain.—A judicial investigation being ordered, it was ascertained
that the fowl which the woman buried as well as the remains of the other
fowls which were thrown upon the dunghill, had been carried off. But on
searching the dunghill more carefully afterwards, the contents of one of
the crops, which had been taken out and examined by the lodger, were
discovered in the rubbish; and in the mass Mr. Jamieson detected a
considerable quantity of arsenic.

This incident happened in 1836. More lately the same gentleman met with
another extraordinary attempt of the same kind. A farmer, about to be
married, gave directions for killing in the evening some fowls which
were to be sent to the house of his bride where the ceremony was to take
place. The killing of them however was accidentally delayed; and next
morning, on the hen-house door being opened, the fowls ran furiously to
the well, drank water incessantly, and died in an hour. On examining the
bodies, Mr. Jamieson found arsenic in large quantity in their crops and
gizzards.

On each of these occasions a particular individual came under suspicion;
but the evidence against them was too slight to justify the authorities
in bringing a formal charge; and consequently the proceedings did not go
farther. In the former instance the evidence in favour of the flesh of
poisoned animals being sometimes poisonous is strong; and the history of
the woman’s case, although death seems to have been caused directly by
apoplexy, renders it probable that even dangerous results might accrue.

The preceding remarks will enable the medical witness to know under what
circumstances accidental observations or intentional experiments on
animals furnish satisfactory proof.

Before quitting the subject, however, I have to add, that there is
another purpose, besides procuring direct evidence, to which experiments
with animals may be applied with great propriety;—namely, the settling
disputed questions regarding the physiological and pathological
properties of a particular poison. The science of toxicology is not yet
by any means so perfect, but in particular cases topics may arise, which
have not hitherto been investigated, and which it may be necessary to
determine by experiment. Experiments on animals instituted for such
purposes by a skilful toxicologist are not liable to any important
objection. On the trial of Charles Angus at Liverpool in 1808, for
procuring abortion and murder by poison, a trial of great interest,
which will be referred to more particularly afterwards, it appeared from
the evidence of the crown witnesses, that the poison suspected,
corrosive sublimate, could not be discovered in the stomach by certain
methods of analysis; and that, although corrosive sublimate is a
powerful irritant, the villous coat of the stomach was not inflamed. But
then it was proved by experiments made by one of their number, Dr.
Bostock, that animals might be killed with corrosive sublimate without
the stomach being inflamed, and without the poison being discoverable
after death by the tests he used in the case.[119] An attempt was made
on the side of the prisoner to throw out this line of evidence as
incompetent, on the ground of the discrepant effects of poisons on man
and on the lower animals. But it was admitted by the judge, on the plea
that it was only to illustrate a general physiological fact, and not to
infer proof of poisoning. The importance of experiments on animals to
settle incidental physiological questions has lately been again
acknowledged in a very pointed manner in an English court of law: for a
set of experiments, to settle the question of the rapidity with which
hydrocyanic acid acts, was instituted before the trial by the medical
witnesses, at the request of the judge who was to try the case.[120]


                  SECTION V.—_Of the Moral Evidence._

It is not my object to treat under this head of the moral evidence
generally, which is required to establish a charge of poisoning. But as
it is well known that in criminal trials medical witnesses have for the
most part nothing to do with the moral proof, while at the same time in
cases of poisoning the medical and moral circumstances are always
intimately interwoven and apt to be confounded together, it is necessary
for me to specify those particulars of the moral evidence, which either
require some medical skill to appreciate them, or fall naturally under
the cognizance of the physician in his quality of practitioner. I shall
enter into greater details under this section than may perhaps appear to
the medical reader necessary, chiefly that I may redeem the pledge given
in the introduction to the lawyer and general reader, and endeavour to
show how powerful an instrument a medico-legal investigation may become
in skilful hands, for throwing light on almost every branch of the
evidence.

The moral or general proof in charges of poisoning is almost always
circumstantial only. The circumstances of which it usually consists
relate, 1. To suspicious conduct on the part of the prisoner before the
event, such as dabbling with poisons when he has nothing to do with them
in the way of his profession, or conversing about them, or otherwise
showing a knowledge of their properties not usual in his sphere of
life:—2. To the purchase or possession of poison recently before the
date of the alleged crime, and the procuring it in a secret manner, or
under false pretences, such as for poisoning rats when there are none on
his premises, or for purposes to which it is never applied:—3. To the
administration of poison either in food, drink, medicine, or
otherwise:—4. To the intent of the prisoner, such as the impossibility
of his having administered the poison ignorantly, or by accident, or for
beneficial purposes, alleged or not alleged:—5. To the fact of other
members of the family besides the deceased having been similarly and
simultaneously affected:—6. To suspicious conduct on the part of the
prisoner during the illness of the person poisoned,—such as directly or
indirectly preventing medical advice being obtained, or the relations of
the dying man being sent for, or showing an over-anxiety not to leave
him alone with any other person, or attempting to remove or destroy
articles of food or drink, or vomiting matter which may have contained
the poison, or expressing a foreknowledge of the probability of speedy
death:—7. To suspicious conduct after the person’s death, such as
hastening the funeral, preventing or impeding the inspection of the
body, giving a false account of the previous illness, showing an
acquaintance with the real or supposed effects of poison on the dead
body:—8. To the personal circumstances and state of mind of the
deceased, his death-bed declaration, and other particulars, especially
such as tend to prove the impossibility or improbability of suicide:—9.
To the existence of a motive or inducement on the part of the prisoner,
such as his having a personal quarrel with the deceased, or a hatred of
him,—his succeeding to property by his death, or being relieved of a
burthen by it,—his knowing that the deceased was with child by him.

Upon many of the particulars now enumerated, important evidence may be
derived from the medical part of the investigation; and not unfrequently
such evidence can be collected or appreciated only by means of a
medico-legal inquiry.

1 and 2. On the first two articles, suspicious conduct or conversation
on the part of the prisoner before the crime, and the possession or
purchase of poison by him, little or nothing need be said. The medical
witness may of course be asked whether the conduct or conversation
proved betokens an unusual acquaintance with poisons and their effects.
And his opinion may be referred to regarding the nature of suspected
articles found in the prisoner’s possession. As to the purchase of
arsenic under the false pretence of poisoning rats, it may be observed,
that a great deal more stress is usually laid on such evidence than it
seems to deserve; for there are few houses, in the country particularly,
which are not more or less infected by them. On the other hand, too
little weight is attached to the circumstance of the purchaser not
having warned his household of poison being laid. Such conduct ought in
my opinion to be accounted extremely suspicious; for so far as I have
remarked, the fear with which unprofessional persons regard the common
poisons is such, that I can hardly believe any master of a house would
actually lay poison without warning the servants and other inmates of
his having done so.

3. The next article, which relates to the proof of the administration of
poison, will require some details.

Direct proof of the administration of poison by the actual giver is very
rarely attainable, that part of the transaction being for the most part
easily concealed. The proof of this point is justly accounted, however,
a very important part of the evidence; nay, on some recent trials in
this country the prosecution has failed apparently for want of such
evidence, although the case was complete in every other particular. It
is generally constituted by a chain of circumstances, and these are
often strictly medical, as will now be shown by a few examples.

In the first place, pointed evidence as to the individual who gave the
poison may be derived from the chemical investigation,—for example, from
the comparative results of the analysis of the poisoned dish, and of the
articles of which it consisted. I am indebted to my colleague, Dr.
Alison, for the following excellent illustration from the case of
William Muir, who was condemned at Glasgow in 1812 for poisoning his
wife. In the course of the day on which she took ill she was visited by
a farmer of the neighbourhood, who had studied physic a little in his
youth. He learned from her that she had breakfasted on porridge a short
time before she felt herself ill, and that she suspected the porridge to
have been poisoned. He immediately procured the wooden bowl or _cap_ in
which the cottagers of Scotland keep the portion of meal used each time
for making the porridge; and finding in it some meal, with shining
particles interspersed, he wrapped a sample in paper, and took the
proper measures for preserving its identity. He then secured also a
sample from the family store in a barrel. The two particles were
produced by him on the trial; and from experiments made in court the
late Dr. Cleghorn was enabled to declare, that the meal from the bowl
contained arsenic, and that the meal from the barrel did not. These
facts, besides proving that the woman had next to a certainty taken
arsenic in the porridge, likewise, in conjunction with other slight
moral circumstances, established that the poison had been mixed with the
meal in the house, and on the morning when the deceased took ill, before
any stranger entered the house. The procedure of this farmer was
precisely that which ought to be followed by the medical practitioner in
a similar conjuncture.

An instance of an opposite description related by M. Barruel also
deserves notice, as showing how evidence of this kind may afford, in
otherwise suspicious circumstances, a strong presumption of accidental
poisoning. Sixteen people near Bressières in France having been severely
affected with vomiting and colic immediately after dinner, the bread,
which was suspected, was examined by Barruel, and found to contain a
little arsenic. The flour of which the bread was made had been taken
from a large store of it, which, on being examined, was also found to be
similarly impregnated. As it was extremely improbable that any one
either could or would poison so large a mass of flour, to attain any
malicious object, it was inferred that the arsenic had been mixed with
it accidentally, and that the accident might have arisen from grain
having been taken by mistake to the flour-mill to be ground, which had
been intended originally for seed, and sprinkled with arsenic to destroy
insects.[121]

It may be worth while observing, in the present place, that in the
instance of poisoned wine very important evidence may be obtained by
examining whether the wine with which the cork is impregnated contains
any traces of the poison. This method of investigation occurred to me in
a very singular case of poisoning with arsenic in champagne, which
happened in a baronet’s family in Scotland. In this instance, however,
such analysis was proved to be unnecessary; for the gentleman himself
brought the bottle from his cellar, broke the wires and drew the cork,
immediately before the wine was drunk.[122]

All evidence of the like nature, though it is at present often procured
from other sources, should, for obvious reasons, be invariably
collected, if possible, with the aid of a medical person. If again a
medical man is called to a patient evidently affected with suspicious
symptoms, and finds himself obliged to declare such to be his opinion,
his thoughts, as soon as he has given directions for the treatment,
should be turned towards that part of the evidence, for the securing of
which he is naturally looked to as the person best qualified by previous
education and his opportunities at the moment. With this view,
therefore, having ascertained in what articles it is possible for poison
to have been administered, he should at once endeavour to secure the
remains of the particular portion partaken of by his patient, as well of
the general dish, if it is an article of food, and of the ingredients of
which the dish was ostensibly made, not forgetting the salt with which
it was seasoned. A case occurred some years ago in the north of
Scotland, in which arsenic was administered in porridge by mixing it
with the salt.

It is of great consequence, before proceeding to analyze such articles,
for example suspected dishes,—to be particular in investigating every
thing connected with the cooking, serving, and eating of them. By doing
so, not only will the chemical analysis be facilitated, but likewise
facts in it will be accounted for, which might otherwise prove
embarrassing, and even lead to the drawing of false conclusions from the
result of the analysis. This statement is very well exemplified by the
following incident which occurred to myself. In 1827 a family in
Portobello were poisoned by the maid-servant; and it was believed, that,
for the sake of a trick, she had, while carrying to the oven the beef
subsequently used at dinner, maliciously mixed with it tartar-emetic or
some other poison. One-half of the beef having been preserved, and two
persons of the family having been very severely affected, Dr. Turner and
I, to whom the case was remitted, made little doubt that we should
discover the poison by chemical analysis: but we did not. Being
subsequently employed by the sheriff to inquire into the particulars, I
found that the poison had been mixed with the gravy, which had been
consumed almost to the last drop,—that the gravy had been poured over
the beef,—that the upper half of the beef had been eaten,—and that the
remainder which we analysed had been transferred upon a different plate
from that on which it was served for dinner. These particulars accounted
sufficiently for the poison not having been discovered.

Another mode in which the chemical part of the inquiry may contribute to
discover the individual who administered the poison is by a comparative
examination of the persons of the deceased and the accused. The
following very pointed illustration has been published by MM. Ollivier
and Chevallier of Paris.—A woman who lived on bad terms with her husband
was found dead on a roadside the morning after having been seen drunk in
his company in the neighbourhood. The mouth, throat, and gullet were
proved by a careful analysis to be corroded with nitric acid, the stains
and traces of which were also found on various parts of her dress, and
on the hair, neck, and arms, but not on her hands, and not lower down
the alimentary canal than the upper fourth of the gullet. Ollivier,
suspecting from these appearances, that she had not taken the acid
voluntarily, requested to see the husband; whereupon there were found on
his coat, trousers, and hands, a great number of stains, which, like
those on the deceased, were proved by chemical analysis to have been
produced by nitric acid. Here it was scarcely possible to avoid
inferring, that the man got these stains while endeavouring to force his
intoxicated wife to take the poison Marks of nail scratches were also
observed round the mouth and on the throat; whence it was reasonably
inferred, that, having failed in his original plan, he had suffocated
her with his hands.[123]

While these illustrations are given of the conclusiveness of the
chemical evidence in fixing the administration of poison on a particular
individual, it is essential likewise to observe that the same kind of
evidence may be at times equally conclusive of the innocence of a person
unjustly suspected. This obvious and important application of a chemical
inquiry is forcibly suggested by the following particulars of an
incident related by M. Chevallier:—An individual was accused by a woman
of having tried to poison her; and she represented that he had put the
poison into her soup, while it stood from one day to another in an iron
pot. On making a careful analysis of some of the soup which remained,
Chevallier found it so strongly impregnated with copper, that, supposing
the sulphate was the salt mixed with the soup, ten ounces must have
contained twenty-two grains. It then occurred to him, that it was
important to examine the iron pot, in which the poisoned soup was
represented to have been kept; for the probability was that a large
quantity of the copper, if any salt of that metal had really been
contained in the soup, would have been thrown down by the superior
affinity of the iron, and consequently that a coppery lining would be
found on the inside. He was led, however, to anticipate that no copper
would be found there, because there was no iron dissolved in the soup,
as would have been the case if copper had been precipitated from it by
the iron of the pot. And accordingly he not only found no copper lining
the inside of the pot; but likewise, on following the process described
by the accuser as the one pursued in cooking the soup and in
subsequently poisoning it, he satisfied himself by express trial that
there was nothing in the circumstances of the case which could have
prevented the iron from exerting its usual action on the salts of
copper. These conclusions, coupled with certain facts of general
evidence, proved substantially that the suspected person had nothing to
do with the crime charged against him; and he was therefore
discharged.[124] A case somewhat similar will be related under the head
of Imputed Poisoning.

In the second place, evidence as to the person who administered the
poison may be procured by considering the commencement of the symptoms,
in relation to the time at which particular articles have been given in
a suspicious manner by a particular individual. The import of facts of
this nature can be properly appreciated only by the medical witness; for
he alone can be acknowledged as conversant with the symptoms which
poisons produce, the intervals within which they begin to operate, and
the circumstances in which their operation may be put off or
accelerated.

Few cases will occur in which it is not possible to procure evidence of
the kind, when diligently sought for. It is often too very decisive in
its operation on judicial proceedings. In the case of Margaret Wishart
tried at the Perth Spring Circuit in 1827 for poisoning her blind
sister, a man who lodged with the prisoner and cohabited both with her
and with the deceased, appeared at first from general circumstances to
be implicated in the crime. He had left the house, however, on the
morning of the day before that on the evening of which the deceased took
ill; and he did not return till after her death. Now her illness
commenced suddenly and violently; and arsenic was the poison which
caused it.[125] It was quite clear, therefore, that the poison could not
have been administered, at least in a dangerous dose, so early as the
day before she was taken ill; and such I stated to be my opinion, on a
reference from the Lord Advocate. The evidence being also otherwise
insufficient, the man was set at liberty. In the case of Mrs. Smith
tried here in February of the same year, this branch of the evidence was
made the subject of question under more doubtful circumstances. The
deceased certainly died of poisoning with arsenic, and the prisoner was
strongly suspected of being the poisoner for many reasons, and among
others because, on the evening before the morning on which the deceased
took ill, the prisoner gave her in a suspicious manner a white-coloured
draught. Here the possibility of the draught having been the cause of
the symptoms must be admitted. But as they did not appear for eight
hours after the draught was taken, I stated in my evidence that it was
improbable the dose, if it contained arsenic at all, contained a
quantity sufficient to cause the violent symptoms and death which
followed.[126]

The correspondence in point of time between the appearance of symptoms
of poisoning, and the administration of suspicious articles by an
individual, constitutes still more decisive proof in a set of cases, in
which it is of great value, as the chemical evidence is generally
defective,—namely, where poisoning is attempted with repeated moderate
doses. If the several renewals or exacerbations of illness correspond
with the periods when suspicious articles have been given by the same
individual, the circumstantial evidence of the administration may be
even tantamount to direct proof. Thus, on the trial of Miss Blandy for
the murder of her father, it was proved, that Mr. Blandy on several
occasions, after the prisoner received certain suspicious powders from
her lover, was taken ill with vomiting and purging; and that on two
occasions recently before his death, when he got from his daughter a
bowl of gruel which contained a gritty sediment, he was attacked after a
very short interval with pricking and heat in the throat, mouth,
stomach, and bowels,—with sickness, vomiting, gripes, and bloody
diarrhœa.[127] Here the proof of administration by the prisoner was
complete.

These examples will show how the evidence of a particular person’s
criminality may be affected by the relation subsisting in point of time
between the commencement of the symptoms and the suspicious
administration of particular articles. But farther, the special period
at which the symptoms begin may even at times supply strong evidence of
his instrumentality, although there may be no direct proof from general
evidence of his having been concerned in administering anything whatever
in a suspicious manner. This statement is well exemplified by the case
of Mrs. Humphreys, who was convicted at the Aberdeen Autumn Circuit in
1830 for poisoning her husband, by pouring sulphuric acid down his
throat while he was asleep. It was clearly proved, as will be seen under
the head of sulphuric acid, that the deceased died of this poison; and
the administration was brought home to the prisoner in the following
singular manner. The only inmates of the house were the deceased, the
prisoner, and a maid-servant. The deceased got a little intoxicated one
evening at a drinking party in his own house; and after his friends all
left the house, and the street-door was barred inside, he went to bed in
perfect health, and soon fell fast asleep. But he had slept scarcely
twenty minutes, when he suddenly awoke with violent burning in his
throat and stomach; and he expired in great agony towards the close of
the second day. Now sulphuric acid, when it occasions the violent
symptoms observed in this instance, invariably excites them in a few
seconds, or in the very act of swallowing. It was, therefore, impossible
that the man could have received the poison at the time he was drinking
with his friends; and as he knew he had not taken any thing else
afterwards, and it was fully proved that he had been asleep before his
illness suddenly began,—it followed that the acid must have been
administered after he fell asleep, the accomplishment of which was
rendered easy by a practice he had of sleeping on his back with his
mouth wide open. But, after he gave the alarm, the door was found barred
as when he went to bed. Consequently no one could have administered the
poison except his wife or servant; and it was satisfactorily proved,
that no suspicion could attach to the latter. Such was one of the
principal train of circumstances, which, as it were by a process of
elimination, led to the inference that the wife was undoubtedly the
person who administered the poison. Other circumstances of a similar
tendency were also derived from the medical evidence; but these it is
unnecessary to detail at present. I have related the particulars of the
whole case fully elsewhere.[128] The prisoner strenuously denied her
guilt after being sentenced, but confessed before her execution.

4. The next article in the moral evidence relates to the intent of the
person who is proved to have administered poison. When the
administration is proved, little evidence is in general required to
establish the intent. It is sufficient that the giver knew the substance
administered was of a deadly nature; and in regard to any of the common
poisons this knowledge is sufficiently constituted by his simply knowing
its name.

In some cases, however, the exact nature of the poison is not
established with certainty; and then something else may be required to
prove the prisoner’s knowledge, and through that knowledge his intent.
In the case of Charles Munn, formerly alluded to [p. 50], arsenic was
the poison presumed to have been taken by the deceased. But the purchase
or possession of it by the prisoner was not for some time satisfactorily
established; neither was there any chemical evidence, the deceased
having lived forty days and upwards after taking the poison. It was
proved, however, that whatever it was which had been administered, the
prisoner knew very well that what he gave was deleterious; because he
persuaded the deceased, who was pregnant by him, to take it by assigning
to it properties which no drug either possesses, or is so much as
thought by the vulgar to possess. On one occasion he persuaded her that
it would show whether she was with child, and on another that it would
prevent people from knowing she was with child. In such cases, then,
good evidence may be derived from the arguments used by the giver to
persuade his victim to take the poison; and sometimes, as in the
instance now mentioned, it will lie with the medical witness to inform
the court whether or not the reasons assigned are false.

Sometimes it has been pleaded by the prisoner that he gave the poison by
mistake. In all such cases, if he descends to particulars, which he
cannot help doing, there is every likelihood that the falsehood of the
defence will be made evident by the particulars of the story not
agreeing with other particulars of the moral or medical evidence. At
present it is only necessary to allude to inconsistencies in his story
with the medical facts. No general rules can be laid down on the method
of investigating a case with a view to evidence of this kind: I must be
satisfied with an illustration from an actual occurrence. On the trial
of Mr. Hodgson, a surgeon, at the Durham Autumn Assizes in 1824, for
attempting to poison his wife, it was clearly proved, that pills
containing corrosive sublimate, and compounded by the prisoner, were
given by him to her in place of pills of calomel and opium, which had
been ordered by her physician. But it was pleaded by him, that, being at
the time intoxicated, he had mistaken, for the shop-bottle which
contained opium, the corrosive-sublimate bottle which stood next it.
This was certainly an improbable error, considering the opium was in
powder, and the sublimate in crystals. But it was not the only one which
he alleged he had committed. Not long after his wife took ill, the
physician sent the prisoner to the shop to prepare for her a laudanum
draught, with water for the menstruum. When the prisoner returned with
it, the physician, in consequence of observing it to be muddy, was led
to taste it, before he gave it to the sick lady: and finding it had the
taste of corrosive sublimate, he preserved it, analyzed it, and
discovered that it did contain that poison. The prisoner stated in
defence, that he had a second time committed a mistake, and instead of
water had accidentally used for the menstruum a corrosive-sublimate
injection, which he had previously prepared for a sailor. This was
proved to have been impossible; for the injection contained only five
grains to the ounce, while the draught, which did not exceed one ounce,
contained fourteen grains.[129]

I believe it must be allowed, that, as the medical inquiries preparatory
to trial are commonly conducted without the inspector being made
acquainted with the moral circumstances in detail, it is rarely possible
for him to foresee what points should be attended to, with the view of
illustrating the intent. But the case now related will show that it is
impossible for him to render his inquiries too minute or comprehensive;
and more particularly, it shows the propriety of ascertaining, whenever
it is possible, not only the nature but likewise the quantity of the
poison.

5. The next article among the moral circumstances,—the simultaneous
illness of other members of the family besides the person chiefly
affected,—depends for its conclusiveness almost entirely upon the
researches and opinion of the medical witnesses.

The fact, that several persons, who partook of the same dish or other
article, have been seized about the same time with the same symptoms,
will furnish very strong evidence of general poisoning. A few diseases,
such as those which arise from infection or from atmospheric miasmata,
may affect several persons of a family about the same time; and
hysteria, and epilepsy, have been communicated to several people in
rapid succession.[130] But I am not aware, that, among the diseases
which resemble well marked cases of poisoning either with irritants or
with narcotics, any one ever originates in such a way as to render it
possible for several persons in a family to be attacked simultaneously,
except through the merest and therefore most improbable accident.
Cholera perhaps is an exception. But when cholera attacks at one time
several people living together, it arises from bad food, and is properly
a variety of poisoning. In such cases, too, the fallacy may in general
be easily got the better of, by finding that the store or stock, from
which the various articles composing the injurious meal have been taken
was of wholesome quality.

Hence it may be laid down as a general rule, that, perhaps if two, but
certainly if three or more persons, after taking a suspected article of
food or drink, are each affected with symptoms, furnishing of themselves
presumptive evidence of poisoning, and have been seized nearly about the
same time, and within the interval after eating within which poisons
usually begin to act,—the proof of poisoning is decisive. Several late
cases might, in my opinion, have been decided by this rule. Thus it
might have decided the important case of George Thom tried at Aberdeen
in 1821 for poisoning the Mitchells, and likewise that of Eliza Fenning,
about whose condemnation some clamour was made in London in 1815. In
both instances, as will be mentioned under the head of arsenic, the
symptoms were developed so characteristically, that from them alone
poisoning with arsenic might have been inferred almost to a certainty.
But even if the symptoms had been somewhat less characteristic, all
doubt of general poisoning was set aside by the fact, that four persons
in the former case, and five in the latter, were similarly and
simultaneously affected, and all of them at an interval after eating,
which corresponded with the interval within which arsenic usually begins
to act.

Sometimes it happens, that while one or more of a party at a certain
meal suffer, others escape. Such an occurrence must not be hastily
assumed as inconsistent with poison having been administered at that
meal. For the guilty person may have slipped the poison into the portion
taken by the individual or individuals affected.

If it be proved that all who ate of a particular dish have suffered, and
all who did not have escaped, the kind of moral evidence now under
review becomes strongest of all. It is well for the medical jurist to
remember also, that such evidence is very useful in directing him where
chiefly he should look for poison.

At other times it happens that the several people affected, suffer in
proportion to the quantity taken by each of a particular dish. Too much
importance ought not to be attached to the absence of that relation; for
it has been already mentioned that habit, idiosyncrasy, and the state of
fulness of the stomach at the time, will modify materially the action of
poisons. But when present, it will often form strong evidence.—A good
illustration of what is now said may be found in the case of Thomas
Lenargan, tried in Ireland for the murder of his master, Mr. O’Flaherty.
He had for some time carried on an amour with O’Flaherty’s wife; and
afterwards, to get rid of the troublesome surveillance of the husband,
contrived to despatch him by poison. The crime was not suspected for two
years. Among the facts brought out on the trial the most pointed were,
that O’Flaherty’s daughter and two servants were affected at the same
time with the very same symptoms as himself; that they had partaken of
the same dish with him; that the severity of their several complaints
was in proportion to the quantity each had taken; and that others of the
family, who did not eat it, were not affected.[131]

Another remarkable instance of this kind has been recorded by Morgagni.
A clergyman, while travelling in company with another gentleman and two
ladies, was setting out one afternoon to resume his journey after dining
at an inn, when he was suddenly taken ill with violent pain in the
stomach and bowels, and soon after with vomiting and purging. One of the
ladies was similarly affected, but in a less degree; and likewise the
other gentleman, though in a degree still less: but the other lady did
not suffer at all. Morgagni found, that this lady was the only one of
the party who had not tasted a dish of soup at the commencement of
dinner. But he was puzzled on finding that the gentleman who suffered
least had taken the largest share of the soup, while the clergyman had
taken less than either of the two that were seized along with him. He
then remembered, however, that in the district where the accident
happened, it was the custom to use scraped cheese with the soup in
question; and on inquiry he was informed that they had each added to the
soup a quantity of cheese proportioned to the severity of their illness.
Here, therefore, Morgagni was led to suspect the presence of poison; and
accordingly, after the whole party had fortunately recovered, the
innkeeper acknowledged, that in the hurry of preparation, he had served
up to his guests cheese seasoned with arsenic to poison rats.[132] This
interesting anecdote shows, that the truth in such cases is not always
to be discovered without minute inquiry and considerable adroitness. In
the case of poisoning with arsenic in wine formerly alluded to,—where
all the individuals at table, to the amount of six, were severely
affected during dinner,—the soup was the article suspected, because all
had partaken of it; and, accordingly, the soup and vomited matter were
sent to me for analysis. On detecting a trace of arsenic in the vomited
matter, but none in the soup, I suggested that some other article might
have been used in common by the party, and mentioned the wine as a
probable article of the kind. It turned out that all had drunk a single
glass of champagne from a particular bottle; and in the wine remaining
in this bottle arsenic was found in the proportion of half a grain per
ounce.[133]

Cases of this nature are so instructive that no apology need be made for
mentioning one example more which lately came under my own notice. In
the case of Mary Anne Alcorn, convicted here in the summer of 1827, of
having administered poison to her master and mistress (a case already
referred to for another purpose, p. 75), it was proved that a white
powder was introduced in a suspicious manner into the gravy of baked
beef, which gravy was subsequently poured over the beef. Now the master
of the family dined heartily on beef, potatoes and rice-pudding, and
mixed the greater part of the beef gravy with his pudding; the mistress
ate moderately of the first slices of the beef, took very little gravy,
even to the beef, and none at all to the pudding; a little girl, their
niece, dined on pudding alone, without gravy; and the prisoner dined
after the family on the beef and potatoes. Accordingly the master
suffered so severely as for two or three days to be in danger of his
life, the mistress was also severely, but by no means so violently
affected, the little girl did not suffer at all, and the servant had
merely slight pain and sickness at stomach. The evidence thus procured
was exceedingly strong, more particularly when coupled with the fact,
that the beef used was half of a piece, the other half of which had been
used by the family two days before, without any ill consequences.

6. The next article of the moral evidence relates to suspicious conduct
on the part of the prisoner during the illness of the person poisoned.
Under this head it is necessary merely to state what I conceive to be,
with reference to the present branch of the proof, the duty of the
medical practitioner who happens to attend a case of poisoning.

In such a conjuncture he is undoubtedly placed in a situation of some
delicacy. But on considering the matter attentively, good reasons will
appear why he should adopt the course, which, I believe, our courts of
justice will expect of him, and keep some watch over the actions of any
individual who is suspected of having committed the crime. On the one
hand, no one else is by education and opportunities so capable of
remarking the motions of the different members of the family
dispassionately, without officiousness, and without being observed. And
on the other hand, it is undoubtedly a part of his private duty as
practitioner, to protect his patient against any farther criminal
attempts, as well as part of his public duty to prevent the vomited
matter and other subjects of analysis from being secretly put away or
destroyed. No one can be so occupied without many accessary particulars
coming under his notice. And certain it is, that on several trials the
practitioner has contributed, with great credit to himself, a
considerable part of the pure moral proof. For an example of discreet
and able conduct under these trying circumstances, the reader will do
well to refer to that of Dr. Addington, the chief crown witness, both as
to medical and moral facts, in the case of Miss Blandy.[134] It is
almost unnecessary to add, that in acting as now recommended, the
physician must conduct himself with circumspection, in order to avoid
giving unnecessary offence, or alarming the guilty person.

7, and 9. On the seventh article, which respects the conduct of the
prisoner after the death of the deceased, and on the ninth, which
relates to the existence of a motive or inducement to the crime, nothing
need be said here. But on the

8th article of the moral evidence,—comprehending the death-bed
declaration of the deceased, his state of mind, his personal
circumstances and other points which prove the possibility or
impossibility of voluntary poisoning—a few remarks are required, because
an important and little understood part of the practitioner’s duty is
connected with this branch of the proof.

The question as to the possibility of the poisoning being voluntary is
one upon which the medical attendant will be expected to throw some
light, and into which he will also naturally inquire for his own
satisfaction. In doing so his attention will be turned to circumstances
purely moral, which may not only decide that question, but may also
criminate a particular individual. His inquiries must therefore be
conducted with discretion, and for obvious reasons should be confined as
much as possible to the patient himself. They are to be conducted not so
much by putting questions, as by leading him to disburden his mind of
his own accord; and it is well to be aware, that there is no one of whom
a patient is so ready to make a confident on such an occasion as his
medical attendant.

If disclosures of consequence are made, and the attendant should feel it
his duty to look forward to the future judicial proceedings and to the
probability of his appearing as a witness, he ought to remember the
general rule is, that his account of what the patient told him is not
evidence in the eye of the law, unless it was told under the
consciousness of the approach of death. Of late, however, the rigour of
this principle in law has been occasionally departed from in Scottish
practice; and in regard to medical facts ascertained in the way here
mentioned, many strong reasons might be assigned for such relaxation.
Evidence of the kind is technically called the death-bed declaration of
the deceased, and is justly accounted very important.

Here it is right to take notice of a part of the death-bed evidence,
although it does not properly belong to the question of suicide, because
it should always be collected if possible by the medical attendant, and
with much greater care than is generally bestowed on it even by him—I
mean the history of the symptoms previously to his being called in. On
this part of the history, including particularly the time and manner in
which the illness began, medical conclusions of extreme consequence are
often subsequently founded: On a single fact or two may depend the fate
of the prisoner. It is not enough, therefore, in my opinion, that such
evidence formed a part of the death-bed declaration. If a fact derived
at second hand from the deceased, and stated too by him from memory, is
a material element of any of the medical opinions on the trial, it is of
much importance that the information be procured by a medical man; and
that the person who procured it, whether professional or not, was aware
at the time of the probability of its becoming important. Such evidence,
although not collected with these precautions, is admissible; but I have
so often had occasion to witness the carelessness with which the
previous history of cases is inquired into both in medical and
medico-legal practice, that I do not see how it is possible to put trust
in evidence of the kind, unless it bear marks of having been collected
with care, and under an impression of its probable consequence. These
statements are well illustrated by the following example:—On the trial
of Mrs. Smith for poisoning her maid-servant with arsenic, it was proved
that some drug was administered by the prisoner in a suspicious manner
on a Tuesday evening. Now it appeared at the trial improbable that this
drug contained a fatal dose of arsenic, because to her fellow-servants,
of whom one slept with her, and others frequently visited her, the
deceased did not appear to be ill at all for eight hours after, or
seriously ill for nearly a day. On the contrary, however, a surgeon, who
was called to see her on the following Saturday, a few hours before her
death, deposed that, according to information communicated by herself,
she had been ill with sickness, vomiting, purging, and pain in the
stomach and bowels since the Tuesday evening. This evidence, if it could
have been relied on, would have altered materially the features of the
case, as it would have gone far to supply what all the medical witnesses
considered defective, namely, proof of the administration. But at the
time the surgeon made his inquiries, he did not even suspect that the
girl laboured under the effects of poison. Neither he therefore nor his
patient could have been impressed with that conviction of the importance
of the information communicated, which was necessary to insure its
accuracy, particularly as it related to a matter usually of so little
consequence in ordinary medical practice as the precise date of the
commencement of an illness; and it would consequently have been rash to
adopt it in face of more direct and contrary evidence. Any one who
examines the details of this trial as I have reported them, will at once
see how much the case turned on the point now alluded to.[135]




                              CHAPTER III.
             OF IMAGINARY PRETENDED, AND IMPUTED POISONING.


The present seems the most convenient place for noticing the general
mode of procedure by which the medical jurist may detect cases of
imaginary, feigned, and imputed poisoning. It is by no means easy to lay
down rules for the investigation of cases suspected to be of such a
kind. But an attempt will be made to state the leading points to be
attended to, and to illustrate them by the circumstances of a few
examples of each variety.

_Imaginary poisoning_ should rarely be the occasion of deception or
embarrassment. The same wandering of the imagination which has led to a
belief of injury from poison, will commonly also lead to such
extravagant notions relative to the mode of administration and the
symptoms, as will infallibly point out the true nature of the case to
one who is well acquainted with the real effects of poisons. It is easy,
nevertheless, to conceive cases which may be embarrassing; and
certainly, in every instance, the physician should proceed in his
inquiries with caution.

It appears to me that in the first place, without seeming to take up at
once the conviction of his patient, he should scrupulously abstain from
treating it lightly, and should on the whole act rather as if he
suspected poison had been given. Allowing his patient therefore
apparently credit for the truth of his suspicions, the medical attendant
should request him to give a full history of existing symptoms, of their
origin and progress, of their relation in point of time to various
meals, and of the mode and vehicle in which the supposed poison was
administered. No unprofessional person can possibly go through such a
narrative, without stating many circumstances which are wholly
irreconcilable with the idea of poisoning generally, and still more of
the administration of a particular poison.

I have met with two instances of imaginary poisoning, the nature of
which was thus at once made obvious by a host of impossibilities in the
narrative of the patient. One of these may be here given as an example.
An elderly lady, who had certain expectancies of the death of a
relation, conceived that the family of her relative had resolved to
defraud her of her supposed rights. She afterwards imagined that an
attempt was made to poison her, and camphor was the poison she fixed on
as the article which had been administered. In its general or moral
particulars the narrative was all plausible and suspicious enough; but
unluckily for its consistency, she stated that the poison could only
have been given in wine,—that she did not remark any particular taste in
the wine,—that her illness did not begin till the day after she took it;
and although she alleged, without any leading question on my part, that
camphorous perspiration was exhaled on the subsequent day, the whole
train of symptoms differed entirely in every other respect from a case
of poisoning, and resembled closely in their origin and progress a case
of slight general fever. The incompatibility of her story with the idea
of poisoning with camphor will be readily understood by referring to
what is afterwards said of the effects of that substance.

_Feigned_ or _pretended poisoning_ is more apt to escape suspicion, and
when suspected is commonly more difficult to develope satisfactorily;
for the actor has it in his power to lay his plans with care, and even
to become acquainted with the properties of the poisons whose effects he
intends to feign. Still he can rarely enact his part so well as to
deceive a skilful physician both by existing symptoms and by his history
of their origin and progress; much less can he contrive his scheme so
adroitly that it shall not be unfolded by the refinements of chemical
analysis.

The investigation of such a case will be directed of course in the first
instance to the state and progress of the symptoms. Here, as in
imaginary poisoning, it is of moment to conceal from the individual the
suspicion entertained of his falsehood. For even if a person who has
actually taken poison knows he is unjustly suspected of feigning, it is
not improbable that he might try to mend his story with impossibilities,
and so lead the physician into error. In a case of feigned poisoning an
excellent mode of investigation is, after hearing out the individual’s
own story, to put a number of questions involving an alternative answer,
one alternative being compatible and the other incompatible with the
alleged nature of his illness. No unprofessional person can stand such a
system of interrogation, if skilfully pursued. Not only will his answers
be often wrong; but likewise his manifest perplexity how to answer will
of itself supply evidence of falsehood.

In the next place, great attention must be paid to the chemical
analysis. A person who feigns poisoning will commonly produce the
poisoned remains of a dish, or some other article, which he represents
himself to have swallowed. Sometimes the substance contained in it will
prove on analysis not to be poison at all, as in an instance I remember
reading some years ago in a London newspaper of pretended poisoning with
arsenic, where the dregs of a bowl of gruel contained, not arsenic, but
finely pounded glass. Sometimes the quantity of a real poison contained
in the remains of a dish may indicate, in what is said to have been
swallowed, a portion wholly incompatible with the mildness or severity
of the symptoms. Sometimes the vomited matter, even the matter first
vomited, may not contain any of the alleged poison. Sometimes poison
found in matter alleged to have been vomited may yield compounds during
analysis which are not animalized, showing that it never was in the
stomach. Sometimes the quantity of poison contained in such matter may
be greater than that alleged to have been taken. Sometimes the quantity
contained in the first matter vomited may be less than that contained in
what is vomited or said to be vomited subsequently. By these and many
other such inconsistencies the falsehood of the story may be
unequivocally unfolded.

The following example will illustrate some of the rules now laid down. A
young married female, in the seventh month of pregnancy, having been
discovered by her friends to be secretly addicted to dram-drinking,
appeared to be much annoyed in consequence of the discovery; and one
evening was found apparently very ill by her husband on his return from
work. She represented that she had taken arsenic with a view to
self-destruction, that she was in great torture, and that she was sure
she must soon die. It was accordingly found, on reference to a
neighbouring apothecary, that she had the same forenoon purchased about
a drachm and a half of arsenic for the pretended purpose of poisoning
rats; and in the bottom of a teacup, in which she said she mixed it,
there was left a small quantity of white powder, that proved on analysis
to be pure oxide of arsenic. Notwithstanding these strong facts, the
mildness of the symptoms and the composure with which she complained of
her tortures led her friends to suspect she was feigning. On
investigating her case I first ascertained, in farther corroboration of
her story, that the powder was nowhere to be found. But she then stated
in reply to questions involving an alternative answer, that the arsenic
had a sour taste, and that the pain began in the lower part of the
belly, and spread upwards. She likewise said that she vomited a mouthful
or two into a chamber-pot twenty minutes after taking the poison; that
she vomited no more till the apothecary was sent for, who gave her
emetics of sulphate of zinc, carefully preserving the discharges; and
that she only vomited when emetics were given. When I first saw her,
five hours after the alleged date of the taking of the arsenic, the skin
was warm and moist, the face full and flushed, the pulse frequent and
firm, the muscular strength natural. The chamber-pot contained only a
small quantity of the fæces of a child and apparently a little water,
but no vomited matters, and no white powder. The fluid discharged in
presence of the apothecary was found on careful analysis to contain a
large quantity of zinc, but not an atom of arsenic. She gradually
recovered from the illness under which she laboured at the time I saw
her, and in two days she admitted she was quite well, but continued to
insist that she had taken the poison.—M. Tartra has related a singular
case of the same kind, where a young woman feigned poisoning with nitric
acid, and was not detected for several days.[136]

_Imputed poisoning_ differs in general from feigned poisoning only in so
far as the symptoms which are feigned are imputed to the agency of
another.

The imputation of the crime of poisoning by feigning or actually
producing the symptoms, and contriving that poison shall be detected in
the quarters where in actual cases it is usually sought for, has been
not unfrequently attempted. Two important continental cases have already
been referred to for other purposes [pp. 66, 76]; and I may here relate
the heads of two English cases, which are of great interest, and will
serve to illustrate the mode of procedure in such circumstances.

The first of these, which I have related elsewhere in detail,[137] is a
striking example of the power of science in eliciting the truth, and
redounds highly to the credit of Mr. Thackrah, the medical gentleman who
conducted the investigation.

Samuel Whalley was indicted at York Spring Assizes in 1821, for
maliciously administering arsenic to Martha King, who was pregnant by
him. The woman King swore, that the prisoner, after twice trying, but in
vain, to prevail on her to take drugs for the purpose of procuring
abortion, sent her a present of tarts, of which she ate one and a
half,—that in half an hour she was seized with symptoms of poisoning
with some irritant poison,—and that she continued ill for a long time
after. Mr. Thackrah found arsenic in the tarts that remained untouched,
and likewise in some matter that was vomited in his presence after the
administration of an emetic, as well as in other vomited matters which
were preserved for him between his first and second visits. Her
appearance, however, did not correspond with the complaint she made of
her sufferings, her pulse and tongue were natural, and on careful
investigation the following inconsistencies were farther detected. 1.
She said she felt a coppery taste in the act of eating the tarts, a
taste which arsenic certainly does not possess. 2. From the quantity of
arsenic in the tarts which remained she could not have taken above ten
grains, while even after repeated attacks of vomiting, the alleged
matter subsequently preserved contained nearly fifteen grains. 3. The
matter first vomited contained only one grain, while the matter alleged
to have been vomited subsequently contained fifteen grains. 4. The time
at which these fifteen grains were alleged to have been vomited was not
till between two and three hours after the symptoms began; in which case
the symptoms would before that time have been in all probability
violent. The prisoner was acquitted, and the prosecutor and another
woman who corroborated her deposition afterwards confessed that they had
entered into a conspiracy to impute the crime to him, because he had
deserted her on finding she was too intimate with other men.

Another case not less interesting in its details was communicated to me
by my colleague Dr. Traill, who was consulted by the medical attendant,
Mr. Parr of Liverpool. A man accused his sister-in-law of administering
poison in his tea. He stated that he was seized with pain in the stomach
and uneasiness in the head half an hour after taking the tea; and when
visited soon after, the countenance was anxious, the skin pallid, the
pulse frequent, the throat red; and while Mr. Parr was examining the
throat, a quantity of matter was vomited, containing a white, gritty,
crystalline substance, which was afterwards ascertained to be oxalic
acid. The following circumstances, however, proved that the poison could
not have been given in the tea. The man alleged that he remarked in the
very first mouthful an acrid taste, followed by sweetness, which is not
the taste of oxalic acid. Notwithstanding this warning, he drank the
greater part of the tea. He stated that the poison was dissolved in the
tea, yet he vomited some oxalic acid in the solid form. Granting he was
mistaken in supposing the whole poison dissolved, the quantity swallowed
must in that case have been large; and nevertheless the symptoms were
mild, though no vomiting took place for about an hour, and next day he
was almost well. Four other individuals had tea at the same time from
the same tea-pot, without sustaining any harm; and what remained of the
infusion did not contain any oxalic acid. Finally, his niece took what
he left of his tea in the cup, without remarking any unusual taste; and
in the unwashed cup not a trace of oxalic acid could be detected. It was
quite plain, therefore, that the man’s accusation was false; and certain
points of general evidence, coupled with the medical facts, afterwards
proved that he must have taken the oxalic acid himself.

It has been alleged, that attempts have been made to impute the crime of
poisoning by introducing poisonous substances into the body after death;
and although I have not been able to find any actual instance of such
ingenious atrocity mentioned by authors, it must be acknowledged to be
quite possible; and the medical jurist should therefore be prepared for
the requisite investigations. Every case may be clearly made out by
attending to the relative effects of poisons on the dead and on the
living tissues;—a subject which will receive some notice under the head
of the principal poisons in common use.




                              PART SECOND.
                         OF INDIVIDUAL POISONS.




                               CHAPTER I.
                   OF THE CLASSIFICATION OF POISONS.


After the preliminary observations on General Poisoning, I proceed next
to treat of Poisons Individually. The subsequent remarks will be
confined in a great measure to the most common poisons, which will be
examined minutely. The rest being mere objects of curiosity, and hardly
ever taken by man either intentionally or by accident, it will be
sufficient to point out their leading properties.

It may be well to point out in the first instance the poisons in most
general use. These will appear from the following Tables. The first is
compiled from a Parliamentary Return of the cases of fatal poisoning
brought before the coroners of England in two years ending with 1838.

        1. _Arsenical_               White arsenic       185
                                     Yellow arsenic        1
                                                          —— 186
        2. _Acids_                   Sulphuric acid       32
                                     Nitric acid           3
                                     Oxalic acid          19
                                                          ——  54
        3. _Mercurials_              Corrosive sublimate  12
                                     White mercury         1
                                     Turbith-mineral       1
                                     Mercury (?)           1
                                                          ——  15
        4. _Other mineral irritants_ Tartar-emetic         2
                                     Sulphate of iron      1
                                     Chloride of tin       1
                                     Subacetate of lead    1
                                     Bichrom. of potash    1
                                     Percussion powder     1
                                     Carbonate of potash   1
                                     Black-ash             1
                                                          ——   9
        5. _Veget. irritants_        Colchicum             3
                                     Hellebore             1
                                     Savin                 1
                                     Cayenne               1
                                     Castor seeds          1
                                     Morison pills         1
                                                          ——   8
        6. _Anim. irrits._           Cantharides           2
        7. _Opium_                   Opium or Laudan.    180
                                     Opium & nitric acid   1
                                     Poppy-syrup           4
                                     Godfrey’s Cordial     6
                                     Morphia               1
                                     Acetate of morphia    1
                                                          —— 193
        8. _Hydrocyanic acid_        Med. Hydroc. acid    27
                                     Do. and Laudanum      1
                                     Ess. oil of Almonds   5
                                     Bay-leaves            1
                                                          ——  34
        9. _Other veget. Narcotics_  Nux-vomica            3
                                     Strychnia             2
                                     Belladonna            2
                                     Hemlock               1
                                     Monkshood             2
                                     Spirits               4
                                     Fungi                 4
                                                          ——  18
       10. _Narcot. gases._          Coal-gas                  2
       11. Unascertained                                      22
                                                             ———
                                            Total            543

In France, in seven years, from 1825 to 1831, inclusive, there were 216
trials for poisoning, at which 273 persons were charged with the crime,
and only 102 condemned. In 94 cases occurring between November 1825 and
October 1832, the substances employed were as follows.[138]

                         Arsenic             54
                         Orpiment             1
                         Verdigris            7
                         Corrosive sublimate  5
                         Fly-powder           3
                         Tartar-emetic        1
                         Sulphate of zinc     1
                         Acetate of lead      1
                         Cerusse              1
                         Mercurial ointment   1
                         Cantharide
                         Nux-vomica           4
                         Opium                1
                         Sulphuric acid       1
                         Nitric acid          1
                         Unascertained        5

In the subsequent seven years there were 218 trials, and 153 prisoners
condemned. Among 194 of these the following were the poisons used.[139]

                        Metallic arsenic      5
                        Arsenious acid      132
                        Arsenite of copper    1
                        Compounds of copper  13
                        Corrosive sublimate  10
                        Artificial orpiment   3
                        Sulphate of zinc      1
                        Tartar-emetic         1
                        Cerusse               1
                        Sulphuric acid        5
                        Nitric acid           2
                        Muriatic acid         1
                        Hydrocyanic acid      1
                        Ammonia               1
                        Belladonna            1
                        Opium                 3
                        Morphia               1
                        Nux-vomica            1
                        Cantharides          10

In Denmark, in five years ending with 1835, there were 99 cases of
poisoning of all sorts, 16 by arsenic, 74 by sulphuric or nitric acid, 4
by potash, 1 by an unascertained caustic substance, 2 by opium, 1 by
litharge, and 1 by copper. Only 5 cases, namely, 3 by arsenic and 2 by
sulphuric acid, were cases of murder, or attempt to murder.[140]

The classification of poisons has hitherto defied the ingenuity of
toxicologists. Formerly it was thought sufficient to arrange them in
three great classes, according as they are derived from the mineral, the
vegetable, or the animal kingdom. It is evident, however, that the only
sound basis of arrangement is their action on the animal economy; for
such a classification is the only one which can be useful in practice.
Now, when we consider what has been said on their mode of action, or the
symptoms produced in consequence of that action, it must at once be
perceived, that no system founded on either of these circumstances can
be logically correct. It would be very desirable, if their mode of
action could be adopted as the basis of arrangement; but both reasoning
and experience have proved this to be impracticable. One very distinct
class indeed might be formed of purely local poisons, comprehending the
mineral acids, the fixed alkalies, and one or two of their chemical
compounds. But a vast proportion of the other poisons which act locally
have also a general or remote action; and on the other hand there are
few of the latter description which do not likewise act locally. Hence
if all which possess this double action were arranged in one class, that
class would include nine-tenths at least of known poisons; so that, in
truth, the labour of classification would still remain to be overcome.

It would be even more fruitless to attempt an arrangement of poisons
according to their medium of action; for no sure criterion is known, by
which a poison acting through direct transmission of an impulse along
the nerves can be distinguished from one that acts by entering the
blood.

Neither is the embarrassment of the toxicologist materially less, if he
attempts to classify poisons according to the symptoms they induce in
man. This is the principle now generally followed, and which in common
with others I shall pursue. But the reader will be at no loss to
discover that the partitions which separate the classes are exceedingly
slight, and that very many poisons might be arranged without impropriety
in either of two classes.

The preceding statements show the impossibility of founding a good
system of arrangement on the only basis which can be acknowledged
philosophical and practical; and consequently, that, as the science of
toxicology now stands, we must altogether despair of forming one that
shall be even moderately satisfactory.

On the whole I see no reason for deviating from the classification
adopted in the first edition of the present work, being a modification
of that previously followed by Professor Orfila. In this classification
poisons are divided into irritants, narcotics, and narcotic-acrids.

The class of irritants includes all poisons whose sole or predominating
symptoms are those of irritation or inflammation; the narcotics those
which produce stupor, delirium, spasms, paralysis, and other affections
of the brain and nervous system; and the narcotico-acrids those which
cause sometimes irritation, sometimes narcotism, sometimes both
together. Some writers still adopt a fourth class, called septics,
because they give rise to putrefaction in the living body. But modern
physiology will scarcely sanction the continuance of such a class of
poisons. For assuredly no substance can cause putrefaction in the living
body.




                              CHAPTER II.
                              CLASS FIRST.
                     ON IRRITANT POISONS GENERALLY.

The class of irritant poisons comprehends all whose sole or predominant
action consists in exciting irritation or inflammation. That is, it
comprises both those which have a purely local, irritating action, and
likewise many which also act remotely, but whose most prominent feature
of action still is the inflammation they excite wherever they are
applied.

This subject will be introduced with an account of the general symptoms
and morbid appearances caused by the irritants, and a comparison of
these with the symptoms and morbid appearances of the natural diseases
which are chiefly liable to be confounded with irritant poisoning, or
mistaken for it.


SECTION I.—_Of the Symptoms of the Irritant Poisons, compared with those
                         of natural diseases._

The symptoms caused by the irritating poisons, taken internally, are
chiefly those of violent irritation and inflammation of one or more
divisions of the alimentary canal.

The mouth is frequently affected, especially when the poison is easily
soluble, and possesses a corrosive as well as irritating power. The
symptoms referrible to the mouth are pricking or burning of the tongue,
and redness, swelling and ulceration of the tongue, palate, and inside
of the cheeks.

The throat and gullet are still more frequently affected; and the
affection is commonly burning pain, sometimes accompanied with
constriction and difficulty in swallowing, and always with redness of
the visible part of the throat and gullet.

The affection of the throat and mouth precedes every other symptom when
the poison is an active corrosive, and more particularly when it is
either a fluid poison or is easily dissolved. Nay, sometimes burning
pain of the mouth, throat, and gullet occurs during the very act of
swallowing.—On the contrary if the poison is soluble with difficulty,
and is only an irritant, not a corrosive, and still more if it is only
one of the feebler irritants, the throat is frequently not affected
sooner than the stomach, occasionally not at all.

The stomach is the organ which suffers most invariably from the
operation of irritant poisons. The symptoms referrible to their
operation on it are acute and general burning pain, sometimes
lancinating or pricking pain,—sickness, vomiting, tenderness on
pressure, tension in the upper part of the belly, and occasionally
swelling. Of these symptoms the sickness is generally the first to
develope itself. In the instance of corrosive irritants pain commonly
commences along with it. The matter vomited is at first the contents of
the stomach, afterwards tough mucus, streaked often with blood and
mingled with bile, frequently clots of purer blood. The powerful
corrosives affect the stomach the moment they are swallowed; irritants
which are either liquid or very soluble also affect it very soon; but
the more insoluble irritants, such as arsenic, generally do not begin to
act till half an hour or even more than a whole hour has elapsed.—The
stomach may be affected without any other part of the alimentary canal
participating in the injury; but much more frequently other parts suffer
also, and in particular the intestines.

The action of irritant poisons on the intestines is marked by pain
extending over the whole belly, sometimes even to the anus. This pain,
like that of the stomach, is often a sense of burning; but it is also
frequently a pricking or tearing pain, and still more frequently a
twisting, intermitting pain like that of colic. It is seldom attended
with much swelling, but often with tension, and tenderness of the whole
belly; and at times the inflammatory state of the mucous coat of the
intestines is clearly indicated by excoriation of the anus and prolapsus
of the rectum, which is of a bright red colour. The pain of the bowels
is most generally attended by purging, rarely with constipation,
frequently with tenesmus. The matter discharged, after the alimentary
and feculent contents have passed, is chiefly a mucous fluid, often
abundant, often also streaked with blood or mixed with considerable
quantities of blood. In some cases the intestines are affected when no
other part of the alimentary canal suffers, not even the stomach. But
much more generally the stomach and intestines are affected together.

In a few very aggravated cases of poisoning with the irritants the whole
course of the alimentary canal, from the throat to the anus, is affected
at one and the same time.

The symptoms now briefly enumerated are accompanied in almost every
instance with great disturbance of the circulation—quick, feeble
pulse—excessive prostration of strength,—coldness, and clammy moisture
of the skin.

The other symptoms, which are often united with the preceding, do not
belong to the irritants as a class. Perhaps, however, among the symptoms
of the class may be mentioned those of irritation and inflammation of
the windpipe and lungs, and those of irritation in the urinary organs. A
great number of the irritant poisons cause hoarseness, wheezing
respiration, and other signs which indicate the spreading of the
inflammation of the throat to the windpipe: some likewise cause darting
pains throughout the chest: and not a few are very apt to cause
strangury and other signs of inflammation of the urinary passages.

Of the effects of the irritants when applied externally little need be
said at present. Their most striking external symptoms will be noticed
under the head of one of the orders of this class, the vegetable acrids.
In the chapter on the local action of poisons some account was given of
the several effects which are produced by the application of poisons to
the skin. It is there stated that some produce merely redness, that
others cause blistering, that others bring out a crop of deep-seated
pustules, that others corrode the tissues chemically, and so give origin
to a deep slough, and that others excite spreading inflammation of the
cellular tissue under the skin and between the muscles.

Such is a general view of the symptoms caused by the irritant poisons.
This topic will be afterwards taken up in detail under the head of the
several species. At present an important subject remains for
consideration, namely, the natural diseases whose effects are apt to be
mistaken for the effects of poison. The remarks now to be made might be
extended to many diseases. In fact, they might be extended to all which
prove fatal suddenly, for all such diseases are apt in peculiar
circumstances to give rise to a suspicion of poisoning. But those only
will be here noticed which occasion the greatest embarrassment to the
medical jurist, and which are most likely to come under his review in
courts of law. They are the following:—Distension and rupture of the
stomach; rupture of the duodenum, biliary ducts, uterus, or other organs
in the belly; the effects of drinking cold water; bilious vomiting and
common cholera; malignant cholera; inflammation of the stomach;
inflammation and perforation of the intestines; inflammation of the
peritonæum; spontaneous perforation of the stomach; melæna and
hæmatemesis: colic, iliac passion and obstructed intestine.

1. _Distension of the Stomach._—Mere distension of the stomach from
excessive gluttony may cause sudden death. Generally indeed the symptoms
and appearances in the dead body show that death is the consequence of
apoplexy; but sometimes not. In order to preserve the continuity of the
succeeding remarks on the diseases of the stomach which imitate
poisoning, it may be useful to consider in the present place all the
varieties of the effects of distension.

Excessive distension of the stomach, then, sometimes causes sudden death
by inducing apoplexy, which is commonly of the congestive kind,—that is,
without rupture of vessels. Mérat has related an instructive case of
this kind. A man in good health, while greedily devouring an excellent
dinner, became suddenly blue and bloated in the face; a clammy sweat
broke out over his body; and he died almost immediately. On dissection
the stomach was found enormously distended with food, and the vessels of
the brain were so gorged, that the brain appeared too large to be
contained within the skull.[141]

There is reason, however, to suppose that death from distension is the
consequence not always of apoplexy,—but sometimes of an impression on
the stomach itself. Sir Everard Home relates the case of a child, who,
being left by its nurse beside an apple-pie, was found dead a few
minutes afterwards, and in whose body no appearance of note could be
discovered, except enormous distension of the stomach with the pie.—A
still more distinct case in point forms the subject of a medico-legal
report by Wildberg. A corpulent gentleman died suddenly fifteen minutes
after dinner; and as he lived on bad terms with his wife, a suspicion
arose that he had been poisoned. His wife said that he fell asleep
immediately after dinner; but had not slept many seconds, when he
suddenly awoke in great anguish, called out for fresh air, exclaimed he
was dying, and actually expired before his physician, who was instantly
sent for, could arrive. Wildberg found the stomach so enormously
distended with ham, pickles, and cabbage-soup, that, when the belly was
laid open, nothing could be seen at first but the stomach and colon.
Some white powder, found on the villous coat of the stomach, was at
first suspected to be arsenic; but it proved on analysis to be merely
magnesia, which the gentleman had been in the habit of taking
frequently. The diaphragm was pushed high into the chest by the
distended stomach. There was not any particular congestion in the brain.
Wildberg very properly ascribed death to simple over-distension of the
stomach.[142]—In all such cases the symptoms may be suspicious; but when
carefully considered they can scarce be said to resemble closely the
effects of irritant poisoning; and at all events the appearances in the
dead body will at once distinguish them.

2. _Rupture of the Stomach_ is not a common occurrence; but it sometimes
imitates in its symptoms the effects of the irritant poisons.

It is generally the consequence of over-distension, combined with
efforts to vomit. The cause of it seems to be, that the abrupt turn
which the gullet makes in entering an excessively distended stomach acts
as a valve, so that the contents cannot be discharged by vomiting. A
case of this kind is related by M. Lallemand in his Inaugural
Dissertation at Paris in 1818.[143] A woman convalescent from a tedious
attack of dyspepsia, being desirous to make amends for her long
privations as to diet, ate one day to satiety. Ere long she was seized
with a sense of weight in the stomach, nausea, and fruitless efforts to
vomit. Then she all at once uttered a piercing shriek, and exclaimed
that she felt her stomach tearing open; afterwards she ceased to make
efforts to vomit, soon became insensible, and in the course of the night
she expired. In the fore part of the stomach there was a laceration five
inches long; and a great deal of half-digested food had escaped into the
cavity of the abdomen. The coats of the body of the stomach were
healthy; but the pylorus or opening into the intestines was indurated;
which had been the cause of her dyspepsia.

In other cases of death from rupture the laceration is caused not by the
accumulation of food, but by the accumulation of gases arising from
depraved digestion, constituting a disease almost the same as that which
attacks cattle that have fed on wet clover. A singular example of this
rare affection, in which death was preceded by the symptoms of irritant
poisoning, has been noticed by Professor Barzelotii.[144]—Another case,
which appears to have been of the same kind, is mentioned in a late
French journal. A child, a twelvemonth old, after eating cabbage-soup,
died during the night unperceived by its mother. On the body being
examined, a great quantity of fetid gas escaped from the abdomen, and a
smooth laceration like an incised wound, three inches in length, was
found in the lesser arch of the stomach.[145]

In other cases, however, it is not easy to say what occasions the
injury. An instance, for example, has been related, where the accident
followed the drinking of a little shrub and water. The individual, a man
of middle age, who had been long liable to fits of severe pain in the
stomach, going off with vomiting, was suddenly seized the day after one
of his fits with violent pain in the epigastrium, extreme tenderness and
tension of the muscles, and for a short time with violent vomiting. In
seventeen hours he expired. On dissection a dark-brown fluid was found
in the cavity of the belly, and the fore part of the stomach presented a
laceration four inches long. There were likewise several lacerations,
one of them three inches long, which intersected the peritonæal coat
alone.[146] A case probably similar in nature has been described by Dr.
Roberts of London, that of a man who died of convulsions in five hours,
and presented after death a long rent in the stomach, with escape of its
contents into the general cavity of the belly.[147]

Another rare variety of rupture of the stomach must also be particularly
noticed, because the course of the symptoms imitates very closely a case
of poisoning with the irritants. It is _partial rupture_,—or laceration
of the inner coat only. A very interesting case of that description has
been related by Mr. Chevallier. A youth of fourteen, on the evening
after a Christmas feast, at which he ate and drank heartily, was
attacked with violent and frequent vomiting. Next morning he said he
felt as if the blood in his heart was boiling, he was unable to swallow,
the pulse became irregular, and pressure on the heart or stomach gave
him excruciating agony. These symptoms continued till the following day,
when he vomited two pounds of blood at successive intervals, and soon
afterwards expired. The inner coat of the stomach was torn in many
places, and that of the duodenum was lacerated almost completely round.
No other disease existed in the bowels or elsewhere.[148]

Some of the cases now mentioned could hardly be distinguished from the
effects of certain irritant poisons by the symptoms only. But the morbid
appearances in the stomach will at once determine their real nature.

Rupture of the stomach, it may be observed, does not always occasion the
symptoms hitherto related. Sometimes it causes instant death. Thus a
healthy coal-heaver in London, while attempting to raise a heavy weight,
suddenly cried out, clapped his hand over his stomach, drew two deep
sighs, and died on the spot. On dissection a lacerated hole was found in
the stomach, big enough to admit the thumb; and the stomach did not
contain any food.[149] This case, along with those of Dr. Roberts and
Mr. Weekes, will show that rupture may take place without previous
distension.

3. _Rupture of the Duodenum_ is a very rare accident from internal
causes. The following instance resembles considerably the symptoms of
irritant poisoning. A gentleman, 48 years old, quarrelled violently with
another while playing billiards immediately after dinner. Soon
afterwards he was seized suddenly with violent pain in the stomach,
vomiting, cold extremities, and a failing pulse; and he died very soon.
The mucous coat of the duodenum was found much inflamed, and four inches
and a half from the pylorus there was a lacerated hole involving a third
of the circumference of the gut.[150]

4. Under the next head may be classed rupture of the other organs of the
belly. _Rupture of the Biliary Ducts_ for example, an extremely rare
accident, has been known to imitate the symptoms of irritant poisoning,
as the following case will show.—An elderly lady, after a slight attack
of jaundice, was seized with violent pain in the stomach, and vomiting
recurring in frequent fits, and in seventeen hours with extreme
tenderness, tension of the muscles, coldness of the skin, and failure of
the pulse. She expired in twenty-four hours; and after death the hepatic
duct was found torn across, a gall-stone lay at the opening of the
cystic duct, the peritonæum was here and there inflamed, and three
pounds of blood and bile were effused into the cavity of the
abdomen.[151]—The nature of such cases will be always apparent on
dissection, but by no means always from the symptoms.

In like manner _rupture of the uterus or its appendages_ may in certain
circumstances occasion similar symptoms, and so be mistaken for the
operation of poison. A striking example of the kind once came under my
notice. A middle-aged woman much addicted to drinking, and on that
account living on indifferent terms with her husband, was suddenly
seized at two in the afternoon with pain in the belly, afterwards with
vomiting and purging, then with extreme exhaustion and coldness of the
extremities; and at ten in the evening she expired. A suspicion of
poisoning having arisen in the neighbourhood, a judicial inspection was
ordered by the sheriff of Linlithgowshire, where the case happened; and
the examination was entrusted to her medical attendant, Mr. Robertson,
and myself. On inquiry, it was found that she had taken nothing whatever
after breakfasting at eight in the morning, six hours before; and
farther, that the pain had begun violently in the lower part of the
belly. These two circumstances alone were almost, if not altogether,
incompatible with the idea of irritant poisoning having been the
occasion of death. But all doubt was completely removed by the
inspection of the body; for the lower part of the belly was filled with
a great quantity of clotted blood, which had proceeded from the rupture
of a Fallopian conception.

5. The next accident which may be noticed on account of its being liable
to be mistaken for the effects of poison is _sudden death from drinking
cold water_.

In Britain the most common form of death from this cause appears to have
been instant death, arising from the impression on the stomach. It is
not an uncommon thing for people to drop down instantaneously and die on
the spot, in consequence of drinking freely of cold water or other
fluids while over-heated.[152] There is an interesting report on a case
of this kind by Pyl in his Memoirs and Observations. The individual had
been quarrelling with a companion, and in the height of a fit of violent
passion swallowed a glass of beer; when he dropped down senseless and
motionless, and died immediately. His wife suspecting the administration
of poison, demanded a judicial inquiry; but nothing was found in the
body to account for death. Pyl therefore came to the conclusion that the
man died from the sudden impression caused by the cold beer.[153] Dr.
Currie, after quoting several instances of the like kind, relates the
following remarkable case which occurred to himself. A young man, having
just sat down, panting and bathed in sweat, after a severe match at
tennis, drank greedily from a pitcher of water fresh drawn from a
neighbouring pump. Suddenly he laid his hand on his stomach, bent
forward, became pale, breathed laboriously, and in a few minutes
expired.[154]

But when combined with exposure to a burning sun, as in hot climates,
drinking cold water when the body is over-heated seems often to excite
along with irritation in the stomach congestive apoplexy. Dr. Watts has
given a good account of these effects as they occurred in the
neighbourhood of New York during the hot season of 1818. During the
summer of that year the thermometer often stood in the shade so high as
92°; and the labourers in consequence could not be restrained from
drinking frequently and excessively of cold water. Many were attacked
with pain in the stomach, sickness, giddiness, and fainting; next with
difficult breathing, and rattling in the throat; then with apoplexy; and
not a few perished.[155] These symptoms are very like the effects of
some narcotico-acrid poisons.

Lastly, drinking cold water sometimes causes symptoms more nearly allied
to those of the pure irritants. Thus some persons, on eating ices, or
drinking iced-water, or cold ginger-beer in the hot days of summer, are
attacked with violent colic. Others in the like circumstances are
attacked with violent fits of vomiting.[156] Haller has even mentioned
an instance of a man, who after swallowing a large draught of cold water
while over-heated, was seized with symptoms of acute gastritis, and died
in fifteen days: and in the dead body the stomach was found gangrenous
and ulcerated at its fundus.[157] M. Guérard relates a similar case,
that of a quarter-master who, swallowing iced-beer after a hurried
journey in a hot day, was attacked in six hours with shivering, then
with heat and tightness in the pit of the stomach, vomiting of every
thing he took, anxiety, thirst and frequency of the pulse; next with
extreme prostration, cessation of pain, hiccup, and lividity of the
face; and he expired in five days. Signs of inflammation were found in
the stomach, such as great redness internally, with spots of
extravasation, and a blackish matter like what he vomited.[158] Cholera
has also been sometimes referred to the same cause. In the hot summer of
1825 it was remarked that a great number of persons who used to frequent
a particular coffee-house in the Palais-Royal at Paris, and the owner
among the rest, were severely affected with cholera. Poison being
suspected to be the cause, a judicial inquiry was instituted. It was
proved, however, that similar accidents had been observed at other
coffee-houses, in other cities, and likewise in former hot seasons; and
when the whole medical evidence was referred to a commission of
physicians and chemists, they gave their opinion, that the disease was
owing to the incautious use of ices and iced-water in an unusually hot
summer.[159] Perhaps cholera arising thus may prove fatal. The following
extraordinary case, which appears to have been of this nature, was
communicated to me by the late Dr. Duncan, junior. A bookbinder in this
city, previously in excellent health, rose one morning at six to kindle
his fire, and took a large draught of cold water from a pitcher used in
common by the whole family. He went immediately to bed again,
complaining of pain in the pit of the stomach, and extreme anxiety, and
affected with incessant vomiting. In twelve hours he died without any
material change in the symptoms, and no disease whatever could be
detected in the dead body. Dr. Duncan satisfied himself from general
circumstances, that poisoning was quite out of the question; so that,
however extraordinary it may appear, his death could be accounted for in
no other way than by ascribing it to the cold water.—Hoffmann says he
was acquainted with instances where fatal inflammatory fever was induced
by drinking too freely of cold water, and a suspicion of poisoning in
consequence excited.[160]

6. _Of Bilious Vomiting and Simple Cholera._—Of all the diseases which
are apt to be confounded with the effects of the irritant poisons, there
is none which it is of so much importance that the medical jurist should
be able to distinguish as cholera. A trial for poisoning with the common
poisons hardly ever occurs, but an attempt is made to ascribe death to
that disease; for it is very frequent, and its symptoms bear a close
resemblance to those of the principal poisons of the class we are now
considering.

It is unnecessary to give here a detailed account of the symptoms of
simple cholera. There is the same burning pain in the stomach and bowels
as in irritant poisoning, the same incessant vomiting and frequent
purging, the same tension and tenderness of the belly, the same sense of
acridity in the throat, and irritation in the anus, the same depression
and anxiety, the same state of the pulse.

It would be wrong, however, to infer from these resemblances that the
two affections are always undistinguishable. Some cases of irritant
poisoning certainly cannot be distinguished by their symptoms from
cholera. Many other cases are similarly circumstanced, because their
particulars cannot be accurately collected. But there is no doubt that
in others the distinction between poisoning and cholera may be drawn by
the physician who has been able to ascertain the symptoms in detail. At
present those points of difference only will be noticed which relate to
the irritants as a class; others will be mentioned under the head of
poisons individually.

The first difference is, that in cholera the sense of acridity in the
throat does not precede the vomiting, as it sometimes does in poisoning.
In cholera this sensation is caused by the vomited matter irritating the
throat, or perhaps by the irritation in the stomach being propagated
upwards by continuity of surface. But, whatever may be its cause, it is
certain that the sense of acridity or burning sometimes remarked in
cholera never begins before the vomiting. In many cases of poisoning,
though certainly not in all, it is the first symptom.—The next
difference is, that in cholera the vomiting is never bloody. I have been
at some pains to investigate this point: and I have been unable to find
any instance of the cholera of this country, which has been accompanied
with sanguinolent vomiting; neither is such a symptom mentioned in any
accounts I have read of malignant cholera. This article of diagnosis
will, of course, be open to correction from the experience of other
practitioners. Lastly, a material difference is, that the simple cholera
of this country very seldom proves fatal so rapidly as poisoning with
the irritants usually does. Death from irritant poisoning is on the
whole seldom delayed beyond two days and a half, and frequently happens
within thirty-six hours, sometimes within six hours, or even less.
Malignant cholera frequently proves fatal in as short a time; but with
regard to the cholera of this country, I believe it may be laid down as
a rule hitherto unshaken by all the controversy to which the subject has
given rise,—that death is not often caused by it at all, and that death
within three days is very rare indeed. A few cases of death within that
period, nay, even within twelve hours, have certainly occurred; but
their great rarity is obvious from the fact, that many practitioners of
experience have not met with a single instance, and others with only one
case in the course of a long practice. Dr. Duncan, senior, mentioned to
me a case, the only one of the kind he had met with, which commenced
soon after the individual ate a sour orange in the Edinburgh theatre,
and which proved fatal in twelve hours. Dr. Duncan, junior, also met
with a single case, which was the instance already noticed of cholera
produced by drinking cold water. Dr. Abercrombie also once, and once
only, met with a case fatal within two days.[161] Mr. Tatham, a late
writer on this subject, met with an instance which proved fatal in
twelve hours.[162] Dr. Burne of London has likewise related an instance
of death within fifteen hours occurring in a child.[163] And I was
informed in 1831 of a case at Leith which ended fatally in twenty-six
hours, and was at first supposed by the unprofessional inhabitants of
the place to be an instance of epidemic or malignant cholera. My
colleagues, Drs. Home, Alison, and Graham, never met with an instance
fatal in so short a time as two or three days; at a meeting of the
Medico-Chirurgical Society of this city, none of the members present
could remember to have seen such a case;[164] and of the witnesses who
were brought to swear to this point on a well-known trial, all of them
physicians of extensive practice, not one could depose that such a case
had ever come within his personal observation.[165] It has been stated
however in a controversial publication written by the late Dr.
Mackintosh of this place, that the author had seen many cases fatal
within the period now mentioned.[166] This is incomprehensible. For my
own part, I cannot help repeating, as the result of the whole inquiry,
that simple cholera rarely causes death in this country, in the period
within which irritant poisoning commonly proves fatal,—that,
consequently, every case of the kind will naturally be apt to lead, in
peculiar circumstances, to suspicion of poisoning,—and that in charges
of poisoning, rapid death under symptoms of violent irritation in the
alimentary canal, like those of cholera, must always be considered an
important article of a chain of circumstantial or presumptive evidence.

7. _Of Malignant Cholera._—The history of this disease affords a fair
promise that, in so far as British practitioners are concerned, it may
ere long be excluded from the list of those which imitate irritant
poisoning. Meanwhile, however, malignant cholera must be allowed to
bear, in its essential symptoms and their course, a marked resemblance
to poisoning with the irritants. So much indeed is this the case that
some authors have actually compared its phenomena to the effects of
arsenic, tartar-emetic, and other powerful acrids. In many cases the two
affections are undoubtedly not so distinguishable by symptoms as to
warrant a physician to rely on the diagnosis in a medico-legal inquiry.
But in many other instances the distinction may be drawn satisfactorily.
Thus the uneasiness in the throat which sometimes attends cholera never
precedes the vomiting. The vomiting in cholera is never bloody. The
colour and expression of the countenance and whole body are peculiar. In
frequent instances the early signs which resemble poisoning are followed
by a secondary stage, sometimes of simple coma, sometimes of typhoid
fever, which a practised person may easily distinguish from the
secondary phenomena produced by some irritants. Lastly, no mistake can
arise where the patient, before presenting the symptoms common to both
affections, experiences violent burning pain or certain tastes, during
or immediately after the swallowing of food, drink, or some other
article.

8. _Of Inflammation of the Stomach._—Chronic inflammation of the stomach
is a common disease; which, however, on account of the slowness of its
course, is not liable to be confounded with the ordinary effects of
irritant poisons. Acute inflammation, on the contrary, follows precisely
the same course as that of irritant poisoning. But great doubts may be
entertained whether true acute gastritis ever exists in this country as
a natural disease. Several of my acquaintances, long in extensive
practice, have stated to me, that their experience coincides entirely
with that of Dr. Abercrombie, who observes he has “never seen a case
which he could consider as being of that nature.”[167] An important
observation of the same purport has been made by M. Louis, one of the
most experienced and accurate pathologists of the present time. He says,
that during six years’ service at the hospital of La Charité, during
which he noticed the particulars of 3000 cases and 500 dissections, he
did not meet with a single instance of fatal primary gastritis. The
disease only occurred as a secondary affection or complicating some
other disease which was the cause of death.[168] So far as I have
hitherto been able to inquire among systematic authors, the descriptions
of idiopathic acute gastritis appear to have been taken from the
varieties caused by poison.

The following are the only specific accounts I have hitherto met with of
an affection of the nature of idiopathic acute gastritis; and the reader
will be at no loss to perceive that in each of them it admits of being
viewed differently. The first two are the cases of inflammation referred
by Haller and Guérard to drinking cold water incautiously [p. 100]. The
next is a remarkable incident related by Lecat, and occurring in 1763. A
girl, nineteen years old, was attacked while in good health with
shivering, faintness, acute pain in the belly, cold extremities and
imperceptible pulse; and she died in sixteen hours. The stomach was
found red, and checkered with brownish patches and gangrenous pustules
(probably warty black extravasation): yet it was supposed to have been
ascertained that she had not taken any thing deleterious.[169] This
narrative is certainly to appearance pointed. But when it is added, that
the girl’s mother was attacked about the same time with precisely the
same symptoms and died in four hours, I think the reader, when he also
considers the imperfect mode in which chemical inquiries were then
conducted, will by no means rest satisfied with Lecat’s assurance that
nothing deleterious was swallowed. The last is an equally singular case
given by Dr. Hastings, of Worcester, where poisoning with cantharides
was suspected. A young lady, liable to indigestion, but at the moment in
better health than usual, was attacked with sickness before breakfast
and after it with vomiting. Three days elapsed before she was seen by
her medical attendant, who found her sinking under incessant vomiting,
severe pain in the loins, strangury, bloody urine, and swelling of the
clitoris, attended with red extravasation of the eyes, and a red
efflorescence on the skin. Death followed next day amidst convulsions;
and there was found in the dead body extravasation of blood between the
kidneys and their outer membrane, into the pelvis of each kidney, and
into the bladder,—redness of the bronchial membrane, and gorging of the
air-cells with blood,—and general redness of the inside of the stomach,
with numerous extravasated spots in the submucous coat.[170] It seems to
have been clearly proved at the coroner’s inquest that poisoning was
here out of the question. But the case appears rather to have been one
of renal irritation or inflammation than of gastritis, and the affection
of the stomach secondarily merely.

The question as to the possibility of acute gastritis being produced by
natural causes is one of very great interest to the medical jurist. For
its possible occurrence is the only obstacle in the way of a decision in
favour of poisoning, from symptoms and morbid appearances only, in
certain cases by no means uncommon, which are characterised by signs of
violent irritation during life, early death, and unequivocal marks of
great irritation in the dead body, namely, bright redness, ulcers, and
black, granular, warty extravasation. In regard to these effects, it may
with perfect safety be said, that they can very rarely indeed all arise
from natural causes; and for my own part, the more the subject is
investigated, the more am I led to doubt whether they ever arise in this
country from any other cause than poison. The possible occurrence of a
case of the kind from natural causes must be granted. But this
concession ought not to take away from the importance of the contrary
fact as one of the particulars of a chain of circumstantial proof.

In whatever way the fact as to the existence of idiopathic acute
gastritis may eventually be proved to stand, an important criterion of
this disease, as of cholera, will be that the sense of burning in the
throat, if present at all, does not precede the vomiting.

9. _Inflammation of the Intestines_ in its acute form is more common
than inflammation of the stomach, as a natural disease. It is generally
accompanied, however, with constipation of the bowels. Acute enteritis,
unless we choose with some pathologists to consider cholera as of that
nature, is very rarely attended with purging.

There is a variety of intestinal inflammation, observed only of late by
pathologists,[171] but now well known, which bears a close resemblance
to the effects of the irritants. It is a particular variety of
ulceration commonly situated near the end of the small intestines,
accompanied at first with trifling or insidious symptoms, and
terminating suddenly in perforation of the gut. It begins with
tubercular deposition under the mucous membrane in roundish patches.
Then an ulcer appears on the middle of one or more of these patches,
gradually spreads over them, and at the same time penetrates the other
coats. At last when the peritoneal coat alone is left, some trifling
accident ruptures it, the fæcal matters escape into the sac of the
peritonæum, and the patient dies in great agony in the course of one or
two days, or in a few hours. Such cases, if not distinguished by the
symptoms, will be at once recognized by the morbid appearances.
Perforation of the intestines, with similar symptoms, also takes place
without the previous tubercular deposit, by simple ulceration of the
coats.[172]

Another form of intestinal inflammation may also be here particularized,
because it imitates the effects of the irritants in the cases in which
they prove slowly fatal. It is a form of aphthous ulceration of the
mucous membrane of the alimentary canal, which appears to affect almost
every part of it from the throat downwards, and begins commonly in the
throat. I once met with a remarkable case in which it appeared in the
form of little white ulcers in the back of the throat, and gradually
travelled downwards to the stomach and from that to the
intestines,—being characterized by burning pain in every one of its
seats, and successively by difficulty of swallowing, by sickness,
vomiting, and tenderness of the stomach, and finally by purging. Such
cases resemble the slow forms of poisoning with arsenic. But they differ
in attacking the several divisions of the alimentary canal in turn,
while in the examples of poisoning with arsenic now alluded to, the
whole canal from the mouth to the anus is affected simultaneously. Dr.
Abercrombie has described a similar disorder, which he appears to have
occasionally seen affecting both the stomach and intestines at the same
time; but he seems to doubt whether it ever occurs as an idiopathic
disease, or independently of some co-existing or preceding fever or
local inflammation.[173]

10. _Inflammation of the Peritonæum_, or lining membrane of the belly,
will not require many remarks. When acute, it is rarely attended in its
early stage by vomiting; rarely also by irregular action of the
intestines, and never by diarrhœa; and it is at once distinguished in
the dead body by unequivocal marks of peritonæal inflammation, which are
very seldom caused by irritant poisons.[174]

11. The subject of _Spontaneous Perforation of the Stomach_ is an
important topic for the medical jurist, because both the symptoms before
death and the appearances in the dead body are occasionally very like
the effects of some of the most active irritant poisons. The following
is a statement of the most material facts hitherto ascertained on this
subject; but it must be premised that a good deal of obscurity still
hangs over some parts of it.

Spontaneous perforation of the stomach is of three kinds. One is the
last stage of some varieties of scirrhus. The indurated membrane
ulcerates, the ulcer penetrates first the villous, then the muscular,
and at last the outer or peritoneal coat, so that the contents of the
stomach escape into the belly. The symptoms of the perforation are a
sense of something giving way in the pit of the stomach, acute pain
gradually extending over the whole abdomen, great tenderness and
tension, excessive prostration, and death commonly within twenty-four
hours. The symptoms which precede the perforation in general clearly
indicate organic derangement of the stomach, namely, aggravated
dyspepsia of long standing. Several cases of this description may be
seen in a thesis by M. Laisné,[175] a pupil of Professor Chaussier. Two
characteristic cases have been published by Dr. Crampton;[176] and Mr.
Alfred Taylor has referred to several others, the stomachs of which are
preserved in Guy’s Hospital Museum, and gives the particulars of some
which had occurred in the practice of that institution or to his
friends.[177] Occasionally no symptom exists prior to the perforation,
as in an instance related by Dr. Kelly of a stout healthy servant, who
was suddenly seized with excruciating pain in the stomach and expired in
eighteen hours, and in whose body the stomach was found perforated in
the middle of an extensive thickening and induration of the villous
coat.[178]

The second variety of perforation takes place by simple ulceration
without previous scirrhus. In one of Dr. Crampton’s papers will be found
some remarks by Mr. Travers, along with a case of this kind. The subject
of it was a man of a strumous habit, who enjoyed good health, till one
day at dinner he was suddenly attacked with acute pain in the pit of the
stomach, and died in thirteen hours. The stomach was found perforated in
the centre of a superficial ulcer of the mucous coat, occupying
two-thirds of the ring of the pylorus.[179] This case shows that the
present variety of perforation may take place without the preliminary
organic disease being indicated by any symptom. The circumstances under
which it commenced are peculiarly important in relation to the medical
jurisprudence of poisoning. Another case which has been lately described
with great exactness by M. Duparcque, was preceded only by very trivial
dyspeptic symptoms. Here the whole mischief arose from a small ulcer
eight lines long and five in breadth on the inside of the stomach, and
not more than a line and a half in diameter at the perforation through
the peritonæum.[180] Several excellent examples of the same disease have
been related by Dr. Abercrombie.[181] In one of these the ulcer in the
centre of which the perforation had been formed, was not bigger than a
shilling, and the rest of the stomach quite healthy. A very instructive
case of a similar nature, but of unusual duration, has been related by
Mr. Alfred Taylor. A young woman, after suffering for some time from
nausea and constant craving for food, but inability to indulge it, and
occasionally from pain in the stomach, was attacked suddenly with the
usual symptoms of perforation, and died forty-two hours afterwards. The
villous coat of the stomach, though generally healthy, presented at the
lesser curvature several small elevated points, and in the middle of two
of these a sharply-defined ulcer, one affecting the mucous coat only,
while the other, which was half an inch in diameter where it affected
the mucous coat, perforated the muscular and peritonæal coats by a hole
no bigger than a crow-quill.[182] A case still more remarkable has been
also related by the same author, where the circumstances naturally gave
rise to a strong suspicion of poisoning. A young female in a noble
family, subject to slight dyspepsia, was suddenly attacked, three hours
after a meal, with violent vomiting and pain in the belly. Collapse soon
ensued, and in fifteen hours she died, under so strong suspicions of
poisoning that various antidotes were administered. This suspicion was
in some measure borne out by proofs of an intrigue having been carried
on between her and a male person in the house, and by the discovery
after death of the signs of recent sexual intercourse. On examining the
cavity of the abdomen, however, there was found, at the upper and back
part of the stomach near the pylorus, an oval perforation, half an inch
wide, surrounded by a firm, smooth, almost cartilaginous margin, without
any inflammation near it. Mr. Taylor properly points out, that the
sudden occurrence of such violent symptoms so long after a meal is
incompatible with the action of any poison which could cause perforation
in fifteen hours; and that the characters of the perforation were those
of a natural disease long latent. He could not detect a trace of any
poison in the stomach.[183]—In some cases, as in that of M. Duparcque,
the pain at the moment the perforation is completed is not at first
violent, because the close proximity of some adjoining organ, such as
the liver, prevents the contents of the stomach from escaping for a
time, so that inflammation of the peritonæum is but gradually developed.

The third variety of spontaneous perforation is of a much more singular
kind. It is produced not by ordinary ulceration, but by a jelly-like
softening of the coats. The gelatinization sometimes extends over a
great extent of surface, affecting chiefly the villous coat, so that the
aperture through the other membranes is surrounded by extensive
pulpiness of the internal membrane. It is seldom accompanied by
vascularity. Its symptoms are exceedingly obscure. In adults there is
very rarely any symptom at all till the perforation is complete;[184] in
children, as appears from a paper by Dr. J. Gairdner of this city, and
another by Dr. Pitschaft, a German author,[185] the early symptoms
indicate an obscure chronic gastritis. The nature of this singular
disease will be discussed in the section on the morbid appearances. At
present it may merely be observed, that the injury caused to the coats
of the stomach seems to be precisely the same with the gelatinization,
which is sometimes found after death in persons who had no symptoms of
an affection of the stomach, and which is ascribed by John Hunter,[186]
and most British pathologists, to the solvent action of the gastric
juice in the dead body. This disease is well described by Laisné in his
thesis formerly quoted. The following is a good example: a young lady,
previously in good health, was awakened at three one morning with
excruciating pain in the stomach, which nothing could alleviate. She
expired seven hours after; and on dissection two holes were found in the
back part of the stomach, surrounded with much softening of the villous
coat.[187] Another case will be mentioned in page 118.—The appearances
produced by this disease have been mistaken for the effects of corrosive
poisons.

12. The _gullet_ may be perforated in a similar manner either with or
without symptoms. Under the head of the morbid appearances (119) two
instances will be mentioned in which there were no corresponding
symptoms. In the following case symptoms did pre-exist. A man, six weeks
after being bit by a dog, which was killed without its state of health
having been ascertained, was attacked with a sense of strangling,
impossibility of swallowing, delirium, excessive irritability, glairy
vomiting; and he died within twenty-four hours. The gullet, a little
above the diaphragm, was perforated by a hole two-thirds of an inch in
diameter, with thin edges; and effusion had taken place into the
posterior mediastinum.[188]

13. _Perforation of the alimentary canal by worms_ may here also be
noticed shortly as a disease liable in careless hands to be confounded
with irritant poisoning. This is far from being a common accident, and
very rarely takes place during life. In most of the cases in which it
has been witnessed the symptoms antecedent to death were those not of
irritant, but of narcotic poisoning, and were then owing simply to the
great accumulation of worms in the alimentary canal. On this subject the
reader is referred to the article Epilepsy in the introductory remarks
on the effects of the narcotic class of poisons. But at times the
symptoms have been like those of irritant poisoning. Thus the following
is a case of perforation by worms during life giving rise to all the
phenomena and symptoms of peritonæal inflammation. A soldier at
Mauritius was seized with slight general fever and severe pain, at first
in the pit of the stomach, and afterwards over the whole belly, which on
the third day began to enlarge. A tendency to suppression of urine and
costiveness ensued, then bilious vomiting; and he died on the fourth
day, the belly having continued to increase to the end. On dissection,
several quarts of muddy fluid were found in the sac of the peritonæum,
the viscera were agglutinated by lymph, a round worm was discovered
among the intestines between the navel and pubes, and the ileum was
perforated six inches from the colon by a hole corresponding in size
with the worm.[189]—A singular case, not however fatal, but which
confirms the fact, that worms may make their way through the intestines
and other textures during life, is mentioned in Rust’s journal. A woman
after a tedious illness first vomited several lumbrici, and was then
seized with a painful swelling in the left side, which in the process of
time suppurated, and discharged along with the purulent matter three
other worms of the same species.[190] Another instance of the same kind,
where the perforation of the gut succeeded strangulated hernia, and was
followed by the discharge of two lumbrici and ultimate recovery, is
detailed in the Revue Médicale.[191]

Symptoms like those of narcotico-acrid poisoning may be caused by worms
without perforation. A girl, eight years old and in excellent health,
was suddenly seized with violent colic pains, vomiting, bloody stools,
tenderness and swelling of the belly, followed by convulsions and coma,
and proving fatal in seven hours. No other explanation of the case could
be discovered on dissection except the presence of several hundred
ascarides in the intestines and thirteen in the stomach.[192]

14. The next diseases to be mentioned are melæna and hæmatemesis, or
purging and vomiting of pure or of altered blood.

It is hardly possible to mistake them for poisoning, as the pain which
accompanies them is seldom acute, and the discharge of blood generally
profuse.

15. The last are _colic_, _iliac passion_, and _obstructed intestine_.
As the symptoms of some poisons are the same with those of colic, it is
of course sometimes impossible to distinguish the natural disease from
the effects of poison by attending to the abdominal symptoms only. But
the distinction in severe cases of poisoning may almost always be drawn
from collateral symptoms and extraneous circumstances.—The iliac passion
is distinguished by a complete reversion of the vermicular motion of the
intestines in consequence of which the fæces are often discharged by
vomiting. I am not aware that stercoraceous vomiting is ever caused by
poisoning.—A case has been recorded in Corvisart’s journal, in which
iliac passion, originating in obstruction of the ileum by hardened
fæces, and proving fatal in twenty-six hours, gave rise to a judicial
inquiry into the possibility of poisoning.[193] Another instance, that
led to a strong suspicion of poisoning, has been lately published by M.
Rostan, in which there was continued vomiting and pain of abdomen,
proving fatal in two days, and arising from the small intestines being
obstructed by an adventitious band.[194] In this case the first
inspectors failed to observe the true cause of the symptoms; but Rostan
and Orfila, who were appointed to examine the body a second time,
discovered the constriction, and were unable to find any poison in the
stomach by analysis. Stercoraceous vomiting occurred during life; which
might have been held sufficient to settle the real nature of the
case.—Obstruction of the intestines arising from twisting of the gut,
intussusception, foreign bodies, or strangulated hernia, is easily known
by the seat where the pain begins, by the obstinate constipation, and
also by the excessive enlargement of the belly,—which last, however, is
rather an equivocal symptom.

The preceding observations will enable the medical jurist to determine,
how far a diagnosis may be drawn from the symptoms between poisoning
with the irritant and the diseases which resemble it. It will be
remarked that the most embarrassing disease, on account of its
frequency, and peculiar symptoms, is cholera. Cholera, however, may be
recognised in some instances even considered in regard to the irritants
as a class; and we shall presently find that it may be distinguished
still better from the effects of some individual poisons.


   SECTION II.—_Of the Morbid Appearances caused by Irritant Poisons,
           compared with those of certain natural diseases._

The next subject for consideration is the morbid appearances produced by
the irritants as a class, together with those of a similar nature, which
arise from natural causes.

The powerful irritants, which are not corrosives, produce simply the
appearances characteristic of inflammation of the alimentary canal in
its various stages,—in the mouth, throat, and gullet vascularity, and
also, if the case has lasted long enough, ulceration;—in the stomach,
vascularity, extravasation of blood under and in the substance of the
villous coat and likewise into the cavity of the organ, abundant
secretion of tough mucus, deposition of coagulable lymph in a fine
network, ulceration of the membranes, occasionally perforation,
preternatural softness of the whole or of part of the villous coat, and
on the other hand sometimes uncommon hardness and shrivelling of that
coat; in the intestines vascularity, extravasation, and
ulceration.—Sometimes several of these appearances are to be seen in the
whole alimentary canal at once. In poisoning with arsenic or corrosive
sublimate it is no unusual thing to meet with redness or ulceration of
the throat, great disease in the stomach, vascularity of the small
intestines, ulcers in the great intestines, and excoriation of the
anus.—When the poison is an active corrosive much more extensive ravages
are sometimes caused, particularly in the stomach. After poisoning by
the mineral acids, for example, the whole mucous membrane of the stomach
is at times found wanting; nay, large patches of the whole coats may be
wanting, and the deficiency supplied by the adhesion of the margin of
the aperture to the adjoining viscera, and the conversion of the outer
membrane of these viscera into an inner membrane for the stomach.

Of the appearances here briefly enumerated the particulars will be
related partly under what is now to be said of the appearances arising
from natural causes, which are liable to be confounded with the effects
of poisons, partly under the head of individual poisons.


 _Of redness of the stomach and intestines from natural causes, and its
            distinction from the redness caused by poisons._

Simple redness of the alimentary mucous membrane in all its forms,
whether of mere vascularity, or actual extravasation, not only does not
distinguish poisoning from inflammatory disorders of natural origin, but
will even seldom distinguish the effects of poison from those of
processes that occur independently of disease, and subsequent to death.
On the subject of real inflammation, as distinguished from redness
originating after death, or pseudo-morbid redness, as it is commonly
termed,—a subject of great consequence to the medical jurist,—the reader
may consult with advantage a paper by Dr. Yelloly,[195] an essay by MM.
Rigot and Trousseau,[196] or that of M. Billard.[197] The former authors
proved by experiment, that various kinds of pseudo-morbid redness may be
formed, which cannot be distinguished from the parallel varieties caused
by inflammation; that these appearances are formed after death, and not
till three, five, or eight hours after it; that they are to be found
chiefly in the most depending turns of intestines, and in the most
depending parts of each turn, or of the stomach; and that after they
have been formed, they may be made to shift their place, and appear
where the membrane was previously healthy, by simply altering the
position of the gut. M. Billard, on the other hand, has laid down their
characters, and made a minute arrangement of the several kinds. He has
divided them into ramiform, capilliform, punctated, striated, laminated,
and diffuse redness,—terms which need hardly be explained. I must be
content with merely referring to these sources of information for a
particular account of the appearances in question. But it may be right
at the same time to quote an instance of the most aggravated form of
pseudo-morbid redness, in order to convince the reader that all forms
may equally arise from the same causes. Among other example, then, which
have been related of laminated redness, or redness in patches from
extravasation, M. Billard mentions the case of a man who hanged himself,
and in whose body was found, on the mucous membrane of the small
intestine where it lay in the right flank, “a large, amaranth-red patch,
six finger-breadths wide, covered with bloody exudation, and not
removable by washing:” and in the lower pelvis there was a similar patch
of even larger dimensions.[198]

Although morbid and pseudo-morbid redness of the inner coat of the
alimentary canal cannot be distinguished from one another by any
intrinsic character, M. Billard thinks this may be done by attending to
collateral circumstances. According to his researches, redness is to be
accounted inflammatory only when it occurs in parts not depending in
position, or is not limited to such parts: when the mesenteric veins
supplying the parts are not distended, nor the great abdominal veins
obstructed at the time of death; when the reddened membrane is covered
with much mucus, particularly if thick, tenacious, and adhering; when
the mucous membrane itself is opaque, so that when dissected off and
stretched over the finger, the finger is not visible; when the cellular
tissue which connects that membrane with the subjacent coat is brittle,
so that the former is easily scratched off with the nail.

Some observations may be here also made on another appearance, allied to
the present group, but which there is strong reason to believe always
indicates some violent irritation at least, if not even irritation from
poison only, in the organ where it is found. It is an effusion under the
villous coat of the stomach, and incorporation with its substance, of
dark brownish-black, or as it were charred, blood; which is thus altered
either by the chemical action of the poison, or by a vital process. In
many cases of poisoning with the mineral acids, oxalic acid, arsenic,
corrosive sublimate, and the like, there are found on the villous coat
of the stomach little knots and larger irregular patches and streaks,
not of a reddish-brown, reddish-black, or violaceous hue, like
pseudo-morbid redness, but dark-grayish-black, or brownish-black, like
the colour of coal or melanosis,—accompanied too with elevation of the
membrane, frequently with abrasion on the middle of the patches, and
surrounded by vascularity. This conjunction of appearances I have never
seen in the stomach, unless it had been violently irritated; and several
experienced pathologists of my acquaintance agree with me in this
statement. It bears a pretty close resemblance to melanosis of the
stomach;[199] but is distinguished by melanotic blackness being arranged
in regular abruptly-defined spots, and still better by melanosis not
being preceded by symptoms of irritation in the stomach.

Referring to what was already said under the head of the symptoms of
gastritis [p. 102], I must again express my doubts whether the
appearances now described ever arise in this country from natural
disease. In the intestines they are sufficiently familiar to the
physician, as arising from idiopathic enteritis, and from dysentery. But
in the stomach their existence as the effect of natural disease is very
doubtful.

Another kind of coloration of the inner membrane of the stomach, which
may be shortly alluded to, because it has actually been mistaken for the
effect of irritation from poison, although by no means like it,—is
staining of the membrane with a reddish, brownish, yellowish, or
greenish tint, observed in bodies that have been kept some time, and
produced by the proximity of the liver, spleen, or colon if it contains
fæces. No unprejudiced and skilful inspector could possibly mistake this
appearance for inflammation. But under the impulse of prejudice it has
been considered such, and imputed to poison. On the occurrence of such
stains an attempt was made by the French to ascribe to poison the death
of the republican general Hoche. He died rather suddenly on his way from
Frankfort to join his troops; and as poisoning was suspected, the body
was opened in the presence of three French army-surgeons, and a French
and two German physicians. The only appearance of note in the alimentary
canal was two darkish spots on the villous coat of the stomach. The
surgeons drew up a report which imputed his death to poison; but the
physicians refused to sign it; and other medical people who were
subsequently added to the commission decided with the latter.[200] The
surgeons probably would not have been so hasty, if they had not known
that the result of their complaisance would have been the levying of a
heavy fine on the inhabitants.

The last kind of discoloration of the inner coat which requires mention
is dyeing from the presence of coloured fluids in the contents. A
remarkable instance has been recorded where redness of this nature was
mistaken for inflammation, and the death of the individual in
consequence ascribed at first to poison. A person long in delicate
health died suddenly after taking a laxative draught; and the stomach,
as well as the gullet, being found on dissection red and livid in
various places, it was hastily inferred by his medical attendants, that
these appearances were the effect of poison, and that the apothecary had
committed some fatal error in compounding the draught. But another
physician, who was acquainted with the deceased, although he did not
attend him professionally, strongly suspected he had died a natural
death; and happening to know he was in the practice of taking a strong
infusion of corn-poppy, inferred that the supposed signs of inflammation
were merely stains arising from the habitual use of this substance.
Accordingly, on making the experiment, he found that in dogs to which a
similar infusion was given, appearances were produced identically the
same.[201]

_Of the effusion of mucus and lymph from natural causes._—The abundant
secretion of tough mucus in the stomach is a sign of that organ having
been irritated. But the effusion of lymph is more characteristic. This
may be produced by natural inflammation as well as by irritating
poisons. As arising from either cause, however, it is rare; and
certainly by no means so common as would be supposed from what is said
in systematic works; for tough mucus has been often mistaken for it.
Reticulated lymph adhering to the villous coat, and accompanied with
corresponding reticulated redness of that coat, such as I have seen in
animals poisoned with arsenic or oxalic acid, is an unequivocal sign of
inflammation.

_Of idiopathic ulcers and perforation of the stomach and intestines, and
their distinction from those caused by poison._—Both ulceration and
perforation may be produced by natural disease. In the ulceration
produced by poisons there is generally speaking nothing to distinguish
it from natural ulcers; but that caused by some poisons, such as iodine,
is said to differ by the surrounding coloration of the membrane; and
when the ulcer is caused by a sparingly soluble poison in a state of
powder, such as arsenic, the cavity of the ulcer is sometimes filled
with the powder. Perforation is a rare effect of the simple irritant
poisons; but it is often caused by corrosives. It is imitated by two of
the varieties of perforation from natural disease.

The form of natural perforation caused by a common ulcer is precisely
the same as that caused by the simple irritants, and is incapable of
being distinguished, except when it is attended with scirrhus.

By far the most remarkable variety, however, of spontaneous perforation
is that which takes place, without proper inflammatory action, from
simple gelatinizing of the coats. It is very apt to be mistaken, and in
a celebrated trial, which will be immediately noticed, was actually
mistaken for the effect of corrosive poison.

It may be situated on any part of the stomach, but is oftenest seen on
the posterior surface. It is sometimes small, more often as big as a
half-crown, frequently of the size of the palm, and occasionally so
great as to involve an entire half of the stomach. Sometimes there is
more than one aperture. The margin is of all shapes, commonly fringed,
and almost always formed of the peritoneum, the other coats being more
extensively dissolved. In one instance, however, the peritonæal surface
was on the contrary the most extensively destroyed;[202] and in a case
which occurred in the infirmary here, and was pointed out to me by the
late Dr. W. Cullen, the peritonæum alone was extensively softened, and
partly dissolved, so as to lay the muscular coat bare on its outer
surface. The gelatinization therefore sometimes, though very rarely,
begins on the outside of the stomach. Internally the whole is surrounded
by pulpiness of the mucous coat, generally white, occasionally bluish or
blackish, never granulated like an ulcer, very rarely vascular; and when
vascular, the blood may be squeezed out of the loaded and open vessels.
The organs in contact with the hole are also frequently softened. Thus
an excavation is sometimes found in the liver or spleen; or the
diaphragm is pierced through and through. The margins of the latter
holes are without any sign of vascular action, but are generally
besmeared with a dark pulpy mass, the remains of the softened tissue.
The pulp never smells of gangrene; with which, indeed, this species of
softening is wholly unconnected. The edge of the hole in the stomach
never adheres to the adjoining organ; yet, even when the hole is very
large, the contents of the stomach have not always made their escape.
Often the dissolution of the coats is incomplete. John Hunter and
others, indeed, have said that a stomach is rarely seen without more or
less solution of the mucous coat.[203] The best account of the
appearances in this state is given by Jaeger of Stuttgardt.[204]

The circumstances under which this extraordinary appearance occurs are
singularly various. Professor Chaussier and the French pathologists
conceive it to be always a morbid process constituting a peculiar
disease; and doubtless cases have occurred in which death appears to
have arisen from the stomach being perforated during life by
gelatinization.[205] But it has been found much more frequently, when
death was clearly the consequence of a different disease, and when there
did not exist during life a single sign of disorder in the stomach. Thus
it has been found in women who died of convulsions after delivery,—in
children who died convulsed or of hydrocephalus,—after death from
suppuration of the brain, both natural and the result of violence,—from
coma following an old ulcer of the back, which communicated with the
spinal canal,—from diseased mesenteric glands,—from phthisis,—from
nervous fever,—and after sudden death from fracture of the skull or
hanging:[206] and in all of these circumstances it has occurred without
any previous symptom referrible to a disorder in the stomach.

The opinions of pathologists are divided as to its nature. The French
conceive it arises from a morbid corrosive action, which, however, may
extend after death, in consequence of the fluids acquiring a solvent
power. Hunter ascribed it entirely to the solvent power of the gastric
juice after death. There are difficulties in the way of both doctrines.
A full examination of the whole inquiry, which is one of much interest
and considerable complexity, would be misplaced in this work; but some
remarks are called for, by reason of the important medico-legal
relations of the subject, and the uncertainty in which it is at present
involved.

In the first place, then, it appears difficult, if not impossible, to
comprehend how a vital erosive action can account for the perforations
observed after death from diseases wholly unconnected with the stomach,
and unattended during life by any symptom of disorder in that organ.
For, not to dwell on other less weighty arguments,—on the one hand,
there is during life no symptom of perforation, an accident which if
deep stupor be not present at the same time is always attended with
violent symptoms when it arises from any cause but gelatinization,—and
on the other hand, there is frequently no escape of the contents of the
stomach into the cavity of the abdomen, though the hole is of enormous
size, and its edge not adherent to the adjoining organs.—All such
perforations, however, are perfectly well accounted for, on the other
theory, by what is now known of the properties of the gastric juice.
This will appear from the following exposition.

The power of the gastric juice to dissolve the stomach and other soft
animal textures was long thought to be fully proved by the well-known
researches of Spallanzani,[207] Stevens,[208] and Gosse.[209] In later
times doubts were entertained on the subject in consequence of negative
results having been obtained by other experimentalists, more especially
by Montégre.[210] But these apparently discrepant facts and opinions
have been reconciled by the ulterior experiments of Tiedemann and Gmelin
on digestion;[211] who found that the nature and quality of the fluid
secreted by the stomach vary much in different circumstances,—that, when
its villous coat is not subjected to some stimulus, the fluid which
lines it is not acid, and does not possess any particular solvent
action,—but that when the membrane is stimulated by the presence of food
or other sources of excitement, the quality of the secretion is
materially changed, for it becomes strongly acid and is capable of
dissolving alimentary substances both in and out of the body. And still
more lately the solvent power of the proper gastric juice over the
stomach, and its capability of producing perforation in animals after
death, have been established in the most satisfactory manner by Dr.
Carswell,[212] who has shown by a series of incontrovertible facts,—that
in the rabbit when killed during the digestion of a meal, and left for
some hours afterwards in particular positions, all the phenomena of
spontaneous gelatinized perforations observed at times in man, may be
easily produced at will,—that acidity of the gastric juice is an
invariable circumstance when such perforations are remarked,—and that
the appearances in question as they occur in the rabbit are the result
of chemical action alone, and occur only after death. Thus, then, the
physiological experiments of Tiedemann and Gmelin, together with the
investigations of Carswell, not merely establish positively the fact,
that the stomach may be perforated after death by the gastric juice, but
likewise account clearly for the negative results obtained by other
experimentalists. For example, passing over earlier experiments, they
explain sufficiently the negative results obtained by Dr. Pommer of
Heilbronn,[213] an experimentalist of some reputation in Germany; for,
falling into the error of some of the less recent experimentalists on
this subject, he made his observations on animals killed slowly by
starving,—in which circumstance there is no proper gastric juice in the
stomach, and consequently no solvent action can exist.

These statements relative to the causes and phenomena of gelatinized
perforation in the stomach supply the strongest possible presumption
which analogy can furnish, that a great proportion of spontaneous
gelatinized perforations in the human subject are owing to the action of
the gastric juice after death. And this presumption is increased to
something not far removed from demonstration by the circumstance, that
in man the process of softening has actually been traced extending in
the dead body. This interesting fact was first noticed by Mr. Allan
Burns.[214] In the body of a girl who died of diseased mesenteric glands
he found an aperture in the fore part of the stomach with the usual
pulpy margin, and the liver in contact with the hole uninjured. In two
days more the liver opposite the hole had become pulpy, and its
peritonæal coat quite dissolved; and the back part of the stomach
opposite the hole was also dissolved, so that only its peritonæal coat
remained. Dr. Sharpey has communicated to me a similar observation. On
finding in the body of a child the stomach perforated and gelatinized,
but the adjoining organs uninjured, he sewed up the body, to show the
appearances to some of his friends next day. By that time the peritonæal
surfaces of the spleen and left kidney were found much softened and
pulpy where they lay in contact with the hole in the stomach. I have
since met with a similar occurrence where the perforation affected the
duodenum (p. 120).

It must be admitted, then, that the action of the gastric juice after
death is quite sufficient to account for the greater number of
gelatiniform perforations in the human stomach.

But in the second place, it seems scarcely possible to explain every
perforation of the kind in this way. The solvent action of the gastric
juice for example, affords no explanation of a singular case related by
M. Récamier,[215] where, after death in the secondary stage of
small-pox, the stomach was transparent and brittle, and perforated in
the splenic region by a gelatinized hole large enough to admit the
fist,—although the fluid in the stomach was subsequently found incapable
of dissolving another stomach, and almost destitute of free acid. And
still less will the solvent action of the gastric juice account for such
cases as those of Laisné and Gastellier, quoted in pp. 107–8, or the
French medico-legal case to be mentioned in p. 118,—where death is
preceded by a short illness, indicating a violent disorder of the
stomach, and sometimes even characterized by all the marked symptoms of
perforation. In the last description of cases, which are comparatively
very rare, it seems necessary to admit that the gelatinization takes
place during life; unless, indeed, it be supposed that the stomach is
first perforated during life by ordinary ulcerative absorption, and then
gelatinized after death, in consequence of the irritation existing
before death having given rise to an unusual secretion of gastric juice.

Passing now to the differences between these gelatinized perforations,
and the perforations caused by corrosive poisons, it may in the first
instance be observed, that the margin of a corroded aperture is
sometimes of a peculiar colour,—for example, yellow with nitric acid,
brown with sulphuric acid or the alkalis, orange with iodine. But a much
better, perhaps indeed an infallible criterion, and one of universal
application, is the following. Either the person dies very soon after
the poison is introduced, in which case vital action may not be excited
in the stomach: or he lives long enough for the ordinary consequences of
violent irritation to ensue. In the former case, as a large quantity of
poison must have been taken, and much vomiting cannot have occurred,
part of the poison will be found in the stomach: In the latter case, the
poison may have been all ejected; but in consequence of the longer
duration of life, deep vascularity, or black extravasation must be
produced round the hole, and sometimes too in other parts of the
stomach; changes which will at once distinguish the appearance from a
gelatinized aperture. There is no doubt that the stomach may be
perforated by the strong corrosives, and yet hardly any of the poison be
found in the stomach after death. Thus in a case related by Mertzdorff
of poisoning with sulphuric acid, where life was prolonged for twelve
hours, he could detect by minute analysis only 4½ grains of the acid in
the contents and tissue of the stomach. But then the hole was surrounded
by signs of vital reaction, and so was the spleen upon which the
aperture opened.[216] Judging from what I have often seen in animals
killed with oxalic acid, which is the most rapidly fatal of all
corrosives, so that little time is allowed for vital action, and also
several times in persons who had died quickly from the action of
sulphuric acid, I believe no poison can dissolve the stomach, without
such unequivocal signs of violent irritation of the undissolved parts of
the villous coat, as will secure an attentive observer from the mistake
of confounding with these appearances the effects of spontaneous
erosion. Spontaneous erosion is very generally united with unusual
whiteness of the stomach, and there is never any material vascularity.

Resting on the description now given of the spontaneous and poisonous
varieties of corrosion, it is an easy matter to decide a controversy,
which at the time it occurred made a great deal of noise, and upon which
the opinions of toxicologists have been unnecessarily divided. It is the
question regarding death by poison which occurred in the trial of Mr.
Angus at Liverpool in 1808 for the murder of his housekeeper Miss Burns.
The poison suspected was corrosive sublimate. The symptoms were those of
irritation in the alimentary canal,—vomiting, purging, and pain. In the
dead body there was not any particular redness either of the intestines
or of the stomach. But on the fore part of the stomach an aperture was
found between the size of a crown piece and the palm of the hand; it had
a ragged, pulpy margin; and the dissolution of the inner coat extended
two inches from it all round the hole. No mention is made of adhesion or
coloration of the margin. This description, it will be remarked, answers
exactly that given above of spontaneous gelatinized perforation; and the
absence of the signs of vital action around the hole and in the rest of
the stomach is incompatible with the effects of a strong corrosive
poison, unless death had occurred very soon after it was swallowed.
This, however, was out of the question; for then the poison would have
been found in the stomach,—which it was not.[217]

The case of Angus is not the only instance in recent times of
spontaneous perforation having given rise to an opinion by medical men
in favour of poisoning, and consequently to a criminal trial. Six years
afterwards a similar incident occurred in France. A young woman near
Montargis having died of a short illness, and a large erosion having
been found in the stomach after death, six practitioners, on a view of
the parts, and without referring to the antecedent symptoms or
attempting an analysis of the contents of the stomach, declared that she
died of the effects of some corrosive poison. The husband and
mother-in-law, against whom there does not appear to have been a shadow
of general evidence, were therefore imprisoned and subsequently tried
for their lives. Luckily, however, an intelligent physician of the town
saw the error of the reporters, and after vainly endeavouring to
persuade them to revise their opinion, was the means of the case being
remitted to the medical faculty of Paris. That distinguished body, with
Professor Chaussier at its head, gave a unanimous and decided opinion,
not only that there was not any proof of poisoning, but likewise that
the woman could have died of nothing else than spontaneous perforation.
The leading features of the medical evidence will at once show how
indefensible the conduct and opinion of the original reporters were. The
last meal taken by the woman before she became ill, and the only one at
which poison could have been administered by the prisoners, was her
supper; her illness did not begin till past six next morning; the
symptoms were mortal coldness, fainting, general pains, headache, pain
in the stomach, purging and colic, without vomiting, and she died after
twenty-four hours’ illness; the morbid appearances were general redness
of the stomach, softening and pulpy destruction of a third part of its
posterior parietes, and nevertheless the presence in the stomach of a
pint and a half of fluid matter, containing evidently the remains of
soup taken by the woman after she felt unwell. On the decision of the
Parisian faculty the prisoners were discharged; and the original
reporters were deservedly handled with great severity in several
publications that appeared not long after.[218]

_Of perforations of the Gullet and Intestines from natural causes, and
their distinctions from those produced by poisons._—The intestines, and
sometimes even the gullet, may be perforated by the same erosive or
solvent process as the stomach. Thus Mr. Allan Burns observes, that in
four plump children, whose previous history he could not learn, he found
every part of the alimentary canal, from the termination of the gullet
down to the beginning of the rectum, reduced to a gluey, transparent
pulp, like thick starch. The bodies were quite free from putrefaction;
but the abdomen exhaled a very sour smell when opened. No other organic
derangement could be detected.[219] The particulars of a similar case,
with an account of the symptoms, have been lately published by Mr.
Smith, a London surgeon. In the body of a child who died of protracted
diarrhœa subsequent to weaning, the whole intestines, from the duodenum
to the sigmoid flexure of the colon, were found fourteen hours after
death gelatinous, semitransparent, and so soft and brittle that they
could not bear their own weight, but tore when lifted between the
fingers. The stomach and rectum were healthy.[220] I lately met with the
following instance, where the erosion clearly took place after death. In
the body of a girl who died within twelve hours of poisoning with
red-precipitate, the stomach and duodenum were found much inflamed, but
quite entire and firm three days after death. Eighteen days afterwards,
when I had an opportunity of examining these organs, their textures
remained firm everywhere, except a few inches below the pylorus, where I
found two apertures in the duodenum, each as big as a crown, and
surrounded by extensive jelly-like softening.

The following case from Laisné’s treatise shows that the gullet may be
also dissolved in the same way. A woman three days after delivery was
attacked with puerperal peritonitis, and died in four days. In the belly
were found the usual morbid appearances of peritonitis: but in addition
there was in the lower part of the gullet a large oval aperture two
inches long, which penetrated through the posterior mediastinum into the
lungs.[221] Another singular instance of the same kind has already been
mentioned under the head of the symptoms (see p. 107). Another has been
described by Dr. Marshall Hall. In a child who died of bronchitis, an
opening was found in the gullet about the size of a pea, so that the
canal of the gullet communicated with the sac of the pleura; and several
veins appeared also to have been opened.[222] The stomach was likewise
perforated.

It is not difficult to draw the distinction between these perforations
and the effects of poison. The throat and gullet may be partially
disorganized or corroded by the strong corrosives; but they are very
rarely penetrated, since the greater part of the poison must pass into
the stomach or be rejected by vomiting. Destruction of the mucous coat
is a common consequence, and stricture occasionally follows; but I have
hitherto met with only one instance among the innumerable published
cases of poisoning with the mineral acids, alkalis, and other
corrosives, where the gullet was perforated. In that case the
perforation was the result of slow ulceration from poisoning with
sulphuric acid, where life was prolonged for two months.[223]
Perforation from simple corrosion never occurs. The intestines are never
perforated by chemical corrosion from within, for either the poison is
in a great measure expelled from the stomach by vomiting, or the pylorus
contracts and prevents the passage of every poison that is sufficiently
concentrated to corrode. Both the small and great intestines might be
corroded from without, in consequence of the poison escaping through a
hole in the stomach. I am not acquainted, however, with any case of the
kind where, intestinal perforation has occurred.

When the intestines are pierced by true ulceration, it is impossible to
tell whether it arose from natural disease or an irritant poison.

The mode of forming a diagnosis between the symptoms and appearances of
irritant poisoning and those of natural disease being thus explained,
the different species of poisons which have been arranged in the class
of irritants will now be considered in their order.

The irritant class of poisons may be divided into five orders: the acids
and their bases; the alkalies and their salts; the metallic compounds;
the vegetable and animal irritants; the mechanical irritants. In a short
appendix some substances will be mentioned which are not usually
considered poisonous, but are capable of causing violent symptoms when
taken in large doses.

The greater number of poisons included in the first order have a very
powerful local action. Most of them possess true corrosive properties
when they are sufficiently concentrated. Most of them likewise act
remotely. One of them, oxalic acid, is evidently not so much an irritant
as a narcotico-acrid; but since its most frequent action as seen in man
is irritation, it seems inexpedient to break the natural arrangement for
the sake of logical accuracy. This is far from being the only instance
where the toxicologist is compelled to violate the principles of
philosophical classification.

In the present Order are included four of the mineral acids, the
sulphuric, nitric, muriatic and phosphoric, with their bases,
phosphorus, sulphur, and chlorine: To these may be added iodine and
bromine, with their compounds, and also oxalic and acetic acid, two of
the vegetable acids.




                              CHAPTER III.
                  OF POISONING WITH THE MINERAL ACIDS.


Of the mineral acids, the most important, because the most common, are
_sulphuric_, _hydrochloric_, and _nitric_ acids. They are remarkably
similar in their effects on the animal economy. Phosphoric acid is of
much less consequence, and will be noticed cursorily.

Sulphuric acid (_vitriolic acid_, _vitriol_—_oil of vitriol_),
hydrochloric acid (_muriatic acid_,—_spirit of salt_) and nitric acid
(_aqua-fortis_), have been long known to be possessed of very energetic
properties; and consequently cases of poisoning with them have often
been observed. The instances of the kind hitherto published have been
chiefly the result of suicide; a considerable number have originated in
accident; and, however extraordinary it may appear, a few have been
cases of murder. Tartra, in an excellent memoir on the subject of
poisoning with nitric acid, quotes an instance of a woman having been
poisoned while in a state of intoxication by that acid being mixed with
wine and poured down her throat.[224] Valentini has related the case of
a woman who was killed by frequent doses of sulphuric acid given under
the pretence of administering medicines.[225] In 1829 an hospital
servant was condemned at Strasbourg for trying to murder his wife in
like manner, by first making her ill with tartar-emetic and then giving
her sulphuric acid in syrup, under the pretence of curing her.[226] At
the Aberdeen autumn circuit in 1830 a woman Humphrey was convicted of
murdering her husband by pouring the same acid down his throat while he
lay asleep with his mouth open.[227] On the whole, considering the
powerful taste and excessively acrid properties of these poisons, it is
probable that they will seldom be resorted to for the purpose of making
away with another person, who is an adult, and in a state of
consciousness. Of late, however, there have been several instances in
our country of murder committed on infants in this barbarous manner. A
woman Malcolm was executed here in 1808 for murdering her own child, an
infant of eighteen months, by pouring sulphuric acid down its
throat;[228] another woman Clark was tried for the same crime at Exeter
in 1822; a man was executed lately at Manchester for murdering in the
same way his son, a child four years and a half old;[229] and the
particulars of an interesting trial will be presently noticed, that of
Overfield, who was executed at Shrewsbury in 1824, for poisoning his
child in the like manner.[230]

In a medico-legal point of view, the mineral acids are interesting on
another account. Of late a new crime has arisen in Britain, the
disfiguring of the countenance by squirting oil of vitriol on it. It
originated in Glasgow, during the quarrels in 1820, between masters and
workmen regarding the rate of wages,[231] and became at last so
frequent, that the Lord Advocate, in applying for an act of Parliament
to extend the English Stabbing and Maiming act to Scotland, added a
clause which renders the offence now alluded to capital. In 1828 a woman
Macmillan was tried here and condemned under that act.[232] The crime
afterwards became common in England. Three cases were noticed in the
newspapers as having occurred in London, in November, 1828; and two
others near Manchester in the spring of 1829. It is now much less
frequent.

The mineral acids are also very interesting on scientific grounds. They
afford the purest examples of true corrosive poisons, their poisonous
effects depending entirely on the organic injury they occasion in the
textures to which they are applied. It is of use to set out, in
investigating the effects of poisons, by determining the phenomena
presented under such circumstances. When made aware of the rapidity with
which other irritating poisons prove fatal, and the slight signs they
commonly leave of their operation, one cannot fail to be struck with
discovering what the animal frame will sometimes endure from these the
most violent of all irritants, and nevertheless recover.

In laying down the mode of determining by chemical evidence a case of
supposed poisoning with any of the three mineral acids mentioned above,
it will be unnecessary to notice any of their chemical properties,
except those from which their medico-legal tests are derived.

The only common properties that require notice are, their power of
reddening the vegetable blue colours, for showing which litmus-paper is
commonly used, and is most convenient: and their power of staining and
corroding all articles of dress, especially such as are made of wool,
hair, and leather. This last property is specified, though a familiar
one, because it always forms important evidence in criminal cases. In
order to give precision to such evidence, it is necessary to remember,
that if the article of dress is a coloured one, it is generally rendered
red by the mineral acids; but that the vegetable acids also will redden
most articles of dress, although they do not corrode them.


                  I.—OF POISONING WITH SULPHURIC ACID.

Sulphuric acid is extensively employed in very many trades, is used even
for some domestic purposes, and is consequently familiar to every one.
Hence it is the mineral acid which has been most commonly used as a
poison, especially for committing suicide. Of 35 cases of poisoning with
the mineral acids which occurred in England in the years 1837 and 1838,
32 were caused by this acid (p. 90).


             SECTION I.—_Of the Tests for Sulphuric Acid._

Sulphuric acid is known as a poison chiefly in the form of the
concentrated commercial acid. But a few cases of poisoning have also
been produced by blue-liquor or the solution of indigo in strong
sulphuric acid; and one instance[233] has been recorded of poisoning
with the aromatic sulphuric acid of the Pharmacopœias, which is an
infusion of aromatics in a mixture of sulphuric acid, ether and alcohol.
In the following remarks on its tests, it will be sufficient to consider
it _first_ in the concentrated form,—_secondly_, in a state of simple
dilution,—and _thirdly_, when mixed with various impurities, more
especially with vegetable and animal matter. The acid solution of indigo
may be known by the tests for the concentrated acid, and its blue
colour, removable by a solution of chlorine; and the aromatic sulphuric
acid may be distinguished by its odour and the tests for the diluted
acid.

1. _When concentrated_ it is oily-looking, colourless, or brownish from
having acted on organic particles, without odour, much heavier than
water, and capable of quickly corroding animal substances. If from these
properties, and its effect in reddening litmus, its exact nature be not
considered obvious, it may be heated with a few chips of copper; when
sulphurous acid is disengaged and may be readily recognised by its
odour.

2. _When diluted_, it may be distinguished from all ordinary acids by
solution of nitrate of baryta occasioning a heavy white precipitate of
sulphate of baryta, which is insoluble in nitric acid. Selenic and
sulphurous acids, however, and also, as Mr. Alfred Taylor informs me he
has lately found, the fluo-silicic acid, are similarly acted on in all
respects. But selenic and fluo-silicic acids in all forms, and
sulphurous acid in a state of solution, are so seldom met with, being
known only in the laboratory of the scientific chemist, that they can
scarcely be considered sources of fallacy. Sulphuric acid may at once be
distinguished from sulphurous acid, by the latter possessing a peculiar
pungent odour. From the two other acids it may be distinguished by
collecting and drying the barytic precipitate, mixing this with
charcoal, converting it into sulphuret of barium by heating it in a
platinum spoon before the blowpipe, and then adding diluted muriatic
acid to the sulphuret, so as to disengage sulphuretted hydrogen
gas,—which again is easily known by its odour, or its property of
blackening paper dipped in solution of acetate of lead. A much more
important source of fallacy than these is the possible presence of a
bisulphate in solution, or a neutral sulphate along with any other free
acid; for these substances will present the same reactions with litmus
and barytic salts as free sulphuric acid itself. Much has been published
lately upon this point; but the difficulty has not yet been
satisfactorily overcome. It may be got rid of indeed by proving, that no
bisulphate or neutral sulphate is present. Their absence may be shown by
no solid residuum being left on evaporating the suspected fluid, or at
least no more than a mere haziness, owing to the sulphate of lead which
commercial sulphuric acid always contains in small quantity. Or as
Orfila suggests, we may establish their absence still better by
concentrating the fluid, and finding that neither carbonate of soda,
which would cause a precipitate with earthy or metallic bases, nor
chloride of platinum, which would do so with potash or ammonia in
combination, nor fluo-silicic acid, which precipitates soda salts, has
any effect when applied to separate portions of the subject of inquiry.
But suppose it appears in the course of these trials that one or more
bases are actually present, how is it to be settled whether the
sulphuric acid, indicated by litmus and a salt of baryta, is really free
or not? To this question I must reply, that no method has yet been
proposed, which is at once satisfactory and easily available. Mr. Alfred
Taylor proposes to concentrate the fluid, and agitate it with alcohol,
in the hope that the alcohol will remove sulphuric acid, and not a
sulphate, from the water.[234] But it removes sulphuric acid from a
bisulphate even when dry, and still more when a little water is present.
Orfila[235] proposes, in the case of sulphuric acid in vinegar,—where
there is both a vegetable acid and a neutral sulphate of lime,—to
concentrate to a sixth, and agitate the residuum with four times its
volume of sulphuric ether, in the expectation that this fluid will
remove the free acid alone, and separate it from sulphates. But
notwithstanding the authority of his name for the fact, pure ether will
not remove sulphuric acid from a watery fluid; and etherized alcohol,
which does remove it, takes it away also, like alcohol itself, from
bisulphates. These results I have observed in some careful trials made
along with Dr. Douglas Maclagan. I suspect, therefore, that where
sulphates or bisulphates do exist, there is no absolutely satisfactory
way of determining whether free sulphuric acid also co-exists, except by
a quantitative analysis, for ascertaining whether the amount of acid and
of bases corresponds with this supposition or not. And it is scarcely
necessary to add, that so operose a method is scarcely applicable to
ordinary medico-legal investigations.

3. It is seldom that the medical jurist is called on to search for
sulphuric acid in either of the states already mentioned. Much more
generally it has mingled with and acted on various organic substances.
The circumstances in which it has usually to be sought for in the
practice of medical jurisprudence are twofold,—on the one hand, in
stains on clothes,—and on the other, in vomited matter, the contents of
the stomach, or organic mixtures generally.

_Process for analyzing stains on clothes._—When sulphuric acid is thrown
upon your clothes, it produces a permanent red, reddish-brown, or
yellowish stain, destroys the cloth entirely or renders it brittle, and
in consequence of its strong attraction for water keeps the stain long
in a moist state. In the course of the decomposition of the cloth a part
of the acid is itself decomposed, sulphurous acid being disengaged. But
it is an important medico-legal fact, that after a time the change
either goes on very slowly, or is arrested altogether, possibly by the
dilution of the acid with moisture from the atmosphere; and that
consequently it may be discovered in a free state in stains after a much
longer interval than would _à priori_ be expected. In the case of
Macmillan formerly alluded to, Dr. Turner and I, who were employed by
the crown to examine the different injured articles of dress, found on a
man’s hat, stock, shirt-collar and coat many discoloured and corroded
spots, which were sour to the taste fourteen days after the crime was
committed; in the subsequent case of Mrs. Humphrey I discovered
six-tenths of a grain of free sulphuric acid in two small spots on a
blanket seven weeks after the crime; and from an express experiment on
the same blanket with two drops of acid of known strength, it appeared
that only one-half of the acid disappeared in seven weeks. It may
therefore be inferred, that, in every instance where stains have been
produced by concentrated sulphuric acid on clothes, at least on woollen
clothes, and no attempt has been made to remove the remaining acid by
washing or neutralization, a sufficient quantity will be present even
after several weeks to admit of being satisfactorily detected by
chemical analysis.

The following are the steps of the process which appear to me the most
delicate and equivocal. Cut away the stained spots; boil them for a
minute or two in several successive small portions of distilled water;
and filter if necessary. Next prove the acidity of the fluid by litmus,
and likewise by the taste if the quantity of solution is large enough to
allow of so coarse a test being used; and with a few drops ascertain the
existence of sulphuric acid in one form or another by nitrate of baryta
and nitric acid, as mentioned in the process for the pure diluted acid.
If no precipitate appears, the search for sulphuric acid is at an end.
But if a precipitate is produced, ascertain the absence of bisulphates
and sulphates by proving the absence of bases, according to the method
described in the process for the simple diluted acid. If, however, bases
be found in material proportion to the acid, the analysis is subject to
all the difficulties mentioned above in speaking of the detection of the
diluted acid in similar circumstances.

_Process for the contents of the stomach and other complex
mixtures._—When sulphuric acid has been mixed with various mineral and
organic substances, it may in no long time cease to exist in the free
state. Part may be decomposed by organic matter in the way formerly
mentioned. Or the whole may be neutralized at once by earthy or alkaline
carbonates, administered purposely as antidotes. Or it may also be
neutralized more slowly by the gradual development of ammonia in
consequence of the decay of the animal matter co-existing in the
mixture. Thus in a case mentioned by Mertzdorff of a child killed in
twelve hours with sulphuric acid, the contents of the stomach did not
redden litmus, but on the contrary had an ammoniacal odour; and they
contained a considerable quantity of a soluble sulphate, probably the
sulphate of ammonia.[236] In like manner MM. Orfila and Lesueur found
that when this acid was left some months in a mixture which contained
putrefying azotized matter, it was gradually neutralized by
ammonia.[237] It appears from Orfila’s latest researches,[238] that in
most cases of acute poisoning with this substance some free acid will be
found in the contents or tissues of the stomach, provided alkalis or
earths were not given as antidotes, and the examination of the body be
made before decay sets in.

The detection of sulphuric acid in complex organic mixtures, simple
though it appears at first sight, is one of the most difficult problems
in medico-legal chemistry. The difficulty arises from a variety of
sources,—from the probable presence of neutral sulphates along with free
hydrochloric, acetic, or some other acid,—the possible presence of a
bisulphate,—the occasional neutralization of the sulphuric acid by
antidotes given during life, or ammonia evolved during decay after
death,—or its neutralization, together with the development of a
different free acid, by its having displaced this acid from a salt
existing in the mixture.

The subject was investigated in most of its relations in the last
edition of the present work, and a process proposed which overcame some
difficulties, but left others untouched. The inquiry has been since
undertaken also by M. Devergie and Professor Orfila, but with most
success in Germany by Dr. Simon.[239] The result of all these researches
is, that a satisfactory process for detecting sulphuric acid in organic
mixtures still remains to be discovered. Meanwhile the most eligible
method appears to me to be the following.

a. _If the mixture be acid_, add distilled water, if necessary, boil,
filter, and test a few drops of the fluid with nitrate of baryta,
followed by nitric acid. If there be no precipitate, the search for
sulphuric acid is at an end. If a precipitate form, distil the fluid
from a muriate of lime or oil bath, at a temperature not above 240°,
till the residuum acquire a thick syrupy consistence; and preserve apart
the last sixth of the distilled liquor. In this liquor test for
hydrochloric acid by litmus-paper and nitrate of silver, and for acetic
acid by litmus-paper, and the odour and taste of the liquid. If these
acids be not in the distilled fluid, they are not in the residuum. In a
portion of this residuum search for nitric acid, and in another portion
for oxalic acid, by the processes for these poisons in complex mixtures.
If all these acids be thus proved to be absent, it is most unlikely that
the acidity of the mixture is owing to any other but sulphuric acid,
especially in the case of the contents or textures of the stomach.

Dilute now what remains of the syrupy extract, and add nitrate of baryta
with nitric acid. If a precipitate arise, there is a strong presumption
that the acidity of the mixture was owing either to a bisulphate or to
free sulphuric acid. And between these the question may be almost
settled, first by the probability or improbability of a bisulphate
having come in the way, and secondly, by the symptoms and morbid
appearances. The result however cannot justify more than a presumptive
opinion.—But if hydrochloric, acetic or nitric acid be indicated in the
subject of analysis, or an acid sulphate, the whole process is vitiated,
and it is scarcely possible to arrive at any trustworthy conclusion.

The difficulties adverted to above have been made the ground-work of
various processes; which however seem to me all imperfect.—It has been
proposed to divide the mixture into two equal parts, to precipitate one
directly by a barytic salt, to do the same with the other after drying
and incinerating it, to compare the weight of the precipitates, and to
infer the presence of free sulphuric acid if the former is more than
double the latter. Various objections however may be brought against
this check, not the least serious being its difficulty in ordinary
hands, whenever the precipitates are none of them considerable.—Simon
proposes to exhaust the residuum of evaporation with absolute alcohol,
in the hope that free sulphuric acid will alone be taken up;[240] but he
himself found that neutral sulphates are dissolved partially; and
besides, alcohol removes sulphuric acid from bisulphates.—Orfila
proposes to remove free sulphuric acid by agitating the concentrated
liquor with sulphuric ether, and separating and evaporating off the
ether; for he holds that all neutral and acid salts of sulphuric acid
are insoluble in ether.[241] This proposal is unaccountable. Simon
stated in his paper three years before, that ether does not remove
sulphuric acid from watery fluids containing it. And Dr. Douglas
Maclagan and I, on inquiring into the matter, found that we could not,
by means of ether, separate a particle of sulphuric acid from an ounce
of rice soup and mucilage to which ten drops of the acid had been added.
The process of Orfila for establishing the absence of bases in a simple
watery solution is applicable to organic mixtures also, after
incineration. But if bases be present in material quantity, all the
difficulties now in question remain in full force.

b. _When the mixture is neutral_, sulphuric acid may be detected in it
by the first steps of the preceding process. But the inference, that it
once existed free can only be drawn when the subject of examination is
not in a state of decay, when the quantity of sulphate of baryta
obtained is considerable, when the administration of an antidote is
proved, and when the ashes after incineration contain the antacid base
which is said to have been administered. Even then the inference is only
presumptive.


 SECTION II.—_Of the Mode of Action of Sulphuric Acid, and the Symptoms
                         caused by it in Man._

It was formerly observed that the action of the strong mineral acids is
independent of the function of absorption. They act by the conveyance
along the nerves of an impression produced by the irritation or
destruction of the part to which they are applied. There is very little
difference between the three acids in the symptoms they excite or the
action they exert.

When sulphuric acid is introduced directly into a vein it causes death
by coagulating the blood. Thus, when Professor Orfila injected in the
jugular vein of a dog half a drachm diluted with an equal weight of
water, he observed that the animal at once struggled violently,
stretched out its limbs, and expired; and on opening the chest
immediately, he found the heart and great vessels filled with coagulated
blood.[242]—Nitric acid and hydrochloric acid act in the same way.

If, on the other hand, they are introduced into the stomach, the blood
as usual remains fluid for some time after death; the symptoms are
referrible almost solely to the abdomen; and in the dead body the
stomach is found extensively disorganised, and the other abdominal
viscera sometimes inflamed. If the dose be large, and the animal
fasting, death may take place in so short a time as three hours: but in
general it lives much longer.[243]

When the strong mineral acids are applied outwardly, they irritate,
inflame, or corrode the skin. The most rapid in producing these effects
is the nitric, or rather the nitrous acid. The strong, fuming nitrous
acid even causes effervescence when dropped on the skin.

Orfila has proved that sulphuric acid, as well as the two other mineral
acids, is absorbed; for they may be detected in the urine, when they are
introduced either into the stomach or through a wound.[244] He could not
succeed, however, in detecting any of them in the liver or spleen; in
which organs it will be seen, hereafter, that various other poisons may
be discovered by chemical analysis. But Mr. Scoffern seems to have found
sulphuric acid in the kidney, even although the individual survived the
taking of the poison nearly two days.[245] It is also worthy of remark,
that, as will be proved presently, these acids may pass through the
coats of the stomach by transudation, and so be found on the surface of
the other organs in the belly.

Toxicology is indebted to M. Tartra for the first methodic information
published respecting the symptoms caused in man by sulphuric acid and
the other mineral acids:[246] but many important additional facts have
been made known by numberless cases of poisoning which have since
appeared, chiefly in the periodic journals.

The symptoms caused by all the three acids are so nearly the same, that
after a detailed account of those occasioned by sulphuric acid, it will
not be necessary to add much on the subject under the head of nitric and
muriatic acid.

M. Tartra considers that four varieties may be observed in the effects
of the mineral acids. 1. Speedy death from violent corrosion and
inflammation; 2. Slow death from a peculiar organic disease of the
stomach and intestines; 3. Imperfect recovery, the person remaining
liable ever after to irritability of the stomach; 4. Perfect recovery.

1. The most ordinary symptoms are those of the first variety,—namely,
all the symptoms that characterise the most violent gastritis,
accompanied likewise with burning in the throat, which is increased by
pressure, swallowing, or coughing;[247]—eructations proceeding from the
gases evolved in the stomach by its chemical decomposition;—and an
excruciating pain in the stomach, such as no natural inflammation can
excite. The lips are commonly shrivelled, at first whitish, but
afterwards brownish in the case of sulphuric acid. Occasionally there
are also excoriations, more rarely little blisters. Similar marks appear
on other parts of the skin with which the acid may have come in contact,
such as the cheeks, neck, breast, or fingers; and these marks undergo
the same change of colour as the marks on the lips. I had an opportunity
of witnessing this in the case of the man who was disfigured by the
Macmillans (p. 122) with sulphuric acid. He was cruelly burnt on the
face as well as on the hands, which he had raised to protect his face;
and the marks were at first white, but in sixteen hours became brownish.
The inside of the mouth is also generally shrivelled, white, and often
more or less corroded; and as the poisoning advances, the teeth become
loose and yellowish-brown about the coronæ. The teeth sometimes become
brown in so short a time as three hours.[248] Occasionally the tongue,
gums, and inside of the cheeks are white, and as it were polished, like
ivory.[249] There is almost always great difficulty, and sometimes
complete impossibility, of swallowing. In the case of a child related by
Dr. Sinclair, of Manchester, fluids taken by the mouth were returned by
the nose; and the reason was obvious after death; for even then the
pharynx was so much contracted as to admit a probe with difficulty.[250]
On the same account substances taken by the mouth have been discharged
by an opening in the larynx which had been made to relieve impending
suffocation. The matter vomited, if no fluids be swallowed, is generally
brownish or black, and at first causes effervescence, if it falls on a
pavement containing any lime. Afterwards this matter is mixed with
shreds of membrane, which resemble the coats of the stomach, and
sometimes actually consists of the disorganised coats, but are generally
nothing more than coagulated mucus. The bowels are obstinately costive,
the urine scanty or suppressed; and the patient is frequently harassed
by distressing tenesmus and desire to pass water. The pulse all along is
very weak, sometimes intermitting, and towards the close imperceptible.
It is not always frequent; on the contrary, it has been observed of
natural frequency, small and feeble in a patient who survived fifteen
days.[251] The countenance becomes at an early period glazed and
ghastly, and the extremities cold and clammy. The breathing is often
laborious, owing to the movements of the chest increasing the pain in
the stomach,—or because pulmonary inflammation is also at times
present,—or because the admission of air into the lungs is impeded by
the injury done to the epiglottis and entrance of the larynx. To these
symptoms are added occasional fits of suffocation from shreds of thick
mucus sticking in the throat, and sometimes croupy respiration, with
sense of impending choking.

Such is the ordinary train of symptoms in cases of the first variety.
But sometimes, especially when a large dose has been swallowed, instead
of these excruciating tortures, there is a deceitful tranquillity and
absence of all uneasiness. Thus, in the case of a woman who was poisoned
by her companions making her swallow while intoxicated aqua-fortis mixed
with wine, although she had at first a good deal of pain and vomiting,
there were subsequently none of the usual violent symptoms; and she died
within twenty hours, complaining chiefly of tenesmus and excessive
debility.[252] Occasionally eruptions break out over the body:[253] but
their nature has not been described.

Death is seldom owing to the mere local mischief, more generally to
sympathy of the circulation and nervous system with that injury.
According to Bouchardat death arises from the acid entering the blood in
sufficient quantity to cause coagulation.[254] But although this
certainly happens sometimes to the blood in the vessels of the stomach
and adjacent organs, as will be proved under the head of the morbid
appearances, there is no evidence that the same takes place throughout
the blood-vessels generally, or in the great veins and heart in
particular. Bouchardat’s proofs of the detection of sulphuric acid in
the blood are not satisfactory.

The duration of this variety of poisoning with the acids is commonly
between twelve hours and three days. But sometimes life is prolonged for
a week[255] or a fortnight;[256] and sometimes too death takes place in
a very few hours. The shortest duration among the numerous cases of
adults mentioned by Tartra is six hours;[257] but Dr. Sinclair, of
Manchester, has related a case which lasted only four hours and a
half;[258] a man lately died in the Edinburgh Infirmary within four
hours; and Professor Remer of Breslau once met with a case fatal in two
hours.[259]

The quantity required to produce these effects has not been ascertained,
and must be liable to the same uncertainty here as in other kinds of
poisoning. The smallest fatal dose of sulphuric acid I have hitherto
found recorded was one drachm. It was taken with sugar by mistake for
stomachic drops by a stout young man, and killed him in seven days.[260]
An infant of twelve months has been killed in twenty-four hours by half
a tea-spoonful, or about thirty minims.[261] A man has recovered after
taking six drachms.[262]

2. The second variety of symptoms belong to a peculiar modification of
disease, which is described by Tartra in rather strong language. It
begins with the symptoms already noticed; but these gradually abate. The
patient then becomes affected with general fever, dry skin, spasms and
pains of the limbs, difficult breathing, tension of the belly,
salivation, and occasional vomiting, particularly of food and drink.
Afterwards membranous flakes are discharged by vomiting, and the
salivation is accompanied with fœtor. These flakes are often very like
the mucous membrane of the stomach and intestines; and such they have
often been described to be. More probably, however, they are of
adventitious formation; for the mere mucous coat of the alimentary canal
cannot supply the vast quantity that is evacuated. There is no doubt,
however, that the lining membrane of the alimentary canal is
occasionally discharged. Dr. Wilson has mentioned an instance of the
ejection by coughing of about nine inches of the cylindrical lining of
the pharynx and gullet six days after sulphuric acid was taken.[263]
Sometimes worms are discharged dead, and evidently corroded by the
poison.[264] Digestion is at the same time deranged, the whole functions
of the body are languid, and the patient falls into a state of marasmus,
which reduces him to a mere skeleton, and in the end brings him to the
grave. Death may take place in a fortnight, or not for months. In one of
Tartra’s cases the patient lived eight months. The vomiting of
membranous flakes continues to the last.

3. The third variety includes cases of imperfect recovery. These are
characterized by nothing but the greater mildness of the primary
symptoms, and by the patient continuing for life liable to attacks of
pain in the stomach, vomiting of food and general disorder of the
digestive function.

4. The last variety comprehends cases of perfect recovery, which are
sufficiently numerous even under unpromising appearances. From the
average of 55 cases recorded by Tartra it appears that the chances of
death and recovery are nearly equal. Twenty-six died, 19 of the primary,
7 of the secondary disorder. Twenty-nine recovered, and of these
twenty-one perfectly. Suicidal are for obvious reasons more frequently
fatal than accidental cases.

Tartra has not taken notice in his treatise of another form of poisoning
with the strong acids,—in which the injury is confined to the gullet and
neighbouring parts. In Corvisart’s Journal there is the case of a man,
who began to drink sulphuric acid for water while intoxicated, but
suddenly found out his error before he had swallowed above a few drops;
and consequently the chief symptoms were confined to the throat. After
his physician saw him he was able to take one dose of a chalk mixture;
but from that time he was unable to swallow at all for a fortnight.[265]
Martini likewise met with a similar instance of complete dysphagia from
stricture in the gullet caused by sulphuric acid.[266] His patient
recovered.

It also appears exceedingly probable, that the strong acids may cause
death, without reaching the stomach or even the gullet, by exciting
inflammation and spasm of the glottis and larynx. Such an effect may
very well be anticipated from an attempt to commit murder with these
poisons; as the person, if he retains consciousness at the time, may
become aware of their nature before he has swallowed enough to injure
the stomach.

Thus, Dr. A. T. Thomson says in 1837, that he once met with the case of
a child, who, while attempting to swallow strong sulphuric acid by
mistake for water, died almost immediately, to all appearance from
suffocation caused by contraction of the glottis; and it was ascertained
after death that none of the poison had reached the stomach.[267]
Professor Quain describes a similar case, occurring also in a child,
where impending death was prevented by artificial respiration, and acute
bronchitis ensued, which proved fatal in three days. In this instance
thickening of the epiglottis and great contraction of the upper opening
of the larynx showed the violent local injury inflicted there,
inflammation could be traced down the trachea into the bronchial tubes,
but no trace of injury could be detected in the gullet and stomach.[268]
In a very interesting and carefully detailed case by Mr. Arnott, where
the poison taken was the nitric acid, the injury was confined in a great
measure to the gullet and larynx,—the stomach, which was distended with
food at the time, being very little affected. The chief symptoms at
first, besides great general depression, were croupy respiration and
much dyspnœa, which became so urgent, that laryngotomy was performed,
and with complete relief to the breathing. But the patient nevertheless
rapidly sunk under the symptoms of general exhaustion, and died in
thirty-six hours without presenting any particular signs of the
operation of the poison on the stomach; and the traces of action found
there after death were trifling.[269]

The importance of the fact established by these cases will appear from
the following medico-legal inquiries. A Prussian medical college was
consulted in the case of a new-born child, in which the stomach and
intestines were healthy, and did not contain poison, but in which the
cuticle of the lips was easily scraped off, the gums, tongue, and mouth
yellowish-green, as if burnt, the velum and uvula in the same state, the
rima glottidis contracted, and the epiglottis, larynx, and fauces
violently inflamed. The College declared, that a concentrated acid had
been given, and that death had been occasioned by suffocation. Sulphuric
acid was found in the house; and the mother subsequently confessed the
crime.[270] A case was formerly quoted (p. 75), where MM. Ollivier and
Chevallier found traces of the action of nitric acid on the lips, mouth,
throat and upper fourth of the gullet, but not lower. In this instance
the reporters came to the opinion from the absence of injury in the more
important parts of the alimentary canal, as well as from the marks of
nail scratches on the neck, and the gorged state of the lungs, that
death had been produced by strangling, after an unsuccessful attempt by
the forcible administration of nitric acid. It is quite possible,
however, that death might quickly ensue from the effects of the poison
on the throat and gullet. In the course of the judicial inquiries M.
Alibert stated that he had known repeated instances of death from
swallowing nitric acid, although none of it reached lower down than the
pharynx. Ollivier in his paper doubts the accuracy of this statement;
but the cases quoted above show clearly that such injury may be done to
the glottis as will be adequate of itself to occasion death.[271]

It seems farther not improbable that, among the terminations of
poisoning with the strong mineral acids, scirrhous pylorus must also be
enumerated. This is a very rare effect of the action of corrosive
poisons. But M. Bouillaud has related an instance of death from
scirrhous pylorus in its most aggravated shape, which supervened on the
chronic form of the effects of nitric acid, and which proved fatal in
three months.[272]

In some circumstances the stomach seems to acquire a degree of
insensibility to the action of the strong acids. Tartra, in alluding to
what is said of certain whisky-drinkers acquiring the power of
swallowing with impunity small quantities of the concentrated acids, has
related the case of a woman at Paris, who, after passing successively
from wine to brandy and from that to alcohol, at last found nothing
could titillate her stomach except aqua-fortis, of which she was seen to
partake by several druggists of veracity.[273] The fire-eating
mountebanks too are said to acquire the same power of endurance; but
much of their apparent capability is really legerdemain. On the other
hand, a very extraordinary sensibility to the action of the diluted
mineral acids has been supposed to exist in the case of infants at the
breast,—so great a sensibility, that serious symptoms and even death
itself have been ascribed to the nurse’s milk becoming impregnated with
sulphuric acid, in consequence of her having taken it in medicinal
doses. By two writers in the London Medical Repository griping pains,
tremors and spasms have been imputed to this cause;[274] and a writer in
the Medical Gazette says he has seen continued griping, green diarrhœa
and fatal marasmus ensue,—apparently, he thinks, from ulceration of the
gastro-intestinal mucous membrane.[275] Without questioning the great
delicacy and tenderness of that membrane in infants, I must nevertheless
express my doubts whether so small a quantity taken by a nurse,
amounting in the cases in question only to four or six drops a day,
could really produce fatal or even severe effects on her child.

Sulphuric acid is not less deadly when admitted into the body through
other channels besides the mouth. Thus, it may prove fatal when
introduced into the rectum. A woman at Bruges in Belgium had an
injection administered, in which, being prepared hastily in the middle
of the night, sulphuric acid had been substituted by mistake for
linseed-oil. The patient immediately uttered piercing cries, and passed
the remainder of the night in excessive torture. In the morning the
bed-clothes were found corroded, and a portion of intestine had
apparently come away; and she expired not long afterwards.[276]

Death may also be occasioned by the introduction of this acid into the
ear. Dr. Morrison relates a case of the kind, where nitric acid, which
is analogous in action, was poured by a man into his wife’s ear, while
she lay insensible from intoxication. She awoke in great pain, which
continued for two or three days. In six days an eschar detached itself
from the external passage of the ear; and this was followed by profuse
hemorrhage, which recurred daily more or less for a month. On the day
after the eschar came away, and without any precursory symptom
referrible to the head, she was attacked with complete palsy of the
right arm, and in eight days more with tremors and incomplete palsy of
the rest of that side of the body. These symptoms subsequently abated;
but they again increased after an imprudent exertion, and she died in a
state of exhaustion seven weeks after the injury. The whole petrous
portion of the temporal bone was found carious, but without any distinct
disease of the brain or its membranes.[277]

Sulphuric acid and the other mineral acids are equally poisonous when
inhaled in the form of gas or vapour; and they then act chiefly by
irritating or inflaming the mucous membrane of the air-passages and
lungs. For some observations on their effects in this form both on
plants and animals the reader may refer to the Chapter on Poisonous
Gases.

Sulphuric acid belongs to the poisons alluded to under the head of
General Poisoning,—of whose operation satisfactory evidence may be
occasionally drawn from symptoms only. If immediately after swallowing a
liquid which causes a sense of burning in the throat, gullet, and
stomach, violent vomiting ensues, particularly if the vomited matter is
mixed with blood; if the mouth becomes white, and stripped of its lining
membrane, and the cheeks, neck, or neighbouring parts show vesications,
or white, and subsequently brown excoriated spots;—if the clothes show
red spots and are moist and disintegrated there,—I cannot see any
objection to the inference, that either sulphuric or muriatic acid has
been taken. In this opinion I am supported by a good authority, Dr.
Mertzdorff, late medical inspector at Berlin.[278]


   SECTION III.—_Of the Morbid Appearances caused by Sulphuric Acid._

The outward appearance of the body in cases of Tartra’s first variety in
the action of the acids is remarkably healthy; every limb is round,
firm, and fresh-looking.

On the lips, fingers, or other parts of the skin, spots and streaks are
found where sulphuric acid has disorganized the cuticle. These marks are
brownish or yellowish-brown, and present after death the appearance of
old parchment or of a burn; sometimes there are little blisters.[279]

The lining membrane of the mouth is more or less disorganized, generally
hardened, and whitish or slightly yellowish. The pharynx is either in
the same state, or very red or even swelled. The rima glottidis, as in
the case described by Dr. Sinclair and in that of Mr. Arnott, is
sometimes contracted, the epiglottis swelled, or on the contrary
shrivelled, and the commencement of the larynx inflamed.[280] The gullet
is often lined with a dense membrane, adhering firmly, resembling the
inner coat, but probably in general a morbid formation; and the
subjacent tissue is brown or red. Sometimes, however, the inner coat or
epithelian of the gullet loses its vitality, and is detached in part or
altogether. In Mr. Arnott’s case the pharynx and upper gullet were lined
by a pale lemon-coloured membrane, which in the lower two-thirds of the
canal was completely detached and was plainly the œsophageal membrane;
in the case related by Mertzdorff, the whole inner coat of the gullet,
as well as that of the throat, epiglottis, and mouth, was stripped from
the muscular coat;[281] and in Dr. Wilson’s case (p. 131), which proved
fatal in ten months, the upper third of the gullet shone like an old
cicatrix, and the lower two-thirds were narrowed, vascular, and softened
on the surface.[282] In a few rare cases of chronic poisoning with the
mineral acids the gullet is found perforated by an ulcerative
process;[283] but it is never perforated by their corrosive action in
quickly fatal cases. Occasionally the gullet is not affected at all,
though both the mouth and the stomach are severely injured; and an
instance has even been published where the acid, in this instance the
nitric, left no trace of its passage downwards till near the
pylorus.[284]

The outer surface of the abdominal viscera is commonly either very
vascular or livid, or bears even more unequivocal signs of inflammation,
namely, effusion of fibrin and adhesions among the different turns of
intestine; and these appearances may take place although the stomach is
not perforated.[285] The cause of this appearance, which is seldom
observed in poisoning with other irritants, more especially with the
metallic irritants, is that the acid passes through the membranes of the
stomach by transudation during life,—as will be proved immediately. It
must be observed, that the peritonæum is sometimes quite natural after
death from sulphuric acid, even although the stomach was perforated. I
have seen this in a case which proved fatal in twelve hours. An
important appearance in the abdomen, to which less attention has been
hitherto paid than it deserves, is gorging of the vessels beneath the
peritonæal membrane of the stomach and adjoining organs with dark,
firmly coagulated blood, arising from the acid having transuded through
the membranes and acted on the blood chemically. My attention was first
turned to this appearance by an interesting case, which I saw in 1840 in
the Royal Infirmary of this city, and of which an able account has been
published by Dr. Craigie.[286] The whole vessels of the stomach were
seen externally to be most minutely injected and gorged, and the blood
in them was coagulated into firmly-cohering cylindrical masses, as if
the vessels had been successfully filled with the matter of an
anatomical injection. This appearance was also observed in the superior
mesenteric arteries, in the omental vessels, and over the greater part
of the mesentery. It was occasioned by the chemical action of the acid
coagulating the colouring matter and albumen; for the clotted blood was
strongly acid to litmus-paper. So too was the peritoneal surface of the
stomach, omentum and intestines. And the acid had transuded through the
stomach and into the omentum and tissues of the intestines during life;
for in the first place, there was no perforation of the stomach, and
secondly, I ascertained that there was no free acid either in the matter
discharged from the stomach before death after the free administration
of antacids, or in the contents of the stomach obtained at the
examination of the dead body.

The stomach, if not perforated, is commonly distended with gases. It
contains a quantity of yellowish-brown or black matter, and is sometimes
lined with a thick paste composed of disorganized tissue, blood and
mucus. The pylorus is contracted.

The mucous membrane is not always corroded. If the acid was taken
diluted, the coats may escape corrosion; but there is excessive
injection, gorging, and blackness of the vessels, general blackness of
the membrane, sometimes even without softening, as in a case related by
Pyl of a woman who first took aqua-fortis and then stabbed herself.[287]
More commonly, however, along with the blackness there is softening of
the rugæ or actual removal of the villous coat, and occasionally regular
granulated ulceration with puriform matter on it.[288] The stomach is
not always perforated. But if it is, the holes are commonly roundish,
and the coats thin at the margin, coloured, disintegrated, and
surrounded by vascularity and black extravasation. In some rare cases
there is no mark of vital reaction except in the neighbourhood of the
aperture. A case of this kind is related by Mertzdorff: The margin of
the hole was surrounded to the distance of half an inch with apparent
charring of the coats, and this areola was surrounded by redness; but
the rest of the stomach was grayish-white.[289] I examined with the late
Dr. Latta of Leith a similar case, where the limitation of the injury
was evidently owing to the stomach having been at the time filled with
porridge. The patient, a child two years old, died in twelve hours; and
on the posterior surface of the fundus of the stomach, towards the
pylorus, there was a hole as big as a half-crown, which was surrounded
to the distance of an inch with a black mass formed of the disorganized
coats, and of incorporated charred blood. But the rest of the stomach
was quite healthy. The most remarkable instance of chemical destruction
of the coats yet known to me is a case mentioned by Mr. Watson of this
city, where suicide was effected by cutting the throat about half an
hour after two ounces of sulphuric acid had been swallowed. The
individual was at first thought to have died simply of the wound of the
throat. But on dissection the usual signs of acid poisoning were found;
and among other effects, it was observed that nearly three-fourths of
the stomach had been entirely destroyed.[290] The perforation, if the
patient lives long enough, is generally accompanied with a copious
effusion into the belly of the usual muddy liquor of peritonitis; and
the outer surface of the viscera feels unctuous, as if from a slight
chemical action of the acid on them. The acid has actually been found in
the contents poured out from the stomach into the sac of the
peritonæum.[291]

One would expect to find the acid always in the stomach when it is
perforated. Nevertheless it is sometimes almost all discharged. In
Mertzdorff’s case, that of an infant who was killed in twelve hours, a
hole was found in the stomach ¾ths of an inch in diameter, and the
contents of the stomach were effused into the belly: yet by a careful
analysis the whole acid he could procure from the contents and tissues
together was only 4½ grains. Sometimes of course the disappearance of
the acid may be owing, as in Dr. Craigie’s case, to the effectual
administration of antacids during life.

The inner coat of the duodenum often presents appearances closely
resembling those of the stomach. Sometimes, however, as in the case just
related from Mertzdorff, and in the infant I examined, the inner coat of
the small intestines is not affected at all, probably because in such
rapid cases the pylorus retains a state of spasmodic contraction till
death or even after it.

The urinary bladder is commonly empty. The thoracic surface of the
diaphragm is sometimes lined with lymph, indicating inflammation of the
chest. In the case which was fatal in two hours [p. 131], Professor
Remer found the surface of the lungs, as well as that of the liver and
spleen, brown and of a leathern consistence, and the tissue beneath
scarlet;—appearances which he thinks arose from the acid penetrating in
vapour and acting chemically. I have not found this appearance mentioned
by any other writer; but I have seen it in animals poisoned with oxalic
acid. The blood in the heart and great vessels has been several times
seen forming a firm black clot. Kerkring[292] relates an instance of the
kind; in Dr. Latta’s case the appearance was very distinct; and it is
dwelt on strongly in a recent paper by M. Bouchardat.[293] Bouchardat
thinks this state of the blood is simply the effect of the absorbed
acid; but coagulation of the blood in the heart and great vessels,—a
striking appearance in contradiction to what is observed after death
from most other poisons,—is more probably the healthy state of the
blood, and not the effect of the particular poison.

The general appearance of the body of those who have died of the second
or chronic variety of poisoning with the acids, is that of extreme
emaciation. The stomach and intestines are excessively contracted: The
former has been found so small as to measure only two inches and a half
from the cardia to the pylorus, and two inches from the lesser to the
greater curvature.[294] Tartra says the intestines are sometimes no
thicker than a writing quill. They are in other respects sound
outwardly, except that they sometimes adhere together.

Internally the pylorus is contracted. In a case of slow poisoning, fatal
in three months, which has been described by Dr. Braun of Fürth, the
chief appearance besides excessive emaciation was a thickening of the
coats round and behind the pylorus to such a degree that the opening of
the pylorus was formed of an almost cartilaginous ring several lines
broad, and only wide enough to pass a quill.[295] There are spots over
the stomach apparently of regenerated villous tissue, smoother and
redder than the natural membrane. At the points where the stomach
adheres to the neighbouring organs, its coats are sometimes wanting
altogether, so that when its connections are torn away, perforations are
produced. The other parts of the body are natural.

It may in some circumstances be necessary to determine from the
appearances in the dead body whether sulphuric acid has been the
occasion of death or has been introduced into the body after death. This
may always be easily done. If a few drachms of sulphuric acid be
injected into the anus immediately after death, and the parts be
examined in twenty-four hours, it will be found, that wherever the acid
touches the gut, its mucous coat is yellowish and brittle, its muscular
and peritonæal coats white, as if blanched, and the blood in the vessels
charred; the injury is confined strictly to the parts actually touched,
is surrounded by an abrupt line of demarcation, and shows no sign of
inflammatory redness. Nitric acid produces nearly the same effects. The
whole tunics are yellow, and the disorganization is greater. For these
facts we are indebted to Orfila.[296]

In closing this account of the morbid appearances, some observations
will be required on the force of evidence derived from them; because
circumstances may exclude all other branches of medical proof. In many
instances both of acute and of chronic poisoning with the strong acids,
I conceive, contrary to the general statements of most systematic
writers on modern medical jurisprudence, that distinct evidence might be
derived from morbid appearances only. Thus, what fallacy can intervene
to render the following opinion doubtful? In a case several times
alluded to as described by Mertzdorff, there were vesicles and brown
streaks on the lips, neck, and shoulders, similar to the effects of
burning,—almost total separation of the lining membrane of the mouth,
throat, epiglottis, and gullet,—perforation of the stomach, with a
margin half an inch wide, which was extensively charred, and surrounded
by a red areola. From the appearances alone Mertzdorff declared that the
child must have been poisoned with sulphuric acid. Perhaps he should
have said sulphuric or muriatic acid.

Or take the case of Richard Overfield, who was condemned at Shrewsbury
Assizes in 1824 for murdering his own child, a babe three months old, by
pouring sulphuric acid down its throat. In the dead body the following
appearances were found: The lips were blistered internally and of a dark
colour externally; the gullet was contracted and its inner coat
corroded; the lining membrane of the mouth and tongue of a dull white
colour; the great curvature of the stomach corroded and converted into a
substance like wet brown paper; the stomach perforated and a
bloody-coloured fluid in the sac of the peritonæum.[297] If to these
appearances be added the fact that the child’s dress was reddened, what
is there to prevent the medical jurist from declaring, without reference
to chemical evidence, that this case must have been one of poisoning by
sulphuric acid or some other mineral acids?

In like manner in the case of Mrs. Humphrey, who was condemned at
Aberdeen in 1830 for murdering her husband by pouring sulphuric acid
down his throat while he was asleep, there was found, on examining the
dead body, two brown spots on the outside of the lips,—whiteness of the
inside of the lips and of the gums,—glazing of the palate,—redness, with
here and there ash-coloured discoloration, of the uvula, posterior part
of the throat, pharynx and epiglottis,—abrasion of most of the inner
coat of the gullet,—erosion and dark-red ulceration of the inner coat of
the stomach in winding furrows. When to these appearances it is added,
that the man was in good health only forty-seven hours before death, and
was taken ill instantaneously and violently with burning pain in the
throat and stomach,[298] it is not easy to see what other opinion could
be formed of the case, unless that he died of poisoning with a mineral
acid, and probably with sulphuric acid.

Among the appearances justifying an opinion where chemical evidence
happens to be wanting, not the least important seems to me to be the
peculiar turgescence and induration of vessels under the peritonæum of
the stomach and neighbouring organs, occasioned by the chemical
coagulation of blood in them. It is an appearance, which, when once
seen, cannot be confounded with any natural morbid phenomenon I have
ever witnessed.

I am far from desiring to encourage rashness of decision, or to revive
the loose criterions of poisoning relied on in former times. But there
cannot, in my opinion, be a rational doubt that in the instance of
sulphuric acid there may often be distinct exceptions to the general law
regarding the feebleness of the evidence from morbid appearances; and
that a witness would certainly be guilty of thwarting the administration
of justice, if, relying on general rules, he refused to admit such
exceptions. What natural disease could produce appearances like those
described above? Assuredly no form of spontaneous perforation bears any
resemblance to that caused in most cases of death from sulphuric acid;
nor is it easy to mention any combination of natural diseases which
could produce the peculiar conjunction of appearances remarked in the
case of the man Humphrey.


    SECTION IV.—_Of the Treatment of Poisoning with Sulphuric Acid._

Since this acid and the other mineral acids act entirely as local
irritants, it may be inferred that their poisonous action will be
prevented by neutralizing them. But in applying that principle to the
treatment it is necessary to bear in mind their extremely rapid
operation; for if much time is lost in seeking for an antidote,
irreparable mischief may be caused before the remedy is taken. Should it
be possible then to administer chalk or magnesia without delay, these
are the antidotes which ought to be preferred; but it may be well for
the physician to remember, that in the absence of both he may at once
procure a substitute in the plaster of the apartment beat down and made
into thin paste with water. M. Chevallier, in a paper on the antidotes
for the mineral acids, quotes five cases of poisoning with sulphuric
acid and two with nitric acid, where life seems to have been saved by
the speedy and free administration of magnesia, although in some cases
so large a quantity as two ounces of the poison had been
swallowed.[299]—A solution of soap is another antidote of no small
value. While the antidote is in preparation, the acid should be diluted
by the free use of any mild fluid, such as milk or oleaginous
matters.—The alkaline bicarbonates are also excellent antidotes; but
their carbonates are ineligible, being themselves possessed of corrosive
properties. In a paper on poisoning with the mineral acids by Dr.
Lunding of Copenhagen, the author is disposed to ascribe the large
proportion of deaths in his practice to the system pursued in the
Copenhagen hospital of administering carbonate of potass as an antidote
daily for weeks together.[300] On the other hand however it may be
mentioned, that in a late memoir, on this description of poisoning Dr.
Ebers of Breslau endeavours to show, that there is no reason to dread
the administration of the alkaline carbonates, even the carbonate of
potash, provided they be given with mucilaginous fluids and syrup in a
rather concentrated form; and he gives three cases illustrative of the
good effects of this mode of treatment, which he maintains to be free of
all danger, and preferable to every other antidotal method, because the
remedy may be administered in small volume,—an advantage possessed by it
especially over chalk or magnesia.[301]

After the proper antidote has been given to a sufficient extent, the use
of diluents ought to be continued, as they render the vomiting more
easy.—Some have recommended the stomach-pump for administering antidotes
and diluents; but this is unnecessary. When it is wished to evacuate the
stomach, there is an advantage in allowing it to do so by its own
efforts, if possible; because the evacuation is accomplished in this way
more completely than by the stomach-pump. Besides, if the patient cannot
swallow fluids, still less can he suffer the tube of the stomach-pump to
be introduced. On several occasions, indeed, it has been found
impracticable to introduce it.[302]

The treatment of the surpervening inflammation does not differ from that
of inflammation of the stomach. Where there is great difficulty of
breathing, evidently from obstruction of the larynx, and where the
absence of abdominal pain, tension or vomiting affords a presumption
that little injury has been done to the stomach, laryngotomy appears an
advisable remedy, and has been known to give very great relief.[303] But
the patient may nevertheless die soon of the sympathetic disorder of the
circulation.


                   II.—OF POISONING WITH NITRIC ACID.

Nitric acid is more frequently used as a poison abroad than in this
country. But even in Britain it is not an uncommon cause of severe
accidents and death.


                    _Of the Tests for Nitric Acid._

1. _When concentrated_, nitric acid is easily known by the odour of its
vapour, which is peculiar. When pure, the acid as well as its vapour is
colourless; when mixed with nitrous acid it is of various tints, and
generally yellow. The acid of commerce is at times rendered impure by
sulphuric acid, a circumstance which must be attended to in applying the
subsequent tests.—The simplest test for nitric or nitrous acid is the
action of copper, lead, or tin. If any of these metals in small
fragments, or powder, be thrown into either acid previously diluted with
an equal volume of water, an effervescence takes place, which in the
case of lead or copper is much accelerated by heat; nitric oxide gas is
disengaged; and ruddy fumes of nitrous acid gas are formed when the gas
comes in contact with the oxygen of the air. Another characteristic
test, which has the advantage of being applicable on an extremely small
scale, is morphia, the alkaloid of opium. This substance is turned in a
few seconds to a beautiful orange-red colour by nitric acid, and after
longer contact forms with it a bright yellow solution. No other acid has
this effect. Muriatic acid, as Dr. O’Shaughnessey has remarked,[304]
does not act at all on morphia, and sulphuric acid chars and blackens
it. When nitric acid is added to a solution of narcotin in sulphuric
acid, the colour of the solution is changed from yellow to
blood-red.[305] When it is added to a solution of proto-sulphate of
iron, the solution becomes brown, and the addition of sulphuric acid
then alters the colour to violet.[306] When it is added even in the most
minute proportion to sulphuric acid, the addition of a few particles of
the alkaloid brucia will render the whole fluid red, passing gradually
to yellow.[307]—Many other characteristic tests might be mentioned; but
those now specified are more than enough.

2. _In a diluted state_ this acid is not so easily recognised as the
other mineral acids, for it does not form any insoluble salt or
precipitate with bases.

The most convenient process consists in first ascertaining the acidity
of the fluid, then neutralizing it with potass, evaporating to dryness,
and heating the residue in a tube with sulphuric acid. The vapour
disengaged, if abundant, may be known by its orange colour in the tube
and its odour. But if small in quantity it is best to distil over the
vapour in a proper apparatus, and to subject the condensed product to
the tests of morphia, narcotin dissolved in sulphuric acid, and
proto-sulphate of iron dissolved in water. A convenient tube for the
purpose is that represented in Fig. 3; into which the materials are
introduced by the funnel, Fig. 4. The wide part of the tube may then be
drawn out in the spirit-lamp flame to any length or fineness that may be
necessary, so as to conduct the vapour into another tube as a condenser,
or directly into the substances to be used as tests.

3. _When in a state of compound mixture_, nitric acid, like sulphuric
acid in similar circumstances, may be after a time partly decomposed and
partly neutralized; and when the matter with which it is mixed belongs
to either of the organic kingdoms, more particularly to the animal
world, its decomposition is more rapid than that of sulphuric acid.
Still it is an important fact, that some of the acid may be discovered
after a considerable interval. M. Ollivier detected it in various stains
on the skin at least a day after it had been applied;[308] Dr.
O’Shaughnessey detected it in a stain on cloth sent to him from Ireland
to Edinburgh;[309] and I have found it in stains made on broad-cloth
with detached drops seven weeks before.

_Process for Stains._ Nitric acid produces on the skin a yellow stain,
which gradually becomes dirty orange, and finally of a dirty
yellowish-brown; but in all of these states it is at once rendered for a
time lively yellow by the action of ammonia. I am not aware that any
other yellow stain is similarly affected. Stains on cloth are generally
yellow, reddish-yellow, or brownish-yellow, and are attended with more
or less disintegration of the texture of the cloth. The method of
analyzing all these stains is as follows:—The stained parts is to be
boiled in a few drachms of pure water several times in succession; and
the liquid is then filtered, and may be subjected to litmus-paper for
the purpose of ascertaining its acidity. It is then to be rendered
neutral, or for the sake of greater facility, feebly alkaline, by adding
a few drops of a diluted solution of caustic potass, after which the
whole is evaporated to dryness, and in a vapour-bath, if practicable.
The residuum is then to be decomposed by sulphuric acid in the same way
as recommended above for the simple diluted acid.—Orfila thinks it
advantageous to let the stains macerate for some hours in a solution of
bicarbonate of soda rather than to boil them in water. In that case,
however, it is necessary to ascertain the acidity of the stains with
litmus-paper before proceeding to macerate them.

_Process for Mixtures._ The detection of nitric acid in compound
mixtures, such as the contents of the stomach, is not so easy a matter
as its detection in stains; and indeed a sure and delicate process is
still a desideratum in medico-legal chemistry. The process varies, as in
the case of sulphuric acid, according as the subject of analysis is acid
or neutral.

a. _If the mixture be acid_, and the proportion of the acid
considerable, it maybe detected without difficulty. It is merely
necessary to ascertain the acidity of the mixture by litmus-paper, to
neutralize with potass, water being added if necessary, and then to
filter and evaporate to a convenient degree of concentration. Crystals
will form on cooling, which may be decomposed by sulphuric acid in the
usual way. But the medical jurist ought not to flatter himself with the
expectation of meeting often with a proportion large enough to admit of
being discovered by so coarse a method of analysis. In general the
crystallization of the nitrate of potass is prevented by co-existing
animal or vegetable matter. When the proportion appears inconsiderable,
therefore, a different process must be pursued. In preparing the former
edition of this work, the present topic was investigated with some care,
and a method suggested which appeared to me at that time more effectual,
delicate, and conclusive than any previously made public. Since then
Professor Orfila has also investigated the subject attentively, and
after trying various methods, has ended in adopting one which is
substantially the same as that now referred to, but without a
precaution, which seems to me essential for success in certain probable
enough circumstances.[310] I am therefore disposed to retain my former
process, with some variations and additions in the details.

Macerate the subject of analysis for a few hours in distilled water,
if it be not already liquid enough; and then boil for a few minutes,
and filter it. Ascertain now whether the fluid be acid to litmus; and
if it be so, neutralize it with solution of potash, or as Orfila
suggests, with a solution of the purer salt, the bicarbonate of soda.
Evaporate gently, to obtain crystals if possible; and if these do not
tend to the cubical form, distil them with sulphuric acid, and proceed
as directed for nitric acid simply diluted. If crystals do not appear,
or their form tend to the cube,—in which case chloride of sodium is
present,—redissolve the whole residue of evaporation in distilled
water; add a slight excess of a warm solution of acetate of silver, to
throw down organic matter and the chlorine of any chlorides that may
be present; filter and evaporate to dryness, and distil the residuum
with sulphuric acid, applying as usual to the vapour the tests of
litmus-paper and morphia,—also, as Orfila proposes, the solution of
narcotin in sulphuric acid, and proto-sulphate of iron in water,—and
if the quantity of vapour be great enough, the sense of smell and the
action of copper with the condensed vapour.

b. _If the mixture be neutral_, proceed exactly as above, except that it
becomes unnecessary to neutralize the liquid with potash or bicarbonate
of soda. This variety in the process will be principally required, where
earths or alkalis have been administered as antidotes.

The process now detailed requires a word or two of commentary.—Organic
matter is inconvenient because it prevents the nitrate of potash or soda
in the mixture from crystallizing. But it will not prevent the evolution
of nitric acid vapour by distillation with sulphuric acid, even although
the material be a simple extract without crystals. At the same time it
is better to get rid of as much organic matter as possible, if distinct
crystals be not obtained by evaporation. A more serious difficulty,
however, to which Orfila does not advert, arises from the co-existence
of a chloride. For, in that case, distillation with sulphuric acid may
disengage not nitric acid, but chlorine, in consequence of the reaction
which takes place between the nitric and hydrochloric acids in the act
of being liberated. This is a more important reason for purifying the
liquid by acetate of silver before subjecting it to concentration; but
in addition, by removing organic matter, this precaution increases the
chance of crystals of nitrate of potash or soda being obtained. Its
necessity, where a chloride co-exists, will appear from the following
experiment. Four drops of nitric acid neutralized with potass were mixed
with six ounces of strong barley-broth; from which half an ounce of
limpid fluid was procured by filtration. One-half of this evaporated to
dryness gave a crystalline residue, which, heated with sulphuric acid in
a tube, emitted a strong odour of chlorine; and the moisture which
bedewed the tube scarcely affected morphia. The residuum of the other
half of the filtered fluid was redissolved, treated with acetate of
silver, again filtered, and evaporated to dryness; and the residue was
gently heated in a tube with sulphuric acid. An odour of nitric acid was
now disengaged, and the moisture on the tube close to the mixture turned
a fragment of morphia to bright orange-red.

Acetate of silver is prepared by mixing strong solutions of acetate of
potass and nitrate of silver, draining and compressing between folds of
bibulous paper the crystalline precipitate which forms, dissolving this
precipitate by agitating it in boiling water, and finally crystallizing
the salt again by refrigeration. The crystals, which are sparingly
soluble in cold water, should be then separated, slightly washed with a
little water, and again dried by compression. When put to use, a
solution should be made by agitating the salt in boiling water, because
at low temperatures water retains very little of the salt; but actual
ebullition should be avoided, because acetate of silver is thus quickly
decomposed.

In all medico-legal analyses for nitric acid, care must be taken that
the different reagents used are free of this acid, and also of nitrates.
Sulphuric acid often contains a little nitric, or rather nitrous acid;
which may be discovered by the sulphuric acid becoming brown or dark-red
when a solution of proto-sulphate of iron is gently poured over it in a
test-tube; and which may be removed either by boiling the acid with a
few grains of sugar, according to the formula of the Edinburgh
Pharmacopœia, or, as Orfila directs, by boiling it with sulphate of
ammonia.


SECTIONS II. III. IV.—_Of the Action, Symptoms, Morbid Appearances, and
               Treatment of Poisoning with Nitric Acid._

All the observations made on these topics under the head of sulphuric
acid apply, with few exceptions, to the nitric acid also. A few
statements therefore on the peculiarities ascertained to exist in the
latter case are all that will be required in the present sections.

Nitric acid is not less powerful as a corrosive and irritant than
sulphuric acid. It will act with energy as an irritant even when
considerably diluted, for example with six or eight parts of water or
even more.—The lips which are rendered at first whitish by all the
acids, and eventually brownish by sulphuric acid, becomes soon yellow
with nitric acid. The tongue too sometimes acquires a yellow colour
instead of a white glazed appearance; but this character is not
invariable.—All spots caused by it on the skin become speedily yellow,
and long retain this hue; or if the tint become dull, which generally
happens in a few days, it is enlivened and the yellow colour restored
for a time, by ammonia, potash, soda, or soap.—An important fact, for
which toxicology is indebted to Professor Orfila, is that the acid may
be often found in the urine, both when it had been swallowed, and when
it had been introduced through the medium of the cellular tissue.[311]
It is to be discovered by the process for compound mixtures. Orfila adds
that he has hitherto been unable to find it in the liver or spleen.

A difference of tint in the lining membrane of the mouth and gullet is
the only difference observed in the morbid appearances caused by nitric
and sulphuric acid. The former sometimes renders these parts yellow; but
this appearance is far from being invariable.

The treatment in both instances is the same in every respect.


               III.—OF POISONING WITH HYDROCHLORIC ACID.

This acid occurs more rarely than any of the other mineral acids in
medico-legal cases; a fact which appears singular enough on considering,
that it is a powerful corrosive, and more perhaps in the hands of the
working-classes than any other.


            SECTION I.—_Of the Tests for Hydrochloric Acid._

Like the other acids, hydrochloric acid occurs in the concentrated
shape, in a state of simple dilution, and mixed with various matters,
especially from organic kingdoms.

1. Hydrochloric acid, _in its concentrated state_, is colourless, if
pure, but yellowish as usually sold; and it is easily known by the
peculiar appearance and odour of its fumes. A convenient additional
test, which, however, is not absolutely distinctive, is the formation of
white vapour when a rod dipped in it is brought near another dipped in
ammonia. If any farther evidence be desired, the strong acid must be
diluted with water, and examined by the tests for it in a diluted state.

2. _When diluted_, it is recognised with facility, first by
litmus-paper, and then by the nitrate of silver, which forms with it a
dense, white precipitate, the chloride of silver. This is soluble in
ammonia, reappears on neutralizing the ammonia by nitric acid, and is
not redissolved by a large excess of nitric acid, even aided by heat.
Its permanence under an excess of nitric acid distinguishes it from
every other silver salt, but the cyanide; which again is known by
disappearing when boiled with a large excess of the acid.

3. In the last edition of this work I proposed for the detection of
hydrochloric acid in _compound organic mixtures_ a process, to which
Professor Orfila has since made an important addition,[312] and which
the investigations of that toxicologist, as well as my own, lead me to
suppose superior to any other yet suggested, although it is not entirely
free from objection. This process divides itself into two, according as
the subject of analysis is acid or neutral; but in the latter case its
indications are of dubious import.

a. If the matter to be examined be acid, boil it with water if
necessary, filter, and distil it with a gentle heat till the residue
acquire the consistence of a very thin syrup. Subject the distilled
liquor to the tests for diluted hydrochloric acid. It will seldom be
found there, however, because it is apt to be retained by the
co-existence of organic matter. If it be not found, add to the thin
extract in the retort a slight excess of a strong solution of tannin,
filter, and distil the filtered liquid by means of a hot bath of
solution of hydrochlorate of lime (consisting of two parts of
crystallized salt and one of water,)—taking care that the temperature of
the bath never exceeds 240°; and stop the distillation just before the
residuum becomes dry. Examine now the distilled liquor with the tests
for diluted hydrochloric acid.

Hydrochloric acid has a tendency to adhere with obstinacy to organic
matters, especially when these are abundant; and therefore Orfila
properly proposes to remove organic principles as far as possible by
precipitating them with solution of tannin. I have found, as he did,
that the acid may be obtained by distillation after this measure, when
it could not be obtained previously.—Orfila objects to the process
however that hydrochlorate of ammonia will pass over in the
distillation. But I have not found this to be the fact, when the
temperature did not rise above 240°; which in his experiments seem to
have been considerably exceeded.—A more important fallacy is, that
hydrochloric acid will be indicated by the process in a mixture which
contains both a neutral chloride, such as common salt, and sulphuric
acid. This fallacy can only be obviated by ascertaining that sulphuric
acid is not present.—But the most important fallacy of all is, that free
hydrochloric acid constitutes an essential part of the gastric juice,
and an ingredient of the secretions of the stomach in various states of
disordered digestion.[313] It is not easy to see how this fallacy can be
obviated, unless the acid be obtained in large quantity; nor am I
prepared to say what quantity would justify the conclusion, that the
acid had been derived from an external source. Dr. Prout once found
between four and five grains of pure acid in sixteen ounces of the fluid
of water-brash.[314] The quantity of hydrochloric acid is to be known by
drying, heating and weighing the chloride of silver thrown down in the
distilled fluid by nitrate of silver, and allowing 100 parts of
concentrated commercial acid for 145 of chloride.

b. When the mixture is neutral, hydrochloric acid can be no longer
detected in it without the aid of sulphuric acid to decompose the
chloride that has been formed. This should be added to the filtered
fluid obtained after organic matter has been separated by solution of
tannin. Hydrochloric acid will then distil over.—It is seldom however
that the discovery of the acid in this way will warrant the conclusion,
that it had ever existed free in the mixture whence it is obtained. For
it may have proceeded from chlorides contained in the subject of
analysis from the first, more especially chloride of sodium, which
exists in small quantity in all animal fluids and solids, and more
largely in many articles of food and drink. The only circumstance indeed
in which the detection of hydrochloric acid by decomposition with
sulphuric acid will yield any evidence,—and even then the evidence will
only be presumptive,—is when it is known that an earth or alkali was
given as an antidote, and when the alkali or earth which was used is
found in the suspected substance.


SECTION II.—_Of the Action and Symptoms produced by Hydrochloric Acid._

Hydrochloric acid has been found by Professor Orfila to exert the same
action as sulphuric and nitric acids; but it is a less powerful
corrosive and irritant.—In the gaseous state, it is a most destructive
poison to vegetables, as will be shown in the article on the Poisonous
Gases.

The symptoms it occasions in man are very like those produced by
sulphuric acid. As few cases however of poisoning with this substance
have yet been published, its effects are not so well known as those of
the other powerful acids; and it may therefore be right to mention the
leading particulars of some of the cases which are met with in
authors.—Mr. Quekett has related the case of a man, who, on arriving at
home one day, told the woman he lodged with that he had poisoned himself
with spirit of salt, but presented at the moment so little sign of
uneasiness, that she at first scarcely believed him. In a short time
however he suddenly became faint and fell down. On being removed to the
London Hospital, magnesia and milk were given, about three hours after
the acid had been taken; but no relief was experienced. He suffered
intense thirst, complained of excessive pain in the stomach and throat,
and expired in about fifteen hours.[315]—Mr. J. F. Crawfurd of Newcastle
has related a still more rapid case which was occasioned by two ounces
of an equal mixture of hydrochloric acid and “tincture of steel,”
probably the tincture of chloride of iron. Vomiting occurred soon
afterwards, but subsequently ceased; there was no complaint made either
of pain or heat anywhere, or of thirst; and questions were answered
intelligently. But the pulse was imperceptible, and the muscles of the
extremities contracted; and death took place in five hours and a
half.[316]—Orfila mentions that an hospital patient, affected with
inflammation of the brain after a fall on the head, having got by
mistake from his nurse 45 grammes, or two fluid ounces, of hydrochloric
acid, was attacked with acute pain in the stomach, efforts to vomit,
hiccup, extreme restlessness, a small pulse, a fiery red tongue,
blackness of the lips, and a burning skin; and next day he died in a
state of constant delirium, and covered with a cold clammy sweat.[317]

These cases present nearly the same violence and variety of action with
that which results from the two other acids.


 SECTION III.—_Of the Morbid Appearances caused by Hydrochloric Acid._

The morbid appearances are on the whole similar to what are caused by
sulphuric acid. In Mr. Quekett’s case the stomach outwardly was
leaden-coloured and its vessels gorged with black blood; the intestinal
peritonæum injected and speckled with fibrinous effusion; the villous
coat of the stomach lined with yellow, curdled milk, and itself
irregularly black here and there, as if charred, and in some places
softened and corroded, so that a rent was made in handling it; the inner
membrane of the duodenum similarly affected, and also even the jejunum,
though more irregularly. The contents of the stomach were not acid, and
did not contain any chloride.—In Mr. Crawfurd’s case the villous coat
presented black elevated ridges, as if charred, and the furrows between
were scarlet-red; black granular extravasation had taken place at many
points into the submucous tissue; similar appearances were seen in the
duodenum and jejunum; and the lower part of the gullet looked as if it
had been cauterized.—In the case related by Orfila the gullet and
pharynx were red, and at one or two places excoriated; the stomach
inflamed externally, and its inner membrane spotted with gangrenous (?)
patches, and very brittle; the duodenum thickened, and the jejunum
perforated by a round worm.




                              CHAPTER IV.
 ON POISONING WITH PHOSPHORUS AND THE OTHER BASES OF THE MINERAL ACIDS.


_Of Poisoning with Phosphorus_.—The only other mineral acid that
deserves mention is the phosphoric. It possesses properties nearly
analogous, and hardly inferior to those of the three acids already
mentioned. On its own account, however, it does not merit any notice
here, since it is much too rare to be within reach of a person who
intends to give or take poison. But it must be attended to, because it
is formed in the course of the action of a more common poison,
phosphorus. An attempt has actually been made to perpetrate murder by
means of this substance. A woman at Mengshausen tried to poison her
husband by putting into his soup a mixture of phosphorus, flour, and
sugar, used for poisoning rats. But the soup having been kept warm on
the stove, the man’s suspicions were excited by its phosphorescence, and
phosphorus was detected in it.[318]

Orfila found that two drachms of phosphorus given to dogs in fragments
caused death in twenty-one hours, that the whole stomach and intestines
were more or less inflamed, and that the phosphorus had lost much of its
weight, though vomiting had been prevented by a ligature on the gullet;
in fact the poison was partly oxidated. In a state of minute division,
as when dissolved in oil, twenty-four grains caused death in less than
five hours with all the symptoms of the most acute irritant poisoning;
and after death the stomach was found extensively corroded, and
perforated by two holes.[319] Other experimentalists have found that
half a grain melted in hot water could kill a dog;[320] and that water,
in which phosphorus had been simply received in the process for
preparing it, proved in small quantities fatal to poultry.[321]

There is no doubt, therefore, that phosphorus is a dangerous poison to
animals. Its effects on man have not been often witnessed; but the
observations hitherto made will show that it is not less injurious to
him than to the lower animals. A grain and a half have actually proved
fatal to man, as appears from a case mentioned by M. Worbe.[322] The
subject of the case was a stout young man who took a grain and a half in
hot water, after having previously taken half a grain without sustaining
injury. In seven hours, and not till then, he was attacked with pain in
the stomach and bowels, then with incessant vomiting and diarrhœa,
excessive tenderness and tension of the belly,—all the symptoms in short
of irritant poisoning; and he died exhausted in twelve days. Another
fatal case somewhat similar in its circumstances has been related by M.
Julia-Fontenelle.[323] An apothecary, after taking in one day first a
single grain and then two grains of phosphorus without experiencing any
particular effects, swallowed next day three grains at once in syrup. In
the evening he felt generally uneasy, from a sense of pressure in the
belly, which continued for three days; and then he was also seized with
violent, continual vomiting of a matter which had an alliaceous odour.
On the seventh day he had also spasms, delirium, and palsy of the left
hand; and death speedily ensued.—Dr. Maier of Ulm relates a singular
case occasioned by a portion of lucifer-match composition having been
swallowed intentionally. Vomiting and pain in the belly ensued, then
anxiety, restlessness, and excessive thirst, and death in about fifteen
hours.[324]—M. Martin-Solon relates the case of a patient, affected with
lead palsy, who having taken considerably less than a grain in the form
of emulsion, was attacked with burning along the gullet and in the
stomach, mucous vomiting, tenderness of the belly, general coldness and
feebleness of the pulse. Afterwards the pulse became imperceptible, the
limbs neuralgic, the intellect clouded, and the breathing stertorous;
and he died in little more than two days.[325]—In the only other case I
have hitherto found recorded death took place in forty hours, and the
symptoms were violent pain in the stomach and continual vomiting,
together with the discharge by clysters of small fragments of
phosphorus, which were discovered by their shining in the dark, and
subsequently by the appearance of burnt spots on the bed-linen. In this
case, which is described by Dr. Flachsland of Carlsruhe,[326] the
quantity of the poison taken was not ascertained. The patient, a young
man, took it on bread and butter at the recommendation of a quack, to
cure constipation, general debility, and impotence.

At one time it was the custom to give small doses of phosphorus in
medical practice; but the uncertainty and occasional severity of its
operation have perhaps properly expelled it from most modern
pharmacopœias. Among other properties ascribed to it in medicinal doses,
it is said to be a powerful aphrodisiac: No such symptom occurred in the
first of the fatal cases just related, or is mentioned in any of the
others; but there is no doubt that medicinal doses sometimes produce it.

As to the morbid appearances, the same changes of structure may be
expected as in the instance of the mineral acids generally. In Worbe’s
case quoted above, the skin was generally yellow, and here and there
livid; the lungs gorged with blood; the muscular coat of the stomach
inflamed, but the other coats not, except near the two extremities of
the organ, where they were black. In Flachsland’s case much fluid blood
was discharged from the first incisions through the skin of the belly;
the omentum and outside of the stomach and intestines were red; the
villous coat of the stomach presented an appearance of gangrenous
inflammation (probably black extravasation only); the inner membrane of
the duodenum was similarly affected; the great intestines were
contracted to the size of the little finger; the mesenteric glands
enlarged; and the kidneys and spleen inflamed. In Maier’s case the
peritonæum and omentum were dry and vascular, the stomach and small
intestines pale, the great intestines contracted, almost empty,
brownish-red, and here and there inflamed, the liver large, and the
blood everywhere liquid. The contents of the caput cœcum had an odour of
phosphorus, and here were found two yellowish lumps weighing eight
grains, which shone when rubbed, exhaled a phosphoric odour, and
contained 0·6 of a grain of phosphorus. In Martin-Solon’s case the
gullet was cherry-red and its epithelian brittle, the villous coat of
the stomach grayish and brittle, the solid viscera in the abdomen soft,
and the cerebral membranes congested.

_Phosphorous acid_, the effects of which have been examined
experimentally by Professor Hünefeld of Greifswalde, differs in its
operation from phosphoric acid. Twenty-five grains had no effect on a
rabbit; but a drachm caused difficult breathing, restlessness, bloody
vomiting, slight convulsions, and death in twelve hours; and the stomach
was found not much injured. The urine contained phosphoric acid.[327]

_Of Poisoning with Sulphur._—It does not appear that sulphur, which
resembles phosphorus in many particulars, bears any resemblance to it in
physiological properties;—which may be ascribed to its not being
susceptible of spontaneous acidification. It certainly possesses,
however, slight irritating properties. It is often given as a purgative,
which is sufficient to prove that it is not altogether inert; and the
veterinary school at Lyons found that a pound killed horses by producing
violent inflammation, recognizable during life by the symptoms, and
after death by the morbid appearances.[328]

_Of Poisoning with Chlorine._—Chlorine in its gaseous state acts
powerfully as an irritant on the windpipe and lungs, and on that account
will be noticed under the head of the poisonous gases. But even in
solution it retains to a certain degree its poisonous qualities. Orfila
says that five ounces of a strong solution of chlorine will kill a dog
in twenty-four hours, if it is kept in the stomach by a ligature, and
that two ounces diluted with twice its volume of water will prove fatal
in four days;—that the symptoms are those of irritation of the
stomach;—and that in the former case he found general redness and
blackness—in the latter ulceration of its villous coat.[329]


                       OF POISONING WITH IODINE.

Iodine is a poison of more consequence than chlorine, both because it is
becoming a more common article, and because it is more violent in its
effects on the animal economy.

_Tests of Iodine._—Iodine when pure is a solid substance easily known by
its scaly form, its resemblance in colour and resplendence to polished
iron, its peculiar odour, the violet fumes it forms when heated, and the
fine blue colour it produces with a solution of starch. It is very
sparingly soluble in water, but readily so in rectified spirit and in
aqueous solutions of certain salts, more especially the iodide of
potassium. Its ordinary forms in the shops are iodine itself, the
tincture, and the compound solution, where the solvent is a solution of
iodide of potassium in water. It stains the skin brownish-yellow; but
the stain is not permanent. Its fumes are intensely irritating to the
nostrils, throat, and lungs.

When dissolved in water or in solutions of neutral salts, it
communicates to the fluid a yellowish-brown or reddish-brown colour,
which is destroyed by sulphuretted hydrogen, because the iodine is
converted into hydriodic acid. In the colourless fluid thus formed, if
treated with chlorine,—or in the original brown fluid without
chlorine,—a solution of starch, obtained by ebullition and subsequently
cooled, produces a fine blue colour and precipitate; and these, if the
solution be sufficiently diluted, disappear on boiling, reappear on
sudden cooling, and are removed permanently by a stream of sulphuretted
hydrogen. This is a very delicate and characteristic system of tests.
The best mode of using chlorine for decomposing hydriodic acid is to let
it descend in the gaseous form from the mouth of a bottle of
nitro-hydrochloric acid upon the fluid to be examined; In this way an
excess is easily avoided, which bleaches out the blue colour. Sulphuric
acid, though often recommended for the purpose, does not act unless it
contains nitrous acid,—from which however the sulphuric acid of commerce
is seldom quite free.

When mingled with organic substances, the discovery of it is a matter of
some nicety; because many substances of this nature, especially in the
living body, quickly convert it into hydriodic acid.[330] Hence few
cases can occur in medico-legal practice, where iodine will be
discoverable in its free state. The following method of analysis will
meet all possible cases.

_Process for Compound Mixtures._—Add water if necessary, and filter. If
either the fluid or solid part is little or not at all coloured, test it
with cold solution of starch, assisting the action of the test on the
solid part by trituration in a mortar. If a blue colour be struck, which
disappears under ebullition, and reappears under refrigeration alone, or
on subsequently allowing chlorine gas to descend on the surface of the
fluid, there can be no doubt of the existence of iodine.—If the colour
of the suspected mixture after filtration is so deep that the action of
the starch cannot be expected to yield characteristic appearances, then
both the solid and fluid parts should be agitated with a third of their
volume of ether; and after the ethereal solution has arisen to the
surface, it is to be removed and tested with solution of starch. The
blue colour will be now perhaps struck, because the ether, in carrying
off the iodine from the mixture, leaves many coloured organic principles
behind.

Should free iodine not be thus detected, strong presumptive evidence may
still be procured of its actual presence, or of its having been at one
time present, by continuing the examination with the view to detect
hydriodic acid. This is described in p. 159.

By following this method of analysis, I have found that one grain of
iodine of potassium, which is equivalent to three-quarters of a grain of
iodine, may be easily discovered in six ounces of urine,—a fluid as
complicated as can well be conceived.

The process adopted by Professor Orfila is so nearly the same with this,
as scarcely to require being detailed. He uses nitric acid instead of
chlorine for decomposing the hydriodic acid. Chlorine, however, is the
most delicate reagent for the purpose, if it be used in the way
described above.

_Action of Iodine and Symptoms in Man._—Iodide has a twofold action, one
local and irritating, the other general, and produced only when it has
been administered long in frequent small doses.

Orfila remarked that in doses of two drachms it excited in dogs symptoms
of irritation in the stomach; that death slowly ensued in seven days,
without the symptoms having ever become very violent; and that the
villous coat of the stomach was here and there yellow, had also patches
of yellow mucus lining it, and exhibited numerous little ulcers of a
yellow colour. He could not observe much injury from iodine introduced
into the cellular tissue; and more lately, Dr. Cogswell remarked that in
this way it merely induces phlegmonous inflammation and the usual
consequences.[331]

An important circumstance in regard to the physiology and medical
jurisprudence of this poison and its compounds is, that it may
undoubtedly be detected in the blood, both when a single large dose has
been taken, and in those persons who have used it for some time
medicinally. Cantu, an Italian experimentalist, discovered iodine in
such circumstances in the blood, sweat, urine, saliva and milk;[332] and
Bennerscheidt, a German chemist, also found it in the blood, when it had
been employed outwardly.[333] In the latter instance it could not be
detected in the serum, but it was detected in the crassamentum by means
of starch. Some interesting facts of the same nature have also been
ascertained by Dr. O’Shaughnessey, from which it appears that even in
acute poisoning with this substance, satisfactory proof of its
administration may be procured several days afterwards by analysing
certain secretions. In a dog poisoned with iodine, he detected the
poison in forty minutes in the urine, and occasionally in the same
secretion so late as the fifth day, when it died. It is singular,
however, that he could not find it in the same quarter on the third day,
although it existed at that time abundantly in the saliva.[334] In these
experiments the iodine was always found in the form of hydriodic acid,
having been converted into that compound in the alimentary canal. This
change takes place with such rapidity, that on one occasion, in the
vomited matter discharged by a dog fifteen minutes only after the
administration of iodine, Dr. O’Shaughnessey could find no iodine, but a
large quantity of hydriodic acid.[335] Orfila has found it not only in
the urine, but likewise in the liver of animals.[336]

Considerable uncertainty prevails as to the circumstances in which we
may expect iodine to be detected in the organs or secretions of persons
who have taken it. Thus it has been stated by an Italian physician, Dr.
Cristin, that in many individuals affected with dropsy, struma,
epilepsy, and other diseases, he had sought for iodine to no purpose in
the urine, bronchial mucus, and other excretory fluids.[337]

With regard to its operation on man, Orfila says, he has tried the
effects of four or six grains on himself, and that he found this dose
produce a sense of constriction in the throat, sickness, pain in the
stomach, and at length vomiting and colic. There is no doubt, therefore,
that in larger doses it will prove a dangerous irritant to man as well
as to dogs. Accordingly, Dr. Gairdner has noticed the case of a child
four years old, who died in a few hours after taking about a scruple in
the form of tincture;[338] but he has not mentioned the symptoms. Dr.
Jahn of Meiningen mentions a case where an over-dose produced violent
pain in the belly, vomiting, profuse bloody diarrhœa, coldness and
blanching of the skin, rigors, quivering of the sight and rapid
pulse.[339] Two similar cases are related in a recent French journal; in
one, which was produced by a drachm and a half of the ioduretted
solution of hydriodate of potass, nausea, with acute pain and sense of
burning in the pit of the stomach, followed immediately; in an hour
there was vomiting of a yellowish matter which had the taste of iodine;
excessive restlessness ensued, with headache, giddiness and paleness of
the countenance; and these symptoms were not entirely dissipated for
five days.[340] In the other case two drachms and a half of iodine were
swallowed for the purpose of self-destruction. A sense of dryness and
burning from the throat down to the stomach was immediately produced;
lacerating pain in the stomach and fruitless efforts to vomit succeeded;
and in an hour, when the relater of the case first saw the patient,
there was suffusion of the eyes, excessive pain and tenderness of the
epigastrium, and sinking of the pulse. Vomiting, however, was then
brought on by warm water; copious yellow discharges, possessing the
smell and taste of iodine, took place; and in nine hours the patient was
well.[341]

There is a singular uncertainty, however, in the action of one or more
large doses. Magendie says he has taken two drachms of the tincture,
containing about ten grains of iodine, without injury;[342] Dr. Gully,
that he has given three times as much daily for some time; Dr. Kennedy,
that he gave an average of twelve grains daily in the form of tincture
for eighty days without observing any effect at all; and Mr. Delisser,
that he has given a patient thirty grains in a day without injury.[343]
Dr. Samuel Wright met with the case of an infant, not more than three
years old, who took three drachms of the tincture at once, and suffered
only from attempts to cough, some retching and much thirst.[344]

It further appears that in medicinal doses, such as a quarter of a
grain, frequently repeated, it is a dangerous poison, unless its effects
are carefully watched. For in consequence of accumulation in the system,
or gradually increasing action, it produces when long used some very
singular and hazardous symptoms; and like mercury, foxglove, and some
other poisons, it may be taken long without effect, and at length begin
to operate suddenly. The symptoms which it then occasions are sometimes
those of irritation; namely, incessant vomiting and purging, acute pain
in the stomach, loaded tongue, rapid and extreme emaciation, violent
cramps and small frequent pulse. These symptoms may continue many days,
and even when subdued to a certain extent, vomiting and cramps are apt
to recur for months after.[345] A fatal case of this form of affection
has been related by M. Zink, a Swiss physician. His patient, after
taking too large doses of iodine for about a month, was seized with
restlessness, burning heat of skin, tremors, palpitation, syncope,
excessive thirst, a sense of burning along the gullet, frequent purging
of bilious and black stools, priapism, and tremulous pulse. The symptoms
of local inflammation went off in a few days; but those of general fever
continued; and he died after six weeks’ illness.[346] Another fatal case
has been described in Rust’s Journal. The leading symptoms were pain in
the region of the liver, loss of appetite, emaciation, quartan fever,
diarrhœa, excessive weakness; and after the emaciation was far advanced
a hardened liver could be felt. The patient appears to have died of
exhaustion.[347] From this case, and another of which the appearances
after death will be presently noticed, it is not improbable that iodine
possesses the power of inflaming the liver.

In another and more common affection, the patient is attacked with
tremors, at first slight and confined to the fingers, afterwards violent
and extending to the whole muscles of the arms and even of the trunk. At
the same time there is excessive and rapidly increasing weakness, a
sense of anxiety and sinking, a total suspension of the function of
digestion, rapid and extreme muscular emaciation, tendency to fainting,
and violent continued palpitation,[348] accompanied sometimes with
absorption of the testicles in man, and of the mammæ in females. In the
midst of these phenomena the curative powers of the poison over the
disease for which it has chiefly been used, namely, goître, are
developed. It has been remarked in particular, that the diminution of
the goître keeps pace with the diminution of the breasts, though at
times either effect has been developed without the other. An instance is
related in Rust’s Journal of a female, whose breasts began to sink after
she had used iodine for four months; and in four weeks hardly a vestige
of them remained; but her goître was not affected.[349] An American
physician, Dr. Rivers, has twice noticed barrenness apparently induced
by the prolonged use of iodine; and as in these instances the females
were young and previously very prolific, but ceased to bear children
from the time the iodine was used, his observations seem worthy of
attention.[350] Dr. Jahn[351] specifies among the leading effects of the
poison when slowly accumulated in the body,—absorption of the
fat,—increase of all the excretions,—dinginess of the skin, with
frequent clammy sweat,—hurried anxious breathing,—diuresis and an
appearance of oil floating in the urine,—increased discharge of fæces,
which are unusually bilious, but free of mucus,—increased secretion of
semen,—increased menstrual discharge,—swelling of the subcutaneous veins
and lividity of the lips,—feebleness of the pulse, with superabundance
of serosity in the blood,—impaired digestion and diminished secretion of
saliva and mucus. This affection, which, in conformity with the name he
has given it, may be termed Iodism [_Iodkrankheit_], he contrasts with
mercurialism, the constitutional effect of the accumulation of mercury
in the body; and he considers the former not more unmanageable than the
latter. The dose required to produce these effects are very various.
Some people appear almost insensible to its action; in one instance,
nine hundred and fifty-three grains were taken in daily portions varying
from two to eighteen grains, without any bad effect;[352] and I have
known an average of four grains daily taken for fifteen months, with the
effect only of increasing the appetite. On the other hand, Dr. Gairdner
has seen severe symptoms commence when half a grain was taken three
times a day for a single week;[353] and Coindet has seen bad effects
from thirty drops of the solution of ioduretted hydriodate taken daily
for five days.[354]

Iodine and iodide of potassium in medicinal doses have been supposed by
Dr. Lawrie to be capable of exciting in certain constitutions an
affection resembling _cynanche laryngea_ in its symptoms, consisting of
inflammation of the salivary glands, glottis, and other adjacent parts,
and proving sometimes fatal.[355] This property is doubtful; but several
instances have been published of profuse salivation and soreness of the
mouth during a course of iodine; it is apt to cause chronic irritation
of the Schneiderian membrane; and some think that it may affect in like
manner the bronchial membrane in the lungs.[356]

_Morbid Appearances from Iodine._—The only account I have seen of the
appearances left in the body after death from slow poisoning with iodine
is contained in the essay of Dr. Zink. In a second fatal case which came
under his notice he found enlarged abdomen from distension of the
intestines with gases, enlargement of the other viscera and serous
effusion into the peritonæum; adhesion of the viscera to one another;
redness of the intestines, in some places approaching to gangrenous
discoloration; redness and excoriation of the peritonæal coat of the
stomach, and also of its villous coat; enlargement and pale rose-red
coloration of the liver. In the chest serum was found in the sac of the
pleura. The gullet was contracted in diameter, and red internally.


                 ON POISONING WITH IODIDE OF POTASSIUM.

To these remarks on iodine a few observations may be added on the iodide
of potassium, one of its compounds, which is now generally substituted
in medicine for the simple substance. The tests and actions of this
poison have been examined by M. Devergie; and more lately its
medico-legal chemistry has been investigated by Dr. O’Shaughnessey and
Professor Orfila.

It is sold in the shops of various degrees of purity. Pure iodide of
potassium is in white crystals, tending to the cubical form, permanent
in the air, possessing a faint peculiar odour, and easily soluble in
both water and rectified spirit. Another variety has the same form, but
possesses an odour of iodine, is often yellowish in colour, and
deliquesces slightly in moist air. This contains an excess of iodine,
but may be otherwise pure. A third variety is impure. It presents less
tendency to assume a crystalline form, is more or less deliquescent,
dissolves but partially in alcohol, and when dissolved effervesces with
acids. The principal ingredient in this article is carbonate of potass;
and sometimes the proportion of iodide is inconsiderable. In one
specimen I procured 74·5 per cent. of carbonate of potass, 16 of water,
and only 9·5 of iodide of potassium.

In the solid state the iodide of potassium may be known by the effect of
strong sulphuric or nitric acid, which turns it brown with
effervescence, and when aided by heat disengages violet fumes of iodine.

In solution many tests will detect it, such as chlorine, nitric acid,
corrosive sublimate, acetate of lead, protonitrate of mercury, muriate
of platinum, and starch with chlorine or nitric acid. Chlorine or nitric
acid forms a brown or orange-coloured solution by disengaging iodine.
Corrosive sublimate forms a fine carmine-red precipitate, the biniodide
of mercury; acetate of lead a fine yellow precipitate, the iodide of
lead; protonitrate of mercury a yellow protiodide of mercury, which
gradually fades into a dirty brown. Solution of starch, followed by
chlorine in solution or in vapour, strikes a deep blue colour, which, if
the fluid is sufficiently diluted, disappears on boiling, reappears on
sudden cooling, and is permanently removed by a stream of sulphuretted
hydrogen gases. Of these tests the most characteristic is starch with
chlorine; and it is also extremely delicate. Too much chlorine however
bleaches the blue colour away.

In compound mixtures most and sometimes all of these tests are useless.
If the mixture is deeply coloured, none will act characteristically. If
carbonate of potass be present in such proportion as is often met with
in the shops, the tests cannot be trusted to.

_Process for Compound Mixtures._—The following method of analysis is
applicable to all mixtures, organic and inorganic. Add water, if
necessary, and filter; and if the fluid which passes through is
tolerably free from colour, test a little of it with solution of starch
and chlorine. If the colour is too deep to admit of this trial, or the
test on trial does not act, unite the fluid and solid parts and transmit
sulphuretted hydrogen to convert any free iodine into hydriodic acid.
Drive off the excess of gas, supersaturate with a considerable excess of
potass, filter, and evaporate to dryness. Char the residue at a low red
heat in a covered crucible; pulverize the charcoaly mass, and exhaust
with water. This solution will probably act characteristically with
starch and chlorine; but on the whole it is better in the first instance
to remove some of the salts by evaporating to dryness, and exhausting
the residuum with alcohol. The alcoholic solution contains the
hydriodate of potass, with some other salts; and on being evaporated to
dryness, a residuum is left, on which, when dissolved in water, the
starch and chlorine will act characteristically. No other test is
necessary; and frequently no other test will act, on account of
co-existing salts.

I have found that a grain of iodide of potassium may thus be easily
detected in six ounces of urine, which must be considered a very
complicated fluid. In the solution ultimately procured nitrous acid
struck a pale brown tint, and on the addition of solution of starch a
dark-blue precipitate was formed; which, after being sufficiently
diluted, disappeared under ebullition, leaving a colourless fluid. On
cooling, no change took place; but on the subsequent addition of a drop
of sulphuric acid, the blue colour and precipitation were immediately
restored. No other reagent acted characteristically, although there was
a sufficient quantity of solution to try the starch test ten times at
least.

Dr. O’Shaughnessey has proposed a more complex method by precipitation
with chloride of platinum.[357] Professor Orfila says it is sufficient
to boil and filter the suspected matter, and to heat first the liquid
and then the solid part with solution of chloride, when violet vapours
of iodine are disengaged, which may be condensed and subjected to
various tests.[358] I have not compared this method with the one I have
been in the practice of using; but, notwithstanding the strong
assurances of its proposer, its superiority in point of delicacy seems
dubious, although no one can deny its simplicity.[359]

_Action and Symptoms in Man._—From the experiments of Devergie on
animals, iodide of potassium seems to be in large doses an irritant,
though not a powerful one. Two drachms in an ounce of water killed a dog
in three days with violent vomiting, and signs of irritation were found
in the stomach, namely, black extravasated spots and ulcers in the
middle of them. A solution injected into the cellular tissue caused only
local inflammation. Injected into the jugular vein in the dose of four
grains, it produced tetanus and death in a minute and a half.[360] The
latter investigations of Dr. Cogswell confirm essentially these results.

Discrepant accounts have been given of the effects of iodide of
potassium on man. When first introduced into medicine, it was conceived
to be an active poison, not much inferior to iodine itself. Many however
have since had an opportunity of observing that it is in general by no
means so energetic. Its medicinal doses were gradually raised from one
grain to five, ten, twenty grains; and at last Dr. Elliotson gave to not
a few patients so much as two, four, or even six drachms daily in
divided doses, without observing any remarkable effect.[361] These and
other similar observations however were made at a period when the salt
used in British practice was much adulterated, often indeed containing
eighty or ninety per cent. of impurity; at the same time it does appear
that large doses of a pure salt have been occasionally taken with
impunity. On the other hand it has evidently in some instances acted
with great force. Mr. Alfred Taylor mentions a case, on the authority of
Mr. Ericksen, where five grains produced alarming dyspnœa, attended with
inflammation of the nostrils and conjunctiva of the eyes.[362] An
instance has been published where twelve grains in four doses occasioned
shivering, vomiting, purging, general fever, and extreme prostration;
and the purging continued for some days.[363] Dr. Moore Neligan informs
me he met with the case of an elderly lady in 1841, who, on taking three
five-grain doses for two days, while labouring under irregular gout, was
seized with severe headache, thirst, and swelling of the face; which
symptoms were succeeded in two days by swelling of the tongue,
ulceration of the gums, and profuse salivation for a week. Dr. Lawrie
says he has known two grains and a half given thrice in one day,
followed by great dyspnœa and irritation in the throat; and is even
inclined to think that death resulted on two occasions from repeated
medicinal doses.[364] It would farther appear from some important
researches made in France, that the protracted use of iodide of
potassium in small doses with the food may produce serious derangement
of the health,—swelling of the face, headache, urgent thirst,
inflammation of the throat, violent colic pains, and frequently bloody
diarrhœa. A disease characterized by the symptoms now described appeared
repeatedly as an epidemic a few years ago in various parts of France,
and spread so widely in one parish, that not less than a sixth of the
whole population were attacked. After several careful investigations, it
seems to have been fully proved that the affection was owing to the use
of salt fraudulently adulterated with an impure salt, obtained from kelp
after the separation of carbonate of soda, and consequently impregnated
with an appreciable proportion of hydriodate of potass.[365]

It is difficult to arrive at any satisfactory conclusions from these
statements as to the nature and energy of the action of this salt as a
poison. But on the whole it appears to be not in general very active;
and the few instances of unusual activity which have occurred may
probably be put to the account of idiosyncrasy. The most remarkable of
its idiosyncratic effects from medicinal doses are salivation, and a
series of symptoms which imitate sometimes catarrh, and sometimes a cold
in the head. I do not know any facts to warrant the general statement of
M. Devergie that 18 or 30 grains may constitute a fatal dose.[366] The
present question is far from being unimportant in a medico-legal point
of view. Mr. A. Taylor mentions the heads of a case, very dubious
however in its nature, where it was suspected that a single dose of six
grains of iodide of potassium had been the occasion of death.[367]

It is important to remember in medico-legal researches, that iodide of
potassium may be detected in the blood, liver, spleen, muscles, urine,
and other textures and secretions; and especially that it may be found
in the urine, when it may no longer exist in the alimentary canal or in
vomited matters. These interesting facts have been clearly proved by the
researches of Wöhler,[368] Stehberger,[369] O’Shaughnessey,[370] and Dr.
Cogswell.[371]

_Of Poisoning with Bromine._—This singular substance is not an object of
much interest in relation to medical jurisprudence, because it is rare,
and only to be met with in the laboratory of the chemist. Hence,
although it appears to be a poison of some activity, it scarcely
requires to be dwelt on particularly.

It is easily known from all other substances by its fluidity, its great
density, which is thrice as great as that of water, its reddish-brown
colour by reflected, and blood-red colour by transmitted light, the
orange fumes which occupy the upper part of a bottle partly filled with
it, and its intensely acrid suffocating vapour, which is so irritating
that an incautious inhalation is followed by all the phenomena of severe
coryza and catarrh. Its odour, however, apart from its acridity, is very
far from being so disagreeable as its discoverer in naming it seems to
have imagined. In its properties it bears a close resemblance to
chlorine and iodine.

The toxicological effects and medico-legal relations of bromine have
been examined by M. Barthez,[372] Dr. Butske,[373] Dr. Dieffenbach,[374]
and Dr. M. Glover.[375]

M. Barthez has given the following process for detecting bromine in
compound mixtures, such as the contents of the stomach or vomited
matter. First separate the fluid matter by filtration, and subject it to
the action of chlorine, which will produce a fine orange colour. Should
this effect not result, or the change of colour be observed by the deep
tint of the fluid, treat the solid matter with solution of caustic
potass; filter and add what passes through to the former fluid;
evaporate to dryness and char by a red heat; act on the residue with
distilled water. The solution contains the bromide of potassium, and is
therefore turned orange-red by chlorine. The orange tint, whether struck
at once in the fluid part of the mixture, or after carbonization and
solution of the residue, is removed by agitation with ether; and the
etherial solution of bromine in its turn loses colour when treated with
solution of caustic potass, hydro-bromate of potass being again formed.

M. Barthez found, that a solution of twelve grains injected into the
jugular vein of a dog, sometimes occasioned immediate tetanus and death;
and that the heart was gorged with clotted blood. Sometimes however even
seventeen drops did not prove fatal, but produced merely restlessness,
difficult breathing, dilated pupil, frequency of the pulse, and
sneezing. Dieffenbach remarked similar effects in the rabbit: The animal
either died immediately, or soon recovered altogether. In a cat, after
the injection of twelve drops of a concentrated solution into its
jugular vein, death took place in fifteen minutes; but in another from
which a little blood was drawn after the symptoms were fully formed,
complete recovery gradually ensued. Butske found a horse suffer so much
from mortal prostration immediately after five grains dissolved in two
ounces of water were injected into its jugular vein, that he supposed it
was about to die; but it quickly revived, and ultimately got quite well.
Dr. Glover obtained similar results. When recovery took place, the
leading symptoms were panting, sneezing, discharge from the nostrils,
rigors and debility.

When introduced into the stomach of dogs, M. Barthez found that twenty
drops on a full stomach had no particular effect; that thirty drops
occasioned vomiting, and temporary acceleration of the pulse and
breathing; and that from forty to sixty drops on an empty stomach
brought on violent vomiting, sneezing, cough, dilated pupil and
prostration, succeeded in a few hours by languor without any other
symptom, and by death in four or five days. In the dead body he remarked
numerous little ulcers of the villous coat, some of which had an
ash-gray appearance at the bottom, while others were covered with a
black slough, easily removed by friction. When the gullet was tied to
prevent vomiting, less doses proved more quickly fatal. He likewise
observed that the matter vomited in these experiments, even a few
minutes after the administration of the poison, had no appearance or
odour of bromine; whence it is reasonable to conclude, that, as in the
instance of iodine, a chemical change takes place with the aid of
certain vital operations, so that the bromine becomes hydrobromic
acid.—The experiments of Dr. Butske assign to it more activity as a
poison than those now related. For he found that a dog died in a day
from taking only five grains dissolved in two ounces of water; and the
symptoms were laborious breathing, loud cries, and convulsions. In the
dead body he found the stomach internally chequered with bloody
extravasation, and filled with bloody mucus, the duodenal mucous
membrane universally injected, but the rest of the alimentary canal in a
healthy state.—Dr. Glover remarked in such cases, besides the usual
symptoms of an irritant action on the stomach, coryza, sneezing,
salivation and difficult breathing. Sixty minims killed a cat in
seventeen minutes, two fluid drachms a dog in five hours and a half, ten
grains a rabbit in five minutes. A dog twice got twenty grains in
solution and recovered, but died after a third dose of the same amount.
Another got twenty grains in solution every two or three days for a
month without injury. In some of these experiments hydrobromic acid was
detected in the blood and urine.

Little is yet known of the effects of bromine on man. Butske found that
a drop and a half in half an ounce of water produced a sense of heat in
the mouth, gullet, and stomach, and subsequently colic pains; and that
two drops and a half in an ounce of mucilage excited, in addition to the
preceding symptoms, great nausea, hiccup, and increased secretion of
mucus. On the other hand M. Fournet, who gave doses gradually increasing
from two to sixty drops daily for many weeks, observed that the lowest
doses excited itching in the hands and feet, and sometimes colic; that
an increase in the quantity caused heat in the chest and nausea; and
that forty-five drops occasioned also severe burning and sense of
acidity in the stomach, which however were temporary. The appetite was
in general rather improved, and the body became more plump.[376]—Bromine
appears on the whole to be a pure local irritant. It acts most
energetically when most thoroughly dissolved in water.

_Hydrobromic acid_ seems from the experiments of Dr. Glover to be a pure
irritant and corrosive, allied in action and energy to hydrochloric
acid. The same experimentalist found that _bromine of potassium_ in the
dose of forty grains had sometimes little or no effect on dogs when
injected into the blood-vessels, while in other instances less doses
cause speedy death by paralysing the heart. Barthez observed that half a
drachm in solution produced dulness and depression in dogs, but no other
bad effect; and that two drachms retained in the stomach by tying the
gullet occasioned death in three days with symptoms of irritant
poisoning. M. Maillet observed that two ounces of this salt in the form
of ointment, administered to a dog by rubbing it over his nose, and
letting him lick it off and swallow it, had no effect whatever.[377]




                               CHAPTER V.
                     OF POISONING WITH ACETIC ACID.


Acetic acid, although in its ordinary state undoubtedly possessed of
little activity as a poison, has nevertheless proved in some
circumstances deleterious, and capable of occasioning death even in the
human subject. It exists in various forms. The most common is ordinary
vinegar, in which it is much diluted. Another common form is the
pyroligneous vinegar, pyroligneous acid, or pyroligneous acetic acid, as
it is variously called, which when impure has a reddish-brown colour,
but when pure is almost or altogether colourless, and the strength of
which is much greater than that of common vinegar. What is called proof
vinegar has a density about 1005, and contains about four per cent. of
concentrated acid. The pyroligneous acid sold in the shops of this town
has a density about 1035, and contains about 25 per cent.; but the
pyroligneous acid of the London Pharmacopœia is stronger, for its
density is 1050, and 100 parts contain about 50 of the strong acid. A
third form is the concentrated or pure acetic acid of the apothecary,
which is familiarly known as the chief ingredient and menstruum of a
common perfume, aromatic vinegar.


               SECTION I.—_Of the Tests for Acetic Acid._

In all its forms acetic acid is easily known by its very peculiar odour,
together with its acid reaction on litmus. But if farther evidence of
its nature be required, it will be requisite to neutralise the fluid
suspected to contain it with carbonate of potass, and then to procure
the acetate of potass by evaporation. This salt is known by its extreme
tendency to deliquesce, and by a concentrated solution in water,
yielding, when distilled with sulphuric acid, a fluid possessing the
peculiar odour and pungency of concentrated acetic acid.

When in a state of compound admixture with organic substances, such as
the contents of the stomach, it has been proved by late researches of
Orfila,[378] that this acid may be present in considerable proportion
without distinctly reddening litmus. For such mixtures the following
process of analysis, devised by the Parisian professor, will be found
convenient and effectual. The fluid being put into a retort with a
receiver attached, the retort is to be heated in a muriate of lime bath
till the residuum be dry. The distilled fluid may then be tested
tentatively for sulphuric and muriatic acids; and these being proved to
be absent, the acidity and peculiar smell of the liquid will supply
strong presumption of the presence of acetic acid. This presumption may
be turned to certainty by forming acetate of potass, as already directed
for the pure diluted acetic acid.

Orfila has omitted in his paper a serious fallacy to which this, as well
as every process for the detection of acetic acid in the contents of the
stomach is exposed,—namely, that the natural secretions of the stomach,
according to the researches of many physiologists, but more especially
in recent times those of Tiedemann and Gmelin in Germany, and those of
Leuret and Lassaigne in Paris, frequently contain a small proportion of
acetic acid. Hence, the inference in favour of the introduction of
acetic acid into the stomach from without, founded on the process
related above, is only legitimate when the quantity discovered is
considerable.—The medical jurist ought also to keep in mind that vinegar
is a common remedy with the vulgar for many diseases, and especially for
poisoning.


    SECTION II.—_Of the Effects of Acetic Acid on Man and Animals._

In the first edition of this work, it was stated that acetic acid could
scarcely be considered a poison. And in illustration, a case was
mentioned which fell under my own notice,—that of a gentleman, who
during dinner swallowed at a draught about eight ounces of vinegar by
mistake for beer, and who nevertheless sustained no harm although he
retained it all, and as the only measure of precaution, swallowed after
it an equal quantity of port wine. In farther confirmation of what is
here mentioned, it may be added, that an ounce of acid equal in strength
to the pyroligneous vinegar, has been found by Schubarth of Berlin to
produce very little effect when administered to a dog. The animal merely
frothed a little at the mouth; cried and became restless for a time;
then had one or two attacks of vomiting; and in an hour appeared quite
well again.[379] Nay, it has even been found by Pommer of Heilbronn,
that a considerable quantity of diluted acetic acid may be injected into
the blood without causing any mischief. He injected six drachms of
distilled vinegar into the femoral vein of one dog, and an ounce into
the jugular vein of another, but observed no effect whatever, except a
slight labour of respiration for a short time afterwards.[380]

It appears, however, from some experiments performed by Professor Orfila
on occasion of a judicial case to be mentioned presently, that all the
forms of acetic acid will prove injurious and even fatal to dogs, if
given in sufficient quantity and prevented from being discharged by
vomiting. An ounce of pyroligneous vinegar, administered to dogs of
middle size, and retained in the stomach by a ligature on the gullet,
produces efforts to vomit, evident suffering, prostration of strength,
and death in five, seven, or nine hours. An ounce of concentrated acetic
acid occasioned death in one hour and a quarter; and four or five ounces
of common vinegar proved fatal in ten or fifteen hours. These
experiments would make it appear that acetic acid is scarcely less
active as an irritant poison than even the mineral acids.[381] They are
in some measure confirmed by the prior experiments of Schubarth; who
operated, however, with an impure reddish-brown pyroligneous acid, and
was led to ascribe its energy to the presence of some empyreumatic oil,
because he found, as was already remarked, that a pure acid of equal
strength appeared almost inert. From half an ounce to an ounce of the
impure acid given to dogs, caused fruitless efforts to vomit, sometimes
free vomiting, occasionally great flow of tears, always weakness in the
hind-legs, and feeble, irregular pulse, and death either in two days
without any new symptom of consequence, or more rapid death in four or
five hours, with previous convulsions, and sometimes insensibility.[382]
These experiments were made with an acid which neutralized 50 grains of
carbonate of lime per ounce, consequently contained at least 50 grains
of concentrated acid, or about a tenth of its weight.

To these observations it may be added, that according to the experiments
of Hébréart, a small quantity of acetic acid dropped into the windpipe,
produces hissing respiration, rattling in the throat, and death in three
days from true croup.[383]

In all the preceding experiments distinct evidence was obtained in the
dead body of the irritant action of the poison. The stomach contained
brownish-black blood, the villous coat was blackish, and the subjacent
cellular tissue injected with black blood; sometimes there was an
appearance of erosion on the surface of the villous coat; and in the
instance of the concentrated acid perforations were found. In the
experiments of Hébréart the lining membrane of the windpipe was covered
with a fibrinous pseudo-membrane, exactly as after croup.

Although acetic acid in its various forms is daily in the hands of every
body, one case only of poisoning with it in the human subject has
hitherto been made public. It is described by MM. Orfila and
Barruel.[384] A girl was seen in a village near Paris at eleven at night
apparently intoxicated. Five hours afterwards she was found lying on the
ground in great agony; and after complaining of pain in the stomach and
experiencing several attacks of convulsions, she expired. On the
subsequent examination of the body considerable lividity was observed on
the skin of the depending parts. The back of the tongue was brownish and
leathery, and the inner membrane of the gullet blackish-brown,
intersected by a fine network of vessels. The stomach presented
internally several large, black, firm elevations, owing to the injection
of coagulated blood into the submucous cellular tissue; and elsewhere it
had a grayish-white tint, with here and there a reddish colour; but the
mucous membrane was perfectly entire. The cavity contained above eight
ounces of a thick, blackish fluid; and a thicker pulpy matter of the
same colour adhered firmly to the villous coat. The intestines were
healthy, and so also were the other organs in the belly and chest. The
uterus contained a fœtus two months and a half old. The contents of the
stomach were subjected to a careful analysis by MM. Orfila and Barruel,
who found that they did not contain any appreciable quantity of free
sulphuric or muriatic acid, or of any of the common metallic poisons;
and by the process of analysis formerly described, they succeeded in
separating from the impure mass three drachms of a pure, and tolerably
concentrated acetic acid, besides two drachms more from the contents of
the intestines. As the residue of the distillation left behind in the
retort did not yield any bitter principle to boiling alcohol, so as to
countenance the idea of a vegetable alkaloid having been given along
with the acetic acid, they inferred that this acid had been swallowed
alone; and the experiments of Orfila on dogs, performed for the
occasion, induced them to conclude that it was the cause of death.

To these observations it is only farther necessary to add, that the
concentrated acid is a powerful irritant and even corrosive when applied
externally; which properties are owing to its power of dissolving many
of the soft animal solids.[385]




                              CHAPTER VI.
                     OF POISONING WITH OXALIC ACID.


The last poison of this order is oxalic acid. It is a substance of very
great interest; for it is a poison of great energy, and in this country
is in common use for committing suicide, and has been often taken by
accident for Epsom salt.

It is certainly ill adapted for the purposes of the murderer; for
although it might be easily given to a sick person instead of a laxative
salt, yet its real nature would betray itself too soon and too
unequivocally for the chief object of the prisoner,—secrecy.
Nevertheless, attempts of the kind have been made. At the trial of James
Brown for assaulting his wife, held at the Middlesex Autumn Assizes
1827, it was brought out in evidence that he had previously tried to
poison her by giving her oxalic acid in gin;[386] and Mr. Alfred Taylor
says he is acquainted with two similar cases, where an attempt was made
to administer it in tea.[387]

It was first made known as a poison by Mr. Royston in 1814.[388] Its
properties have been examined by Dr. A. T. Thomson of London,[389] and
Dr. Perey of Lausanne;[390] in 1823, the whole subject of poisoning with
oxalic acid in its medico-legal relations was examined by Dr. Coindet of
Geneva and myself;[391] and in 1828, another experimental inquiry, which
confirms most of the results we obtained, was published by Dr. Pommer of
Heilbronn.[392]


               SECTION I.—_Of the Tests for Oxalic Acid._

Oxalic acid is commonly in small crystals of the form of flattened
six-sided striated prisms, transparent, colourless, free of odour, very
acid to the taste, and permanent in the air. Two other common vegetable
acids, the citric and tartaric acids, present a totally different
crystalline form. In general appearance it greatly resembles the
sulphate of magnesia, for which it has been so often and so fatally
mistaken. So close, indeed, is the resemblance, that repeatedly, on
desiring several persons to point out which was the poison and which the
laxative, I have found as many fix on the wrong as on the right parcel.
The sulphate of magnesia has of course a very different taste, being
strongly bitter. Various plans have been devised for preventing the
accident to which this unlucky resemblance has given rise. The best of
them imply the use of a safeguard by the patient before he takes his
laxative draught. It seems to have escaped the notice of those who have
proposed the plans in question, that, if accidents are to be prevented
in this manner, by far the simplest and most effectual security will be
to let the public know, that a laxative salt ought always to be tasted
before being swallowed. Its solubility has been much overrated by some
chemists. It does not appear to me soluble in less than eleven parts of
water.

In determining the medico-legal tests for oxalic acid, it will be
sufficient to consider it in two states,—dissolved in water,—and mixed
with the contents of the stomach and intestines or vomited matter. If
the substance submitted to examination is in the solid state, the first
step is to convert it into a solution.

1. In the form of a pure solution, its nature may be satisfactorily
determined by the following process.

The acidity of the fluid is first to be established by its effect on
litmus-paper.—A small portion is next to be tested with ammonia, which,
if the solution of the acid be sufficiently concentrated, will produce a
radiated crystallization, as the oxalate of ammonia formed is much less
soluble than oxalic acid itself. This property, according to Dr.
O’Shaughnessey, distinguishes it from every other acid.[393] The
remainder of the fluid is next to be subjected to the following
reagents.

_Hydrochlorate of lime_ causes a white precipitate, the oxalate of lime;
which is dissolved on the addition of a drop or two of nitric acid,—and
is not dissolved when similarly treated with hydrochloric acid, unless
the acid is added in very large proportion.

The easy solubility of the oxalate of lime in nitric acid distinguishes
the precipitate from the sulphate of lime, which the present test might
throw down from solutions of the sulphates, and which is not soluble in
a moderate quantity of nitric acid without the aid of heat. The
insolubility of the oxalate of lime in hydrochloric acid on the other
hand distinguishes the precipitate from the tartrate, citrate, carbonate
and phosphate of lime, which the test might throw down from any solution
containing a salt of these acids. The last four precipitates are
redissolved by a drop or two of hydrochloric acid; but the oxalate is
not taken up till a large quantity of that acid is added.

_Sulphate of lime_ in solution causes a white precipitate with oxalic
acid, and not with any other.[394]

_Sulphate of copper_ causes a faint bluish-white, or greenish-white
precipitate, which is not redissolved on the addition of a few drops of
hydrochloric acid. The precipitate is the oxalate of copper. It is
redissolved by a large proportion of hydrochloric acid.

This test does not precipitate the sulphates, hydrochlorates, nitrates,
tartrates, citrates. But with the carbonates and phosphates it forms
precipitates resembling the oxalate of copper. The oxalate, however, is
distinguished from the carbonate and phosphate of copper by not being
redissolved on the addition of a few drops of hydrochloric acid.

_Nitrate of silver_ causes a dense, white precipitate, the oxalate of
silver; which, when collected on a filter, dried and heated, becomes
brown on the edge, then fulminates faintly and is dispersed.

The object of the supplementary test of fulmination is to distinguish
the oxalate of silver from the numberless other white precipitates which
are thrown down by the nitrate of silver from solutions of other salts.
The property of fulmination, which is very characteristic, requires, for
security’s sake, a word or two of explanation, in consequence of the
effect of heat on the tartrate and citrate of silver. The citrate when
heated becomes altogether brown, froths up, and then deflagrates,
discharging white fumes and leaving an abundant, ash-gray, coarsely
fibrous, crumbly residue, which on the farther application of heat
becomes pure white, being then pure silver. The tartrate also becomes
brown and froths up, but does not even deflagrate, white fumes are
discharged, and there is left behind a botryoidal mass, which, like the
residue from the citrate, becomes pure silver when heated to redness.
Another distinction between the oxalate and tartrate is that the former
continues permanent at the temperature of ebullition, while the latter
becomes brown. The preceding process or combination of tests will be
amply sufficient for proving the presence of oxalic acid, free or
combined, in any fluid, which does not contain animal or vegetable
principles.

2. The only important modifications in the analysis rendered necessary
by the admixture of organic principles, occur in the case of the
contents of the alimentary canal or vomited matters.

Dr. Coindet and I proved, that oxalic acid has not any chemical action
with any of the common animal principles except gelatin, which it
rapidly dissolves;—and that this solution is of a peculiar kind, not
being accompanied with any decomposition, either of the acid or of the
gelatin.[395] Consequently oxalic acid, so far as concerns the tissues
of the stomach or its ordinary contents, is not altered in chemical
form, and remains soluble in water.

In such a solution, however, a variety of soluble principles are
contained, which would cause abundant precipitates with two of the tests
of the process,—sulphate of copper and nitrate of silver; so that the
oxalates of these metals could not possibly be detached in their
characteristic forms. The process for a pure solution, therefore, is
inapplicable to the mixtures under consideration.

But changes of still greater consequence are effected on the poison by
exhibiting antidotes during life. It is now generally known, that the
proper antidotes for oxalic acid are magnesia and chalk. Each of these
forms an insoluble oxalate; so that if either had been given in
sufficient quantity, no oxalic acid will remain in solution, and the
proofs of the presence of the poison must be sought for in the solid
contents of the stomach or solid matter vomited.

The following process for detecting the poison will apply to all the
alterations which it may thus have undergone.

_Process for Compound Mixtures._—If chalk or magnesia has not been given
as an antidote, the suspected mixture is to be macerated if necessary
for a few hours in a little distilled water, then filtered, and the
filtered fluid neutralized with carbonate of potass. If on the other
hand chalk or magnesia has been given, the mixture is to be left at rest
for some time, and the supernatant fluid then removed. This fluid, if
not acid, may be thrown away; but if acid, it may be treated as already
directed for a suspected mixture, where chalk or magnesia has not
obtained entrance. After the removal of the supernatant liquid, pick out
as many solid fragments of animal or vegetable matter as possible; and
add as much pure water to the insoluble residue as will give the mass a
sufficiently thin consistence. Add now to the mixture about a twentieth
of its weight of carbonate of potass, and boil gently for two hours, or
till the organic matter is all dissolved. While dissolution thus takes
place, a double interchange is effected between the elements of the
carbonate of potass on the one hand, and those of the earthy oxalate on
the other, so that an oxalate of potass will at length exist in
solution. The fluid when cold is next to be filtered, then rendered very
faintly acidulous with nitric acid, then filtered and rendered very
faintly alkaline with carbonate of potass, and filtered a third time. At
each of these steps some animal matter will be thrown down.

From this point onwards the process proceeds in the same way, whatever
may have been the original form in which the acid existed in the
mixture; for the oxalate of lime or magnesia in the second case is
converted into oxalate of potass.

Add now the solution of acetate of lead to the fluid as long as any
precipitate is formed. Collect the precipitate on a filter, wash it
well, and dry it by compression between folds of bibulous paper. Remove
this precipitate, which consists of oxalate of lead and organic matter
in union with oxide of lead, and rub it up very carefully while damp
with a little water in a mortar. Transmit sulphuretted hydrogen gas
briskly for an hour, so that the whole white precipitate shall be
thoroughly blackened; filter and boil. In this manner is formed a
sulphuret of lead, which retains a great deal of animal matter; and the
oxalic acid being set free, is found in the solution tolerably pure.
Filtration before boiling is an essential point in this step, to prevent
animal matter being dissolved by the water from the sulphuret of lead.
More animal matter may still be separated by evaporating the liquid to
dryness at 212°, keeping it at that temperature for a few minutes, and
redissolving and filtering. The solution will now exhibit the properties
of oxalic acid.

I have found that when this process was applied to a decoction of an
ounce of beef in six ounces of water, with which one grain of anhydrous
oxalic acid had been mixed, all the tests acted characteristically on
the solution ultimately procured. I have farther found, that when two
grains of oxalate of lime, which correspond with one grain of oxalic
acid, were mixed with a similar decoction in which some fragments of
beef were purposely left to complicate the process, a solution was
eventually obtained, which gave with muriate of lime a white precipitate
insoluble in a little muriatic acid, with sulphate of copper a
greenish-white precipitate also insoluble in a little muriatic acid, and
with nitrate of silver a white precipitate which fulminated and was
almost all dispersed, but left a little charcoal, owing to its
containing a small proportion of animal matter. In a case which lately
happened in London, every test acted as here described, except that the
oxalate of lime did not fulminate, owing to the presence of organic
impurities.[396] In order to try the test of fulmination in such
circumstances, it is essential to dry the precipitated oxalate of silver
thoroughly before raising the temperature to the point at which
fulmination usually occurs.

The process now recommended is both delicate and accurate. An objection
has been advanced against it,—that acetate of lead will throw down
chloride of lead as well as the oxalate of lead; that both will
subsequently be decomposed by the sulphuretted-hydrogen? and that the
hydrochloric acid thus brought into the solution with the oxalic acid
will be precipitated by the nitrate of silver, and form a mixture of
salts which will not fulminate characteristically.[397] This objection
is not well founded. Chloride of lead being soluble in thirty parts of
temperate water, it will seldom be thrown down from such fluids as occur
in medico-legal inquiries; and besides it is easily removed, as I have
ascertained, by washing the precipitate with moderate care on the
filter.

Professor Orfila has advanced another objection,—that the process will
yield all the indications mentioned above, if binoxalate of potash be
present, or sorrel-soup, which contains a little of that salt.[398] The
objection is valid, were these substances apt to come in the way. But
the binoxalate of potash is not put to any medicinal use in Britain, and
English cookery does not acknowledge the “soupe à l’oseille.” The
process he recommends to meet the difficulty, an important one in
France, is the following: 1. Having made a watery solution as above,
evaporate nearly to dryness, agitate the residue with cold pure alcohol,
repeatedly during a period of several hours; decant the tincture, and
repeat this step with more alcohol; evaporate to obtain crystals, if
possible; dissolve these again in cold pure alcohol, and crystallize a
second time by evaporation. If crystals do not form on first
concentrating the alcoholic solution, evaporate it till a pellicle
begins to form, agitate the residue with cold pure alcohol, and
concentrate again to obtain crystals. Lastly, examine the crystals by
the tests for pure oxalic acid. The object of these steps in the process
is to separate binoxalate of potass, oxalate of magnesia and oxalate of
lime, which, he says, are all either not soluble, or very sparingly so,
in absolute alcohol. 2. More oxalic acid may be got by acting with
distilled water on the matter left by the action of alcohol, evaporating
this watery solution nearly to dryness, agitating the residuum with cold
alcohol as before, and so on. 3. The preceding operations may have left
oxalate of magnesia and oxalate of lime unacted on by the water among
the solids remaining on the filter. The former compound may be dissolved
out by cold hydrochloric acid diluted with four times its volume of
water; and by an excess of pure carbonate of potass, the oxalate of
magnesia in the solution is converted into insoluble carbonate of
magnesia and soluble oxalate of potass, from which oxalic acid is to be
obtained by a salt of lead and sulphuretted-hydrogen, as explained in my
own process. 4. Oxalate of lime, which may still remain, is to be sought
for by boiling the residuum of the action of hydrochloric acid with
solution of bicarbonate of potash, so as to obtain here also an oxalate
of potass in solution. I have not had an opportunity of trying this
method. But I find, that, contrary to Orfila’s statement, binoxolate of
potass, though sparingly soluble in cold alcohol of the density of 800,
is sufficiently so to vitiate the principle on which the process is
founded.

Caustic potass must not be used for decomposing oxalate of lime or
magnesia, because the pure alkali, as Gay-Lussac has shown, produces
oxalic acid in acting on animal substances at a boiling temperature.
Carbonate of potass has no such effect.

The discovery of oxalic acid in the form of oxalate of lime in the
stomach or vomited matter is exposed to a singular fallacy, if a
material quantity of rhubarb has been taken recently before death, or
before the discharge of the vomited matter. For according to the
researches of M. Henry of Paris, rhubarb root always contains some
oxalate of lime, and some samples yield so much as 30 and even 33 per
cent.[399]


SECTION II.—_On the Action of Oxalic Acid and the Symptoms it causes in
                                 Man._

The action of oxalic acid on the animal economy is very peculiar.

When injected in a state of concentration into the stomach of a dog or
cat, it causes exquisite pain, expressed by cries and struggling. In a
few minutes this is succeeded by violent efforts to vomit; then by
sudden dulness, languor, and great debility; and death soon takes place
without a struggle. The period which elapses before death varies from
two to twenty minutes, when the dose is considerable,—half an ounce, for
example. After death the stomach is found to contain black extravasated
blood, exactly like blood acted on by oxalic acid out of the body; the
inner coat of the stomach is of a cherry-red colour, with streaks of
black granular warty extravasation; and in some places the surface of
the coat is very brittle and the subjacent stratum gelatinized,
evidently by the chemical action of the poison.[400] If the stomach is
examined immediately after death, little corrosion will be found,
compared with what is seen if the inspection be delayed a day or
two.[401]

Such are the effects of the concentrated acid. When considerably
diluted, the phenomena are totally different. When dissolved in twenty
parts of water, oxalic acid, like the mineral acids in the same
circumstances, cease to corrode; nay it hardly even irritates. But,
unlike them, it continues a deadly poison; for it causes death by acting
indirectly on the brain, spine, and heart. The symptoms then induced
vary with the dose. When the quantity is large, the most prominent
symptoms are those of palsy of the heart; and immediately after death
that organ is found to have lost its contractility, and to contain
arterial blood in its left cavities. When the dose is less the animal
perishes after several fits of violent tetanus, which affects the
respiratory muscles of the chest in particular, causing spasmodic fixing
of the chest and consequent suffocation. When the dose is still less,
the spasms are slight or altogether wanting, and death occurs under
symptoms of pure narcotism like those caused by opium: the animal
appears to sleep away.

This poison acts with violence, and produces nearly the same effects to
whatever texture of the body it is applied. It causes death with great
rapidity when injected into the sac of the peritonæum, or into that of
the pleura; it acts with still greater quickness when injected into a
vein; and it also acts when injected into the cellular tissue beneath
the skin, but with much less celerity than through any other channel.
Eight grains injected into the jugular vein of a dog occasioned almost
immediate death: Thirty-three grains injected into the pleura killed
another in twelve minutes. The same quantity did not prove fatal, though
it caused violent effects, when retained in the stomach by a ligature on
the gullet. One hundred and sixty grains injected under the skin of the
thigh and belly did not prove fatal for about ten hours. The symptoms
were nearly the same in every case.[402]

It is probable from the facts now stated, that oxalic acid, when not
sufficiently concentrated to occasion death by the local injury
produced, acts on the nervous system through the medium of the blood.
Nevertheless it is a remarkable circumstance that it cannot be detected
in that fluid. Mention has already been made of an experiment performed
by Dr. Coindet and myself (p. 22), where even after the injection of
eight grains of oxalic acid into the femoral vein, and the consequent
death of the animal in thirty seconds, none of the poison could be
detected in the blood of the iliac vein or vena cava. Similar results
have been more lately obtained by Dr. Pommer. In dogs killed by the
gradual injection of from five to thirty grains into the femoral vein,
he never could detect the poison in the blood of the right side of the
heart or great veins, except in the instance of the largest doses, where
a little could be detected near the opening in the vein. Dr. Pommer’s
experiments likewise agree with those of Dr. Coindet and myself as to
the absence of any change in the physical qualities of the blood.[403]
When to these circumstances it is added that very small quantities of
oxalic acid may be detected in blood, into which it has been introduced
immediately after removal from the body by venesection, it appears
reasonable to conclude that the poison is quickly decomposed in the
blood by vital operations.

According to Orfila, however, it may be detected in the urine, in which
crystals of oxalate of lime form on cooling, and more may be obtained on
the addition of hydrochlorate of lime. Yet he could not detect any
oxalic acid in the liver or spleen.[404]

In man the most prominent symptoms hitherto observed have been those of
excessive irritation, because it has been almost always swallowed in a
large dose and much concentrated.

It is the most rapid and unerring of all the common poisons. The London
Courier contains an inquest on the body of a young man who appears to
have survived hardly ten minutes;[405] an equally rapid case of a young
lady, who poisoned herself with an ounce, is mentioned in the St.
James’s Chronicle;[406] and few of those who have died survived above an
hour. This rule, however, is by no means without exception. Mr. Hebb has
described a case which did not prove fatal for thirteen hours;[407] Dr.
Arrowsmith of Coventry has favoured me with the particulars of a very
interesting case which lasted for the same period: and Mr. Frazer has
accurately described another, in which, after the patient seemed to be
doing tolerably well, an exhausting fever, with dyspepsia and singultus,
carried him off in twenty-three days.[408]

Among the fatal cases the smallest dose has been half an ounce; but
there can be little doubt that less would be sufficient to cause death.
Dr. Babington of Coleraine has published a case where very severe
effects were produced by only two scruples.[409]

Very few persons have recovered where the quantity was considerable.

In every instance in which the dose was considerable, and the solution
concentrated, the first symptoms have been immediate burning pain in the
stomach, and generally also in the throat. But when the dose was small,
more particularly if the solution was also rather diluted, the pain has
sometimes been slight, or slow in commencing. Mr. Hebb’s patient, who
took only half an ounce dissolved in ten parts of water, and diluted it
immediately after with copious draughts of water, had not any pain in
the belly for six hours.

In general, violent vomiting follows the accession of pain, either
immediately, or in a few minutes; and it commonly continues till near
death. Some, however, have not vomited at all, even when the acid was
strong and in a large dose; and this is still more apt to happen when
the poison has been taken much diluted. The man last mentioned did not
vomit at all for seven hours, except when emetics were administered. The
vomited matter, as in this man’s case, and in that of Mr. Frazer’s
patient, is sometimes bloody. Instant discharge of the poison by
vomiting does not always save the patient’s life: A woman who swallowed
two ounces died in twenty minutes, although she vomited almost
immediately after taking the poison.[410]

The tongue and mouth occasionally become inflamed if the case lasts long
enough. In an instance of recovery, which happened not long ago in St.
Thomas’s Hospital, London, the tongue was red, swollen, tense and
tender, the day after the acid was swallowed.[411]

Death commonly takes place so soon, that the bowels are seldom much
affected. But when life is prolonged a few hours, they are evidently
much irritated. Dr. Arrowsmith’s patient, who lived thirteen hours, had
severe pain in the bowels and frequent inclination to go to stool, and
Mr. Hebb’s patient, who also lived thirteen hours, had a constant,
involuntary discharge of fluid fæces, occasionally mixed with blood.
Bloody diarrhœa is very common in dogs.

The signs of depressed circulation are always very striking. In general
the pulse fails altogether, it is always very feeble, and the skin is
cold and clammy. Contrary to the general fact, however, I once remarked
in a dog the pulsation of the heart so strong as to be audible at a
distance of several yards.

In some cases nervous symptoms have occurred, but in none so distinctly
as in animals that have taken the diluted acid. It should be remarked,
however, that few published cases contain good histories of the
symptoms; since they commonly come to an end before being seen by the
physician. Convulsions appear to have occurred in some instances either
at the time of death or soon before it. In the slower cases various
nervous affections have been observed. A girl, who swallowed by mistake
about two drachms, and did not vomit till emetics were given, complained
much at first of pain, but afterwards chiefly of great lassitude and
weakness of the limbs, and next morning of numbness and weakness there
as well as in the back. This affection was at first so severe that she
could hardly walk up stairs; but in a few days she recovered
entirely.[412] Analogous effects took place in Mr. Hebb’s patient and in
Dr. Arrowsmith’s case. The first thing the former complained of was
acute pain in the back, gradually extending down the thighs, occasioning
ere long great torture, and continuing almost till the moment of death.
Dr. Arrowsmith’s patient had the same symptoms, complained more of the
pain shooting down from the loins to the limbs than of the pain in the
belly, and was constantly seeking relief in a fresh change of posture.
Mr. Frazer’s patient had from an early period a peculiar general
numbness, approaching to palsy. Dr. Babington’s patient, who took two
scruples by mistake for tartaric acid in an effervescing draught,
suffered, after the first twenty-four hours, chiefly from headache,
extreme feebleness of the pulse, and a sense of numbness and tingling or
pricking in the back and thighs. In a recent case described by Mr.
Tapson, which occurred in London, and where it was supposed, but on
insufficient grounds,[413] that so much as two ounces had been taken,
violent symptoms of irritation in the alimentary canal came on as usual,
but soon afterwards a sense as if the hands were dead, loss of
consciousness for eight hours, and then lividity, coldness, and almost
complete loss of the power of motion in the legs; which symptoms were
not entirely removed for fifteen days. In a case related by Mr. Alfred
Taylor, where death was caused by seven drachms in fifteen or twenty
minutes, there was first violent vomiting, then severe pain in the
stomach, and finally clammy perspiration and convulsions, with two or
three deep inspirations before death.[414] The effects in this case came
very near those generally observed in animals.

In Dr. Arrowsmith’s case two symptoms occurred, which I have not seen
mentioned in any other. The first was an eruption or mottled appearance
of the skin in circular patches, not unlike the roundish red marks on
the arms of stout healthy children, but of a deeper tint. The second was
the poisoning and death of leeches applied to the stomach. “They were
healthy,” says Dr. Arrowsmith in the notes with which he obligingly
furnished me, “small, and fastened immediately. On looking at them in a
few minutes I remarked that they did not seem to fill, and on touching
one it felt hard and immediately fell off, motionless and dead. The
others were all in the same state. They had all bitten and the marks
were conspicuous; but they had drawn scarcely any blood. They were
applied about six hours after the acid was taken.” This curious fact
illustrates the observations formerly quoted from Vernière’s experiments
[p. 67]. It will be observed that the leeches were applied several hours
after the poison was swallowed, and in a case in which the acid was
largely diluted in the stomach;—so that it might have entered the blood
and been diffused throughout the body before the observation was made.


    SECTION III.—_Of the Morbid Appearances caused by Oxalic Acid._

The external appearance of the body is commonly natural. In one instance
the cellular tissue was distended with gases ten hours after death.[415]
Violent marks of irritation have been commonly found in the stomach; and
sometimes that organ has been even perforated.[416] It is probable that
the extensive destruction of the coats noticed by some authors has taken
place in part after death from the action of the acid on the dead
tissues.—The usual conjunction of morbid appearances is well described
by Mr. Hebb. The mucous coat of the throat and gullet looked as if it
had been scalded, and that of the gullet could be easily scratched off.
The stomach contained a pint of thick fluid. This is commonly dark, like
coffee-grounds, as it contains a good deal of blood. The inner coat of
the stomach was pulpy, in many points black, in others red. The inner
membrane of the intestines was similarly but less violently affected.
The outer coat of both stomach and intestines was inflamed. The lining
membrane of the windpipe was also very red.—The appearances have also
been excellently described in the case published by Mr. Alfred Taylor.
The inside of the gullet was pale, as if boiled, strongly corrugated and
brittle, and covering a ramification of vessels filled with consolidated
blood. The stomach presented externally numerous vessels in the same
state; and its villous coat was pale, soft, brittle, but here and there
injected with vessels. The duodenum and part of the jejunum were red,
the other intestines natural, the liver, spleen, and kidneys congested.
The stomach contained a brownish jelly, in which gelatin was detected,
as well as oxalic acid. The blood was fluid every where except in the
vessels of the gullet and stomach.[417] The consolidated condition of
the blood there was evidently owing to the local action of a strong
acid, and is the same with what has been observed in poisoning with the
mineral acids.—In Mr. Frazer’s patient the whole villous coat of the
stomach was either softened or removed, as well as the inner membrane of
the gullet, so that the muscular coat was exposed; and this coat
presented a dark gangrenous-like appearance, being much thickened and
highly injected.

Although these signs of violent irritation are commonly present, it must
at the same time be observed, that some cases have occurred where the
stomach and intestines were quite healthy. In a girl who died about
thirty minutes after swallowing an ounce of the acid, no morbid
appearance whatsoever was to be seen in any part of the alimentary
canal.[418] In the case of a girl, described by Mr. Anderson, where
death took place in twenty minutes, there was no appearance but
contraction of the rugæ of the gullet and stomach, one spot of
extravasation in the latter and doubtful softening of its villous
coat.[419]

The state of the other organs of the body has not been taken notice of
in published cases. In several instances, as in Mr. Taylor’s case, the
blood in the veins of the stomach is described as having been black and
as it were charred; probably by the chemical action of the acid after
death.


     SECTION IV.—_Of the Treatment of Poisoning with Oxalic Acid._

The chief part of the treatment of this kind of poisoning is obvious. On
account of its dreadful rapidity, remedies cannot be of material use
unless they are resorted to immediately after the acid has been
swallowed. Emetics may be given, if vomiting is not already free; but
time should never be lost in administering them if an antidote is at
hand. In particular it is necessary to avoid giving warm water with a
view to accelerate vomiting, unless it is given very largely; for
moderate dilution will promote the entrance of the poison into the
blood, if it has not the effect of immediately expelling it.

The principal object of the practitioner should be to administer as
speedily as possible large doses of magnesia or chalk suspended in
water. Chalk has been given with great advantage in several cases,[420]
and magnesia has also been of service.[421] As no time should be lost,
the plaster of the apartment may be resorted to, when chalk or magnesia
is not at hand. These substances not only neutralize the acid so as to
take away its corrosive power, but likewise render it insoluble, so as
to prevent it from entering the blood. There appears no particular
reason for using the stomach-pump when antidotes are at hand. But
fashion seems to have authorised the employment of this instrument for
every kind of poison.[422] Alkalis are inadmissible. As might be
inferred from the general statements formerly made on the effect of
chemical changes on poisons [p. 28], the alkalis, as they form only
soluble salts, will not deprive oxalic acid of its remote or indirect
action; and instances are not wanting of their inutility in actual
practice.

Oxalic acid is one of the poisons alluded to under the head of General
Poisoning,—of whose operation distinct evidence may sometimes (though
certainly not always) be found in the symptoms. If a person, immediately
after swallowing a solution of a crystalline salt, which tasted purely
and strongly acid, is attacked with burning in the throat, then with
burning in the stomach, vomiting particularly of bloody matter,
imperceptible pulse and excessive languor, and dies in half an hour, or
still more in twenty, fifteen, or ten minutes, I do not know any fallacy
which can interfere with the conclusion, that oxalic acid was the cause
of death. No parallel disease begins so abruptly and terminates so soon;
and no other crystalline poison has the same effects.

_Poisoning with the Oxalates._—Oxalic acid is one of the best examples
of a poison that acts through all its soluble chemical combinations. Dr.
Coindet and I found that the oxalates of potash and ammonia are little
inferior in energy to the acid. They do not corrode, indeed, and
scarcely ever irritate; but they produce tetanus and coma, like the
diluted acid. Half a drachm of oxalic acid neutralized with potass will
kill a rabbit in seventeen minutes; ninety grains of neutral oxalate of
ammonia will kill a strong cat in nine minutes.[423] The binoxalate of
potash, the most familiar of the salts of oxalic acid, was not tried by
us. But the preceding facts would leave little doubt of its being a
poison.

Since the last edition of this work was published several cases have
occurred which amply confirm the results of experimental inquiry. In Dr.
Babington’s case alluded to above, the greater part of the oxalic acid
had been neutralized by bicarbonate of soda [p. 176].—Mr. Tripier has
communicated the particulars of a case in which half an ounce of the
binoxalate of potash was taken by mistake for bitartrate of potash in
hot water, and caused death in eight minutes, after an attack of violent
pain and convulsions.[424]—A young woman at Bordeaux was attacked with
frequent vomiting after a dose of a drachm and a half of the same salt
dissolved in a ptisane. Next morning a similar dose caused bloody
vomiting and acute pain at the pit of the stomach; and a third dose the
following day excited delirium, more violent vomiting, and death in the
course of an hour.[425]—A girl in London swallowed about an ounce of the
same salt dissolved in hot water. Sickness and faintness ensued, with
imperceptible pulse, cold, clammy skin, rigors, scalding of the mouth
and throat, pain in the back, soreness of the eyes, redness of the
conjunctivæ, and dilatation of the pupils. Afterwards there was
reaction, with a full frequent pulse, hot skin, flushed countenance,
headache, thirst, and tenderness of the abdomen. She recovered under the
use of chalk, external heat, ether and opium draughts, leeches and
sinapisms to the belly, and carbonate of ammonia.[426]

No account has yet been published of the morbid appearances in man.

The proper antidote is sulphate of magnesia. Failing this, weak milk of
lime may be given with advantage.

_Appendix on Tartaric and Citric Acid._—These two acids may be taken in
considerable quantities without injury. Dr. Coindet and I gave a drachm
of each in solution to cats, without observing that the animals suffered
any inconvenience.[427] Dr. Sibbald, a surgeon of this place, has
informed me of an instance in which a patient of his took in twenty-four
hours six drachms of tartaric acid, having by mistake omitted the
carbonate of potass sent along with the acid to make effervescing
draughts; and yet he did not suffer any more inconvenience then the cats
on which Dr. Coindet and I experimented.

Pommer, however, found that tartaric acid is scarcely less active than
oxalic acid when injected into the blood. When fifteen grains
dissolved in half an ounce of water were injected into the femoral
vein of a dog in four doses, difficult breathing and discharge of
fæces and urine were produced after each operation, and death speedily
ensued without any other particular symptom. As in the instance of
oxalic acid, the blood in the great veins was not apparently changed
in any of its physical qualities. The heart continued contractile long
after death, while in the case of oxalic acid its contractility was
suddenly extinguished.[428]




                              CHAPTER VII.
                   OF THE ALKALIS AND ALKALINE SALTS.


The second order of the class of irritants comprehends the alkalis, some
of the alkaline salts, and lime. The species which it includes are
little allied to one another except in chemical composition; and in
particular they are little allied in physiological properties. It
appears impossible, however, to make a better arrangement than that
proposed by Orfila, which will therefore be here followed.

Most of the poisons of the second order are powerful local irritants.
Some of them likewise act indirectly on distant organs; and a few are
more distinguished by their remote than by their local effects. This
order may be conveniently divided into two groups,—the one embracing the
two fixed alkalis with their carbonates, nitrates, and chlorides, and
also lime,—the other ammonia, with its salts, and likewise the alkaline
sulphurets.

The action of the first group is purely irritant and strictly local.
When concentrated, the fixed alkalis and their carbonates produce
chemical decomposition, softening the animal tissues, and reducing them
eventually to a pulpy mass; which change depends on their possessing the
power, as chemical agents, of dissolving almost all the soft solids of
the body. When much diluted, they produce inflammation, without
corroding the textures; and it does not appear that they are even then
absorbed in such quantity as to prove injurious to any remote organ. The
action of the alkaline nitrates and of lime is that of irritants only;
at least their chemical action is obscure and feeble.


              _Of the Fixed Alkalis and their Carbonates._


                     _Section_ I.—_Of their Tests._

_Potass_ in its caustic state, as usually met with in the shops, forms
little gray-coloured cylinders or cakes which have a radiated,
crystalline fracture, and an excessively acrid caustic taste, and feel
soapy if touched with the wet finger. It deliquesces rapidly in moist
air, and then attracts carbonic acid from the atmosphere. It is easily
fused by heat, and is exceedingly soluble in water. The solution has a
strong alkaline reaction on vegetable colours, restoring reddened litmus
to blue, turning syrup of violets or infusion or red cabbage to green,
and rendering infusion of turmeric brown. It is distinguished from the
alkaline earths when in solution, by not precipitating with carbonic or
sulphuric acid, and from soda by the tests to be presently mentioned for
its carbonate.

_Carbonate of potash_ [subcarbonate, salt of tartar], is usually sold,
when pure, in small white grains, formed by melting the salt and
stirring it rapidly as it cools. In its impure state it is called in
this country potashes, and when somewhat purified, pearl ash. It has
then a mixed grayish, yellowish, or bluish colour, and is sold in
crumbly lumps of various sizes. In every state it is deliquescent and
very caustic. It cannot be crystallized. It gives out carbonic acid gas
with the addition of any stronger acid, such as sulphuric, muriatic, or
acetic acid. Its solution precipitates yellow with the chloride of
platinum, gives a crystalline precipitate with perchloric acid, when the
salt forms not less than a fortieth or fiftieth part,—is similarly acted
on by a considerable excess of tartaric acid, if the salt constitute
about a thirtieth of the fluid,—and yields with the soluble salts of
baryta a white precipitate soluble in nitric acid.

_Soda_ resembles potass closely in chemical as well as physiological
properties; and the _carbonate_ bears the same resemblance to the
carbonate of potass. The chief differences are the following. The
carbonate of soda is easily crystallized, and effloresces on exposure to
the air. A solution in twenty parts of water yields no precipitate with
either perchloric acid or an excess of tartaric acid, because there is
no sparingly soluble perchlorate or bitartrate, as in the case of
potash. Its solution is precipitated by antimoniate of potash, because
the antimoniate of soda is very sparingly soluble. All its salts remain
unaffected by the chloride of platinum, because their base cannot form
like potass an insoluble triple salt with the reagent. The acetate of
soda is permanent in the air, while the acetate of potass is one of the
most deliquescent salts known. In trying this last test, which is very
characteristic, care must be taken to avoid an excess of acid in the
acetate of soda by expelling it at a temperature of 212°, otherwise the
salt is as deliquescent as the acetate of potass.—Another difference is,
that the chloride of sodium, being nearly as soluble in temperate as in
boiling water, crystallizes with difficulty and but sparingly by cooling
a concentrated boiling solution; while the chloride of potassium is much
more soluble in hot than in cold water, and crystallizes easily and
abundantly when a concentrated boiling solution is cooled down.

_Process for Potash and its Carbonate in Organic Mixtures._—The
following method has been lately recommended for the detection of potash
and its carbonate in complex organic mixtures. Ascertain that the
mixture is alkaline in its action on litmus-paper and turmeric-paper,
and that it is not ammoniacal in odour. Distil to one-third; ascertain
that it has still an alkaline reaction, and evaporate to dryness in a
porcelain basin. Agitate the residue, when cold, with absolute alcohol;
boil, pour off the liquor, and filter it while hot. Repeat this with the
residuum and more alcohol. Distil off most of the alcohol, and evaporate
to dryness. Raise the heat to char the residuum, continue the heat as
long as vapours come off, remove the charcoaly matter, and incinerate it
for forty-five minutes in a silver crucible. Try to separate potash from
what remains by means of absolute alcohol; and if this do not succeed,
remove carbonate of potash by boiling water. In either case search for
potash by litmus-paper, turmeric-paper, chloride of platinum, and
perchloric acid.[429]

The conclusiveness of this process depends upon the fact, that absolute
alcohol cannot dissolve from solid organic substances such a proportion
of lactate, tartrate, acetate, sulphate, or phosphate of potash, or
chloride of potassium, as to be acted on by chloride of platinum or
perchloric acid.[430]—It is to be observed that carbonate of potash
singly is insoluble in absolute alcohol; but it becomes soluble in that
fluid, when it is conjoined with various organic matters. Hence it is
that this process, intended fundamentally for caustic potash alone, is
applicable to carbonate of potash also.

_Process for Soda and its Carbonate in Organic Mixtures._—These
substances may be separated by the method just described for potash. If
the alcoholic solution of the extract of the suspected matter be
alkaline in its action on litmus, and be afterwards found to contain
soda or its carbonate, the evidence of these substances having been
derived from without is satisfactory, because the carbonate of soda
contained in many animal matters cannot be so detached. But if no
indications of the presence of soda be thus obtained, it is not enough
that soda be found in the alcoholic solution of the incinerated
alcoholic extract, because the natural carbonate of soda of animal
matter may be separated in that manner.[431]


 SECTION II.—_Of the Action of the fixed Alkalis, and the Symptoms they
                             cause in Man._

The action of the two fixed alkalis and their carbonates on the animal
system is so nearly the same, that the facts which have been ascertained
in respect to one of them will apply to all the rest. The operation of
potass and its carbonate has been carefully investigated by Professor
Orfila,[432] and by M. Bretonneau of Tours.[433]

When caustic potass is injected in minute portions into the veins, it
instantly coagulates the blood. Five grains, according to Orfila, will
in this way kill a dog in two minutes. But when small doses either of
potash itself, or its carbonate, or indeed any of its salts are used,
Mr. Blake found, that without coagulating the blood, they arrested the
action of the heart in ten seconds, if injected into the jugular vein;
and that when they were injected into the carotid artery, they
occasioned in four seconds signs of great obstruction in the capillary
circulation, and arrestment of the heart’s action in thirty-five
minutes, through means of this effect. Next to the salts of baryta he
thought the potash salts the most powerful on the heart’s action of all
those he tried.[434] When introduced into the stomach potash acts
powerfully as an irritant, and generally corrodes the coats of that
organ. Thirty-two grains given by Orfila to a dog caused pain in the
gullet, violent vomiting, much anguish, restlessness, and death on the
third day. On dissection he found the inner coat of the gullet and
stomach black and red; and near the pylorus there was a perforation
three-quarters of an inch wide, and surrounded by a hard, elevated
margin. The observations of Bretonneau are in some respects different.
When potass was swallowed by dogs in the dose of 40 grains, he found
that the animals, after suffering for some time from violent vomiting,
always died sooner or later of wasting and exhaustion; and that the
action of the poison was confined chiefly to the gullet, which was
extensively destroyed and ulcerated on its inner surface. But when the
gullet was defended by the potass being passed at once into the stomach
in a caustic holder, larger doses, even several times repeated, did not
prove fatal. The usual violent symptoms of irritation prevailed for two
or three days; but on these subsiding, the animals rapidly recovered
their appetite and playfulness, appearing in fact to be restored to
perfect health. Yet there could be no doubt that the stomach all the
while was severely injured; for in some of the animals, which were
strangled for the sake of examination several weeks after they took the
poison, the villous coat was found extensively removed, and even the
muscular and peritonæal coats were here and there destroyed and
cicatrized. Bretonneau farther adds, that ten or fifteen grains
introduced into the rectum caused death sooner than three times as much
given by the mouth.

The carbonate of potass possesses properties similar in kind, but
inferior in degree to those of the caustic alkali. Two drachms given by
Orfila to a dog killed it in twenty-five minutes, violent vomiting and
great agony having preceded death. The stomach was universally of a
deep-red colour on its inner surface.

Potash and its carbonate are absorbed in the course of their action, and
may be detected by Orfila’s process in the liver, kidneys, and
urine.[435]

The actions of soda and its carbonate seem on the whole the same with
those of potash; but they are not so energetic. In one respect however
soda and its salts differ most materially from those of potash. For
while the latter, when admitted directly into a vein, act by arresting
the action of the heart, soda and its salts, according to the inquiries
of Mr. Blake, have no such effect, but cause death by obstructing the
circulation of the pulmonary capillaries, and preventing the return of
blood from the lungs to the left side of the heart. This conclusion
seems to flow from the following facts. The respiration becomes in a few
seconds laborious and soon ceases, whilst the heart continues to beat
vigorously: arterial pressure is greatly reduced, while venous pressure
is much increased owing to accumulation of blood in the right side of
the heart: after death the lungs are found congested and often full of
froth: and the heart continues contractile, very turgid in the right
side, but quite empty of blood in its left cavities.[436]

Poisoning with the caustic alkalis is rare. In 1842, a lady suffering
from inflammation of the bowels took an ounce of solution of potass by
mistake for kali-water, or a solution of bicarbonate of potash
surcharged with carbonic acid. She suffered severely at the time, and
died in a fortnight, probably of the conjunct effects of her disease and
the poison.[437] This is the only case I have found in print of
poisoning with a caustic alkali. But the effects of their carbonates
have been several times witnessed, and appear to resemble closely those
of the concentrated mineral acids.

The symptoms are in the first instance an acrid burning taste, and rapid
destruction of the lining membrane of the mouth; then burning and often
constriction in the throat and gullet, with difficult and painful
deglutition; violent vomiting, often sanguinolent, and tinging vegetable
blues green; next acute pain in the stomach and tenderness of the whole
belly; subsequently cold sweats, excessive weakness, hiccup, tremors and
twitches of the extremities; and ere long violent colic pains, with
purging of bloody stools and dark membranous flakes. So far the symptoms
are nearly the same in all cases; but in their subsequent course several
varieties may be noticed.

In the worst form of poisoning death ensues at an early period, for
example within twenty-four hours, nay even before time enough has
elapsed for diarrhœa to begin. A case of this kind, which has been very
well described by Mr. Dewar of Dunfermline, and which arose from the
patient, a boy, having accidentally swallowed about three ounces of a
strong solution of carbonate of potass, proved fatal in twelve hours
only.[438] Here death was owing to the general system or some vital
organ being affected through sympathy by the injury sustained by the
alimentary canal.

In the mildest form, as in a case related by Plenck[439] of a man who
swallowed an ounce of the carbonate of potass, the symptoms represent
pretty nearly an attack of acute gastritis when followed by
recovery,—the effects on man being then analogous to those observed by
Bretonneau in animals, when the poison was introduced into the stomach
without touching the gullet.

But a more common form than either of the preceding is one, similar to
the chronic form of poisoning with the mineral acids, in which constant
vomiting of food and drink, incessant discharge of fluid, sanguinolent
stools, difficulty of swallowing, burning pain from the mouth to the
anus, and rapid emaciation, continue for weeks or even months before the
patient’s strength is exhausted; and where death is evidently owing to
starvation, the alimentary canal being no longer capable of assimilating
food. Two characteristic examples of this singular affection have been
recorded in the Medical Repository,[440] and a third, of which the event
has not been mentioned, but which would in all likelihood end fatally,
has been communicated by M. Jules Cloquet to Orfila.[441] Of the two
first cases, which were caused by half an ounce of carbonate of potass
having been taken in solution by mistake for a laxative salt, one proved
fatal in little more than a month, the other three weeks afterwards. In
Cloquet’s case, at the end of the sixth week the membrane of the mouth
was regenerated; but the gullet continued to discharge pus, and the
stools were purulent and bloody.

Another form perhaps equally common with that just described, and not
less certainly fatal, commences like the rest with violent symptoms of
irritation in the mouth, gullet, and stomach; but the bowels are not
affected, and by and by it becomes apparent that the stomach is little
injured; dysphagia or even complete inability to swallow, burning pain
and constriction in the gullet, hawking and coughing of tough, leathery
flakes, are then the leading symptoms; at length the case becomes one of
stricture of the œsophagus with or without ulceration; the bougie gives
only temporary relief, and the patient eventually expires either of mere
starvation, or of that combined with an exhausting fever. Mr. Dewar has
related a very striking example of this form of poisoning with the
alkalis.[442] His patient, after the first violent symptoms had
exhausted themselves, which took place in sixteen or eighteen hours,
suffered little for four or five days till the sloughs began to separate
from the lining membrane of the mouth, throat, and gullet. The affection
of the gullet then became gradually predominant, and terminated in
stricture, of which she appears to have been several times so much
relieved as to have been thought in a fair way of recovery. After
repeatedly disappointing Mr. Dewar’s hopes of a successful issue by her
intemperance in the use of spirituous liquors, she died of starvation
about four months after swallowing the poison. Sir Charles Bell has
noticed three parallel cases, and has given delineations of the
appearance in the gullet of two of them.[443] One of his patients did
not die till twenty years after swallowing the poison, which in this
instance was soap-less; yet he does not hesitate to ascribe the
stricture to that cause, and says death arose purely from starvation.

The carbonate of soda, though a salt in very common use, has not
hitherto been the cause of accident, which has found its way into print.
It is plainly much less actively corrosive than carbonate of potass, and
is therefore probably in every sense less energetic.


 SECTION III.—_Of the Morbid Appearances caused by the fixed Alkalis._

The morbid appearances caused by potass, soda, and their carbonates
differ with the nature of the case.

In the boy who died in twelve hours Mr. Dewar found the inner membrane
of the throat and gullet almost entirely disorganized and reduced to a
pulp, with blood extravasated between it and the muscular coat. The
inner coat of the stomach was red, in two round patches destroyed, and
the patches covered with a clot of blood;—its outer coat, as well as all
the other abdominal viscera, was sound.

In the two chronic cases mentioned in the Medical Repository the
mischief was much more general, the whole peritonæum being condensed,
the omentum dark and turgid, the intestines glued together by lymph, the
external coats of the stomach thick, the villous coat almost all
destroyed, what remained of it red and near the pylorus ulcerated, and
the pyloric orifice of the stomach plugged up with lymph so as barely to
admit a small probe.

In Mr. Dewar’s patient who died of stricture of the gullet the
intestines were sound, the inner surface of the stomach red especially
towards the cardia, the inner and muscular coats of the gullet thickened
and firmly incorporated together by effused lymph, the inner coat here
and there wanting, the passage of the gullet every where contracted, and
to such a degree about two inches above the cardia as hardly to pass a
common probe. In Sir C. Bell’s cases the appearances were similar.

Orfila says he is led to conclude from a great number of facts that of
all corrosive poisons potass is the one which most frequently perforates
the stomach.[444] This appearance, however, has not been mentioned in
any case of poisoning in the human subject.


  SECTION IV.—_Of the Treatment of Poisoning with the fixed Alkalis._

In the treatment of poisoning with the alkalis the first object is
evidently to neutralize the poison. This may be done either with a weak
acid, or with oil. Of the acids the acetic in the form of vinegar is
most generally recommended, as it is not itself injurious. A successful
case in very unpromising circumstances, where two ounces and a half of
carbonate of potash had been taken by mistake for cream of tartar, and
where the antidote was not administered for half an hour, has been
related by M. Liégard of Caen. Great relief was experienced to the
burning in the throat and stomach, the chilliness, difficult breathing,
and frequent efforts to vomit, which were the first symptoms; and after
repeated alternations of collapse and reaction, convalescence was
established in eight days.[445]—M. Chereau thinks that for the mineral
alkalis and their carbonates fixed oil is a preferable antidote to
vinegar; and he has given the heads of two cases of poisoning with large
doses of carbonate of potass, in which the free employment of almond oil
prevented the usual fatal consequences. It appears to act partly by
rendering the vomiting free and easy, partly by converting the alkali
into a soap. It must be given in large quantity, several pounds being
commonly required.[446] For the subsequent treatment the reader may
consult the paper of Mr. Dewar, which contains many useful hints on the
management of the most complex description of cases.




                             CHAPTER VIII.
                  OF POISONING WITH NITRATE OF POTASS.


The _nitrate of potass_ [nitre, saltpetre, sal-prunelle], is a dangerous
poison. It has been often mistaken for the saline laxatives, especially
the sulphate of soda, and has thus been the source of fatal accidents.


       SECTION I.—_Of the Chemical Tests for Nitrate of Potass._

It exists in commerce and the arts in two forms, fused and crystallized.
The fused nitre [sal-prunelle] is sold in little button-shaped masses,
spheres of the size of musket-balls, or larger circular cakes, of a
snow-white tint. The crystallized salt [sal-petre] is sold in whitish,
sulcated crystals, which are often regular and large. They are six-sided
prisms, more or lest flattened, and terminated by two converging planes.
In both forms nitre has a peculiar, cool, but sharp taste.

Its chemical properties are characteristic. In the solid form, it
animates the combustion of burning fuel, and yields nitrous fumes when
heated with strong sulphuric acid. In solution it is precipitated yellow
by the chloride of platinum, and yields, when not greatly diluted, a
crystalline precipitate with perchloric acid. The crude salt of commerce
contains chloride of sodium; and hence the odour disengaged by sulphuric
acid may be mixed with that of chlorine or hydrochloric acid gas. When
mixed with any vegetable or animal infusion by which it is coloured,
crystals may sometimes be easily procured in a state of sufficient
purity by filtration and evaporation. But if not, then the same process
must be resorted to with that formerly recommended for nitric acid (p.
143), the first step of neutralization with potass being of course
dispensed with.—A process nearly the same with this has been suggested
by M. Kramer of Milan. He proposes to free the liquid in part of animal
matter by adding acetate of lead, transmitting sulphuretted-hydrogen
through the filtered fluid to remove any excess of lead, boiling the
fluid after another filtration, and then proceeding with acetate of
silver to remove chlorides, as in the process I have adopted. In this
way he found nitre even in the blood.[447]


  SECTION II.—_Of the Action of Nitrate of Potass and its Symptoms in
                                 Man._

This substance forms an exception to the general law formerly laid down
with regard to the effect of chemical neutralization on the local
irritants. Both its acid and its alkali are simple irritants; yet the
compound salt, though certainly much inferior in power, is still
energetic. Nay, the experiment of Orfila and the particulars of some
recently published cases tend even to prove, that the action of its
alkali and acid is materially altered in kind by their combination with
one another; for, besides inflaming the part to which it is applied,
nitre has at times produced symptoms of a secondary disorder of the
brain and nerves.

The experiments of Orfila upon dogs show that on these animals it has a
twofold action, the one irritating, the other narcotic. He found that an
ounce and a half killed a dog in ninety minutes when the gullet was
tied, and a drachm another in twenty-nine hours: that death was preceded
by giddiness, slight convulsions, dilated pupil, insensibility and
palsy; that after death the stomach was externally livid, internally
reddish-black, and the heart filled in its left cavities with florid
blood; that when the gullet was not tied the animals recovered after
several attacks of vomiting, and general indisposition for twenty-four
hours; and that when the salt was applied externally to a wound it
excited violent inflammation, passing on to gangrene, but without any
symptom which indicated a remote or indirect operation.[448] Mr. Blake
found that this salt, when injected into the veins of a dog in the dose
of fifteen grains dissolved in twenty-four parts of water, causes sudden
depression and arrestment of the action of the heart, and death in less
than a minute; but that, like other salts of potash, it has no influence
on the capillaries of the lungs, though a powerful effect in obstructing
the systemic capillary system.[449]—When taken in the ordinary way, it
is absorbed in the course of its action, and has been detected both in
the blood and the urine by Kramer of Milan.[450]

As to its effects on man, it must first be observed, that considerable
doses are necessary to cause serious mischief. In the quantity of one,
two, or three scruples, it is given medicinally several times a day
without injury; and Dr. Alexander found by experiments on himself, that
an ounce and a half, if largely diluted, might thus be safely
administered in the course of twenty-four hours.[451] Sometimes, too,
even large single doses have been swallowed with impunity. A gentleman
of my acquaintance once took nearly an ounce by mistake for Glauber’s
salt, and retained it above a quarter of an hour: nevertheless, except
several attacks of vomiting, no unpleasant symptom was induced. M.
Tourtelle has even related an instance where two ounces were retained
altogether and caused only moderate griping, with considerable purging
and flow of urine.[452] Resting on such facts as these Tourtelle, with
some physicians in more recent times,[453] has maintained that nitre is
not a worse poison than other saline laxatives; and some practitioners
of the present day have consequently ventured to administer it for the
cure of diseases, in the quantity of half an ounce in one dose.[454] It
is not easy to say, why these large doses are at times borne by the
stomach without injury,—whether the cause is idiosyncrasy, or a
constitutional insensibility engendered by disease, or some difference
in the mode of administering the salt. But at all events, the facts
which follow will leave no doubt that in general it is a dangerous and
rapid poison in the dose of an ounce.

Dr. Alexander found that, in the quantity of a drachm or a drachm and a
half, recently dissolved in four ounces of water, and repeated every
ninety minutes, the third or fourth dose caused chilliness and stinging
pains in the stomach and over the whole body; and these sensations
became so severe with the fourth dose, that he considered it unsafe to
attempt a fifth.[455]

Two cases which were actually fatal have been described in the Journal
de Médecine for 1787, the one caused by one ounce, the other by an ounce
and a half. In the latter the symptoms were those of the most violent
cholera, and the patient died in two days and a half;[456] in the former
death took place in three hours only, and in addition to the symptoms
remarked in the other there were convulsions and twisting of the
mouth.[457] In both the pulse failed at the wrist, and a great tendency
to fainting prevailed for some time before death. Dr. Geoghegan has
communicated to Mr. Taylor a case where an ounce and a half taken by
mistake caused severe pain in the stomach, vomiting, and death in two
hours.[458]

Similar effects have been remarked in several cases which have been
followed by recovery. A woman in the second month of pregnancy,
immediately after taking a handful of nitre in solution, was attacked
with pain in the stomach, swelling of the whole body and general pains;
she then miscarried, and afterwards had the usual symptoms of gastritis
and dysentery, united with great giddiness, ringing in the ears, general
tremors and excessive chilliness. She seems to have made a narrow
escape, as for three days the discharges by stool were profuse, and
composed chiefly of blood and membranous flakes.[459] Dr. Falconer has
related another instance, where also the patient’s life seems to have
been in great danger. The quantity taken was two ounces, and it was
swallowed in half a pint of warm water by mistake instead of a laxative
salt. Violent pain in the belly was immediately produced, in half an
hour frequent vomiting, and in three hours a discharge of about a quart
of blood from the stomach. After the administration of gruel and butter
the symptoms began to subside; but they receded slowly; and even six
months afterwards the man, though otherwise in good health, had frequent
pain in the stomach and flatulence.[460] In the case of a female in the
second month of pregnancy, described by Dr. Butter, miscarriage did not
take place, although the symptoms were very violent and lasting. The
quantity taken was two ounces. The symptoms were first bloody vomiting,
afterwards dysentery, which continued seven days; and on the tenth day a
nervous affection supervened exactly like chorea, and of two months’
duration.[461] The effects of the poison in the latter period of this
woman’s illness tend to establish the existence of a secondary operation
on the nervous system. But this kind of action is more strongly pointed
out by the following cases. Three puerperal women in the Obstetric
Hospital of Pavia got each an ounce of nitre by mistake for sulphate of
magnesia. Two, who vomited immediately, did not suffer. The third, who
retained the salt fifteen minutes, had pain in the stomach and vomiting,
followed by paleness of the countenance, stiffness of the jaw, some
stupor, and convulsive movements of the limbs; which symptoms continued
till next day, when she gradually recovered.[462] A German physician,
Dr. Geiseler, met with an instance, in which the only disorder produced
appeared to depend on derangement of the cerebral functions. A woman,
after swallowing an ounce of nitre instead of Glauber’s salt, lost the
use of speech and the power of voluntary motion, then became insensible,
and was attacked with tetanic spasms. This state lasted till next day,
when some amelioration was brought about by copious sweating. It was
not, however, till eight days after, that she recovered her speech, or
the entire use of her mental faculties; and the palsy of the limbs
continued two months.[463] Her case resembles the account given by
Orfila of the effects of nitre on animals.


 SECTION III.—_Of the Morbid Appearances caused by Nitrate of Potass._

The morbid appearances observed in man are solely those of violent
inflammation of the stomach and intestines. In Laflize’s case, which
proved fatal in three hours, the stomach was distended, and the contents
deeply tinged with blood; its peritonæal coat of a dark-red colour
mottled with black spots; its villous coat very much inflamed and
detached in several places. The liquid contents gave satisfactory
evidence of nitre having been swallowed; for a portion evaporated to
dryness deflagrated with burning charcoal. In Souville’s patient, who
lived sixty hours, the stomach was every where red, in many places
checkered with black spots, and at the centre of one of these spots the
stomach was perforated by a small aperture. The whole intestinal canal
was also red. In Dr. Geoghegan’s case, the stomach contained bloody
mucus, and its villous coat was brownish-red, and here and there
detached. He could not detect any nitre in it.




                              CHAPTER IX.
          OF POISONING WITH THE ALKALINE AND EARTHY CHLORIDES.


There can be little doubt that the _chlorides_ of _soda_, _potass_, and
_lime_ are active poisons; but the first two have alone been hitherto
carefully investigated by physiological experiments.

The two alkaline chlorides are usually seen in the form of colourless
solutions. That of potass is little known in this country; but that of
soda is familiar to all in the shape of Fincham’s chloride of soda or
bleaching liquid. The chloride of lime, which is best known of them all,
is usually in the form of a dry powder, deliquescent, and acrid,
commonly termed bleaching powder. All these substances are easily known
by their peculiar odour of chlorine, and the copious disengagement of
that gas on the addition of sulphuric acid.

The action of chloride of soda on the animal body has been examined by
Segalas, who infers that it is an irritant poison, which, however, at
times occasions symptoms of an affection of the nervous system. He
remarked that three ounces of the solution, commonly sold in Paris under
the name of Labarraque’s disinfecting liquid, caused immediate death by
coagulating the blood in the heart, when injected into a vein in a dog.
Two ounces introduced into the peritonæum excited palpitation, oppressed
breathing, constant restlessness, and death in ten minutes; and three
drachms did not prove fatal for some hours, tetanic spasms being
produced in the first instance, and peritonæal inflammation being found
after death. One ounce introduced into the stomach of a dog excited
immediate vomiting, and no farther inconvenience; and two ounces
retained by a ligature on the gullet brought on violent efforts to
vomit, from which the animal was gradually recovering, when it was
killed in twenty-four hours for the sake of observing the appearances.
The stomach was found generally inflamed and interspersed with dark,
gangrenous-like spots.[464]

I am not acquainted with any case of poisoning with these substances in
the human subject. But it is probable that symptoms of pure irritation
and inflammation will occur, and that moderate doses may prove fatal.




                               CHAPTER X.
                        OF POISONING WITH LIME.


Lime, the last poison of the present group, is a substance of little
interest to the toxicologist, as its activity is not great.

Its physical and chemical properties need not be minutely described. It
is soluble, though sparingly, in water; and the solution turns the
vegetable blues green, restores the purple of reddened litmus, gives a
white precipitate with a stream of carbonic acid gas, and with oxalic
acid a very insoluble precipitate, which is not redissolved by an excess
of the test.

Its action is purely irritant. Orfila has found that a drachm and a half
of unslaked lime, given to a little dog, caused vomiting and slight
suffering for a day only, but that three drachms killed the same animal
in five days, vomiting, languor, and whining being the only symptoms,
and redness of the throat, gullet, and stomach, the only morbid
appearances.[465]

Though a feeble poison, it has nevertheless proved fatal in the human
subject. Gmelin takes notice of the case of a boy who swallowed some
lime in an apple-pie, and died in nine days, affected with thirst,
burning in the mouth, burning pain in the belly, and obstinate
constipation.[466] A short account of a case of this kind of poisoning
is also given by Balthazar Timæus. A young woman, afflicted with pica or
depraved appetite, took to the eating of quicklime; and in consequence
she was attacked with pain and gnawing in the belly, sore throat,
dryness of the mouth, insatiable thirst, difficult breathing and cough;
but she recovered.[467] It is well known that quicklime also inflames
the skin or even destroys its texture, apparently by withdrawing the
water which forms a component part of all soft animal tissues. When
thrown into the eyes it causes acute and obstinate ophthalmia, which may
end in loss of sight. On this account it will belong, I presume, to the
poisons included in the Scottish act against disfiguring or maiming with
corrosives.




                              CHAPTER XI.
                OF POISONING WITH AMMONIA AND ITS SALTS.


The second group of the order of alkaline poisons, including ammonia
with its salts, and the sulphuret of potass, have a double action on the
system, analogous to that possessed by many metallic poisons. They are
powerful irritants; but they produce besides, through the medium of the
blood, a disorder of some part of the nervous system; and their remote
is sometimes more dangerous than their local action. The nervous
affection produced by ammonia and the sulphuret of potass closely
resembles tetanus, and therefore depends probably on irritation of the
spinal column.

_Of the Chemical tests for the Ammoniacal Salts._—Ammonia is when pure a
gaseous body; but as commonly seen, it exists in solution in water,
which dissolves it in large quantity. The solution has the usual effects
of alkalis on vegetable colours, with the difference, however,—that the
changes of colour are not permanent under the action of heat. It forms a
yellow precipitate, as potass does, with chloride of platinum. It may at
once be distinguished from other fluids by its peculiar pungent odour,
which is possessed by no other substance except its carbonate.

Various _carbonates_ are known in chemistry, but the only one known in
commerce or met with in the shops is the sesqui-carbonate
(subcarbonate—smelling salt—volatile salt—hartshorn). It is solid,
white, fibrous, and has the same odour as pure ammonia. Its solution
differs little in physical properties from the pure liquid ammonia; but,
unlike it, is precipitated by the salts of lime.

The _hydrochlorate_ (muriate of ammonia—sal-ammoniac)—is known by its
solid, white, crystalline appearance; its ductility; its volatility; and
by the effect of caustic potass and nitrate of silver, the former of
which disengages an ammoniacal odour, while the latter causes in a
solution of the salt a white precipitate, the chloride of silver.

_Of the action of the Ammoniacal Salts, and their effects on man._—To
determine the action of ammonia on the animal system, Professor Orfila
injected sixty grains of the pure solution into the jugular vein of a
dog. Immediately the whole legs were spasmodically extended; at times
convulsions occurred; and in ten minutes it died. The chest being laid
open instantly, coagulated florid blood was seen in the left ventricle,
and black fluid blood in the right ventricle of the heart. No unusual
appearance was discernible any where else except complete exhaustion of
muscular irritability.[468] The experiments of Mr. Blake also show that
ammonia introduced in large doses into the veins acts by suddenly
extinguishing the irritability of the heart. Small doses first lower
arterial pressure from debility of the heart’s action, and then increase
it by obstructing the systemic capillaries. When injected into the aorta
from the axillary artery, it causes great increase of arterial pressure,
owing to the latter cause; and then arrests the heart, while the
respiration goes on. Four seconds are sufficient for the ammonia to pass
from the jugular vein into the heart, so as to be discovered there by
muriatic acid causing white fumes.[469] Half a drachm of a strong
solution, introduced by Orfila into the stomach of a dog and secured by
a ligature on the gullet, caused at first much agitation. But in five
minutes the animal became still and soporose; after five hours it
continued able to walk; in twenty hours it was found quite comatose; and
death ensued in four hours more. The only morbid appearance was slight
mottled redness of the villous coat of the stomach. A third dog, to
which two drachms and a half of the common carbonate were given in fine
powder, died in twelve minutes. First it vomited; next it became
slightly convulsed; and the convulsions gradually increased in strength
and frequency till the whole body was agitated by dreadful spasms; then
the limbs became rigid, the body and head were bent backwards, and in
this state it expired, apparently suffocated in a fit of tetanus.[470]

Several cases of poisoning with ammonia or its carbonate have occurred
in the human subject. Plenck has noticed shortly a case which proved
fatal in four minutes, and which was caused by a little bottleful of
ammonia having been poured into the mouth of a man who had been bitten
by a mad-dog.[471] The symptoms are not mentioned, but it is probable,
from the rapidity of the poisoning, that a nervous affection must have
been induced. More generally, however, the effects are simply irritant;
and the seat of the irritation will vary with the mode in which the
poison is given. If it is swallowed, the stomach and intestines will
suffer; if it is imprudently inhaled in too great quantity, inflammation
of the lining membrane of the nostrils and air-passages will ensue.
Huxham has related a very interesting example of the former affection,
as it occurred in a young man, who had acquired a strange habit of
chewing the solid carbonate of the shops. He was seized with great
hemorrhage from the nose, gums, and intestines; his teeth dropt out;
wasting and hectic fever ensued; and, although he was at length
prevailed on to abandon his pernicious habit, he died of extreme
exhaustion, after lingering several months.[472] But the most frequent
cases of poisoning with ammonia have arisen from its being inhaled, and
thus exciting bronchial inflammation. An instructive instance of the
kind has been related by M. Nysten. A medical man, liable to epilepsy,
was found in a fit by his servant, who ignorantly tried to rouse him by
holding assiduously to his nostrils a handkerchief dipped in ammonia. In
this way about two drachms appear to have been consumed. On recovering
his senses, the gentleman complained of burning pain from the mouth
downwards to the stomach, great difficulty in swallowing, difficult
breathing, hard cough, and copious expectoration, profuse mucous
discharge from the nostrils, and excoriation of the tongue. The
bronchitis increased steadily, and carried him off in the course of the
third day, without convulsions or any mental disorder having
supervened.[473] A case precisely similar is related in the Edinburgh
Medical and Surgical Journal. A lad, while convalescent from an attack
of fever, was seized with epilepsy, for which his attendant applied
ammonia under his nose “with such unwearied, but destructive
benevolence, that suffocation had almost resulted. As it was, dyspnœa
with severe pain of the throat and breast, immediately succeeded; and
death took place forty-eight hours afterwards.”[474] A third instance
has been recorded of analogous effects produced by the incautious use of
ammonia as an antidote for prussic acid. The patient had all the
symptoms of a violent bronchitis, accompanied with redness and scattered
ulceration of the mouth and throat; but he recovered in thirteen
days.[475] A fourth case, similar to the preceding, has been related by
M. Souchard of Batignolles. A druggist, who inhaled while asleep the
fumes of ammonia from a broken carboy, awoke in three-quarters of an
hour, with the mucous membrane of the mouth and nostrils corroded, and a
bloody discharge from the nose. A severe attack of bronchitis followed,
during which he could not speak for six days; but being actively treated
with antiphlogistic remedies, he recovered.[476]—An extraordinary case
has been published by Mr. Paget of death from injecting ammonia into the
blood-vessels. A solution weak enough to allow of the nose being held
over it was injected into a nævis in a child two years old. An attack of
convulsions immediately followed, and in a minute the child
expired.[477]

Nysten’s case is the only one in the human subject in which the _morbid
appearances_ were ascertained. The nostrils were blocked up with an
albuminous membrane. The whole mucous coat of the larynx, trachea,
bronchi, and even of some of the bronchial ramifications, was mottled
with patches of lymph. The gullet and stomach showed red streaks here
and there; and there was a black eschar on the tongue, and another on
the lower lip.

_Of Poisoning with Hydrochlorate of Ammonia._—The effects of the
hydrochlorate of ammonia on animals have been examined by Professor
Orfila and Dr. Arnold; but I have not yet met with any instance of its
operation as a poison on man. When given to dogs it irritates and
inflames the parts it touches, and causes the ordinary symptoms of local
irritation. But it also acts remotely. For, first, like arsenic, and
other poisons of the third order of irritants, it produces inflammation
of the stomach, in whatever way it is applied to the body,—Orfila having
found that organ affected when the salt was applied to the subcutaneous
cellular tissue;[478] and, secondly, according to the experiments of
Arnold, it causes, when swallowed, excessive muscular weakness, slow
breathing, violent action of the heart, and tetanic spasms,—effects
which cannot arise from mere injury of the stomach. Half a drachm will
thus kill a rabbit in eight or ten minutes;[479] and two drachms a small
dog in an hour.[480]




                              CHAPTER XII.
               OF POISONING WITH THE ALKALINE SULPHURETS.


The liver of sulphur, or sulphuret of potass of the pharmacopœias, the
last poison of this order to be mentioned, is allied to the ammoniacal
salts in action. It is of no great consequence in a toxicological point
of view in this country, being put to little use; but several accidents
have been caused by it in France, where it is employed for manufacturing
artificial sulphureous waters; and farther, its properties should be
accurately ascertained, because till lately it was erroneously resorted
to as an antidote for some metallic poisons.

_Chemical Tests._—It has a grayish, greenish, or yellowish colour when
solid; its dust smells of sulphuretted hydrogen, which is also
copiously disengaged from it by the mineral acids: and it forms with
water a yellow solution of the same odour.—In composite fluids it may
be detected by heating it with acetic acid, and passing the disengaged
gases through solution of acetate of lead, in which a black
precipitate of sulphuret of lead is produced, from the action of
sulphuretted-hydrogen.[481]

_Action and Symptoms._—Orfila found that a solution of six drachms and a
half, secured in the stomach of a dog by a ligature on the gullet,
caused death by tetanus in seven minutes, without leaving any morbid
appearance in the body; that inferior doses caused death in the same
manner, but at a later period, and with symptoms of irritation in the
alimentary canal, which also was seen red, black, or even ulcerated
after death; that a solution of twenty-two grains injected into the
jugular vein killed a dog in two minutes, convulsions having preceded
death, and the heart being found paralysed immediately after it; and
that a drachm and a half thrust in small fragments under the skin
occasioned death in thirteen hours with coma and extensive inflammation
of the cellular tissue.[482] There can be no doubt, therefore, that
liver of sulphur is a true narcotic acrid poison.—It is absorbed, and
may be detected in the blood, liver, kidneys, and urine by Orfila’s
process.[483]

Orfila has collected three cases of poisoning in the human subject with
this substance;[484] and a fourth has been related by M. Cayol.[485] Of
these cases two proved fatal in less than fifteen minutes; and the
symptoms were acrid taste, slight vomiting, mortal faintness, and
convulsions, with an important chemical sign, the tainting of the air
with the odour of sulphuretted-hydrogen. The dose in one case was about
three drachms. The two other patients, who recovered, were for some days
dangerously ill. The symptoms were burning pain and constriction in the
throat, gullet, and stomach; frequent vomiting, at first sulphureous,
afterwards sanguinolent; purging, at first sulphureous; sulphureous
exhalations from the mouth; pulse at first quick and strong, afterwards
feeble, fluttering, and almost imperceptible; in one case sopor; finally
severe inflammation of the gullet, stomach and intestines, which abated
in three days. One of these patients took four drachms of sulphuret of
soda, the other two ounces of sulphuret of potass; but it is probable,
that the latter dose was partly decomposed by long keeping.

_Morbid Appearances._—The morbid appearances in the two fatal cases were
great lividity of the face and extremities, and exhaustion of muscular
contractility immediately after death; the stomach was red internally,
and lined with sulphur; the duodenum also red; the lungs soft, gorged
with black fluid blood, and not crepitant.

_Treatment._—The most appropriate treatment consists in the instant
administration of any diluent, then of frequent doses of the chloride of
soda, and lastly the antiphlogistic mode of subduing inflammation. The
chloride of soda or lime decomposes sulphuretted hydrogen, the
disengagement of which is the probable cause of death in the quickly
fatal cases.[486]




                             CHAPTER XIII.
                       OF POISONING WITH ARSENIC.


The third order of the irritant class of poisons includes the compounds
of the metals. These are of great importance to the medical jurist. They
are frequently used for criminal purposes; they give rise to the
greatest variety of symptoms; and the medical evidence on trials
respecting them, while much skill is required on the part of the witness
to collect it, is also the most conclusive.

It must not be inferred from their being arranged in the class of
irritants that their action is merely local. In fact this is the case
with a very few of them only, which produce chemical corrosion. The
greater number likewise act indirectly on organs at a distance from the
part to which they are applied. Nevertheless the most prominent symptoms
generally produced by them are those of violent local irritation; so
that they may be justly considered in the place which has been assigned
them.

The poisons included in this order are the oxides and salts of arsenic,
mercury, copper, antimony, tin, silver, gold, bismuth, iron, chrome,
zinc, barium, lead. Many other metals also form poisonous compounds with
various acids and other bodies; but these are so rare as to be merely
objects of physiological curiosity.

Of all the varieties of death by poison, none is so important to the
medical jurist as poisoning with arsenic. On account of the shameful
facility with which it may be procured in this country, even by the
lowest of the vulgar, and the ease with which it may be secretly
administered, it is the poison most frequently chosen for the purpose of
committing both suicide and murder. In 1837 and 1838 no fewer than 186
cases of fatal poisoning with arsenic were known to have occurred in
England alone (see p. 90). Of 221 cases of murder by poison in France
during ten years subsequent to 1829, in which the poison given was
ascertained, there were 149 where the substance administered was
arsenic.[487] It is fortunate, therefore, that there are few substances
in nature, and perhaps hardly any other poison, whose presence can be
detected in such minute quantities and with so great certainty.


    SECTION I.—_Of the Chemical Tests for the Compounds of Arsenic._

Metallic arsenic has an iron-gray colour, a specific gravity of 8·308,
and a crystalline fracture. It is very brittle. It has a strong tendency
to oxidate, so that it undergoes this change in air, in water, and even
in alcohol. In air, particularly when moist, it becomes rapidly
tarnished, a black powder being formed, which some have regarded as a
regular protoxide.[488]—When exposed to heat, metallic arsenic is
usually said to sublime at the temperature of 356° F.; but according to
some late experiments by Dr. Mitchell of Philadelphia this does not
happen under a low red heat, luminous in the dark.[489] In close vessels
it condenses unchanged; but when heated in the open air, it passes to
the state of white oxide, and rises in white fumes. This substance is a
sesquioxide, consisting of two equivalents of metal and three of oxygen.
Another oxide likewise exists, which contains two equivalents of metal
and five of oxygen, and, possessing strong acid properties, is
denominated arsenic acid. The sesquioxide and arsenic acid unite with
bases, and produce compounds which, with the exception of those they
form with the alkalis, are mostly insoluble. Metallic arsenic unites
with sulphur in two proportions, forming an orange-red and a
sulphur-yellow compound. The compounds of arsenic have very little
chemical action with vegetable and animal principles.

Of the compounds which arsenic thus forms, those which it will be
necessary to particularize are the following:—1. The protoxide of
Berzelius, or _fly-powder_. 2. The arsenious acid, or _white arsenic_.
3. The arsenite of copper, or _mineral green_. 4. The arsenite of potass
as contained in _Fowler’s solution_. 5. The arsenite of potass; 6. The
various sulphurets, pure and impure, namely, _realgar_, _orpiment_, and
_king’s yellow_; and 7. Arseniuretted-hydrogen gas.


                     _Of the Tests for Fly-powder._

This substance is rarely known as a poison in Britain, but is a familiar
poison in France and Germany, under the names of _Poudre à mouches_, and
_Fliegenstein_. Of late it has been occasionally used in Scotland for
poisoning rats.

It is a fine grayish-black powder, formed by exposing powdered arsenic
for a long time to the air; but it also frequently contains fragments of
the metal. It is usually considered by chemists to be a mixture of
metallic arsenic and its white oxide.

It is acted on by water, the white oxide being found ere long in
solution by its proper tests. Oxidation and solution, however, are also
effected upon pure metallic arsenic in the same manner. A thousand
grains of water take up a grain in the course of half an hour when
boiled on the metal.[490]

A very simple and decisive test for fly-powder is derived from the
effect of heat. If it is heated in a tube two substances are sublimed,
first a white crystalline powder, and then a bright metallic crust, the
former being the white oxide, the latter the metal. The metallic crust
thus formed possesses physical properties, which distinguish arsenic
from all other substances, capable of being sublimed by a low heat: The
surface next the tube is very like polished steel, being a little darker
in colour, but equal in brilliancy and polish; and the inner surface is
either brilliantly crystalline to the naked eye, like the fracture of
cast-iron, or has a dull grayish-white colour, but appears crystalline
before a common magnifying lens of four or five powers. If these
characters be attended to, particularly the appearance of the inner
surface, it appears to me scarcely possible to mistake for an arsenical
crust any other substance which can be sublimed by any of the methods
for subliming arsenic.

If a farther test should be desired, it is only necessary, as was first
proposed by Dr. Turner of London,[491] to chase the crust up and down
the tube with the spirit-lamp flame till it is all oxidated, when little
octaedral crystals of adamantine lustre are formed, on which, either
with the naked eye or with the aid of a common lens, triangular facettes
may be distinguished.

The niceties to be attended to in applying the preceding tests will be
considered presently under the head of the next compound, the
sesquioxide.


                 2. _Of the Tests for Arsenious Acid._

Arsenious acid, the sesquioxide, or white oxide of arsenic, usually
called white arsenic, or simply arsenic, is the most common and
important of all the arsenical preparations.

It is met with in the shops in two forms,—as a snow-white gritty powder,
and in solid masses generally opaque, but sometimes translucent. When
newly sublimed it is in translucent or even almost transparent masses of
a vitreous lustre, conchoidal fracture and sharp-edged. By keeping it
becomes opaque and white. The nature of the change has not been
determined; but some alteration is certainly effected, for Guibourt, who
has examined both varieties with care, found that the opaque variety is
more soluble in water than the other. He adds that the former is
alkaline, the latter acid, in its action on litmus paper; but I have
always found the opaque variety acid.[492] The powder soon becomes
analogous to the opaque variety of the oxide in mass.

The oxide of arsenic has a specific gravity of 3·729, according to the
experiments of Dr. Ure,—of 3·529 when opaque, according to Mr. Alfred
Taylor, and 3·798, when translucent. Very incorrect notions prevail as
to its taste. It was long universally believed to be acrid,[493] and is
described to be so in many systematic works and express treatises; but
in reality it has little or no taste at all. The reader will find some
details on this point in a paper I published in the Edinburgh Medical
and Surgical Journal.[494] In the present work it is sufficient to
observe, that I have repeatedly made the trial, and seen it made at my
request by several scientific friends, and that, after continuing the
experiment as long, and extending the poison along the tongue as far
back, as we thought safe, all agreed that it had scarcely any taste at
all,—perhaps towards the close a very faint sweetish taste. It appears
to me that the experiments made on that occasion might have set at rest
the question as to the taste of arsenic, and corrected an important
error long committed by systematic authors in chemistry as well as
medical jurisprudence. And accordingly in this country the truth is
generally known.[495] Professor Orfila, however, continues to repeat the
error; for even in the last edition of his Toxicologie he says it has “a
rough, not corrosive, slightly styptic taste, perceptible not for a few
seconds, but persistent, and attended with salivation.”[496] These
sensations must be either imaginary or the indications of an organ
peculiarly constituted. It is impossible to make satisfactory
experiments with safety on its impressions on the back of the palate.
But we may rest assured that in general it makes no impression there at
all; for it has been often swallowed unknowingly with articles of food.
Not a few have in such circumstances noticed merely its grittiness, and
thought there was sand in their food. Two instances only am I hitherto
acquainted with, where an acrid sensation would seem really to have been
experienced in the act of eating or swallowing. In one of these, noticed
in Rust’s Journal, the individual who was poisoned, could not finish the
poisoned dish on account of its unpleasant, very peppery taste.[497] In
the other case, which was lately communicated to me by Mr. Hewson of
Lincoln, the individual, who was poisoned by arsenic dissolved in his
tea-kettle,—happening in the first instance to wash his mouth with the
water,—observed at the time to his daughter, that it had a very odd
taste; which subsequently was called a burning taste. These facts,
however, are evidently not altogether satisfactory. It is not improbable
that, in an _ex post facto_ description, the reporters, as others in the
same circumstances have clearly done[498], confounded the subsequent
inflammation with mere taste in the act of chewing or swallowing. At all
events it is absolutely certain that the great majority of people who
have been poisoned with arsenic remarked in taking it either no taste at
all, or merely a roughness owing to the gritty condition of its powder.

The oxide of arsenic when subjected to heat is sublimed at 380°, or,
according to Dr. Mitchell, 425° F.[499] and condenses in the form of a
crystalline powder, which, if the operation is performed slowly and on a
small quantity proportioned to the size of the tube, evidently consists
of little, adamantine octaedres.—When it is mixed with carbonaceous
matter and heated, it is reduced, and the metal is sublimed. This
constitutes the test of reduction, which, when conducted with due care,
may be rendered singly a certain proof of the presence of arsenic.

Water dissolves it. Its solubility is a point of some medico-legal
importance; for a doubt may arise whether the quantity of a solution
that has been swallowed contained a sufficient dose to cause severe
symptoms or death. Different statements have gone forth on this head.
Klaproth found, that a thousand parts of temperate water take up only
two parts and a half,—and that a thousand parts of boiling water take up
77·75 parts or a thirteenth, and retain on cooling 30 parts or a
thirty-third of their weight.[500] Guibourt found a difference between
the transparent and opaque varieties; for a thousand parts of temperate
water dissolved in thirty-six hours 9·6 of the transparent, 12·5 of the
opaque variety; and the same quantity of boiling water dissolved of the
transparent variety 97 parts, retaining 18 when cooled, but of the
opaque variety took up 115 and retained on cooling 29.[501] More lately
Mr. Alfred Taylor observed that temperate water, simply poured on the
opaque oxide and left for seventy-two hours, contained one grain in a
thousand, but if often agitated, 8·5 grains; that boiling water,
occasionally agitated for the same period, contained 9·27 or 9·54
grains; that water, boiling gently for an hour dissolved 31·5, and on
cooling and resting for three days retained 17; that with violent
ebullition for an hour, it took up 46·3, and retained 24·7 grains on
cooling and resting for three days; that a saturated boiling solution
after six months contained 24 or 26 grains; and that a saturated boiling
solution of the transparent oxide contained 46 or 47·5 grains, and on
cooling and resting for two days retained 18·7 or 13·4 grains.[502] It
is impossible to account for these discrepancies; for all the
experimentalists conducted their investigations with care, and with a
view to the medico-legal question stated above. Hahnemann farther
remarked, that at the temperature of the blood a thousand parts of water
dissolve ten parts with the aid of ten minutes’ agitation;[503] and
Navier, that boiling water kept for an hour on it, and decanted off in
the way an infusion is usually made, dissolves 12·5 grains in every
thousand.[504]

Its solubility is impaired by the presence of organic principles. When
mixed with mucus or milk it dissolves, according to Hahnemann, with
great difficulty; and I have found that a cup of tea, left beside the
fire at a temperature of 200° for half an hour upon two grains of the
oxide, does not take up entirely even that small quantity. An important
consequence of the fact now mentioned is, that when swallowed in the
solid state, little or no arsenic may be found in the fluid contents of
the stomach. In a case which occurred to Scheele three grains of solid
arsenic were found in the contents, but hardly a trace in solution.[505]
It would be wrong, however, to suppose that it is never found in the
fluid contents. For, not to mention the observations of others, I have
myself often detected it in the fluid part of the stomach in persons
poisoned by arsenic.

The solution of oxide of arsenic in boiling water yields minute crystals
on cooling, which, when their form is defined, are octaedres. In this
state, on account of its whiteness and brilliancy, it exceedingly
resembles pounded sugar. By spontaneous evaporation I have procured in
twelve months fine octaedres nearly as large as peas. These do not
become opaque by keeping, like the sublimed masses.

A difference of opinion prevails as to the action of the oxide on
vegetable colours. This is a matter of no great consequence to the
medical jurist; but it is right not to leave a disputed point without
some notice. Guibourt says the transparent variety faintly reddens
litmus, while the opaque variety faintly restores to blue litmus
previously reddened.[506] My own experiments are at variance with these
statements: I have always found that the solution of the powder, which
is of the opaque variety, faintly reddens litmus, and does not alter
reddened litmus.

The remaining chemical properties of the oxide, which it is necessary
for the medical jurist to know, will be mentioned under what is now to
be said of the principal test by which its presence may be ascertained.
Under this head will be noticed, first the tests for the solid oxide,
secondly, those for its solution, and lastly, the method of detecting it
when mingled with vegetable or animal solids and fluids, such as the
contents and tissues of the stomach.


             _Of the Tests for Arsenic in the solid state._

The most characteristic and simple test for oxide of arsenic in its
solid state, either pure or mixed or combined with inorganic substances,
is its reduction to the metallic state.

Various methods have been at different times proposed for employing the
test of reduction. In the ruder periods of analytic chemistry we find
Hahnemann recommending a retort as the fittest instrument, and stating
ten grains as the least quantity he could detect.[507] Afterwards Dr.
Black substituted a small glass tube, coated with clay and heated in a
choffer; and in this way he could discover a single grain.[508] In a
paper published in the Edinburgh Medical and Surgical Journal, I showed
how to detect a sixteenth of a grain; and afterwards even so minute a
quantity as a hundreth part of a grain.[509]

The process is performed in a glass tube; which, when the quantity of
the oxide is very small, should not exceed an eighth of an inch in
diameter, and may be conveniently used of the form first recommended by
Berzelius, and represented in Fig. 3.—The best material for reducing the
oxide is recently ignited charcoal, if the quantity of suspected
substance be very small. For when any of the ordinary alkaline fluxes is
used, more than half of the arsenic is retained, probably in the form of
an arseniuret of the alkaline metalloid. But when the quantity of matter
for analysis is considerable, charcoal is inconvenient, as it is apt to
be projected up the tube on the application of heat; and an alkaline
flux is on that account preferable. For this purpose soda-flux,—made by
grinding crystals of carbonate of soda with an eighth of their weight of
charcoal, and then heating the mixture gradually to redness, so as to
drive off all water,—is better than the more familiar black flux, which
contains carbonate of potash; because the latter attracts much moisture
when kept for some time.—If the quantity operated on is large it should
be mixed with the flux before being introduced into the tube; if it is
small, it may be dropped into the tube and covered with charcoal. The
materials are to be introduced along a little triangular gutter of stiff
paper, if the tube is large; but with a small tube it is preferable to
use the little glass funnel represented in Fig. 2, to which a wire is
previously fitted, for pushing the matter down when it adheres. The
material should not be closely impacted. Heat is best applied with the
spirit-lamp, first to the upper part of the material, with a small
flame, and then to the bottom of the tube, the flame being previously
enlarged. A little water, disengaged in the first instance, should be
removed with a roll of filtering paper, before a sufficient heat is
applied to sublime the metal. As soon as the dark crust begins to form,
the tube should be held steady in the same part of the flame. With these
precautions a well defined crust will be procured with facility.

The characters of the crust have been mentioned already under the head
of fly-powder (p. 199). They are distinct even in crusts weighing only a
300th of a grain. A crust of this weight, a tenth of an inch broad and
four times as long, may show characteristically all the physical
characters of an arsenical sublimate a hundred times larger.

The fallacies to which the test has been supposed to be liable
(excluding at present that part of it which consists in the oxidation of
the metal, and which renders it quite unimpeachable), are the
following.— Dr. Paris says he has known an instance where a person, “by
no means deficient in chemical address, mistook for it a deposit of
charcoal,”[510] and I have known the same mistake happen in the hands of
one of my pupils, a beginner in the study of medico-legal chemistry. The
outer surface of a charcoal crust may be mistaken for arsenic by a
careless person; but with ordinary care it is quite impossible to err if
the inner surface be examined, for that of charcoal is brown, powdery,
and perfectly dull.—It has been suggested to me and has been stated in
print,[511] that the preparations of antimony yield by reduction a
sublimate resembling closely an arsenical crust. But in consequence of
repeated trials I am certain that no preparation of antimony, reduced
either by charcoal or the black flux with the fullest red heat of the
blowpipe will yield any metallic sublimate; and the same facts were
observed by the late Dr. Turner.—It has even been said by Mr. Donovan
that the action of the flux on glass which contains lead causes a stain
similar to an arsenical crust.[512] If it be meant by this observation,
that the lead contained in the glass usually gives that part of the tube
which contains the flux a glimmering appearance and impairs its
transparency, the author is correct: but it is impossible that a
sublimate can be so formed.—Dr. Mitchell of Philadelphia in an elaborate
paper on the process of reduction seems to consider the crust
undistinguishable from that formed in similar circumstances by
cinnabar.[513] Crusts of cinnabar, however, do not present the peculiar
character possessed by the internal surface of arsenic.—Zinc, it is
said, may be sublimed in its metallic state; but the sublimation of zinc
requires a full white heat; which in the process for arsenic cannot be
generated.—Tellurium, cadmium, and potassium sublime at a lower heat;
but these metals are so exceedingly rare, that it is quite unnecessary
to particularize the characters of their sublimates.—Lastly, it is said
that a crust may be produced from arsenic contained in the glass of the
tube. A few years ago MM. Ozanam and Idt of Lyons detected arsenic in
the remains of a body which had been seven years interred; but
subsequently M. Idt imagined he had discovered that the glass used in
the analysis contained arsenic, and yielded it by the process of
reduction. He accordingly retracted his original opinion; and the person
accused of administering the poison was acquitted. An extended inquiry,
however, was in consequence undertaken by the Parisian Academy of
Medicine at the request of the French government. And the result was
that no arsenic could be detected in the glass tubes used by MM. Ozanam
and Idt; and that although arsenic is sometimes used in glass-making,
and a trace of it may be retained in some opaque glasses or enamels, it
cannot be detected by any process of analysis in any of the clear glass
met with in commerce,[514] the whole arsenic being volatilized during
the manufacture of the glass.

It may therefore be safely laid down that the appearances exhibited by a
well-formed arsenical crust, even in the minute quantity of a 300th part
of a grain, are imitated by no substance in nature which can be sublimed
by the process for the reduction of arsenic.

But should farther evidence be required as to the nature of the crust,
this may be obtained by subjecting it to oxidation by heat.

The best method of doing so is to heat the ball containing the flux
deprived of arsenic, to attach a bit of glass tube to its end, and to
draw this gently off in the spirit-flame, taking care to prevent the
flux being driven forward on the crust. This being done, the whole
crust, or, if it is large, a portion of it, is to be chased up and down
the tube with a small spirit-lamp flame till it is all converted into a
white powder. In order to show the crystalline form of the powder
distinctly, let the flame be reduced to the volume of a pea by drawing
in the wick, and let the part of the tube containing the oxide be held
half an inch or an inch above it. By repeated trials sparkling crystals
will at length be formed, which are octaedres,—the crystalline form of
arsenious acid. The triangular facettes of the octaedres may be
sometimes seen with the naked eye, though the original crust was only a
fiftieth of a grain or even less; and they may be always seen with a
lens of four powers, the tube being held between the eye and a lighted
candle or a ray of sunshine, either of which is preferable to diffuse
daylight for making this observation.—For the success of the oxidation
test it is indispensable that the inside of the tube be not soiled with
an alkaline flux: because the alkali would unite with the oxide. It is
also requisite not to heat the tube suddenly to redness before the oxide
is sublimed; because then the oxide is apt to unite with the glass,
forming a white, opaque enamel. The physical characters of the sublimed
oxide are so delicate and precise, that they may be accurately
distinguished, even when those of the metallic crust are obscure, owing
to its minuteness. Sometimes too, the metal may be so scanty that it is
oxidated at once in the act of subliming, and never presents the
appearance of a metallic crust. Although the characters of the
crystalline oxide in either of these cases are very precise and
distinctive, it may be right to subject it to a farther test when the
metal is not previously exhibited with its characteristic properties.
For this purpose it is sufficient to cut away with a file the portion of
the tube which contains the sublimate, to boil it in another tube with a
few drops of distilled water till the sublimate disappear, and then to
test the solution with one of the fluid tests to be presently described,
the ammoniacal nitrate of silver.

After all that has been recently written as to the old and newer
processes for detecting arsenic, I must nevertheless avow my conviction,
that for solid arsenic no test is, for medico-legal purposes, at once so
satisfactory, convenient, and delicate as the test of reduction,
especially with the addition of the supplementary test of oxidation.
That other methods are still more delicate may be readily granted. But
where the suspected substance is in the solid form, what possible
occasion can there be for a method more delicate than one which will
detect a 300th part of a grain? A method ten times less so would meet
every case in actual practice.—A variety of supplementary tests have
been proposed. But they are all greatly inferior in facility, or
conclusiveness, or both, to the process of oxidation, and ought
therefore to be expelled from medico-legal practice,—not even excepting
the alliaceous odour of metallic arsenic in the act of subliming, a
character, the fallaciousness of which was long ago pointed out by
myself as well as others, and to which a preposterous importance has
been attached in some late inquiries. The reader will find in the last
edition of this work an attempt to estimate the value of various tests
supplementary to that of reduction. This disquisition is now omitted, as
it seems no longer necessary.


            _Of the Tests for Oxide of Arsenic in Solution._

Oxide of arsenic in a state of solution may be detected in one of four
ways; by what are called the liquid tests; by precipitating it with one
of these, and subliming metallic arsenic from the precipitate, which
method is usually termed the reduction process; by Marsh’s method, which
consists in disengaging it in the form of arseniuretted-hydrogen gas,
and decomposing the gas by combustion; or by the method of Reinsch, in
which metallic arsenic is deposited on the surface of copper, and then
separated by heat for farther examination.

_Process by Liquid Reagents._—The first method is by the employment of
several liquid tests, which cause in the solution peculiar precipitates.
Many such tests have been proposed; but the most characteristic and
precise are _hydrosulphuric acid_, _ammoniacal nitrate of silver_, and
_ammoniacal sulphate of copper_. The indications of each of the three
tests must concur, otherwise, in a medico-legal case, no one can be
entitled to speak with certainty to the existence of arsenic. But when
they do concur, the evidence is unimpeachable. When this method of
analysis is followed, corresponding experiments ought always to be made
with the water that is used for diluting or otherwise preparing the
subject of examination, or with distilled water, if the article be
already sufficiently aqueous. This precaution is necessary on account of
the risk of accidental impregnation of the water or other reagents with
arsenic.[515]

_Hydrosulphuric acid_ [sulphuretted-hydrogen] is obtained by decomposing
proto-sulphuret of iron with diluted sulphuric acid in such an apparatus
as is represented at Fig. 5. And the gas may be either applied directly
to the suspected fluid, or condensed in distilled water, and thus kept
in store for occasional use in the liquid shape. Before applying this
test, the suspected fluid must be acidulated with acetic or hydrochloric
acid; because an excess of alkali prevents the action. And if an acid be
indicated by litmus in the fluid, neutralization, or slight
supersaturation, with potash must be effected, before adding acetic or
hydrochloric acid; for if the acidity should happen to be owing to an
excess of sulphuric or nitric acid, the test is decomposed, and
yellowish-white sulphur deposited.—These precautions being taken,
hydrosulphuric acid occasions a sulphur-yellow or lemon-yellow
precipitate. If the arsenical solution, however, be very weak, a yellow
colour merely is struck, because the precipitate, which is
sesqui-sulphuret of arsenic, is dissolved by the excess of the test; but
it separates after ebullition, or a few hours’ exposure to the air.
Co-existing animal and vegetable principles sometimes enable the fluid
to retain a minute portion even after ebullition, so as to acquire a
yellow milkiness; but they do not in any case prevent the test from
producing the yellow colour. Acidulation with acetic or hydrochloric
acid favours its subsidence in all cases; and according to Mr. Boutigny,
alkaline sulphates, muriates and nitrates have the same effect.[516]
Hydrosulphuric acid is so delicate as to act on the oxide in a hundred
thousand parts of water. The proper colour of the precipitate is lemon
or sulphur-yellow; which, when vegetable or animal matter is present,
acquires a shade of white or brown.

It is not liable to any material fallacy. The salts of cadmium yield
with it precipitates nearly of the same colour: but they are exceedingly
rare; and the precipitate, unlike sulphuret of arsenic, is insoluble in
ammonia.—The salts formed by selenic acid, if decomposed by another
acid, also yield yellow precipitates; but these salts are extremely
rare.—The salts of peroxide of tin give a dirty grayish-yellow
precipitate; which however ammonia turns brown.—A lead solution
acidulated with hydrochloric acid gives at first a yellow precipitate;
but this becomes brownish-black when more gas is transmitted.[517] The
contents of the human intestines sometimes yield a yellowish precipitate
though no arsenic be present; and it is dissolved, like sulphuret of
arsenic, by ammonia.[518] The tartrate of antimony and potash
(tartar-emetic) does not form, as was once thought, any source of
fallacy, the antimonial precipitate having always a tint of orange-red;
besides it is not, like sulphuret of arsenic, soluble in carbonate of
ammonia.—Other fallacies exist, unless the test be used with the
precautions mentioned above. But these need not enumeration here.

_Ammoniacal nitrate of silver_ is prepared by precipitating the oxide of
silver by means of ammonia, from a solution of nitrate of silver or
lunar caustic in ten parts of water, and then redissolving the
precipitate nearly, but not entirely, by adding gradually an excess of
ammonia. When thus prepared, it causes, even in a very diluted solution
of the oxide of arsenic, a lively lemon-yellow precipitate of arsenite
of silver; which passes to dark brown under exposure to the light.—The
action of this test is prevented by nitric, acetic, citric, or tartaric
acid in excess, particularly by the first and last. It is also prevented
by an excess of ammonia; and in very diluted solutions by the nitrate of
ammonia. These facts will suggest the necessity of certain obvious
precautions. Its action is obscured by the co-existence of various
salts, which singly cause a white precipitate with nitrate of silver;
for the yellow colour is then much lessened in intensity. The only one
of these requiring special notice, because it occurs in very many of the
fluids which are likely to be subjected to the researches of the medical
jurist, is common sea-salt, the chloride of sodium. The best way of
getting rid of the difficulty is to use in the first instance, not the
ammoniacal nitrate, but the simple nitrate of silver, as long as any
white precipitate falls down, to add a slight excess of that test, and
then, after subsidence, to drop in ammonia. No arsenic is thrown down by
the first steps of this process; but if any be present, it is
subsequently thrown down in the form of the yellow arsenite of silver,
on the addition of ammonia. This simple mode of getting rid of chloride
of sodium was first proposed by Dr. Marcet.[519]—Ammoniacal nitrate of
silver is of no use as a test for a moderately diluted solution of the
oxide of arsenic, if vegetable or animal matter be present; either the
colour of the precipitate is essentially altered, or no precipitate is
formed at all.[520]

If the presence of arsenic is to be inferred only when the full
lemon-yellow colour of the precipitate is developed, this test is not
liable to any material fallacy. The presence of a phosphate, a serious
obstacle according to an old way of using the silver test, is not a
source of fallacy in the instance of the ammoniacal nitrate; for the
yellow phosphate of silver is so soluble in the ammonia of the test,
that it is not thrown down unless the phosphatic solution is very
strong.—The silver test, which is extremely delicate, was proposed by
Mr. Hume, a chemist of London; and in its improved state was suggested
by the late Dr. Marcet. Various foreign authors have fallen into the
error of supposing that nitrate of silver without an alkali precipitates
oxide of arsenic: without an alkali, pure nitrate of silver gives no
precipitate, or at most a bluish-white or yellowish-white haze when both
solutions are strong.

_Ammoniacal sulphate of copper_ is prepared by the same process with the
last test, sulphate of copper being substituted for nitrate of silver.
It is a test of very great delicacy. It causes in solutions of the oxide
of arsenic an apple-green or grass-green precipitate of the arsenite of
copper. The particular tint is altered apparently by trifling
circumstances; but after the precipitate has stood some hours it always
assumes a tint intermediate between apple-green and grass-green. The
operation of this test is prevented by hydrochloric, nitric, sulphuric,
acetic, citric, and tartaric acids in excess; and also by an excess of
ammonia. These difficulties are obviated by manifest precautions. It is
also prevented, according to Hünefeld, by muriate, nitrate, and sulphate
of ammonia;[521] and by almost all vegetable infusions and animal
fluids, when the oxide of arsenic is not abundant: these difficulties
cannot be obviated. Even when not prevented by such fluids, its
operation is often obscured, the precipitate not possessing its
characteristic colour.

Ammoniacal sulphate of copper is more open to fallacies than the silver
test. Of these the most important is that in some organic fluids it
strikes a green precipitate, like the arsenite of copper, though arsenic
be not present.[522] The solution of bichromate of potass is turned
green but not precipitated by it.

On reviewing all that has now been stated regarding the liquid tests for
arsenic, it will appear that there is no single test on which absolute
reliance can be placed; but that the fallacies to which they are liable
are generally remote, and each of them applicable to one test only.
Hence if each of the three reagents, applied with due care, gives a
precipitate of the characteristic tint, the proof of the presence of
arsenic is decisive.

This particular view of the indications of the liquid tests, however
obvious it may seem, has been often overlooked by the numerous chemists
and medical jurists who have written for and against them. The
antagonists of the tests have been content with proving how so many
fallacies lie in the way of each, that no dependence can be put in any
one of them: They have not considered that the fallacies attached to one
are obviated by the conjunct indications of the others.

I am of opinion therefore that the analysis for arsenic by liquid
reagents has been unjustly neglected in the present day. It is an
exceedingly convenient method, and one of extreme delicacy, because by
using small tubes it is easy to operate with precision on very minute
portions of a suspected fluid. It is also perfectly conclusive, so far
as chemical knowledge now goes. On a remarkable trial a few years ago in
this country, a distinguished chemist, who, as witness for the prisoner,
was made by counsel to throw discredit on the liquid tests individually,
nevertheless admitted to the counsel for the prosecution, that no other
substance in nature but arsenic could produce the same effects as it
with the whole three tests in succession.

_Reduction process._—The process by reduction of arsenic to the metallic
state, as applied to the poison in a state of solution, consists in
separating the whole arsenic by a liquid test in such a state as to
admit of the precipitated compound being subjected to the process of
reduction and sublimation. The best method of the kind is a modification
of one described by me in 1824.[523] This consists in throwing down the
whole arsenic in the form of sulphuret by means of hydrosulphuric acid,
converting the sulphuret by the process of reduction to the metallic
state, and oxidating the metal thus procured. The hydrosulphuric acid is
preferred to other liquid reagents, because the precipitate it forms,
while possessing a very characteristic colour, is also more bulky than
those caused by the other tests, and is therefore more easily
collected,—and because its action is not liable to be prevented or
obscured by so many disturbing causes. The steps of the process are the
following:—

The fluid to be examined must be acidulated with acetic or hydrochloric
acid. If the fluid be neutral or alkaline, the acid may be added at
once. If on the other hand the fluid redden litmus, and the acid be
either unknown or a mineral acid, potash must first be added in a slight
excess, and then the alkali must be supersaturated with acetic or
hydrochloric acid. The reasons for these precautions are stated under
hydrosulphuric acid as a liquid reagent. The fluid being thus prepared,
it is subjected to a stream of hydrosulphuric acid gas for ten or
fifteen minutes. The first portions of the gas turn the arsenical
solution to a bright lemon-yellow colour, and the subsequent portions
throw down a yellow flocculent sulphuret of arsenic. If the proportion
of oxide in solution is small, a yellowness or yellow milkiness only is
caused, owing to the sulphuret being soluble in an excess of
hydrosulphuric acid. But on expelling that excess by boiling, a distinct
precipitate and colourless fluid are produced. The precipitate is then
to be collected thus. The precipitate is allowed to subside, and the
supernatant fluid being withdrawn, the remainder is poured into a
filter. When all the fluid has passed through, the portions of
precipitate on the upper part of the filter are washed down to the
bottom. The filter is then gently compressed between folds of bibulous
paper, and the sulphuret removed with the point of a knife before it
dries, and dried in little masses on a watch-glass by the side of a
chamber-fire, or still better in a vapour-bath. In this way it is very
easy to collect a twenty-fifth part of a grain of the sulphuret. Another
method which takes more time, but will enable the least skilful person
to collect extremely small quantities, is to allow the sulphuret to
subside in the original fluid in which it is formed, to pour off the
supernatant liquid, and pour the remainder into a small glass tube, Fig.
7. After the precipitate has thoroughly subsided, the supernatant liquid
is to be withdrawn, and its place filled up with boiling water. The
operation of alternate subsidence and affusion being repeated a
sufficient number of times, the last portions of water should be gently
driven off by heat, and wiped off the inside of the tube as the drops
condense on it. Finally, the bottom of the tube, with the precipitate
attached, is to be cut away with the file, and broken into small
fragments with the view of preserving the whole sulphuret for the
process of reduction. The sulphuret having been collected in either of
these ways, it is now to be dropt into the tube, Fig. 3, and covered by
means of the funnel, Fig. 4, with soda-flux. The process in other
particulars is the same with that for reducing solid oxide of arsenic.

This method of investigation gives extremely precise results, because it
presents the poison successively in three distinct forms, as sulphuret,
metal, and crystallized oxide, all of which possess very prominent and
characteristic external properties. It is also a method which is capable
of detecting very minute quantities of oxide of arsenic. And it has the
advantage over the process by liquid reagents of being applicable to
organic fluids. It was accordingly followed in most medico-legal
researches until the recent discovery of the methods of Marsh and
Reinsch.

In order to render it quite satisfactory, it is necessary to go through
the steps of the analysis at the same time with distilled water, lest
any of the reagents used should accidentally contain arsenic.

_Process of Marsh._—This method consists in disengaging arsenic from the
solution in the form of arseniuretted-hydrogen gas, burning the gas in
such way as to obtain either metallic arsenic or oxide of arsenic, and
subjecting the product to various tests.

I have called this beautiful method of analysis Marsh’s process, because
it appears to me that injustice has been done its discoverer both by
himself and those who have since investigated the subject, when they
denominated it merely a test. Medico-legal analysis stood in no need of
a new test for arsenic, but very much of an easy and infallible method
of detaching minute quantities of it in a state of purity from simple
and compound fluids, so as to admit of its being accurately examined. It
is this important object, and not strictly speaking a new test, that has
been attained through means of the discovery of Mr. Marsh.

His discovery consists in the observation, that, if hydrogen gas be
disengaged by the action of sulphuric acid or zinc in a fluid containing
arsenic dissolved in any form, arseniuretted-hydrogen gas is disengaged
along with the hydrogen; and that if the two gases be burnt together in
a fine flame, metallic arsenic is deposited on a white porcelain surface
held in the flame, and oxide of arsenic if the porcelain be held
immediately above it.[524] The production of a brilliant mirror-like
crust in the former case, and of a white powdery one in the other,
constituted Marsh’s test as originally proposed; and it was at first
conceived to furnish unimpeachable evidence of the detection of arsenic.
Afterwards many inquirers, and among them the discoverer himself, became
satisfied that certain fallacies stand in the way of a conclusion based
on such simple premises. Various supplementary tests were in consequence
proposed. And at length it seems to be agreed, that the proper mode of
applying Marsh’s discovery is to employ a succession of tests, of which
that originally pointed out by him is the first. A vast variety of
methods of analysis founded on this principle have been proposed by
British and continental chemists. It would be tedious and unprofitable
to discuss or even to state them here. The reader will probably be
satisfied with a reference to the most important of them[525] and with a
description of that process, which appears to me, from repeated trials
in medico-legal practice, to be at once most convenient, delicate, and
conclusive.

Let the liquid to be examined be introduced into a Döbereiner’s lamp
[Fig. 10], or an apparatus constructed with a bottle and a funnel upon
the same principle [Fig. 11]; and dilute the liquid with distilled
water, until the lower cavity of the apparatus be nearly full, leaving
space however for the tube of the funnel, a fragment of zinc, and some
sulphuric acid. Put in a cylinder or rod of zinc, _a_; and then add
sulphuric acid until a moderate effervescence ensue. Close the junction
of the two vessels, and then, allowing a little gas to escape at _c_,
shut the stop-cock, and let the gas fill the vessel A, by driving the
liquid up into B. Having meanwhile fitted by a cork to the exit-tube,
_c_, the glass tube, _d e_, which is loosely stuffed with raw cotton at
the end _d g_, and has a bent plate of copper or tinned iron hung over
it at _f_,—open the stop-cock, allow a little gas to escape so as to
expel the air in _d e_, and then kindle the gas at _e_, which must be
contracted to a capillary opening. Keep the flame low, and hold the
surface of a white porcelain vessel across the middle of it for a few
seconds. If no stain be produced on the porcelain, there is no arsenic
in the fluid. If a stain be formed, regulate the escape of gas by the
stop-cock so that the fluid may not rise above the middle of the lower
vessel of the apparatus, and apply the heat of a spirit-lamp flame to
the tube _d e_ on the left hand of the plate _f_, the purpose of which
is to prevent the heat being communicated beyond that point. By and by,
if there be arsenic in the fluid, a brilliant metallic ring will appear
beyond _f_, owing to decomposition of arseniuretted-hydrogen gas. As
soon as the crust is thick enough to present its properties
characteristically, withdraw the spirit-lamp; place the tube _e h_ so
that the flame at _e_ shall be completely within the ball, _i_; let the
tube incline very slightly in the direction from _k_ to _l_; and allow a
stream of cold water to trickle down upon the portion _k l_, which
should be wrapped in a single layer of calico. Oxide of arsenic will
gradually condense, partly in white powder or minute sparkling crystals
in the ball and between _i_ and _k_, and partly between _k_ and _l_ in
the form of a solution, which collects at the bend _l_. The solution
which may be increased in quantity by boiling a little distilled water
upon the powder in the ball and bend _i k_, is then to be subjected in
small portions to the three liquid reagents, ammoniacal nitrate of
silver, ammoniacal sulphate of copper, and hydrosulphuric acid.

Some experience is required to apply this process successfully. But with
due attention it furnishes conclusive evidence with great delicacy and
precision. A solution containing only a millionth part of oxide of
arsenic will part with it readily in the form of arseniuretted-hydrogen;
and the slightest trace of that gas in the hydrogen is indicated by the
method recommended above.—The process is compounded of Mr. Marsh’s
original discovery, the supplementary test of reduction in the exit-tube
recommended by Berzelius,[526] and the formation and examination of the
oxide proposed by myself.[527]—With certain precautions and modes of
manipulating, it is applicable to the most complex organic fluids, as
well as to simple solutions.

The discovery of Mr. Marsh had not been long made before the test in its
original simple form was found liable to divers important fallacies. It
appeared, for example, that antimony yields very nearly the same
appearance of metallic crust and of white powder, according to the
position of the porcelain in the flame; that some porcelains glazed with
oxide of zinc are similarly stained by a flame of simple hydrogen gas;
that a great variety of metallic salts, if spirted up into the
exit-tube, undergo reduction in the flame, and cause imitative stains on
the porcelain; that iron-salts seems to form stains from the same
chemical action as what occurs in the case of arsenic; and that certain
compounds of phosphorous acid with ammonia and animal matter, or even
mere animal matters themselves, will in some circumstances produce a
stain more or less similar to that which is occasioned by arsenic.

There is no doubt, that the resemblance of most of these spurious stains
to an arsenical crust has been much exaggerated. But still the
similarity is sufficient to satisfy every impartial judge, that the mere
production of a brilliant metallic, or white powdery stain, or both,
upon porcelain, is not conclusive evidence of the detection of arsenic
in medico-legal inquiries. It is strong presumptive evidence; and the
non-production of such stains is absolute proof that arsenic is not
present. But in order to obtain irrefragable proof of its presence, the
substance which forms the crusts and stains must be subjected to farther
examination. And such is the object of the supplementary methods in the
process detailed above. That process is perfectly free of fallacy. No
substance yet known but arsenic can yield the succession of phenomena
which have been detailed. My opinion farther is, that the process may be
safely simplified by withdrawing Berzelius’s supplementary test of
reduction in the exit-tube, and retaining the test of oxidation only,
with the examination of the oxide by liquid reagents. I have retained
the former in deference to the opinion expressed by a committee
appointed by the French Institute, who examined the whole subject with
unwearied zeal, but who, it may be observed, seem never to have had in
their view the check-test of oxidation; which, with the consecutive
tests, is superior in conclusiveness to the check of reduction only.

_Reinsch’s process_, like the former, has been inconveniently called a
new test for arsenic. The fact discovered by Dr. Reinsch is valueless as
supplying a mere test; but it forms the ground-work of the best process
of all yet proposed for the detection of arsenic in solution. The
discovery is, that arsenic in solution is deposited in the metallic
state upon copper-leaf, when the fluid is acidulated with hydrochloric
acid, and heated till it boils gently or is about to do so; and that by
heating the copper gently in a glass tube the arsenic is sublimed from
it in the form of oxide or metal according to the quantity present.[528]

This method is so simple and easy as scarcely to require any detailed
explanation. The fluid should contain about a tenth of its volume of
hydrochloric acid. It must be heated near ebullition before the copper
is introduced, otherwise the copper becomes tarnished, though arsenic be
not present. Copper-leaf, or copper-plate worn thin by the action of
diluted nitric acid, or fine copper gauze, is the best form for use. In
the feeblest solutions ten or fifteen minutes elapse before arsenic is
visibly deposited, and forty minutes should be allowed for strong
deposition; but in strong solutions, the action takes place in a few
seconds. The result is a thin, brittle brilliant, steel like coating of
metallic arsenic. As soon as the deposit is formed, the copper is to be
removed, dried with a gentle heat, cut into small shreds, and heated
with a spirit-lamp in the smallest glass tube that will conveniently
contain the whole; upon which a metallic ring of arsenic is sometimes
sublimed, but more generally a ring of small sparkling crystals. These
are first to be examined as to their form with a common pocket lens; and
then dissolved in boiling distilled water, after shaking out the copper,
so that a solution may be obtained and subjected to the liquid reagents,
especially the ammoniacal nitrate of silver as being the readiest and
most delicate. In all medico-legal inquiries it is necessary to perform
a preliminary experiment with distilled water and the hydrochloric acid
used, lest the acid contain arsenic.

The process here described is one which I have followed with great
facility, certainty and despatch in several medico-legal cases.[529] It
is extremely delicate; for it will detect at least a 250,000th part of
arsenic in solution; and it removes from the fluid every particle of
arsenic, because none can be afterwards discovered by means even of
Marsh’s method. It is not subject to any fallacy. The mere formation of
a brilliant coating on the copper is not evidence of arsenic being
present; for as Reinsch himself ascertained, solutions of bismuth, tin,
zinc, and antimony produce a coating more or less similar to an
arsenical one. But the farther steps of the process entirely put aside
all these sources of error. The non-formation of a metallic tarnish of
copper, however, is perhaps not absolute proof of the absence of
arsenic. For, according to a late statement by Drs. Fresenius and Von
Babo,[530] “all nitrates, and various salts of mercury and other metals,
render the separation of arsenic by copper difficult or even
impossible.” The authors of this objection, although the paper is
otherwise elaborate and detailed, have not given any particulars in
illustration of so important a criticism.


        _Of the Tests for Oxide of Arsenic in Organic Mixtures._

The present is by far the most important of the conditions under which
it may be necessary to search for arsenic in medico-legal cases; for in
nine cases out of ten the subject of analysis is either some article of
food or drink, the contents or tissues of the stomach, or the textures
of other organs of the body into which the poison has been carried by
absorption.

Accordingly much attention has been paid to this subject for some years
past, and many valuable methods of analysis have been suggested, more
especially since the recent discovery that arsenic, like many other
poisons, undergo absorption, and is diffused by the circulation
throughout the body generally. It was proved by me in 1824,[531] that
the tests for arsenic, at that time in general use, are so fallacious
when applied to complex organic mixtures as to be unfit for medico-legal
investigations except merely as trial-tests; and a process was proposed,
which has since undergone various modifications from others as well as
myself. This process, in the form in which it was adopted in the last
edition of the present work, is still applicable to a great proportion
of cases; and indeed a recent modification of it has been thought by
Drs. Fresenius and von Babo to be superior even yet to every other in
all circumstances.[532] But two new methods are at present generally
preferred, and probably not without reason. At least they have been much
employed and with great success in numerous medico-legal researches,
where the quantity of arsenic was to all appearance extremely small, and
the subject of examination most complex and troublesome to bring within
the sphere of analysis. And in particular they have been successfully
employed to detect arsenic in those organs of the human body into which
it can obtain admission only through the medium of absorption.

In the following statement I shall describe four processes only, that of
Reinsch, by which the arsenic is first separated as a crust on
copper,—that of Marsh, who first detaches it in the form of
arseniuretted-hydrogen,—my own method, which consists in obtaining in
the first instance a sulphuret of arsenic,—and that of Drs. Fresenius
and von Babo, which has the same foundation.

_Process of Reinsch._—This is the simplest and easiest of all. Remove in
the first place any white or gray powder which can be detached from the
mixture; and either subject it to the process of reduction by charcoal
or soda-flux, as described at p. 203, or dissolve it in boiling
distilled water and subject the solution to the three liquid reagents,
p. 207, or if there be enough, examine it in both ways. If arsenic be
thus obtained, it is seldom necessary to proceed any farther. But if
not, cut all soft solids into small fragments, add distilled water if
necessary, then add hydrochloric acid to the amount of a tenth of the
whole mixture, and more if the subject of analysis be decayed and
ammoniacal, so that there may be a decided excess of acid. Boil gently
for an hour, or until all soft solids be either dissolved or broken down
into fine flakes and grains. Filter through calico; bring the filtered
fluid again to the boiling point; and then proceed as described for
Reinsch’s method in simple arsenical solutions [p. 214].

The only important precaution to be attended to in employing this
process is to take care that the water, hydrochloric acid, and calico
are free of accidental impregnation with arsenic. This is guarded
against by applying the process to them in the first instance. I have
lately employed this method of analysis with success in two medico-legal
cases where the bodies had been buried for several months, and where the
quantity of arsenic must have been very minute. Satisfactory evidence
was obtained from a sixth part of the stomach, and also from the same
proportion of the liver.

_Process of Marsh._—The chief difficulties in applying the process of
Marsh to complex organic mixtures arise from the tendency of oxide of
arsenic to adhere with obstinacy to some organic principles in the solid
state, and from the liability of the gas disengaged in the apparatus to
raise organic fluids in a fine froth, which breaks up slowly, and is
therefore apt to pass over into the exit-tube. Many contrivances have
been devised, to meet these difficulties, especially by the French
chemists and toxicologists, whose attention was turned earnestly to the
subject by the investigations carried on in certain late criminal trials
of great interest and importance. The various devices now alluded to
were subjected to trial in 1841 by a Committee of the French Institute;
who came to the opinion that the following method suggested by MM.
Flandin and Danger is the most convenient and comprehensive.[533]

Heat the organic matter with a sixth of its weight of strong sulphuric
acid; when complete solution has taken place, concentrate the fluid to a
friable almost dry charcoal; add a little concentrated nitric acid
gradually to this when cold, and again evaporate to dryness; then act on
the residue with boiling distilled water, and a solution of a
reddish-brown colour is obtained, which may be used in such an apparatus
as that of Döbereiner without risk of obstruction from froth.—The
arseniuretted-hydrogen, thus disengaged along with the hydrogen gas, is
to be submitted to the succession of tests described in speaking of
Marsh’s process for detecting arsenic in a state of simple solution [p.
212].

This method of investigation is exceedingly precise and conclusive. The
sulphuric acid aided by heat destroys organic matter sufficiently to
prevent frothing in the apparatus and dissolves out arsenic from a state
of combination with organic principles; and nitric acid afterwards
converts any arsenic in the half-charred mass into the soluble arsenic
acid. It has been employed with success in various medico-legal
proceedings in France. It answers well for detecting oxide of arsenic in
the viscera, muscles, and other parts of the body into which the poison
has been conveyed through absorption.

_Process by Hydrosulphuric Acid._—This method may be employed in two
ways, according as the object is merely to prove the presence of oxide
of arsenic, or to ascertain also its quantity.

a. If proof of its presence be all that is wanted, cut any soft solids
into small pieces, add distilled water if necessary, boil for half an
hour, let the decoction cool, and filter it. Add a little acetic acid to
the filtered fluid, and if any precipitate form, filter again. Evaporate
to dryness, first by ebullition, afterwards over the vapour-bath.
Dissolve the residuum again in repeated portions of boiling distilled
water, and filter the solution. If it be not acid to litmus-paper add
more acetic acid, and transmit hydrosulphuric acid gas through the fluid
until an excess be indicated by the sense of smell after agitation, Then
expel the excess of gas by boiling; and if the precipitate of sulphuret
of arsenic do not subside readily add a little of a strong solution of
hydrochlorate of ammonia, which will facilitate subsidence. When the
precipitate has fallen to the bottom, withdraw the supernatant fluid
with the pipette, Fig. 8; and replace it with a little boiling distilled
water. Lastly, collect the precipitate on a filter, and proceed as by
the reduction process with soda-flux for oxide of arsenic, in a state of
simple solution.

This method answers very well for ordinary cases where the quantity of
arsenic is not extremely minute. But I have met with instances in
medico-legal practice where the process of Reinsch, as well as that of
Marsh, succeeded in detecting the poison in sources to which the method
by hydrosulphuric acid had been applied without avail; because
apparently the organic matter existing in solution prevented the action
of the gas, or, as Orfila thinks, because boiling water will not in all
circumstances remove oxide of arsenic from the textures of the animal
body which are impregnated with it. In particular I doubt whether this
method is sufficiently delicate to detect arsenic in those organs and
textures into which it has been conveyed in cases of poisoning through
absorption into the blood.—Another objection is its tediousness. The
first filtration, if the substance to be examined be the stomach or its
contents, may take two days; and one way or another the analysis can
seldom be completed within four days. Reinsch’s process may be brought
to a conclusion in two hours or less, even in the most difficult
circumstances.

b. The last process to be mentioned, is one based, like the previous
one, upon the precipitation of arsenic in the form of sulphuret, but
with very material modifications, the purpose of which is to enable the
analyst to separate the whole arsenic in a state of purity, so as to
ascertain the exact amount of the poison in the mixture. This method has
been recently proposed by Drs. Fresenius and von Babo.[534]

Cut any soft solids into small pieces, put the whole into a porcelain
basin, add as much hydrochloric acid as equals the probable weight of
the dry matter in the mixture, and then water enough to form a thin
pulp. Heat the basin over the vapour-bath, adding every five minutes
about half a drachm of chlorate of potass, and stirring frequently,
until the liquid become clear-yellow, homogeneous, and thin. Add now two
drachms more of the chlorate; filter through linen, washing the residuum
on the filter with boiling water; concentrate to a pound; add a strong
solution of sulphurous acid till its odour predominates, and expel the
excess of it by heat. The liquid is now ready for the transmission of
hydrosulphuric acid gas, which should be transmitted in a slow stream
for twelve hours. Wash away any sulphuret adhering to the tube by means
of ammonia, and add the solution to the principal liquid; which is next
to be left at a gentle heat about 80° F., in a vessel covered with
paper, till the sulphureous smell entirely disappear. The precipitate,
which contains organic matter as well as sulphuret, is then to be
collected on a paper filter, washed, and dried with the filter over the
vapour-bath. The animal matter is next destroyed, and the sulphuret
converted into arsenic acid, by dropping on it fuming nitrous acid till
the whole is moistened, drying the product thoroughly over the
vapour-bath, moistening the residuum with concentrated sulphuric acid,
heating the mixture again in the vapour-bath for two or three hours, and
raising the heat afterwards gradually in a sand-bath to 300° F., till a
charred brittle mass be obtained. This is to be heated over the
vapour-bath with twenty parts of distilled water, filtered, and washed
with boiling water on the filter till what passes through ceases to
redden litmus. The solution, which ought to be colourless, is next
acidulated with hydrochloric acid, and treated as formerly with
hydrosulphuric acid gas. When the sulphuret has been collected on a
small filter, diluted ammonia is to be sent through the filter as long
as it dissolves any sulphuret, and is to be received in a weighed
porcelain basin, in which the ammonia and water are to be driven off at
a temperature not exceeding 212°. The sulphuret which is alone left may
now be weighed by again weighing the basin; and one grain of sulphuret
is equivalent to 0·803 of a grain of oxide of arsenic.—The authors add
an elaborate process for obtaining from this the whole arsenic by
reduction. But such a proceeding is unnecessary. It is sufficient in
medico-legal inquiries to ascertain by the simpler method given above
[p. 204], that it does yield by reduction with soda-flux a true
arsenical crust, and that this yields by oxidation white, sparkling
crystals with triangular facettes.

After a comparative trial of the most esteemed process, Drs. Fresenius
and von Babo state that they found the one now described as delicate as
any other, and the only method by which the quantity of oxide of arsenic
can be ascertained with accuracy.—The hydrochloric acid used at the
commencement enables the water to dissolve compounds of arsenic which
water alone will not act on; and it farther facilitates solution by
breaking up or dissolving organic textures. The addition of chlorate of
potash prevents the escape of oxide of arsenic during the subsequent
evaporation; which is apt to happen when hydrochloric acid is present.
The subsequent addition of sulphuric acid converts arsenic acid into
arsenious acid, in which shape the sulphuret of arsenic is more readily
formed by the action of hydrosulphuric acid gas, when organic matter
co-exists in the solution. The steps for destroying organic matter
thrown down with the sulphuret at its first formation require no further
commentary: They are the most important particulars in the process for
its main object,—the determination of the quantity of pure
sesqui-sulphuret, and, through it, of the sesquioxide originally in the
subject of analysis.


    _Of certain alleged Fallacies in the case of Organic Mixtures._

Before taking leave of the detection of arsenic in organic mixtures, it
is necessary to notice certain alleged fallacies in the way of every
process, arising from arsenic obtaining admission into the subject of
analysis through other means than its intentional addition or its
introduction as a poison into the body. This topic, one of paramount
importance in medico-legal chemistry, has lately undergone careful
investigation during and since the notorious trial of Madame Lafarge.
The results are the following:—

It has been alleged that arsenic may obtain accidental admission into
the subject of analysis, 1, because the reagents used in the processes
may be adulterated with arsenic; 2, because the material of the
apparatus may contain it; 3, because it may have existed in antidotes
administered during life; 4, because it sometimes forms a constituent
part of the human body in the natural state; and 5, because it exists in
the soil of some churchyards.

1. _Arsenic may exist as an adulteration in some reagents._—It must be
apt to occur in _sulphuric acid_, when that substance is prepared with
pyritic sulphur, which commonly contains some sulphuret of arsenic; and
it has actually been found in abundance in the acid by various
experimentalists, and in England for the first time by Dr. Rees.[535] It
may be detected by transmitting hydrosulphuric acid gas through the
diluted acid; and it may be effectually removed in the same way,[536]
the acid being afterwards filtered in a funnel whose throat is
filled with asbestus, and the excess of gas being expelled by
heat.—_Hydrochloric acid_ may contain arsenic, because it may have been
prepared with an arsenicated sulphuric acid. The impurity may be
detected and removed in the same way as in that substance. Nitric acid
seems not apt to be similarly adulterated;[537] but it may be tested by
Marsh’s process, after neutralizing the acid with potash, and adding
more sulphuric acid than is required to decompose the nitre thus formed.
_Zinc_ occasionally contains a little arsenic, which will be evolved in
Marsh’s process. Dr. Clark of Aberdeen says zinc is scarcely ever free
of a trace of arsenic; and it has been occasionally detected by others.
Orfila, however, very seldom found so much as to be discoverable by
Marsh’s test applied continuously for a great length of time.[538] A
committee of the French Institute came to the same conclusion.[539] M.
Jaquelain, acting under the directions of Professor Dumas, could not
detect an atom in any French specimen of zinc, or its carbonate or
silicated oxide, as met with in commerce.[540] Lastly, Mr. Brett
satisfied himself that no British or foreign zinc he could obtain
indicated the presence of arsenic by a process capable of detecting a
5000th of that metal in zinc.[541] It is an obvious inference from all
these inquiries that no difficulty can be experienced in obtaining zinc
so pure as to exhibit not a trace of arsenic by Marsh’s method. Neither
is there any difficulty in obtaining sulphuric, muriatic, and nitric
acid free of that adulteration.

But at the same time it is equally obvious, that in medico-legal
analyses, unless the reagents used be previously known to be free of
arsenic, they ought invariably to be subjected in the first instance to
the process, whatever it may be, which the analyst proposes to employ
for detecting arsenic in a suspected substance.

2. _Arsenic may be present in some articles of chemical
apparatus._—Arsenic has been detected in the metal of cast-iron
pots,[542] which Orfila and others have proposed to employ in certain
analyses on the large scale, as, for example, when the poison is sought
for in the whole soft solids of the human body. It is denied, however,
that any of that arsenic can be dissolved out of cast-iron by the
process which has been followed in such circumstances.[543]

The primary fact, and the qualification of it, are in my opinion of
equally little medico-legal importance. It is not likely that such
enormous masses of material will ever be operated on again, as those
which were made use of in some late, French trials, and for which great
iron pots were found indispensable;—because it has been proved that
absorbed arsenic is chiefly to be met with in particular organs or
secretions, such as the liver and urine. Besides, a false importance has
been attached to the enthusiastic analyses of the whole human carcase,
with which some French chemists have been astounding the minds of the
scientific world, as well as the vulgar, on the occasion of certain late
trials for poisoning. I confess I could not find fault with a jury, who
might decline to put faith in the evidence of poisoning with arsenic,
when the analyst, after boiling an entire body, with many gallons of
water, in a huge iron cauldron, making use of whole pounds of sulphuric
acid, nitric acid, and nitre, and toiling for days and weeks at the
process, could do no more than produce minute traces of the poison. What
man of common sense will believe, that, with such bulky materials and
crude apparatus, it is possible to guard to a certainty against the
accidental admission of a little arsenic? At all events I am much
mistaken if any British jury would condemn a prisoner on such
evidence,—or any British chemist find fault with them for declining to
do so.

3. _Arsenic may have existed in antidotes administered during life._—It
is now generally known, that the only chemical antidote for arsenic is
the hydrated sesquioxide of iron. But this substance appears
occasionally to contain a little arsenic, obviously derived from the
compound of iron whence the oxide is prepared.[544] Such an adulteration
must be rare in what is prepared by the ordinary processes, according to
which the oxide of arsenic ought to remain in solution. The only
effectual mode, however, of guarding against this source of error, when
the antidote has been administered, is to examine a portion of the stock
whence the patient was supplied, by dissolving it in an excess of
sulphuric acid, and subjecting it to Marsh’s test.

4. _Arsenic sometimes exists naturally in the human body._—This
startling proposition was first advanced by M. Couerbe, and by Professor
Orfila soon afterwards.[545] The latter subsequently stated, that it
exists only in the bones, and not in any of the soft solids.[546] It is
now clear, however, that both of these experimentalists must have
committed an error. Orfila himself admits that his early researches are
vitiated by the subsequent discovery of arsenic in some kinds of
sulphuric acid;[547] and all recent attempts by others to obtain his
results have failed. Thus MM. Flandin and Danger could not detect
arsenic in any part of the human body, when it had not been
administered:[548] Pfaff was unable to detect an atom of it in the bones
of man or the lower animals by Orfila’s own process:[549] Dr. Rees was
equally unsuccessful:[550] and in 1841 a committee of the French
Institute, who superintended the performance of an analysis in three
cases by Orfila, reported that he failed in every instance to find a
trace of arsenic, by a process which could detect a 65th part of a grain
intentionally mixed with an avoirdupois pound of bones.[551]

There is the strongest possible presumption, therefore, that human bones
never contain any arsenic. And besides, supposing they did, the source
of fallacy would be utterly insignificant; for, when it becomes
necessary to search for arsenic absorbed into the textures of the body,
it is never necessary to have recourse to the bones.

5. _Arsenic may exist in the soil of churchyards._—This proposition too
was first announced by Professor Orfila, who found a little in the
churchyard of Villey-sur-Tille, near Dijon, and of the Bicêtre,
Mont-Parnasse, and New Botanic Garden at Paris.[552] And although MM.
Flandin and Danger afterwards denied they could ever find any,[553] a
committee of the Parisian Academy of Medicine reported that Orfila
proved before them the accuracy of his statement.[554] But the arsenic
exists in a state in which it cannot be dissolved out by boiling water:
It has been hitherto separable only by boiling the churchyard mould with
concentrated sulphuric acid. Hence it cannot pass by percolation through
a coffin into a body; and consequently it becomes a source of fallacy
only when the coffin has been broken up in the course of time, and the
mould lies in actual contact with the organs to be analysed.[555]

It plainly appears, then, that most of the fallacies alleged against the
validity of the evidence derived from the discovery of arsenic within
the human body in cases of poisoning have no real existence; and that
those which are real can easily be provided against by simple and
obvious precautions.


                        3. _Arsenite of Copper_.

The arsenite of copper [Scheele’s-green, Mineral-green] deserves notice,
because it is in use as a pigment, and has actually been used as a
poison. Dr. Duncan once detected it in pills, given to a pregnant female
with the view of procuring abortion; in Paris it has been detected in
sweetmeats, having been used to give them a fine green colour;[556] and
Mr. Ainley of Bingley in Yorkshire informs me he found it to constitute
a pigment sold by London pastry-cooks under the name of emerald-green
for colouring preserves, and which in his practice had proved poisonous
to children who had eaten apple-tarts coloured with it.

It is a compound of arsenious acid and deutoxide of copper, is sold in
powder or pulverulent cakes, and has a pale grass-green colour. Its
nature may be ascertained by heating it in a glass tube. Crystals of
oxide of arsenic sublime, and oxide of copper remains, which, on being
dissolved in nitric acid, yields a fine violet-blue solution with
ammonia.

The mineral-green of the shops, however, is seldom arsenite of copper.
The substance sold in Edinburgh under that name, although believed by
colourmen to be a preparation of arsenic, is not the arsenite of copper,
but a mixture of hydrated oxide of copper and carbonate of lime; which
will be mentioned more particularly under the head of the poisons of
copper.

_Process for Organic Mixtures._—The suspected mixture is to be heated
with a little hydrochloric acid and well stirred. The arsenite being
thus dissolved, the solution is to be allowed to cool and then filtered.
A stream of hydrosulphuric-acid gas will now cause a dark-brown or
yellowish-brown muddiness or precipitate, which is a mixture of
sulphuret of copper and sulphuret of arsenic. The precipitate being
separated after boiling, and properly cleansed by the process of
subsidence and affusion, or if it is large, by washing on a filter, the
two sulphurets are to be separated by ammonia, which dissolves sulphuret
of arsenic but leaves the sulphuret of copper; and the sulphuret of
arsenic may be recovered from the filtered fluid by expelling the
ammonia with heat. The sulphuret of arsenic is next to be reduced as
directed at page 211; and the sulphuret of copper examined as
recommended under the head of copper.


                        4. _Arsenite of Potass_.

This salt is an object of some importance to the medical jurist, as it
forms the basis of a common medicine, Fowler’s Solution, or the
Tasteless Ague Drop. This preparation contains in every ounce four
grains of arsenious acid. It has a brownish-red colour, and an odour of
lavender. It is strongly alkaline to litmus. When acidulated with
hydrochloric acid, hydrosulphuric-acid gas causes in it a dirty
brownish-yellow precipitate; and Reinsch’s process will detach arsenic
from it upon copper in a state capable of being subjected to the usual
tests [see p. 214].


                       5. _Arseniate of Potass._

This substance is so rarely met with as to be an object of little
consequence to the medical jurist: nevertheless I have found in the
course of reading two instances of poisoning with it. A very dangerous
and tedious case has been related by Professor Bernt, which arose from
too great a quantity having been given medicinally by an ignorant
druggist;[557] and a case of accidental poisoning with it has been
related in the London Medical Repository.[558] A singular account too
has been published of the accidental poisoning of seven horses with it
at Paris. They all died, most of them with the symptoms and morbid
appearances of well-marked inflammation of the alimentary canal.[559]

When solid it forms tetraedral prismatic crystals, acuminated by four
planes. It is very soluble in water, fuses at a red heat, and on cooling
concretes into a crumbly, foliaceous mass, having a pearly lustre. It is
easily known by the effect of the process of reduction—of the nitrate of
silver, the salts of copper, and sulphuretted-hydrogen. Heated with
charcoal in a tube it gives off metallic arsenic in the usual manner;
but a stronger heat is required than for the reduction of the arsenious
acid. Dissolved in water and treated with nitrate of silver it yields a
brick-red precipitate, the arseniate of silver. With the salts of copper
its solution gives a pale bluish-white precipitate, the arseniate of
copper. With sulphuretted-hydrogen gas, preceded by acidulation with
muriatic acid, and transmitted for a considerable length of time, it
yields the yellow sulphuret of arsenic. When in solution it yields
arsenic both by Reinsch’s process and the method of Marsh.


                    6. _The Sulphurets of Arsenic._

In the arts various substances are known which contain a compound of
sulphur and arsenic. In the first place, two pure sulphurets are known
in chemistry and in painting, the one of a fine orange colour, and known
by the name of realgar, the other of a rich sulphur-yellow, and termed
orpiment. Secondly, the name of orpiment is familiarly given to a
pigment in more general use than either of the former, which has a less
lively colour, and consists of pure orpiment with a large admixture of
arsenious acid. Lastly, orpiment also forms a great proportion of
another common pigment, King’s yellow.

The orange-red sulphuret (realgar, risigallum, Σανδαραχη, sandaracha),
is chiefly a natural production. It is solid, of a bright orange-red
colour, and composed of small shining scales, so soft as to be scratched
with the nail. It is composed of one equivalent of metal and one of
sulphur. Its best chemical characters are the disengagement of metallic
arsenic when it is heated in a tube with potass or the black flux; and
its undergoing sublimation unchanged when heated alone in a tube.

The yellow sulphuret (orpiment, auripigmentum, αρσενικον), is both a
natural production, and the result of many chemical operations. The
sulphuret thrown down from solutions of arsenic by sulphuretted-hydrogen
is quite conformable in physical and chemical characters with the
natural orpiment. Natural orpiment, when in mass, consists of broad
scales of much brilliancy and of a rich yellow colour. It is composed of
two equivalents of metal and three of sulphur. Its most striking
chemical characters are the same with those of realgar, from which it is
distinguished chiefly by its colour.

It has been stated by Hahnemann in his elaborate work on Arsenic, that
the pure sulphurets are somewhat soluble in water,—that native orpiment
is soluble in 5000 parts of water with the aid of ebullition, and that
artificial orpiment by precipitation is soluble in 600 parts.[560]
Hahnemann, however, was mistaken in supposing that the water dissolved
these sulphurets. It does not dissolve, but decomposes them. Very lately
M. Decourdemanche has found that, by slow action in cold water, and much
more quickly with the aid of heat, the arsenical sulphuret is decomposed
by virtue of a simultaneous decomposition of the water, hydrosulphuric
acid being evolved and an oxide of arsenic remaining in solution. And he
has farther remarked, that this change is promoted by the presence of
animal and vegetable principles dissolved in water.[561] These facts are
interesting, as they explain certain apparent anomalies to be noticed
presently in the physiological properties of the sulphurets.

The common orpiment of the shops is not a pure sulphuret like the
natural orpiment, but a much more active substance, a mixture of
orpiment and arsenious acid. It is made by subliming in close vessels a
mixture of sulphur and oxide of arsenic. It is met with in the shops in
two forms, in that of a fine powder possessing a yellow colour with a
faint tint of orange, and in that of concave masses composed of layers
of various tints of white, yellow and orange, commonly also lined
internally with tetraedral white pyramidal crystals. Till lately it was
accounted a variety of sulphuret, and some ingenious conjectures were
made as to the cause of its superior energy over the other sulphurets as
a poison. But M. Guibourt has proved that it always contains oxide of
arsenic, and is commonly impregnated with it to a very large amount,
some parcels containing so much as 96 per cent.[562] The inner surface I
have often seen lined with large crystals of pure oxide. In a very
interesting account by Dr. Symonds of Bristol, describing the case of
Mrs. Smith, for whose murder a woman Burdock was executed in that city a
few years ago, it is stated that artificial orpiment was the poison
given, that death took place in a very few hours, and that a sample from
the druggist’s shop where the poison was bought contained on an average
79 per cent. of oxide of arsenic.[563]

Another impure sulphuret, a good deal used in painting, and a favourite
poison in this country for killing flies, is King’s yellow. It is sold
in the form of a light powder or in loose conical cakes. It has an
intense sulphur-yellow colour. This substance is soluble, though not
entirely, in water, both cold and warm, and forms a colourless solution,
from which, on cooling, or by evaporation, a yellow powder separates. In
this respect it differs essentially from the pure sulphurets. The
solution is not acted on by reagents in the same way as the solution of
arsenious acid. Lime-water and hydrosulphuric acid have no effect on it,
the ammoniacal nitrate of silver causes a copious dirty brown, and the
ammoniacal sulphate of copper a scanty, dirty lemon-yellow precipitate.
I have not seen any account of the mode of preparing it or an analysis
of its composition. But according to my own experiments it contains a
large proportion of sulphuret of arsenic, a considerable proportion of
lime, and about 16 per cent. of sulphur. Its nature is best shown by the
following method of analysis. Let the powder be agitated in diluted
ammonia till the colour becomes white. The filtered fluid contains the
sulphuret of arsenic, which, on addition of an acid, falls down, and may
be separated and reduced in a tube with the black flux. The remaining
white powder, well freed from adhering sulphuret by washing, is next to
be agitated in diluted acetate or hydrochloric acid and again filtered.
The solution on being neutralized precipitates abundantly with oxalate
of ammonia and the alkaline carbonates, showing that lime was taken up
by the acid: and, as the acid operates without effervescence, the lime
must have been in the caustic state. The powder which remains after the
action of the acid will be found to fuse with a gentle heat and to burn
almost entirely away with a blue flame, emitting sulphureous vapours.
These experiments make it obvious that King’s yellow contains sulphuret
of arsenic, caustic lime, and free sulphur; and in all probability the
lime exists in the form of a triple sulphuret of lime and arsenic.

All the preparations containing the sulphuret of arsenic are interesting
to the medical jurist, but particularly the two impure sulphurets last
mentioned. The King’s yellow above all should be carefully studied,
because on account of its frequent employment as a fly-poison it has
been the source of fatal accidents. It was likewise taken intentionally
a few years ago in this city, and proved fatal in thirty-six hours. Dr.
Duncan also, while he was Professor of Medical Jurisprudence, met with
an instance of an attempt to poison by mixing King’s yellow with tea;
and at the Glasgow Spring Circuit of 1822 a woman was tried for
poisoning her child with it.

_Process for Organic Mixtures._—If sulphuret of arsenic be present in
such mixtures in appreciable quantity, the particles, owing to their
intense yellow colour, will be visible in any mass which has not the
same tint. From this state of admixture they may be removed by adding
caustic ammonia which dissolves sulphuret of arsenic; and the solution,
on being acidulated with muriatic acid, will deposit the sulphuret
sufficiently pure for undergoing the process of reduction.

Sulphuret of arsenic sometimes exists in small quantity in the stomach,
although the poison was given in the form of oxide; for a portion of the
oxide is subject to be converted into the sulphuret by hydrosulphuric
acid gas evolved in the stomach after death.[564] In every instance of
the kind yet carefully examined a large proportion of the oxide has
remained unacted on, although the intense colour of the mixed sulphuret
makes it appear as if that were the only compound present.


                      7. _Arseniuretted-Hydrogen._

This compound presents the form of a colourless gas, possessing a fetid
garlicky odour, a density of nearly 2·7, and great virulence as a
poison. It is mentioned here, because accidental poisoning with it has
happened occasionally within a few years, chiefly owing to the
occasional adulteration of sulphuric acid with arsenic, and the
liability of the arsenic to form arseniuretted-hydrogen when such
sulphuric acid is used to prepare hydrogen gas. Dr. O’Reilly has
mentioned a melancholy instance of a young chemist losing his life in
this way.[565] Dr. Schlinder of Greifenberg has related another, which
did not prove fatal.[566] And it is well known that the German chemist
Gehlen lost his life by accidentally breathing arseniuretted-hydrogen
while engaged in examining its chemical properties.[567] It is an
inflammable body; and its presence in any other gas is easily detected
by burning it according to the method of Marsh.


  SECTION II.—_Of the Action of Arsenic and the Symptoms it excites in
                                 Man._

It is now generally admitted that arsenic produces in the living body
two classes of phenomena,—or that, like the narcotico-acrids, it has a
twofold action. One action is purely irritant, by virtue of which it
induces inflammation in the alimentary canal and elsewhere. The other,
although it seldom occasions symptoms of narcotism properly so called,
yet obviously consists in a disorder of parts or organs remote from the
seat of its application.

It is also the general opinion of toxicologists, that arsenic occasions
death more frequently through means of its remote effects than in
consequence of the local inflammation it excites. In some cases indeed
no symptoms of inflammation occur at all; and in many, although
inflammation is obviously produced, death takes place long before it has
had time to cause material organic injury. Nevertheless in some, though
certainly in comparatively few instances, the local action, it must be
admitted, predominates so much, that the morbid changes of the part
primarily acted on are alone adequate to account for death.

Its chief operation being on organs remote from the part to which it is
applied, a natural object of inquiry is, whether this action results
from the poison entering the blood, and so passing to the remote organs
acted on, or simply arises from the organ remotely affected sympathizing
through the medium of the nerves with the impression made on the organ
which is affected primarily. On this question precise experiments are
still wanted. The general opinion has for some time been that it acts
through the blood. And this view has of late been strengthened by
indisputable evidence, that the poison does enter the blood, and is
diffused by it throughout the body.

For a long period chemists sought in vain for arsenic in the animal
tissues and secretions at a distance from the alimentary canal. Such was
the position of matters at the date of the last edition of this work; in
which the failure was ascribed to the methods of analysis then known not
being delicate enough to discover the small quantity of arsenic which
disappears by absorption in cases of poisoning.[568] That statement is
now referred to, because in a late controversy in France an attempt was
made, by an erroneous quotation of this work, to deprive Professor
Orfila of the honour, which is due to him alone, of having recently been
the first to demonstrate the possibility of detecting arsenic throughout
the organs and secretions generally of the bodies of men and animals
poisoned with it.

This most important discovery, pregnant alike with interesting
physiological deductions and valuable medico-legal applications, was
first announced by him to the Parisian Academy of Medicine in January,
1839; when he stated that arsenic is absorbed in such quantity in cases
of poisoning as to admit of being discovered by an improved process of
analysis in various organs and fluids of the body, such as the liver,
spleen, kidneys, muscles, blood, and urine.[569] In November, 1840, he
proved these facts to the satisfaction of a committee of the
academy.[570] And since then they have been confirmed by others, not
merely in express experiments, but likewise in the familiar experience
of medico-legal practice. The situations where arsenic is met with in
largest quantity are the liver, the spleen, and the urine, but above all
the liver. The precise circumstances in which it may be found in one or
another of these quarters have not yet been determined. But in most
cases of acute arsenical poisoning where the search has been made at
all, it has proved successful in the liver. In two late instances I have
readily found arsenic by the process of Marsh or Reinsch in the liver
after four months’ interment.

Since arsenic then is clearly absorbed into the blood, it becomes an
interesting question whether the organization of the blood is thereby
changed. This question cannot be answered with confidence. But in all
probability the blood does undergo some change in its _crasis_; for in
most cases of acute poisoning that fluid is found after death in a
remarkable state of fluidity [see Section on the Morbid Appearances];
and Mr. James observed that if venous or arterial blood be received into
a solution of arsenic, instead of coagulating in the usual way, a
viscous jelly first forms, and lumpy clots separate afterwards.[571]

Our knowledge of the affection induced by the remote action of arsenic
is in some respects vague. Toxicologists have for the most part been
satisfied with calling it a disorder of the general nervous system. When
employed to designate the state of collapse which accompanies or forms
the chief feature of acute cases of poisoning with arsenic, this term is
misapplied. The whole train of symptoms is that not of a general nervous
disorder, but simply of depressed action of the heart. That this is the
chief organ remotely acted on in such cases farther appears probable
from certain physiological experiments, in which it has been remarked,
that immediately after rapid death from arsenic the irritability of the
heart was exhausted or nearly so, while that of the intestines, gullet,
and voluntary muscles continued as usual.[572] As to the singular
symptoms which often arise in the advanced stage of lingering cases, the
term, disorder of the general nervous system, is more appropriately
applied to them. They clearly indicate a deranged state sometimes of the
brain, sometimes of particular nerves.

Arsenic belongs to those poisons which act with nearly the same energy
whatever be the organ or texture to which they are applied. The
experiments of Sproegel,[573] repeated by Jaeger,[574] and by Sir
Benjamin Brodie,[575] leave no doubt, that when applied to a fresh wound
it acts with at least equal rapidity as when swallowed. Although in such
circumstances the signs of irritation are often distinct, yet the
symptoms are on the other hand sometimes more purely narcotic than by
any other mode of administering it,—Sir B. Brodie in particular having
observed loss of sense and motion to be induced, along with occasional
convulsions. Arsenic likewise acts with energy when applied to the
conjunctiva of the eye, as was proved by Dr. Campbell. It acts too with
great energy when inhaled in the state of vapour into the lungs, or in
the form of arseniuretted-hydrogen. It farther acts with violence
through the mucous membrane of the vagina, producing local inflammation,
and the usual constitutional collapse. These facts were determined
experimentally by the Medical Inspectors of Copenhagen on the occasion
of a singular trial which will be noticed afterwards. Arsenic also acts,
as may easily be conceived, when injected into the rectum. And farther,
it acts as a poison, when it is applied to the surface of ulcers, yet
certainly not under all circumstances. Its power of acting through the
unbroken skin has been questioned. Jaeger found that, when it was merely
applied and not rubbed on the skin of animals, it had no effect.[576]
But some cases will be afterwards mentioned which tend to show that the
reverse probably holds in regard to man. According to the last-mentioned
author, who is the only experimentalist that has hitherto examined the
subject consecutively, arsenic is most active when injected into a vein,
or applied to a fresh wound, or introduced into the sac of the
peritonæum; it is less powerful when taken into the stomach; it is still
less energetic when introduced into the rectum; and it is quite inert
when applied to the nerves.

It is a striking fact in the action of that poison that, whatever be the
texture in the body to which it is applied, provided death do not ensue
quickly, it almost always produces symptoms of inflammation in the
stomach; and on inspection after death traces of inflammation are found
in that organ. In some instances of death caused by its outward
application, the inflamed appearance of the stomach has been greater
than in many cases where it had been swallowed. Sproegel met with a good
example of this in a dog killed by a drachm applied to wounds. The whole
stomach and intestines, outwardly and inwardly, were of a deep-red
colour, blood was extravasated between the membranes, and clots were
even found in the stomach.[577]

Of the different preparations of arsenic, it may be said in general
terms, that those are most active which are most soluble. In conformity
with what appears to be a general law in toxicology, the metal itself is
inert. It is difficult to put this fairly to the test, because it is not
easy to pulverize the metal without a sufficient quantity being oxidated
to cause poisonous effects. Bayen and Deyeux, however, found that a
drachm carefully prepared might be given in fragments to dogs without
injuring them; and they once gave a cat half an ounce without any other
consequence than temporary loss of flesh.[578] Its alloys are also
inert. The same experimentalists found it inactive when combined with
tin; and Renault likewise found it inactive when united with sulphur and
iron in the ore mispickel, or arsenical pyrites.[579]

It is probable that all the other preparations of arsenic are more or
less deleterious.

A difference of opinion prevails as to the power of the sulphurets.
Various statements have been published on the subject. But it may be
sufficient to observe, that in consequence of the poisonous properties
of the sulphurets having been imputed to the oxide, with which they are
often adulterated,—Professor Orfila made some experiments with native
orpiment and realgar, and with the sulphuret procured by
sulphuretted-hydrogen gas (which are all pure sulphurets); and he found
that in doses varying from 40 to 70 grains they all caused death in two,
three, or six days, whether they were applied to a wound, or introduced
into the stomach.[580] It may appear at first view singular that the
sulphurets, being insoluble, should be poisonous; but the apparent
anomaly vanishes on considering the experiments of M. Decourdemanche
formerly noticed; which prove that in animal fluids the sulphurets are
rapidly changed into the oxide (see p. 225). The sulphurets, however,
are much less active than the preparations in which the metal exists
already oxidated. Yet in sufficient doses they will prove rapidly fatal.
In the Acta Germanica there is the case of a woman who was killed in a
few hours by realgar, mixed by her step-daughter in red cabbage
soup.[581] The common artificial orpiment procured by sublimation is
very active, in consequence of the oxide mixed with it. Renault found
three grains killed a dog in nine hours.[582]

Among the less active preparations of arsenic may also be enumerated
such of the arsenites and arseniates as are not soluble in water. They
have not indeed been actually tried. But there can be little doubt that
they will prove poisonous; because, though insoluble in water, they are
probably somewhat soluble in the animal juices. We may infer from their
sparing solubility, even in these menstrua, that they will be less
active than the preparations now to be mentioned, which are more
soluble.

These are the alkaline arsenites and arseniates, arsenic acid, arsenious
acid, the black oxide or fly-powder, and arseniuretted-hydrogen. With
regard to arsenic acid, and the alkaline arseniates and arsenites, it is
probable, from their effects in medicinal doses, that they are as active
as the white oxide, if not more so. But they have not been particularly
examined, as they are not objects of great interest to the medical
jurist.

The fly-powder or black oxide is very active. Renault found that four
grains killed a middle-sized dog in ten hours.[583] It has been likewise
known to prove quickly fatal to man. In a French journal there is a case
related which ended fatally in sixteen hours;[584] and in the Acta
Germanica is an account of four persons, who died in consequence of
eating a dish of stewed pears poisoned with it, and of whom three died
within eighteen hours.[585] The dose is not mentioned; but it is
probable from the collateral circumstances that it was not considerable.

Arseniuretted-hydrogen is probably the most active of all arsenical
compounds. The celebrated German chemist Gehlen, having accidentally
inhaled a small portion of it, died in nine days with the usual symptoms
of arsenical poisoning. In Dr. O’Reilly’s case, which proved fatal in
seven days, it was computed that the equivalent of twelve grains of
oxide had been inhaled. And Dr. Schlinder’s patient had inhaled a
quantity of gas corresponding with only an eighth of a grain of
sesquioxide; yet he appears to have made a narrow escape.[586]

It is of some consequence to settle with precision the power of the
white oxide. Witnesses are often asked on trials how small a quantity
will occasion death? It is obvious that this question admits only of a
vague answer: It can be answered at all only in reference to concomitant
circumstances, and even then but presumptively. Nevertheless, it is
right to be aware what facts are known on the subject.

It has been stated by various systematic authors that the white oxide
will prove fatal to man in the dose of two grains. Hahnemann says in
more special terms, that in circumstances favourable to its action four
grains may cause death within twenty-four hours, and one or two grains
in a few days.[587] But neither he nor any of the other authors alluded
to have referred to actual cases. Foderé knew half a grain cause colic
pains in the stomach and dysenteric flux, which continued obstinately
for eight days;[588] and I have related an instance where six persons,
after taking each a grain in wine during dinner, were seriously and
violently affected for twelve hours.[589] Mr. Alfred Taylor mentions
three similar cases occasioned by arsenic accidentally taken in port
wine after dinner,—one, an infant of sixteen months who got about a
third of a grain, another, a lady who took a grain and a half, and the
third, a gentleman, who had two grains and a half,—in all of whom
violent vomiting, and prostration, without pain, occurred for three or
four hours; and the gentleman of the party did not recover for several
days.[590] M. Lachèse mentions his having met with a number of cases of
poisoning from small doses taken in bread or soup; whence he concludes,
that an eighth of a grain taken in food may cause vomiting;—that a
quarter of a grain or twice as much taken once only causes vomiting,
colic, and prostration,—that the same quantity repeated next day renews
these symptoms in such force as to render the individual unfit for work
till three or four days afterwards,—and that four such doses, taken at
intervals during two days, that is between one and a half and two grains
in all, excite acute gastro-enteritis and may prove fatal, since two
individuals who had taken this much died, one in seven weeks, the other
three weeks later.[591] The smallest fatal dose I have found recorded
elsewhere is four grains and a half; and death ensued in six hours
only.[592] But the subject was a child, four years old, and the poison
was taken in solution. Alberti mentions the case of a man who died from
taking six grains; but I am unacquainted with the particulars, not
having seen the original account.[593] Two children, whose cases are
alluded to in the Proceedings of the Academy of Medicine of Paris, died,
the one in two days, the other a day later, after taking rather less
than sixteen grains. The former was four years and a half old, the
latter seven years.[594] Valentini alludes to a case where thirty grains
of the oxide in powder killed an adult in six days.[595] The effects of
medicinal doses, which seldom exceed a quarter of a grain without
causing irritation of the stomach, and the fatal effects of somewhat
larger doses on animals, Renault having found that a single grain in
solution killed a large dog in four hours,[596] must convince every one
that the general statement of Hahnemann cannot be very wide of the
truth. Mr. Taylor thinks his own cases mentioned above throw doubt over
this inference. But it must be remembered, that his patients had dined
just before taking the poison.

It is not improbable that the activity of oxide of arsenic is impaired
by admixture with other insoluble powders. M. Bertrand, conceiving from
some experiments on animals that he had found an antidote for arsenic in
charcoal powder, took no less than five grains of the oxide mixed with
that substance, and he did not suffer any injury, although his stomach
was empty at the time, and he did not vomit.[597] But Orfila afterwards
showed, that other insoluble powders, such as clay, have the same
effect; that no such powder can be of any use if not introduced into the
stomach till after the arsenic is swallowed; and that they appear to act
solely by enveloping the arsenical powder and preventing it from
touching the membrane of the alimentary canal.[598] Although M.
Bertrand’s discovery will not supply the physician with an antidote, the
medical jurist will not lose sight of the interesting fact, that, by
certain mechanical admixtures, arsenic in moderate doses may be entirely
deprived of its poisonous quality. A singular case of recovery from no
less a dose than sixty grains, which happened in the case of an American
physician, probably comes under the same head with the experiments of
Bertrand,—a large quantity of powder of cinchona-bark having been
swallowed along with the arsenic. In this case, however, the symptoms
were severe for three days.[599]

The tendency of habit to modify the action of arsenic is questionable.
So far as authentic facts go, habit has no power of familiarizing the
constitution to its use. One no doubt may hear now and then of
mountebanks who swallow without injury entire scruples or drachms of
arsenic, and vague accounts have reached me of patients who took
unusually large doses for medicinal purposes. But as to facts of the
former kind, it is clear that no importance can be attached to them; for
it is impossible to know how much of the feat is genuine, and how much
legerdemain. With respect to the latter facts, I have never been able to
ascertain any precise instance of the kind; and so far as my own
experience goes, the habit of taking arsenic in medicinal doses has
quite an opposite effect from familiarizing the stomach to it.

Oxide of arsenic being sparingly soluble, its operation is often much
influenced by the condition of the stomach as to food at the time it is
swallowed. If the stomach be empty, it adheres with tenacity to the
villous coat and acts with energy. If the stomach be full at the time,
the first portions that come in contact with the inner membrane may
cause vomiting before it can be diffused, so that the whole or greater
part is discharged. One remarkable case of this nature has been quoted
in page 29. In another, where severe symptoms did supervene, and
recovery was ascribed to the use of magnesia as an antidote, the
favourable result seems to have been really owing to the circumstance,
that the patient had supped heartily not long before taking the
arsenic.[600] An extraordinary case related by Mr. Kerr, in which nearly
three-quarters of an ounce were retained for two hours without causing
any serious mischief, probably comes under the same category; for the
arsenic was taken immediately after a meal, and the stomach was cleared
out by emetics.[601]

In the following detail of the symptoms caused by arsenic in man, its
effects when swallowed will be first noticed; and then some remarks will
be added on the phenomena observed when it is introduced through other
channels.

The symptoms of poisoning with arsenic may be advantageously considered
under three heads. In one set of cases there are signs of violent
irritation of the alimentary canal and sometimes of the other mucous
membranes also, accompanied with excessive general depression, but not
with distinct disorder of the nervous system. When such cases prove
fatal, which they generally do, they terminate for the most part in from
twenty-four hours to three days. In a second and very singular set of
cases there is little sign of irritation in any part of the alimentary
canal; perhaps trivial vomiting or slight pain in the stomach, but
sometimes neither; the patient is chiefly or solely affected with
excessive prostration of strength and frequent fainting; and death is
seldom delayed beyond the fifth or sixth hour. In a third set of cases
life is commonly prolonged at least six days, sometimes much longer, or
recovery may even take place after a tedious illness; and the signs of
inflammation in the alimentary canal are succeeded or become
accompanied, about the second or fourth day or later, by symptoms of
irritation in the other mucous passages, and more particularly by
symptoms indicating a derangement of the nervous system, such as palsy
or epilepsy. The distinctions now laid down will be found in practice to
be well defined, and useful for estimating in criminal cases the weight
of the evidence from symptoms.

1. In one order of cases, then, arsenic produces symptoms of irritation
or inflammation along the course of the alimentary canal. Such cases are
the most frequent of all. The person commonly survives twenty-four
hours, seldom more than three days; but instances of the kind have
sometimes proved fatal in a few hours, and others have lasted for weeks.
On the whole, however, if the case is much shorter than twenty-four
hours, or longer than three days, its complexion is apt to be altered.
In the mildest examples of the present variety recovery takes place
after a few attacks of vomiting, and slight general indisposition for a
day or two.

In regard to the ordinary progress of the symptoms, the first of a
decisive character are sickness and faintness. It is generally thought
indeed that the first symptom is an acrid taste; but this notion has
been already shown to be erroneous. For some account of the sensations
felt in the act of swallowing the poison, the reader may refer to what
has been stated in p. 200. There is no doubt, that in the way in which
arsenic is usually given with a criminal intent, namely, mixed with
articles of food, it seldom makes any impression at all upon the senses
during the act of swallowing.

In some instances the sickness and faintness, particularly when the
poison was taken in solution, have begun a few minutes after it was
swallowed. Thus in a case mentioned by Bernt, in which a solution of
arseniate of potass was taken, the symptoms began violently in fifteen
minutes;[602] in one related by Wildberg, where the oxide was given in
coffee, the person was affected immediately on taking the second
cup;[603] in one related by Mr. Edwards, the patient was taken ill in
eight minutes,[604] in one mentioned by M. Lachèse of Angers, violent
symptoms commenced within ten minutes after the poison was swallowed
with prunes;[605] in a case communicated to me by Mr. J. H. Stallard of
Leicester, the symptoms set in with violence ten minutes after it was
taken dissolved in tea; nay, in a case of poisoning with orpiment in
soup, mentioned by Valentini, the man felt unwell before he had finished
his soup, and set it aside as disagreeable.[606] It is a mistake
therefore to suppose, as I have known some do, that arsenic never begins
to operate for at least half an hour. Nevertheless it must be admitted,
that in general arsenic does not act for half an hour after it is
swallowed.—On the other hand, its operation is seldom delayed beyond an
hour. The following, however, are exceptions to this rule. Lachèse in
the paper quoted above mentions an instance where the interval was two
hours, and where the issue was eventually fatal. The arsenic had been in
very coarse powder. Mr. Macaulay of Leicester has communicated to me a
case where the individual took the poison at eight in the evening, went
to bed at half-past nine, and slept till eleven, when he awoke with
slight pain in the stomach, vomiting, and cold sweats. In this instance
the dose was seven drachms, and death took place in nine hours. M.
Devergie has related a similar case of poisoning with the sulphuret,
where the symptoms did not begin for three hours; and here too the
patient fell asleep immediately after swallowing the poison.[607]
Professor Orfila has noticed an instance, to be quoted afterwards, where
there appears to have been scarcely any symptom at all for five
hours[608] (p. 243). I suspect we must also consider as an instance of
the same kind the case which gave occasion to the trial of Mrs. Smith
here in 1827. A white draught was administered in a suspicious manner at
ten in the evening; the girl immediately went to bed; and no symptoms
appeared till six next morning, from which time her illness went on
uninterruptedly.[609] In three of the preceding cases it will be
remarked that sleep intervened between the taking of the poison and the
invasion of the symptoms; and it is therefore not improbable that the
reason of the retardation is the comparative inactivity of the animal
system during sleep.—In voluntary poisoning, as in a case related by Dr.
Roget, a slight attack of sickness or vomiting occasionally ensues
immediately after solid arsenic is swallowed, and some time before the
symptoms commence regularly.[610]

The observations now made will often prove important for deciding
accusations of poisoning; for pointed evidence may be derived from the
commencement of the symptoms, after a suspected meal, corresponding or
not corresponding with the interval which is known to elapse in
ascertained cases. The reader will see the effect of such evidence in
attaching guilt to the prisoner in the case of Margaret Wishart, which I
have detailed elsewhere.[611] In the trial of Mrs. Smith, the want of
the correspondence just mentioned contributed greatly to her acquittal;
for the symptoms of poisoning did not begin till more than eight hours
after the only occasion on which the prisoner was proved to have
administered any thing in a suspicious manner. As I was not at the time
acquainted with any parallel case except that recorded by Orfila, I
hesitated to ascribe the symptoms to the draught; and consequently, as
the other medical witnesses felt the same hesitation on the same
account, the proof of administration was considered to have failed. I am
not sure that I should have now felt the same difficulty. The
intervening state of sleep probably affords an explanation of the long
interval; and the cases noticed by Mr. Macaulay and M. Devergie are
parallel, though the interval in them was certainly not so great.—There
is a limit, however, to the possible interval in such cases. It seems
impossible that the action of the poison shall be suspended for three
entire days. Yet death has been ascribed to arsenic in such
circumstances. A child 3½ years old having swallowed eight grains with
bread and butter, but being soon made to vomit forcibly by emetics,
presented no decided symptom at the time, or for three days more; but on
the fourth day difficult breathing ensued, with anxiety of expression,
frequency of the pulse, and heat of the skin; and next day death took
place. There was no morbid appearance found in the body.[612] I do not
know of any parallel instance of death from arsenic, and cannot admit
that the poison was the cause of the symptoms and fatal event.

Soon after the sickness begins, or about the same time, the region of
the stomach feels painful, the pain being commonly of a burning kind,
and much aggravated by pressure. Violent fits of vomiting and retching
then speedily ensue, especially when drink is taken. There is often also
a sense of dryness, heat, and tightness in the throat, creating an
incessant desire for drink; and this affection often precedes the
vomiting. Occasionally it is wanting, at other times so severe as to be
attended with suffocation and convulsive vomiting at the sight of
fluids.[613] Hoarseness and difficulty of speech are commonly combined
with it. The matter vomited is greenish or yellowish; but sometimes
streaked or mixed with blood, particularly when the case lasts longer
than a day.

In no long time after the first illness diarrhœa generally makes its
appearance, but not always. In some cases, instead of it, the patient is
tormented by frequent, ineffectual calls: in others the great intestines
are scarcely affected. About this time the pain in the stomach is
excruciating, and is often likened by the sufferer to a fire burning
within him. It likewise extends more or less downwards, particularly
when the diarrhœa or tenesmus is severe; and the belly is commonly tense
and tender, sometimes also swollen, though not frequently,—sometimes
even on the contrary drawn in at the navel.[614] When the diarrhœa is
severe, the anus is commonly excoriated and affected with burning
pain.[615] In such cases the burning pain may extend along the whole
course of the alimentary canal from the throat to the anus. Nay at times
the mouth and lips are also inflamed, presenting dark specks or
blisters.[616]

Sometimes there are likewise present signs of irritation of the lungs
and air-passages,—almost always shortness of breath (which, however, is
chiefly owing to the tenderness of the belly),—often a sense of
tightness across the bottom of the chest, and more rarely decided pain
in the same quarter, darting also through the upper part of the chest.
Sometimes pneumonia has appeared a prominent affection during life, and
been distinctly traced in the dead body.[617]

In many instances, too, the urinary passages are affected, the patient
being harassed with frequent, painful and difficult micturition,
swelling of the penis, and pain in the region of the bladder, or, if a
female, with burning pain of the vagina and excoriation of the
labia.[618] Sometimes the irritation of the urinary organs is so great
as to be attended with total suppression of urine, as in a case related
by Guilbert of Montpellier, in which this symptom continued several
days.[619] During the late contentions among chemists, physiologists,
and physicians, occasioned by the case of Madame Lafarge, it was alleged
by Flandin and Danger that in animals the urine is always suppressed, by
Orfila that it is always secreted, by Professor Delafond of the Alfort
Veterinary School, that it is never suppressed, but always diminished,
and sometimes even to a sixth of the natural quantity.[620] There is,
however, no invariable rule in the matter. And in fact, urinary symptoms
are seldom present unless the lower bowels are likewise strongly
irritated; but are then seldom altogether wanting. They are rarely well
marked in cases of the present variety, unless life is prolonged three
days or more.

When symptoms of irritation of the alimentary canal have subsisted a few
hours, convulsive motions often occur. They commence on the trunk,
afterwards extend over the whole body, are seldom violent, and generally
consist of nothing else than tremors and twitches. Cramps of the legs
and arms, a possible concomitant of every kind of diarrhœa, is
peculiarly severe and frequent in that caused by arsenic.

The general system always sympathizes acutely with the local
derangement. The pulse commonly becomes very small, feeble and rapid
soon after the vomiting sets in; and in no long time it is often
imperceptible. This state is naturally attended with great coldness,
clammy sweats, and lividity of the feet and hands. Another symptom
referrible to the circulation which has been observed, though, very
rarely, is palpitation.[621]

The countenance is commonly collapsed from an early period, and almost
always expressive of great torture and extreme anxiety or despair; the
eyes are red and sparkling; the conjunctiva often so injected as to seem
inflamed; the tongue and mouth parched; and the velum and palate
sometimes covered with little white ulcers.

Delirium sometimes accompanies the advanced stage, and stupor also is
not unfrequent. Coma occasionally precedes death, as in Mr. Stallard’s
case (p. 235), in which the symptoms of irritation, at first very
violent, gradually gave place in two hours to complete insensibility,
proving fatal in two hours more. Very often, however, the patient
remains quite sensible to the last. Death in general comes on calmly,
but is sometimes preceded by a paroxysm of convulsions.[622] In some
cases it takes place quite unexpectedly, as if from sudden deliquium, as
in a case mentioned by Dr. Dymock of this city. The patient, a girl who
had taken two ounces intentionally, rose from her bed without help two
hours and a half afterwards, went to a chair at the fireside, and had
scarce sat down when she expired.[623]

Various eruptions have at times been observed, especially in those who
survive several days; but they are more frequent in the kind of cases to
be considered afterwards, in which life is prolonged for a week or more.
The eruptions have been variously described as resembling petechiæ, or
measles, or red miliaria, or small-pox. In the case already quoted from
Guilbert a copious eruption of miliary vesicles appeared on the fifth
day, and for fifteen days afterwards. They were attended with
perspiration and abatement of the other symptoms, and followed with
desquamation of the cuticle. Another external affection which may be
noticed is general swelling of the body. Several cases of this nature
have been described by Dr. Schlegel of Meiningen; and in one of them the
swelling, particularly round the eyes, appears to have been
considerable.[624]

In some cases of the kind now under consideration a short remission or
even a total intermission of all the distressing symptoms has been
witnessed, particularly when death is retarded till the close of the
second or third day.[625] This remission, which is accompanied with
dozing stupor, is most generally observed about the beginning of the
second day. It is merely temporary, the symptoms speedily returning with
equal or increased violence. Sometimes the remission occurs oftener than
once, as in a case related in the London Medical and Physical Journal.
The patient, a child seven years old, lived thirty-six hours in a state
of alternate calm and excitement; and during the state of calm no pulse
was to be felt at the wrists.[626]—So far as at present appears a long
intermission is impossible.

In cases such as those now described death often occurs about
twenty-four hours after the poison is swallowed, and generally before
the close of the third day. But on the one hand life has been sometimes
prolonged, without the supervention of the symptoms belonging to a
different variety of cases, for five or six days,[627] nay perhaps even
for several weeks. And, on the other hand, the symptoms of irritation of
the alimentary canal are sometimes distinct, although death takes place
in a much shorter period than twenty-four hours. Metzger has related a
striking case, fatal in six hours, in which the symptoms were acute
colic pain, violent vomiting, and profuse diarrhœa;[628] and Wildberg
has related a similar case fatal in the same time.[629] Hohnbaum
describes another fatal in five hours;[630] and I met with as brief a
case in this city in 1843, where all the usual symptoms of irritation in
the stomach and bowels were violent. These symptoms were also present at
first in Mr. Stallard’s case, which was fatal in four hours; Pyl has
recorded one, where all the signs of irritation in the stomach and
intestines were present, except vomiting, and which proved fatal in
three hours;[631] and Dr. Dymock met here with a similar instance which
lasted only two hours and a half.[632] This is one of the shortest
undoubted cases of poisoning from arsenic I have hitherto found in
authentic records. Dr. Male mentions one, which was fatal in four
hours;[633] Wepfer another equally short;[634] Johnston another fatal in
three hours and a half;[635] and I shall presently mention others
without symptoms of irritation which ended fatally in two, five, or six
hours [p. 242].[636] Wibmer has even quoted a case fatal in half an
hour; but there seems to have been some doubt whether the poison taken
was arsenic.[637]

Such is an account of the symptoms of poisoning by arsenic in their most
frequent form. It will of course be understood, that they are liable to
a great variety as to violence, as well as their mode of combination in
actual cases;—and that they are by no means all present in every
instance. The most remarkable and least variable of them all, pain and
vomiting, are sometimes wanting. A case, in which pain was not felt in
the stomach, even on pressure, although the other symptoms of
inflammation were present, has been briefly described in the Medical
Repository.[638] A similar case fatal in fourteen hours and a half,
where there was much vomiting and some heat in the stomach, but no pain
or tenderness, has been related by Dr. E. Gairdner.[639] Another very
striking example of this anomalous deficiency has been detailed by Dr.
Yellowly. A lad sixteen years old died twenty-one hours after swallowing
half an ounce of the white oxide; and the presence of inflammation was
denoted all along by sickness, vomiting, purging, and heat in the
tongue; yet he never complained of pain, neither did he ever seem to his
friends to suffer any. Another anomaly in the case was, that the pulse,
contrary to what is usual, was very slow: twelve hours after he took the
poison, the pulse was 40, and two hours before death it was so slow as
30.[640] These deviations from the ordinary course of the symptoms are
taken notice of merely to put the practitioner on his guard, and prevent
the medical jurist from drawing hasty conclusions. Upon the whole, they
are rare; and the symptoms of poisoning by arsenic are in general very
uniform.

2. The second variety of poisoning with arsenic includes a few cases in
which the signs of inflammation are far from violent or even altogether
wanting, and in which death ensues in five or six hours or a little
more,—at a period too early for inflammation to be always properly
developed. The symptoms are then generally obscure, and are referrible
chiefly to the mode of action, which is probably the cause of death in
most cases,—a powerful debilitating influence on the circulation, or on
the nervous system.

These symptoms occasionally amount to absolute narcotism, as in some of
the animals on which Sir B. Brodie experimented. Thus, when he injected
a solution of the oxide into the stomach of a dog, the pulse was
rendered slow and intermitting; the animal became palsied in the
hind-legs, lethargic, and in no long time insensible, with dilated
pupils; and soon afterwards it was seized with convulsions, amidst which
it died, fifty minutes after the poison was administered.[641] In man
the symptoms very seldom resembled so closely those of the narcotic
poisons. In Mr. Stallard’s case, however, formerly mentioned, the
symptoms of irritation which appeared at first speedily gave place to
complete insensibility for two hours before death (pp. 235, 238), a
similar instance has been related in Henke’s Journal. A young man who
got an arsenical solution from an old woman to cure ague, was attacked
after taking it with vomiting and loud cries, afterwards with incoherent
talking, then fell into a deep sleep, and finally perished in
convulsions in five hours.[642]

In some cases of the kind now under consideration, one or two attacks of
vomiting occur at the usual interval after the taking of the poison; but
it seldom continues. The most uniform and remarkable affection is
extreme faintness, amounting at times to deliquium. Occasionally there
is some stupor, or rather oppression, and often slight convulsions. Pain
in the stomach is generally present; but it is slight, and seldom
accompanied with other signs of internal inflammation. Death commonly
takes place in a few hours. Yet, even when it is retarded till the
beginning of the second day, the faintness and stupor are sometimes more
striking features in the case than the symptoms of inflammation in the
stomach.

This variety of poisoning has been hitherto observed only under the
three following circumstances,—when the dose of poison was large,—when
it was in little masses,—or when it was in a state of solution. The mode
in which the first and last circumstances operate is evident; they
facilitate the absorption of a large quantity of arsenic in a short
space of time, so that its remote action begins before local
inflammation is fully developed. But it is not easy to see how any such
effect can flow from the arsenic being in little masses. It is also to
be observed that none of the circumstances here mentioned is invariable
in its operation. An instance is related in Rust’s Magazine, of the
customary signs of irritation having been produced even by the
solution.[643]

On the whole, the present variety of poisoning is rather uncommon, and
indeed, although the attention of the profession was pointedly called to
it even in the first edition of the present work, its existence does not
seem to be so generally known as it ought to be.[644] It may be right
therefore to specify the cases which have been published.

In the Medical and Philosophical Journal of New York,[645] is related
the case of a druggist, who swallowed an ounce of powdered arsenic at
once, and died in eight hours, after two or three fits of vomiting,
with slight pain and heat in the stomach.—A similar case has been
related by Metzger. A young woman died in a few hours, after suffering
from trivial diarrhœa, pain in the stomach and strangury; her death
was immediately preceded by slight convulsions and fits of
suffocation; and on dissection the stomach and intestines were found
quite healthy. Half an ounce of arsenic was found in the
stomach.[646]—A third case similar in its particulars to the two
preceding was submitted to me for investigation by the sheriff of this
county in 1825. The subject, a girl fourteen years of age, took about
ninety grains, and died in five hours, having vomited once or twice,
complained of some little pain in the belly, and been affected towards
the close with great faintness and weakness. The stomach and
intestines were healthy.[647]—A fourth case allied to these is
succinctly told in the Medical and Physical Journal. The person
expired in five hours; and vomiting never occurred, even though
emetics were given.[648]—A fifth has been related by M. Gérard of
Beauvais. The subject was a man so addicted to drinking, that his
daily allowance was a pint of brandy. When first seen, there was so
much tranquillity, that doubts were entertained whether arsenic had
really been swallowed; but at length he was discovered actually
chewing it. This state continued for nearly five hours, when some
vomiting ensued: coldness of the extremities and spasmodic flexion of
the legs soon followed; and in a few minutes more he expired.[649]—A
sixth and very singular case of the same kind has been described by
Orfila. The individual having swallowed three drachms at eight in the
morning, went about for two hours bidding adieu to his friends and
telling what he had done. He was then prevailed on to take emetics and
diluents, which caused free, easy vomiting. He suffered very little
till one, when he became affected with constricting pain and burning
in the stomach, feeble pulse, cold sweats, and cadaverous expression,
under which symptoms he died four hours later.[650] Orfila justly
designates this case as the most extraordinary instance of poisoning
with arsenic that has come under his notice.—A seventh is related by
Mr. Holland of Manchester where death took place in the course of
eight or nine hours, and the symptoms were at first some vomiting,
afterwards little else but faintness, sickness, a sullen expression,
and a general appearance which led those around to suppose the
individual intoxicated.[651]—Professor Chaussier has described a still
more striking case than any yet mentioned. A stout middle-aged man
swallowed a large quantity of arsenic in fragments and died in a few
hours. He experienced nothing but great feebleness and frequent
tendency to fainting. The stomach and intestines were not in the
slightest degree affected during life; and no morbid appearance could
be discovered in them after death,[652]—A similar instance not less
remarkable has been communicated to me by Mr. Macauley of Leicester,
where the individual died with narcotic symptoms only within two hours
after taking nearly a quarter of a pound of arsenic.—Another fatal in
four hours has been described by Mr. Wright, where the symptoms were
vomiting under the use of emetics, great exhaustion, feeble hurried
pulse, cold sweating, drowsiness and finally stupor. In this case the
quantity of arsenic taken was about an ounce.[653]—Another of the same
nature is recorded by Morgagni. An old woman stole and ate a cake,
which had been poisoned with arsenic for rats. She died in twelve
hours, suffering, says Morgagni, rather from excessive prostration of
strength than from pain or convulsions.[654]—The following case
related by M. Laborde is most remarkable in its circumstances. A young
woman was caught in the act of swallowing little fragments of arsenic,
and it afterwards appeared that she had been employed most of the day
in literally cracking and chewing lumps of it. When the physician
first saw her the countenance expressed chagrin and melancholy, but
not suffering. After being forced to drink she vomited a good deal,
but without uneasiness. Two hours afterwards her countenance was
anxious; but she did not make any complaint, and very soon resumed her
tranquillity. Five hours after the last portions of the poison were
taken she became drowsy, then remained perfectly calm for four hours
more, and at length on trying to sit up in bed, complained of slight
pain in the stomach, and expired without agony. A clot of blood was
found in the stomach.[655]—Dr. Platner of Pavia describes a case,
fatal probably in five hours, where the symptoms were a tranquil,
melancholic expression, great coldness, paleness of the features, slow
languid pulse, retarded respiration, and suppression of urine, but no
pain or swelling of the belly, and no diarrhœa till near death, when
there was one copious fluid evacuation.[656]—Lastly, Dr. Choulant has
related the case of an elderly female who got a thimbleful of arsenic
in soup, and died in eleven hours, affected with occasional, easy
vomiting, uneasiness, thirst, and undefinable uneasiness in the chest,
but without pain of any kind, or any other complaint.[657]

The cases of which an abstract has here been given, will, it is
apprehended, be sufficient to correct the erroneous impression of
many,—that arsenic, when it proves fatal, always produces violent and
well-marked symptoms. It will of course be understood that cases of the
present kind pass by insensible shades into those of the first
class,—the following, for example, being intermediate between the two. A
young man had frequent vomiting and diarrhœa, which were supposed to
depend on indigestion merely, as the countenance was calm, without any
appearance of suffering, the appetite tolerable, and the abdomen quite
free of tenderness. The pulse, however, quickly sunk, the voice failed,
and death took place in eleven hours; and on dissection about twenty
grains of arsenic were found in the stomach with strong signs of
inflammation.[658]—In a case communicated to me by a former pupil, Mr.
Adams of Glasgow, that of a woman who died five hours after taking six
drachms of arsenic, there was some vomiting not long after she swallowed
it; but subsequently she presented no prominent symptoms except a
ghastly expression, redness of the eyes, a fluttering pulse and extreme
prostration, until within half an hour before death, when the action of
an emetic and the stomach-pump was followed by severe burning pain.

3. The third variety of poisoning with arsenic places in a clear point
of view its occasional action on the nervous system. This occurs chiefly
in persons who, from having taken but a small quantity, or from having
vomited soon after, are eventually rescued from destruction; but it has
also been met with in some cases where death ensued after a protracted
illness.

In such cases the progress of the poisoning may be divided into two
stages. The first train of symptoms is exactly that of the first or
inflammatory variety, and is commonly developed in a very perfect and
violent form. In the second stage the symptoms are referrible to nervous
irritation.

These generally come on when the former begin to recede; yet sometimes
they make their appearance earlier, while the signs of inflammation in
the alimentary canal continue violent; and more rarely both classes of
symptoms begin about the same period. The nervous affection varies in
different individuals. The most formidable is coma; the slightest, a
peculiar, imperfect palsy of the arms or legs, resembling what is
occasioned by the poison of lead; and between these extremes have been
observed epileptic fits, or tetanus, or an affection resembling
hysteria, or mania. As these affections are of much interest, in respect
to the evidence of poisoning from symptoms, it may be well to relate in
abstract a few characteristic examples of each.

A good example of epilepsy supervening on the ordinary symptoms of
inflammation has been minutely related by Dr. Roget. A girl swallowed a
drachm of arsenic, and was in consequence attacked violently with the
usual symptoms of irritation in the whole alimentary canal. After being
ill about twenty-four hours, she experienced several distinct remissions
and had some repose, attended with fainting. In twelve hours more she
began to improve rapidly; the pain subsided, her strength and spirits
returned, and the stomach became capable of retaining liquids. So far
this patient laboured under the common effects of arsenic. But a new
train of symptoms then gradually approached. Towards the close of the
second day she was harassed with frightful dreams, starting from sleep,
and tendency to faint; next morning with coldness along the spine,
giddiness, and intolerance of light; and on the fourth day with aching
of the extremities and tingling of the whole skin. These symptoms
continued till the close of the sixth day, when she was suddenly seized
with convulsions of the left side, foaming at the mouth, and total
insensibility. The convulsions endured two hours, the insensibility
throughout the whole night. Next evening she had another and a similar
fit. A third, but slighter fit occurred on the morning of the tenth;
another next day at noon; and they continued to return occasionally till
the nineteenth day. For some time longer she was affected with tightness
across the chest and stomach complaints; but she was eventually restored
to perfect health.[659]

A characteristic set of similar cases, which occurred in London in 1815,
has been related in a treatise on arsenic by Mr. Marshall.[660] They
were the subject of investigation on the trial of Eliza Fenning, a
maid-servant, who attempted to poison the whole of her master’s family
by mixing arsenic with a dumpling, and whose condemnation excited an
extraordinary sensation at the time, as many persons believed her to be
innocent. Five individuals partook of the poisoned dish, and they were
all violently seized with the usual inflammatory symptoms. But farther,
one had an epileptic fit on the first day, which returned on the second,
and he had besides frequent twitches of the muscles of the trunk, a
feeling of numbness in one side, and heat and tingling of the feet and
hands. Another had tremors of the right arm and leg on the first day,
and several epileptic fits in the course of the night. During the next
fifteen days he had a paroxysm every evening about the same hour; which
returned after an intermission of eight days, and frequently for several
months afterwards.

In the following set of cases the nervous symptoms exhibited a singular
combination of delirium, convulsions, tetanus, and coma, such as is
frequently met with in paroxysms of hysteria; but the cases are probably
not pure examples of poisoning with arsenic, for liver of sulphur was
administered as a remedy to a considerable amount. Three servant girls
in one of the Hebrides ate a mixture of lard, sugar, and arsenic, which
had been laid for destroying rats. The ordinary signs of irritation in
the stomach ensued, but on the following morning were greatly mitigated.
They were then ordered twelve grains of liver of sulphur every other
hour. Soon afterwards the inflammatory symptoms became more severe, the
root of the tongue swelled and inflamed, and in the afternoon two of
them lost the power of speech and swallowing, and were attacked with
locked-jaw and general convulsions. The third had not locked-jaw, but
was otherwise similarly, affected. On the morning of the third day one
of the two former was found comatose, with continuance of the locked-jaw
and occasional return of convulsions; and on being roused by venesection
and the cold affusion, she complained of headache and heat in the
throat. The sulphuret of potass, which had been discontinued on account
of the locked-jaw, was then resumed. On the evening of the fourth day
the headache increased, and the patient became delirious and
unmanageable. The cold affusion, however, soon restored her again to her
senses, and from that time her recovery was progressive. In the other
patients the symptoms were similar, but less violent. In these instances
the evidence of an injury of the nervous system was decisive; but it may
be doubted whether the symptoms were not, in part at least, owing to the
sulphuret of potass, which has been already described as an active
poison, capable of inducing convulsions and tetanus. Its properties were
not generally known in this country at the time the cases in question
happened.[661]

Sometimes the convulsions caused by arsenic assume the form of pure
tetanus. At least a case of this affection is noticed by Portal.[662] He
has given only a mere announcement of it; and I have not hitherto met
with a parallel instance in authors.

A common nervous affection in the advanced stage of the more tedious
cases of poisoning with arsenic is partial palsy. Palsy in the form of
incomplete paraplegia is a very common symptom even of the early stage
in animals, and has been also sometimes observed during that stage in
man. The paralytic affection, however, is more frequent in the advanced
stage; and in those persons who recover, an incomplete paralysis of one
or more of the extremities, resembling lead palsy, is often the last
symptom which continues.

Dehaen relates a distinct example of this disorder occurring in a female
who took a small quantity of arsenic by mistake. The ordinary signs of
inflammation were soon subdued, and for three days she did well; but on
the fourth she was attacked with cramps, tenderness, and weakness of the
feet, legs and arms, increasing gradually till the whole extremities
became at length almost completely palsied. At the same time the cuticle
desquamated. But the other functions continued entire. The power of
motion returned first in the hands, then in the arms, and she eventually
recovered; but eleven months passed before she could quit the hospital
where Dehaen treated her.[663]

An excellent account of a set of similar cases has been given by Dr.
Murray of Aberdeen. They became the subject of judicial inquiry on the
trial of George Thom, who was condemned in 1821 at the Aberdeen autumn
circuit for poisoning his brother-in-law. Four persons were
simultaneously affected about an hour after breakfast with the primary
symptoms of poisoning with arsenic, and some in a very violent degree.
But besides these symptoms, in all of them the muscular debility was
great; and in two it amounted to true partial palsy. One of them lost
altogether the power of the left arm, and six months after, when the
account of the cases was published, he was unable to bend the arm at the
elbow-joint. The other had also great general debility and
long-continued numbness and pains of the legs.[664]

An interesting case of the same nature with these was lately submitted
to me on the part of the crown. A man after taking arsenic was attacked
with vomiting, purging, and other symptoms of abdominal irritation,
which were mistaken for dysentery. Five days afterwards he began to
suffer also from feebleness of the limbs; amounting almost to palsy.
Subsequently an improvement slowly took place; but he continued to
suffer under irritative fever, diarrhœa, and faintness. Several weeks
later the diarrhœa abated, but he had great stiffness, numbness, and
loss of power in the joints of the hands and feet. Two months after he
first took ill, and while he was slowly recovering from this paralytic
affection, arsenic was again administered and proved fatal in eighteen
hours.

Another, somewhat similar to the preceding, has been related by M.
Lachèse of Angers. Two people took about half a grain in soup twice a
day for two days, and were attacked with the usual primary symptoms. One
of them died in ten weeks, gradually worn out, but without any
particular nervous affection. The other was seized with convulsions, and
afterwards with almost complete palsy of the limbs.[665]—A well-marked
case of the same nature has been noticed by Professor Bernt. It was the
case formerly alluded to as arising from an over-dose of the arseniate
of potass. The paralytic affection consisted in the loss of sensation
and of the power of motion in the hands, and of the loss of motion in
the feet, with contraction of the knee-joints. The issue of the case is
not mentioned.[666]—Dr. Falconer observes in his essay on Palsy, that he
had repeatedly witnessed local palsy after poisoning with arsenic, and
alludes to one instance in which the hands only were paralysed, and to
two others in which the palsy spread gradually from the fingers upwards
till the whole arms were affected.[667]—On the whole, then, local palsy
is the most frequent of the secondary effects of arsenic.

It is sometimes very obstinate, as the cases related by Dehaen and
Murray will show. But it even appears to be sometimes incurable. For in
the German Ephemerides there is related the case of a cook, who after
suffering from the usual inflammatory symptoms, was attacked with
perfect palsy of the limbs, and had not any use of them during the rest
of her life, which was not a short one.[668]

Occasionally, instead of being palsied, the limbs are rigidly bent and
cannot be extended.[669] They were contracted, as well as palsied in the
case noticed by Bernt.

The last nervous affection to be mentioned is mania. The only instance I
have hitherto found of that disease arising from arsenic is related by
Amatus Lusitanus. He has not recorded the particulars of the case, but
merely observes that the individual became so outrageously mad as to
burst his fetters and jump out of the window of his apartment.[670]
According to Zacchias, Amatus was not very scrupulous in his adherence
to fact in recording cases.

The preceding remarks contain all that is known with certainty of the
effect of arsenic on man when it is swallowed. Independently of the
obvious nervous disorders which succeed the acute symptoms, other morbid
affections of a more obscure character and chronic in their nature have
been sometimes observed or supposed to arise from this poison.—Among
these the most unequivocal is dyspepsia. Irritability of the stomach,
attended with constant vomiting of food, has been occasionally noticed
for a long time after. Wepfer has described two cases in which the
primary symptoms were followed, in one by dyspepsia of three years’
standing, in the other by emaciation and an anomalous fever, which ended
fatally in three years.[671]—Hahnemann farther adds, that in the
advanced stage the hair sometimes drops out, and the cuticle
desquamates, accompanied occasionally with great tenderness of the
skin;[672] and Wibmer mentions a case of the kind, where not the cuticle
and hair only, but likewise even the nails, fell off.[673] Desquamation
of the cuticle and dropping of the nails are at times produced by the
continued use of arsenic in medicinal doses.—Other effects have likewise
been ascribed to its employment medicinally. Thus passing over what was
stated by its opponents at the time when its introduction into the
materia medica was made the subject of controversy over Europe,
Broussais maintained that it causes chronic inflammation of the stomach
or intestines;[674] and Dr. Astbury inferred, from an instance which
fell under his notice, that it may bring on dropsy.[675] Neither of
these ideas is supported by the general experience of the profession;
and although some persons even of late have alleged that those, who take
it medicinally to any material amount, invariably die soon after of some
chronic disease,[676] there cannot be a doubt, that, under proper
restriction, it is both an effectual and a safe remedy.—A case where
salivation, with fetor and superficial ulceration of the gums, seemed to
have been produced by arsenic, was lately published in an English
Journal.[677]

In the present place may also be considered the supposed effects of the
celebrated _Aqua Toffana_ or _Acquetta di Napoli_, a slow poison, which
in the sixteenth century, was believed to possess the property of
causing death at any determinate period, after months for example, or
even years, of ill health, according to the will of the poisoner.

The most authentic description of the aqua Toffana ascribes its
properties to arsenic. According to a letter addressed to Hoffman by
Garelli, physician to Charles the Sixth of Austria, that Emperor told
Garelli, that, being governor of Naples at the time the aqua Toffana was
the dread of every noble family in the city, and when the subject was
investigated legally, he had an opportunity of examining all the
documents,—and that he found the poison was a solution of arsenic in
_aqua cymbalariæ_.[678] The dose was said to be from four to six drops.
It was colourless, transparent, and tasteless, like water.

Its alleged effects are thus eloquently described by Behrends, a writer
in Uden and Pyl’s Magazin. “A certain indescribable change is felt in
the whole body, which leads the person to complain to his physician. The
physician examines and reflects, but finds no symptom, either external
or internal,—no constipation, no vomiting, no inflammation, no fever. In
short, he can advise only patience, strict regimen, and laxatives. The
malady, however, creeps on; and the physician is again sent for. Still
he cannot detect any symptom of note. He infers that there is some
stagnation or corruption of the humours, and again advises laxatives.
Meanwhile the poison takes firmer hold of the system; languor,
wearisomeness and loathing of food continue; the nobler organs gradually
become torpid, and the lungs in particular at length begin to suffer. In
a word, the malady is from the first incurable; the unhappy victim pines
away insensibly, even in the hands of his physician; and thus is he
brought to a miserable end through months or years, according to his
enemy’s desire.”[679] An equally vigorous and somewhat clearer account
of the symptoms is given by Hahnemann. “They are,” says he, “a gradual
sinking of the powers of life, without any violent symptom,—a nameless
feeling of illness, failure of the strength, slight feverishness, want
of sleep, lividity of the countenance, and an aversion to food and drink
and all the other enjoyments of life. Dropsy closes the scene, along
with black miliary eruptions, and convulsions, or colliquative
perspiration and purging.”[680]

Whatever were its real effects, there appears no doubt it was long used
secretly in Italy to a fearful extent, the monster who has given her
name to it having confessed that she was instrumental in the death of no
less than six hundred persons. It has been already stated, however [p.
40], that she owed her success rather to the ignorance of the age than
to her own dexterity. At all events, the art of secret poisoning cannot
now be easily practised. Indeed even the vulgar dread of it is almost
extinct. Partly on account of the improvement in general knowledge and
chiefly in consequence of the subtility and precision, which the
refinement of modern physic and chemistry have introduced into
medico-legal inquiries, it is rare that the suspicious scrutiny of the
world now “recognizes in the accounts of the last illness of popes and
princes the effects of poison insidiously introduced into the
body.”[681]

I may add in conclusion, that I was consulted a few years ago on the
part of the crown in a case which considerably resembled the effects
ascribed in former times to the aqua Toffana, except that it was more
acute in its character and swifter in its progress. As this case will
probably be found to represent pretty nearly the usual effects of
moderate doses frequently repeated, it is here given in some detail.

A woman of indifferent character married a young man in circumstances
which led to a breach between him and his relatives; but the pair
appeared to live on good terms with one another. Eighteen months after
the marriage she was attacked with sickness and faintness; and on the
fourth day of this illness, while she was recovering, the symptoms
unexpectedly increased, and she seemed very unwell. On the fifth day she
became extremely weak, and suffered much from yellow vomiting. On the
seventh, when she was first visited by a medical man, she had frequent
vomiting, burning in the stomach, a yellow tongue, flushed countenance,
hot skin, and hurried pulse. On the ninth the throat was sore and red,
and the expression anxious; and next day the soreness was greater,
affected the nose and mouth also, and was attended with excoriation of
the lips and nostrils, swelling of the glands of the throat, dimness of
sight, and great exhaustion. On the eleventh day, while previously again
getting better, she became much worse, and suffered greatly from
excessive vomiting, pain in the stomach, and an increase of the other
symptoms. On the thirteenth she was very hoarse, and despaired of
recovery. Next day she was occasionally incoherent, and had twitches of
the facial muscles; the hands and face were swelled, the eyelids dingy,
the conjunctivæ injected, and the nails blue. On the morning of the
fifteenth there was for two hours violent delirium and fierce maniacal
excitement, which were succeeded by coma, and this by death in the
course of the evening. There was no diarrhœa, or urinary complaint, and
no paralysis or eruption on the skin. A variety of circumstances of a
general nature, which it would be out of place to enumerate here,—the
detection of arsenic in various articles of which the woman had
partaken, and in which the arsenic had been dissolved sometimes simply,
sometimes with the aid of an alkali,—together with the fact, that the
body five months after death was found preserved from decay, as it is
now well known to be in most cases of arsenical poisoning,—left little
doubt that the woman died of the effects of arsenic taken in several
small doses at distant intervals, although none could be detected in the
stomach or intestines. The case did not go to trial, owing to the death
of an essential witness.

The effects of arsenic on man, when introduced into the living body
through other channels besides the stomach, will now require some
observations. It is necessary for the medical jurist to be well
acquainted with them, because there is hardly an accessible part of the
human body to which this poison has not been applied either accidentally
or by design. When some account was given of its comparative action on
the different tissues of animals, it was observed that arsenic acts when
applied to a wound or ulcer, to the peritonæal membrane, to the eye, and
to the vagina. On man it has been known to act through an ulcer or
wound, the inner membrane of the rectum, the membrane of the vagina, the
membrane of the air-tubes, the membrane of the nose, and even the sound
skin.

Many persons have been poisoned by the application of arsenic to
surfaces deprived of the cuticle, such as blistered surfaces, eruptions,
ulcers, or wounds. When applied in this manner it commonly induces both
local inflammation and constitutional symptoms. Amatus Lusitanus relates
the case of a young man, who, against the advice of his physician,
anointed an itchy eruption of the skin with an arsenical ointment, and
next day was found dead in bed.[682] A similar case, not so rapidly
fatal, has been recorded by Wepfer. A girl, affected with psoriasis of
the scalp, had it rubbed with a liniment of butter and arsenic. In a
short time she was seized with acute pain and swelling of the whole
head, fainting-fits, restlessness, fever, delirium, and she died in six
days.[683] Zitmann has noticed the cases of two children, eight and ten
years of age, who were killed by the application of an arsenical
solution to a similar eruption of the head.[684] And Belloc relates the
case of a woman who, trying to cure an inveterate itch with an arsenical
lotion, was attacked in consequence with severe erysipelas of the whole
body, succeeded by tremors and gradual exhaustion of the vital powers,
ending fatally in two years.[685] M. Errard of Injurieux in France
lately met with two cases, where, in consequence of a freshly blistered
surface being dressed with a cerate made with the stearine of
arsenicated candles (see p. 256), local pain, nausea, pain in the
stomach, urgent thirst, redness of the tongue, involuntary contractions
of the muscles of the extremities, and weakness and irregularity of the
pulse came on; and one person died within twenty-four hours, while the
other recovered, chiefly because the dressing caused so much pain that
the patient could not keep it on long.[686]

Next as to ulcers; M. Roux has noticed the case of a girl, who was
killed by the application of the arsenical paste to an ulcer of the
breast, and in whom the constitutional symptoms were strongly marked,
although the quantity of the poison must have been very small. The
preparation used, which contains only a twenty-fourth of its weight of
arsenic, was applied for a single night on a surface not exceeding an
inch and a half in diameter. Yet she complained next day of violent
colic and vomited frequently, the countenance soon became collapsed, and
she died two days afterwards in great anguish.[687] Another instance of
the like kind is related in the Annales d’Hygiène, where death arose
from an arsenical ointment ignorantly applied for scirrhous breast over
a large surface of the skin stripped of the cuticle by a blister. The
particular symptoms and their duration are not stated; but there was
violent irritation of the stomach.[688] Another fatal case, related by
Dr. Küchler, arose from the application of Frêre Cosme’s powder to a
soft fungoid tumour on the temple, which discharged serum usually and
blood upon slight pressure. About a drachm and a half of arsenic mixed
with fifteen grains of other powders was applied. Severe inflammation
spread round the tumour next day; and soon afterwards, the patient was
attacked with great difficulty of breathing, thirst, pains in the belly,
and purging, then with difficulty in swallowing from swelling of the
base of the tongue, delirium, cold sweating, and extreme debility; and
death ensued in four days.[689]

There is a singular uncertainty in the effects of arsenic when applied
to ulcerated surfaces. Some persons, like Roux’s patient, are obviously
affected by a single application; while others have had it applied for a
long time without experiencing any other consequences than the formation
of an eschar at the part. Two causes have been assigned for these
differences, and probably both are founded on fact. One, which has been
assigned by Mr. Blackadder, is the relative quantity of arsenic applied.
He says he never witnessed but one instance of its acting
constitutionally, although he often applied it to sores; and he imputes
this success to his having always used a large quantity. For he
considers that by so doing the organization of the part is quickly
destroyed, and absorption prevented,—but that if the quantity be small,
as in the mode practised by Roux, it will cause little local injury and
readily enter the absorbing vessels.[690] Another unequivocal cause is
pointed out by Harles in his treatise on arsenic. While treating of its
therapeutic properties, and noticing the controversy that prevailed last
century throughout Europe respecting the propriety of its outward
application, he remarks that it may be applied with safety to the
abraded skin, to common ulcers, to wounded surfaces, and to malignant
glandular ulcers, even when highly irritable, provided the part be not
recently wounded, so as to pour out blood.[691] The reason of this is
obvious; the application of the poison to open-mouthed vessels is the
next thing to its direct introduction into a vein. It is some
confirmation of Harles’s opinion, that Roux, whose patient was so easily
affected, recommends that before arsenic is applied to an ulcer, a fresh
surface be made by paring away the granulations; and that Küchler’s
patient had an ulcer which did not discharge pus, but serum, and was
easily made to bleed.

In the cases related above it will be remarked that the symptoms vary in
their nature. Sometimes the chief disorder is inflammation, spreading
over and around the eruption or ulcer, sometimes inflammation of the
alimentary canal, sometimes an affection of the nervous system. In
general the sufferings of the patient both from the local inflammation
and constitutional symptoms are very severe. But this rule has its
exceptions. In Pyl’s Memoirs there is the history of a child who died
four days after an itchy eruption of the whole body had been washed with
an arsenical solution, and signs of vivid inflammation were found after
death in many parts; yet she appears to have complained only of
headache.[692] Occasionally too, without exciting either inflammation of
the part, or disorder of the stomach, or a general injury of the nervous
system, it seems to give rise to partial palsy of the muscles adjoining
the seat of its application. An extraordinary case is noticed in an
American Journal, in which the prolonged use of an arsenical preparation
for destroying a tumour on the right side of the neck, was followed by
complete palsy of the muscles of the neck and arm of that side.

In the next place, poisoning has been perpetrated by introducing arsenic
into the fundament with an injection.[693] Foderé has noticed a case of
this kind, which happened in France, and was communicated to him by a
physician of Thoulouse. A lady under medical treatment for some trifling
illness, died unexpectedly under symptoms of poisoning; and it was
discovered that her servant, after unsuccessfully attempting to despatch
her by dissolving arsenic in her soup, had ultimately succeeded by
administering it repeatedly in injections.[694] There is no doubt that
by this mode all the usual effects of arsenic may be induced; and on
account of the facility with which the colon and rectum may be
evacuated, it is not likely that the poison will be found in the gut
after death, if the individual did not die in a few hours after its
administration.

In the third place, women have also died of poisoning by arsenic
introduced into the vagina. Two examples of this revolting crime are on
record. One of them occurred in 1799, in the Department of the Ourthe in
France. A middle-aged female was seized with vomiting, diarrhœa,
swelling of the genitals and uterine discharge; and she expired not long
after. Before her death she told two of her neighbours, that her husband
had some time before tried to poison her by putting arsenic in her
coffee, and had at length succeeded by introducing a powder into her
vagina while in the act of enjoying his nuptial rights. The vulva and
vagina were gangrenous, the belly distended with gases, and the
intestines inflamed.[695]

The other case, which happened in Finland in 1786, gave rise to an
excellent dissertation on the subject by Dr. Mangor, at that time
medical inspector for Copenhagen. A farmer near Copenhagen lost his wife
suddenly under suspicious circumstances, and six weeks afterwards
married his maid-servant. In a few years he transferred his affections
to another maid-servant, with whose aid he endeavoured to poison his
second wife. For some time his attempts proved abortive; till at last
one morning, after coïtion, he introduced a mixture of arsenic and flour
on the point of his finger into the vagina. She took ill at mid-day and
expired next morning; and the murderer soon after married his guilty
paramour. But a few years had not elapsed before he got tired of her
also; and one morning, after the conjugal embrace, he administered
arsenic to her in the same way as to her predecessor. About three in the
afternoon, while enjoying good health, she was suddenly seized with
shivering and heat in the vagina. The remembrance of her former
wickedness soon awoke the suspicions of the unhappy woman, and she wrung
from her husband a confession of his crime. Means were resorted to for
saving her life, but in vain: She was attacked with acute pain in her
stomach and incessant vomiting, then became delirious, and died in
twenty-one hours. After death grains of arsenic were found in the
vagina, although frequent lotions had been used in the treatment. The
labia were swollen and red, the vagina gaping and flaccid, the os uteri
gangrenous, the duodenum inflamed, the stomach natural. In the course of
the judicial proceedings which arose out of these two cases, Dr. Mangor
made experiments on mares, with the view of settling the doubts which
were entertained as to the likelihood of arsenic proving fatal in the
manner alleged; and the results clearly showed that, when applied to the
vagina of these animals, it produces violent local inflammation and
fatal constitutional derangement.[696]

In the fourth place, poisoning by arsenic through the bronchial membrane
or membrane of the air-passages is a comparatively rare accident, which
can take place only in consequence of arsenical gases or vapours being
incautiously breathed. The effects of oxide of arsenic when introduced
in this way are described from personal experience by Otto Tachenius, a
chemist of the sixteenth century.

“Once,” said he, “when I happened to breathe incautiously the fumes of
arsenic, I was surprised to find my palate impressed with a sweet, mild,
grateful taste, such as I never experienced before. But in half an hour
I was attacked with pain and tightness in the stomach, then with general
convulsions, difficult breathing, an unspeakable sense of heat, bloody
and painful micturition, and finally with such an acute colic as
contracted my whole body for half an hour.” By the use of oleaginous
drinks he recovered from these alarming symptoms; but during all the
succeeding winter he had a low hectic fever.[697]

Balthazar Timæus relates a similar case which came under his notice. An
apothecary of Colberg, while subliming arsenic, had not been careful
enough to avoid the fumes; and was soon after seized with frequent
fainting, tightness in the præcordia, difficult breathing,
inextinguishable thirst, parched throat, great restlessness, watching,
and pains in the feet. He had afterwards profuse daily perspiration and
palsy of the legs; and several months elapsed before he got entirely
well.[698] The same author says that the famous Paracelsus, being one
day put out of temper by an acquaintance, made him hold his nose over an
alembic in which arsenic was subliming; and that the object of this
severe joke nearly lost his life in consequence. Wibmer quotes the heads
of several cases where swelling of the tongue, headache and giddiness,
nausea, and an oppressive sense of constriction in the throat, were
occasioned by the incautious inhalation of arsenical fumes.[699] The
following extraordinary case, closely allied to malignant cholera in its
early stage, has been ascribed by the reporter Dr. Welper of Berlin to
the inspiration of arsenical fumes,—with what probability I am not
prepared to say. A stout healthy man, who in the forenoon had freely and
for some time exposed himself to the steam from a vessel where he was
boiling several ounces of orpiment in water, was attacked at night with
sickness, and next morning with extreme weakness and some difficulty of
breathing. These symptoms were greatly relieved by an emetic. But
towards evening the extremities became ice-cold and very stiff, the
breathing much oppressed, the pulse very hurried, and imperceptible
except in the neck, the mouth and throat dry, and the tongue rigid; but
the mind remained clear, though anxious and afraid of impending
dissolution. His state of collapse was removed in twelve hours by
fomentations, and in no long time he recovered entirely except from the
dyspnœa, which continued more or less till a few years afterwards, when
he died of hydrothorax.[700]

The slighter effects of arsenic are said to have been repeatedly
observed of late in this country from inhaling the products of the
combustion of arsenicated candles,—an article of recent invention, in
which arsenic, to the extent of three or four grains and a half in each
candle, is introduced for the purpose of hardening the stearine chiefly
used in manufacturing them. It is unnecessary to say, that such candles
are prejudicial and ought to be prohibited. In a set of experiments made
to try their effects by Messrs. Everitt, Bird, and Phillips in 1838,
birds were killed in no long time, and small quadrupeds were severely
affected, when kept in an apartment lighted with them.[701]

Analogous to the effects of inhaling oxide of arsenic are those lately
observed from the incautious inhalation of arseniuretted-hydrogen gas.
Gehlen the chemist died of this accident, but no particular account has
been published of the symptoms he suffered. Two cases, however, have
been detailed within a few years. In one of these, which has been
related by Dr. Schlinder, of Greifenberg, the individual inhaled in
forty minutes about half a cubic inch of the gas, which is equivalent to
about an eighth of a grain of arsenic. In three hours he became affected
with giddiness, and soon afterwards with an uneasy sense of pressure in
the region of the kidney, passing gradually into acute pain there and
upwards along the back. General shivering ensued, with coldness of the
extremities, and gouty-like pains in the knees, shoulders, and elbows.
The hands and lower half of the fore-arms, the feet and legs nearly to
the knees, the nose and region of the eyebrows, felt as if quite dead,
but without any diminution of muscular power. There was also acute pain
in the stomach and belly generally, painful eructation of gas, and
occasional vomiting of bitter, greenish-yellow mucus. The most
tormenting symptom, however, was the pain in the kidneys, which soon
became attended with constant desire to pass water, and the discharge of
deep reddish-brown urine, mixed with clots of blood. The whole
expression of the countenance was altered, the skin becoming dark brown,
and the eyeballs sunk, yellow, and surrounded by a broad livid ring.
Warm drink brought out a copious sweat and removed the sense of
numbness; but next day there was little change otherwise in the
symptoms, except that the urine was no longer mixed with clots, and that
the hair on the benumbed parts had become white. On the third day the
pains had abated, and the urine became clear; but there was hiccup, an
excited state of the mind, and a feeling as if a great stone lay in the
lower belly. In seven days he was much better. In the third week the
whole glans and prepuce became covered with little pustules which were
followed by small ulcers. It was not till the close of the seventh week
that he recovered completely.[702] Dr. O’Reilly has related the
following case, which arose from the inhalation of hydrogen gas
impregnated with arseniuretted-hydrogen in consequence of the sulphuric
acid used for dissolving zinc having contained arsenic. Mr. Brittan, a
Dublin chemist, wishing to ascertain the effects of hydrogen on the
body, proceeded to inhale 150 cubic inches of it. Immediately after the
second inhalation, he was seized with confusion, faintness, giddiness
and shivering, and passed a stool, as well as two ounces of bloody
urine, but without any pain. Pain in the limbs followed, and in two
hours frequent vomiting and dull pain in the stomach. The pulse at this
time was 90, the skin cold, and the voice feeble. Ammonia, laudanum, and
emollient clysters gave him little relief. During the subsequent night
there was frequent vomiting and no urine; the face became
copper-coloured, and the rest of the body greenish; there was tenderness
of the epigastrium and hiccup; but he was free of fever. On the third
day there was diarrhœa and still no urine; but the jaundice had
disappeared. On the fourth the breath was ammoniacal, and somnolency had
set in. On the fifth the skin became again deeply jaundiced, and the
face was œdematous; no urine had yet been discharged, and the bladder,
examined with the catheter, was found empty. On the evening of the
seventh day he expired. On examination of the body, two pints of red
serum were found in the pleural cavities; the lungs were sound, the
heart pale and flaccid, the liver indigo-blue, the gall-bladder
distended with bile, the kidneys also indigo-blue, the stomach empty,
and its villous coat brittle, with here and there inflamed-like spots on
it, the bladder empty, the brain bloodless, the cellular tissue
generally anasarcous. Arsenic was detected in the pleural serum. By an
approximate calculation it was supposed that the hydrogen this gentleman
inhaled had contained the equivalent arsenic of twelve grains of the
oxide.[703]

It would appear that arsenic acts with great rapidity and force when
respired in any form.

Poisoning through the lining membrane of the nostrils is a still rarer
accident than that last mentioned. There is a distinct example of it in
the German Ephemerides, which arose from an arsenical solution having
been used by mistake as a lotion for a chronic discharge from the
nostrils. The individual was attacked with a profuse discharge from the
nostrils, and then with stupor approaching to coma. Weakness of sight
and of memory continued after sensibility returned; and he died two
years afterwards, death having been preceded for some time by
convulsions.[704]

Arsenic when applied to the sound skin of animals does not easily affect
them. The experiments of Jaeger formerly noticed prove that no effect is
produced, if the poison is simply placed in contact with the skin. Nay
even when rubbed into it with fatty matters it does not operate with
energy; for in that case, according to the experiments of Renault, it
causes sometimes a pustular eruption, sometimes an eschar, but never any
constitutional disorder.[705] It is more energetic, however, when
applied to the more delicate skin of the human subject. Some experiments
were made by Mr. Sherwen on himself with the view of proving this;[706]
but they are not satisfactory. The following facts, however, will show
that it may produce through the sound skin all the ordinary signs of
poisoning. Desgranges, a good authority, relates the case of a woman who
anointed her head with an arsenical ointment to kill lice, and, after
using it several days, was attacked with erysipelas of the head and
face, attended with ulceration of the scalp, swelling of the salivary
and cervical glands, and inflammation of the eyes. There were likewise
violent constitutional symptoms,—much fever, fainting, giddiness,
vomiting and pain in the stomach, tenesmus, and ardor urinæ, tremors of
the limbs, and even occasional delirium. Afterwards the whole body
became covered with an eruption of white papulæ, which dried and dropt
off in forty-eight hours. She recovered gradually; but appears to have
made a narrow escape. Her hair fell out during convalescence.[707] A
similar instance is recorded in the Acta Germanica for 1730. A schoolboy
having found in the street a parcel of arsenic, his mother mistook it
for hair powder; and as he had to deliver a valedictory speech at school
next day, she advised him to powder himself well with it in the morning.
This he accordingly did. In the middle of his speech he was attacked
with acute pain of the face; and a fertile crop of pustules soon broke
out upon it. The head afterwards swelled much, and the pustules spread
all around it; he was tormented with intolerable heat in the scalp; and
the hair became matted with the discharge into a thick scabby crust.
This crust separated in a few weeks, and he soon recovered
completely.[708] Schulze, a German physician, has related no fewer than
five cases of the same description, all arising from arsenic having been
mistaken for hair powder; and one of them proved fatal. Two of the cases
were slight. The other persons had the same violent inflammation of the
head as Desgranges’s patient and the German schoolboy. In the fatal case
death took place in twenty-one days; and on dissection, besides other
morbid appearances, the scalp was found gangrenous and infiltered with
fluid blood, and the stomach much inflamed.[709] The two survivors, who
were severely ill, it is well to add, were not attacked with the
erysipelas of the scalp till six days after they powdered themselves.
Sproegel mentions a fatal case from fly-powder having been applied in
like manner to the head; and Wibmer quotes another, but not fatal, where
from the same cause great swelling of the head and face arose, followed
by erysipelas of the face, neck, and belly, and a papular eruption on
the hands which continued five days.[710]

From the statements now made, it is evident that arsenic applied to
various parts of the external surface and natural apertures of the body,
will prove poisonous, and will often act with a certainty and rapidity
not surpassed by its effects when taken internally. Many of the cases
furnish a striking confirmation of a circumstance formerly noticed with
respect to its action,—namely, that it produces signs of irritation in
the stomach, in whatever manner it is introduced into the body. In some
instances, indeed, the signs of inflammation in the stomach were quite
as distinct as in the cases previously described, where the poison was
taken internally.

The subject of the symptoms caused by arsenic will now be concluded with
a few remarks on the strength of the evidence which they supply.

The present doctrine of toxicologists and medical jurists seems
generally to be, that symptoms alone can never supply decisive proof of
the administration of arsenic. This opinion is certainly quite correct
when applied to what may be called a common case of poisoning with
arsenic, the symptoms of which are little else than burning pain in the
stomach and bowels, vomiting and purging, feeble circulation, excessive
debility, and speedy death. All these symptoms may be caused by natural
disease, more particularly by cholera; and consequently every sound
medical jurist will join in condemning unreservedly the practice which
prevailed last century of deciding questions of poisoning in such
circumstances from symptoms alone. But modern authors appear to have
overstepped the mark, when they hold that the rule against deciding from
symptoms does not admit of any exceptions. For there are cases of
poisoning with arsenic, not numerous certainly, yet not very uncommon
neither, which can hardly be confounded with natural disease; and, what
is of some consequence, they are precisely those in which the power of
deciding from symptoms alone is most required, because chemical evidence
is almost always wanting. Either the peculiar combination of the
symptoms is such as cannot arise from natural causes, so far at least as
physicians are acquainted with them: or these symptoms occur under
collateral circumstances, which put natural causes almost or altogether
out of the question.

Thus, let the medical jurist consider in the first place, the symptoms
occasionally observed in those who survive five, six or ten days; let
him exclude for the present the secondary nervous affections; and
instead of a compounded description, which may be objected to as apt to
convey a false and exaggerated idea of the facts, let him take an actual
example. In a paper by Dr. Bachmann on some cases of poisoning with
arsenic, there is a minute account of the case of a lady who was
poisoned by her maid with fly-powder and white arsenic, and whose
symptoms were those of universal inflammation of the mucous membranes.
After suffering two days from retching and vomiting, colic pains and
purging, these symptoms suddenly became more violent, and attended with
oppressed breathing and hoarseness so that she could hardly make herself
be heard,—with vesicles on the palate, burning pain in the throat, and
excessive difficulty in swallowing,—with spasm and pain of the bladder
in passing water,—and with extreme feebleness of the pulse. Three days
afterwards the symptoms increased still more. She complained of
intolerable burning and spasms of the throat, which, as well as the
mouth, was excessively inflamed,—of violent burning pain in the stomach
and bowels,—of burning in the fundament and genitals, both of which were
inflamed even to gangrene,—of indescribable anxiety and anguish about
the heart; and she died the following day, death being preceded by
subsultus, delirium, and insensibility.[711] Or take the case in the
trial of Miss Blandy. On two successive evenings, immediately after
taking some gruel which had been prepared by the prisoner, Mr. Blandy
was attacked with pricking and burning of the tongue, throat, stomach,
and bowels, and with vomiting and purging. Five days after, when the
symptoms were fully formed, he had inflamed pimples round the lips, and
a sense of burning in the mouth; the nostrils were similarly affected;
the eyes were bloodshot and affected with burning pain; the tongue was
swollen, the throat red and excoriated, and in both there was a
tormenting sense of burning; he had likewise swelling, with pricking and
burning pain of the belly; excoriations and ulcers around the anus and
intolerable burning there; vomiting and bloody diarrhœa; a low,
tremulous pulse, laborious respiration, and great difficulty in speaking
and swallowing. In this state he lingered several days, death
supervening nine days after the first suspected basin of gruel was
taken.[712] Can the symptoms, in these two cases, attacking, as they
did, at one and the same time, the whole mucous membranes, be imitated
by any natural combination of symptoms? Viewing the endless variety and
wonderful complexity of the phenomena of disease, the practitioner will
probably, and with justice, reply that a natural combination of the kind
is possible. But if his attention is confined, as in strictures it ought
to real occurrences,—if he is required to speak only from actual
experience, personal or derived, it is exceedingly questionable whether
any one could say he had ever seen or read of such a case. At all
events, if a medical witness had to give his opinion from symptoms only
in such a case as that of Mr. Blandy, or that described by Bachmann, he
would certainly be justified in declaring that poisoning was highly
probable; and, admitting general poisoning to be proved, he would, it is
likely, fix on arsenic as the substance which could most easily produce
the effects.

Let him next, however, take also into consideration the nervous
affections that sometimes either immediately follow the inflammation of
the mucous membranes, or become united with it when it has existed a few
days; and confining his attention still to actual occurrences, let him
reflect on the symptoms in Dr. Roget’s case, in which there was first
violent inflammation of the whole alimentary canal, and then regular and
obstinate epilepsy (p. 245), or on those in Dehaen’s patient, in whom
the nervous disorder was partial palsy (p. 247). On reconsidering these
narratives, still greater reason will appear for doubting whether such a
combination of simultaneous, and in the present instance also
consecutive symptoms, ever arise from natural causes. It is difficult to
conceive a fortuitous concurrence of natural diseases producing at the
same moment that variety and complexity of disorder which occur in the
primary stage of the cases alluded to; and it would surely be a still
more extraordinary combination which should farther add the supervention
of epilepsy or partial palsy from a natural cause, at the exact period
at which it appears as the secondary stage of poisoning with arsenic.
All that any practitioner could say is, that a concurrence of the kind
is within the bounds of possibility. He must be compelled to admit that
it is in the highest degree improbable, and likewise that it could
hardly take place from natural causes without the real causes of the
symptoms being clearly indicated.

But to conclude, there are likewise collateral circumstances connected
with the symptoms, which, taken along with the symptoms themselves, will
sometimes place the fact of poisoning with arsenic beyond the reach of a
doubt. Thus, if a person were taken several times ill with symptoms of
general inflammation of the mucous membranes, after partaking each time
of a suspected article of food or drink, the proof of the administration
of arsenic would be very strong indeed; and it would be unimpeachable if
at length a nervous affection succeeded at the usual period. Or above
all, suppose several persons, who have partaken of the same dish, are
seized about the same time with nearly the same symptoms of irritation
of the mucous membranes. The proof of general poisoning would then be
unequivocal. And if one or more of them should afterwards suffer from a
nervous disorder, little hesitation ought to be felt in declaring that
arsenic is the only poison which could have caused their complaints.

These views are of more practical consequence than may at first sight be
thought. The doctrine which has been here espoused might have been
applied to decide two criminal cases which at the time made a great
noise in this country. One was the case of Eliza Fenning (p. 245). Here
five persons were simultaneously attacked with symptoms, more or less
violent, of inflammation of the whole alimentary canal; and in two of
them epileptic convulsions appeared before the inflammatory symptoms
departed. The other was the case of George Thom (p. 247). Here four
persons were at one and the same time seized with the primary symptoms
in an aggravated form; and in two of them, as these symptoms abated,
obstinate partial palsy came on. On both trials, then, it might have
been stated from the symptoms alone that poison had been given, and that
arsenic was the only poison hitherto known to be capable of producing
such effects.

In applying this doctrine to parallel instances two precautions must be
attended to. On the one hand, care must be taken to ascertain, as may
always be done, that the simultaneous symptoms of general irritation in
the alimentary canal, arising soon after a meal, are not owing to
unsound meat having been used in preparing it. And on the other hand,
which is of more consequence, the symptoms on which so important an
opinion is founded, must be strongly marked and well ascertained by a
competent person. The signs of irritation in the mucous membranes must
be really general and unequivocal; and those of a disorder of the
nervous system must be likewise developed characteristically. Care must
be taken in particular to distinguish symptoms of the latter class from
others which approach to them in nature, and are the ordinary sequels of
natural disease: for example, the true palsy caused by arsenic must not
be confounded with the numbness and racking pains in the limbs, which
occasionally succeed cholera.

With these precautions the evidence from symptoms may in certain cases
be decisive of the question of poisoning with arsenic. And it is of
moment to observe, as has been already hinted, that, although such cases
are numerous, they are precisely of the kind in which it is most
essential to the ends of justice that the symptoms should, if possible,
supply evidence enough to direct the judgment; for the characteristic
symptoms referred to occur chiefly when the patient either recovers or
survives many days, and where consequently the chemical evidence,
usually procured from the examination of the contents of the stomach, is
almost always wanting.


      SECTION III.—_Of the Morbid Appearances caused by Arsenic._

The morbid appearances caused by arsenic will next require some details.
In treating of them the same plan will be pursued as in the preceding
section: the various morbid appearances left by it will first be
mentioned in their order; and the subject will then be wound up with
some remarks on the force of the evidence from these appearances, as
they are usually combined in actual cases.

In the first instance, there are some cases in which little or no morbid
appearance is to be seen at all. These all belong to the second variety
of poisoning, which is characterized by the absence of local
inflammation, and the presence of symptoms indicating an action on the
heart, or some other remote organ. In such circumstances death takes
place before a sufficient interval has elapsed for inflammation to be
developed.

Several examples of the absence of diseased appearances in the dead body
are to be found in authors. Thus in Chaussier’s case formerly quoted (p.
243), in that related by Metzger (p. 242), in another related by
Etmuller, which was fatal in twelve hours,[713] and in a fourth related
by Professor Wagner of Berlin, where life was also prolonged for twelve
hours under incessant vomiting,[714] there was positively no morbid
alteration at all. Such was also the state of the whole alimentary canal
in the extraordinary case related by Orfila (p. 243). In the case quoted
from the Medical and Physical Journal (p. 242), there was merely a
slight redness at the pyloric end of the stomach. In the case of the
American grocer too, there was only a little redness. In Mr. Wright’s
case (p. 243), there was scarcely any morbid appearance,—nothing more
than two small vascular spots and a minute ecchymosis. In that which
fell under my own notice (p. 242), the villous coat of the stomach was
of natural firmness, and had an exceedingly faint mottled-cherry-red
tint, barely perceptible in a strong light; and the rest of the
alimentary canal, as well as the body generally, was quite healthy.

Although in these examples the morbid appearances were trifling or
undistinguishable, it must not be supposed that the same happens in all
cases of rapid death from arsenic. In Gérard’s case, where the usual
irritant symptoms were wanting, and which proved fatal in five hours,
there was dark redness of the whole villous coat of the stomach. In Mr.
Holland’s case, fatal in eight or nine hours (p. 243), the stomach was
of an intense purple colour at its pyloric end, and contained bloody
mucus; and the mucous coat of the cœcum presented extensive softening
and congestion. Mr. Alfred Taylor refers to three cases observed by Mr.
Forster of Huntingdon, in which the mucous coat of the stomach was
highly inflamed, though death took place in 6½, 3½, and 2 hours
only:[715] in Mr. Hewson’s case, fatal in five hours, the whole stomach
was exceedingly vascular, and presented both spots of extravasation, and
several small erosions (p. 201). In a case alluded to at p. 239 as
having fallen under my own observation, and which was also fatal in five
hours, the whole villous coat of the stomach was intensely red, except
where the folds of the rugæ protected it from contact with the poison;
and the prominences of the rugæ presented corroded spots of ecchymosis.
In Dr. Dymock’s case, fatal in two hours and a half, the stomach, which
I had an opportunity of examining, presented on its mucous coat many
scarlet patches, and here and there a purplish appearance (p. 240).
Lastly, an instance is related by Pyl of this poison proving fatal in
three hours, and leaving nevertheless in the dead body distinct signs of
inflammation in the stomach.[716]

In the ordinary cases in which death is delayed till the second day or
later, a considerable variety of diseased appearances has been observed.
They are the different changes of structure arising from inflammation in
the alimentary canal, in the organs of the chest, and in the organs of
generation—together with certain alterations in the state of the blood
and condition of the body generally.

The first set of appearances to be mentioned are those indicating
inflammation of the alimentary canal, viz., redness of the throat and
gullet,—redness of the villous and peritonæal coats of the stomach,
blackness of its villous coat from extravasation of blood into it,
softening of the villous coat, ulceration of that as well as of the
other coats, effusion of coagulable lymph on the inner surface of the
stomach, extravasation of blood among its contents,—finally, redness and
ulceration of the duodenum and other parts of the intestinal canal, and
more particularly of the rectum; to which may also be added, though not
properly a morbid phenomenon, certain appearances put on by the arsenic
which remains undischarged.

Redness of the throat and gullet is not common, at least it does not
often occur in the descriptions of cases. Jaeger, however, says that in
his experiments he usually found redness at the upper and purplish
stripes at the lower end of the gullet:[717] and Dr. Campbell likewise
found the gullet red in animals,[718] Similar appearances have also been
remarked in man. In the case of a man who lived eight days, Dr. Murray
found the gullet very red;[719] in that of a woman who lived scarce
seven hours, Dr. Booth observed the gullet inflamed downwards very
nearly to the cardia;[720] and Wildberg has reported two cases of the
same nature, in one of which it is worthy of remark that the poisoning
lasted only six hours.[721] On the whole, it appears probable that
inflammation of the throat and gullet would be found more frequently in
the reports of cases, if it was more carefully looked for.

Redness of the inner coat of the stomach is a pretty constant effect of
arsenic, when the case is not very rapid. All the varieties of redness,
formerly mentioned among the effects of the irritant poisons generally,
may be produced by arsenic. There is nothing, however, in the redness
caused by this poison, any more than in the redness of inflammation
generally, by which it is to be distinguished from the pseudo-morbid
varieties. (See p. 110.)

It is singular, that, however severe the inflammation of the inner
membrane of the stomach may be, inflammatory redness of the peritonæal
coat is seldom found. Yet inflammatory vascularity does occur sometimes
on the peritonæal coat. Sproegel found it in animals;[722] and it was
present in the case of the girl Warden, whose death gave rise to the
trial of Mrs. Smith.[723] Dr. Nissen, a Danish physician, has related
another case in which the external coat of the stomach appeared as if
minutely injected with wax. But the patient had been attacked with
incarcerated hernia during the progress of his illness, and the whole
peritonæal membrane was in consequence inflamed.[724] A common
appearance when the internal inflammation is well marked, and one often
unwarily put down as inflammation of the peritonæum, is turgescence of
the external veins, sometimes so great as to make the stomach look
livid.

Blackness of the villous coat from effusion of altered blood into its
texture is sometimes met with. When the colour is brownish-black, or
grayish-black, not merely reddish-black, when the inner membrane is
elevated into firm knots or ridges by the effusion, and the black spots
are surrounded by vascularity or other signs of reaction, the
appearances strongly indicate violent irritation. I have already said
that such appearances are never imitated by any pseudo-morbid
phenomenon.

One of the most remarkable appearances occasionally observed in the
stomach in those instances where the body has been buried for at least
some weeks before examination, is the presence of bright yellow patches,
of various sizes, which appear as if painted with gamboge, and obviously
arise from the oxide of arsenic diffused throughout the tissues having
been decomposed and converted into sulphuret of arsenic by the
sulphuretted-hydrogen disengaged during putrefaction. I have witnessed
this appearance in several cases. In the case mentioned at p. 247, where
the body had been buried twenty days, numerous brilliant yellow patches
were visible on the villous coat of the stomach. In the case of a female
who was poisoned about the same time with that man, and, as was
suspected, by the same individual, the body was not examined till three
months after interment; and here broad, bright, yellow patches,
disappearing under the action of ammonia, were found under the
peritonæal coat of the left end of the stomach, the adjoining great
intestine, and also the muscular parietes of the abdomen. In the case of
Mr. Gilmour, for whose murder his wife was tried a few months ago in
this city, but acquitted,—and who undoubtedly died of poisoning with
arsenic, howsoever administered,—there were found fourteen weeks after
death numerous yellow streaks and patches both on the inner surface of
the stomach, on its outer surface under the peritonæum, on the adjoining
transverse colon, and on the small intestines in contact with the
stomach. From these and other parallel facts which have been
occasionally noticed by the periodical press, it seems probable that the
appearance in question is common in bodies which have been some time
buried. It is an extremely important part of the pathological evidence.
I doubt whether natural causes can occasion any appearance similar to
it. And indeed, what is it but the effect of a chemical test applied to
the poison by nature?

The next appearance which may be mentioned is unnatural softness of the
villous coat of the stomach. This coat has certainly been often found,
after death from arsenic, unusually soft, brittle, and easily separable
with the nail.[725] But the same state occurs in dead bodies so often
and so unconnected with previous symptoms of irritation in the stomach,
that it cannot with any certainty be assumed as the effect of irritation
when it is found subsequently to such symptoms. So far from softening
and brittleness being a necessary effect of the irritation produced by
arsenic, it is a fact that a condition precisely the reverse has been
also noticed. In a case which I examined, the villous coat, except where
it had been disintegrated by effused blood and ulceration, was strong
and firm; and the rugæ were thickened, raised and corrugated, as if
seared with a hot iron.[726] Metzger once found the mucous membrane
dense, thickened, and the rugæ like thick cords.[727] Pyl too once met
with the same appearance, and ascribes the thickening to gorging of
vessels;[728] and in a case related by Dr. Wood of Dumfries, where I had
an opportunity of examining the stomach, this appearance was present in
a remarkable degree, and it clearly arose from elevation of the villous
coat by effusion of blood under it.[729] Remer, in his edition of
Metzger’s Medical Jurisprudence, says he once met with an instance where
the stomach was shrivelled like a bladder subjected to boiling
water.[730]

Sometimes the villous and also more rarely the other coats of the
stomach are found actually destroyed and removed in scattered spots and
patches. This loss of substance is occasionally owing to the same action
which causes softening and brittleness of the villous coat,—the action,
however, having been so intense as to cause gelatinization. That such is
the nature of the process appears from the breach in the membrane being
surrounded by gelatinized tissue, and not by an areola of inflammatory
redness. Of this species of destruction of the coats I have seen a
characteristic example.[731] But in other cases the loss of substance is
owing to a process of ordinary ulceration, as is proved by the little
cavities having a notched irregular shape, and being surrounded both by
a red areola and a margin of firm tissue. This was the character of the
ulcers in the case of Warden, which I have described elsewhere.[732]
Destruction of the coats of the stomach by ulceration is not a very
common consequence of poisoning with arsenic, as death frequently takes
place before that process can be established. It does not often occur,
unless the patient survive nearly two days. Mr. Alfred Taylor, however,
mentions a case fatal in seventeen hours where he found ulceration of
the stomach, and another fatal in ten hours where several small ulcers
were seen on the lesser curvature, and two nearly circular ones as big
as a sixpence.[733] Mr. Hewson too informs me he found many eroded spots
even in his case which proved fatal in five hours (p. 56). I suspect,
however, that spots of healthy membrane surrounded by vascular redness
are sometimes mistaken for ulcers in such cases; for indeed nothing can
more exactly resemble them. In many general works on Medical
Jurisprudence, and in some express treatises on arsenic, it is stated
that this poison may cause complete perforation of the stomach.[734] But
this effect is exceedingly rare. I have related one distinct example of
it;[735] Professor Foderé has briefly alluded to a case he witnessed
which proved fatal in two days and a half;[736] I have likewise found in
an account of a trial in North America, an instance in which the stomach
was perforated by numerous small holes, so that when held before the
light it appeared as if riddled like a sieve;[737] but I have not been
able to find in medical authors any farther authority for the general
statement. Destruction of the coats of the stomach as produced by
arsenic has been variously described by authors under the terms erosion,
corrosion, dissolution, ulceration. But the correct mode of describing
it appears to be by the terms gelatinization, or ulceration, according
to the nature of the diseased action by which it is induced. At all
events it is necessary to beware of being misled by the terms erosion,
corrosion, and the like, which all convey the idea of a chemical action;
while it is well ascertained that a chemical action either does not
exist at all between arsenic and the animal tissues, or, if it has
existence, tends to harden and condense rather than to dissolve or
corrode them. Arsenic is not a corrosive.

Another species of destruction of the coats of the stomach, which will
require a little notice, is sloughing or gangrene. This appearance
occurs frequently in the narratives of the older writers; but it has not
been enumerated in the list of morbid appearances at the commencement of
this section, because its existence as one of the effects of arsenic is
problematical. It has not been witnessed so far as I know by any recent
good authority. Those who have mentioned it have probably been misled by
the appearance put on by the black extravasated patches, when they are
accompanied by disintegration of the villous coat and effusion of clots
of black blood on its surface—an appearance which resembles gangrene
closely in everything but the fetor. Sir B. Brodie has stated that Mr.
John Hunter has preserved in his museum, as an example of a slough of
the villous coat caused by arsenic, which turned out on examination to
be nothing else than an adhering clot.[738] It is clear too, that, when
Mr. James speaks of having found “several gangrenous patches” on the
villous coat of the stomach, and “patches of sphacelus” in the
intestines, on examining the body of a notorious French criminal,
Soufflard, who poisoned himself with arsenic in prison in 1839, he
mistook for gangrene what was merely extravasation; for the man lived
only twelve hours.[739]

Various secretions have been found on the inner surface of the stomach.
The mucous secretion of the inner membrane is generally increased in
quantity. Frequently it is thin, but viscid, as in its natural state;
but sometimes it is both abundant and solid, as if coagulated; and then
it forms either a uniform attached pellicle, or loose shreds floating
among the contents.[740] In both forms it has been mistaken for the
mucous membrane itself. I believe this increased secretion and
preternatural firmness of the gastric mucus cannot take place without
some irritating agent being applied to the stomach. Both may occur
without any other sign of inflammation in the mucous membrane. In a case
of suicide after seduction which came under my notice in this city in
1843, and which proved fatal in five hours [p. 239], the mucus in the
stomach, which was very abundant, put on the appearance of curdled milk,
owing to its being rendered opaque and white by the large quantity of
finely powdered arsenic diffused through it; and it was actually
mistaken for curdled milk by several medical men.—Sometimes the matter
effused is true coagulable lymph. This is rarely seen as the effect of
arsenic. I have remarked it, however, very distinctly in dogs, and Dr.
Baillie saw it once in the human subject.[741] It is of course quite
decisive of the presence of inflammation. It is known from tough mucus,
to which it bears some resemblance, by its reticulated disposition, and
by the threads of the reticulation corresponding with inflamed lines on
the stomach beneath.

Another very common appearance is the presence of a sanguinolent fluid,
or even actual blood in the cavity of the stomach. In several of the
cases which have come under my own notice, the subject of analysis was a
thick, dirty brownish-red fluid, evidently containing a large proportion
of blood; and many other examples of the same nature are on record.[742]
In Laborde’s case formerly mentioned actual clots were found among the
contents; in the instance of a woman who died in five days, as related
by Zittmann, half a pound of coagulated blood was found in the
stomach;[743] and in another case mentioned by Professor Bernt, the
stomach contained no less than three pounds of black ichor mixed with
clots of blood.[744] A good deal of reliance has been placed on bloody
effusion in proof of the administration of arsenic or some other active
irritant. It is of some importance, as it appears not to be an effect of
that irritation which causes cholera.

Among the appearances observed in the stomach the presence of arsenic
may be included, though not properly speaking a morbid appearance. Under
the head of the medical evidence of poisoning generally it was stated,
that many causes conspire to remove from the stomach during life poisons
which have actually caused death. In addition to the illustrative cases
there alluded to, I may here also refer to an interesting case
communicated to me by Mr. J. H. Stallard, and already noticed for a
different purpose [p. 235]. Arsenic in no large quantity had been
swallowed in tea, and death took place in four hours only. Here none of
the poison could be detected by Marsh’s process, either in the contents
of the stomach, or in its tissues, or in the liver.—In the instance of
arsenic, however, the operation of the causes which tend to remove the
poison is prevented by various circumstances, in particular by its
insolubility and firm adhesion to the stomach. Hence it happens, that
even after long-continued vomiting a portion still generally remains
behind, either in the contents of the stomach or in its tissues.
Sometimes the arsenic exists dissolved in the contents; more commonly it
is present there in the solid form; and is then either in loose
particles, or enveloped in coagulated mucus,[745] or in little clots of
blood,[746] or is wrapped up in the more solid parts of the
contents.[747] Frequently it adheres to the coats of the stomach, and is
then either scattered in the form of fine dust or collected in little
knots. The adhering particles are always covered by mucus; they are
often surrounded by redness of the membrane or by effused blood; and
sometimes they are imbedded in little ulcers.—A remarkable appearance
which the arsenic sometimes puts on is a brilliant yellowness of its
surface, owing to its conversion into the sulphuret. This appearance
existed in six cases which have come under my own notice, first in one
related in the Edinburgh Medico-Chirurgical Transactions,[748] next in
the instance of Margaret Warden,[749] again in the case of a young woman
whose death gave rise to the trial of John Lovie held at Aberdeen in the
Autumn Circuit of 1827, again in a case described by Dr. Wood, which I
had an opportunity of examining;[750] and lastly, in two others which I
had occasion to examine in 1842 and 1843. In one of these, the case of
Mr. Gilmour, adverted to at p. 265, Drs. Wylie and M’Kinlay, who
examined the body in the country, found the inner surface of the stomach
thickly sprinkled with small yellow particles, some of which were very
bright. In all of these cases oxide was found, as well as the sulphuret
of arsenic. In the case related by Dr. Nissen [p. 264], a similar yellow
appearance, observed on the surface of the arsenic, was ascribed with
justice to the action of sulphuretted hydrogen-water, which had been
given as an antidote during life.[751] In a very important case examined
here a few years ago by my colleague Dr. Traill, and which will be
noticed more particularly for a different purpose afterwards, this
conversion of the oxide into sulphuret had taken place to a great extent
[p. 277]. In every instance of the kind yet examined, however, the
conversion has been only partial, so that a large proportion of oxide
could easily be detected by the usual process.

Care must be taken not hastily to consider as arsenic every white powder
which may be found lining the inside of the stomach. Many other white
powders may obtain entrance from without; and besides, small, white,
shining, pulverulent scales, not unlike finely powdered arsenic, but
rarely composed of animal matter, sometimes form naturally on the mucous
coat of the stomach and intestines. In a medico-legal report published a
few years ago, Professor Orfila has noticed two instances in which these
scales were mistaken for arsenic;[752] in another published not long
after he mentions that he found white particles which crackled when
bruised, and appeared brilliant before the microscope, and which
nevertheless were not arsenic.[753] Buchner too says he is acquainted
with an instance where, in a medical inspection on account of a
suspicion of poisoning, the villous coat of the stomach was found lined
with a white granular substance which presented the properties of a fat
and contained no mineral admixture;[754] and in the case of Warden I
remarked a similar appearance, which, as arsenic was found in the
stomach, I was disposed to consider a sprinkling of that poison, until
the contrary was ascertained by analysis. The present caution,
therefore, is not superfluous.

In a few cases the stomach is the only situation where morbid
appearances are visible, even though life has been prolonged for so much
as two days. This state of matters is well exemplified by a French case
of death in forty-three hours, where the stomach presented much redness
and extravasated patches, but where the intestines, the larynx and the
contents of the head and chest were in a natural condition.[755] Such
limitation, however, of the diseased appearances are rare.

Redness of the mucous membrane of the intestines is often present when
the stomach is much inflamed. Dissolution of the mucous coat is much
less frequent in the intestines than in the stomach. Ulceration
occasionally occurs in lingering cases. In the case of Mitchell, which
has been several times alluded to, the inner coat of the duodenum was
dark-red, pulpy, thickened, easily separable; and on a spot as big as a
crown piece, both the inner and the muscular coats were wanting.[756]
Perforation of the small intestine was found in a case communicated to
me by Mr. Sandell, and detailed at page 277. But as the person survived
only eight hours, and had laboured under symptoms of disease in the
bowels for some days before taking the arsenic, it is unlikely that this
appearance, which has not been observed, to my knowledge, in any other
instance, arose from the action of the poison.

The signs of inflammation are seldom distinct in the small intestines
much lower down than the extremity of the duodenum; and they do not
often affect the colon. But the rectum is sometimes much inflamed,
though the colon, and more particularly the small intestines, are not.
Dr. Male mentions, that in man he has found the rectum abraded,
ulcerated, and even redder than the stomach itself;[757] and Dr. Baillie
also notices two cases in which the lower end of the rectum was
ulcerated.[758] A common appearance in lingering cases is excoriation of
the anus,[759] and it is said that even gangrene has been produced.[760]

A late writer draws attention to the fact that in the only two fatal
cases he had seen the whole colon was contracted to an extraordinary
degree;[761] and this state is mentioned in other cases. The appearance
deserves notice; but of course whatever empties the colon thoroughly
will have the same effect.

The chief appearances in the alimentary canal have now been mentioned.
The next quarter in which deceased appearances are to be met with is the
cavity of the chest. Here are sometimes seen redness of the pleura,
redness and congestion of the lungs, redness of the inner surface of the
heart, and redness of the lining membrane of the windpipe.

Redness of the diaphragmatic part of the pleura, or even of the whole of
that membrane, has been at times observed; as one would expect, indeed,
from the pectoral symptoms which occasionally prevail during life.
Inflammation of the lungs themselves has also been noticed. Dr. Campbell
twice found great congestion of blood in the lungs of animals poisoned
by the application of arsenic outwardly.[762] Sproegel likewise found
the pleura, pericardium, and whole lungs deeply inflamed in
animals.[763] Dr. Venables found the pleura of a bright crimson colour
in some poultry maliciously poisoned with arsenic,—more redness there
indeed than in the stomach.[764] Mr. James says that in his experiments
on animals he constantly found the lungs much gorged with blood, unless
when death occurred quickly; but that he could see no evidence of the
congestion being inflammatory.[765] A distinct example of advanced
pneumonia in man is related in Pyl’s Magazine: the patient died after
vomiting and purging incessantly for eight days; and on dissection the
lungs were found “in the highest state of inflammation; and so congested
as to resemble a lump of clotted blood.”[766] A distinct case of the
same nature is related in Henke’s Journal; this patient had obvious
pneumonic symptoms during life; and in the dead body the lungs were
found so gorged, that, on being cut into, nothing could be seen but
clotted blood in their cellular structure.[767] In a case formerly
adverted to [p. 252] of death from arsenic applied externally for
scirrhus, excessive congestion was found in the lungs, “both lungs being
completely gorged with blood, and presenting all the characters of
pulmonary apoplexy.”[768] In another described by Dr. Booth of
Birmingham, where death occurred in seven hours only, the lungs
presented sufficient congestion to have completely impeded
respiration.[769]

It has been alleged that the inner surface of the heart has been found
red from inflammation. In a case examined judicially at Paris by Orfila,
the left cavities of the heart were of a mottled red hue, and in the
ventricle were seen many small crimson specks which penetrated into the
muscular part of the parietes. The right cavities had a deep
reddish-black tint, and the ventricle of that side contained specks like
those in the other, but more faint. Orfila adds, that he had previously
seen the same appearance in animals.[770] These observations are not
satisfactory. There is no evidence that the observer drew the
distinction between the redness of inflammation, and that produced by
the dyeing of the membrane with blood after death. The subject was
afterwards brought before the Royal Academy of Medicine at Paris by M.
Godard, who had also observed the appearance in question in a person
killed by arsenic, and who dwelt strongly on it as characteristic of
this species of poisoning. It was distinctly proved, however, by many
members present that the appearance arises from various other
causes.[771]

The inner membrane of the windpipe is said to be sometimes affected with
inflammatory redness. Jaeger found it so in animals;[772] and the
symptoms referrible to the windpipe during life would lead us to expect
the same thing in man.

The organs of generation are occasionally affected. The penis in the
male and the labia in the female have been found distended and black; in
an interesting case related by Bachmann the external parts of generation
(in a female) were surrounded by gangrene;[773] and in a case related in
Pyl’s collection the inside of the uterus and Fallopian tubes was
inflamed.[774] It is probable that signs of inflammation in the internal
organs of generation will be found if there have been corresponding
symptoms during life. But in truth this part of the pathology of
poisoning with arsenic has not been particularly attended to.

To complete this account of the morbid appearances of the mucous
membranes, it may be added that the conjunctiva of the eyes frequently
presents vascularity and spots of extravasation.[775]

It now only remains, under the head of the morbid appearances produced
by arsenic, to mention certain alterations that are said to take place
in the state of the blood and general condition of the body.

With regard to the state of the blood Sir B. Brodie observes in general
terms, that in animals killed by arsenic it is commonly fluid.[776]
Harles, on the authority of Wepfer, Sproegel, and Jaeger, says it is
black, semi-gelatinous, and sometimes pultaceous.[777] Novati alleges
that the blood after death is without exception black and liquid as
after cholera, of a blackish-purple tint that colours linen
reddish-brown, viscid, opaque, and without any trace of
coagulation.[778] In a fatal case related by Wildberg the blood was
everywhere fluid.[779] This condition, however, is not uniform; for Dr.
Campbell found the blood coagulated in the heart of a rabbit;[780] and
Wepfer found it also coagulated in the dog.[781]

It has been stated by some authors in medical jurisprudence that the
dead body occasionally exhales an aliaceous odour, resembling that of
sublimed arsenic. This is a very questionable statement. The only fact
of the kind worth mentioning is one brought forward by Dr. Klanck, as
occurring in the course of certain experiments, which will presently be
noticed, on the antiseptic virtues of arsenic. Several animals which had
been killed with arsenic are said to have exhaled an odour like that of
sublimed arsenic from three to eight weeks after death.[782]

A great discordance of opinion at one time prevailed among authors, as
to the influence of arsenic on the putrefactive process in the bodies of
those poisoned with it. The vulgar idea, borrowed probably from the
ancient classics, that the bodies of those who have been poisoned decay
rapidly, was till lately the prevalent doctrine of medical men, and even
of medical jurists; and it was applied to arsenic as well as other
poisons. Even so lately as 1776 we find Gmelin stating in his History of
Mineral Poisons, that the bodies of those who have died of arsenic pass
rapidly into putrefaction, that the nails and hair often fall off the
day after death, and that almost the whole body quickly liquefies into a
pulp.[783] A similar statement has been made in 1795 by a respectable
author, Dr. John Johnstone.[784] It appears that this rapid or premature
decay does really occur in some instances. Thus in a case related by
Plattner of death from arsenic administered as a seasoning for
mushrooms, the body had a very putrid odour the day after death.[785]
Loebel also asserts he found by experiments on animals, that after death
from arsenic putrefaction took place rapidly, even in very cold
weather.[786]

In other instances the body probably decays in the usual manner. For
example, in Rust’s Magazin is related the case of a child who died in
six hours of poisoning with arsenic, and in whose body, fourteen days
after death, the integuments were found considerably advanced in
putrefaction, and the liver and kidneys beginning to soften.[787] In the
case of a man who died in two days, and in whose body arsenic was found
by MM. Chapeau and Parisel throughout many of the tissues, “putrefaction
was so far advanced eight days after death as to render the examination
of parts obscure.”[788] And in the course of some experiments on dogs
poisoned with the oxide Dr. Seeman found the usual changes after five
months’ interment.[789]

But it has been proved in recent times that in general arsenic has
rather the contrary tendency—that, besides the antiseptic virtues which
it has been long known to exert when directly applied in moderate
quantity to animal substances, it also possesses the singular property
of enabling the bodies of men and animals poisoned with it both to
resist decay unusually long, and to decay in an unusual manner. The
observations and inquiries which have been made abroad on this subject
were little known any where else than in Germany before the publication
of the earlier editions of the present work; but parallel examples have
been since met with both in Britain and France; and in this country the
importance of the subject is generally appreciated.

The first occasion on which the antiseptic property of arsenic was
brought under public notice was about the beginning of the present
century, in the course of the trial of the widow of a certain
state-councillor, Ursinus of Berlin. Some time before that Dr. Welper,
then medical inspector in the Prussian capital, having remarked that the
body of a person poisoned with arsenic remained quite fresh for a whole
week in summer, he attended carefully to the subject at every
opportunity, and invariably, he says, found that the body resisted
putrefaction. Not long after making this remark, he was concerned in
1803, by virtue of his office, in the investigations in the case of the
widow Ursinus. This lady having been discovered in an attempt to poison
her servant, suspicions arose regarding the previous sudden death of
three persons in her family, her husband, a young officer who had
carried on an amour with her, and an aunt from whom she derived an
inheritance. They had all died in mysterious circumstances, and the lady
had been their only nurse. Dr. Welper disinterred the bodies of the
husband and aunt, which had been buried, the former two years and a half
before at Berlin, the latter half a year afterwards at Charlottenberg;
and he found them not putrid, but dried up; and specks of an appearance,
which is described as being gangrene, but which was probably warty
extravasation, were visible in the stomach. Arsenic could not be
detected.

He afterwards got Dr. Klanck, his acquaintance, to make some express
experiments on animals; and the results were strikingly conformable. In
dogs poisoned with arsenic and left for two months sometimes buried in a
damp cellar, sometimes exposed to the air of the cellar, the flesh and
alimentary canal were red and fresh, as if pickled; and though the place
where the carcases were subsequently buried again was flooded for eight
months after, the intestines were eventually found entire and red, the
fat converted into adipocire, and most of the muscles unaltered,—those
only being soft and greasy which were directly acted on by the water.
From a set of comparative experiments which were made on dogs killed by
blows, or poisoned by corrosive sublimate, or by opium, Klanck found,
that, after being buried in the same place, and for the same space of
time the whole soft parts of the carcases were converted into a greasy
mass. In a subsequent year he repeated his experiments, the bodies,
however, being this time left exposed to the air of the cellar. The
experiments were commenced in the month of August. In ten days there
appeared slight signs of incipient putrefaction; a faint putrid smell
was exhaled, and all flies that settled on the carcase died. This state
continued for eight or ten weeks without increasing. After that the soft
parts began to grow firmer and drier, and at the same time the putrid
odour was succeeded by a smell like that of garlic, which became
insupportably strong when the carcases were removed into warm air. The
bodies, three years afterwards, still continued dry and undecayed.[790]

A similar set of facts was again brought before the public between 1809
and 1811, during the criminal proceedings in a case like that of the
widow Ursinus, tried first at Bayreuth and afterwards by appeal at
Munich. A lady near Bayreuth died of five days’ illness, under symptoms
of violent general irritation of the alimentary canal. Some months
afterwards a variety of circumstances having raised a suspicion that she
had been poisoned by her maid, Margaretha Zwanziger, a judicial
investigation was set on foot; the consequence of which was, that the
same woman came under suspicion of having also previously poisoned
another lady and a gentleman with whom she had been successively in
service. The bodies of the three people were accordingly disinterred,
one of them five months, another six months, and the third fourteen
months after death. In all of them the external parts were not properly
speaking putrid, but hard, cheesy, or adipocirous; in the last two the
stomach and intestines were so entire as to allow of their being tied,
taken out, cut up, and handled; and in one a sloughy spot was found in
the region of the pylorus. Arsenic was detected in two of the bodies by
Rose’s process of analysis.[791]

The next example to the same effect which will be mentioned is perhaps
the most satisfactory of all, because it was the result of an express
experiment on the human subject. Dr. Kelch of Königsberg buried the
internal organs of a man who had died of arsenic, and whose body had
remained without burial till the external parts had begun to decay; and
on examining the stomach and intestines five months after, he found that
the hamper in which they were contained was very rotten; but that “they
had a peculiar smell, quite different from that of putrid bowels, were
not yet acted on by putrefaction, but as fresh as when first taken from
the body, and might have served to make preparations. They had lost
nothing of their colour, glimmer, or firmness. The inflamed spots on the
stomach had not disappeared, and the small intestines also showed in
some places the inflammatory redness unaltered.”[792]

In a recent French case, although the degree of preservation was less
remarkable, the other circumstances are so striking as to render it well
worthy of notice. In this instance the body was disinterred after having
been seven years in the ground, in a high situation and sandy soil. The
coffin, which was of oak, had become dry and brittle, and no moisture
appeared on the inside. The body was entire: the head, trunk, and limbs
retained their situation; but the organs of the chest and belly were
converted into a brown soft mass of the consistence of plaster, which
lay on each side of the spine. In this mass MM. Ozanam and Idt, the
medical inspectors, succeeded in discovering by chemical analysis a
considerable quantity of arsenic.[793]

M. Ollivier describes another French case, where the body had been
buried for three years, and was found so completely dried up that the
trunk weighed only two pounds. The integuments were entire, dark-brown,
and of a faint odour like decayed wood. The organs of the chest and
belly were confounded together in a foliaceous membranous mass, in which
the liver only could be distinguished, but in an exceedingly shrivelled
state. Arsenic was detected in the membranous matter by MM. Barruel and
Henri. The preservative power of the arsenic was promoted in this case
by the sandy nature of the soil.[794]

In the case of the girl Warden, which has been several times alluded to,
the internal organs were also preserved somewhat in the same manner as
in the German cases. The body had been buried three weeks; yet the
mucous coat of the stomach and intestines, except on its mere surface,
was very firm, and all the morbid appearances were consequently quite
distinct. Nay, three weeks after disinterment, except that the
vascularity had disappeared, the membranes and the appearances in them
remained in the same state.[795] A similar case has been recorded by
Metzger. It is that of an old man who died of six hours’ illness, and in
whose stomach three drachms of arsenic were found. The body had been
kept ten days in February before burial, and was disinterred eight days
after that; yet there was not the slightest sign of putrefaction any
where.[796] A parallel case was described by myself in the Edinburgh
Medico-Chirurgical Transactions;[797] and I have met with three others
of the same kind since.

In a very important case, that of Mrs. Smith, which was made the subject
of investigation at Bristol in December, 1834, the body was also found
in a state of great preservation, modified, however, by adipocirous
decomposition, owing to the presence of water in the coffin. The body
had been fourteen months interred. The internal parts, especially of the
head and neck, were here and there decayed somewhat or converted into
adipocire, the muscles and internal organs entire, though more or less
shrivelled, the alimentary tube remarkably preserved, “every part being
almost as distinct as if the inspection had been made at a very short
period after death,” “the mucous membrane sufficiently tenacious to be
lifted by the forceps in as large flakes as usual;” and the reporters,
Drs. Riley and Symonds, Messrs. Herapath and Kelson, seem to have had no
difficulty in ascertaining the absence of vascularity, extravasation, or
even abrasion of the inner membrane. Artificial orpiment, the
preparation proved to have been given [see p. 225], was found in the
stomach by Mr. Herapath, and the quantity appeared to be about half a
drachm.[798]

A similar instance, very remarkable in all its circumstances, was
investigated here in 1834 by my colleague Dr. Traill to whom I am
indebted for the particulars. The master of a foreign vessel died in
about twenty-four hours, apparently of malignant cholera, at a small
port in the neighbourhood of Edinburgh: and the body was forthwith
buried. A suspicion, however, having arisen in his native country that
he had been poisoned by his mate, an inquiry was instituted at the
request of the foreign government; and the body was disinterred five
months after death. The face and neck was swollen, black, and decayed;
but the rest of the body was quite free of the usual signs of
putrefaction. The skin was white and firm, the muscles fresh, the lungs
crepitating, the liver and spleen much shrivelled, the stomach and
intestines entire throughout their whole tissues, and capable of being
handled freely without injury. On the mucous coat of the stomach several
dark patches of extravasation were found, likewise several spots and
large patches which presented on their surface a firmly adhering bright
yellow crust; and the contents of the stomach consisted of a
considerable quantity of yellow sandy matter of the consistence of
paste. The contents and adhering crusts were found to consist chiefly of
oxide of arsenic partially converted into sulphuret. In this instance,
as in that last described, the coffin contained water, owing to its
having laid in a sandy soil resting on clay.

An important case of the same nature was communicated to me in 1843 by
Mr. Sandell of Potton, Bedfordshire, and afterwards published by Mr.
Hedly of Bedford. A man Dazley at Wrestlingford, affected with symptoms
of gastro-enteric irritation for five or six days, was seized with
sickness, vomiting, heat and constriction in the throat, and great
weakness, about an hour after getting a white powder from his wife; and
in eight hours he expired, without any suspicion of unfair usage arising
at the time. Suspicions, however, being entertained afterwards, the body
which had not been examined at first, was disinterred in five months,
during the month of March. The countenance was so entire as to be
recognisable. Adipocire had been formed in many places. The stomach and
intestines were “in a most perfect state of preservation,” as if death
had taken place only a few days previously. The stomach presented yellow
patches on its outer and inner surface,—was generally red over its
villous coat, which had also been abraded near the cardiac end,—and,
together with the small intestines, was lined with white powder and
contained more of it enveloped in much red mucus. This powder proved to
be arsenic. About the middle of the small intestines a small ulcerated
opening was found, through which some arsenic had escaped.[799]

The following cases which have come under my own notice during the last
five years are also worthy of observation. In a case submitted to me on
the part of the crown in 1841, which has been adverted to above for
another purpose [p. 265], the body after being three months interred was
found with the head and face decayed and putrid; but the muscular
substance was little changed; and the inspectors were particularly
struck with the state of preservation of the body, and also with the
very distinct state of inflammation seen over almost the whole external
and internal surfaces of the alimentary canal,—a description, the
accuracy of which I had afterwards an opportunity of verifying. In the
case of Mr. Gilmour (p. 265), whose body had been buried 101 days, the
external parts were more decayed; but the alimentary canal appeared
equally entire both to the original inspectors, Drs. M’Kinlay and Wylie,
and likewise to myself three weeks later. But the following instance, in
which I was consulted in 1839, is the most remarkable one of the kind
that has hitherto occurred to me; because the observations then made
were the result of an express experiment in a medico-legal
investigation. The history of this case, which arose from small doses of
arsenic frequently administered, has been already given above in some
detail [p. 250]. Arsenic not having been detected in the contents or
tissues of the stomach, and the trial of the individual suspected of
giving the poison being necessarily postponed for some months, I
recommended that a third examination of the body,—for it had been twice
disinterred for inspection within ten days after death,—should be made
at as distant an interval as possible, in order to ascertain whether it
underwent preservation from decay. It was accordingly disinterred again,
five months after death. It had an ammoniacal, but not a putrid odour.
The skin was here and there covered with a thin sebaceous matter, at one
or two places stripped of the epidermis, but for the most part natural
in appearance, firm, and elastic. The nails were loose. The muscles of
the head and near the tops of the scapulæ were adipocirous, on the chest
and abdomen obscurely fibrous in texture and hardened, but elsewhere
unaltered, and “in the lower extremities so perfect that they might have
been used for an anatomical demonstration.” The liver and lungs were
also in a state of good preservation, and the latter crepitated when
cut. The other viscera had been removed at the previous examinations.

It may be added that the experiments of Klanck on dogs adverted to above
have been more recently repeated by Hünefeld on rabbits and mice, with
precisely the same results. The animals were sometimes left in the air,
at other times buried, and generally in a moist place. In every instance
putrefaction made more or less progress at first; but in a few days a
peculiar garlicky odour arose, from which time the progress of decay
seemed to be arrested; and the bodies underwent a process of hardening
and desiccation which completely preserved them.[800]

On considering attentively the illustrations now given, the toxicologist
can hardly doubt that in some cases arsenic has appeared both to retard
and to modify putrefaction in the bodies of persons poisoned with it.

Assuming arsenic to have been the cause of the preservation of the
bodies, it becomes a point of consequence to account for its effect, and
more particularly to reconcile that effect with what has certainly been
noticed in other cases of poisoning with the same substance, namely,
ordinary rapidity of decay, if not actually an increased tendency to
putrefaction.

At the outset of this part of the inquiry some light may be thrown upon
it by separating the local from the general operation of arsenic.

Arsenic is a good preservative of animal textures when it is directly
applied to them in sufficient quantity. This is well known to stuffers
of birds and beasts, was experimentally ascertained by Guyton
Morveau,[801] and has come also under my observation.[802] It is now
likewise known to be an excellent substance for preserving bodies, when
injected in the form of solution into the blood-vessels.

Hence, if in a case of poisoning the arsenic be not discharged by
vomiting, and the patient die soon, it will act as an antiseptic on the
stomach at least, perhaps on the intestines also; while the rest of the
body may decay in the usual manner. This is very well shown in a case
examined by Dr. Borges, medical inspector at Minden, fourteen weeks
after death. The stomach and intestines were firm, of a grayish-white
colour, and contained crumbs of bread, while all the other organs in the
belly were pulpy, and the external parts adipocirous.[803] It is also
equally well exemplified in a case that happened at Chemnitz so early as
1726, and which was examined five weeks after burial. The skin was every
where very putrid, but the stomach and intestines were perfectly
fresh.[804] In the case of Warden the appearances were precisely the
same. Three weeks after burial the Dundee inspectors found the external
parts much decayed, yet three weeks later the stomach and intestines
were found by myself in a state of almost perfect preservation. A
striking experiment performed by Dr. Borges on a rabbit will likewise
illustrate clearly the fact now under consideration. The rabbit was
killed in less than a day with ten grains of arsenic, and its body was
buried for thirteen months in a moist place under the eaves of a house.
At the end of this period it was found, that “the skin, muscles,
cellular tissue, ligaments and all the viscera, except the alimentary
canal, had disappeared, without leaving a trace; but the alimentary
canal from the throat to the anus, along with the hair and the bare
bones, was quite entire.”[805]

In all of these cases arsenic was found in the body. In the rabbit
experimented on by Dr. Borges, above five grains of arsenic were
separated in the form of a metallic sublimate.

But, on the contrary, if the arsenic is all or nearly all discharged by
vomiting, not only the body generally, but likewise even the stomach and
intestines, may follow the usual course of decay. Accordingly, in the
case of the child formerly quoted (273), where the body putrified in the
usual manner, only four grains and a half of arsenic had been taken; and
as it was swallowed in a state of solution and caused violent vomiting,
it must have been almost all ejected. Nay, in such circumstances, the
alimentary canal, in consequence of its unnatural supply of moisture and
incipient disorganization, may decay somewhat faster than other parts.
Thus Dr. Murray observed in the case of a man formerly mentioned (264),
who lived under violent gastritic symptoms for seven days, and vomited
much, that the stomach, which was removed for more minute examination,
decayed so rapidly that in twenty-four hours an examination was
impracticable, while the body in general rather resisted
putrefaction.[806]

The preceding statements on the differences in the state of preservation
of the body after poisoning with arsenic are not then incapable of some
explanation. Nevertheless, it must be granted that the reasons assigned
will not account for all the apparent cases of the preservative powers
of arsenic. And especially they will not explain how the whole body has
sometimes resisted decay altogether, and become as it were mummified. It
is impossible to ascribe this preservation to the spelling power of the
arsenic diffused throughout the body in the blood; the quantity there
being extremely small. Consequently if the preservation of the bodies is
not occasioned by some accidental collateral cause (a mode of accounting
for the phenomena which seems inadmissible), this property of arsenic
must depend on its causing, by some operation on the living body, a
different disposition and affinity among the ultimate elements of
organized matter, and so altering the operation of physical laws on it.
There appears no sound reason for rejecting this supposition, especially
as it is necessary to admit an analogous change of affinities as the
only mode of accounting for a still more incomprehensible violation of
the ordinary laws of nature,—the spontaneous combustion, or
preternatural combustibility, of the human body.

The following judicious observations by Harles on this subject are
worthy of attention:—“In regard,” says he, “to this singular property of
arsenic, now no longer doubtful, it should be remembered that certain
circumstances will limit or impair it, while others will favour or
increase it;—circumstances, for example, connected with the soil of the
burying-ground, or the air of the vaults where the bodies are deposited.
Different soils and different conditions of the air will materially
affect the decomposition of all bodies indiscriminately, and will
therefore affect likewise the antiseptic properties of arsenic. For it
would be absurd to ascribe to arsenic the power of preventing
putrefaction in all circumstances whatsoever,—a power which those who
make use of it for preserving skins know very well it does not possess,
and a power possessed by no antiseptic whatever, not even by
alcohol.”[807]

An important consequence of the preservative tendency of arsenic is,
that in many instances the body in this kind of poisoning may be found
long after death in so perfect a state as to admit of an accurate
medico-legal inspection and a successful chemical analysis. In one of
his cases Dr. Bachmann detected arsenic in the stomach fourteen months
after interment; Dr. Borges had no difficulty in detecting it in an
animal after thirteen months; Mr. Herapath discovered it after
fourteen months in the human body; M. Henry detected it after three
years and a half, and obtained no less than seven grains of metallic
arsenic from the shrivelled viscera;[808] and MM. Ozanam and Idt found
it after the long interval of seven years.—The late experiments of
Orfila and Lesueur confirm the fact that arsenic may remain long in
contact with decaying animal matter, and yet continue in such a state
as to be easily detected.[809] It might be supposed that the poison
would pass off partly in the gaseous state by being converted into
arseniuretted-hydrogen, partly in the liquid state by becoming
arsenite of ammonia, a very soluble compound. But the fact
nevertheless is, that, notwithstanding these reasons for its
disappearance, it may be detected after the lapse of several years.

Under the head of the diseased appearances left by arsenic in the dead
body, every change of structure has now been described which has been
mentioned by authors and supported by trustworthy statements. Another
set of appearances may still be noticed; but they are here separated
from the rest, because the author who first notices them has not been
supported in the statement by any special observations of his own, or by
an adequate number of facts observed by others. In an elaborate essay on
a case of poisoning by Professor Seiler of Wittemberg, it is said in
general terms that arsenic may cause gorging of the vessels of the
brain, effusion of serum into the ventricles, inflammation of the brain,
and even extravasation of blood.[810] Turgescence of vessels is
mentioned in several published cases, and I have myself met with it. But
it is seldom so considerable as to attract attention. In the following
instance, however, which has been related by Dr. Hofer of Biberach the
evidence of cerebral congestion was unequivocal. A man addicted to
intoxication, but enjoying good health otherwise, was attacked after
supper with sickness, vomiting, and pain in the belly. On going to bed
he fell soon quiet; and six hours after he took ill, he was found dead.
Arsenic was detected in the stomach, and in what he vomited; and
considerable redness was seen on the villous coat of the stomach. But
the most remarkable appearances were gorging of the cerebral vessels,
adhesion of the dura mater to the membranes beneath, and the effusion of
eight ounces of serosity into the lateral ventricles.[811] The only
instance I am acquainted with to justify the opinion that extravasation
of blood into the brain may occur from poisoning with arsenic, is the
remarkable case of apparent death from eating poultry poisoned with
arsenic, which was communicated to me by Mr. Jamieson of Aberdeen. The
individual, after suffering under the usual primary symptoms, became
apoplectic after a fit of sneezing, and died three days afterwards; and
in the dead body, besides other signs of disease in the brain, a recent
clot of blood was found in the right anterior lobe. (See p. 69.)

It is quite unnecessary to notice lividity of the skin among the signs
of poisoning with arsenic, except for the mere purpose of reminding the
medical jurist that, although it has been sometimes much relied on as a
sign of death from arsenic, it is not of the slightest importance as a
sign either of that or of any other kind of poisoning. (See p. 51.)

The action of arsenic on the alimentary canal after death will now
require a few remarks; the purpose of which is to prepare the medical
inspector for investigating attempts to impute the crime of poisoning to
innocent persons, by introducing arsenic into the dead body. Such
attempts, according to Orfila, have been made; but I am not acquainted
with any actual instance.

The action of arsenic on dead intestine has been fully examined by the
last mentioned author. If it is introduced into the anus immediately
after death, and allowed to remain there twenty-four hours, the mucous
membrane in contact with it becomes of a lively red colour, with darker
interspersed patches as if from extravasation. The other coats are
natural; and so is the mucous membrane itself wherever the poison does
not actually touch it. Consequently the margin of the coloration is
abrupt and well defined. When the arsenic is not introduced till
twenty-four hours after death, the part to which it is actually applied
presents dark patches, while the rest of the membrane is quite
healthy.[812]

The appearance of redness in the former case is probably the result of
lingering vitality. The cause of the dark appearance in the latter it is
not easy to comprehend.

When arsenic has been applied, during life, the redness, if it has had
time to begin at all, extends to some distance from the points with
which the poison has been in contact, and passes by degrees into the
healthy colour of the surrounding membrane.

On reviewing what has been said of the pathological appearances caused
by arsenic, it must appear that the medical jurist can never be supplied
from this source alone with satisfactory evidence of the cause of death.
But in some circumstances the evidence may amount to a strong
probability of one variety or another of irritant poisoning. Mere
redness, conjoined or not with softening of the mucous membrane, may
justify suspicion only. But if there should be found in the body of a
person who has died of a few days’ illness, redness, black warty
extravasation, and circumscribed ulcers of the villous coat of the
stomach,—effusion of blood or bloody clots among the contents of that
organ,—also redness of the intestines, more especially redness and
ulceration of the colon and rectum,—and redness of the pharynx, or of
this along with the gullet,—the proof of poisoning with some irritant
will amount to a strong presumption. At least it is difficult to mention
any natural disease which could produce in so short a time such a
conjunction of appearances as this; which arsenic and other analogous
poisons sometimes occasion.


       SECTION IV.—_On the Treatment of Poisoning with Arsenic._

It was formerly proved that arsenic acts in all its forms of chemical
combination, which have been hitherto tried, and nearly in the ratio of
their solubility. This general fact is conformable with the law laid
down as to the influence of chemical changes on the energy of poisons
which enter the blood [p. 37]. Hence every supposed chemical antidote
must be useless, which does not render the arsenic insoluble not only in
water, but likewise in the contents and secretions of the stomach.

The antidotes chiefly trusted to until recent times, such as vinegar,
sugar, butter and other oily substances, lime-water, bitter decoctions,
and the like, have now justly fallen into disuse. The liver of sulphur
or sulphuret of potassium, which maintained its character for some time
longer on account of its chemical action with oxide of arsenic in
solution, is not more efficacious. The experiments of Renault on the
counter-poisons for arsenic, confirmed by the subsequent researches of
Orfila, have proved that the arsenical sulphuret formed by solutions of
the liver of sulphur is scarcely less active than the oxide itself.[813]

It appears that fine impalpable powders, though inert as physiological
agents, and destitute of any true chemical action with oxide of arsenic,
may nevertheless prove useful in certain limited circumstances. Thus Mr.
Hume of London and others have apparently found some advantage in the
administration of large doses of magnesia.[814] If this substance be of
any use at all, which is doubtful, it can act only by covering the
arsenical particles with its fine insoluble powder, and so preventing
them from coming in contact with the surface of the stomach; for in its
state of magnesia it has no chemical action with oxide of arsenic.
Another remedy of the same nature is charcoal powder, which was proposed
in 1813 with much confidence by M. Bertrand.[815] That it has some
efficacy when swallowed along with the poison seems to admit of no
doubt; for the proposer of it himself swallowed five grains of arsenic
in one dose along with charcoal in a state of emulsion, and sustained
little inconvenience of any kind. In all probability it acts merely by
enveloping the particles of arsenic. But it may possibly be also of
service, if recently exposed to heat, by the superficial attraction it
exerts over substances in solution; through means of which property it
will remove many soluble substances from a fluid, and render them
insoluble. Charcoal, however, has been proved to be destitute of all
efficacy when not administered till after the arsenic is swallowed. The
one must be given along with the other, otherwise it is useless.[816]

For some time past the formation of an insoluble arsenite has been aimed
at by most experimentalists who have endeavoured to discover an antidote
for arsenic. But in general the arsenites, though very insoluble in
water, are sufficiently so in weak acids or in organic fluids, so that
they are soluble enough in the juices of the stomach to enter the blood
in such quantity as to prove fatal. The only exception now admitted to
exist is the arsenite produced when a solution of oxide of arsenic is
brought in contact with the hydrated sesquioxide of iron. The compound
thus formed is held to be insoluble in the secretions of the stomach;
and consequently the hydrated sesquioxide of iron is usually regarded as
a true antidote.

The substance, the Ferrugo of the Edinburgh Pharmacopœia,—a compound
which differs little from the older preparation, the rust of iron, when
not deprived of its combined water,—was announced in 1834 by Drs. Bunsen
and Berthold as an effectual remedy even when given some time after the
arsenic is swallowed.[817] Their experiments were repeated with variable
success. Similar results were obtained by MM. Soubeiran and Miquel, as
well as MM. Orfila and Lesueur, in some experiments on dogs, and by M.
Boullay on the horse.[818] The last experimentalist found that the
effects of a dose adequate ta occasion death are almost entirely
prevented in the horse by giving the oxide of iron either immediately
after the poison, or within four hours. Results of the same nature were
obtained in this country by Mr. Donald Mackenzie.[819] Others, however,
such as Mr. Brett[820] and Mr. Orton,[821] have failed to observe any
antidotal virtues, and even deny that the sesquioxide of iron can remove
oxide of arsenic from a state of solution. But in 1840 the causes of
these discrepant statements were explained by Dr. Douglas Maclagan,[822]
who found, in corroboration of the remarks of Drs. Bunsen and Berthold,
as well as various French authorities, that the oxide must be given in
large quantity, and that the failures of some were owing to the quantity
used having been too small. He ascertained, that, in order to remove one
part of arsenic from a state of solution, twelve parts of oxide of iron
in the moist state are necessary, and sixty parts if it be previously
dried; that the arsenic so appropriated is with difficulty removed from
the insoluble matter even by boiling; and that, as the discoverers of
this antidote first stated, the preparation made by precipitating the
sesquioxide of iron by means of ammonia, is a more active form than any
other. As the oxide prepared in this way always contains ammonia, and
the proportion necessary for removing the arsenic is far greater than
what is required to constitute a simple arsenite of iron, it is
reasonable to infer that the ammonia forms a part of the insoluble
compound actually produced. At all events the action of the antidote
would appear to be chemical, and not mechanical, as has been thought by
many, and as was stated to be probable in the last edition of this work.
In confirmation of these views, and as a fact worthy of farther
investigation on its own account, it is worthy of notice, that,
according to Dr. Duflos, the acetate of sesquioxide of iron answers
equally well as an antidote with the sesquioxide itself. It precipitates
both arsenious and arsenic acid from every state of solution, and always
the more quickly the more the solution is diluted; and the co-existence
of acetic acid is no obstacle to this action taking place.[823]—More
recently Professor Orfila has called in question the absolute efficacy
generally ascribed to the sesquioxide of iron. He alleges that the
arsenical compound formed, though insoluble in water, is soluble to some
extent in the gastric juices, and is consequently a poison to animals;
that the sesquioxide is therefore only partial in its operation as a
remedy; but yet that the influence of the animal fluids in the stomach
in counteracting it may be overcome by giving it in excess, so that, as
fast as the compound is dissolved, it is thrown down again.[824]

The cases of the successful employment of this antidote in the human
subject, which have appeared in the periodical press during the last
eight years, are so numerous, that its utility can scarcely be called in
question, whatsoever may be its precise mode of action. The hydrated
sesquioxide of iron ought therefore to be kept in readiness in every
druggist’s establishment; for it cannot be prepared when wanted without
great loss of time. The quickest way to make it is to dissolve the
common anhydrous sesquioxide, formerly miscalled carbonate of iron, in
diluted sulphuric acid aided with a gentle heat; to decompose the hot
solution with an excess of strong ammonia; to filter off the fluid by
means of a cloth filter and wash the precipitate well with warm water;
and then to let it drain thoroughly and to squeeze out more of the water
by expression. It should be kept in this state, and not allowed to dry.

In regard to all antidotes for arsenic, it must be observed, that they
can seldom be otherwise employed than in unfavourable circumstances. If,
as most generally happens, the poison has been taken some time before
medical aid is obtained, its powder is diffused over the surface of the
stomach, adheres with tenacity to the villous coat, and excites the
secretion of tough mucus, through which it is with difficulty reached by
any antidote possessing a chemical action with it. In all cases,
therefore, it is advisable to promote vomiting occasionally, if not
already full and free, so as to aid the stomach in clearing itself of
the secreted mucus.

If the existence of a chemical antidote for arsenic be doubtful, much
less is there any one known of that rarer denomination which operates by
exciting in the system an action contrary to that established by the
poison.

A good deal, however, may be done by general medical treatment to
improve the chance of recovery. If vomiting should be delayed, as often
happens, for half an hour or more, advantage ought to be taken of the
opportunity to administer an emetic of the sulphate of zinc, with the
view of withdrawing the powder in mass before it is diffused over the
stomach; and for the same purpose milk should be drunk both before and
after vomiting has begun, as it appears to be the best substance for
enveloping the powder, and so procuring its discharge. The patient
should never be allowed to exhaust his strength in retching without a
little milk or other fluid in his stomach to act on. At the same time,
there is probably some justice in the opinion expressed by a late writer
on this subject, that large draughts of diluents are injurious; and
that, unless the stomach is allowed to contract fully and frequently on
itself, it cannot discharge from its surface the mucous secretion, in
which the powder of arsenic is in general closely enveloped.[825] The
stomach-pump, although it has been applied to cases of poisoning with
arsenic, does not possess any advantage whatever over emetics or the
natural efforts of nature, and is less effectual in expelling the mucus
which envelopes the poison. Even emetics are unnecessary, when full
vomiting is caused by the poison itself. If milk in sufficient quantity
cannot be procured, strong farinaceous decoctions will probably prove
useful.

Supposing the poison to have been removed from the stomach, or that the
patient has been put on the course which appears best fitted to
accomplish that end,—two objects remain to be accomplished, namely, to
allay the inflammation of the alimentary canal, and to support the
system under that extraordinary depression which it undergoes in the
generality of cases. Were it not for the latter of these objects, the
treatment would be both obvious and frequently successful. But it is
highly probable that the active remedies, to which the physician trusts
in internal inflammations generally, and which are urgently called for
by the inflammation caused by arsenic, cannot be enforced with the
requisite vigour, on account of the remote depressing effects also
produced by this poison on the body.

Nevertheless, it is certain that in a few even very aggravated cases the
purest and most vigorous antiphlogistic treatment has been resorted to
with success. Dr. Roget’s patient, whose case was formerly referred to
for another purpose, seems to have been saved by venesection; and at all
events, the amelioration effected was unequivocal. In the Medical
Repository there is another good example of the beneficial effects of
blood-letting carried even to a greater extent than in Roget’s
case;[826] and in the Medical and Physical Journal[827] a third instance
will be found, which after the first twenty-four hours assumed the form
of pure gastritis, and was treated as such with success. Blood-letting
ought not to be practised till the poison is nearly all discharged from
the stomach, because it promotes absorption by causing emptiness of the
blood-vessels.

Orfila has lately advocated the use of blood-letting, on the ground that
it tends to remove from the system a portion of the poison which
circulates with the blood, and is the main source of danger to life. He
has endeavoured to show by experiments on animals, that doses adequate
to cause death may be given without this result following, if depletion
be vigorously enforced along with other treatment. And he has related a
case of recovery in the human subject under unfavourable circumstances,
where blood-letting was practised five times, and on every occasion with
marked relief.[828]

It is not probable that any material advantage will be derived from
topical blood-letting, at least in the early stage, because if depletion
is to be of use at all, it must be carried at once to a far greater
extent than it is possible to attain by local evacuants. Blisters on the
abdomen will prove useful auxiliaries in the advanced stage.

While many have advocated the employment of blood-letting and other
antiphlogistics, and have used them with apparent advantage, Rasori was
of opinion, and more recently Giacomini has strenuously maintained that
the proper treatment in all cases of arsenical poisoning is the purely
stimulant method. The remedy recommended by the latter is a mixture of
eight ounces of beef-tea and two ounces of wine. These notions are
evidently dictated by the prevailing pathological delusions of the
Italian school. Although upheld in some measure by a Report of the
Parisian Academy of Medicine upon some experiments by M. Rognetta on
this subject,[829] Professor Orfila subsequently proved, that the
practice recommended is utterly useless, if not even hurtful.[830] At
the same time no one who has ever seen a case of poisoning by arsenic
can doubt that it is often necessary to counteract the overwhelming
languor of the circulation by the moderate use of stimulants.

Opium in repeated doses will prove useful, when the poison has been
removed, and the inflammation subdued by blood-letting. And I conceive
that to the form of gastritis, caused by arsenic, may be applied a
method of treatment by anodynes, which has been successfully used in
acute inflammation generally,—the free administration of opium
immediately after copious depletion. For the safe employment of this
method, however, it is essential that the arsenic be completely removed
from the stomach and intestines. And from the results of many cases
there must always be great reason to apprehend, that, before the
treatment can be with propriety resorted to, the patient’s strength will
be exhausted.

The harassing fits of vomiting which often continue long after the
poison has been discharged from the stomach are best removed by opium in
the form of clyster, or rubbed over the inside of the rectum in the form
of ointment with the finger.

The use of laxatives is particularly required in all cases in which
there is tenesmus instead of diarrhœa, or where, in the latter stages,
diarrhœa is succeeded by constipation; and castor oil is the laxative
generally preferred. While diarrhœa is present, and the evacuations are
profuse or the intestines have been thoroughly emptied, laxatives are
unnecessary or even hurtful; but emollient clysters are advisable, and
opium in the form of enema or suppository. In short, so far as regards
the intestinal affection, the treatment of the acute stage of dysentery
is to be enforced.

Professor Orfila lays great stress on the employment of diuretics after
the stomach has been cleared out, and founds this practice on his
observations which show that arsenic is absorbed into the blood, and
gradually discharged by the secretions, especially the urine. Experience
seems to confirm theory. Dogs, after receiving a small dose, adequate to
occasion death, recovered under the active administration of diuretics.
Having ascertained that this animal was constantly killed in a period
varying from thirty to forty-eight hours by two grains applied to a
wound, provided no remedies were employed, he tried the diuretic method
with six which had been thus poisoned; and all of them recovered.[831]
The diuretic he recommends is a mixture of ten pounds of water, five of
white [French] wine, a bottle of Selzer water, and three ounces of
nitre; the dose of which is two wine-glassfuls frequently.[832] This
method has been followed with success in the human subject. M. Augouard
relates a case where 230 grains produced in half an hour all the usual
symptoms, which he immediately proceeded to treat by administering a
grain and a half of tartar-emetic, to excite full vomiting. Having
accomplished this object, he gave frequent doses of decoction of mallow
“strongly salpetred,” which in seven hours excited so profuse a diuresis
that in the ensuing ten hours no less than eighteen imperial pints was
discharged. At the close of this period a material amendment took place,
and recovery was complete in fifteen days.[833] It may be observed,
however, that it is sometimes impossible to excite diuresis.[834]

Little need be said of the practice to be pursued in the advanced stages
of poisoning with arsenic, when convalescence has begun. The principal
object is to support the system by mild nourishment, avoiding at the
same time stimulant diet of every kind, but especially spirituous and
vinous liquors. Whatever may be the difference of results obtained with
the antiphlogistic mode of cure, the opposite system has been invariably
detrimental in the advanced stage.

The treatment of the nervous and dyspeptic affections, which may
supervene after the symptoms of local inflammation have ceased, is not a
fit object of review in this work, as it would lead to great details.




                              CHAPTER XIV.
                       OF POISONING WITH MERCURY.


The next genus of the metallic poisons includes the preparations of
mercury. Some of these are hardly less important than the arsenical
compounds. They act with equal energy, produce the same violent
symptoms, and cause death with the same rapidity. They have therefore
been often given with a criminal intent; and have thus become the
subject of inquiry upon trials. In another respect, too, they claim the
regard of the medical jurist: their effects on the body, when
insidiously introduced in the practice of the arts in which mercury is
used, form a branch of that department of medical police, which treats
of the influence of trades on the health.


 SECTION I.—_Of the Chemical History and Tests for the preparations of
                               Mercury._

Mercury is a fluid metal, exceedingly brilliant, of a silver-white
colour, and of the specific gravity 13·568.

When heated to about 660° F. it sublimes, and on cooling it condenses
unchanged. If this experiment is made in a small glass tube, the metal
forms a white ring of brilliant globules, which may be made to coalesce
into a single large one. In this way its physical properties may be
recognised, though the quantity is exceedingly minute.

Two oxides of this metal, a protoxide and peroxide, exist in combination
with acids. A bluish-gray or grayish-black protoxide is separated from
the salts of the protoxide by the fixed alkalis. The peroxide has an
orange-red colour, and is the common red precipitate of the apothecary.
Mercury unites with sulphur in two proportions. The proto-sulphuret,
which is black, is formed from the salts of the protoxide by the action
of sulphuretted-hydrogen: the bisulphuret is the well known pigment,
cinnabar or vermilion. Mercury likewise unites with chlorine in two
proportions, forming an insoluble protochloride and a soluble
bichloride, the former calomel, the latter corrosive sublimate. It
likewise unites with cyanogen. Mercury also unites in the state of
protoxide and peroxide with the acids. Several compound salts are known
to the chemist, but few occur in commerce or the arts.

Among the compounds resulting from the action of this metal with other
substances, those which require notice in a toxicological treatise are
the following:—1. The binoxide or _red precipitate_; 2. The bisulphuret
or _vermilion_; 3. The protochloride or _calomel_; 4. The bichloride or
_corrosive sublimate_; 5. The sulphate or _Turbith mineral_; 6. The
_bicyanide_ or prussiate of mercury; and 7. The _nitrates_ of mercury.
Its other compounds are of little consequence to the toxicologist.


                        1. _Of Red Precipitate._

Red precipitate, when well prepared, is in the form of fine powder or
small, brilliant, heavy scales of a scarlet or orange colour. It
consists of 101 mercury and 8 oxygen. It is insoluble in water.

It is easily distinguished from all other substances by the action of
heat. If a little of it is heated in a small glass tube, it becomes dark
brown, and on cooling recovers its original colour. But if the heat be
raised higher, metallic globules are sublimed, and oxygen gas is
disengaged. The escape of oxygen may be ascertained by plunging to the
bottom a small bit of burning wood, when the combustion will be observed
to be enlivened.


                           2. _Of Cinnabar._

Cinnabar or vermilion, the bisulphuret of mercury, usually exists in the
arts in the form of a fine, heavy, red powder, of a peculiar tint, which
is termed from this substance vermilion-red. In mass its structure is
coarsely-fibrous, and its colour reddish-brown; and it has some lustre.
When thrown down from a solution of corrosive sublimate by
sulphuretted-hydrogen, or the alkaline hydrosulphates, it forms a black
powder, which acquires a red tint by being sublimed. It is composed of
101 metal and 16 sulphur.

It is distinguished from other substances by the operation of heat, and
by the effects of reduction with iron filings. Heated alone in a tube it
sublimes without change. Its colour, indeed, which is fugacious under
heat unless particular manipulations are used, becomes darker and dingy;
but its lustre and crystalline texture are retained. Heated with iron
filings in a tube, it gives off globules of mercury; and the existence
of sulphuret of iron in what remains may be proved by the escape of
sulphuretted-hydrogen on the addition of diluted sulphuric acid.


                        3. _Of Turbith Mineral._

The Turbith mineral, or subsulphate of the binoxide of mercury, exists
in the form of a bright lemon-yellow, heavy powder. It is soluble in
2000 parts of water, and has an acrid taste.

It may be known by the effects of heat. When heated in a tube, globules
of mercury are sublimed, and at the same time sulphurous acid gas is
disengaged, as may be ascertained by the smell. But a better method of
proving the existence of sulphuric acid in it is to expose it to the
action of a solution of caustic potass: The potass separates from it the
brownish-yellow peroxide, and appropriates the sulphuric acid, which may
be found in the solution by acidulating with nitric acid, and then
adding hydrochlorate of baryta, when a heavy, snow-white precipitate of
sulphate of baryta will form. The nitric acid used in this process must
be quite pure, and free of sulphuric acid, which the acid of commerce
often contains.


                            4. _Of Calomel._

Calomel (muriate, mild muriate, chloride, protochloride of mercury), is
commonly met with in the shops in the form of a heavy powder, having a
faint yellowish-white colour, and no taste or smell. In mass it forms
compact, fibrous, translucent, shining cakes of great density. It is
insoluble in water.

It is distinguished by the effects of heat, and those of the solution of
caustic potass. Heated in a tube it sublimes unchanged, and condenses in
a crystalline or crumbly mass. The solution of caustic potass or soda
turns it at once black, disengaging protoxide of mercury and acquiring
hydrochloric acid, the presence of which is proved by neutralizing the
solution with nitric acid, and adding nitrate of silver, when a heavy
white precipitate is formed, the chloride of silver. In applying this
process, care must be taken to employ potass quite free of muriates, and
nitric acid free of muriatic acid. Ammonia also renders calomel powder
black, but the action and product are much more complex in their nature.


                      5. _Of Corrosive Sublimate._

Corrosive sublimate (oxymuriate, corrosive muriate, bichloride of
mercury), is by far the most important of the mercurial poisons, as it
is both the most active of them, and the one most frequently used for
criminal purposes. It is commonly met with in the form of a heavy,
snow-white powder, or of small, broken crystals, or in white, compact,
concave, crystalline cakes. It is permanent in the air; but in the
sunshine is slowly decomposed, a gray insoluble powder being formed. It
readily crystallizes, and the common form of the crystals is the
quadrangular prism. Its specific gravity is 5·2. Its taste is strongly
styptic, metallic, acrid, and persistent; and its dust powerfully
irritates the nostrils. It is soluble, according to Thenard, in 20,
according to Orfila, in 11 parts of temperate water, and in thrice its
weight of boiling water. Its solution faintly reddens litmus. It is more
soluble in alcohol than in water, boiling alcohol dissolving its own
weight, and retaining when it cools, a fourth part. It is also very
soluble in ether, so that ether will remove it from its aqueous
solution. Corrosive sublimate may become the subject of a medico-legal
analysis in three states. It may be in the solid form; it may be
dissolved in water along with other mineral substances; and it may be
mixed with vegetable and animal fluids or solids.


       _Of the Tests for Corrosive Sublimate in the solid state._

Corrosive sublimate in the solid state is distinguished from other
substances by the action of the heat, and the effects of solution of
caustic potass. Subjected to heat alone it sublimes in white acrid
fumes; and if the experiment is made in a little tube, it condenses
again unaltered in a crystalline cake. Treated with solution of caustic
potass, it becomes yellow, the binoxide being disengaged, and
hydrochloric acid uniting with the potass, as may be proved by nitrate
of silver, after filtration and neutralization with nitric acid. The
yellow colour of the binoxide which is separated in this process
distinguishes corrosive sublimate from calomel, which is also decomposed
by the potass solution, but yields a black protoxide. Caustic soda has
the same effect. Not so caustic ammonia: Ammonia blackens calomel, but
does not change the colour of corrosive sublimate, as it forms with it a
white triple salt, commonly called white precipitate.

The process here described is the best and simplest method of
determining chemically the nature of corrosive sublimate in its solid
state. But two other tests may also be mentioned, as they have been a
good deal used. A very good test is the process of reduction with
potass, by which globules of mercury are sublimed, and a chloride of
potassium left in the flux, as may be proved by the action of nitrate of
silver on the solution of the flux previously neutralized with nitric
acid. This test alone will not distinguish corrosive sublimate from
calomel: The solubility of the former must be taken into
account.—Another satisfactory test is the solution of protochloride of
tin. Corrosive sublimate, when left for some time in this solution,
first becomes grayish-black, and ere long its place is supplied by
globules of mercury,—the chlorine being entirely abstracted by the
protochloride of tin, which consequently passes to the state of a
bichloride. Calomel is similarly affected.


     _Of the Tests for Corrosive Sublimate in a state of Solution._

Two processes may be mentioned for the detection of corrosive sublimate
in mineral solutions,—a process by reduction, and a process by liquid
tests.

_Reduction process._—In order to procure mercury in its characteristic
metallic state from a solution of corrosive sublimate, the following
plan of procedure will be found the most delicate and convenient. Add to
the solution, previously acidulated with hydrochloric acid if very weak,
a little of the protochloride of tin, which will be seen presently to be
a liquid reagent of great delicacy. If the solution is not darkened
there is not present an appreciable quantity of mercury. If mercury is
present a bluish-gray or grayish-black precipitate falls down, owing to
the chemical action already particularized. After ebullition, this
precipitate is to be allowed to subside, first in a tall glass vessel
suited to the quantity of the solution, and afterwards in the small
glass tube, Fig. 7, the superincumbent fluid being previously decanted
off as far as possible. After it has subsided in the tube, the remaining
fluid is withdrawn with the pipette, Fig. 8; water is poured over it;
and this is withdrawn again after the precipitate has subsided a third
time. The bottom of the tube is then cut off with a file, and the
moisture which remains is driven off with a gentle heat. When this is
accomplished, the powder, which is nothing else than metallic mercury,
sometimes runs into globules. Should it not do so, the bit of tube is to
be broken in pieces and heated in the tube, Fig. 1, when a brilliant
ring of fine globules will be formed. If the globules are too minute to
be visible to the naked eye, the tube is to be cut off with the file
close to the ring; and the globules may then be easily made to coalesce
into one or more of visible magnitude by scraping the inside of the tube
with the point of a penknife.

This process is not recommended as preferable to the plan by liquid
reagents which is next to be mentioned, and which is both more easily
put in practice, and at the same time quite as satisfactory. It is
related chiefly because it forms the ground-work of a process for
detecting mercury in mixed animal or vegetable fluids. It will be
remarked that the process does not prove with what acid the mercury was
combined in the solution. But this is a defect of little consequence;
for the only other soluble salts of mercury ever met with in the arts,
namely, the nitrate, acetate, and cyanide, are too rare to be the source
of any material fallacy; and are besides all equally poisonous with
corrosive sublimate.

_Process by Liquid Tests._—The process by liquid reagents consists in
the application of several tests to separate portions of the solution.
The tests which appear to me the most satisfactory are hydrosulphuric
acid gas, hydriodate of potass, protochloride of tin, and nitrate of
silver.

1. _Hydrosulphuric acid gas_ transmitted in a stream through a solution
of corrosive sublimate causes a dark, brownish-black precipitate, the
bisulphuret of mercury. When the solution is not very diluted, the gas
forms a whitish or yellowish precipitate before the blackening
commences,—an effect which, according to Pfaff, distinguishes the salts
of the peroxide of mercury from all other metals that are thrown down
black from their solutions by sulphuretted-hydrogen.[835] The cause of
this is that the particles of sulphuret first formed acquire a thin
covering of corrosive sublimate by that property which chemists of late
have termed superficial attraction. Hydrosulphuric acid is a very
delicate test of the presence of mercury. It will detect corrosive
sublimate, where its proportion is only a 35000th of the solution.[836]

This test is not alone sufficient, unless reliance be placed on Pfaff’s
criterion, which is rather a trivial one; for hydrosulphuric acid
occasions a black precipitate in other metallic solutions, for example,
in solutions of lead, copper, bismuth and silver. In mixed organic
fluids its action is not liable to be prevented; but the precipitate
formed is often kept intimately suspended, as in the instance of milk.
It may be conveniently used in the form of hydrosulphate of ammonia.
This test produces a dark-brown precipitate, which is said to pass
slowly to a bright cinnabar red; but I have not been able to observe any
transformation of the kind.

_Hydriodate of Potass_ causes in solutions of corrosive sublimate a
beautiful pale scarlet precipitate, which rapidly deepens in tint. The
precipitate is the biniodide of mercury. This is a test of great
delicacy when skilfully used, as it acts where the salt forms only a
7000th of the solution (Devergie). Care must be taken, however, not to
add too much of the test, because the precipitate is soluble in an
excess of the hydriodate, or too little, because the precipitate is also
soluble in a considerable excess of corrosive sublimate.

The action of hydriodate of potass is not liable to any important
ambiguity: no other iodide resembles in colour the biniodide of mercury.
It is not a certain test, however, when other salts exist in solution
along with corrosive sublimate. Chloride of sodium, nitrate of potass,
and probably also other neutral salts possess the power of dissolving
the precipitate. Sulphuric and nitric acids, even considerably diluted,
oxidate and dissolve the mercury, and disengage iodine, which colours
the fluid reddish-brown. When corrosive sublimate is dissolved in
coloured vegetable infusions or animal fluids, the hydriodate of potass
cannot be relied on, the colour of the precipitate being altered, as in
infusion of galls, or the action of the test being suspended altogether,
as by milk.

_Protochloride of Tin_ causes first a white precipitate, which, when
more of the test is added, gives place to a grayish-black one. In very
diluted solutions the colour struck is grayish or grayish-black from the
beginning. In such solutions Devergie has found it useful to acidulate
with hydrochloric acid before adding the test. The chemical action here
is peculiar. The white powder thrown down at first is protochloride of
mercury; a part of the chlorine of the bichloride of mercury having been
abstracted by the protochloride of tin, which becomes in consequence the
bichloride. On more of the test being added these changes are repeated,
the chlorine is removed from the protochloride of mercury, and metallic
mercury falls down. This test is one of extreme delicacy, affecting
solutions which contain only an 80,000th of salt. It is prepared by
acting on tin powder or tinfoil with strong hydrochloric acid aided by a
gentle heat. The solution must be kept carefully excluded from the air;
otherwise bichloride of tin is formed, which does not act at all on the
solution of corrosive sublimate.

The protochloride of tin is not liable to any fallacy. Neither is it
liable to be suspended in its action by the co-existence of other saline
substances. It causes precipitates with almost all animal and most
vegetable fluids. But when corrosive sublimate is present, even in very
small proportion, the precipitate is always darker than when no
mercurial salt exists in solution, and frequently has its proper
grayish-black tint. This property, as will presently be seen, is the
foundation of a process for the detection of mercury in all states of
admixture with organic matters.

_Nitrate of Silver_ causes a heavy white precipitate, the chloride of
silver, which darkens under exposure to light. This is a test for the
chlorine of the corrosive sublimate, but not for the mercury, and is a
necessary addition to the three former tests in order to determine how
the mercury is kept in solution. It acts with very great delicacy.

It is of no use, however, when chlorine or hydrochloric acid is present
either free or combined with other bases. It is not of use, therefore,
in animal fluids and vegetable infusions, because very many of them,
besides organic principles which form white precipitates with this test,
contain a sensible proportion of hydrochlorate of soda.

Although the preceding liquid reagents when employed conjunctly are
amply sufficient for determining the presence of corrosive sublimate in
a fluid, many other tests hardly less characteristic and delicate have
been used by medical jurists. These will now be shortly mentioned.

1. _Lime-Water_ throws down the binoxide of mercury in the form of a
heavy yellow powder. The precipitate first thrown down is lemon-yellow,
an additional quantity of the test gives it a reddish-yellow tint, and a
still larger quantity restores the lemon-yellow. This test is
characteristic, but not so delicate as those already mentioned.—2.
_Caustic Potass_ has precisely the same effect as lime-water, except
that the tint of the precipitate is always yellow—3. _Caustic Ammonia_
causes a fine, white, flocculent precipitate of intricate composition,
commonly called precipitate. It is a very delicate test; but ammonia
likewise causes a white precipitate in other metallic solutions.—4.
_Carbonate of Potass_ causes a brisk-red precipitate, by virtue of a
double decomposition, the precipitate being carbonate of mercury.—5. The
_Ferro-cyanate of Potass_ causes at first a white precipitate, the
ferro-cyanide of mercury. The precipitate becomes slowly yellowish, and
at length pale-blue, owing, it is believed, to the admixture of a small
quantity of iron with the corrosive sublimate.—6. _A polished plate of
Copper_ immersed in a solution of corrosive sublimate becomes in a few
seconds tarnished and brownish; and in the course of half an hour a
grayish-white powder is formed on its surface. This powder, according to
Orfila,[837] is a mixture of calomel, mercury, and a copper amalgam. If
it is wiped off, and the plate then rubbed briskly where tarnished, it
assumes a white argentine appearance.—7. _A little Mercury_ put into a
solution of corrosive sublimate is instantly tarnished on the surface;
the solution in a few seconds becomes turbid, a heavy grayish
precipitate is formed, and in no long time with the aid of agitation the
whole corrosive sublimate is removed from the solution. The powdery
precipitate is a mixture of finely divided mercury and calomel; the
former being derived from the surface of the mercury, and the latter
produced by the corrosive sublimate uniting with a larger proportion of
the metal to form the protochloride.—8. _A solution of Albumen_ causes a
white precipitate, which is soluble in a considerable excess of the
reagent. The nature of this precipitate will be discussed presently.—A
_slip of Gold_ aided by galvanism, becomes silver-white in the solution,
in consequence of the formation of an amalgam. When the solution is
concentrated, it may be thus tested by simply putting a few drops on a
bit of gold, and touching the gold through the solution with an iron
point, as recommended by Mr. Sylvester and Dr. Paris.[838] When the
solution is very weak, a different method is necessary, and a process
for the purpose has been proposed by M. Devergie, which appears so
delicate, accurate, and at the same time simple, a mode of detecting
traces of mercury in very weak solutions, as to deserve detailed notice.
A thin plate of gold, and another of tin, a few lines broad, and two or
three inches long, being closely applied to one another by silk threads
at the ends, and then twisted spirally, this galvanic pile is left for
twenty-four or thirty-six hours in the solution previously acidulated
with muriatic acid; upon which the gold is found whitened, and mercury
may be obtained in globules by heating the gold in a tube. Distinct
indications may be obtained by this method, where the corrosive
sublimate forms but an 80,000th of the water.[839] For facility of
application, an important condition is, that the quantity of fluid
should not exceed three or four ounces, because in a larger quantity the
pile of the size stated above cannot remove the whole mercury. Somewhat
similar to this is the galvanic method of Mr. Davy of Dublin. He
proposes to place the suspected solution in a platinum crucible with
hydrochloric acid, diluted with its own weight of water, to excite
galvanic action by immersing in the fluid a plate of zinc, and to
sublime and collect the reduced mercury, by washing the crucible,
heating it over a spirit-lamp, and condensing the mercurial vapours on a
plate of glass placed over the mouth of the crucible.[840]


_Of the Tests for Corrosive Sublimate when mixed with Organic Fluids and
                                Solids._

The process for detecting corrosive sublimate in mixtures of organic
fluids and solids, such as the contents of the stomach, is now to be
described. But some remarks are previously required on the chemical
relations subsisting between this poison and various principles of the
vegetable and animal kingdoms.

These relations are important in a medico-legal point of view on several
grounds. On the one hand, the chemical changes which corrosive sublimate
undergoes often alter so much the action of its tests, as to render
necessary a process of analysis materially different from any hitherto
described. And on the other hand, these chemical changes, of which some
take place rapidly, others slowly, will hinder the corrosive sublimate,
more or less completely, from exerting its usual operation on the animal
system; so that it may thus either accidentally fail to act as intended,
or be checked in its operation by antidotes administered for the
purpose.

It appears from the researches of M. Boullay, confirmed by those of
Professor Orfila, that various vegetable fluids, extracts, fixed oils,
volatile oils and resins, possess the power of decomposing corrosive
sublimate. According to M. Boullay, a part of the chlorine is gradually
disengaged in the form of hydrochloric acid, and the salt is
consequently converted into calomel, which is deposited in a state of
mixture or combination with vegetable matter.[841] Some vegetable fluids
produce this change at once, others not for some hours, others not for
days, and only when aided by a temperature approaching ebullition. For
example, a strong infusion of tea, mixed with a solution of a few grains
of corrosive sublimate, becomes immediately muddy, and an insoluble
cloud separates in half an hour. But the remaining fluid slowly becomes
muddy again, and in eight days a considerable precipitate is formed.
Both precipitates contain mercury; the former, I find, contains 31 per
cent. On the other hand, an infusion of galls in like circumstances does
not become muddy for six or seven hours. A solution of sugar does not
undergo any change after being mixed with a solution of corrosive
sublimate for months at the ordinary temperature of the atmosphere; but
at the temperature of ebullition Boullay has found that the usual
changes ensue, though to no great extent.

The experiments of Professor Taddei of Florence have farther shown, that
the property of decomposing corrosive sublimate is possessed in an
eminent degree by one of the vegetable solids, gluten. If the salt in
solution is properly mixed with a due proportion of gluten of wheat,
that is, about four times its weight, the water will be found no longer
to contain any mercury, while the gluten becomes whitish, brittle, hard,
and not prone to putrefaction. A ternary compound is formed, the
protochloride of mercury and gluten.[842] This change is effected with
rapidity.

The researches of Berthollet,[843] repeated and extended by Professor
Orfila,[844] have also shown that the same property is possessed by most
animal fluids and solids. Among the soluble animal principles, albumen,
caesin, osmazôme, and gelatin possess it in a high degree, but above all
albumen, the action of which has been examined with some care, as it
supplies the physician with the most convenient and effectual antidote
against the effects of the poison.

If a solution of albumen, for example that procured by beating white of
eggs in water, is dropped by degrees into a solution of corrosive
sublimate, a white flaky precipitate is immediately thrown down, which
when separated and dried forms horny masses, hard, brittle, and
pulverizable. The precipitate is soluble in a considerable excess of
albumen; so that wherever albumen abounds in any fluid, to which
corrosive sublimate has been added, a portion of the mercury will always
be found in solution. The precipitate is also soluble in a considerable
excess of corrosive sublimate. The dry precipitate I have found to
contain 6 per cent. of metallic mercury.

The action of casein as it exists in milk is precisely the same. A
solution of corrosive sublimate, poured into a large quantity of milk,
causes no change; but if the proportion of salt be considerable, a flaky
coagulum is formed, and the milk becomes clear. The principles, osmazôme
and gelatin, are similar in their effects, though not quite so powerful.
Urea has no chemical action with corrosive sublimate. Of the compound
animal fluids, blood and serum have the same effects as albumen.

Many insoluble animal principles, as well as all the soft solids of the
animal body, act in the same manner with vegetable gluten. Fibrin, for
example, coagulated albumen, or coagulated casein, acts precisely in the
same way. Muscular fibre, the mucous and serous membranes, the fibrous
textures, and the brain, have all the same effect: they become firmer,
brittle, white, and a white powder detaches itself from their surface,
which contains mercury and animal matter. This chemical action, which
Taddei has proved to take place in the living[845] as well as in the
dead body, is the source of the corrosive property of the poison, as was
first pointed out by Berthollet in his essay formerly quoted.

In all of the compounds thus formed by vegetable and animal substances,
the presence of mercury is easily proved by boiling the powder in a
solution of caustic potass. The organized matter is dissolved; a heavy,
grayish-black powder is formed, which is protoxide of mercury; and if
this be collected in the way formerly described, it forms running
quicksilver when heated.

A difference of opinion prevails as to the nature of the changes
effected by the mutual action of corrosive sublimate and organic matter.
For example, in the instance of the action of albumen, which has been
most carefully examined, Berzelius and Lassaigne[846] regard the
precipitate as a compound of bichloride of mercury with albumen.
Professor Rose and Dr. Geoghegan[847] have proved it, in their opinion,
to be a compound of binoxide of mercury and albumen without any
chlorine. And according to Boullay it is composed of albumen in union
with calomel.[848] Lassaigne says he has found it to be a compound of
ten equivalents of albumen with one of mercury, or 93·33 per cent. of
the former, and 6·67 of the latter.[849] The compound with fibrin he
considers to be analogous in composition.

With regard to the changes induced by these effects of organized matter
on the operation of the liquid tests for corrosive sublimate, it will in
the first place be manifest that the poison may thus be wholly removed
from their sphere of action: it may be thrown down as an insoluble
substance, on which any process by liquid tests hitherto mentioned will
of course fail to act. But secondly, even when a moderate quantity does
remain in solution, the operation of the liquid tests, as formerly
noticed under the head of each, will be materially modified. It is of
some moment for the medical jurist to remember, that by reason of the
slowness with which the changes in question sometimes takes place, the
poison may exist abundantly in solution at one time, and yet be present
only in small quantity after an interval of some hours or days.

_Process for Organic Mixtures._—Various processes have been proposed for
detecting corrosive sublimate in organic mixtures. The first I shall
mention is one proposed by myself in former editions of this work. It is
a double one; of which sometimes the first part, sometimes the second,
sometimes both may be required. The first removes the corrosive
sublimate undecomposed from the mixture, which may be accomplished when
its proportion is considerable; the second, when the proportion of
corrosive sublimate is too small to admit of being so removed, separates
from the mixture metallic mercury; and the analyst will know which of
the two to employ by using the protochloride of tin as a trial-test in
the following manner.

A fluid mixture being in the first instance made, if necessary, by
dividing and bruising all soft solids into very small fragments, and
boiling the mass in distilled water, a small portion is to be filtered
for the trial. If the protochloride of tin causes a pretty deep ash-gray
or grayish-black colour, the first process may prove successful; if the
shade acquired is not deep, that process may be neglected, and the
second put in practice at once.

_First branch of the Process._—In order to remove the corrosive
sublimate undecomposed, the mixture, without filtration, is to be
agitated for a few minutes with about a fourth part of its volume of
sulphuric ether; which possesses the property of abstracting the salt
from its aqueous solution. On remaining at rest for half a minute or a
little more, the etherial solution rises to the surface, and may then be
removed by suction with the pipette (Fig. 8). It is next to be filtered
if requisite, evaporated to dryness, and the residue treated with
boiling water; upon which a solution is procured that will present the
properties formerly mentioned as belonging to corrosive sublimate in its
dissolved state. This branch of the process is derived from one of
Orfila’s methods.

_Second branch of the Process._—If the preceding method should fail, or
shall have been judged inapplicable, as will very generally be the case,
the mixture is to be treated in the following manner. In the first
place, all particles of seeds, leaves, and other fibrous matter of a
vegetable nature, are to be removed as carefully as possible. This being
done, the mixture, without undergoing filtration, is to be treated with
protochloride of tin as long as any precipitate or coagulum is formed.
If there were solid animal matters in the mixture, besides being cut and
carefully bruised as directed above, they should also be brought
thoroughly in contact with the salt of tin by trituration. The mixture,
even if it contains but a very minute proportion of mercury, will
acquire a slate-gray tint, and become easily separable into a liquid and
coagulum. The coagulum is to be collected, washed and drained on a
filter; from which it is then to be removed without being dried; and
care should be taken not to tear away with it any fibres of the paper,
as these would obstruct the succeeding operations. The mercury exists in
it in the metallic state for reasons formerly mentioned.

The precipitate is next to be boiled in a moderately strong solution of
caustic potass contained in a glass flask, or still better in a smooth
porcelain vessel glazed with porcelain; and the ebullition is to be
continued till all the lumps disappear. The animal and vegetable matter,
and oxide of tin united with them, will thus be dissolved; and on the
solution being allowed to remain at rest, a heavy grayish-black powder
will begin to fall down in a few seconds. This is chiefly metallic
mercury, of which, indeed, globules may sometimes be discerned with the
naked eye or with a small magnifier.

In order to separate it, leave the solution at rest under a temperature
a little short of ebullition for fifteen or twenty minutes, or longer,
if necessary. Fill up the vessel gently with hot water without
disturbing the precipitate, so that a fatty matter, which rises to the
surface in the case of most animal mixtures, may be skimmed off first
with a spoon, and afterwards with filtering paper. Then withdraw the
whole supernatant fluid, which is easily done on account of the great
density of the black powder. Transfer the powder into a small glass
tube, and wash it by the process of affusion and subsidence till the
washings do not taste alkaline. Any fibrous matter which may have
escaped notice at the commencement of the process, and any lumpy matter
which may have escaped solution by the potass, should now be picked out.
The black powder is the only part which should be preserved. If the
quantity of powder is very minute, an interval of twelve hours should be
allowed for each subsidence, and the tube represented in Fig. 7 should
be used.

Lastly, the powder is to be removed, heated, and sublimed, as in the
last stage of the process described in page 293, for detecting corrosive
sublimate in a pure solution.

The second branch of this process is very delicate. I have detected by
it a quarter of a grain of corrosive sublimate mixed with two ounces of
beef, or with five ounces of new milk, or porter, or tea made with a
liberal allowance of cream and sugar. I have also detected a tenth part
of a grain in four ounces of the last mixture, that is in 19,200 times
its weight.

It may be applied successfully and without difficulty to a very large
majority of medico-legal cases. The only difficulty in the way of
applying it to all organic mixtures whatever arises from the occasional
presence of some vegetable matters, such as seeds, leaves, ligneous
fibre and the like, which are insoluble in caustic potass, and which may
therefore be left behind with the mercurial precipitate, and obstruct
the subsequent sublimation of the metal. This difficulty may be
sometimes got rid of, as recommended above, by picking such matters out
of the mixture before the protochloride of tin is added. No mercury is
lost by so doing, for none of it is united with these vegetable matters:
corrosive sublimate does not form any chemical compound with them as it
does with other vegetable matters soluble in caustic potass, and with
the soft animal solids. When the particles are too small to admit of
being thus removed, or cannot be afterwards removed during the process
of washing the black powder, which is left after the action of
potass—the analyst must be content with the increased facility of
sublimation derived from the abstraction of other vegetable and animal
admixtures, and take care to use a tube of greater length and with a
larger ball than usual. If the sublimate is too much obscured by
empyreumatized matter to exhibit distinctly its metallic, globular
appearance, the portion of the tube is to be broken off, and scraped,
washed, and boiled with a little rectified spirit in a tube. If the
globules do not then become visible, a second sublimation will render
them distinct. This supplemental operation, however, will be very seldom
required; and the process given above will be found to apply to a great
majority of instances.

Various objections brought against this process by reviewers and others
were noticed in previous editions of this work. The result of the
investigation is, that, though not by any means a perfect process, it is
one of the most convenient and certain, and least fallacious of all yet
proposed. The first step for separating corrosive sublimate by ether in
the undecomposed state,—which is borrowed from a suggestion of Professor
Orfila, will seldom succeed; for the poison is seldom present in
sufficient quantity.

It must be observed that this as well as every other method yet proposed
for discovering corrosive sublimate in compound mixtures merely
indicates the presence of mercury, and does not point out its state of
combination. More especially, in the case of the contents of the
stomach, if mercury be not obtained from the filtered fluid, it is
impossible to know whether what is detected in the solid matter only may
not have proceeded from calomel given medicinally. This objection can be
obviated solely by sufficient evidence that calomel was not
administered; at least the different criterions laid down by Professor
Orfila for distinguishing calomel in the alimentary canal from the
products of the decomposition of corrosive sublimate do not appear
sufficiently precise, or commonly applicable.[850]

Various processes for detecting corrosive sublimate in organic mixtures
have been proposed by others. But none of these seem to me preferable to
the method detailed above, with the exception of one which has been
lately proposed by Professor Orfila, and which is particularly deserving
of notice, because, although complex, he has found it sufficiently
manageable and delicate for detecting mercury in the animal textures and
secretions, into which it has obtained admission through the medium of
absorption in cases of poisoning with the compounds of mercury. Like the
previous process, however, it merely detects mercury, and cannot point
out the state of combination in which mercury was administered, or mixed
with the substance examined.

If the suspected matter be sufficiently liquid, boil for a few minutes
and filter; acidulate the product with a few drops of hydrochloric acid;
and immerse some slips of copper-leaf in it for a few hours. Should they
be tarnished, dissolve oxide and chloride of copper from the surface by
means of ammonia; wash them and press them between folds of filtering
paper; cut them in pieces, and heat these in a glass tube. Globules of
mercury may be obtained or not. In either case, let the liquid, in which
the plates were first immersed, be evaporated to dryness over the
vapour-bath; add to the residue a sixth of sulphuric acid in a retort
with a receiver; and heat gently till a nearly dry carbonaceous mass be
obtained. Boil this with an ounce and a half of nitro-hydrochloric acid
[Edin. Pharm.], until the charcoal be again nearly dry. Heat what
remains with boiling distilled water, filter, apply to a small part of
the liquid the copper test as just described, and try whether corrosive
sublimate can be detached from the remainder by means of sulphuric ether
(p. 299). The distilled fluid in the receiver may contain corrosive
sublimate in considerable proportion, relatively to what existed in the
subject of analysis. In order to discover it, boil the liquid for
fifteen minutes with nitro-hydrochloric acid; transmit chlorine gas for
an hour, filter, and evaporate to dryness over the vapour-bath; dissolve
the residue in water, and search for corrosive sublimate both by copper
plates, and by agitation with ether.

If mercury be not thus detected, proceed to the solid matter left on the
filter, by which the subject of analysis was in the first instance
separated into a liquid and solid part. Examine this by evaporation to
dryness over the vapour-bath, and charring with sulphuric acid in a
retort with a receiver attached; and then subject the product to the
same steps as those detailed above for the dried residuum of the liquid
part.

If the materials for analysis be soft solids, especially the stomach,
intestines, liver, and the like, commence at once with the process of
charring with sulphuric acid. In the case of the urine, examine both the
liquid and sediment. Filter the liquid, transmit chlorine to excess, let
the product rest twenty-four hours, filter, evaporate to dryness,
dissolve the residue in water acidulated with hydrochloric acid, and
test the solution both with copper-leaf and by agitation with ether.
Heat the sediment with nitro-hydrochloric acid as directed above, and
then proceed as with the liquid portion of the urine.[851]

Some other processes, but probably inferior to that of Professor Orfila,
will be found in the last edition of this work. It seems unnecessary to
reproduce them here.


                     6. _Of Bicyanide of Mercury._

The bicyanide of mercury is a compound of mercury and cyanogen. It is
usually sold in the form of white, opaque, heavy, crystals, which are
rhomboidal prisms. It has a disagreeable, corrosive, metallic taste. It
is easily known from every other substance by the effects of heat. If a
small quantity of it, previously well dried, be introduced into a glass
phial to which a small tube is fitted by means of a cork, on the
application of heat the salt becomes black; mercury is sublimed, and
condenses in globules on the upper part of the phial; and a gas escapes,
which has the odour of prussic acid, and burns with a beautiful rose-red
flame.


                    7. _Of the Nitrates of Mercury._

The nitrates of mercury are used in some of the arts, but have so rarely
been the cause of injury to man that they are of little medico-legal
importance. I am acquainted with only one case of poisoning with
them.[852]

There are two nitrates, the protonitrate and pernitrate. 1. The
protonitrate is in transparent colourless crystals, entirely soluble in
water with the aid of a slight excess of nitric acid; and the solution
is precipitated black by the alkalis, black by sulphuretted-hydrogen,
white by muriatic acid, and yellow by hydriodate of potass. The crystals
when heated discharge fumes of nitrous acid, and when the whole acid is
driven off the red oxide is left, which by farther heat is converted
into metallic mercury. 2. The pernitrate is similarly affected by heat.
Its crystals form white or yellowish needles. Water decomposes them,
separating an insoluble yellowish subnitrate, and dissolving a
supernitrate, which is precipitated yellow by the alkalis, black by
sulphuretted-hydrogen, carmine-red by the hydriodate of potass. Copper
separates mercury from both nitrates; and so does gold or platinum when
aided by a galvanic current.


   SECTION II.—_Of the mode of Action of Mercury and the Symptoms it
                            excites in Man._

The effects of mercury on the animal body are more diversified than
those of any other poison. It acts on a great number of important
organs, and in consequence the phenomena of its action are
proportionately various. It is not surprising, therefore, that some
ambiguity still prevails as to its mode of action and the circumstances
by which the action is regulated.

The attention of toxicologists in their physiological researches has
been chiefly turned to the more active preparations of mercury, and
especially to corrosive sublimate, when given in such quantity as to
prove fatal in a few days at farthest. The more immediate and prominent
properties of corrosive sublimate have consequently received some
elucidation. But its qualities as a slow poison, as well as the
analogous operation of the less active compounds of mercury, have not
been experimentally examined with the same care: indeed it is
questionable whether the phenomena of the latter description as they
occur in man can be studied with much advantage by means of experiments
on animals.—In treating of the mode in which the compounds of mercury
act, the most convenient method will be to consider at present its
action in the form of corrosive sublimate in large doses as ascertained
by late experiments, and to reserve the consideration of the general
action of mercurial poisons at large till their effects on man have been
fully described.

The mode of action of corrosive sublimate has been examined particularly
by Sir B. Brodie in 1812;[853] by Dr. Campbell in 1813,[854] by M. Smith
in 1815,[855] by M. Gaspard in 1821,[856] and more lately by Professor
Orfila.[857] The following is a short analysis of their experiments and
results.

The leading phenomena remarked by Sir B. Brodie, on large doses being
introduced into the stomach, were very rapid death, corrosion of the
stomach, and paralysis of the heart. In rabbits and cats, from six to
twenty grains, injected in a state of solution into the stomach,
produced in a few minutes insensibility and laborious breathing, then
convulsions, and death immediately afterwards,—the whole duration of the
poisoning varying from five to twenty-five minutes. After death the
inner membrane of the stomach was gray, brittle, and here and there
pulpy,—changes precisely the same with those produced by corrosive
sublimate on the dead stomach. When the chest was opened immediately
after death, the heart was found either motionless or contracting
feebly; and in both circumstances the blood in its left cavities was
arterial.

These experiments make it evident that the brain was acted on as well as
the heart, and that the immediate cause of death was stoppage of the
heart’s action. But they do not show whether the action takes place
through absorption, or by a primary nervous impression transmitted along
the nerves.

I am not acquainted with any other experiments of consequence on the
operation of corrosive sublimate when introduced into the alimentary
canal. But some interesting observations have been made by Campbell,
Smith, Gaspard, and Orfila severally as to its effects when applied to
the cellular tissue or injected at once into the blood of a vein. It
follows from their researches, taken along with those of Sir B. Brodie,
that, like arsenic, corrosive sublimate is an active poison, to whatever
part or tissue in the body it is applied.

Campbell, Smith, and Orfila all agree in assigning to it dangerous
properties, when it is applied to a wound or the cellular tissue of
animals. Even in the solid state, and in the dose of three, four, or
five grains only, it causes death in the course of the second, third,
fourth, or fifth day. The symptoms antecedent to death are generally
those of dysentery; and corresponding appearances are found after death,
namely, redness, blackness, or even ulceration of the villous coat of
the stomach and rectum, the intermediate part of the alimentary canal
being sound. This poison, therefore, has, like arsenic, the singular
power of inflaming the stomach and intestines, even when it is
introduced into the system through a wound.

But this is not its only property in such circumstances. According to
Smith and Orfila, it also possesses the power of inflaming both the
lungs and the heart. Orfila found the lungs unusually compact and
œdematous in some parts; and Smith observed on their anterior surface
black spots, elevated in the centre, evidently the consequence of
effusion of blood. As to the heart, in one of Smith’s experiments black
spots were found in its substance, immediately beneath the lining
membrane of the ventricles; and Orfila invariably found in one part or
another of the lining membrane, most commonly on the valves, little
spots of a cherry-red or almost black colour; nay, on one occasion he
observed these spots so soft that slight friction made little cavities.
The production of pneumonia by corrosive sublimate when applied to a
wound appears well established; but the appearances assumed as
indications of carditis are equivocal, since they may have arisen simply
from dyeing of the membrane of the heart in the fluid part of the blood
after death.

The researches of Gaspard were confined to the effects of the poison
when injected at once into the blood. They show still more clearly its
tendency to cause inflammation of the lungs; and they prove that through
the channel of the blood, as through the cellular tissue, it is apt to
cause inflammation of the stomach and rectum. The symptoms were
vomiting, bloody diarrhœa, difficult breathing, apparent pain of chest,
and bloody sputa; and death took place in a few seconds or in three or
four days, according to the dose, which varied from one to five grains.
The appearances in the dead body were principally redness in the mucous
membrane of the intestines; and in the lungs, according to the length of
time the animal survived, either black ecchymosed spots, or black
tubercular masses, some inflamed, others gangrenous, others suppurated,
or finally, regular abscesses separated from one another by healthy
pulmonary tissue.[858]

Besides the effects mentioned in the preceding abstract, two of the
experimentalists referred to have likewise observed in animals the same
remarkable operation on the salivary organs which forms so conspicuous a
feature in the action of the compounds of mercury on man. Dr. Campbell
observed mercurial fetor, and M. Gaspard mercurial salivation. Another
writer, Zeller, found that dogs might be made to salivate, but not
graminivorous animals.[859] Schubarth, however, remarked profuse
salivation in a horse, to which twenty-four ounces of strong mercurial
ointment were administered in the way of friction in sixteen days:[860]
and I observed the same symptoms in a rabbit on the sixth day after the
commencement of daily mercurial inunction.

The result of the preceding inquiry is, that corrosive sublimate causes,
when swallowed, corrosion of the stomach, and in whatever way it obtains
entrance into the body, irritation of that organ and of the rectum,
inflammation of the lungs, depressed action and perhaps also
inflammation of the heart, oppression of the functions of the brain,
inflammation of the salivary glands. These phenomena are diversified
enough. But it will presently be found that other organs still are
implicated in its effects on man.

Before proceeding, however, to its effects on man, some notice may be
taken of a question, connected with its mode of action, which has long
been the subject of controversy. The experiments already quoted render
it probable that corrosive sublimate, before it can exert its remote
action, must enter the blood; and the facts to be enumerated under the
next head of the present section will render it probable that the milder
compounds of mercury used in medicine also act in a similar manner.
Physicians and chemists, therefore, long sought to discover this metal
in the solids and fluids of the body while under its influence; and the
failure of some attempts to detect it has naturally led to its presence
throughout the system being called in question by many. This inquiry,
besides its interest in a physiological point of view, is highly
important in respect to medico-legal practice, since it forms a material
branch of the general questions which at present occupy the attention of
medical jurists,—whether poisons that act through the blood should be
sought for by chemical analysis in other parts of the body besides the
stomach, intestines, or other organ to which they have been directly
applied—and in what particular quarters the search should be principally
made.

In the case of mercury, the evidence of the absorption of the poison,
and of its entering the tissues and secretions of the body, is now
unimpeachable. This is chiefly derived from observations and experiments
made on man and animals after the long-continued use of the milder
preparations of mercury; it being imagined that if the poison enters the
blood at all, the greatest quantity will be found under these
circumstances. The facts may be arranged under three heads. Some relate
to the discharge of metallic mercury from the living body during a
mercurial course for medicinal purposes; others to the discovery of
metallic mercury in the dead body after a mercurial course, and others
to the detection of mercury by a careful chemical analysis in the fluids
and solids during life or after death.

Many stories are related by the older authors of the discharge of
running quicksilver from the living body during a mercurial course. Some
of the most authentic of them have been collected by Zeller. In his list
of cases it is stated that Schenkius met with an instance of the
discharge of a spoonful of quicksilver by vomiting; that Rhodius twice
remarked quicksilver pass with the urine; and that Hochstetter once saw
it exhaled with the sweat.[861] Fallopius likewise states, that in
people who had used mercurial inunction for three years, and who had the
bones of the leg laid bare by suppurating nodes, he had seen quicksilver
collected in globules on the tibia; and he speaks of its being the
practice in his day to draw the mercury from the body, when overloaded
with it, by successively amalgamating a bit of gold in the mouth and
heating the amalgam to expel the mercury.[862] With regard to these
statements of the older authors it may be observed that, although their
singularity renders them questionable, they ought not to be rejected at
once, as some have done, merely because corresponding facts have not
been witnessed in modern times; for no one can now-a days have such
opportunities for observation as were enjoyed by Fallopius and his
contemporaries. The experiment of amalgamating gold in the mouth of a
person under a course of mercury has always failed in modern times. But
who can now have an opportunity of making the experiment during a
mercurial course of three years? Besides, the statements quoted above
are not all destitute of modern confirmation. Thus Fourcroy has noticed
the case of a gilder attacked with an eruption of little boils, in each
of which was contained a globule of quicksilver. Bruckmann mentions the
case of a lady who subsequently to a course of mercury remarked after a
dance many small black stains on her breast, and minute globules of
quicksilver in the folds of her shift.[863] And Dr. Jourda has described
in a late French periodical a case where fluid mercury was passed by the
urine. The last fact appears satisfactory in all its circumstances. A
patient had been taking corrosive sublimate for a month in the dose of a
grain, besides using for the first sixteen days a gargle containing
metallic mercury finely divided. Towards the close of the month he
observed on the sill of the window, on which he used to turn up his
chamber-pot after using it, many little globules of mercury, amounting
in all to four grains. Dr. Jourda on learning this observation of his
patient collected some of the urine with care, and after it had stood
some time found in it a black, powdery sediment, which, when separated
and dried, formed little globules of mercury.[864]

The next class of facts in favour of the entrance of mercury into the
blood are derived from the discovery of the metal in the bodies of
persons who had undergone a long mercurial course recently before death.
In the German Ephemerides it is said that no less than a pound of it was
found in the brain and two ounces in the skull-cap of one who had been
long salivated.[865] This is certainly too marvellous a story. But
analogous observations have been made lately. In Hufeland’s Journal it
is mentioned that a skull found in a churchyard contained running
quicksilver in the texture of its bones, and that there is preserved in
the Lubben cabinet of midwifery a pelvis infiltered with mercury, and
taken from a young woman who died of syphilis.[866] An unequivocal fact
of the same nature has been related by Mr. Rigby Brodbelt. In a body of
which he could not learn the history he found mercurial globules as big
as a pin-head lying on the os hyoides, laryngeal cartilages, frontal
bone, sternum, and tibia.[867] Another equally unquestionable fact of
the kind has been supplied by Dr. Otto. On scraping the periosteum of
several of the bones of a man who had laboured under syphilis, he
remarked minute globules issuing from the osseous substance: in some
places globules were deposited between the bone and periosteum, where
the latter had been detached in the progress of putrefaction; and in
other places, when the bones were struck, a shower of fine globules fell
from them.[868] Wibmer observes that Fricke, surgeon to the Hamburg
Infirmary, has obtained mercury by boiling the bones of persons who had
been long under a course of mercurial inunction.[869]

The third and most satisfactory class of facts are the result of actual
chemical analysis. These results were long variable. On the one hand,
Mayer, Marabelli,[870] and Devergie,[871] failed to detect mercury in
the fluids of people under a mercurial course; and I myself,[872] as
well as Dr. Samuel Wright,[873] had no better success in some
experiments on animals. On the other hand, Zeller detected it after
death in the blood and bile, Cantu procured it from the urine, Buchner
found it in the blood, saliva, and urine, and Schubarth extracted it
from the blood. The first experimentalist found that in the blood and
bile of animals killed by mercurial inunction, mercury could be detected
by destructive distillation, but not by any fluid tests.[874] Cantu, by
operating on sixty pounds of urine, taken from persons under the action
of mercury, procured no less than twenty grains of the metal from the
sediment.[875] The experiments of Buchner are very satisfactory. By
destructive distillation of the crassamentum of seven ounces of blood
taken from a patient who was salivated by mercury, he obtained rather
more than a quarter of a grain of globules; two pounds of saliva yielded
in the same way a 200th of a grain; and the urine contained so much that
it became brownish-black with sulphuretted-hydrogen.[876] Buchner
likewise adds, that Professor Pickel of Würzburg procured mercury by
destructive distillation from the brain of a venereal patient who had
long taken corrosive sublimate.[877] Not less satisfactory are the
experiments of Dr. Schubarth. A horse after being rubbed for twenty-nine
days with mercurial ointment to the total amount of eighty ounces, died
of fever, emaciation, diarrhœa, and ptyalism. On the sixteenth day, when
ptyalism had set in, a quart of blood was drawn from the jugular vein,
and after death another quart was collected from the heart, great
vessels and lungs,—extreme care being taken to collect it perfectly
pure. In each specimen there was procured by destructive distillation a
liquor, in which minute metallic globules were visible. A copper coin
agitated in the liquor was whitened; and when the oily matter was
separated by filtration and boiling in alcohol, the residue gave with
nitric acid a solution, which produced an orange precipitate with
hydriodate of potass.

These researches were considered adequate to prove the strong
probability of the absorption of mercurial preparations when introduced
into the animal. But the frequency with which negative results were
obtained by competent inquirers, and in circumstances apparently
favourable, threw an air of doubt over the positive facts, however clear
they seem to be in themselves,—till at length Professor Orfila proved by
a series of careful experiments that the cause of failure must generally
have been the want of a process sufficiently delicate: for in all
ordinary circumstances, by using his process described above, he
succeeded in obtaining mercury in the urine and liver of animals
poisoned with corrosive sublimate, as well as in the urine of patients
who were taking that salt in medicinal doses. He could not detect it,
however, in the blood.[878] Since these investigations, Professor
Landerer of Athens detected mercury in the brain, liver, lungs and
spinal cord of a man who poisoned himself with two ounces and a half of
corrosive sublimate;[879] and M. Audouard has twice found it in the
urine and once in the saliva of persons salivated with mercury, by
simply transmitting chlorine, exposing the liquid to the air for a day,
evaporating it nearly to dryness, dissolving the residue in water
slightly acidulated with hydrochloric acid, immersing copper-leaf for
twenty-four hours, and heating the stained portions in a tube.[880]

The cases of poisoning with the preparations of mercury, which have been
observed in the human subject, may be conveniently arranged under three
varieties. In one variety the sole or leading symptoms are those of
violent irritation of the alimentary canal. In another the symptoms are
at first the same as in the former, but subsequently become united with
salivation and inflammation of the mouth, or some of the other disorders
incident to mercurial erethysm, as it is called. In a third variety the
preliminary stage of irritation in the alimentary canal is wanting, and
the symptoms are from beginning to end those of mercurial erethysm in
one or another of its multifarious forms.

The first variety of poisoning with mercury is remarked only in those
who have taken considerable doses of its soluble salts, particularly
corrosive sublimate. The second is produced by the same preparations.
The third may be caused by any mercurial compound.

1. The symptoms in the first variety are very like what occur in the
ordinary cases of poisoning with arsenic,—namely, vomiting, especially
when any thing is swallowed, violent pain in the pit of the stomach, as
well as over the whole belly, and profuse diarrhœa. But there exist
between the effects of the two poisons some shades of difference which
it is necessary to attend to.

In the first place,—taking corrosive sublimate as the best example of
the preparations which cause this variety of poisoning with mercury,—the
symptoms generally begin much sooner than those caused by arsenic. The
symptoms of irritation in the throat may begin immediately, nay, even
during the very act of swallowing;[881] and those in the stomach may
appear either immediately,[882] or within five minutes.[883]

Secondly, the taste is much more unequivocal and strong. Even a small
quantity of corrosive sublimate, either in the solid or fluid state, and
considerably diluted, has so strong and so horrible a taste, that no one
could swallow it in a form capable of causing much irritation in the
stomach, without being at once made sensible by the taste that he had
taken something unusual and injurious. Occasionally, indeed, persons
thus warned of their danger while in the act of swallowing the poison,
have stopped in time to escape fatal consequences.[884]

Thirdly, the sense of acridity which it excites in the gullet during the
act of deglutition, and throughout the whole course of the subsequent
inflammation of the alimentary canal, is usually much stronger. If the
dose be not small, or largely diluted, or in the solid form, the sense
of tightness, acridity, or burning in the throat and gullet during
deglutition is often far greater than ever occurs at any stage in the
instance of arsenic; and sometimes it is very severe even when corrosive
sublimate is taken in the solid form.[885] The tightness and burning in
the throat often continue throughout the whole duration of the
poisoning; and may be so excessive as to cause complete inability to
swallow,[886] or even to speak.[887] Occasionally the affection of the
throat is the only material injury inflicted by the poison, as in a case
related by Dr. J. Johnstone of a young woman, who tried to swallow two
drachms of corrosive sublimate in the solid state, but was unable to
force it down on account of the constriction it caused in the gullet.
She died in six days of mortification of the throat.[888] The greater
violence of the action of corrosive sublimate on the throat, compared
with that of arsenic, is evidently owing to its greater solubility and
powerful chemical operation on the animal textures.

Fourthly, instead of the contracted ghastly countenance observed in
cases of poisoning with arsenic (but which, it will be remembered, is
not invariable in that kind of poisoning), those who are suffering under
the primary effects of corrosive sublimate have frequently the
countenance much flushed, and even swelled.[889]

Corrosive sublimate seems to occasion more frequently than arsenic the
discharge of blood by vomiting and purging,—obviously because it is a
more powerful local irritant.

It likewise gives rise more frequently to irritation of the urinary
passages. This irritation generally consists in frequent, painful
micturition; but the secretion of urine is often suppressed altogether.
Instances of this kind have been related by Mr. Valentine,[890] by my
colleague, Professor Syme,[891] by an anonymous writer in the Medical
and Physical Journal,[892] by Dr. Venables,[893] by Mr. Blacklock,[894]
and by M. Ollivier, in whose case, however, the poison was the bicyanide
of mercury.[895] In the last three cases the suppression was total, and
continued till death; which did not ensue, in one till eight, in the
next till five, and in the last till nine days after the poison was
taken. Sometimes, as in Ollivier’s case, the urinary irritation is
attended with symptoms of excitement of the external parts, such as
swelling and blackness of the scrotum and erection of the penis.

Another distinction seems to be that corrosive sublimate is more apt
than arsenic to cause nervous affections during the first inflammatory
stage. The tendency to doze, which sometimes interrupts the inflammatory
symptoms caused by arsenic, has been more frequently observed in cases
of poisoning with corrosive sublimate.[896] The same may be said of
tremors and twitches of the extremities. Sometimes the stupor approaches
even to absolute coma;[897] and the twitches occasionally amount to
distinct, nay violent convulsions.[898] In other instances paraplegia
has been witnessed.[899]

Another difference is, that the effects of mercurial irritants are fully
more curable than those of arsenic. Recovery has taken place even after
half an ounce was swallowed, with the effect of inducing both bloody
vomiting and purging.[900] This may depend in part on the greater
solubility of mercurial preparations, so that they are more easily
discharged than arsenic, which often remains in the stomach after days
of continual vomiting,—and in part on corrosive sublimate and other
soluble salts of mercury being converted, in no long time and much more
easily, into comparatively innocuous compounds, either by antidotes
intentionally given for the purpose, or by animal principles in the
secretions and accidental contents of the alimentary canal.

Lastly, deviations from the ordinary course and combination of the
symptoms appear to be more rare in the instance of corrosive sublimate
than in that of arsenic.

To these general statements, it may be right to add the heads of
one or two actual cases, lest an exaggerated idea be conveyed of
the combination of the symptoms as they usually occur. For this
purpose it will be sufficient to refer to a fatal case related by
M. Devergie, to an instance of recovery, without salivation having
supervened, which is contained in Orfila’s Toxicology, and to
another by Dr. Vautier, presenting the mildest possible symptoms
of this variety. In Devergie’s case, the patient, a female,
swallowed three drachms of corrosive sublimate in solution, and
was soon after seized with vomiting, purging, and pain in the
belly. In five hours, when she was first seen by Devergie, the
skin was cold and damp, the limbs relaxed, the face pale, the eyes
dull, and the expression that of horror and anxiety. The lips and
tongue were white and shrivelled; and she had dreadful fits of
pain and spasm in the throat whenever she attempted to swallow
liquids, also burning and pricking along the course of the gullet,
and increase of pain in these parts on pressure. There was
likewise frequent vomiting of mucous and bilious matter, with
burning pain in the stomach and tenderness of the epigastrium on
the slightest pressure. She had farther profuse diarrhœa, with
pricking pain and tenesmus. The pulsation of the heart was deep
and slow, the pulse at the wrist almost imperceptible, and the
breathing much retarded. In eighteen hours these symptoms
continued without any material change; but the limbs were also
then insensible. In twenty-three hours she died in a fit of
fainting, the mind having been entire to the last.[901]—Orfila’s
case was that of a gentleman who drank by mistake an alcoholic
solution of corrosive sublimate, but fortunately was so much
alarmed by its taste while drinking it, that he did not finish the
poisonous draught. Nevertheless, he was instantly attacked with a
sense of tightness in the throat and burning in the stomach, and
then with vomiting and purging. Two hours after the accident
Orfila found him with the face very full and red, the eyes
sparkling and restless, the pupils contracted, and the lips dry
and cracked. There was also acute pain along the whole course of
the alimentary canal, particularly in the throat. The belly was
swelled, and so tender that he could not bear the weight of
fomentation-cloths. The pulse was 112, small and sharp; the skin
intensely hot and pungent; micturition scanty, frequent, and
difficult; the breathing very much oppressed; the purging bilious.
The patient had likewise a tendency to doze, and was affected with
occasional convulsive twitches of the face and extremities, and
with constant cramps in the limbs. Next morning all the symptoms
were sensibly mitigated; and they went on decreasing till
convalescence was established in eight days. In the course of a
few weeks he recovered his usual health, without suffering
salivation.[902]—In Vautier’s case, where sixteen grains had been
swallowed, the patient was immediately attacked with pain in the
throat and stomach, cold extremities, trembling of the arms and
legs, vomiting, paleness of the features, and great feebleness of
the pulse. Vomiting being promoted by frequent draughts of warm
water, and white of egg given subsequently, no further symptoms
ensued, those first excited slowly subsided, and in a few days
recovery took place, without any salivation. Yet it was upwards of
half an hour before any measures could be taken for his
relief.[903]

The only material and common symptom which was wanting in the case now
related was blood in the stools and in the matter vomited. In other
respects they are good examples of the ordinary train of symptoms in
cases of the present variety. For other examples of the same nature the
reader may refer particularly to the paper of Mr. Valentine, who has
described five cases that happened at one time in the same family, the
mother having attempted to poison herself and four children.[904]

It may sometimes be necessary to know the usual duration of this variety
of mercurial poisoning, and also the extremes of its duration. On these
points I have not hitherto had opportunities of consulting a sufficient
number of cases to be able to lay down the general rule with precision.
But, so far as my inquiries go, the ordinary duration in fatal cases is
from twenty-four to thirty-six hours. It is probable that a few may last
three days,[905] but only one instance has come under my notice where
the duration was greater; and in that instance, which is described by
Dr. Venables, life was prolonged under great agony from pain of the
belly, bloody vomiting, diarrhœa and suppression of urine, but without
salivation, for no less than eight days.[906] In cases of recovery the
symptoms of irritation may continue very long, and nevertheless not pass
into the second variety of this kind of poisoning,—a transition,
however, which on the whole is uncommon. In the case of which an
analysis has been given from Orfila’s narrative, and likewise in one of
Mr. Valentine’s patients who recovered, the symptoms all along were
those of irritation in the alimentary canal; there was not any ptyalism,
or other symptom of proper mercurial erethysm.—The shortest duration yet
recorded is two hours and a half. This was in a case related by Dr.
Bigsby of Newark-on-Trent, where a tea-spoonful of a concentrated
solution of nitrate of mercury was swallowed by a lad sixteen years old,
and where the chief symptoms were burning pain from the mouth to the
stomach, tenderness of the whole belly, mucous vomiting, and feculent
purging.[907] In a case which occurred in London, and which has been
published succinctly by Mr. Illingworth, death must have occurred either
as soon, or very shortly afterwards. The dose of corrosive sublimate,
though not positively ascertained, was large.[908] Next to this the
shortest case recorded proved fatal in eleven hours.[909]

2. The second variety of poisoning with mercury comprehends the cases,
which begin, like the former, with irritation in the alimentary canal,
but in which the symptoms of what is called mercurial erethysm gradually
supervene. In fatal cases of this description death sometimes arises
from the primary action of the poison, exactly as in the previous
variety; but in other instances it is owing to general disturbance of
the constitution, or the local devastation, brought on by the secondary
effects.

It is unnecessary to describe here the several forms of mercurial
erethysm which may thus be developed, because they will immediately be
considered under the third variety of mercurial poisoning. It is
sufficient to state in passing that the leading affection is
inflammation of the organs in and adjoining the mouth, and more
particularly of the salivary glands.

But it may be right to endeavour in the present place to fix the period
of the poisoning at which these secondary affections may and usually do
commence. This cannot be done so satisfactorily as might be wished,
because the cases already published which I have been able to examine do
not form a large enough induction. Among the recorded cases I have
hitherto seen, salivation has never been retarded beyond the third
day;[910] but in an instance of suicide by corrosive sublimate which
happened in the Castle of Edinburgh in 1826, and which was communicated
to me by the late Dr. Shortt, the salivation did not begin till the
fourth. Salivation seldom comes on sooner than the beginning of the
second;[911] and the most usual date of its commencement is towards the
close of the second day. There is little doubt that it may be retarded
till a period considerably later than I have yet found recorded. It is
doubtful whether true mercurial salivation ever begins much sooner than
after the first twenty-four hours. Occasionally, however, corrosive
sublimate produces salivation of a different kind, which has been
mistaken for the specific variety caused by mercury. Thus in a paper on
the cure of gonorrhœa by corrosive sublimate in single large doses,
communicated by Mr. Addington of West Bromwich to Dr. Beddoes, it is
stated that a grain and a half, taken at once in half an ounce of
rectified spirit, causes immediately “a great burning in the throat and
stomach, and quickly afterwards a copious salivation, lasting between an
hour and a half and two hours, and amounting frequently to more than a
quart.”[912] These facts have been appealed to by authors in medical
jurisprudence as proving the rapid production of mercurial salivation.
But the effect produced is not the specific ptyalism of mercury; for its
brief duration is scarcely consistent with this supposition. And
farther, the author goes on to observe, that, if the dose be taken on
going to bed, the latter part of the night is passed quietly, and no
inconvenience is felt afterwards, even when the dose is taken five or
six times at intervals of three or four days. The effects here observed
is a sympathetic phenomenon depending on the topical action of the
poison. And such, I have no doubt, has been the nature of the salivation
in several cases of poisoning with corrosive sublimate, which have been
supposed to be at variance with the general rule, that this affection
does not begin till about twenty-four hours have elapsed. Such seems to
have been the nature of the salivation in a case published by Dr.
Perry,[913] that of a girl who was attacked with swelling of the cheeks
and lower lip, burning in the throat, flushed face, feeble pulse, and
cold, clammy extremities after swallowing corrosive sublimate, and who
had a copious flow of saliva in an hour and a half; for there is no
mention made of fetor, and the girl was well enough to leave the
hospital in a few days,—which could scarcely happen if she had been
affected with ptyalism from the constitutional action of mercury.—In
like manner Dr. Alexander Wood has related a case, fatal in fourteen
days, in which the patient said salivation came on in seven hours.[914]
But, notwithstanding Dr. Wood’s argument in support of the patient’s
statement,—for he did not see him till nine days after the poison was
taken,—there is no satisfactory evidence that the salivation was the
true constitutional salivation of mercury, and not simply the result of
its topical action, which seems to have been very severe.—Farther, in an
instance related by Dr. H. Anderson of Belfast, where salivation
appeared to him to begin in nineteen hours, it seems not improbable that
he mistook for mercurial ptyalism the common salivation arising from
inability to swallow on account of sore throat; for this patient too was
quite convalescent in three days.[915]—Mr. Alfred Taylor alludes to a
case in Guy’s Hospital of salivation occurring in four hours; but so
briefly, that its true influence on the present question cannot be
judged of.[916]—On the whole, then, although it is clear that ptyalism
of one kind or another may occur very soon after corrosive sublimate is
swallowed, it remains a matter of doubt, whether the true, specific
ptyalism, depending on the constitutional action of the poison begins
sooner than after an interval of above twenty-four hours.

As to the total duration of this variety in fatal cases, I have found an
instance fatal on the fourth day, salivation having begun on the
second;[917] and Orfila quotes a case from Degner, in which the
gastro-enteritic symptoms were succeeded by ptyalism about the same
period, and which proved fatal in fifteen days.[918] These periods,
however, probably do not form the extremes; for in such cases as the
former death is the consequence of the primary affection, and may
therefore ensue immediately after the secondary stage has begun to
develope itself; and when death arises from profuse salivation, as in
Degner’s patient, or from the ravages committed by ulceration and
gangrene, it may be delayed almost as long as in cases of the third
variety of mercurial poisoning, in which there is no precursory stage of
inflammation in the alimentary canal.

Death may arise, not only from the primary action of the poison, or from
the exhaustion caused by mercurial erethysm, but likewise from
incidental occurrences. Thus, in Dr. Alexander Wood’s case, referred to
above, death arose directly from sudden profuse hemorrhage from the
bowels, to the amount of six pounds.

The present variety of poisoning with corrosive sublimate may be
concluded with the heads of an excellent example related in the Medical
and Physical Journal. The patient, a stout young girl, swallowed soon
after supper a drachm of corrosive sublimate dissolved in beer, and in a
few minutes she was found on her knees in great torture. All the primary
symptoms of this kind of poisoning were present in their most violent
form,—burning in the stomach, extending towards the throat and mouth,
followed in no long time by violent vomiting of a matter at first
mucous, afterwards bilious and bloody; by purging of a brownish, fetid
fluid; suppression of urine and much tenderness of the urethra and
bladder; small, contracted, frequent pulse, anxious countenance, and
considerable stupor, interrupted frequently by fits of increased pain.
All these symptoms were developed in four hours. Subsequently the pain
in the stomach became much easier, but that in the throat much worse. At
length in the course of the second day, the teeth became loose, the gums
tender, the saliva more abundant than natural; profuse ptyalism and
great fetor of the breath ensued, and the patient expired towards the
close of the fourth day.[919]

3. The third variety of poisoning with mercury comprehends all the forms
of what is called mercurial erethysm. Without endeavouring to settle the
precise meaning of this term, which is now used in rather a vague sense,
I shall consider under the present head all the secondary and chronic
effects of mercury. These may be caused by any of its preparations, but
are most frequently seen as the consequence of its milder compounds,
either given medicinally in frequent small doses, or applied
continuously to the bodies of workmen who are exposed by their trade to
its fumes.

The secondary and chronic effects of mercury are multifarious enough in
reality; but if credit were given to all that has been written, and is
still sometimes maintained on this subject, almost every disease in the
nosology might be enumerated under the present head; for there is
scarcely a disease of common occurrence, which has not been imputed by
one author or another to the direct or indirect operation of mercury.
The present remarks, however, will be confined as much as possible to
what is well ascertained, and bears on the medical evidence of poisoning
with mercury, or is important in regard to medical police. With this
view, salivation and its concomitants, the most usual of the secondary
effects of mercury, will first be treated of. Some observations will
then be made on the shaking palsy, or mercurial tremor, which is caused
in those who work with mercury. And in conclusion, a short view will be
taken of the other diseases which are more indirectly induced by this
poison, as well as some which have been ascribed to it on insufficient
grounds. This being done, the mode of action of mercurial poisons will
be resumed, and a description given of their relative effects when
introduced by different channels and in different chemical forms.

_Of Mercurial Salivation._—Mercurial salivation may be caused by any of
the preparations of mercury, and either by a single dose or by
frequently repeated small doses. It may be caused by corrosive sublimate
as the secondary stage of a case which commenced with inflammation in
the alimentary canal; or it may be the first sign of mercurial action,
as in the medicinal mode of administering calomel and blue pill. Even in
the latter case a single dose, and that not large, may be sufficient to
induce ptyalism of the most violent kind. When induced by a single dose
it usually commences between the beginning of the second and end of the
third day, rarely within twenty-four hours. But an extraordinary case is
mentioned by Dr. Bright, where five grains, put on the tongue in
apoplexy and not washed over, excited in three hours most violent
salivation, with such swelling of the tongue that scarifications became
necessary.[920] It commences with a brassy taste and tenderness of the
mouth, swelling, redness, and subsequently ulceration of the gums;
peculiar fetor of the breath; and at last an augmentation is observed in
the flow of the saliva, commonly accompanied with fulness around the
lower jaw. These symptoms increase more or less rapidly. Sometimes they
are very mild; nay, this form of the secondary effects of mercury may
consist in nothing else than brassy taste, tenderness of the mouth,
redness of the gums, and fetor. On the other hand, the symptoms are
often very violent, the salivation being profuse, the face swelled so as
to close the eyes, and almost fill up the space between the jaw and
clavicles, the tongue swollen so as to threaten suffocation, the inside
of the mouth ulcerated, nay gangrenous, and at times the gangrene
extends over the face. It is not uncommon to observe severe and
extensive ulceration without particular increase of the saliva.

These local affections are almost always accompanied with more or less
constitutional disorder. If severe, they are attended with the
symptomatic fever proper to inflammation and gangrene, from whatever
cause they spring. But independently of that, mercurial salivation is
accompanied, and indeed commonly preceded, by a constitutional disorder
or symptomatic fever of its own, which occasionally exhibits some
peculiarities. The mildest affection of the mouth and salivary glands is
very generally preceded by some exaltation of the pulse and temperature,
and other symptoms of fever. But when the local disorder begins
violently, and above all when this takes place by idiosyncrasy from
small doses of mild preparations, there is often great rapidity of the
pulse, irregular action of the heart, and various nervous disorders
possessing the hysteric character,—all of which, except the quick pulse,
will sometimes gradually abate or even disappear, when the salivation is
fairly established.

The phenomena of ordinary mercurial salivation being familiar to every
practitioner, it is unnecessary to quote here any illustrative example;
but the following instance may be given to exemplify its most malignant
forms. A patient of Mr. Potter of Chipping-Ongar, in Essex, after taking
eighteen grains of blue pill in divided doses during three days, was
seized with excessive salivation and great constitutional disturbance,
indicated by offensive evacuations, copious sweating, bleeding from the
nose, purple spots on the skin, dilated pupils, and such severe local
disease that the teeth dropped out, and he expired six days after
mercurial action set in.[921]

As the phenomena of mercurial salivation have been often known to lead
to important evidence and much contrariety of opinion upon trials, it
will be necessary to dwell at some length on some parts of the subject.

In the first instance, then, the dose which is required to bring on
salivation may be noticed. It is needless to mention the ordinary
quantity required in mercurial courses. A more useful object of
consideration is the departure from the ordinary rule. One of the most
common and important of these deviations is excessive sensibility to the
action of mercury, in consequence of which the individuals who have this
idiosyncrasy may be profusely salivated by one or two small doses even
of the mildest preparations. Three grains of corrosive sublimate divided
into three doses have caused violent ptyalism.[922] Fifteen grains of
blue pill, taken in three doses, one every night, have excited fatal
salivation.[923] Nay, two grains of calomel have caused ptyalism,
extensive ulceration of the throat, exfoliation of the lower jaw, and
death.[924] Three drachms of mercurial ointment applied externally have
caused violent ptyalism and death in eight days. On the other hand, it
is well known that some constitutions resist the action of mercurials
very obstinately, so as even sometimes to appear incapable of being
salivated at all. I have more than once met with cases of the last
description, where mercurial courses had been continued for three months
and upwards without avail. It may be added, that, except in
constitutions naturally predisposed to suffer from a few small doses, a
few large doses do not appear apt to excite severe salivation, or even
to cause any at all. This has been clearly shown in the course of the
practice lately introduced of administering calomel in doses of a
scruple. On that subject more will be said by and by. At present I may
mention, that, in conformity with the practice alluded to, I have
several times, in various diseases, given eight or ten grains of calomel
five or six times a day for two or three days together, without
observing that ptyalism was apt to ensue.

The next point to be considered is, whether mercurial salivation can be
confounded with any other affection. In a very difficult case of
poisoning which was tried here in 1817, that of William Patterson for
murdering his wife,[925] it appeared probable that he had given her
repeatedly large doses of calomel. But the proof of this was
circumstantial only, and an important circumstance in the chain of
evidence was a deposition to the occurrence of salivation during the
woman’s illness. This fact, however, rested on the skill and testimony
of a quack doctor only; and the admissibility of such a person to decide
on a point of this nature, will depend on the facility with which the
true mercurial form of salivation can be recognised. This statement will
show the practical object of what is to follow.

Many other causes may excite a preternatural flow of saliva. Several
other poisons may have that effect, for example, preparations of gold,
preparations of copper, antimony, croton-oil, and foxglove: foxglove has
been known to cause violent salivation for three weeks.[926] Opium too
has occasionally excited salivation,[927] and also hydrocyanic acid and
iodide of potassium.

Even a common sore throat, if the swelling and pain are so great as to
render swallowing very difficult and distressing, may be accompanied, as
every physician must have remarked, with a profuse flow of saliva; and
in the ulcerative stage there is also often a fetor that is hardly
distinguishable from the mercurial kind. In the ulceration of the mouth
called _cancrum oris_ there is some salivation with great fetor of the
breath.

Salivation likewise forms an idiopathic disease, and may then be both
profuse and obstinate. Mr. Davies has described a case of spontaneous
ptyalism which had lasted for a fortnight before he was called to see
the patient; and during all that time the quantity of saliva discharged
was two or three pints daily. How long it endured afterwards he does not
mention; but it must have continued for some time, because during his
attendance first one physician and then another were called into
consultation with him. Laxatives slowly removed it. Mr. Davies has not
described the state of the mouth; but the first physician mistook the
salivation for a mercurial one.[928] In the same journal which contains
this case another has been related which lasted four months.[929]
Another very remarkable case has been recorded by Mr. Power. The
patient, a young lady, discharged for more than two years from sixteen
to forty ounces of saliva daily. In the last two cases the mouth was not
affected.[930] Two other instances have been related by M. Bayle, in one
of which the patient was cured after spitting five pounds daily for nine
years and a half; while the other continued to be affected after
spitting profusely for three years. In neither was there any ulceration
of the mouth.[931] An instance has been related by an Italian physician,
Dr. Petrunti, where, in the course of various nervous affections of the
hysteric character, the patient became affected with heat and tightness
in the throat, and so profuse a salivation for two months, that between
three and four pounds were discharged daily.[932] A case somewhat
similar is related in Rust’s Magazin of a man who suffered upwards of
two years from a daily salivation alternating occasionally with a mucous
discharge from the bowels or lungs.[933] M. Guibourt describes the case
of a lady who had an attack of profuse salivation every thirty, forty,
or fifty days, lasting between twenty-four and forty-eight hours, and
unaccompanied with any other affection of the mouth or adjoining parts
except a sense of tightness in the throat.[934] M. Gorham relates an
interesting case of a lady who in three successive pregnancies was
attacked soon after impregnation with excessive ptyalism, which
continued to the extent of between two and four quarts daily until the
period of quickening on two occasions, and on the third till her
delivery; but there was never any fetor or any affection of the
gums.[935] I have likewise met with a singular case where spontaneous
ptyalism accompanied an ulcerated sore throat of the mercurio-syphilitic
kind. The patient had taken mercury to salivation about six months
before coming under my care, and got completely rid of both the sore
throat and salivation. But the sore throat returned, together with the
salivation, two months before I saw him, and the salivation continued
for two months longer to the extent of twenty or even thirty ounces
daily,—the ulcer of the throat during that interval being sometimes
healed up, and again returning as severely as ever. In three weeks more
the discharge rapidly diminished, and ceased. During all the time he was
under my care there was no fetor of the breath, and no redness,
ulceration, or sponginess of the gums. A singular account of an epidemic
salivation which occurred in connection with a continued tertian fever,
has been given in an inaugural dissertation contained in one of Haller’s
Collections. The author, Quelmalz, says that the ptyalism sometimes
continued for three weeks, that it was in one instance as great in
extent as the most violent mercurial salivation, and that it was
accompanied by fetor, superficial ulceration of the mouth, pustules on
the tongue, relaxation of the gums, and looseness of the teeth.[936]

Salivation may likewise be produced by the influence of the imagination.
I have seen a singular example of this. A woman who had a great aversion
to calomel was taking it with digitalis for a dropsical complaint. Some
one having told her what she was using, she immediately began to
complain of soreness of the mouth, salivated profusely, and even put on
the expression of countenance of a salivating person, although she had
taken only two grains. On being persuaded, however, that she had been
misinformed, the discharge ceased gradually in the course of one night.
Two days afterwards she was again told on good authority that calomel
was contained in her medicines, upon which the salivation began again
and was profuse. It did not last above twenty-four hours; but the
symptoms during that period resembled a commencing mercurial salivation
in every thing but the want of fetor and redness of the gums.

In general, mercurial salivation may be easily distinguished from all
the preceding varieties by an experienced practitioner. If its progress
has been traced from the first appearance of brassy taste and fetor to
the formation of ulcers and supervention of ptyalism, no attentive
person can run any risk of mistaking it. Its characters are also quite
distinct at the time salivation just begins. The fetor of the breath and
sponginess and ulceration of the gums at this stage distinguish it from
every other affection. But if the state of the mouth is not examined
till the ulcers have existed several days, the characters of the
mercurial disorder are much more equivocal. They cannot be
distinguished, for example, from some forms of idiopathic ulceration of
the mouth connected with unsoundness of the constitution, and
characterized by extensive sloughing, ptyalism, and gangrenous
fetor.[937] In particular they cannot be distinguished from the effects
of the disease called _cancrum oris_. A few years ago indeed a London
physician was charged, in consequence of this resemblance, with having
killed, by mercurial salivation, a patient to whom it was proved that he
had not given a particle of mercury, and who clearly died of the disease
in question;[938] and a similar case, where fatal mercurial salivation
was suspected, but which was clearly proved on a Coroner’s Inquest to
have been also a case of cancrum oris, has been more lately published by
Mr. Dunn.[939]

For distinguishing these and such other affections from mercurial
salivation Dr. Davidson of Glasgow has lately proposed a character, the
exact scope of which cannot yet be appreciated,—namely, that in true
mercurial salivation there is never any sulpho-cyanic acid in the
saliva; so that sesquichloride of iron does not render it red. The
presence of sulpho-cyanic acid may possibly prove that salivation is not
mercurial; but the converse does not hold good, because other causes
tend to deprive human saliva of its sulpho-cyanic acid.[940]

The next point to be noticed regarding mercurial salivation is, that a
long interval may elapse after the administration of the mercury has
been abandoned, before the effect on the salivary glands and mouth
begins,—mercury in small doses being what is called a cumulative poison,
or a poison whose influence accumulates silently for some time in the
body before its symptoms break forth. Swédiaur has met with instances
where the interval was several months,[941] Cullerier with a case in
which it was three months.[942] It will at once be seen how strongly
such facts may bear on the evidence in a criminal case, where the
administration of mercury in medicinal doses, which have been long
abandoned, is brought forward to account for salivation, appearing weeks
or months after, and giving rise, in conjunction with other
circumstances, to a suspicion of mercurial poisoning of more recent
date.

Another question which has been made the subject of discussion is the
duration of mercurial ptyalism. The medical witness may be required to
give his opinion how long this affection may last after the
administration of mercury has been abandoned. The present question may
be cut short by stating, that there appears to be hardly any limit to
its possible duration. Linnæus met with an instance of its continuing
inveterately for a whole year;[943] Swédiaur says he has known persons
languish for months and years from its effects;[944] and M. Colson knew
an individual who had been salivated for six years.[945] These, however,
are very rare incidents. After an ordinary mercurial course the mouth
and salivary glands generally return to the healthy state in the course
of a fortnight or three weeks.

A fifth question, whether the ptyalism, or, speaking in general terms,
the erethysm of mercury, is susceptible of a complete intermission,
formed a material subject of inquiry, and the cause of much
contradictory statement on a noted criminal trial, that of Miss
Butterfield in 1775 for the murder of her master, Mr. Scawen. She was
accused of administering corrosive sublimate; and it was alleged in her
defence, that the salivation and consequent sloughing of which he died
might have arisen, without the fresh administration of mercury, from the
renewal of a previous ptyalism, which had been brought on by a common
mercurial course, and had ceased two months before the second salivation
began. It appeared that Mr. Scawen was salivated with a quack medicine
from the beginning till the middle of April; and that about the middle
of June he was again seized with violent salivation, of which he died.
It was rendered very improbable, that during the interval between the
two salivations any more mercury had been taken medicinally. The
question then was, whether the original ptyalism could have reappeared
after so long an interval, without the fresh administration of mercury?
The witnesses for the prosecution, gentlemen in extensive practice, said
it could not. But one of the prisoner’s witnesses, Mr. Bloomfield of the
London Lock Hospital, said he had repeatedly known salivation reappear
after a long intermission; that it was quite common for hospital
patients to have a second salivation, when thought well enough to go out
the next dismissal day;[946] that in one case the interval was three
months; and that one of his patients was attacked periodically with
salivation at intervals of six weeks or a month for a whole year. Mr.
Howard, another surgeon of the Lock Hospital, deposed to the same
effect; and the prisoner was acquitted, apparently upon their
evidence.[947]

Notwithstanding what was said by these gentlemen, I believe the
recurrence of mercurial salivation after so long an interval, without
the repetition of mercury, is exceedingly rare. Dr. Gordon Smith, in
alluding to the trial of Miss Butterfield, has mentioned a case which
occurred to the late Dr. Hamilton of this University, and used to be
related by him in his lectures. The interval was so great as four
months.[948] Mr. Green of Bristol has lately described another
unequivocal case, where the interval was six weeks.[949] Dr. Mead says
he met with an instance where the interval was six months;[950] and Dr.
Male mentions another where mercury brought on moderate salivation in
March, and after a long interval excited a fresh salivation in October,
of which his patient died in a few weeks.[951] M. Louyer-Villermé met
with a case, where, in consequence of exposure to cold, a sudden attack
of salivation was caused a twelvemonth after the removal of syphilis by
mercury.[952] Some other cases not less wonderful have been recorded by
M. Colson in his paper on the effects of mercury. He quotes Dr. Fordyce
for the case of a man who had repeated attacks of salivation, with
metallic taste, which lasted for three weeks, although mercury had not
been taken for twelve years; and Colson himself knew a surgeon who had a
regular and violent attack of all the symptoms of mercurialism eight
years after he had ceased to take mercury.[953] It is impossible to
attach credit to such marvellous stories as the last two. Granting the
ptyalism to be really mercurial, it would require much better evidence
than any practitioner could procure, to determine the fact that mercury
had not been given again during the supposed interval. This objection
indeed will apply more or less even to the instances where the alleged
interval did not exceed a few months.

The last point to be noticed regarding mercurial salivation is the
manner in which it proves fatal. Death may ensue from the mildest
preparations, and from the smallest doses, in consequence of severe
salivation being produced by them in peculiar habits. Two instances have
been already mentioned which illustrate both of these statements, and
others might easily be referred to were the fact not familiar.

Death may be owing to a variety of causes. Some of those which have been
assigned are direct and unquestionable in their operation; others
indirect and more doubtful.

The most direct and obvious manner is by extensive spreading gangrene of
the throat, mouth, face, and neck. The late happy changes, introduced
into the treatment of syphilis and other diseases which are benefited by
mercury, render this mode of death rare in the present day. Yet I may
mention that I have seen an example of it in a woman who was salivated
to death, because her medical attendant, a firm believer in the powers
of mercury as an antidote, forgot that the antidote is itself a poison,
if not given in moderation. In general, when gangrene is the cause of
death, it begins within the mouth or in the throat, and spreads from
that till it even reaches the face. But sometimes it begins at once on
the external surface, at a distance from the primary ulcers. An example
of such a progress of the symptoms has been related by Dr. Grattan. A
child ten years old was violently salivated by twenty grains of calomel
given in six days. On the fifth day of the salivation, a little vesicle
appeared on the skin near the mouth on each side, and was the
commencement of a gangrenous ulcer, which spread over the whole cheek,
and proved fatal eight days after its appearance.[954]

Another cause of death appears to be exhaustion from profuse and
protracted discharge of saliva, without material injury of the mouth or
adjoining organs.

A third manner of death which I have witnessed is exhaustion from
laryngeal phthisis; and from the circumstances of the case, I have
little doubt but, in the state to which patients are then sometimes
reduced, death may also take place suddenly from suffocation. My patient
had undergone before I saw him five long salivations for a venereal
complaint, and had latterly been attacked with symptoms of ulceration of
the glottis. This affection went on slowly increasing, and he died of
exhaustion after many weeks of suffering. During this period he was
repeatedly attacked with alarming fits of suffocation, which were
relieved by the hawking of mucous flakes. The symptoms were explained on
dissection by the appearance of extensive ulceration and thickening of
the glottis, and almost total destruction of the epiglottis.

The other causes of death are more indirect, and will be mentioned
presently. They depend on the pre-existence of other diseases, on which
mercury acts deleteriously during the state of erethysm excited by it in
the constitution.

_Of Mercurial Tremor._—The second division of the secondary effects of
mercury comprehends the palsy or tremor, with the collateral disorders
induced in miners, gilders, and other workmen, whose trade exposes them
to the operation of this poison. Under the present head, which might be
treated at considerable length as an important branch of medical police,
I shall confine myself chiefly to an analysis of an interesting essay by
Mérat on the _Tremblement Metallique_, and to some remarks by Jussieu on
the health of the quicksilver miners of Almaden in Spain.

Mérat’s account of the shaking palsy induced by mercury is very
interesting.[955] The disease, he states, may sometimes begin suddenly;
but in general it makes its approaches by slow steps. The first symptom
is unsteadiness of the arms, then quivering, finally tremors, the
several movements of which become more and more extensive till they
resemble convulsions, and render it difficult or impossible for the
patient to walk, to speak, or even to chew. All voluntary motions, such
as carrying a morsel to the mouth, are effected by several violent
starts. The arms are generally attacked first and also most severely. If
the man does not now quit work, loss of memory, sleeplessness, delirium,
and death ensue. But as the nature of the disease soon renders working
almost impossible, he cannot well continue; and in that case death is
rare. The concomitant symptoms of the trembling are a peculiar brown
tint of the whole body, dry skin, flatus, but no colic, no disorder of
respiration, and, except in very old cases, no wasting or impaired
digestion. The pulse is almost always slow.—This description agrees with
a somewhat later account of the disease by Dr. Bateman, as he observed
it in mirror-silverers;[956] and also with some interesting cases
recently published by Dr. Bright.[957]

In general the tremors are cured easily, though slowly, several months
being commonly required. One of Dr. Bright’s patients got almost well in
little more than a fortnight under the use of sulphate of zinc.
Sometimes, however, the trembling is incurable.[958] I have said the
disease is rarely fatal. Mérat quotes three cases only, in one of which
death was owing to profuse salivation and gangrene, in the others to
marasmus. On the whole, those who are liable to the shaking palsy do not
appear liable to salivation. Yet the two affections are sometimes
conjoined, as in three of the cases described by Dr. Bright, and in some
noticed by Mr. Mitchell among the mirror-silverers of London.[959]
Gilders, miners, and barometer-makers are all subject to the disease.
Even those who undergo mercurial frictions may have it, according to
Mérat; and M. Colson, who confirms this statement, quotes Swédiaur as
another authority for it.[960] It is not merely long-continued exposure
to mercurial preparations that causes the shaking palsy: a single strong
exposure may be sufficient; and the same exposure may cause tremor in
one and salivation in another. Professor Haidinger of Vienna some time
ago mentioned to me an accident a barometer-maker of his acquaintance
met with, which illustrates both of these statements. This man and one
of his workmen were exposed one night during sleep to the vapours of
mercury from a pot on a stove, in which a fire had been accidentally
kindled. They were both most severely affected, the latter with
salivation, which caused the loss of all his teeth, the former with
shaking palsy, which lasted his whole life.

In regard to all such workmen, it is exceedingly probable that with
proper care the evils of their trade may be materially diminished. This
appears at least to be the result of the observations made long ago by
Jussieu on the miners of Almaden in La Mancha. Most quicksilver mines
are noted for great mortality among the workmen. But Jussieu maintains
that the trade is not by any means so necessarily or so dreadfully
unhealthy as is represented, or as it really is in some places. The free
workmen at Almaden, he says, by taking care on leaving the mine to
change their whole dress, particularly their shoes, preserved their
health, and lived as long as other people; but the poor slaves, who
could not afford a change of raiment, and who took their meals in the
mine, generally without even washing their hands, were subject to
swelling of the parotids, aphthous sore throat, salivation, pustular
eruptions, and tremors.[961]

_Of the indirect effects of mercurial erethysm._—The last division of
the secondary effects of mercury relates to its indirect action when
concurring with other diseases or predispositions to disease.

Of these effects there are some of which the poison appears to be the
chief, if not even the sole cause. Thus, during the symptomatic fever
which precedes salivation there are sometimes remarked imitative
inflammations, or coma, or affections of the heart, which go off as
salivation is established.

Other effects require the distinct co-operation of collateral causes.
Many inflammatory diseases, not easily excited in ordinary
circumstances, arise readily from improper exposures during salivation,
for example dropsy, pneumonia, phrenitis, iritis, erysipelas, and
various chronic eruptions.

Other effects again require the co-operation of disease, such as
sloughing gangrene supervening on ordinary ulcers during the action of
mercury,—a not uncommon accident. This appears most likely to happen
when the ulcers are constitutional.

Lastly, in conjunction with other diseased morbid actions, either going
on at the same time, or immediately preceding mercurial erethysm, this
poison is apt to occasion some modifications of disease which are rarely
otherwise witnessed. Modifications of the kind have already been traced
in the instances of lues venerea and scrofula; but there is reason to
believe that the same singular property may also exist in relation to
other constitutional disorders.

These observations conclude the inquiry into the symptoms caused in man
by mercurial poisons generally. Returning now to its mode of action, we
have to examine its relative effects through the different animal
textures, and in its various chemical forms.

The result of the previous remarks as to its action on animals, it will
be remembered, was, that its soluble preparations cause when swallowed
corrosion of the stomach, and in whatever way it enters the body
irritation of the stomach and rectum, inflammation of the lungs,
depressed action and perhaps inflammation of the heart, oppression of
the functions of the brain, and inflammation of the salivary glands. All
of these effects have likewise been mentioned in the preceding sketch,
as occurring in a greater or less degree in consequence of its operation
on man.

Mercury acts as a poison on man in whatever way it is introduced into
the body,—whether it be swallowed, or inhaled in the form of vapour, or
applied to a wound, or even simply rubbed or placed on the sound skin.
But the kind of action excited differs according to the channel by which
it is introduced.

The most ordinary and dangerous cases of poisoning arise from the
introduction of corrosive sublimate into the stomach. The poison then
kills by corroding or inflaming the alimentary canal, or by causing
salivation and its concomitants.

When applied to a wound or ulcer corrosive sublimate does not often
occasion dangerous symptoms. Yet it is sometimes a hazardous remedy. It
is not a convenient escharotic even in a concentrated state; for its
escharotic action is not incompatible with its absorption; at all events
it certainly sometimes acts constitutionally through the surface of
wounds and ulcers, and the symptoms brought on in this way are generally
violent. They are the symptoms of mercurial salivation, accompanied at
times with well-marked inflammation of the alimentary canal. When
applied to sores in a diluted state it has also been known to cause
dangerous effects if too long persevered in. A case of the kind has been
related by Mr. Robertson, an army-surgeon. After anointing an itchy
eruption of the arms for seven days with a solution of corrosive
sublimate containing five grains to the ounce, his patient was attacked
with fever, inflammation of the stomach and bowels, and in two days more
with violent salivation.[962] A case of the same nature has been related
by Mr. Sutleffe.[963] His patient, a child, in consequence of having an
eruption of the head washed with a solution of corrosive sublimate, was
attacked with violent salivation, which proved fatal in a few days.
Pibrac has recorded three fatal cases from the free application of
corrosive sublimate to ulcerated surfaces. One of these proved fatal in
five days, another in twenty-four hours, and a third during the night
after the poison was applied. The symptoms generally indicated violent
action on the alimentary canal.[964] In an instance mentioned by Degner,
fatal in twenty-five days, there was also violent irritation of the
stomach; but the chief affection was excessive swelling of the face and
throat, together with profuse ptyalism.[965]

One of the readiest modes of bringing the system under the poisonous
action of mercury is by introducing its preparations into the lungs. It
appears from some experiments by Schlöpfer that the fluid preparations
act rapidly through the lining membrane of the air-passages. Six grains
of corrosive sublimate in solution will thus kill a rabbit in five
minutes.[966] But the effects of mercury through this channel are much
better exemplified when its preparations are inhaled in the form of
vapour. Corrosive sublimate when incautiously sublimed in chemical
experiments has been known to cause serious effects. Dr. Coldstream of
Leith informs me, that while subliming about twenty-four grains of it
with the blowpipe when a student, he and several of his
fellow-apprentices were seized with painful constriction of the throat,
several had headache, and one had sickness and vomiting. The phenomena
produced by the various preparations of mercury in more violent cases,
are sometimes protracted tremors,[967] sometimes severe ptyalism and
tedious dysentery,[968] sometimes salivation and gangrene of the mouth
ending fatally.[969] This last form was produced remarkably in a
chimney-sweeper, after cleaning a gilder’s chimney, during which
operation he felt a disagreeable sense of tightness in the throat.

Several extraordinary instances have happened of poisoning from
long-continued inhalation of the vapours which arise from metallic
mercury. That vapours do arise from metallic mercury of the ordinary
temperature of the atmosphere has been fully proved by Mr. Faraday; who
found, that when a bit of gold was suspended from the top of a phial,
the bottom being covered with a little mercury, the gold soon became
amalgamated.[970] The vapours thus discharged may produce the worst
species of mercurialism, if they are diffused through an apartment
insufficiently ventilated. One of the most striking examples known of
the baneful effects of mercury thus gradually insinuated into the
system, occurred in a well-known accident which befel the ships Triumph
and Phipps. These vessels were carrying home in 1810 a large quantity of
quicksilver saved from the wreck of a ship near Cadiz, when by some
accident several of the bags were burst and the mercury spilled. On the
voyage home the whole crews of both vessels were more or less severely
salivated, two died, many were dangerously ill, all the copper articles
on board became amalgamated, all the rats, mice, cockroaches, and other
insects, as well as a canary-bird and several fowls, and all larger
animals, such as cats, dogs, goats, and sheep were destroyed.[971]

The action of mercury is often violently excited when it is applied to
the skin even not deprived of the cuticle. The effects of mercurial
inunction form a well-known and satisfactory proof of this. Even without
the aid of infriction, the soluble preparations of mercury will excite
mercurial action by being put simply in contact with the skin. Thus it
has been shown by a German physician, Dr. Guérard, that ptyalism may be
induced by a warm bath of corrosive sublimate in the proportion of an
ounce to 48 quarts of water, and that the effect commonly begins after
the third bath with an interval of three days between them.[972] It is
not so generally known that the more active preparations, such as
corrosive sublimate or nitrate of mercury, may, like arsenic, cause
through the sound skin effects almost as violent as through the
alimentary canal. The following pointed illustration is related by Dr.
Anderson. A gentleman affected with rheumatism, was persuaded by a
friend to use a nostrum, which was nothing else than a solution of half
a drachm of corrosive sublimate in an ounce of rum. This was rubbed on
the affected part for several minutes before going to bed. Ere the
friction was ended, he felt a sensation of heat in the part, to which,
however, he paid little attention. But during the night he was attacked
with pain in the stomach, sickness, and vomiting, and soon after with
purging and tenesmus. In the morning Dr. Anderson found him very weak
and vomiting incessantly. The arm up to the shoulder was prodigiously
swelled, red, and blistered. Next day he complained of brassy taste and
tenderness of the gums, and regular salivation soon succeeded.[973]
Another case of much interest has been described by my colleague,
Professor Syme, where a solution of the nitrate was rubbed by mistake
upon the hip and thigh instead of camphorated oil. Intense pain
immediately followed, and afterwards shivering; the urine was suppressed
for five days, without any insensibility, and during its suppression
urea was detected in the blood; ptyalism appeared on the third day,
became very profuse, and was followed by exfoliation of the alveolar
portion of the lower jaw, but recovery nevertheless slowly took
place.[974]

The mere carrying of mercurial preparations for a length of time near
the skin, though not in direct contact with it, may be sufficient to
induce the peculiar effects of the poison, as the following example will
show. A man applied to a German physician, Dr. Scheel, affected with
violent salivation evidently mercurial which proved fatal, but which it
was impossible to trace to its real cause till after death, when a
little leathern bag containing a few drachms of mercury was found
hanging at his breast; and it was then discovered that he had been in
the practice of carrying this bag for six years as a protection against
itch and vermin, and during that period had frequent occasion to renew
the mercury.[975]

The effects of mercury as a poison differ with the chemical form in
which it is introduced into the system.

In its metallic state it is probably inactive. This fact is a material
one for the medical jurist to determine precisely; for running
quicksilver has been given with a criminal intent. A case of the kind
forms the subject of a medico-legal report in Pyl’s Repertory;[976] and
another is mentioned in Klein’s Annals.[977]

It is well ascertained that large quantities of fluid mercury have been
repeatedly swallowed, without any injury or peculiar effect having
followed. In neither of the German cases now referred to was any bad
effect produced; and it has proved equally harmless when given
medicinally to remove obstruction in the intestines. Farther, M. Gaspard
mentions in his paper quoted in a former page, that he has left large
quantities shut up for many hours in the various cavities of the body in
animals, without observing any other result than at times inflammation,
which was evidently owing to the mere presence of a foreign body, and
not to the action of an irritant poison.[978]

It has been already stated, however, that the vapours of metallic
mercury, even at the temperature of the air, produce mercurialism when
inhaled. But then, in all likelihood, some of the metal is oxidated
before being inhaled. At least the chemist knows that the surface of a
mercurial trough soon tarnishes, especially when the mercury is not
pure.

But it may be said that the blue ointment, which is made with running
quicksilver, will not act as a mercurial when rubbed upon the skin. Here
too, however, some oxidation takes place in the making of the ointment.
Mr. Donovan endeavoured to prove that some of the mercury is always
oxidated;[979] and I have generally found a sufficient quantity of oxide
to account for the effects.[980]

It has been farther said, in proof of the poisonous action of
quicksilver in its metallic state,—that patients, who have taken it for
obstructed bowels, have sometimes been salivated. This accident has, I
believe, happened in a few instances where the mercury was retained long
in the body. But such cases are undoubtedly very rare. Zwinger mentions
the case of a man, who took four ounces for colic, and was seized in
seven days with salivation.[981] Laborde relates the particulars of
another instance where seven ounces taken in fourteen days excited
ptyalism, ulceration of the mouth, and great feebleness of the
limbs.[982] In the days of Dr. Dover, when the administration of large
doses of fluid mercury was a fashionable practice for a variety of
purposes, it was alleged to have even sometimes proved fatal; and the
case of an actor is specially mentioned, to whom, when convalescent from
ague, Dover gave mercury to the amount of two pounds in five days, and
who at the close of that period was seized with headache, colic,
restlessness, and costiveness, proving fatal in two days; and the whole
lower intestines were found black and lined with minute metallic
globules.[983] Perhaps then it must be admitted that fluid mercury is
not altogether inactive, speaking medicolegally. But this admission is
no argument in favour of the metal being physiologically a poison;
because in the course of the cases referred to, a part is in all
likelihood oxidated by the oxygen in the intestinal gases. It is said to
have been taken in the dose of an ounce daily for nine months, without
either good or harm resulting.[984]

The question regarding the poisonous qualities of running quicksilver
was carefully investigated some years ago by the Berlin College of
Physicians in a report on the case in Pyl’s Repertory.[985] They observe
that the opinion of Pliny, Galen, Hippocrates, Dioscorides, and many of
the earlier moderns, including even Zacchias, had led to the popular
belief in the deadly properties of fluid mercury; but that this belief
is erroneous; for many surgeons, and among the rest Ambrose Paré, had
given without injury to their patients several pounds of it to cure
obstructed bowels; and in 1515 the Margrave of Brandenburg, over-heated
on his marriage night with love and wine, and rising to quench his
thirst, drank by mistake a large draught of quicksilver without
suffering any harm. Fallopius mentions that he had known instances of
women swallowing pounds of mercury, for the purpose of procuring
miscarriage, and who did not suffer any injury.[986]

The sulphurets of mercury, like the metal, are not possessed of any
deleterious action on the animal body. Orfila found that half an ounce
of the sulphuret, formed in a solution of corrosive sublimate by
sulphuretted-hydrogen, and half an ounce or six drachms of cinnabar, had
no effect whatever on dogs.[987] The sulphurets which have appeared
injurious in the hands of Smith[988] and other previous experimentalists
must therefore have been impure.

Of the compounds of mercury, the red-precipitate and Turbith-mineral act
as irritants, besides possessing the property common to all mercurial
compounds, of causing mercurial erethysm. But they are not escharotics,
though generally termed such. That is, they do not chemically corrode
the animal textures. The effects of red-precipitate have been variable.
Mr. Allison relates the case of a girl who in a fit of jealousy
swallowed thirty grains of it. Being immediately detected, an emetic was
given, which operated freely, and subsequently the stomach-pump was
used; but on neither occasion was any red powder brought away. She was
attacked with burning pain in the stomach, which was removed by opium,
and for a week she had a distaste for food, but no other symptom of
consequence.[989] Mr. Brett has described a case, in which the symptoms
were occasional vomiting, stupor, languid pulse, cold clamminess of the
skin, afterwards severe cramps of the legs, tenderness of the abdomen,
dysuria, and some purging, and on the third day ptyalism; but the
patient recovered.[990] M. Devergie has given a case somewhat similar,
but without any ptyalism having followed the irritant effects of the
poison.[991] In 1840 I was consulted on the part of the Crown in the
case of a girl, who, there was every reason to suppose, had been killed
in twelve hours by red-precipitate. The symptoms towards the close were
pain in the throat, inability to swallow, vomiting, and excessive
prostration; extensive red patches were found on the villous coat of the
stomach after death; and I detected mercury in the solid contents and
likewise in the inner coat of the stomach. The case did not go to trial,
because, although a man by whom she was pregnant came under some
suspicion, it rather appeared that the deceased had herself swallowed
the poison with the view of inducing miscarriage. Dr. Sobernheim has
given the particulars of the case of a young man who died from
swallowing an ounce of red-precipitate. He suffered for some hours from
vomiting, diarrhœa, pain in the stomach, tenderness of the belly, and
colic; next day he had no pain, but coldness, lividity, stiffness, and
an imperceptible pulse; and he expired in thirty-three hours. The poison
was found abundantly in the stomach and duodenum after death, and some
grains of it rested upon little ulcers.[992] As to Turbith-mineral, two
scruples will kill a cat in four hours and a half; and several instances
of violent and even fatal poisoning with it are mentioned by the older
modern authors.[993]

The white precipitate or chloride of mercury and ammonia is probably
also irritant, though inferior in power to the preparations just
mentioned. Two scruples given to a dog occasion vomiting, pain, and some
diarrhœa; and cases are recorded of death in the human subject from less
doses.[994] But there are no recent facts as to the activity of this
compound, and the older cases, which would assign to it very great
energy, are open to the objection that this preparation was in former
times often impure.

The bichloride or corrosive sublimate is a powerful corrosive or
irritant, according to the dose and state of concentration; and it also
excites mercurial erethysm in a violent degree. The nitrates too are
corrosive, and not inferior in activity to the bichloride, as may be
inferred from Dr. Bigsby’s case, noticed at page 314.

The bicyanide or prussiate of mercury, from the researches of Ollivier,
and an interesting case he has published of poisoning with it in the
human subject, appears to resemble corrosive sublimate closely in all
its effects, except that it does not corrode chemically. Twenty-three
grains and a half proved fatal in nine days.[995] M. Thibert has
described a case in which ten grains caused death in the same period of
time.[996] The symptoms in both instances were those of severe
irritation of the stomach, extensive inflammation of the organs in the
mouth, and suppression of urine; and in Thibert’s case a small quantity
of albuminous fluid was discharged from the bladder instead of urine.

The protochloride or calomel, and probably also the protoxide, are the
most manageable of the preparations of mercury for inducing ptyalism.
Calomel is also an irritant; that is, it causes irritation and
inflammation in the alimentary canal when swallowed. This part of its
properties as a poison will require a word or two of explanation.

Calomel is universally employed as a laxative, but to secure this effect
being produced it is commonly combined with other purgatives. When given
alone a few grains will in some constitutions induce a violent
hypercatharsis; and larger, but still moderate, doses have with most
people such a tendency to cause severe griping and diarrhœa as to have
led to the practice of combining it with opium when the object is to
salivate. These considerations clearly establish that calomel, in a
moderate dose of five or ten grains, is an irritant.

It farther appears that in larger doses it is said to have occasionally
produced very violent effects, nay, even death itself, by its irritant
operation. Hoffmann has mentioned two instances where fifteen grains of
calomel proved fatal to boys between the ages of twelve and fifteen. One
of them had vomiting, tremors of the hands and feet, restlessness and
anxiety, and died on the sixth day. The other, he merely mentions, died
after suffering from extreme anxiety and black vomiting.[997] Another
fatal case has been related by Ledelius in the German Ephemerides, which
was caused by a dose of half an ounce taken accidentally. Vomiting soon
ensued, and a sense of acridity in the throat; then profuse diarrhœa to
the extent of twenty evacuations in the day; next excessive prostration
of strength and torpor of the external senses; and death followed in
little more than twenty-four hours.[998] Wibmer quotes Vigetius, an
author of the beginning of last century, for a similar case, likewise
fatal, which was occasioned by half an ounce,—also Hellweg, a writer of
the previous century, for the case of a physician, who took an ordinary
medicinal dose by way of experiment, and died in five hours under all
the symptoms of violent irritant poisoning.[999]

These observations being kept in view, what explanation will the
toxicologist give of the effects which in modern times have been
ascribed to large doses of calomel? It was stated not many years ago by
several East India surgeons, apparently with the universal assent of
their brethren in later times, that this drug in the dose of a scruple
administered even several times a day, is not only not an irritant, but
even on the contrary a sedative;[1000] and that in some diseases, for
example yellow fever, it has been given in the dose of five, ten, or
twenty grains, four or six times a day, till several hundred grains were
accumulated in the body, yet without causing hypercatharsis, nay, with
the effect of checking the irritation which gives rise to black vomit in
yellow fever, and to the vomiting and diarrhœa observed in the cholera
of the East. It is quite impossible for a European physician to doubt
these statements; for all practitioners in hot climates concur in them,
and now that analogous practices have been transferred to Britain,
repeated opportunities have occurred for establishing the fidelity of
the original reporters. Some American physicians, advancing beyond the
Hindostan treatment, have since given calomel in bilious fever in the
dose of forty grains, one drachm, two drachms, and even three drachms,
repeatedly in the course of twenty-four hours for several days
together,—and with similar phenomena. In one instance 840 grains were
given in the course of eight days in these enormous doses. The largest
dose was three drachms; and it was followed by only one copious
evacuation, and that not till after the use of an injection.[1001] This
practice appears not to have been altogether unknown in former times.
Ledelius, the author formerly quoted, states, that he had been
accustomed to give doses of a scruple, and that Zwölffer even gave a
drachm in one dose.[1002]

It must be also added, that while the facts quoted above from Hoffmann,
Ledelius, and others assign to single large doses a powerful and
dangerous irritant action, very different results have been occasionally
observed in recent times where even so large a quantity as one or two
ounces had been taken. Thus, in the case of a lady mentioned by Wibmer,
who took by mistake the enormous quantity of fourteen drachms, although
acute pain in the belly ensued, together with vomiting and purging,
these symptoms were speedily subdued by oleaginous demulcents; and after
a smart salivation, she recovered entirely in six weeks.[1003] Another
case has been related by Mr. H. P. Robarts, where an ounce was swallowed
by a young lady by mistake for magnesia, with no other effect than
nausea at first, rather severe griping and slight tenderness of the
belly afterwards, and subsequently languor, headache and indigestion;
yet the powder was retained two hours.[1004]

It is impossible in the present place to enter into the physiological
action of calomel as a remedy; but every one must be satisfied that,
with all which has been already written, much still remains to be done
before the facts now mentioned can be explained satisfactorily. Can the
violent effects described by Hoffmann, Ledelius and Hellweg have arisen
from the calomel having been imperfectly prepared and adulterated with a
little corrosive sublimate? Or may they be explained by reference to the
fact, that the presence of hydrochlorates in solution, particularly
hydrochlorate of ammonia, tends to convert calomel into corrosive
sublimate.[1005] Mr. Alfred Taylor has made some experiments, to show
that the latter explanation will not suffice.[1006]

Meanwhile, taking the facts as they stand, it is plain that great
caution must be used in ascribing violent irritant properties generally,
or even symptoms of irritant poisoning in a particular case, to large
doses of calomel.

With the view of illustrating the importance of the preceding
observations, it may be useful to mention here the heads of a case
already briefly alluded to for another purpose, the trial of William
Paterson for murder (319).[1007] His wife during the month previous to
her death had two attacks of diarrhœa, with an interval of a fortnight
between them. On the second occasion it became profuse and exhausting,
but without any material pain or considerable vomiting; looseness of the
teeth and salivation ensued, and she died in nine days. On examination
of the body, the anus was found excoriated, the whole intestines
checkered with dark patches, and the stomach red, ulcerated, and spotted
with black, warty excrescences; but the late Dr. Cleghorn of Glasgow
could not detect any poison by chemical analysis. It was proved that the
prisoner, besides procuring, a few months before his wife’s death, a
variety of poisons, such as hydrochloric acid, cantharides, and arsenic,
had also on different occasions during her last illness purchased in a
suspicious manner four doses of calomel varying from 30 to 60 grains
each. Among the various ways in which he was charged with having
poisoned the deceased, that which was best borne out by the general as
well as medical facts consisted in his taking advantage of an existing
inflammation of the mucous membrane of the bowels,—whether arising from
a natural cause or from poison it was in this view of the case
immaterial to inquire,—and keeping up and aggravating the inflammation
by purposely administering at intervals large doses of calomel. On the
trial Dr. Cleghorn and other witnesses gave their opinion that the doses
purchased by the prisoner, if administered, would cause the symptoms and
morbid appearances observed in the case. On the other hand, the late Dr.
Gordon deposed to the effect, that all the symptoms of the case might
arise under the operation of natural disease, and that such doses of
calomel were by no means necessarily injurious; the late Mr. John Bell
deposed, that it had even been given in much larger doses without
injury; and the profession are now well aware, though not at the time of
this trial, that in the very malady alleged by the prisoner to have
carried off the deceased, namely dysentery, the administration of
calomel in repeated large doses is accounted by many a proper method of
cure. The doses purchased by the prisoner were considerably larger, it
is true. But there was not any evidence of his having administered his
purchases in single doses as he got them; and even though there had been
evidence to that effect, it would not remove altogether the difficulty
of deciding the question, as to the irritating action of calomel, on
which the issue of the trial in one view of the case chiefly depended.

It is probable that all the compounds formed by corrosive sublimate with
animal and vegetable substances are feebly poisonous, or at least very
much inferior in activity to corrosive sublimate itself. This has been
shown by Orfila to be the case with the compound formed by albumen.
Sixty grains of this compound, being equivalent to nearly five grains of
corrosive sublimate, produced no bad effect whatever on a dog or a
rabbit.[1008] The same has been satisfactorily proved by Taddei as to
the compound formed by gluten. Twelve grains of corrosive sublimate
decomposed by his emulsion of gluten had no effect whatever on a
dog.[1009] It is important to remark, however, that if there be an
excess of the decomposing principle, so that the precipitate is party
redissolved, the irritant action of the corrosive sublimate is not so
much reduced, though it is still certainly diminished. Orfila has
settled this point in regard to albumen.[1010] The power of producing
mercurial erethysm is possessed by all mercurial compounds whatever, and
among the rest by the compounds now under consideration.[1011]

The present section may now be concluded with a few remarks on the
strength of the evidence derived from the symptoms which are produced by
the compounds of mercury.

If the medical jurist should meet with a case of sudden death like that
of the animals experimented on by Sir B. Brodie, the symptoms alone
could not constitute any evidence of poisoning with corrosive sublimate.
All he could say would be that this variety of poisoning was possible,
but that various natural diseases might have the same effect. This
feebleness in the evidence from symptoms, however, is of little moment;
because the dose must be great to cause such symptoms, and little can be
vomited before death; so that the poison will be certainly found in the
stomach.

Should the patient die under symptoms of general irritation in the
alimentary canal, poisoning may be suspected. But it would be impossible
to derive from them more than presumptive evidence. The suspicion must
become strong, however, if the ordinary signs of irritation in the
alimentary canal are attended with the discharge of blood upwards and
downwards. And the presumption will, I apprehend, approach very near to
certainty,—at least of the administration of some active irritant
poison,—if, at the moment of swallowing a suspected article, and but a
short time before the symptoms of irritation began in the stomach and
bowels, the patient should have remarked a strong, acrid, metallic
taste, and constriction or burning in the throat.

When upon all these symptoms salivation is superinduced, the evidence of
poisoning with corrosive sublimate or some other soluble salt of mercury
is almost unequivocal. That is, if, after something has been taken which
tasted acrid, and caused an immediate sense of heat, pricking, or
tightness in the throat, the characteristic signs of poisoning with the
irritants make their appearance in the usual time, and are soon after
accompanied or followed by true mercurial salivation,—it may be safely
inferred that some soluble compound of mercury has been taken. Before
drawing this inference, however, it will be necessary to determine with
precision all the classes of symptoms, more particularly the nature of
the salivation. It should also be remembered that salivation may
accompany or follow the symptoms of inflammation in the stomach, in
consequence of calomel having been used as a remedy. But if proper
attention be paid to the fallacies in the way of judgment, I conceive
that an opinion on the question of poisoning with corrosive sublimate
may be sometimes rested on the symptoms alone. This is another exception
to the rule laid down by most modern toxicologists and medical jurists
respecting the validity of the evidence of poisoning from symptoms.

For a good example of the practical application of these precepts, the
reader may consult the trial of Mr. Hodgson, for attempting to poison
his wife. In the instance which gave rise to the trial in question, a
violent burning sensation in the throat was felt during the act of
swallowing some pills; in the course of ten minutes violent vomiting
ensued, afterwards severe burning pain along the whole course of the
gullet down to the stomach, next morning diarrhœa, and on the third day
ptyalism. There were many other points of medical evidence which left no
doubt that corrosive sublimate was swallowed in the pills. But even the
history of the symptoms alone would have led to that inference.[1012]


      SECTION III.—_Of the Morbid Appearances caused by Mercury._

The morbid appearances observed in the bodies of persons killed by
corrosive sublimate will not require many details; since most of the
remarks formerly made under the head of the pathology of the irritants
generally, and of arsenic in particular, apply with equal force to the
present species of poisoning. Still there are some peculiarities
deserving of notice, which arise from the greater solubility or stronger
irritant action of corrosive sublimate.

The mouth and throat are more frequently affected than by arsenic; and a
remarkable appearance sometimes observed, and not excited, so far as I
know, by arsenic, is shrivelling of the tongue, with great enlargement
of the papillæ at its root.[1013]

The disorder of the alimentary canal is also usually more general, and
reaches a greater height before death takes place. Sometimes the
irritation and organic injury are confined to the stomach;[1014] but
more commonly the throat, stomach, gullet, rectum, nay, even also the
colon, are affected. The black or melanotic extravasation into the
mucous membrane of the stomach, which has been already several times
described as a common effect of the more violent irritants, is also
produced by corrosive sublimate. In Devergie’s case and in that of Dr.
Venables it was present in a very great degree.[1015]

The coats of the stomach, and also those of the intestines, more
particularly the colon and rectum, have frequently been found destroyed.
So far as I have been able to ascertain, two kinds of destruction of the
coats may be met with,—corrosion and ulceration.

The first is the result of chemical decomposition of the tissues. This
kind is evidently to be looked for only when the quantity has been
considerable and the dose concentrated. Nay even then it is rare. For on
account of the solubility of corrosive sublimate, the facility with
which it is decomposed by the secretions or accidental contents of the
stomach, and the violence and frequency of the vomiting, this poison is
peculiarly liable to be prevented from exerting its corrosive action on
the membranes. Hence it is that proper chemical corrosion of the coats
of the stomach is seldom witnessed in man.

The appearance of this corrosion differs according to the rapidity of
the poisoning. In very rapid cases, for example in animals which have
survived only twenty-five minutes, the villous coat has a dark gray
appearance, without any sign of vital reaction.[1016] But this variety
has never been witnessed in man, in whom the action has been hitherto
much less rapid. In the most rapid cases, such as that of Dr. Bigsby,
which terminated in two hours and a half (314), or those related by Mr.
Valentine, of which one ended fatally in eleven and another in
twenty-four hours, the corrosion was black, like the charring of
“leather with a red-hot coal, and the rest of the stomach scarlet-red or
deep rose-red;—showing that inflammation had set in.” In the former of
these two cases the corrosion was as big as a half-crown, in the latter
three inches in diameter. In a third case, where the patient lived
thirty-one hours, the stomach was perforated.[1017] In the case
described by Dr. Venables, and formerly alluded to, where life was
prolonged for eight days, there was a patch on the under surface of the
stomach as large as two crown-pieces, hard, elevated, and of a very dark
olive or almost black colour, besides very general erosion of the
villous coat.[1018] In all these cases the disintegrated spot was
probably situated where the poison first chiefly lodged.

The corrosion caused by mercury, if examined before the slough is thrown
off, will be found to possess an important peculiarity: the disorganized
tissue yields mercury by chemical analysis. Professor Taddei repeatedly
obtained the metal from the membranes of animals which he had poisoned
with corrosive sublimate.[1019] It is probable that mercury may be thus
detected although death may not have taken place for some time after the
poison was swallowed. For the slough was found adhering in one of Mr.
Valentine’s cases, where life was prolonged for seventy hours; and it
was not entirely removed even in eight days in one of the cases
described by Dr. Venables.

Although, however, it is sometimes possible to find the poison in the
stomach, the medical jurist must not perhaps expect to find it so often
in the present instance as in that of poisoning with arsenic. For on
account of its greater solubility corrosive sublimate cannot adhere with
such obstinacy to the villous coat, and is therefore more subject to be
discharged by vomiting. Nevertheless, the insoluble compound formed by
antidotes may adhere to the coats like arsenic, and so resist the
tendency of vomiting to displace them. In Devergie’s case,
notwithstanding twenty-three hours of incessant vomiting, although no
poison could be detected in the fluid contents of the stomach, it was
distinctly found in small whitish masses that lay between the folds of
the rugæ.[1020]

It may be here farther observed that corrosive sublimate, as well as
other salts of mercury, may undergo in the alimentary canal after death
the same change which is produced in arsenic from the gradual action of
hydrosulphuric acid gas. It may be converted into the sulphuret. I am
not acquainted indeed with any actual instance of such conversion; but
that it may occur we can scarcely doubt, not merely from theoretical
considerations, but likewise because Orfila met with an instance where
calomel taken daily in a case of gastro-cephalitis was discharged by
stool in the form of a black sulphuret.[1021]

Another important consideration is, that corrosive sublimate may be
decomposed and reduced to the metallic state by the admixture of various
substances either given at the same time or subsequently, and the longer
the inspection is delayed, the more complete will be the decomposition
which is accomplished. Iron, zinc, and other metals are the most active
of these substances.[1022]

The other forms of destruction of the coats of the alimentary canal is
common ulceration, either such from the beginning, or what was
originally corrosion converted into an ulcer in consequence of the
disorganized spot being thrown off by sloughing.

I have seen this appearance to an enormous extent in the great
intestines of a man who survived nine days. Numerous large, black,
gangrenous ulcers, just like those observed in bad cases of dysentery,
were scattered over the whole colon and rectum. In this instance, which
occurred to the late Dr. Shortt, the stomach was also ulcerated, but the
small intestines were not.

Sometimes the ulceration seems to be a variety of softening of the
mucous tissue, as in a case described by Dr. Alexander Wood of this
city, which proved fatal in fourteen days, and in which the stomach,
cæcum, and ascending colon presented round, softened, greenish spots
about the size of a sixpence, and accompanied in the stomach with a
tendency to detaching of the membrane in the form of a slough.[1023]

The destruction of the villous coat of the stomach occasioned by
corrosive sublimate and other soluble salts of mercury may be
distinguished from spontaneous gelatinization by one of two characters.
If the slough remains attached, mercury will be detected in it: if
separation has taken place, the ulcer exposed presents surrounding
redness and other signs of reaction.[1024]

All the other effects of inflammation may be produced by corrosive
sublimate, as by arsenic and other irritants. More frequently here than
in the case of arsenic peritonæal inflammation is met with. In
Devergie’s case the external surface of the stomach along both its
curvatures presented the appearance of red points on a violet ground. In
Mr. Valentine’s cases there was much minute vascularity, not only of the
outside of the stomach but also of the whole peritonæum lining the
viscera and inside of the abdomen; and there was even some serous
effusion into the cavity. In Dr. Venables’s case the peritonæal coat of
the stomach was highly vascular and inflamed, and the omentum also
injected.

The urinary organs, and particularly the kidneys, are often much
inflamed by poisoning with corrosive sublimate. Dr. Henry has related a
case in which this poison proved fatal on the ninth day, and where the
left kidney was found to contain an abscess.[1025] In all of Mr.
Valentine’s cases the kidneys were inflamed, and the bladder excessively
contracted, so as not to exceed the size of a walnut. In Ollivier’s
case, caused by the cyanide of mercury, the scrotum was gorged and
black, the penis erected, and the kidneys a third larger than natural.
In the case described by Dr. Venables both kidneys, but especially the
left, were large, flaccid, and vascular, the ureters turgid and purple,
and the bladder contracted, empty, and red internally.

Orfila has observed that the internal membrane of the heart is sometimes
inflamed and checkered with brownish-black spots. Some remarks have been
already made on the light in which this appearance ought to be viewed by
the pathologist (p. 271).

Whatever may be the real state of the fact as to the alleged power of
arsenic to preserve from decay the bodies of those poisoned with it, all
authors agree that corrosive sublimate possesses no such property. Yet
it is well known to be a good antiseptic, when applied topically. The
experiments of Klanck, noticed under the head of Arsenic, prove that
corrosive sublimate at all events does not retard putrefaction in the
bodies of those poisoned with it; and Augustin in his analysis of
Klanck’s researches infers that it even promotes decay.[1026] I have met
with one example in the human subject which seems to confirm Augustin’s
opinion. In the case formerly quoted from the Medical and Physical
Journal, which was fatal in four days, the relater found the body
forty-two hours after death so putrid, though in the month of January,
that the examination of it was very unpleasant, the belly being black,
and a very offensive odour being exhaled.[1027] Little importance,
however, can be attached to a solitary case; for on the contrary Sallin
relates a case where the body of a man supposed to have been poisoned
with corrosive sublimate was found not decayed, but imperfectly
mummified, after sixty-seven days.[1028]

It is unnecessary to detail the proofs to be found in the dead body of
mercurial salivation having existed during life. They are of course to
be looked for in the mouth, and in the adjoining organs. We must not,
however, expect to see much appearance of disease in the salivary
glands; for according to Cruveilhier, in persons who die of mercurial
salivation these glands do not present any trace of inflammation
themselves, but merely serous effusion into the cellular tissue around
them.[1029]

Professor Orfila has made some useful experiments as to the effects of
corrosive sublimate on dead intestine, which it may be proper to notice
in a few words. When applied in the form of powder to the rectum of an
animal newly killed, the part with which it is in contact becomes
wrinkled, and as it were granulated, harder than natural, and of
alabaster whiteness, intermingled with rose-red streaks, apparently the
ramifications of vessels. When the membrane is stretched upon the
finger, the wrinkling disappears. The muscular coat is of a snow-white
colour, and even the serous coat is white, opaque, and thickened. The
parts not in contact with the powder retain their natural appearance,
and the line of demarcation between the affected and unaffected portions
is abrupt. If the powder is not applied till twenty-four hours after
death, the parts it touches become thick, white, and hard; but no red
lines are visible. It is easy to draw the distinction between these
appearances and the effects of corrosive sublimate during life.

Little need be said of the force of the evidence of poisoning with
corrosive sublimate, derived from the morbid appearances. If the gullet,
stomach, and colon be all inflamed and ulcerated, and these injuries
have taken place during a short illness, the presumption in favour of
some form of irritant poisoning will be strong. And the presumption of
poisoning with corrosive sublimate will be strong, if the usual marks of
salivation are also found in the mouth and throat. But such evidence can
never amount to more than a strong presumption or probability.


       SECTION IV.—_Of the Treatment of Poisoning with Mercury._

The treatment of poisoning by the compounds of mercury may be referred
to two heads,—that which is required when irritation of the alimentary
canal is the prominent disorder, and that which is designed to remove
mercurial salivation.

Irritation and inflammation of the alimentary canal are to be treated
nearly in the same way as when arsenic has been the poison swallowed. In
the instance of corrosive sublimate we also possess a convenient and
effectual antidote.

Several substances may be used as antidotes; but those which have
hitherto been most employed are albumen and gluten.

It has been already hinted that albumen, in the form of white of eggs
beat up with water, impairs or destroys the corrosive properties of
bichloride of mercury, by decomposing it and producing an insoluble
mercurial compound. For this discovery and the establishment of albumen
as an antidote, medicine is indebted to Professor Orfila. He has related
many satisfactory experiments in proof of its virtues. The following
will serve as an example of the whole. Twelve grains of corrosive
sublimate were given to a little dog, and allowed to act for eight
minutes, so that its usual effects might fairly begin before the
antidote was administered. White of eight eggs was then given; after
several fits of vomiting the animal became apparently free from pain;
and in five days it was quite well.[1030] According to Peschier the
white of one egg is required to render four grains of the poison
innocuous.[1031] The experiments of the Parisian toxicologist have been
repeated and confirmed by others and particularly by Schloepfer; who
found that when a dose was given to a rabbit sufficient to kill it in
seven minutes if allowed to act uncontrolled, the administration of
albumen, just as the signs of uneasiness appeared, prevented every
serious symptom.[1032] Dr. Samuel Wright has found that if the
administration of albumen is followed up by giving some astringent
decoction or infusion, the beneficial effects are more complete, because
the compound formed is less soluble in an excess of albumen.[1033]

The virtues of albumen have also been tried in the human subject with
equally favourable results. The recovery of the patient, whose case was
quoted formerly (p. 312), from Orfila’s Toxicology, seems to have been
owing in great measure to this remedy. In the Medical Repository another
case is related, in which it Was also very serviceable.[1034] A third
very apposite example of its good effects is related by Dr. Lendrick.
His patient had taken about half a drachm of corrosive sublimate, and
was attacked with most of the usual symptoms, except vomiting. White of
eggs was administered a considerable time afterwards, the beneficial
effects of which were instantaneous and well-marked; and the patient
recovered.[1035] A few years ago Orfila’s discovery was the means of
saving the life of M. Thenard the chemist. While at lecture, this
gentleman inadvertently swallowed, instead of water, a mouthful of a
concentrated solution of corrosive sublimate; but having immediately
perceived the fatal error, he sent for white of eggs, which he was
fortunate enough to procure in five minutes. Although at this time he
had not vomited, he suffered no material harm. Without the prompt use of
the albumen, he would almost infallibly have perished.[1036]

Albumen is chiefly useful in the early stage of poisoning with corrosive
sublimate, and is particularly called for when vomiting does not take
place. But it farther appears to be an excellent demulcent in the
advanced stages.

On a previous occasion, mention was made of a few of the facts brought
forward by Professor Taddei to prove the virtues of the gluten of wheat
as an antidote for poisoning with corrosive sublimate [297, 336], so
that nothing more need be said on the subject in the present place. As
it is difficult to bring the whole of a fluid containing corrosive
sublimate into speedy contact with pulverized gluten, which when put
into water becomes agglutinated into a mass, the discoverer of this
antidote proposes to give it in the form of emulsion with soft soap.
This is made by mixing, partly in a mortar and partly with the hand,
five or six parts of fresh gluten with fifty parts of a solution of soft
soap. And in order to have a store always at hand, this emulsion, after
standing and being frequently stirred for twenty-four hours, is to be
evaporated to dryness in shallow vessels, and reduced to powder. The
powder may be converted into a frothy emulsion in a few minutes.[1037]
Taddei made use of this powder with complete success in the case of a
man who had swallowed seven grains of corrosive sublimate by mistake for
calomel. Violent symptoms followed the taking of the poison; but they
were immediately assuaged by the administration of the antidote; and the
person soon got quite well.[1038] It is probable that wheat flour will
prove an effectual antidote by reason of the gluten it contains. On
agitating for a few seconds a solution of twelve grains of corrosive
sublimate along with three ounces of a strong emulsion of flour, and
immediately filtering,—I find that ammonia and carbonate of potass have
little or no effect, that hydriodate of potass occasions a yellow
precipitate, and that the acrid, astringent taste of the solution is
removed; whence it may be inferred, that the corrosive sublimate is all
decomposed, that little mercury remains in solution, and that what does
remain is in the form of a chloride of mercury and gluten.

When neither albumen nor gluten is at hand, milk is a convenient
antidote of the same kind.

Iron filings would appear to be also a good antidote. MM. Milne-Edwards
and Dumas have found that when they were administered in the dose of an
ounce to animals after twelve or eighteen grains of corrosive sublimate
had remained long enough in the stomach for the symptoms to begin, the
animals recovered from the effects of the poison, and died only some
days afterwards of the effects of tying the gullet, which operation was
necessary to prevent them vomiting. The iron obviously acts by reducing
the corrosive sublimate to the metallic state.[1039]

Meconic acid, the peculiar acid of opium, which will be described under
the head of that poison, is also probably a good antidote. Pettenkoffer
correctly remarks that this acid has a great tendency to form very
insoluble salts with the metallic oxides, particularly with the
deutoxides, and above all when the acid is previously in union with a
base which constitutes a soluble salt.[1040] On this account it must be
a good antidote. Pettenkoffer adds, that the precipitating action of the
meconates is the reason why “the operation of corrosive sublimate on the
animal body is almost entirely prevented by opium.” Opium, however,
cannot be safely used in such quantity as to decompose all the corrosive
sublimate in a case of poisoning; for I find that an infusion of
thirty-three grains is required to precipitate all which can be thrown
down from a solution of five grains of the mercurial salt. I am not
aware of any instances on record where poisoning with corrosive
sublimate has been prevented or cured by opium given so as to decompose
the salt; but a very remarkable case will be related under the head of
Compound Poisoning, where the phenomena of its action were masked and
altered in a singular manner. There is little doubt that the alkaline
meconates must prove valuable antidotes for corrosive sublimate. At
present an effectual barrier to their employment is their rarity; but
they might be rendered more accessible, as a great quantity of meconate
of lime, which is at present put to no use, is formed in the manufacture
of muriate of morphia; and meconate of potass may easily be prepared in
sufficient quantity from the meconate of lime.

It has been alleged by Dr. Buckler of Baltimore, that a mixture of
gold-dust and iron filings is an effectual antidote; but Orfila denies
this statement; and the fact if true would be unimportant, on account of
the improbability of the materials being ever at hand in practice.[1041]

M. Mialhe suggested not long ago as an antidote the proto-sulphuret of
iron prepared by decomposing sulphate of protoxide of iron by
hydrosulphate of ammonia; and Orfila found that it is a perfect chemical
antidote, which altogether prevents the poisonous action of corrosive
sublimate, if administered to animals either before or immediately after
the poison; but he further ascertained that the lapse of ten minutes was
sufficient to render it of no use.[1042] It is difficult, however, to
perceive why in this respect it should differ from white of egg or any
other chemical antidote.

As to the old antidotes for poisoning with corrosive sublimate, such as
the alkaline carbonates, the alkaline hydrosulphates, cinchona, mercury,
charcoal,—Orfila has given them all a fair trial, and found them all
inefficacious. It would appear, however, from a case related in a late
American journal, that frequent doses of charcoal powder have much
effect in soothing the bowels and allaying the inflammation after the
poison is evacuated.[1043]

The treatment of mercurial salivation consists in exposure to a cool
pure air, nourishing diet, and purgatives, if the intestinal canal is
not already irritated. In some of the inflammatory affections it
induces, venesection is required; in others it is hurtful. In some
complaints induced by mercury, as in iritis, the poison appears to be
its own antidote; for nothing checks the inflammation so soon and so
certainly as mercurial salivation.

Dr. Finlay of the United States proposed to check mercurial salivation
by small doses of tartar emetic frequently repeated, so as to act on the
skin;[1044] and Mr. Daniell has recommended large doses of the acetate
of lead as an effectual antidote for the same purpose.[1045] I have
tried both of these plans several times with apparent success. In one
instance particularly, where a severe salivation was threatened by the
administration of six grains of calomel in three doses, and where
profuse salivation, ulceration of the tongue and swelling of the face
actually did commence with violence, the mercurial affection after a few
days rapidly receded under the use of large doses of acetate of
lead.—Dr. Klose, a German physician, says he has found iodine to possess
the property of arresting the effects of mercury on the mouth.[1046] The
iodide of potassium is generally acknowledged to be one of the best
remedies for eradicating the constitutional infirmities left in many by
severe courses of mercury.

A great deal might be said on the treatment of the secondary effects of
poisoning with mercury. But a thorough investigation of the subject
would lead to such details as would be inconsistent with the other
objects of this work.




                              CHAPTER XV.
                        OF POISONING WITH COPPER


Poisoning with the salts of copper was not long ago a common accident,
in consequence of the metal being much used in the fabrication of
vessels for culinary and other domestic purposes, or ignorantly resorted
to by confectioners and others to impart a good colour to sweetmeats and
preserves. Such accidents have been materially diminished in frequency
since the poisonous qualities of the metal, and the circumstances under
which it is acted on by articles of food, have become known.
Nevertheless they are still frequent enough. The diffusion among the
common people of the knowledge of the properties of copper has also
naturally led some persons to have recourse to its preparations for the
purpose of self-destruction. Poisoning with copper has seldom been
caused by the wilful act of another person; for the deep colour of its
compounds and their strong disagreeable taste render it a difficult
matter to administer them secretly. This, however, though difficult, is
not impossible: whatever may be swallowed accidentally, may be also
administered secretly. In 1795 a woman Inglis was tried at Aberdeen for
administering sulphate of copper with intent to poison; but the charge
was not proved.[1047] In 1842 an attempt was made at Béziers in France
to poison a young woman by dissolving this salt in her coffee; but the
first mouthful caused such a sense of constriction in the throat as to
apprize her of something deleterious being present, and she escaped
after suffering from soreness of the mouth, vomiting and cramps.[1048] A
case of imputed poisoning with sulphate of copper has been related at
page 76.


  SECTION I.—_Of the Chemical History and Tests of the Preparations of
                                Copper._

Metallic copper has a special red colour, to which it gives its own
name. Its specific gravity is nearly 9, its hardness considerable, its
tenacity great, its point of fusion about 27° W. or at a full white
heat.

It unites with oxygen in two proportions, forming a yellowish-red
protoxide, and a peroxide, which, when dry, is brownish-black—when
hydrated, azure-blue. It unites also with sulphur in two corresponding
proportions, forming a gold-yellow proto-sulphuret, the natural
copper-pyrites, and a black bisulphuret, which is formed by
sulphuretted-hydrogen in all the solutions of this metal. The peroxide
unites with ammonia. The acids all unite with the oxide and form blue or
green salts, some of which are soluble, some insoluble. The oxide is
frequently mixed with other matters to form various pigments; but in
such compounds the union is generally mechanical, not chemical. Of the
substances thus formed and existing in nature and the arts the following
only require notice here. 1. _Mineral green_, and other pigments formed
with the hydrated oxide. 2. _Natural verdigris_, or the carbonate. 3.
_Blue vitriol_, or the sulphate. 4. _Artificial verdigris_, or the mixed
acetates.


                          1. _Mineral Green._

The description of this substance and its chemical properties must be
introduced with a short account of the tests for the unmixed _peroxide_.
When free of water the peroxide is a brownish-black powder or granular
mass, which is usually procured by decomposing nitrate of copper at a
low red heat. It is easily known by the solvent power of nitric acid,
the blue colour of the filtered solution, and the beautiful deep violet
tint communicated to the solution by an excess of ammonia. The last
property is considered by chemists the most satisfactory proof of the
presence of oxide of copper in a fluid. It is alone quite free of
fallacy, and may be applied to all the soluble and also many insoluble
compounds of copper, provided they are not mixed with a large proportion
of vegetable or animal fluids, in which case the colour is often
greenish.

In the case of the peroxide and of copper poisons generally, the process
of reduction, which has been applied with such delicacy and precision to
arsenical and mercurial poisons, loses all its advantages. The metal
remains in the flux, and intimately diffused; so that of its physical
qualities the colour only can be estimated, and even that but
inaccurately, except in the instance of one compound, verdigris.

The _hydrated peroxide of copper_, when newly formed and well prepared,
has a fine azure-blue colour; but on exposure to a gentle heat, it parts
with its water, and becomes the anhydrous peroxide. It is procured by
precipitating any of the soluble salts of copper by means of caustic
potass. It is at once known by the action of ammonia, which immediately
forms with it a deep violet-blue solution.

_Mineral green_, as already mentioned under the head of Arsenic (p.
223), was originally an arsenical pigment introduced into the art of
colour-making by Scheele, and now sometimes sold in this country by the
name of emerald-green. But the mineral green of the colourist now
contains no arsenic, being a hydrate of peroxide of copper intimately
mixed with a little lime, which is generally carbonated. This variety of
mineral-green probably varies a little in composition. Some parcels I
have found to contain the lime in the state of carbonate; in others the
lime was chiefly caustic.

The best method of determining its nature is to dissolve it in diluted
hydrochloric acid, which leaves only a slight cloudiness from accidental
impurities; and then to transmit through the filtered solution a stream
of sulphuretted hydrogen gas. The copper on boiling is all thrown down
in the form of a black bisulphuret, and hydrochlorate of lime remains in
solution. The lime is then to be detected by its proper tests, after the
solution has been filtered and neutralized (see p. 192). In general this
long process is unnecessary, as the medical jurist may be simply
required to say whether the suspected substance contains copper. In that
case it is only requisite to subject the substance to the action of
ammonia, as if it was hydrated peroxide.

_Verditer_, another green pigment, the basis of which is always oxide of
copper, does not appear to differ essentially in composition from
mineral green. The samples I have examined consist of a large proportion
of hydrated oxide of copper, and a small proportion of carbonate of
lime.


                        2. _Natural Verdigris._

This is a compound of no great importance in a medico-legal point of
view. Nevertheless an instance has been lately published in which it was
taken for the purpose of committing suicide, and was found abundantly in
the stomach.[1049] The carbonate of copper exists naturally in two
states. In one form it constitutes the rust of copper, or natural
verdigris, and is produced as a powdery crust on metallic copper by long
exposure to moist air. It is insipid and insoluble, so that pure water
left in vessels incrusted with it does not become poisonous. It
dissolves with effervescence in sulphuric acid, and without
effervescence in ammonia, forming the usual violet solution. In another
form it exists in the mineral kingdom, constituting the chief part of a
beautiful ore, malachite, and also a considerable proportion of some
blue-copper ores.


                           3. _Blue Vitriol._

Blue vitriol, blue copperas, blue stone, vitriol of copper, as it is
variously called in common speech, is the sulphate of copper. In the
solid form it constitutes large crystals of a deep blue colour, and an
acrid, astringent, metallic taste, efflorescent in dry air, and very
soluble in water. Under the action of heat it first loses its water of
crystallization without undergoing the watery effusion; then its
sulphuric acid is driven off partly unchanged, partly decomposed; and at
last the brown peroxide is left behind in a state of considerable
purity. If carbonaceous matter be previously mixed with the sulphate,
the oxide is decomposed at a low red heat, so that the process of
reduction may be performed in a glass tube. For the reasons formerly
stated, this process does not constitute a convenient or characteristic
test for sulphate of copper. The best mode of ascertaining its nature is
to dissolve it, and then to apply the tests for the solution.

There are many excellent tests for copper in solution. But the four
following are the most delicate and characteristic,—ammonia,
sulphuretted hydrogen, ferro-cyanate of potass, and metallic iron.

1. _Ammonia_ causes a pale azure precipitate, which is redissolved by an
excess of the test, forming a deep violet-blue transparent fluid. If the
solution is very diluted, there is no previous precipitation; the fluid
becomes violet without its transparency being disturbed. This is a
perfectly characteristic test of copper, and one of great delicacy.

2. _Sulphuretted hydrogen gas_ causes a dark brownish-black precipitate,
the sulphuret of copper. This test is one of very great delicacy; but it
is not alone decisive of the presence of copper, since lead, bismuth,
mercury, and silver, are similarly affected by it. A method, however,
will be presently described, by which the precise nature of the
sulphuret may be determined.

The alkaline hydrosulphates, for example the hydrosulphate of ammonia,
answer equally well with sulphuretted-hydrogen. The solution of the
common liver of sulphur throws down, not a black, but a chestnut
precipitate.

3. _Ferro-cyanate of potass_ causes a fine hair-brown precipitate, the
ferro-cyanide of copper. This test is also exceedingly delicate and
characteristic.

4. A polished rod or plate of _metallic iron_, held in a solution of
sulphate of copper, soon becomes covered with a red powdery crust, which
is metallic copper; and ere long the solution is changed in colour from
blue to greenish-yellow. The action is simple; the iron merely displaces
the copper in the solution, in which a sulphate of iron is consequently
formed. This test is characteristic, and even of considerable delicacy.
At the same time other substances may cause a reddish encrustation on
iron by simply rusting it, so that the test cannot be relied on alone.

The four preceding reagents taken together are amply sufficient to prove
the existence of copper in a solution. Three other tests, however, may
be here briefly alluded to.

Caustic potass in a solution not too diluted causes a fine azure-blue
precipitate, the hydrated peroxide of copper.

Oxide of arsenic, with the previous addition of a few drops of ammonia,
causes a fine apple-green or grass-green precipitate, the arsenite of
copper. This test, which is both delicate and characteristic, has been
already fully considered under the head of Arsenic.

The process by fluid reagents, as hitherto laid down, merely proves the
presence of copper, but does not indicate the acid with which the oxide
is combined. In order to determine whether it is sulphuric acid, the
fluid must also be tested with nitrate of baryta followed by nitric
acid: a heavy white precipitate is thus produced, which the excess of
nitric acid does not redissolve.


                       4. _Artificial Verdigris._

_Artificial verdigris_ is a common pigment, which is met with in the
form either of earth-like masses, or of a light powder of a
greenish-blue colour and peculiar disagreeable smell, approaching that
of vinegar. Like blue vitriol it has a strong metallic, astringent
taste. The effect of heat is peculiar. Some acetic acid is in the first
place distilled over; a portion of the acid, however, is decomposed and
reduces the oxide; and a low red heat is sufficient to make the outer
crust of the verdigris distinctly copper-red, when the material is
contained in a glass tube.

Artificial verdigris varies somewhat in composition. Foreign verdigris
contains chiefly the hydrated diacetate, with a little carbonate, oxide,
and even metallic copper, along with particles of the fruit and
fruit-stalks of the grape. British verdigris consists of little else
than the hydrated diacetate. It is known by the following characters.
Ammonia dissolves it almost entirely, forming a deep violet solution.
Diluted sulphuric acid dissolves it, evolving an odour of acetic acid,
and forming a solution of sulphate of copper, which may be known by the
tests for that salt. Boiling water converts it partly into an insoluble
brown powder, which is oxide of copper in union with a small proportion
of acetic acid, and partly into a greenish-blue neutral acetate, which
is dissolved, and may be known by the four tests for sulphate of copper,
and the want of action of nitrate of baryta.

It may be right to notice shortly three other salts of copper, the
nitrate, the ammoniacal sulphate, and the muriate. The _nitrate_ forms a
violet solution, which is acted on by reagents in the same way as the
dissolved acetate, but has not any odour of vinegar. The _ammoniacal
sulphate_ [ammoniated copper—ammoniuret of copper], has been
occasionally used in medicine. It forms, when solid, small scaly
crystals, of an intense violet colour and strong ammoniacal odour; and
when dissolved it retains its peculiar colour even though very much
diluted.—The _muriate_ of copper has a lively grass-green colour, and is
acted on by reagents in the same way as the solution of verdigris.

_Of the corrosion of copper by articles of food and drink._—To these
observations on the chemical history of copper a few remarks must be
added relative to the action of various articles of food or drink upon
the metal. Unpleasant accidents have often happened from the use of
copper vessels in the preparation of food; and it is therefore necessary
for the medical jurist to know the circumstances, so far as they have
been investigated, under which the poison may be dissolved.

Dr. Falconer found, that distilled water kept several weeks on a
polished plate of copper, neither injured its lustre, nor acquired any
taste, nor become coloured with ammonia;[1050] and Drouard afterwards
observed, that distilled water, kept for a month on copper filings, did
not contain any of the metal.[1051] Eller of Berlin, however, remarked,
that water, if it contain a considerable quantity of common salt, as
four ounces in five pounds, or a twentieth part, will give slight traces
of copper after being boiled in a brass pan; and that if the pan be made
of copper, a powder is procured by evaporation, which when treated with
acetic acid yields so much as 20 grains of acetate of copper.[1052] But
it is a singular circumstance, also observed by the same
experimentalist, that if beef of fish be boiled with the usual allowance
of salt, and with the addition also of various vegetable substances, the
liquid does not yield any copper. This observation has been lately
denied by Professor Orfila; who says he found copper deposited on a
plate of iron in salt water in which beef had been boiled, and that he
also obtained copper from the beef itself.[1053] The quantity thus
dissolved, however, must be exceedingly small, if the copper be kept
clean and free of oxide; for copper vessels, although they have often
been the source of fatal accidents, if carelessly used in the
preparation of food, have appeared under careful management to be quite
harmless. An excellent practical confirmation of this will be found in
Michaelis’s Commentaries. He states, that in the Orphan Hospital of
Hallé, the food was in his time prepared in large copper vessels, which
were kept remarkably clean; and that out of a population of eight or
nine hundred he never heard of any one having suffered from symptoms of
poisoning with copper.[1054] Several other saline matters promote the
solution of copper in water. Thus Dr. Falconer found that alum has this
effect when aided by heat; and probably nitre and Epsom salt possess the
same quality.[1055] Their mode of action is not very well known.

It is a common though erroneous idea, that milk, heated or allowed to
stand in a copper vessel, becomes impregnated with the metal. Eller has
shown, that, on the contrary, if the vessel be well cleaned, milk, tea,
coffee, beer, and rain-water, kept in a state of ebullition for two
hours, do not contract the slightest impurity from copper;[1056] and the
same remark has been also made by Dr. Falconer with respect to cabbage,
potatoes, turnips, carrots, onions, rice, and barley.[1057]

But Eller farther remarked, that, if the vessel is not thoroughly clean,
then all acid substances dissolve the carbonate that encrusts it,
especially if left in it for some time. Nay, it appears that some acid
matters, though they do not dissolve clean copper by being merely boiled
in it a few minutes, nevertheless, if allowed to cool and stand some
time in it, will acquire a sensible impregnation.[1058] Dr. Falconer
also observed that syrup of lemons, boiled fifteen minutes in copper or
brass pans, did not acquire a sensible impregnation; but if it was
allowed to cool and remain in the pans for twenty-four hours, the
impregnation was perceptible even to the taste, and was discovered by
the test of metallic iron.[1059] This fact has been farther confirmed by
the researches of Proust,[1060] who states, that, in preparing food or
preserves in copper, it is not till the fluid ceases to cover the metal,
and is reduced in temperature, that solution of the metal begins.
Inattention to this difference has been the cause of fatal accidents, of
which the following case from Wildberg’s Practical Manual will serve as
a good example. A servant left some sour-krout for only a couple of
hours in a copper pan which had lost the tinning. Her mistress and a
daughter, who took the cabbage to dinner, died after twelve hours
illness; and Wildberg found the cabbage so strongly impregnated with
copper, that it was detected by the test of metallic iron.[1061]

Some wines have the same power, by reason of the acid they contain.
Hence Eller found twenty-one grains of the acetate in five pounds of
French white wine, after being boiled in a copper vessel. An epidemic
disease, mentioned by Fabricius, which broke out in 1592 among the
senators of Bern, and a number of their guests who had been invited to a
great entertainment, was supposed to have arisen from a poisonous
impregnation of this kind. The wine used at the feast had been kept cool
in copper vessels immersed in a very cold well. Many of the company were
attacked with dysenteric symptoms, and some died.[1062]

Vinegar also dissolves metallic copper. Dupuytren observed that the
vinegar sold by hawkers in the streets of Paris generally contained
copper from the action of the acetic acid on the stop-cocks of the
little vessels used in retailing it.[1063] Others in like manner have
found copper in vinegar pickles prepared in copper vessels. Thus Dr.
Percival found a strong impregnation of copper in pickled samphire, of
which a young lady ate one morning two breakfast platefuls, and which
proved fatal to her in nine days.[1064] And Dr. Falconer once detected
so large a quantity in some pickled cucumbers bought at a great London
grocer’s, that it was deposited on a plate of iron, and imparted its
peculiar taste and smell to the pickles.[1065] It seems indeed to have
been at one time the custom to make a point of adulterating pickles with
copper; for in many old cookery-books the cook is told to make her
pickles in a copper pan, or to put some halfpence among the pickles to
give them a fine green colour.[1066]

The action of the vegetable acids, and more particularly of vinegar on
copper, depends on the co-operation of the atmospheric air held in
solution by the fluid, and in contact with its surface. Without such
co-operation the copper cannot be oxidated. This fact, which was
determined experimentally by Proust,[1067] will explain the observations
of Eller and Falconer,—that it is not dangerous to boil acidulous
liquids in copper vessels, while it is very unsafe to keep these fluids
cold in the same vessels. In the latter instance the liquid is
impregnated with atmospheric air, while in the former the usual aëriform
contents are driven off by the heat. I must observe, however, in
limitation of Proust’s statement, that strong vinegar, such as the
pyroligneous acetic acid, will become impregnated to a certain extent if
boiled in copper vessels. The action which takes place is the same as
that remarked by him in the case of cold vinegar:[1067] the copper where
it is always covered remains quite bright; but at the edge of the fluid
it becomes oxidated, and the oxide is dissolved by the occasional
bubbling up of the acid.

In the last place, the property of oxidating and uniting with copper is
likewise possessed by fatty matters and oils. According to Falconer,
fatty substances do not act on metallic copper unless they are
rancid.[1068] But Proust is probably more correct when he states, that
they will act, though fresh, provided they are aided by the co-operation
of atmospheric air.[1069] I have found, that, if a plate of copper be
thrust into a mass of fresh butter, its surface becomes dark in
twenty-four hours, and the butter becomes green wherever it is in
contact both with the copper and the air, but not where it covers the
metal closely. In fresh hog’s lard, however, I have found that the whole
lard in contact with the copper becomes blue even at a depth to which
the air can scarcely reach. The action of oils is similar. It is even
probable that they act when hot; for Mr. Travis found that hot oil
became green when kept for only four or five minutes in a copper
vessel.[1070] Dr. Falconer mentions that the property of acting on
copper is possessed in an eminent degree by volatile oils, and
especially by oil of cloves and oil of cinnamon.[1071]

The general result of the preceding observations is, that there is
hardly any article of food or drink which may not become impregnated
with copper if kept in copper vessels, as there are few articles which
do not contain either an acid or some fatty matter; and it farther
appears, that the impregnation will scarcely ever take place during the
boiling of such articles, but only during the preservation of them in a
cold state. It must also be considered, that, independently of these
chemical impregnations, articles of food may be mixed mechanically with
copper, in consequence of the vessels being allowed, through the
carelessness of the cook, to become covered with rust or carbonate,
which is subsequently removed by the friction of the solid parts of any
article that is boiled in them.

In order to prevent accidental impregnations, copper vessels are usually
tinned. The tinning consists of an alloy of tin and lead, which is much
less easily attacked than the copper, and the safety of which is farther
insured by the circumstance, that the substances endowed with the
property of dissolving lead, cannot attack that metal before the whole
tin of the alloy is oxidated.[1072] The tinning of copper, however, has
been found to be but a partial protection, as the tinning is apt to be
worn away without attracting the attention of servants. Hence the use of
copper in the fabrication of kitchen utensils is becoming every day more
and more limited, especially since the manufacture of cast-iron vessels
was brought to perfection in this country.

Many instances might be adduced of the ignorance and carelessness which
prevailed, even not far back in the last century, as to the employment
of copper vessels for culinary purposes. In addition to the instances
already quoted, the following are well deserving of notice. Gmelin was
consulted by the abbot of a monastery, on account of a violent disease
which prevailed throughout the whole brotherhood of monks. The symptoms
were obstinate and severe colic, retching and bilious vomiting,
costiveness, flatus, burning pain in the pit of the stomach, under the
sternum, in the kidneys and extremities, and paralytic weakness in the
arms. On inquiring into the cause of this singular combination of
symptoms, Gmelin found that every vessel in the kitchen, the pots and
pans, and even the milk pails and butter dishes for storing the butter,
were made of copper.[1073] In 1781 an establishment of Jacobin monks at
Paris were all violently affected from a similar error. The cook on a
Friday and the subsequent Saturday, after boiling fish for the dinner of
the monks in a copper pan, and drawing off the water, poured vinegar
over the fish, and left it thus in the pan for a considerable time. On
the evening of Friday several of them were taken severely ill with
headache, acute pain in the stomach and bowels, precordial anxiety,
purging, great feebleness, and cramps in the legs. The rest of them, to
the number of twenty-one in all, were similarly attacked next morning;
and the symptoms continued in most of them for five or six days.[1074]

A singular variety of adulteration with copper was brought not long ago
into public notice on the continent,—namely, the impregnation of bread
with the sulphate of copper, which was used in small quantity for
promoting the fermentation of the dough. This practice was first
detected in some of the towns of Flanders, but was afterwards found to
prevail in France.[1075] Some chemists of reputation have indeed doubted
altogether the existence of the practice; and M. Barruel in particular,
who was consulted on the subject by the Prefecture of Paris, publicly
declared his disbelief, because he remarked that, instead of favouring
the panary fermentation, a very small proportion of sulphate of copper
actually impeded it, and besides gave the bread a greenish colour of
such depth that no customer would take it for a wholesome article.[1076]
Subsequent inquiries, however, have shown that Barruel must have allowed
himself to be misled, probably by using too much of the sulphate of
copper. For the bakers of St. Omer admitted that they practised this
ulceration for the sake of saving their yeast, the proportion required
being an ounce of the salt in two pints of water, for every hundred
weight (_quintal_) of dough, or about an 1800th part.[1077] And it
appears from an interesting set of experiments by M. Meylink, a chemist
of Deventer, that, contrary to the statements of Barruel, sulphate of
copper not only possesses the property of promoting the panary
fermentation, but likewise constitutes in several important respects a
source of adulteration, which ought to be prohibited and strictly looked
after. He found that when he added to half a Flemish pound of dough from
one grain to eight grains of sulphate of copper, fermentation took place
more quickly than in the same dough without such addition, and nearly in
proportion to the quantity of the salt used;—that the adulterated loaves
when taken out of the oven were much better raised, and the loaf with
only one grain of the salt likewise much whiter, than those which were
not adulterated;—that a slight increase, however, in the proportion
rendered the loaf greenish, and gave it a peculiar taste; but especially
that the employment of the salt of copper even in the small proportion
of one grain had the singular effect of bringing about the complete
fermentation of the dough with considerably less loss of weight than
occurs in the common process of baking, the loss in the sound and in the
adulterated loaves being in the proportion of 116 to 100.[1078] It
certainly seems fully proved, then, that the adulteration of bread with
sulphate of copper is an important fraud in more ways than one. Some
doubt may be entertained whether any injury can result to the human body
from even the habitual use of so small a quantity as that employed by
the bakers; and at all events, we may be satisfied that if any bad
effects do result, this can only happen from the continual use of the
adulterated bread for a great length of time. But there can be no doubt
that the practice is a fraud on the public, by enabling the baker to
make his loaves of the standard weight with a less allowance of
nutritive material.

Another important adulteration also indicated by foreign chemists, is
that of syrup made with the coarsest kinds of sugar, and decolorized by
means of sulphate of copper. The colour is removed by adding a solution
of the sulphate to the syrup boiling hot, and decomposing the salt by
lime; but a portion of the salt is often left behind, and in consequence
accidents have arisen from such syrups being used in making various
medicinal preparations.[1079]

_Of the detection of copper in organic mixtures._—As in the instance of
arsenic and mercury, so in that of copper the presence of vegetable and
animal principles interposes material obstacles in the application of
the ordinary tests and methods of analysis. Some substances, such as
albumen, milk, tea, coffee, and the like, decompose the solutions of the
salts of copper, throwing down the oxide of copper in union with various
proximate principles. Others, such as red wine, bile, vomited matter,
and the tissues composing the stomach, although they do not decompose
the soluble copper salts, alter materially the action of reagents on
them. These facts were established long ago by Professor Orfila;[1080]
and various processes were suggested by him, by myself in former
editions of this work, and by various other authors, with the view of
overcoming the difficulties in question.

More lately a fresh difficulty has been started, which has been thought
to render every prior process fallacious, including that which I have
proposed. For it is alleged that copper exists naturally as a
constituent part of many vegetable and animal substances, and more
especially in the organs of the human body. This statement is so
important as to deserve attentive consideration before fixing on a
method of analysis for medico-legal cases.

Some time ago Meissner pointed out the existence of a trace of copper in
some vegetable substances;[1081] and more recently M. Sarzeau alleged
that a minute quantity of this metal, sometimes not above a 1,500,000th
and never exceeding a 120,000th part, may be detected not only in all
vegetable substances, but likewise in the blood, as well as other fluids
and solids of the animal body. Among vegetable substances he examined
with great care cinchona-bark, madder, coffee, wheat and flour; and he
succeeded in separating metallic copper from them all.[1082]

The accuracy of these researches was called in question. By some
chemists the discoveries of Meissner and Sarzeau were confirmed so far
as they relate to vegetable substances. By others the confirmation was
extended to the animal body, and more especially to the human organs and
secretions. Thus M. Devergie says, that, having been struck with the
singular circumstance of two cases occurring to him in a single year,
where analysis indicated copper in the tissues of the alimentary canal
of persons suspected of having died of poison, he was led to inquire,
along with M. O. Henry, whether the metal was contained naturally in the
textures of the human body; and that in the course of many experiments,
although unable to detect any in a solution made by means of weak acetic
acid, he could always find it by the process of incineration.[1083]
Orfila has also repeatedly detected traces of copper in the bodies of
animals not poisoned with the preparations of that metal.[1084]

By other experimentalists opposite results have been obtained, more
especially in regard to animal solids and fluids. In the course of an
inquiry relative to the question, whether poisons pass into the blood, I
failed to detect copper in the blood, muscles, or spinal marrow of
animals, although the method of analysis must have enabled me to
discover extremely minute quantities of that metal. Afterwards M.
Chevreul was unable to detect the slightest trace of copper in beef,
veal, or mutton; nor was he more successful in the case of wheat,
provided care was taken to keep the sample clean.[1085] And more
recently MM. Flandin and Danger have denied that there is any copper
ever found naturally in the body.[1086]

These discrepant results appear to be in a great measure reconciled in
an extensive inquiry into the subject by M. Boutigny; who found that
wheat, wine, cider, and some other substances of a vegetable nature, do
frequently present minute traces of copper, but only when copper is
contained in the manure used in raising the grain, apples, and the like;
that manure from the streets of great towns always contains copper, and
introduces it into vegetable articles grown where such manure is used;
and that the occasional presence of the same metal in animal substances
may be traced either to copper vessels having been employed in preparing
or preserving them, or to the animals producing them having been fed on
vegetables presenting from the causes mentioned above a faint cupreous
impregnation.[1087]—Another fallacy, which may account for the alleged
invariable success of some chemists, has been pointed out by M.
Hiers-Reynaert of Bruges. Having once obtained copper in a specimen of
suspected bread, when he used paper for a filter, but none when he used
linen, he was led to examine various filtering papers, and found that
some kinds contain an appreciable trace of copper.[1088] This important
fact must be attended to in all medico-legal investigations.

On the whole, whatever may be thought of the physiological question,
whether copper forms a constituent of the textures and fluids of
vegetables and animals, it seems well established that this metal is
often present there in minute proportion; and consequently its possible
presence must not be overlooked in medico-legal researches. Fortunately
methods of analysis are known which this source of fallacy does not
affect.

_Process._ The following method embraces all possible cases; and it is
exempt, so far as yet appears, from every source of error.

1. Should the subject of analysis not be a liquid, render it such by
dividing it into small fragments, and boiling it gently for an hour in
distilled water acidulated with acetic acid, which must previously be
ascertained not to contain any copper. If the liquid be not viscid,
filter it at once; but if it be too viscid for filtration, pass it
through a muslin sieve, add two volumes of rectified spirit to it when
cool, and then filter it. Transmit through a small portion of it a
stream of hydrosulphuric acid gas; and if a brownish-black precipitate
or cloud form, subject the whole liquid to the gas. A brown precipitate,
which is sulphuret of copper, will separate either immediately, or after
ebullition and repose for an hour. Collect the precipitate, if abundant,
by filtration, if scanty, by repeated subsidence and affusion. Dry it,
subject it to a low red heat, and then heat it with a little strong
nitric acid, which will convert the sulphuret into the sulphate of
copper. This salt, dissolved out by boiling distilled water, may be
subjected to the tests described above, and especially to ammonia.

2. If the copper be extremely minute in quantity, sulphuretted hydrogen
will not act upon it in a fluid much charged with organic matter. To
meet this possible case, which may occur when the subject of analysis is
an organ of the human body into which the poison has been conveyed by
absorption,—let the liquid be evaporated to dryness, and charred in the
following manner. Heat in a porcelain basin a quantity of nitric acid
equal in weight to the residuum, together with a fifteenth of chlorate
of potash. Add the dry residuum in successive portions of such magnitude
as not to occasion too great effervescence. When it has been all added,
heat the product till it become dark-red and thick. It will then, or
soon afterwards, begin suddenly to char, and at length a thick vapour
will arise in dense clouds; upon which, the charring being complete, the
heat must be withdrawn. Pulverise the carbonaceous mass; boil it with
nitric acid diluted with its own volume of water; and evaporate the
filtered fluid to dryness, so as to expel any excess of acid. Dissolve
the saline residuum, and test the solution with the usual reagents.

The first branch of this process is nearly the same with the one adopted
in the last edition of the present work. The second is derived from a
process lately proposed by Orfila.[1089]

The principles on which it is founded are these. 1. Of the numerous
organic compounds formed by vegetable and animal principles with the
salts of copper, all either dissolve in very weak acetic acid, or part
with their oxide of copper to it. This was pointed out by me in my last
edition. 2, Weak acetic acid, as already mentioned (p. 356), has been
shown by M. Devergie to be incapable of dissolving that copper which is
contained naturally in the tissues, at least so as to render it
discoverable by the subsequent steps of the process. 3, According to
Orfila, copper naturally present in organic substances, is never
indicated by the second branch of the process, provided the charred
product of the action of nitric acid and chlorate of potash be not
heated to incineration. It does not appear why the charring process,
when so conducted, should separate adventitious copper, and not that
which is present naturally. But the empirical fact may be accepted in
the mean time, as it rests on apparently careful experiments.

Orfila does not use acetic acid in the first branch of his process, but
merely infuses the suspected matter in cold water, and if copper be not
thus found, he has recourse to boiling water. But this method introduces
needless complexity; and besides neither maceration, nor boiling with
mere water, will dissolve out the whole oxide of copper. Acidulation
with acetic acid dissolves it all; and Devergie has shown that this
advantage is gained without any additional fallacy arising from the
possible presence of copper as a natural ingredient of the substance
under examination (p. 356).


  SECTION II.—_Of the Action of Copper, and the Symptoms it excites in
                                 Man._

The symptoms caused by copper have at least two varieties in their
character. One class arises from its local action on the alimentary
canal; the other from its operation on distant organs.

This double influence is proved by the experiments of Drouard on
animals, published in his inaugural dissertation at Paris in 1802; and
by those of Orfila in his Toxicology.

When Drouard gave twelve grains of verdigris to a strong dog fasting, he
observed that it caused aversion to food, efforts to vomit, diarrhœa,
listlessness, and death in twenty-two hours; and that the stomach was
but little inflamed. When two grains dissolved in water were injected
into the jugular vein of another dog, it caused vomiting and discharge
of fæces in seven minutes, then rattling in the throat, and death in
half an hour; and there was no particular morbid appearance in the
body.—Half a grain killed another in four days; and in addition to the
preceding symptoms, there was palsy of the hind legs for a day before
death. Six grains of the sulphate introduced into the stomach killed a
dog in half an hour, without producing any appearance of
inflammation.[1090]

These experiments prove that it is not by causing local irritation that
this poison proves fatal. But its mode of action is more distinctly
shown in the later and more accurate experiments of Orfila. He found
that twelve or fifteen grains of the neutral acetate generally killed
dogs within an hour; and that besides the usual symptoms of irritation
in the stomach, they often had insensibility, almost always convulsions,
and immediately before death rigidity, or even absolute tetanus. He
likewise remarked violent convulsions and insensibility when a grain of
this salt was injected into the veins; and death was then seldom delayed
beyond ten minutes. In no case was there any particular morbid
appearance, except loss of contractility in the voluntary muscles.[1091]
More recently results nearly the same have been obtained by
Mitscherlich; and when doses of two drachms of sulphate of copper were
given, he observed after death pale blueness of the villous coat of the
stomach, mingled with brownness,—the apparent effect of chemical
action.[1092]

Allied to these results are those obtained by my late colleague, Dr.
Duncan, and by Mitscherlich, when the sulphate was applied to a wound.
Dr. Duncan observed that death took place in twenty-two hours, and the
body was every where in a healthy state. Mitscherlich found that a
drachm of either sulphate or acetate proved fatal in four hours, with
symptoms of extreme prostration. The experiments of M. Smith, repeated
by Orfila, are at variance with these; for one or two drachms of the
acetate applied to a wound in the thigh of a dog caused only local
inflammation, and no constitutional symptoms.[1093]

It follows from the researches now detailed, that the salts of copper
act in whatever way they are introduced into the system, and the more
energetically, the more directly they enter the blood. The inquiries
of Mr. Blake farther show, that when injected into the blood-vessels,
they act with peculiar force in exhausting muscular irritability, and
occasion death by paralysing the heart if they are injected into a
vein. Six grains of the sulphate injected into the jugular vein of a
dog reduced the force of the heart’s contractions, and fifteen grains
arrested them in twelve seconds, leaving in the dead body distension
of the heart, loss of contractility, and florid blood in the left
cavities. Ten grains injected into the aorta through the axillary
artery caused no sign of obstruction in the capillary system; and
small doses of three or four grains occasioned vomiting, dyspnœa, and
stiffness of the limbs; and immediately after death the muscles had
lost their irritability.[1094]

Copper has been sought for, with variable success, in the blood of
animals poisoned with its salts. Drouard was unable to detect it in the
blood. But this need not excite surprise, because the same physiologist
could not detect it, even when he had injected it into a
vein.—Lebküchner, who published a thesis at Tübingen in 1819, on the
permeability of the living membranes, succeeded in discovering it. He
introduced four grains of the ammoniacal sulphate into the bronchial
tubes of a cat, and five minutes afterwards, when the animal was under
the action of the poison, he drew some blood from the carotid artery and
jugular vein; and he detected copper in the serum of the former, but not
in the latter, by sulphuretted-hydrogen and hydrosulphate of
ammonia.[1095]—Afterwards Dr. Wibmer of Munich also succeeded in
discovering it. In a dog which had taken from four to twenty grains of
the neutral acetate daily for several weeks, he found the metal in the
substance of the liver, but not anywhere else. In the charcoally matter
left by incinerating the liver, nitric acid formed a solution, which
when neutralized gave the characteristic action of the salts of copper
with sulphuretted-hydrogen, ferro-cyanate of potash, and ammonia.[1096]
Fischer also found copper in the blood of a dog which in forty-three
days had got gradually-increasing doses of acetate of copper, till at
length twelve grains were taken daily.[1097] Orfila has recently often
detected copper in the liver, spleen, heart, kidneys, and lungs of
animals poisoned with its salts.[1098] These facts are not all
invalidated by the late discovery of the presence of copper in the
animal tissues of men and animals not poisoned with its preparations.
For in the experiments of Wibmer and of Orfila the quantity found in
cases of poisoning was much larger than in the ordinary state of things;
and the poison was accumulated in particular organs, especially the
liver. The absorption of copper may therefore be considered as fully
substantiated; and it is equally important whether it be regarded as a
physiological or medico-legal fact.

Dr. Duncan’s experiment on its effect when applied to a wound shows that
it may prove fatal when applied externally. Yet in small quantities, the
sulphate is daily used with safety for dressing ulcers.

As to the preparations of copper which are poisonous, it is pretty
certain that, like all other metals, it is not deleterious unless
oxidated, and that its soluble salts are by far the most energetic.
Portal, indeed, has related the case of a woman who, while taking from a
half a grain to four grains of copper filings daily, was seized with
symptoms of poisoning.[1099] But it is probable the filings were
oxidated; for Drouard gave an ounce to dogs without injuring them at
all,[1100] and Lefortier more lately observed that two drachms had no
effect.[1101] The same explanation must be given of the injury sustained
by those artisans who prepare and use what is called “bronze dust” in
printing and paper-staining. If the substance employed be nothing else
than an alloy of copper and zinc, as is alleged, the injurious effects
to be mentioned presently can only be explained on the supposition that
the copper becomes oxidated either before or after coming in contact
with the body. It deserves to be added, that many persons have swallowed
copper coins and retained them for weeks without having any symptoms of
poisoning.

The sulphuret is equally innocuous with the metal if pure; but it
appears probable that it becomes oxidated by long exposure to the air,
and passes into the state of sulphate. Orfila found that an ounce of
recently prepared sulphuret had no effect on a dog; but half an ounce of
a parcel which had been long kept caused vomiting, and yielded a little
sulphate to water.[1102] The power of the oxides has not been
ascertained. They are certainly poisonous; and Lefortier found that both
the red dioxide and black protoxide undergo solution in no long time in
the stomachs of dogs.[1103] The hydrated protoxide is probably more
active. From some experiments made at the hospital of St. Louis in
Paris, it appears that twelve grains will cause nausea, pain in the
stomach and bowels, vomiting and diarrhœa.[1104] There is no doubt that
the carbonate or natural verdigris, the phosphate, and even the
subphosphate, though quite insoluble in water, are capable of acting as
poisons, because Lefortier found that they are soon dissolved in the
stomachs of dogs, and in small doses cause severe vomiting in the course
of fifteen minutes.[1105] But it is chiefly in the soluble salts that we
are to look for the full development of the action of this poison. A
very small quantity of the sulphate will prove fatal; for, as already
noticed, Drouard found that six grains killed a dog in half an hour.

The symptoms caused by the soluble salts of copper in man are, in a
general point of view, the same with those caused by arsenic and
corrosive sublimate. But there are likewise some peculiarities.
According to the cases related by Orfila in his Toxicology, the first
symptom is violent headache, then vomiting and cutting pains in the
bowels, and afterwards cramps in the legs and pains in the thighs.
Sometimes throughout the whole course of the symptoms there is a
peculiar coppery taste in the mouth, and a singular aversion to the
smell of copper. Drouard notices this in his thesis; and says, that,
having himself been once poisoned with verdigris, the smell of copper
used to excite nausea for a long time after.[1106] Another symptom,
which occasionally occurs in this kind of poisoning, and never, so far
as I know, in poisoning with arsenic or corrosive sublimate, is
jaundice. It likewise appears that, when the case ends fatally,
convulsions and insensibility generally precede death.

A set of cases illustrating the slighter forms of poisoning with copper
has been published by M. Bonjean of Chambéry. The cause was the
preparation of an acid confection in a copper vessel. Two women suffered
from severe headache, constriction of the throat, nausea, colic, and
extreme weakness. Two young men, who had eaten the confection more
freely, had for some hours excruciating colic, severe pain in the mouth
and throat, impeded breathing, and hurried irregular pulse; and for
twenty-four hours they suffered severely from headache and prostration
of strength.[1107]

The following case communicated to Professor Orfila by one of his
friends will convey a good idea of the symptoms in severe cases, which
do not prove fatal. A jeweller’s workman swallowed intentionally half an
ounce of verdigris, suspended in water. In fifteen minutes he was
attacked with colic pains and profuse vomiting and purging. When seen by
the physician eight hours afterwards there was not much vomiting, but
frequent eructation of a matter containing verdigris, some salivation, a
small pulse, and blueness about the eyes. In sixteen hours jaundice
began to appear. In the course of the night he was a good deal relieved
from the colic pains by three alvine discharges; and next morning he had
ceased to vomit, and the pain had disappeared. But he complained of a
taste of copper in his mouth, and the jaundice had increased. From this
time he recovered rapidly, and on the fourth day convalescence was
confirmed.[1108]

When the poisoning ends fatally, convulsions, palsy, and insensibility,
the signs in short of some injury done to the brain, are very generally
present. This is illustrated by a good example in Pyl’s Essays and
Observations. It was the case of a confectioner’s daughter, who took two
ounces of verdigris, and died on the third day under incessant vomiting
and diarrhœa, attended towards the close with convulsions, and then with
palsy of the limbs. This case, however, is chiefly valuable for the
dissection, which will be noticed presently.[1109] But two cases of the
same description are related in greater detail by Wildberg in his
Practical Manual, which clearly show the action of this poison on the
brain. They are the cases formerly alluded to of a lady and her daughter
who were poisoned by sour-krout kept in a copper pan. Soon after dinner
they were attacked first with pain in the stomach, then with nausea and
anxiety, and next with eructation and vomiting of a green, bitter, sour,
astringent matter. The pain afterwards shot downwards throughout the
belly, and was then followed by diarrhœa; afterwards by convulsions, at
first transient, then continued; and finally by insensibility. The
daughter died in twelve hours, the mother an hour later.[1110] In these
three cases, although there was not any jaundice noticed during life,
the skin was very yellow after death.—In some instances it would appear
that narcotic symptoms form the commencement and irritant symptoms the
termination of the poisoning. This unusual relation occurs in a case of
recovery related by M. Julia-Fontenelle, and also, though less
remarkably, in a fatal case mentioned by Wibmer. The subject of the
former was a man who intentionally took a solution of copper in vinegar,
prepared by keeping several sous-pieces seven days in that fluid. In
three hours he was found in a state of insensibility, with the jaws
locked, the muscles rigid and frequently convulsed, the breathing
interrupted, and the pulse small and slow. In half an hour he was so far
roused that he could tell what he had done; and soon after taking white
of eggs the convulsions ceased: but next day the belly was hard and
tender, and the repeated application of leeches was required to subdue
the abdominal irritation that ensued.[1111] In the fatal case by Wibmer,
that of a girl of 18, who was poisoned by a dish of beans having been
cooked in a copper vessel, sickness, pain of the belly and vomiting
speedily arose, but were soon followed by convulsions and loss of
consciousness. Next day there was little pain, but extraordinary
paralytic weakness of the arms and legs: the abdomen afterwards became
distended and painful; and death took place in seventy-eight
hours.[1112]—A case where convulsions were produced by two drachms of
blue vitriol is mentioned by Dr. Percival.[1113]—In other instances it
would appear that no nervous affection occurs at all, as in the case of
a young lady related by Percival, who, when poisoned with pickled
samphire containing copper, suffered chiefly from pains in the stomach,
an eruption over the breast, general shooting pains, thirst, a frequent
small pulse, vomiting, hiccup, and purging. Death occurred on the ninth
day, without stupor or convulsions.[1114]

Besides these effects when introduced in considerable doses and in the
form of soluble salts, copper is said to produce other disorders when
applied to the body for a long time in minute quantities and in its
metallic or oxidized state. Among those artisans who work much with
copper various affections are thought to be gradually engendered by
merely handling the metal. Patissier in his treatise on the diseases of
artisans says, that copper-workers have a peculiar appearance which
distinguishes them from other tradesmen,—that they have a greenish
complexion,—that the same colour tinges their eyes, tongue, and hair,
their excretions, and even their clothes through the medium of the
perspiration,—that they are spare, short in stature, bent, their
offspring ricketty, and they themselves old and even decrepit at their
fortieth or fiftieth year.[1115] Mérat also asserts that they are liable
to the painters’ colic, that peculiar disease soon to be noticed as a
common effect of the long-continued application of lead.[1116]

But these notions must be received with some limitation. At least the
alleged effects on copper-workers are by no means invariable. For
copper-workers now-a days in this country and elsewhere are by no means
the unhealthy persons Patissier represents them to be. As to colica
pictonum, it is very rare among them; and possibly the cases noticed by
Mérat might have been produced by the secret introduction of lead into
the body, if indeed they were not cases of common colic.

A very singular set of cases was lately brought under notice by Mr.
Gurney Turner, where poisoning seemed to have been occasioned by the
external application or inhalation of the fine dust used for imitating
gilding by painters, paper-stainers, and porcelain-painters, and which
is said to be essentially brass in a state of fine division. The workmen
who use it, are very apt to be attacked with irritation about the
private parts, and a vesicular eruption about the hairs on the
pubes,—with loss of appetite, tendency to vomiting, and other symptoms
of irritation in the stomach,—with obstinate constipation,—with soreness
and dryness of the throat and irritation in the nose,—and with want of
sleep, and a remarkable greenness of the hair over the whole body.[1117]


       SECTION III.—_Of the Morbid Appearances caused by Copper._

The appearances found in the body after death by poisoning with copper
are chiefly the signs of inflammation.

Where death takes place very rapidly, however, it is probable, that no
diseased appearance whatever will be perceptible. At least this was the
case in the animals experimented on by Drouard and Orfila; and little
doubt can therefore be entertained that the result would be the same
with man also in similar circumstances.

When death ensues more slowly, as in the only fatal cases yet on record
of its action on man, the marks of inflammation coincide with the signs
of irritation during life. The best account I have seen of the morbid
appearances under such circumstances is in the cases related by Pyl, by
Wildberg, by Wibmer, and by Dégrange.

In Pyl’s case the whole skin was yellow. The intestines, particularly
the lesser intestines, were of an unusual green colour, inflamed, and
here and there gangrenous. The stomach was also green; its inner coat
was excessively inflamed; and near the pylorus there was a spot as big
as a crown, where the villous coat was thick, hard, and covered with
firmly adhering verdigris. The lungs are likewise said to have been
inflamed. The blood was firmly coagulated.

In the cases related by Wildberg, which are very like each other, the
skin on various parts, and particularly on the face, was yellow, but on
the depending parts livid. The outer coat of the stomach and intestines
was here and there inflamed; and the inner coat of the former was very
much inflamed, and even gangrenous[1118] near the pylorus and cardia.
The duodenum and jejunum, and likewise the gullet, were in a similar
state. The blood in the heart and great vessels was black and fluid.

In the case of the girl referred to by Wibmer, the skin was
ochre-yellow, the stomach green, much inflamed, especially near the
pylorus, the gullet and intestines also inflamed, the diaphragm red, the
brain healthy, the lungs and heart “gorged with thick blood.”

In the case of poisoning with carbonate of copper described by Dégrange
[p. 348], in which, however, it is probable that death was accelerated
by a fall, there was found congestion of the surface of the brain,
arborescent redness of the gullet and a green sand over its surface,
general greenness of the villous coat of the stomach, with vascularity
of the fundus and points of superficial ulceration, greenness of the
whole intestines, with black vascular ecchymosed spots and softening,
except in the ileum, and redness of the inner surface of the heart.
Copper was detected in the contents of the stomach and intestines.

The intestines have been found perforated by ulceration, and their
contents thrown out into the sac of the peritonæum. Portal has related
one case where the small intestines were perforated, and several where
the perforation was in the rectum, which portion of the intestines, as
well as the duodenum, jejunum, and ileum, was also extensively
ulcerated.[1119]

The existence of verdigris in the form of powder lining the inside of
the stomach after incessant vomiting for three days, is of course an
important circumstance in the inspection of the body. But too much
reliance ought not to be placed on mere bluish or greenish colouring of
the membranes. For Orfila[1120] and Guersent[1121] have both observed,
that the inside of the stomach as well as its contents may acquire these
tints in a remarkable degree in consequence of natural disease.


        SECTION IV.—_Of the Treatment of Poisoning with Copper._

The treatment of poisoning with the salts of copper has been examined in
relation to the antidotes by M. Drouard, M. Marcelin-Duval, Professor
Orfila, and M. Postel.

The alkaline sulphurets were at one time thought to be antidotes for the
poisons of copper, but without any reason. Drouard found that fifteen
grains of verdigris killed a dog in thirty hours, notwithstanding the
free use of the liver of sulphur.[1122]

Afterwards M. Marcelin-Duval was led from his experiments to infer that
sugar was an antidote,[1123] and in the first editions of his Toxicology
Professor Orfila agreed with him, and related some experiments of his
own, which, along with those of Duval, seemed to place the fact beyond
all doubt. Later and more careful experiments, however, satisfied
Orfila, that it only acts as an emollient after the poison has been
removed from the stomach, and that it has no effect at all if the poison
is retained by a ligature in the gullet.[1124] Sugar being thus rejected
as well as the sulphurets, he was led to try the effects of albumen; and
his experiments induced him to recommend that substance as an antidote
in preference to every thing else. He found that the white of six eggs
completely neutralized the activity of between 25 and 36 grains of
verdigris; so that even when the mixture was retained in the stomach by
a ligature on the gullet no effect ensued which could be ascribed to the
poison. He infers that white of egg is the best antidote for poisoning
with copper.[1125] He likewise found the ferro-cyanate of potass not
inferior.[1126]

Since the publication of these inquires the subject has been again
examined by M. Postel, who reverts to the original proposition of Duval,
that sugar is really a good antidote; and he rests this conclusion
partly on direct comparative experiments, showing that it is at least
equally effective with white of egg, and partly on the singular fact
ascertained by him, that sugar, which was believed to decompose the
salts of copper only at the temperature of 212°, does actually
accomplish this decomposition at the temperature of the human body, and
throws down the copper in the form of oxide.[1127]

According to the experiments of MM. Milne-Edwards and Dumas, metallic
iron is likewise a good antidote: they found that when fifteen, twenty,
and even fifty grains of sulphate of copper, acetate of copper, or
verdigris, were given to animals, and an ounce of iron filings
administered either immediately before, or immediately afterwards,—the
gullet being tied to prevent the discharge of the poison,—death did not
ensue for five, six, or even eight days, and consequently proceeded from
the operation on the gullet; and that in one experiment, on the ligature
being removed from the gullet, the opening healed up, and complete
recovery took place.[1128]

Before quitting the subject of the treatment, it is necessary to caution
the practitioner particularly against the employment of vinegar,—a
substance often ignorantly used for this, in common with many other,
species of poisoning. On account of its solvent power over the insoluble
compounds formed by the salts of copper with animal and vegetable
matters, it must be injurious rather than useful.




                              CHAPTER XVI.
                      OF POISONING WITH ANTIMONY.


The fourth genus of the metallic irritants includes the preparations of
antimony. Poisoning with antimonial preparations is not common. They are
employed extensively in medicine, however, and consequently accidents
have sometimes occurred with them. One of them is also often foolishly
used, in the way of amusement, to cause sickness and purging, and
likewise to detect servants who are suspected of making free with their
mistress’s tea-box or whisky-bottle; and in both of these ways alarming
effects have sometimes been produced. In 1837 a woman was tried in
England for attempting to poison a child with tartar-emetic; but the
poison appeared to have been given through ignorance.[1129] In large
doses some of the antimonial compounds may cause death; and one of them,
the chloride of antimony, now very little used in this country, is a
violent corrosive.


 SECTION I.—_Of the Chemical History and Tests for the preparations of
                               Antimony._

Metallic antimony has a bluish-white colour, not liable to tarnish. Its
specific gravity is 6·7. It is easily fused, but is not very volatile.
In certain circumstances, however, it easily undergoes a spurious
sublimation, by being carried along with gases disengaged while it is in
the act of being reduced.

A great number of preparations of antimony were at one time to be found
in the shop of the apothecary; but they are now reduced to a few. Those
which require notice here are the oxide, chloride, and tartar-emetic.

The _oxide_ [sesquioxide] is a white heavy powder, which is best known
by its solubility in tartaric acid, and the effects of the tests for
tartar-emetic on the solution.

The _chloride_ [sesquichloride], as usually seen, is a yellow or reddish
liquid, but when pure is colourless. It is highly corrosive. It is
readily known by the effect of water in decomposing it,—an insoluble
white subchloride being thrown down, and hydrochloric acid remaining in
solution. The latter is detected by nitrate of silver; and the
precipitate is known by being soluble in a solution of tartaric acid,
and then presenting the reactions of tartar-emetic.


                            _Tartar-Emetic._

In its solid state tartar-emetic forms regular tetraedral or more
generally octaedral crystals, which are colourless when pure,
efflorescent, and of a slightly metallic taste. As commonly seen in the
shops it is in the form of a white, or pale yellowish-white powder.

When heated it decrepitates and then chars; and if the heat be increased
the oxide of antimony is reduced by the carbonaceous matter, and little
globules appear, like those of quicksilver in point of colour. The best
way of reducing tartar-emetic is to char it in a porcelain vessel or
watch-glass, and then to increase the heat till the charred mass takes
fire. Or the charred mass may be introduced into a tube and heated
strongly with the blowpipe, after which globules of antimony will be
found lining the bottom of the glass where the material has been. None
of it is ever sublimed. It is not easy to procure distinct globules by
heating tartar-emetic at once in a small tube.

According to Dr. Duncan, tartar-emetic is soluble in three parts of
boiling and fifteen of temperate water. The solution presents the
following characters with reagents.

1. _Caustic potass_ precipitates a white sesquioxide, but only if the
solution is tolerably concentrated. The first portions of the test have
no effect. The precipitate is redissolved by an excess of potass.

2. _Nitric acid_ throws down a white precipitate, and takes it up again
when added in excess.

3. The _Infusion of Galls_ causes a dirty, yellowish-white precipitate;
but it will not act on a solution which contains much less than two
grains per ounce.

4. The best liquid reagent is _Hydrosulphuric acid_. In a solution
containing only an eighth part of a grain per ounce, it strikes an
orange-red colour, which, when the excess of gas is expelled by heat,
becomes an orange-red precipitate; and if the proportion of salt is
greater, the precipitate is thrown down at once.—The colour of the
precipitate is so peculiar as to distinguish it from every other
sulphuret; but if any doubt regarding its nature should occur, it may be
known by collecting it, dissolving it with the aid of gentle heat in
hydrochloric acid, and adding water to the solution; which will then
yield a white precipitate, the sesquioxide of antimony in union with a
little chlorine.

5. When the solution is put into Marsh’s apparatus for detecting arsenic
[p. 211], the flame yields a dark brownish-black, obscurely shining
crust on a surface of porcelain held across it, and a white crystalline
powder if the porcelain be held just above the flame. The dark crust is
antimony, the white one its oxide. The former has only a distant
resemblance to the brilliant stain of arsenic, notwithstanding all that
has been said of their similarity. It is well, however, to use some
other test for distinguishing the two metals besides their appearance;
and the most convenient is a solution of chloride of lime, which
instantly makes an arsenical crust disappear, but does not affect an
antimonial one.

Tartar-emetic, like the soluble salts of mercury and copper, is
decomposed by various organic principles. All vegetable substances that
contain a considerable quantity of tannin have this effect; of which an
example has been already mentioned in the action of infusion of galls.
Decoctions of cinchona-bark decompose it still more effectually. The
animal principles do not act on tartar-emetic, with the exception of
milk, which is slightly coagulated by a concentrated solution. Many
vegetable and animal substances, though they do not decompose it, alter
the operation of the fluid tests. Thus tea, though it does not effect
any distinct decomposition of the salt, will prevent the action of
gall-infusion; and French wine gives a violet tint to the precipitates
with that test and with acids.[1130] Hydrosulphuric acid, however, acts
under all circumstances, and always characteristically, whatever the
colour of the fluid may be. Dr. Turner found that when transmitted
through a diluted solution in tea, porter, broth, and milk, with certain
precautions to be mentioned presently, he procured a precipitate which
either showed its proper colour at once, or did so at the margin of the
filter on which it was collected.[1131]

The circumstances now referred to render it necessary to resort to other
means, besides the simple application of liquid reagents, for the
purpose of detecting tartar-emetic in complex organic mixtures. This
subject has been ably investigated, first by Dr. Turner,[1132] and
afterwards by Professor Orfila.[1133] The result of the researches of
both seems to me to be that the most convenient method yet proposed is
the following.

_Process for Tartar-emetic in Organic Mixtures._—If the subject of
analysis be not already liquid enough, add distilled water. Then
acidulate with a little hydrochloric and tartaric acids; the former of
which throws down some animal principles, while the latter dissolves
readily all precipitates formed with tartar-emetic by reagents or
organic principles except the sulphuret. Filter the product.

1. Subject a small portion of the liquid to a stream of hydrosulphuric
acid gas, and if it be perceptibly coloured orange-red, treat the whole
liquid in the same way; boil to expel the excess of gas, collect the
precipitate, dry it, and reduce it by hydrogen gas in the following
manner. Put the sulphuret in a little horizontal tube, transmit hydrogen
through the tube by means of the apparatus represented in Figure 9, and
when all the air of the apparatus is expelled, apply heat to the
sulphuret with a spirit-lamp. Hydrosulphuric acid gas is evolved, and
metallic antimony is left, if the current of hydrogen be gentle, or it
is sublimed if the current be rapid.—When there is much animal or
vegetable matter present in the sulphuret, the metal is not always
distinctly visible. In that case, dissolve the antimony by the action of
nitric acid on the mixed material and broken fragments of the tube, and
throw down the orange sulphuret again from the neutralized solution by
hydrosulphuric acid.

2. If hydrosulphuric acid do not distinctly affect the liquid, or if no
precipitate be separated after boiling, or so small a quantity as cannot
well be collected,—evaporate the liquid to dryness, char it by means of
nitric acid and chlorate of potash, as directed for copper (p. 357),
boil the carbonaceous mass for half an hour in a mixture of eight parts
of hydrochloric acid and one of nitric acid, and introduce the filtered
solution into the modification of Marsh’s apparatus for detecting
arsenic described in page 204, but without the tube _e h_. Kindle the
gas at _e_, and try whether a black, dull stain, not removable by
solution of chloride of lime, be produced on a surface of porcelain held
across the flame. If no stain be produced, there was no antimony in the
liquid under examination. If the porcelain be stained, apply the heat of
a spirit-lamp flame to the tube _d e_. Antimony will be deposited within
the tube where the heat is applied. In order to ascertain its nature,
break the tube, heat the portion containing the crust with
nitro-hydrochloric acid, evaporate to dryness, dissolve the residue in
hydrochloric acid, decompose a part of this solution with water, and
subject the rest to a stream of hydrosulphuric acid gas, which will
produce the usual orange sulphuret of antimony.

3. If antimony be not indicated in either of these ways in the fluid
part of the subject of analysis, the solid portion may next be subjected
to the second process; but success will very seldom attend the search
when the previous steps have failed.

The first branch of this process,—a slight modification of Dr.
Turner’s,—is a very delicate and satisfactory method of detecting
antimony in organic mixtures. Some practice is required to transmit the
hydrogen gas with the proper rapidity. The gas ought to be allowed to
pass for some time before the spirit-lamp flame is applied, otherwise
the oxygen remaining in the apparatus may cause an explosion, or will
oxidate the metallic antimony, formed by the reduction of the sulphuret.
As soon as the reduction of the sulphuret begins, the tube is blackened
on account of the action of the sulphuretted-hydrogen on the lead
contained in the glass. This obscures the operations within the tube;
but on subsequently breaking it, a metallic button or a sublimate will
be easily seen. When the sulphuret is considerable in quantity and the
gaseous current slow, the metal remains where the sulphuret was; but if
the mass of sulphuret is small and the current rapid, then the metal is
sublimed and condensed in minute scaly brilliant crystals.

The second branch of the process is a modification of the method lately
employed by Professor Orfila for detecting antimony in the textures and
secretions of animals poisoned with tartar-emetic. It is probably more
delicate than the other, but not more satisfactory.

The method of analysis here recommended, as well as every other yet
proposed for organic mixtures, merely detects the presence of antimony.
It does not indicate the state in which the metal was combined. It is a
process in short for antimony in every state of combination.

It is almost unnecessary to observe that when the contents of the
stomach or vomited matters are the subject of analysis, care must be
taken to ascertain that tartar-emetic was not administered as a remedy.


SECTION II.—_Of the Action of Tartar-Emetic, and the Symptoms it excites
                                in Man._

There is little peculiarity in what is hitherto known of the symptoms of
poisoning with tartar-emetic in man. Cases in which it has been taken to
the requisite extent are rarely met with; and it has seldom remained
long enough in the stomach to act deleteriously. But its action on
animals would appear from the experiments of Magendie to be in some
respects peculiar.

He found that dogs, like man, may take a large dose with impunity, for
example half an ounce, if they are allowed to vomit; but that if the
gullet is tied, from four to eight grains will kill them in a few hours.
His subsequent experiments go to prove that death is owing to the poison
exciting inflammation in the lungs. When six or eight grains dissolved
in water were injected into a vein, the animal was attacked with
vomiting and purging, and death ensued commonly within an hour. In the
dead body he found not only redness of the whole villous coat of the
stomach and intestines, but also that the lungs were of an orange-red or
violet colour throughout, destitute of crepitation, gorged with blood,
dense like the spleen, and here and there even hepatized. A larger
quantity caused death more rapidly without affecting the alimentary
canal; a smaller quantity caused intense inflammation there and death in
twenty-four hours; but the lungs were always more or less
affected.[1134]

It is a fact, too, worthy of notice, that in whatever way this poison
enters the body its effects are nearly the same. This is shown not only
by the researches of Magendie already mentioned, but likewise by the
experiments of Schloepfer, who found that a scruple dissolved in twelve
parts of water and injected into the windpipe, caused violent vomiting,
difficult breathing, and death in three days; and in the dead body the
lungs and stomach were much inflamed, particularly the former.[1135] It
farther appears from an experiment related by Dr. Campbell, that, when
applied to a wound, it acts with almost equal energy as when injected
into a vein. Five grains killed a cat in this way in three hours,
causing inflammation of the wound, and vivid redness of the
stomach.[1136] He did not find the lungs inflamed.

Magendie infers from his own researches that tartar-emetic occasions
death when swallowed, not by inflaming the stomach, but through means of
a general inflammatory state of the whole system subsequent to its
absorption,—of which disorder the affection of the stomach and
intestines and even that of the lungs are merely parts or symptoms. The
later experiments of Rayer tend in some measure to confirm these views,
by showing that death may occur without inflammation being excited any
where. In animals killed in twenty-five minutes by tartar-emetic applied
to a wound, he, like Dr. Campbell, could see no trace of inflammation in
any organ of the great cavities.[1137]

Orfila has proved by analysis the important fact that tartar-emetic is
absorbed in the course of its action, and may be detected in the animal
tissues and secretions. He found that, when it is applied to the
cellular tissue of small dogs, two grains disappear before death: That
antimony may be detected by his process given above throughout the soft
textures generally, but especially in the liver and kidneys: but that it
is quickly discharged from these quarters through the medium of the
urine. Hence in an animal that died in four hours he found it abundantly
in the liver and still more in the urine; in one that survived seventeen
hours, the liver presented mere traces of the poison, but the urine
contained it in abundance; and in one that lived thirty-six hours, there
was a large quantity in the urine, but none at all in the liver. He also
ascertained that antimony is generally to be found in the urine of
persons who are taking tartar-emetic continuously in large doses for
pneumonia according to Rasori’s mode of administering it.[1138] These
results have been confirmed by the conjoined researches of Panizza and
Kramer, who found antimony in the urine and blood of a man during a
course of tartar-emetic.[1139] And Flandin and Danger also satisfied
themselves that in animals it may be generally detected in the
liver.[1140]

_Effects on Man._—When tartar-emetic is swallowed by man, it generally
causes vomiting very soon and is all discharged; and then no other
effect follows. But if it remains long in the stomach before it excites
vomiting, or if the dose be large, more permanent symptoms are sometimes
induced. The vomiting recurs frequently, and is attended with burning
pain in the pit of the stomach, and followed by purging and colic pains.
There is sometimes a sense of tightness in the throat, which may be so
great as to prevent swallowing. The patient is likewise tormented with
violent cramps. Among the cases hitherto recorded no notice is taken of
pulmonary symptoms; which might be expected to occur if Magendie’s
experiments are free of fallacy.

The late introduction of large doses of tartar-emetic into medical
practice having excited some doubt as to its poisonous properties, it
becomes a matter of some moment to possess positive facts on the
subject. The following cases may therefore be quoted, which will satisfy
every one that this substance is sometimes an active irritant.

The first is particularly interesting from its close resemblance to
cholera. It occurred in consequence of an apothecary having sold
tartar-emetic by mistake for cream of tartar. The quantity taken was
about a scruple. A few moments afterwards the patient complained of pain
in the stomach, then of a tendency to faint, and at last he was seized
with violent bilious vomiting. Soon after that he felt colic pains
extending throughout the whole bowels, and accompanied ere long with
profuse and unceasing diarrhœa. The pulse at the same time was small and
contracted, and his strength failed completely; but the symptom which
distressed him most was frequent rending cramp in the legs. He remained
in this state for about six hours, and then recovered gradually under
the use of cinchona and opium; but for some time afterwards he was
liable to weakness of digestion.[1141]

The next case to be mentioned, where the dose was forty grains, proved
fatal, although the person vomited soon after taking it. The symptoms
illustrate well the compound narcotico-acrid action often observed in
animals. The poison was taken voluntarily. Before the person was seen by
M. Récamier, who relates the case, he had been nearly two days ill with
vomiting, excessive purging, and convulsions. On the third day he had
great pain and tension in the region of the stomach, and appeared like a
man in a state of intoxication. In the course of the day the whole belly
became swelled, and at night delirium supervened. Next day all the
symptoms were aggravated; towards evening the delirium became furious;
convulsions followed; and he died during the night, not quite five days
after taking the poison.[1142]

Severe effects have also been caused by so small a dose as six grains. A
woman, who swallowed this quantity, wrapped in paper, was seized in half
an hour with violent vomiting, which soon became bloody. In two hours
the decoction of cinchona was administered with much relief. But she had
severe colic, diarrhœa, pain in the stomach, and some fever; of which
symptoms she was not completely cured for five days.[1143] A case has
been published, where a dose of only four grains caused pain in the
belly, vomiting, and purging, followed by convulsions, failure of the
pulse, and loss of speech; and recovery took place very slowly.[1144]
Under the head of the treatment another case will be noticed where half
a drachm excited severe symptoms, and was probably prevented from
proving fatal only by the timely use of antidotes.

While these examples prove that tartar-emetic is occasionally an active
irritant in the dose of a scruple or less, it must at the same time be
admitted to be uncertain in its action as a poison. This appears from
the late employment of it in large doses as a remedy for inflammation of
the lungs. The administration of tartar-emetic in large doses was a
common enough practice so early as the seventeenth century, and was also
occasionally resorted to by physicians between that and the present
time. But it is only in late years that, by the recommendations of
Professor Rasori of Milan,[1145] and M. Laennec of Paris, it has again
become a general method of treatment. According to this method,
tartar-emetic is given to the extent of twelve, twenty, or even thirty
grains a day in divided doses; and not only without producing any
dangerous irritation of the alimentary canal, but even also not
unfrequently without any physiological effect whatever. Doubts were at
one time entertained of the accuracy of the statements to this effect
published by foreign physicians; but these doubts are now dissipated, as
the same practice has been tried, with the same results, by many in
Britain. Rasori ascribes the power the body possesses of enduring large
doses of tartar-emetic without injury, to a peculiar diathesis which
accompanies the disease and ceases along with it. And it is said, that
the same patients, who, while the disorder continues, may take large
doses with impunity, are affected in the usual manner, if the doses are
not rapidly lessened after the disease has begun to give way. The
testimony of Laennec on the subject is impartial and decisive. He
observes he has given as much as two grains and a half every two hours
till twenty grains were taken daily, and once gave forty grains in
twenty-four hours by mistake; that he never saw any harm result; and
that vomiting or diarrhœa was seldom produced, and never after the first
day. The power of endurance he found to diminish, but not, as Rasori
alleges, to cease altogether, when the fever ceases; for some of his
patients took six, twelve, or eighteen grains daily when in full
convalescence.[1146] My own observations correspond with Laennec’s,
except as to the effects of large doses during convalescence, of which
effects I have had no experience. I have seen from six to twenty grains,
given daily in several doses of one or two grains, check bad cases of
pneumonia and bronchitis, without causing vomiting or diarrhœa after the
first day, and also without increasing the perspiration. At the same
time I have twice seen the first two or three doses excite so violent a
purging and pain in the stomach and whole bowels, that I was deterred
from persevering with the remedy. In continued fever too I have
repeatedly found that the doses mentioned above did not cause any
symptoms of irritation in the stomach or intestines.

The large quantities now mentioned have even been sometimes given in a
single dose with nearly the same results. Dr. Christie mentions in his
Treatise on Cholera that he sometimes gave a scruple in one dose with
the effect of exciting merely some vomiting and several watery stools.
But he admits that in one instance symptoms were induced like those of a
case of violent cholera.[1147]

The same large doses have been given by some in delirium tremens without
any poisonous effect being produced. A correspondent of the Lancet has
even mentioned that on one occasion, after gradually increasing the
dose, he at last wound up the treatment, successfully as regarded the
disease, and without any injury to the patient, by giving four doses of
twenty grains each, in the course of twenty minutes.[1148]

These facts are sufficiently perplexing, when viewed along with what
were previously quoted in support of the poisonous effects of
tartar-emetic. On a full consideration of the whole circumstances,
however, I conceive the conclusion which will be drawn is, that this
substance is not so active a poison as was till lately supposed;—that in
the dose of four, six, or ten grains, it may cause severe symptoms, but
is uncertain in its action,—and that although there appears to be some
uncertainty in the effects of even much larger doses, such as a scruple,
yet in general violent irritation will then be induced, and sometimes
death itself.

An instance is related in the Journal Universel of a man who, while in a
state of health, swallowed seventeen grains, and then tried to suffocate
himself with the fumes of burning charcoal. He recovered, though not
without suffering severely from the charcoal fumes; but he could hardly
be said to have been affected at all by the tartar-emetic.[1149] Here
the inactivity of the poison was probably owing to the narcotic effects
of the fumes.

The effects of tartar-emetic on the skin are worthy of notice; but they
have not yet been carefully studied. Some facts tend to show that even
its constitutional action may be developed through the sound skin. Mr.
Sherwen attempted to prove by experiments on himself and two pupils,
that five or seven grains in solution will, when rubbed on the palms,
produce in a few hours nausea and copious perspiration.[1150] His
observations have been confirmed by Mr. Hutchinson.[1151] But Savary, a
French physician, on repeating these experiments, could remark nothing
more than a faint flat taste and slight salivation;[1152] and Mr.
Gaitskell could not remark any constitutional effect at all.[1153]
Sometimes it has appeared to cause severe symptoms of irritant poisoning
when used in the form of ointment to excite a pustular eruption. An
instance of this has been described in a late French Journal.[1154] Nay,
in the Medical Repository there is a case, in which the external use of
tartar-emetic ointment is supposed to have been the cause of death. The
subject was an infant, two years old, who, soon after having the spine
rubbed with this ointment, was seized with great sickness and frequent
fainting, which in forty-eight hours proved fatal.[1155] Considering the
numerous opportunities which medical men have had of witnessing the
effects of tartar-emetic applied in the same manner, and that these are
solitary cases, doubts may be entertained whether the irritant symptoms
in the one case, or the child’s death in the other, were occasioned in
the way supposed.

Although the constitutional action of tartar-emetic is not easily
developed through the sound skin, its local effects are severe and
unequivocal. When applied to the skin it does not corrode, but excites
inflammation, on which account it is much used instead of cantharides.
It does not blister; but after being a few days applied, it brings out a
number of painful pustules; if it be persevered in, the skin ulcerates;
and if it be applied to an ulcerated surface it causes profuse
suppuration, or sometimes even sloughing.

Tartar-emetic is one of the substances which appear to possess the
property of acting on the infant through the medium of its nurse’s milk.
I do not know, indeed, what may be the general experience on this point;
but a French physician, M. Minaret, has published a clear case of the
kind, in the instance of a young woman who was taking tartar-emetic for
pleurisy, and whose infant was attacked with a fit of vomiting
immediately after every attempt to suck the breast.[1156]

There is some reason to suppose, that the vapours of antimony may prove
injurious when inhaled. Four persons, constantly exposed in preparing
antimonial compounds to the vapour of antimonious acid and chloride of
antimony, were attacked with headache, difficult breathing, stitches in
the back and sides, difficult expectoration of viscid mucus, want of
sleep and appetite, mucous discharge from the urethra, loss of sexual
propensity, atrophy of the testicles, and a pustular eruption on various
parts, but especially on the scrotum. They all recovered.[1157]


  SECTION III.—_Of the Morbid Appearances produced by Tartar-emetic._

The morbid appearances caused by tartar-emetic have not been often
witnessed in man.

In M. Récamier’s case there were some equivocal signs of reaction in the
brain. The organs in the chest were healthy. The villous coat of the
stomach, except near the gullet, where it was healthy, was everywhere
red, thickened, and covered with tough mucus. The whole intestines were
completely empty. The duodenum was in the same state as the stomach; but
the other intestines were in their natural condition.

M. Jules Cloquet observed in the body of a man who died of apoplexy, and
who in the course of five days had taken forty grains of tartar-emetic,
without vomiting or purging,—that the villous coat of the stomach had a
deep reddish-violet colour, with cherry-red spots interspersed; and that
the whole small intestines were of a rose-red tint spotted with
cherry-red.[1158]

The only other dissection I have seen noticed is one by Hoffmann. He
says that in a woman poisoned by tartar-emetic he found the stomach
gangrenous, and the lungs, diaphragm, and spleen as it were in a state
of putrefaction.[1159] Little credit can be given to this description.

In animals Schloepfer found the blood always fluid.[1160]


       SECTION IV.—_Of the Treatment of Poisoning with Antimony._

The treatment of poisoning with tartar-emetic is simple. If the poison
be not already discharged, large draughts of warm water should be given
and the throat tickled, to bring on vomiting. At the same time some
vegetable decoction should be prepared, which possesses the power of
decomposing the poison; and none is better or more likely to be at hand
than a decoction of cinchona-bark, particularly yellow-bark. The
tincture is also a good form for giving this antidote. The
administration of bark has been found useful even after vomiting had
continued for some length of time, probably because a part of the poison
nevertheless remained undischarged. Before the decoction is ready, it is
useful to administer the bark in powder. It is alleged, however, by M.
Toulmouche that decoction of cinchona is not nearly so serviceable as
infusion of galls, and that powder of galls is better still.[1161] When
there is reason to believe that the patient has vomited enough, and that
a sufficient quantity of the antidote has been taken, opium is evidently
indicated and has been found useful; but venesection may be previously
necessary if the signs of inflammation in the stomach are obstinate.

The following case related by M. Serres was probably cured by cinchona.
At all events, the effect of the antidote was striking. A man purchased
half a drachm in divided doses at different shops, and swallowed the
whole in a cup of coffee. Very soon afterwards he was attacked with
burning pain in the stomach, convulsive tremors, and impaired
sensibility,—afterwards with cold clamminess of the skin, hiccup, and
some swelling of the epigastrium, but not with vomiting. Decoction of
cinchona was given freely. From the first moment almost of its
administration he felt relief, and began to sweat and purge. Next
morning, however, he vomited, and for some days there were evident signs
of slight inflammation in the stomach; nay, for a month afterwards he
had occasional pricking pains in that region; but he eventually
recovered.[1162] Another and more pointed case has been related by Dr.
Sauveton of Lyons. A lady swallowed by mistake for whey a solution of
sixty grains of tartar emetic. In ten minutes she was seen by her
physician, and at this time vomiting had not commenced. Tincture of bark
was immediately given in large doses. No unpleasant symptom occurred
except nausea and slight colic.[1163]

Orfila considers that the diuretic plan of treatment recommended by him
for arsenic [p. 288] is equally applicable in the case of antimony.
Having ascertained that a grain and a half of tartar-emetic applied to a
wound constantly killed dogs in a period varying from seventeen to
thirty-six hours, if no treatment was employed,—he administered to them
in this way a dose varying from a grain and a half to three grains, and
by then giving diuretics effected a cure in four out of five
instances.[1164]


                        _Chloride of Antimony._

The chloride of antimony [sesquichloride, muriate, or butter of
antimony] being now put to little use and seldom seen except as an
intermediate product obtained in the preparation of other compounds of
antimony, it is rarely met with as the cause of poisoning, and therefore
scarcely deserves notice here, were it not that its effects differ
widely from those of tartar-emetic and other antimonials.

It is easily known by the characters mentioned above. It has not yet
been made the subject of investigation by experiments on the lower
animals. Mr. Taylor has collected three cases of poisoning with it,
which show that it is a powerful corrosive and irritant, and that its
effects, as hitherto witnessed, seem to depend entirely on this action.
In one instance, that of a boy, twelve years old, who swallowed four or
five drachms of the solution by mistake for ginger-beer, the symptoms
were vomiting in half an hour, then faintness and extreme feebleness,
and next day heat in the mouth and throat, difficulty in swallowing,
slight abrasions of the lining membrane of the mouth, and general fever;
but he got quite well in eight days. In the case of another boy, ten
years old, who got about the same quantity by mistake for antimonial
wine, there was an immediate sense of choking and inability to speak,
then vomiting and pain in the throat, next a general state of collapse,
with dilated pupils and a tendency to stupor, and on the subsequent day
bright scarlet patches on the throat, with difficulty of swallowing.
This patient also recovered completely in a few days. The third was the
case of a surgeon who took intentionally between two and three fluid
ounces, and was found in an hour by his medical attendant in a state of
great prostration, and affected with severe efforts to vomit, violent
griping, and urgent tenesmus. Reaction soon ensued, the pain abated, and
the pulse rose to 120; a strong tendency to doze succeeded; and in ten
hours and a half he expired. The whole inside of the alimentary canal,
from the mouth to the jejunum, was black as if charred; the mucous
membrane seemed to have been removed along the whole of this extent of
the canal; and the submucous and peritoneal coats were so soft as to be
easily torn with the finger.[1165]




                             CHAPTER XVII.
 OF POISONING WITH TIN, SILVER, GOLD, BISMUTH, CHROME, ZINC, AND IRON.


Several other metallic compounds produce effects analogous to those of
the preparations of arsenic, copper, mercury, and antimony. But they may
be passed over shortly; because they are little known as poisons, and it
is therefore only necessary that their leading properties be mentioned.
They are the compounds of tin, silver, gold, bismuth, chrome, zinc, and
iron.


                        _Of Poisoning with Tin._

The chlorides of _tin_ are used in the arts of colour-making and dyeing,
and the oxide of tin forms part of the putty-powder used for staining
glass and polishing silver plate.

There are two chlorides, the protochloride and bichloride. They both
form acicular crystals, which are very soluble. It is needless to notice
their tests or chemical history; but in order that the following account
of their effects on man and animals may be understood, it is necessary
to mention, that they are decomposed by almost all vegetable infusions
and animal fluids.

Orfila found, that a solution of six grains of the protochloride
injected into the jugular vein of a dog killed it in one minute,—that
two grains caused death by tetanus in fifteen minutes,—and that so small
a quantity as half a grain caused death in twelve hours, the only
symptoms being somnolency and catalepsy or fixedness of position.

To these dreadful effects when introduced into the blood, its effects
when swallowed are not nearly proportionate. From eighteen to forty-four
grains killed dogs in one, two, or three days, efforts to vomit and
great depression being the only symptoms; and after death the stomach
was found excessively inflamed, and sometimes ulcerated. Its effects
when applied externally are still less violent. Two drachms applied to a
wound merely caused violent inflammation and sloughing of the part, and
death in twelve days, without any internal symptom during life or
appearance after death.[1166]

These phenomena, considered along with the violent symptoms excited when
the poison is injected into the veins, show that, when swallowed or
applied outwardly, it acts only as a local irritant.

Tin is absorbed in the course of its action, and may be detected in the
liver, spleen, and urine, by boiling them in water acidulated with
hydrochloric acid, evaporating the decoction to dryness, charring the
residue by means of nitric acid as directed for copper, treating the
carbonaceous mass with a mixture of twenty parts of hydrochloric acid
and one of nitric acid, evaporating the solution to dryness so as to
expel any excess of acid, dissolving what is left in hydrochloric acid
diluted with twice its volume of water, and then transmitting
hydrosulphuric acid gas. If the precipitated sulphuret of tin has not a
fine yellow colour, it must be heated with a little strong nitric acid;
after which, if the residuum be again dissolved in diluted hydrochloric
acid, a characteristic yellow bisulphuret will be thrown down by
hydrosulphuric acid gas. This process may be applied to all organic
mixtures containing tin.[1167]

The oxide of tin, according to Schubarth, is quite inactive; for he gave
an entire drachm to a dog without being able to observe any effect from
it whatever.[1168] This is what would be expected from its extreme
insolubility. Yet Orfila has stated in the early editions of his
Toxicology, and repeats in that of 1843, but without noticing the
contradictory observations of Schubarth, that one or two drachms of the
oxide occasion in dogs all the phenomena of irritant poisoning, and
prove invariably fatal.[1169]

The metal has been proved by Bayen and Charlard to be inactive.[1170] It
has been given expressly to dogs without any effect being observed; and
it is given in large doses to man for worms, without detriment. No
importance therefore can be attached to some alleged cases of poisoning
with this metal.[1171]

Cases of poisoning with the preparations of tin are rare. Orfila briefly
notices a set of cases which occurred to M. Guersent. Several persons in
a family took the protochloride, in consequence of the cook having
mistaken a packet of it for salt and dressed their dinner with it. They
had all colic, some of them diarrhœa; none vomited; and all recovered in
a few days.[1172] A case is related in the Medical Times of death
apparently caused by so small a quantity as half a tea-spoonful of a
solution of protochloride. The effects were vomiting, acute pain in the
stomach, anxiety, restlessness, thirst, and a frequent, hard, small
pulse. These symptoms increased next day; and on the third day death
took place, preceded by delirium.[1173] As this was a case of suicide,
it is probable that some other poison, or a larger dose of the chloride
of tin was taken.

Little need be said of the morbid appearances. Besides the signs of
violent irritation caused by the poisons of tin in common with other
irritants, Orfila always found in dogs a peculiar tanned appearance of
the villous coat of the stomach. In the case from the Medical Times the
gullet was red, the stomach inflamed externally, and internally
thickened, vascular, and pulpy.


                      _Of Poisoning with Silver._

Of the preparations of _silver_, the only one which requires notice is
the nitrate or lunar caustic.

It exists in two forms,—crystallized in broad, transparent, colourless
tables,—and fused into cylindrical, crystalline, grayish pencils. Both
forms are essentially the same in chemical nature.—The most convenient
tests are, 1, _Hydrochloric acid_, or any hydrochlorate, which even in a
state of extreme dilution causes with it a dense white precipitate,
passing, under exposure to light, into dark brown; and 2, _Ammonia_,
followed by the solution of oxide of arsenic; if the nitrate of silver
is not too much diluted it gives a dark brown precipitate with ammonia,
soluble, however, in an excess of that alkali; and when the solution has
thus been restored, arsenic throws down a lively yellow precipitate,
passing rapidly to brown, if left exposed to the light.

Most organic substances, but in particular all animal fluids, with the
exception of gelatin, decompose nitrate of silver.

It appears from the experiments of Orfila, that, like the chlorides of
tin, the nitrate of silver is a deadly poison when introduced into the
veins; but that, by reason of its facility of decomposition, it cannot
enter the blood through ordinary channels in a quantity sufficient to
develope any remote action. When two grains in solution were injected
into the jugular vein of a dog it died in six minutes, difficult
respiration being the chief symptom; the third part of a grain caused
death in four hours and a half, violent tetanus having preceded death;
and in both animals the blood in the heart was found very black and the
lungs gorged, or vivid red. According to Mr. Blake, the salts of silver
when directly introduced into the blood, do not act on the heart, but
operate by causing obstruction of the capillary system. If they are
injected into the aorta, the systemic capillaries are obstructed, the
nervous system is consequently oppressed, respiration is arrested
through the medium of this nervous oppression, and death takes place by
asphyxia, the heart continuing to beat vigorously. If again they are
injected into a great vein, immediate obstruction of the pulmonary
capillaries takes place, so that the blood ceases to be transmitted to
the left side of the heart.[1174]

To the violent action exerted by nitrate of silver when directly
admitted into the blood, its effects through the medium of the stomach
bear no proportion or resemblance. Thus, when twelve grains of the salt
were introduced into the stomach in the solid state, its effects were so
slight as not to be distinguishable from those of the ligature on the
gullet practised to prevent its discharge by vomiting. When introduced
in a state of solution, however, and in a larger dose, in the dose of 36
grains, for example, it is more energetic. Death ensued in thirty-six
hours, but without any particular symptoms; and in the dead body the
villous coat of the stomach was found generally softened, and corroded
near the pylorus by little grayish eschars like those formed by this
poison on the skin.[1175]

Hence it appears that nitrate of silver does not act remotely, but
simply as a local irritant and corrosive. The corrosion it produces is
incompatible with its absorption in large quantity. This inference is
confirmed by the experiments of Schloepfer, on its effects when
introduced into the trachea. He found that it caused inflammation of the
windpipe, and pneumonia passing on to hepatization of the lungs, but no
symptom referrible to a remote action.[1176] Its pure corrosive
properties have long pointed it out to the surgeon as the most
convenient of all escharotics.

Nitrate of silver is absorbed, however, in the course of its action. It
would seem to be absorbed when it is taken medicinally in frequent small
doses. It is not easy to account otherwise for the singular blueness of
the skin, sometimes observed after the protracted use of lunar caustic
as a remedy for epilepsy and other diseases.[1177] The effects of the
poison on the constitution in such cases are not very well known. It
appears, however, that considerable doses may be taken for a great
length of time without injury, and that the first and only unpleasant
effects produced by its too free administration are such as indicate
simply an injury of the stomach. The only exception to this general
statement I have met with is a case by Wedemeyer, where, after the
remedy had been taken for six months on account of epilepsy, that
disease disappeared, and dropsy, with diseased liver at the same time
commenced, and soon proved fatal. It is probable, however, that the
nitrate of silver had no share in the ultimate event. In this instance
the whole internal organs were more or less blue; and metallic silver,
it is said, was found in the pancreas, and in the choroid plexus of the
brain.[1178] Silver has been found in the urine of persons who were
taking it medicinally. A young man who had used the nitrate for some
time observed that his urine became muddy soon after being passed, and
that the sediment became black if exposed to the light; and when the
sediment was digested in ammonia, chloride of silver was detached by
neutralizing the ammoniacal liquor.[1179]

But it also appears that some nitrate of silver is absorbed when it is
given in a single large dose. For in animals poisoned with it Orfila
found that silver may be detected in the liver and spleen by charring
these organs with nitric acid as in the instance of poisoning with
copper, and then treating the residue with boiling diluted nitric acid,
and adding hydrochloric acid to the solution. He also found silver in
the urine by charring the extract with heat, acting on the charcoal with
ammonia, and saturating the filtered ammoniacal solution,—chloride of
silver being then detached.[1180] These results have been confirmed by
the experiments of Drs. Panizza and Kramer of Milan,[1181] who found
silver in the blood after the administration both of the nitrate and
chloride.

Boerhaave has noticed a case of poisoning with this substance, but in
very brief terms. He says it caused gangrene. Schloepfer in his thesis
notices a case by Dr. Albers of Bremen in which croup was brought on by
a bit of lunar caustic dropping into the windpipe. M. Poumarede has
related an instance of poisoning with an ounce of nitrate of silver in
solution. A few hours afterwards the individual was found insensible,
with the eyes turned up, the pupils dilated, the jaws locked, and the
arms and face agitated with convulsions. A solution of common salt was
immediately given as an antidote. In two hours there was some return of
consciousness, and abatement of the convulsions, but still complete
insensibility of the limbs, with redness of the features, and pain in
the stomach. In eleven hours he could articulate. For thirty-six hours
he continued subject to fits of protracted coma; but he eventually
recovered. Sixteen hours after taking the poison he vomited a large
quantity of chloride of silver.[1182]

The treatment of poisoning with the nitrate of silver is obvious. The
muriate of soda by decomposing it will act as an antidote; and any signs
of irritation left will be subdued by opium.


                       _Of Poisoning with Gold._

_Gold_ in various states of combination was at one time much used in
medicine, and an attempt has been lately made to revive its employment.

Its poisonous properties are powerful, and closely allied to those of
the chlorides of tin and nitrate of silver. In the state of chloride it
occasions death in three or four minutes when injected into the veins,
even in very minute doses; and the lungs are found after death so turgid
as to sink in water. But if swallowed, corrosion takes place; the salt
is so rapidly decomposed, that none is taken up by the absorbents; and
death ensues simply from the local injury.[1183] It has been of late
used in medicine in France as an antisyphilitic; but even doses so small
as a tenth of a grain have been known to produce an unpleasant degree of
irritation in the stomach.[1184]

In the state of fulminating gold, this metal has given rise to alarming
poisoning in former times, when it was used medicinally. Plenck in his
Toxicologia says it excites griping, diarrhœa, vomiting, convulsions,
fainting, salivation; and sometimes has proved fatal.[1185] Hoffmann
likewise repeatedly saw it prove fatal, and the most remarkable symptoms
were vomiting, great anxiety and fainting. In one of his cases the dose
was only six grains.[1186] These compounds are now so little met with
that they need not be noticed in greater detail.


                      _Of Poisoning with Bismuth._

_Bismuth_, in its saline combinations, is also an active poison. One of
its compounds, the trisnitrate, white bismuth, or magistery of bismuth,
is a good deal used in medicine and the arts; and pearl white, one of
the paints used in the cosmetic art, is the tartrate of this metal.

The former substance is an active poison. It is got by dissolving
bismuth in nitric acid, and pouring hot water over the crystals; a
supernitrate being left in solution, and the trisnitrate thrown down in
the form of a white powder.

Orfila found that the soluble part of fifteen grains of the nitrate,
when injected into the jugular vein of a dog, caused immediate giddiness
and staggering, and death in eight minutes. He also remarked that forty
grains mixed with water and introduced into the stomach, caused all the
customary signs of irritation, and death in twenty-four hours; and that
a great part of the villous coat of the stomach was reduced to a pulpy
mass, and likewise exhibited several ulcers.[1187]

Similar effects were produced by the trisnitrate; but a larger dose was
required. Two drachms and a half killed a dog in twenty-four hours; and
redness and eroded spots were found in the stomach.

In some more recent researches Orfila found that the poison is absorbed,
and may be detected, like other metallic poisons, in the liver, spleen,
and urine. The process for this purpose, applicable also to all organic
mixtures, consists in boiling the solids in water acidulated with a
twentieth of nitric acid, evaporating the solution to dryness, charring
the residue with nitric acid, as directed for copper, boiling the
charcoal in diluted nitric acid, and thus obtaining an acid solution of
nitrate of bismuth, which may be known by the effects of water and of
hydrosulphuric acid.[1188]

Orfila remarks, that Camerarius of Tübingen once detected the
adulteration of wine with the oxide of bismuth, and that the bakers in
some parts of England used to render their bread white and heavy by
mixing the trisnitrate with flour; but he has not stated his authority
for this accusation. It may be discovered in any such mixture by
calcining the suspected substance in a crucible, and then separating the
metallic bismuth by means of nitric acid. But the adulteration of bread
with bismuth is very questionable, as there are many cheaper methods for
effecting the purpose, without adding any thing positively deleterious.

The following is the only case with which I am acquainted of poisoning
with the preparations of bismuth in the human subject. A man subject to
water-brash took two drachms of the trisnitrate with a little cream of
tartar by mistake for a mixture of chalk and magnesia. He was
immediately attacked with burning in the throat, brown vomiting, watery
purging, cramps, and coldness of the limbs, and intermitting pulse, and
then with inflammation of the throat, difficult swallowing, dryness of
the membrane of the nose, and a constant nauseous metallic taste. On the
third day he had hiccup, laborious breathing, and swelling of the hands
and face; and suppression of urine was then discovered to have existed
from the first. On the fourth day swelling and tension of the belly were
added to the pre-existing symptoms, on the fifth day salivation, on the
sixth delirium, on the seventh, swelling of the tongue and enormous
enlargement of the belly; and on the ninth he expired. The urine
continued suppressed till the eighth day.—On inspection of the body it
was found that from the back of the mouth to the rectum there were but
few points of the alimentary canal free of disease. The tonsils, uvula,
pharynx, and epiglottis, were gangrenous, the larynx spotted black, the
gullet livid, the stomach very red, with numerous purple pimples, the
whole intestinal canal red, and here and there gangrenous, especially at
the rectum. The inner surface of the heart was bright red. The kidneys
and brain were healthy.[1189]


                      _Of Poisoning with Chrome._

The next metal whose properties deserve notice is _chrome_. As it is now
extensively used in the art of dyeing it is necessary to mention its
effects, more especially as they are singular. They have been
ascertained experimentally with great care by Professor Gmelin of
Tübingen. He found that in the dose of a grain the _chromate of potass_
had no effect when injected into the jugular vein of a dog,—that four
grains produced constant vomiting, and death in six days without any
other striking symptom,—and that ten grains caused instant death by
paralysing the heart. Its effects, when introduced under the skin, are
still more remarkable. It seems to cause general inflammation of the
lining membrane of the air-passages. When a drachm was thrust in the
state of powder under the skin of the neck of a dog, the first symptoms
were weariness and a disinclination to eat. But on the second day the
animal vomited, and a purulent matter was discharged from the eyes. On
the third day it became palsied in the hind legs; on the fourth it could
not breathe or swallow but with great difficulty; and on the sixth it
died. The wound was not much inflamed; but the larynx, bronchi, and
minute ramifications of the air tubes contained fragments of fibrinous
effusion, the nostrils were full of similar matter, and the conjunctiva
of the eyes was covered with mucus. In another dog, an eruption appeared
on the back, and the hair fell off.[1190]

The effects of the salts of chrome on man have not been well
ascertained, but seem to be peculiar. Dr. Schindler of Greifenberg
relates the following case of fatal poisoning with bichromate of potash.
A colourman having swallowed a solution of it, vomiting was brought on
by warm water, soap and oil, and kept up until the discharges ceased to
be yellow. The man got apparently well and passed a quiet night; but
next morning he felt excessively weary, had stitches in his back and
kidneys, passed no urine, and was affected with purging. A restless
night followed. On the subsequent morning, he lay motionless and like
one fatigued to the extremest degree; in which state he died, fifty-four
hours after swallowing the poison. The stomach was healthy, the
intestines reddish, the kidneys gorged with blood and marbled internally
with dark-red patches, and the bladder empty.[1191]—Mr. Wilson of Leeds
has described the case of an elderly man who took the poison in the
evening, and was found dead about twelve hours afterwards, without any
sign of vomiting, purging, or convulsions; and no morbid appearance was
found but redness of the villous coat of the stomach, and an inky-like
fluid in it, containing a large quantity of bichromate of potash.[1192]

To these facts may be added another not less singular, which my late
colleague Dr. Duncan informed me has been observed by the workmen in
Glasgow, who use the bichromate of potass in dyeing. When this salt was
first introduced into the art of dyeing, the workmen who had their hands
often immersed in its solution were attacked with troublesome sores on
the parts touched by it; and the sores gradually extended deeper and
deeper, without spreading, till they sometimes actually made their way
through the arm or hand altogether.[1193]


                       _Of Poisoning with Zinc._

The compounds of _zinc_, which have been long used in considerable doses
in medicine, have sometimes occasioned serious and even fatal effects.
Partly on this account, and partly because one of them, the sulphate of
zinc, being the emetic most commonly used in the treatment of poisoning,
is apt to complicate various medico-legal analyses, it will be proper to
notice both its physiological properties and the mode of detecting it by
chemical means.

The only important compound of this metal is the sulphate or _white
vitriol_. As usually sold in the shops, it forms small, prismatic
crystals, transparent, colourless, of a very styptic metallic taste, and
exceedingly soluble in water. That which is kept by the apothecary is
tolerably pure; but there is a salt sometimes met with in commerce which
contains an admixture of sulphate of iron, and with which the natural
action of the tests for zinc is materially modified.

The solution of the pure salt is precipitated white by the _caustic
alkalis_, an oxide being thrown down, which is soluble in an excess of
ammonia. The _alkaline carbonates_ also precipitate it white, the
carbonate of ammonia being the most delicate of these reagents. The
precipitate is soluble in an excess of carbonate of ammonia, and is not
thrown down again by boiling. The precipitate produced both by the
alkalis and by their carbonates becomes yellow, when heated nearly to
redness; and on cooling it becomes again white. This is a characteristic
property, by which the oxide of zinc may be known from most white
powders. But oxide of antimony is similarly affected. The _ferro-cyanate
of potass_ also causes a white precipitate. A stream of
_sulphuretted-hydrogen_ likewise causes a white precipitate, the
sulphuret of zinc, the colour of which distinguishes the present genus
of poisons from all those previously mentioned, as well as from the
poisons of lead. The precipitate is apt to be suspended till the excess
of gas is expelled by ebullition. The action of this test will not
distinguish sulphate of zinc from the salts of peroxide of iron, by
which white sulphur is disengaged from the gas in consequence of the
peroxide of iron being reduced to the state of protoxide. The same
decomposition takes place wherever there is free chlorine, as in impure
samples of muriatic or nitric acid.

When the sulphate of zinc contains iron, the alkalis throw down a
greenish-white precipitate, the alkaline carbonates a grayish or
reddish-white, the ferro-cyanate of potass a light-blue, but
sulphuretted-hydrogen the usual white precipitate. Tincture of galls,
which merely renders the pure salt hazy, causes a deep violet coagulum
if there is any ferruginous impurity.

The sulphate of zinc is acted on by albumen and milk precisely in the
same manner as the sulphate of copper. The salt is decomposed, and the
metallic oxide forms an insoluble compound with the animal matter.

When the sulphate of zinc has been mixed with vegetable and animal
substances, the action of the tests mentioned above is modified. In such
circumstances I have found the following process convenient.

The mixture being strained through gauze, it is to be acidulated with
acetic acid, and filtered through paper. The acetic acid dissolves any
oxide of zinc that may have been thrown down in union with animal
matter. The filtered fluid is then to be evaporated to a convenient
extent, and treated when cool with sulphuretted-hydrogen gas,—upon which
a grayish or white milkiness or precipitate will be formed. The excess
of gas must now be expelled by boiling, and the precipitate washed by
the process of subsidence and affusion, and collected on a filter. It is
then to be dried and heated to redness in a tube. When it has cooled, it
is to be acted on by strong nitric acid, which dissolves the zinc and
leaves the sulphur. The nitrous solution should next be diluted, and
neutralized with carbonate of ammonia; after which the liquid tests
formerly mentioned will act characteristically. The effect of carbonate
of ammonia, and that of heat on the carbonate of zinc which is thrown
down, ought to be particularly relied on.

I have tried this process with the matter vomited after the
administration of sulphate of zinc, in a case of pretended poisoning,
and found it to answer exceedingly well.

Orfila has lately suggested the following method. Boil the suspected
substance in water, evaporate the filtered decoction to dryness, char
the residuum with nitric acid as directed for copper in similar
circumstances, digest the charcoal in diluted muriatic acid, and subject
the filtered solution to hydrosulphuric acid. If the sulphuret be not
white, but yellowish from iron, heat it with strong nitric acid, dry the
product, and heat it to redness; dissolve it in weak nitric acid; throw
down the oxide of iron by an excess of ammonia, which retains the oxide
of zinc; and then having filtered the fluid, separate the oxide of zinc
by neutralizing the ammonia.[1194]

Orfila has furnished the only accurate information hitherto possessed
regarding the effects of sulphate of zinc on the animal system.[1195] He
found that dogs might be made to swallow 7½ drachms without any
permanent harm being sustained, provided they were allowed to vomit; for
in a few seconds the whole poison was invariably discharged, and the
animals, after appearing to suffer for four or five hours, gradually
recovered their usual liveliness. But the result is different if the
gullet be tied: violent efforts to vomit ensue, and death follows in
three days, the intermediate phenomena being those of local irritation
chiefly, and the appearances in the dead body those of incipient
inflammation of the stomach, without corrosion.—When injected into the
veins, the effect of sulphate of zinc is much more violent, in an
inferior dose. Forty-eight grains occasioned almost instant death; and
half the quantity proved fatal in three minutes. Orfila does not appear
to have ascertained the cause of death in the last two experiments. But
Mr. Blake found that when this salt is injected into the veins in the
dose of three grains, it causes some depression of the heart; that
thirty grains arrest the action of the heart in eight seconds, leaving
that organ exhausted of irritability and full of florid blood in its
left cavities; and that when injected into the arterial system in the
dose of sixteen grains, it seemed not to cause any obstruction of the
capillaries, but to act on the nervous system, producing extreme
prostration, without insensibility or convulsions.[1196] These
experiments, when taken together, show that sulphate of zinc, though a
moderately active irritant, is more indebted for its activity to a
remote operation on some vital organ.

Sulphate of zinc is absorbed in the course of its action; for Orfila has
lately found it by his process for complex mixtures in the spleen,
liver, and urine of animals.[1197]

The effects of the preparations of zinc on man in large doses have not
been particularly studied. In the dose of a scruple or a drachm, the
sulphate is the most immediate emetic known; and it is to be inferred,
that if larger doses are rejected, as is the fact, with equal rapidity,
they will in general cause no more harm than the medicinal dose.

Nevertheless, some people have suffered severely from over-doses of
sulphate of zinc, and a few have even perished. Instead of presenting
here a general view of the symptoms, it will be preferable to relate the
heads of such cases as have been published.

The first to be mentioned is related by Foderé, who, in consequence of
the violent symptoms produced, assigns to the present poison very active
properties. “A patient of mine,” says he, “a custom-house officer,
having got from a druggist six grains of sulphate of zinc to cure a
gonorrhœa, was attacked with inflammation in the lower belly, attended
by retraction of the navel and severe colic, which yielded only to
repeated blood-letting, general as well as local, oleaginous emollients,
opiates, and the warm bath.”[1198] This case is noticed here chiefly to
prevent any one from being misled by it, as it has been quoted by other
medico-legal authors. For assuredly some other cause must have
co-operated before such symptoms could arise; since I have in many cases
given the same dose thrice daily for several days, without ever
observing more than slight sickness; and Dr. Babington once gave
thirty-six grains thrice a day for some weeks with as little
effect.[1199]

Parmentier, the chemist, met with an instance, in which about two ounces
of white vitriol in solution were swallowed by mistake. The countenance
became immediately pale, the extremities cold, the eyes dull, and the
pulse fluttering. The patient, a young lady, then complained of a
burning pain in the stomach, and vomited violently. But potass being now
administered in syrup, the pain ceased, the vomiting gradually abated,
and the lady soon recovered completely.[1200]

In the Journal de Médecine, another instance is related by M. Schueler,
in which a very large dose did not produce material injury. The symptoms
were pain in the stomach and bowels, with vomiting and diarrhœa. They
were dispelled in a few hours by the administration of cream, butter,
and chalk.[1201]

The following is a fatal case recorded by Metzger, but it is not a pure
example of poisoning with zinc, though accounted such by the relater;
for a small quantity of sulphate of copper was mixed with the sulphate
of zinc. Three persons in a family took this mixture, which had been
given them by a grocer in mistake for pounded sugar. They were all
seized with violent vomiting; and a boy twelve years of age died in less
than twelve hours.[1202]

Another and an unequivocal case has been lately recorded in Horn’s
Archiv from Mertzdorff’s experience. No part of the history of the
symptoms is mentioned, except that there had been vomiting. But
Mertzdorff has described carefully the morbid appearances, which are
interesting; and he detected the poison in the stomach by a satisfactory
analysis.[1203]

Two other cases, which are presumed to have arisen from the commercial
sulphate of zinc, and which proved fatal, have been recently published
by Dr. Sartorius of Aachen; but they do not appear to me to have been
satisfactorily traced to this poison, and it is therefore unnecessary to
quote them.[1204]

Dr. Werres of Cologne has related the particulars of three cases of
poisoning with some preparation of zinc in milk-porridge. One of the
persons, a child four years old, was seized with vomiting in three
minutes, and, after frequent violent returns of it, died in convulsions
within eight hours. The others also suffered severely from vomiting, but
recovered.[1205]

It does not appear that workmen who are exposed to the fumes of zinc
ever suffer materially. But there is a case in Rust’s Magazin, which
shows that these fumes are not quite harmless. An apothecary’s
assistant, while preparing philosopher’s wool, incautiously filled the
whole laboratory with it. The same day he was seized with tightness in
the chest, headache and giddiness; next morning with violent cough,
vomiting, and stillness of the limbs; on the third day with a coppery
taste in the mouth, some salivation, gripes, and such an increase of
giddiness that he could not stand. He was then freely purged, after
which a fever set in, ending in perspiration; and he got well in three
weeks.[1206]

From these cases, and the experimental researches of Orfila, it is clear
that the preparations of zinc, though not very active poisons, are
nevertheless far from being innocuous. We are not acquainted with their
effects when long and habitually introduced into the body in small
quantities. About the time when physicians began to study with care the
dangerous consequences of employing lead and copper in the manufacture
of culinary vessels, it was conceived by some that zinc might prove a
safe substitute. It was farther imagined by some military economists in
France, that zinc might be profitably used instead of tinned iron in the
manufacture of canteens and other articles of camp equipage, because the
worn and damaged vessels would sell as old metal at little short of
their original price, while tinned iron as old metal bears no value at
all. But from the experiments of Deyeux and Vauquelin it subsequently
appeared, that in the course of many culinary operations zinc is more
liable to be attacked than either copper or lead;—that water left for
some time in zinc vessels oxidates them, and acquires a metallic
taste;—that if water acidulated with vinegar or lemon-juice is boiled in
zinc, a solution is formed, in which the metal may be detected by its
tests;—and that sea-salt, sal-ammoniac, and even butter, have the power
of dissolving it also.[1207] Some singular inquiries were afterwards
prosecuted by Devaux and Dejaer among the Spanish prisoners at Liége,
with the view of proving, that frequent small quantities of zinc
dissolved in the manner mentioned, and habitually taken with the food,
have no injurious tendency; that even in large doses it can hardly be
accounted poisonous, as it merely gives rise to vomiting and slight
diarrhœa; and that an adulteration to such an amount would always betray
itself by its strong disagreeable taste.[1208] These are certainly
valuable facts, though not quite satisfactory. But it is unnecessary to
inquire minutely into their validity; for, independently of all other
considerations, vessels constructed of zinc are too brittle for domestic
purposes. With regard to the effects of frequent small doses of sulphate
of zinc, the only positive information I can communicate is, that I have
often given medicinally from three to six grains thrice a day for two or
three weeks, without observing any particular effect except in some
persons sickness when the largest doses were taken; and others have
frequently made the same observation.[1209] On the other hand, Dr. Nasse
of Berlin says a patient of his, who had taken twenty grains of oxide of
zinc daily till 3247 grains were swallowed, was attacked with paleness,
emaciation, weakness of intellect, obstinate constipation, coldness and
œdema of the limbs, extreme dryness of the skin, and a thready scarcely
perceptible pulse. But he quickly recovered under the use of laxatives
and tonics.[1210]

Sulphate of zinc is said to have proved fatal when applied externally.
In Pyl’s memoirs there is a case of this nature, which was attributed to
sulphate of zinc having been used as a lotion for a scabby eruption on
the head. The subject was a child, six years old, and otherwise healthy.
The wash, which was a vinous solution, had not been long applied before
the child complained of acute burning pain of the head, which was
followed by vomiting, purging, convulsions, and death in five hours. The
cause of these symptoms, though the particulars of the case were
ascertained judicially by an able medical jurist, Dr. Opitz of Minden,
is nevertheless very doubtful, as daily use is made of the salt for
similar purposes without any such effect. Appearances of congestive
apoplexy were found within the skull; and the reporter ascribes death to
the wash having produced repulsion of the cutaneous disease, and
determination of blood to the head.[1211]

The only opportunities which have occurred of observing the morbid
appearances after poisoning with sulphate of zinc taken internally, are
the cases by Metzger, Mertzdorff, and Werres.

In the first, which was a mixed case, the only appearances of note were
slight inflammation in the stomach, and excessive gorging of the lungs
with fluid blood; from which Metzger oddly enough concludes that the
child was suffocated by the vomiting. In the second case, Mertzdorff
found the stomach and intestines, but particularly the latter,
contracted,—their outer surface healthy—the inner membrane of the
stomach grayish-green, with several spots of effused blood, and
greenish, fluid contents,—the inner membrane of the small intestines
similarly spotted,—the rest of the body quite natural. It has been
already mentioned that Mertzdorff detected the poison in the body. He
found it not only in the contents, but likewise in the coats of the
stomach and intestines. In the third, Werres found a reddish-brown patch
and some vascularity in the stomach.


                       _Of Poisoning with Iron._

In previous editions of this work the preparations of iron were arranged
among those substances which are not usually considered poisonous, but
which may nevertheless prove injurious when taken in large quantity. But
the soluble salts of iron, although not very active, seem sufficiently
so to entitle them to a regular place among poisons; and one of them,
the sulphate, has actually been used, as will presently appear, for the
purpose of committing murder. There are many soluble salts of iron which
in all probability may prove hurtful; but the only ones which have been
brought under notice in medico-legal researches are the sulphate of the
protoxide, and the mixed chlorides.

The sulphate of the protoxide of iron, commonly called green vitriol or
copperas, occurs in commerce in crystals or crystalline masses of
various shades of bluish-green. It is easily known by its colour and its
strong styptic inky taste. When in solution, the iron may be detected by
ferro-cyanate of potash, sulphuretted-hydrogen, and tincture of galls.
Ferro-cyanate of potash causes a blue precipitate, at first pale, but
gradually passing to deep Prussian blue. Sulphuretted-hydrogen has no
effect, but if an alkali, such as ammonia, be added to disengage the
oxide of iron, a black precipitate of sulphuret of iron is immediately
produced. Tincture of galls occasions a deep purplish-black precipitate,
the tannate of iron, and it acts with greater delicacy in very diluted
solutions, if the oxide of iron be disengaged by carbonate of soda.
These tests prove the presence of iron in solution. A white precipitate
under the action of nitrate of baryta will indicate that the oxide is
dissolved by sulphuric acid.

The most familiar form of chloride of iron is the tincture of the
chloride, which sometimes contains only the sesquichloride, sometimes
consists of a mixture of this with the protochloride. It is known by the
three tests for oxide of iron described above, and by nitrate of silver
occasioning a heavy white precipitate, insoluble in nitric acid.

For detecting iron in organic mixtures, where the liquid reagents do not
act satisfactorily, the simplest process is to digest the mixture, if
there be any solid matter, in water acidulated with acetic acid, to
evaporate the filtered liquid to dryness, to incinerate the extract in a
porcelain crucible, to act on the product with diluted sulphuric acid,
and then to treat the solution with the three liquid reagents.

Professor Gmelin found that sulphate of iron merely caused vomiting in
dogs who were made to swallow two drachms of it, that rabbits might take
forty grains without any apparent injury, and that twenty grains in a
state of solution might even be injected into the veins of a dog without
producing any particular symptom.[1212] From these and some other facts
of the like kind it was generally held, that sulphate of iron is not a
poison. But Smith ascertained that a dose of two drachms will prove
fatal to dogs in little more than twenty-tour hours, when it is
introduced into the stomach, and in half that time if applied to a
wound; and that it occasions some redness of the alimentary mucous
membrane, and the effusion of a thick layer of tough mucus. It is
remarkable, however, that, like Gmelin, he found no effect to flow from
the transfusion of a solution of seven grains into the veins, except
transient vomiting and expressions of pain.[1213]

The effects which have been observed in the human subject are
conformable with those witnessed in experiments on the lower animals,
the symptoms being those of pure irritant poisoning. Few illustrative
cases, however, have as yet been made public. In Rust’s Journal there is
the case of a girl, who took as an emmenagogue, an ounce of green
vitriol dissolved in beer, and suffered in consequence from colic pains,
constant vomiting and purging for seven hours, but eventually recovered
under the use of mucilaginous and oily drinks.[1214] A fatal case of
poisoning with this substance occurs in the Parliamentary Returns of
death from poison in England during the years 1837–38 [see p. 90].—Dr.
Combe of Leith has communicated to me an instructive case of fatal
poisoning with the tincture of the chloride of iron, which was taken to
the extent of an ounce and a half by a gardener accidentally instead of
whisky. Violent pain in the throat and stomach, tension and contraction
of the epigastrium, and nausea immediately ensued; afterwards coldness
of the skin and feebleness of the pulse were remarked; and then vomiting
of an inky fluid, with subsequently profuse vomiting of mucus and blood,
and also bloody stools under the use of laxatives. He remained for some
days in a very precarious state, but then began to rally, and in three
weeks resumed his occupation. But in two weeks more Dr. Combe found him
emaciated, cadaverous in appearance, and affected with pains in the
stomach, costiveness, and thirst; in which state he lingered for five
days more, and then died. In the dead body there was found great
thickening towards the pylorus, a cicatrized patch there three inches
long and two inches broad, and another large patch of inflammatory
redness surrounded by a white border. The preparation taken in this
instance contained a third of its volume of hydrochloric acid and a
tenth of its weight of oxide of iron; and consequently some of the acid
was free.

The following remarkable case, in which I was lately consulted on the
part of the Crown, will show that sulphate of iron is a more important
poison than has been commonly thought. Suspicions having arisen in
December, 1840, respecting the death of a child in the county of Fife
about four months before, an investigation was made by the law
authorities; and the body was disinterred and inspected by Mr. Dewar and
Dr. James Dewar of Dunfermline. It was ascertained that the child, a
girl four years of age, and previously in good health, was attacked with
violent vomiting and purging immediately after breakfasting on porridge,
and died in the course of the afternoon of the same day. A boy two years
older, having seen a blue solution put into the porridge, and observing
that the porridge had a bad taste, took only three spoonfuls of it, but
became for a time very sick. The girl, being fed by a woman in the
house, was made to take all her share; and in the course of the day the
same person was seen by two children of the family to give a blue
solution to the sick girl for drink. The woman was proved to have
purchased sulphate of copper, and admitted having bought about this time
both that salt and sulphate of iron, for the alleged purpose of dyeing
some clothes. Poisoning with sulphate of copper was therefore suspected.
On examining the body, which had been buried four months, the Messrs.
Dewar found the external parts considerably decayed,—the stomach soft,
gelatinous, and of a uniform intense black colour through the whole
thickness of its parietes,—the gullet and duodenum similarly affected,
but not so deeply on their outer surface,—the spleen, kidneys, and lower
parts of the liver similarly stained with a black pulp, which could be
wiped off,—and the whole alimentary canal lined with a thick layer of
jet-black mucus, from the pharynx down to the very anus. Inferring that
the cause of this extraordinary blackness was decomposition of sulphate
of copper by hydrosulphuric acid gas disengaged during the decay of the
body, they proceeded to search for that metal in the form of sulphuret
both in the contents and texture of the stomach, but without success:
there was not a trace of copper to be found. Being then led from some
circumstances in the analysis to suspect that the black matter might be
sulphuret of iron, they proceeded to search for that substance, and
ascertained that a large quantity existed both in the textures of the
stomach and in the black mucus which lined it. They further ascertained
that there was no iron in a state capable of being dissolved by water,
but that a much larger quantity of sulphuric acid was associated with
the black matter than could have proceeded from the sulphates naturally
contained in the animal textures or in the mucous secretions. They had
also an opportunity of examining several large buff-coloured stains on
various articles of dress, worn by the child and by the woman at the
time the poisoning was supposed to have happened; and they detected a
large quantity of oxide of iron in all of them. The whole case was
subsequently submitted to me for my opinion, together with a portion of
the stomach, the entire intestines, and several stained articles of
dress. The results of the analysis of the tissues of the stomach, the
black intestinal mucus, and the stains on the cloth were the same in my
hands.—It is not easy to see how any other conclusion could be drawn
from the whole circumstances, than that a soluble preparation of iron
had been administered a short time before death, and that it had been
entirely decomposed and converted into sulphuret of iron by the
evolution of hydrosulphate of ammonia during the decay of the body. In
consequence of important defects in the evidence criminating a
particular individual, and especially because all the essential facts
depended on the testimony of children, who, after the lapse of some
time, did not adhere to their original statement, it was judged improper
to bring this case to a trial.

A few years afterwards another case somewhat similar was submitted by
the law authorities to the same gentlemen, to whom I am indebted for the
particulars. A woman far advanced in pregnancy, and enjoying excellent
health, was suddenly seized about midnight with vomiting and purging,
and died in fourteen hours. Various circumstances having raised
suspicions as to the cause of death, the body was disinterred a few days
after burial, and carefully examined by Mr. Dewar and Dr. Dewar. The
organs were in general healthy. There were some dark-red patches on the
villous coat of the stomach, and a general blush pervaded the whole
alimentary canal, which was empty of every thing but a reddish-brown
mucus. The intestines were in several places irregularly contracted and
hard. The stomach, small intestines, and rectum contained iron in large
quantity, dissolved either by sulphuric or hydrochloric acid. Sulphate
of iron was found in the house.—No trial took place in this instance
either, because there was a want of evidence to attach guilt to any
particular individual, although it was highly improbable that the woman
had taken the poison herself.[1215]

A short notice may here be added of the toxicological effects of the
rarer metals, which have been examined chiefly by Professor Gmelin of
Tübingen.[1216]—Oxide of _osmium_ is nearly as active as arsenic, for a
grain and a half will kill a dog in a few hours by the stomach, and in
one hour through a vein. Twelve grains of hydrochlorate of _platinum_
will kill a dog within a day through the stomach, with symptoms of pure
irritation; and so will half that quantity through a vein.—The
hydrochlorates of _iridium_ and _rhodium_ are rather less active.—The
hydrochlorate of _palladium_ is equally powerful when introduced into
the stomach, and much more so through a vein, for two-thirds of a grain
will kill dogs in a minute.

The salts of other metals appear less active.—_Molybdenum_, in the form
of molybdate of ammonia, seems a feeble poison; thirty grains killed a
rabbit in two hours, but produced in dogs merely some vomiting and
purging; and ten grains injected into the jugular vein did not prove
fatal.—_Manganese_, according to Gmelin, is likewise a feeble poison,
but has peculiar effects. A drachm of the sulphate killed a rabbit in an
hour. Thirty grains swallowed by a dog had no effect. Two drachms thrust
into the cellular tissue had no effect. Twelve grains injected into a
vein occasioned death in five days: and in the dead body, the stomach,
duodenum, and liver were found much inflamed. Manganesic acid, according
to Professor Hünefeld, appears also to act on the liver, but is a feeble
poison. A rabbit received two drachms in three days in doses of ten or
fifteen grains, without presenting any symptom except increased flow of
urine. Being then killed, the liver was found soft, at one part bright
red, elsewhere dark-brownish-red, and it yielded manganese by
incineration.[1217] Some singular observations have been lately
published by Dr. Couper of Glasgow, the purport of which is, that
manganese belongs to the class of insidious, cumulative poisons, and
that it has the property of slowly bringing on, in those who breathe or
handle the oxide, a paraplegic affection which is incurable unless taken
under treatment early. Five cases of the kind occurred subsequently to
1828, in the great chemical manufactory of Tennant and Company, among
the workmen employed in grinding the black oxide of manganese.[1218] On
the other hand, Dr. Thomson of Glasgow has recently stated that an ounce
of sulphate of manganese is an effectual and safe laxative.[1219]
_Uranium_ is an active poison when injected into a vein, for three
grains of the muriate proves fatal instantly; but dogs may swallow
fifteen, or from that to sixty grains without any other effect except
slight vomiting [Gmelin]. _Cobalt_ is more active. Thirty grains of the
oxide occasion death in a few hours through the stomach. Twenty-four
grains of the muriate applied to the cellular tissue excite vomiting.
Three grains of sulphate injected into a vein prove fatal in four
days.—_Tungsten_, _cerium_, _cadmium_, _nickel_, and _titanium_ can
scarcely be considered poisons. _Tungstate_ of ammonia in the dose of a
drachm had no effect when swallowed by a dog; forty grains of tungstate
of soda, which is more soluble, operated as an emetic; but this dose
will prove fatal to rabbits in a few hours. A drachm of the muriate of
_cerium_ had little or no effect on a dog, and half that dose had no
effect on a rabbit. The oxide of _cadmium_ in the dose of twenty grains,
made a dog vomit; and ten grains had no effect at all.[1220] Twenty
grains of sulphate of _nickel_ made a dog vomit; forty grains applied to
the cellular tissue had no effect at all on the general constitution;
but ten grains injected into the jugular vein occasioned immediate death
[Gmelin]. A drachm of _titanic_ acid had no effect on a dog.




                             CHAPTER XVIII.
                        OF POISONING WITH LEAD.


Poisoning with lead is a subject of great consequence in Medical Police,
as well as Medical Jurisprudence. Its preparations have been used for
the purpose of intentional poisoning. At the Taunton Assizes in March,
1827, a servant-girl was tried for attempting to administer sugar of
lead to her mistress in an arrow-root pudding: and although the charge
was not made out, it appeared from the prisoner’s confession that she
really had made the attempt. Sugar of lead has also been often taken by
accident.

In relation to medical police lead is a subject of great importance.
This metal is used in so many forms, and in so many of the arts, and its
effects when gradually introduced into the body are so slow and
insidious, that instances of its deleterious operation are frequently
met with. Such accidents, indeed, are less common now, than they used to
be before the late improvements in chemistry. But they are still
sufficiently frequent to render it necessary for the toxicologist to
investigate the properties of lead attentively.


 SECTION I.—_Of the Chemical History and Tests for the Preparations of
                                 Lead._

The physical characters of lead in its metallic state are familiar to
every one. It is easily known by the dull bluish-gray colour it assumes
when exposed some time to the air, by the brilliant bluish-gray colour
of a fresh surface, and by the facility with which it may be cut. The
compounds which require particular notice are four in number, litharge,
red lead, white lead, sugar of lead, and Goulard’s extract. The first
three are very much used by house-painters and glaziers, the last two
are extensively employed in surgery, and the sugar of lead is also used
in many of the arts.


                     1. _Of Litharge and Red Lead._

_Litharge_ is the protoxide of lead in a state of semivitrification.
_Red lead_ is a compound of two equivalents of protoxide and one of
deutoxide. The former is generally in the form of a grayish-red heavy
powder, sometimes partly crystalline; the latter in the form of a bright
red powder approaching in colour to vermilion. They may be known by
their colour;—by their becoming black when suspended in water and
treated with a stream of sulphuretted-hydrogen gas;—and by litharge
being entirely, and red lead partly, soluble in nitric acid, and forming
a solution which possesses the properties to be mentioned presently for
solutions of the acetate. The chemical actions concerned in these
changes are obvious, except in the instance of nitric acid on red lead.
Here the acid dissolves the protoxide only, and the deutoxide, which
seems to act the part of an acid in the pigment, is separated in the
form of a brown powder.


                          2. _Of White Lead._

_White lead_, which is the carbonate of the metal, is in the form of a
heavy snow-white powder, or in white chalk-like masses. It consists of
variable proportions of the hydrated oxide and neutral carbonate; those
specimens are the whitest which contain most carbonate; and the best
English white lead I find to contain four equivalents of carbonate and
one of hydrated protoxide. The grayer variety, formed by the action of
distilled water on metallic lead, consists of only two of the former to
one of the latter.[1221] It may be known by its being blackened like the
two former compounds by sulphuretted-hydrogen,—by being soluble with
effervescence in nitric acid,—and by becoming permanently yellow when
heated to redness, in consequence of the expulsion of its carbonic acid,
and its conversion into protoxide. These tests, however, apply with
exactness only to the pure carbonate, in which state white lead is not
often met with in the shops. It is generally adulterated with sulphates,
in consequence of which it is only partially acted on by nitric acid,
and does not become distinctly yellow under a strong red heat. Dutch
white-lead contains no less than between 78·5 and 25 per cent. of
impurities insoluble in nitric acid, Venetian white-lead from 11 to 14·5
per cent., Munich white-lead between 1 and 7·5 per cent.[1222] I have
met, however, with perfectly pure specimens in the shops of this city.


                         3. _Of Sugar of Lead._

_Sugar of lead_ is the acetate of this metal. It is sold in the form
either of a white heavy powder, or of aggregated masses of long
four-sided prismatic crystals. It has a sweetish astringent taste, and a
slight acetous odour. It is very soluble.

When in the solid state, it may be known by its solubility in water, and
by the effects of heat. It first undergoes the aqueous fusion, then
abandons a part of its acid empyreumatized, as may be perceived by the
smell, next becomes charred, and finally presents globules of lead
reduced by the charcoal of the acid. The best way of effecting its
reduction on the small scale is to char it, and then direct on the mass
the point of a blowpipe-flame: in an instant globules are developed. It
is not easily reduced in a tube; at least I have never been able to
succeed in that way.

In the fluid state the acetate of lead, as well as all its
soluble salts, may be detected by the following system of
reagents,—hydrosulphuric acid, bichromate of potass, hydriodate of
potass, and metallic zinc,—which are the best of the numerous reagents
yet proposed.

1. _Hydrosulphuric acid_ causes a black precipitate, the sulphuret of
lead. This is a test of extreme delicacy; and it acts in whatever state
of combination the lead exists, whether fluid or solid.

It is preferable to the hydrosulphate of ammonia as a medico-legal test;
for, as Fourcroy observed, the hydrosulphate of ammonia acts on many
sound wines as if they contained lead,[1223] while hydrosulphuric acid
never causes with them a black precipitate, unless they contain either
lead or some other metallic impregnation. It must be remembered that
many other metallic solutions, such as those of mercury, copper, silver
and bismuth, yield a black precipitate with this test.

2. _Chromate of potass_, both in the state of proto-chromate and
bichromate, causes a fine gamboge-yellow precipitate, the chromate of
lead. For the characteristic action of this reagent, it is desirable
that the suspected liquid be neutral. It forms with solutions of the
sulphate of copper a precipitate nearly of the same colour as the
chromate of lead.

3. _Hydriodate of potass_ causes also a lively gamboge-yellow
precipitate, the iodide of lead. The action of this test is impaired in
delicacy by a considerable excess of nitric acid, or acetic acid. These
acids cause a yellow coloration with the test, though no lead be
present.

4. _A rod of zinc_ held for some time in the solution displaces the
lead, taking its place, and throwing down the lead in the form of a
crystalline arborescence. This is a very characteristic test; and also
one of much delicacy; for I have found a small thread of zinc will very
easily detect a twentieth part of a grain of lead dissolved in the form
of acetate in 20,000 parts of water. It acts also on the nitrate of
lead. Its action is impaired or prevented by an excess of acetic or
nitric acid.

These tests are amply sufficient for determining the presence of lead in
a solution, provided they act characteristically. Others have been also
used, however; and it is therefore right to notice them cursorily.

The _alkaline carbonates_ throw down a white precipitate in a very
diluted solution of lead. This test is ineligible, because the alkaline
carbonates cause a white precipitate with many other salts. It might be
rendered decisive, however, by washing the precipitate thoroughly,
suspending it in pure water and transmitting sulphuretted-hydrogen,
which blackens it. No other white carbonate is similarly altered except
those of bismuth and silver, which are rare.

The _soluble sulphates_ likewise cause with solutions of lead a white
precipitate, the sulphate of lead. To this test the same objections
apply as to the carbonates of the alkalis.

The _ferro-cyanate of potash_ causes a white precipitate, the
ferro-cyanate of lead. This is an objectionable test, as many other
substances besides lead are similarly acted on by it.


                        4. _Goulard’s Extract._

Goulard’s extract, the diacetate of lead, is easily distinguished from
the acetate or sugar of lead by the effect of a stream of carbonic acid,
which throws down a copious precipitate of carbonate of lead. The proper
method of analyzing it is to transmit this gas till it ceases to act any
longer, and then to subject the precipitate and solution to the tests
for carbonate of lead, and acetate of lead. Solutions of the common
acetate usually give a scanty white precipitate with carbonic acid, in
consequence of containing a faint excess of oxide.

The presence of vegetable or animal matters may either decompose the
salts of lead, or materially alter the action of the preceding reagents.

It appears from the experiments of Orfila, that most vegetable infusions
possess the power of decomposing them more or less. The acetate
furnishes, for example, an abundant precipitate with infusion of galls,
or with infusion of tea. Almost all animal fluids, with the exception of
gelatin, possess the same property; albumen, milk, bile, beef-tea, all
give with it a copious precipitate. In fluids which do not decompose it
altogether, the colour of the precipitate formed by the tests is so
materially altered, that they cannot be relied on for the detection of
lead. The test, however, which undergoes least alteration is
hydrosulphuric acid.

Before proceeding to the detection of lead in complex organic mixtures,
some remarks will be required on its relations to medical police. Here
the various ways in which it is apt to be insidiously introduced into
the body, chiefly by the action of chemical agents on metallic lead
itself, will come under consideration.


             _Of the Action of Air and Pure Water on Lead._

When lead is exposed to the air it becomes tarnished. This arises from a
thin crust of carbonate of lead being formed; for the crust dissolves
with brisk effervescence in acetic acid. The formation of carbonate is
accelerated by moisture and probably by the presence of an unusual
proportion of carbonic acid in the air.

The action of water on lead, which is of much greater consequence, has
been made the subject of observation by the curious for many ages. The
Roman architect, Vitruvius, who, it is believed, nourished in the time
of Cæsar and Augustus, forbids the use of this metal for conducting
water, because cerusse, he says, is formed on it, which is hurtful to
the human body.[1224] Galen also condemns the use of lead pipes, because
he was aware, that water transmitted through them contracted a muddiness
from the lead, and those who drank such water were subject to
dysentery.[1225] If we trace the sciences of architecture, chemistry,
and medicine downwards from these periods, nothing more will be found
than a repetition of the statements of Vitruvius and Galen, with but a
few particular facts in support of them, till we arrive at the close of
the last and beginning of the present century.

The first person that examined the subject minutely, was Dr. Lambe of
Warwick; who inferred from his researches, that most, if not all, spring
waters possess the power of corroding and dissolving lead to such an
extent as to be rendered unfit for the use of man, and that this solvent
power is imparted to them by some of their saline ingredients.[1226] The
inquiry was afterwards undertaken more scientifically by Guyton-Morveau;
who, in opposition to Dr. Lambe, arrived at the conclusion, that
distilled water, the purest of all waters, acts rapidly on lead by
converting it into a hydrated oxide, and that some natural waters, which
hardly attack lead at all, are prevented doing so by the salts they hold
in solution.[1227] A few years later Dr. Thomson of Glasgow also
examined the subject, and, assenting to Dr. Lambe’s proposition, that
most spring waters attack lead, maintains nevertheless that the lead is
only held in suspension, not in solution; and that the quantity
suspended in such waters, after they have passed through lead pipes,
pumps, and cisterns, is too minute to prove injurious to those who make
habitual use of them.[1228] In the first edition of this work an
extended account was given of an investigation I made into the whole
subject of the action of different waters on lead.[1229] Additional
observations were afterwards published on the same point by Captain
Yorke,[1230] and by Mr. Taylor.[1231] And I have added some new facts in
a late paper.[1232]

The inquiry is of so great practical consequence, that I need not offer
any apology for reproducing it here in detail, with such additions as
ulterior experience and the researches of others enable me to make.
Professor Orfila takes no notice of this important subject, except in a
few lines containing several inaccurate statements.[1233]

Distilled water, deprived of its gases by ebullition, and excluded from
contact with the air, has no action whatever on lead. If the water
contains the customary gases in solution, the surface of the metal,
freshly polished, becomes quickly dull and white. But if the surface of
the water be not at the same time exposed to the air, the action soon
comes to a close.—When the air, on the other hand, is allowed free
access to the water, a white powder appears in a few minutes on and
around the lead; and this goes on increasing till in the course of a few
days there is formed a large quantity of white matter which partly
floats in the water or adheres to the lead, but is chiefly deposited on
the bottom of the vessel. If this experiment be made with atmospheric
air deprived of carbonic acid, the white substance puts on the form of a
fine powder, which I find to be a hydrated oxide; for when dried at
180°F. it gives off water on being heated to redness, and dissolves
without effervescence in weak nitric acid.—But if the surface of the
water be exposed to the open air, the substance formed consists of
minute brilliant pearly scales, which with the aid of a powerful
microscope are seen to be thin equilateral triangular tables, often
grouped into hexaedral tables, or worn at the edges into the form of
rosettes. This substance, which has a pale grayish hue when dried, I
have ascertained to be a carbonate of lead, consisting of two
equivalents of neutral carbonate and one of hydrated protoxide.[1234]
The formation of carbonate takes place with considerable rapidity. In
twelve ounces of distilled water, contained in a shallow glass basin
loosely covered to exclude the dust, twelve brightly polished lead rods
weighing 340 grains, will lose two grains and a half in eight days; and
the lead will then show evident marks of corrosion. The process of
corrosion goes on so long as atmospheric air is allowed to play freely
on the surface of the water. In twenty months I have obtained 120 grains
from an ounce of lead rods kept in 24 ounces of distilled water.

During these changes, a minute quantity of lead is dissolved. This is
best proved by carefully filtering the water, then acidulating with a
drop or two of nitric acid, and evaporating to dryness. I have never
failed to detect lead in the residue by expelling the excess of nitric
acid by heat, dissolving it in distilled water, and applying
hydrosulphuric acid, hydriodate of potass, and chromate of potass to the
solution. The lead is first dissolved in the form of hydrated oxide.
For, if the air admitted to the water be deprived of carbonic acid, a
clear liquid is obtained by filtration, and this is turned brown by
hydrosulphuric acid. But a great part of the hydrate is speedily
separated in the form of carbonate. For the filtered liquid speedily
becomes turbid if exposed to the air; and on evaporating it, the
residuum dissolves in weak nitric acid with brisk effervescence. Captain
Yorke estimates the quantity dissolved when the water is saturated at a
10,000th part.[1235]

By far the greatest part of the lead, however, which disappears, will be
found in the white pearly crystals. This crystalline powder is not,—as
alleged by Guyton-Morveau, and after him by some systematic writers, a
hydrated oxide of lead, but, as stated above, a particular variety of
carbonate, containing more hydrated oxide than exists in common white
lead. At first I thought it was neutral carbonate. Captain Yorke was led
to suppose it hydrated oxide. In 1842 I found that, if it be exposed for
some time to the action of aërated water after the lead has been
removed, it invariably consists of two equivalents of neutral carbonate
and one of hydrated oxide.

It will be inferred from the preceding facts, that distilled water for
economical use should never be preserved in leaden vessels or otherwise
in contact with lead. Even the distilled water of aromatic plants should
not be so preserved, because the essential oil which communicates to
them their fragrance does not take away the power which pure distilled
water possesses of acting on lead. This fact was first announced in the
second edition of the present work. A druggist in Edinburgh requested me
to examine a reddish-gray crystalline, pearly sediment formed copiously
in a sample of orange-flower water. I found this to be carbonate of lead
coloured by the colouring matter of the water, and obviously produced by
the action of the water on lead solder used instead of tin solder, and
coarsely and liberally applied to the seams of the copper vessel in
which the water had been imported from France. The filtered fluid did
not contain a particle of lead. The same observation has been since made
by a French pharmaceutic chemist, M. Barateau, who seems at a loss,
however, to account for the formation of the carbonate of lead.[1236] It
appears from an inquiry of MM. Labarraque and Pelletier, conducted at
the request of the Prefecture of Paris, that the orange-flower water,
which is extensively used there, is often adulterated with lead in
solution. They impute this to careless distillation; for then some of
the decoction is driven over with the distilled liquid, and consequently
produces a fluid which becomes acetous by keeping and dissolves the lead
solder of the _estagnons_ or copper vessels. Pure orange-flower water
does not acidify by keeping.[1237] M. Chevallier in a more recent
investigation arrived at the same results, and found that few specimens
of the orange-flower water of Paris were altogether free of lead.[1238]
In none of these inquiries have the authors adverted to the action of
pure water in forming carbonate of lead.


         _Of the Action of Solutions of Neutral Salts on Lead._

The property which pure aërated water possesses of corroding lead is
variously affected by foreign ingredients which it may hold in solution.

Of these modifying substances none are more remarkable in their action
than the neutral salts, which all impair the corrosive power of the
water. Important practical consequences flow from that action; for it
involves no less than the possibility of employing lead for most of the
economical purposes to which the ingenuity of man has applied that
useful metal. The first experimentalist who made it an object of
attention was Guyton-Morveau; whose experiments are imperfect and in
some respects erroneous. Having found that distilled water corrodes
lead, he proceeded to inquire why no change of the kind takes place in
some natural waters; and being aware that most spring and river waters
differ from that which has been distilled, chiefly in containing
sulphate of lime and muriate of soda, he tried a solution of each of
these salts, and discovered that the addition of a certain quantity of
either to distilled water takes away from it the power of attacking
lead,—that this preservative power is possessed by so small a proportion
as a 500th part of sulphate of lime in the water,—and that the nitrates
are also probably endowed with the same singular property.[1239] Here
his researches terminated.

Extending Guyton-Morveau’s inquiries to other proportions of the same
salts, and likewise to many other neutral salts, I was led to the
conclusion, that all of them without exception possess the power of
impairing the action of distilled water on lead. At least I found this
power to exist in the case of sulphates, muriates, carbonates,
hydriodates, phosphates, nitrates, acetates, tartrates, and arseniates.

The degree of this preservative power differs much in different salts.
The acetate of soda is but an imperfect preventive when dissolved in the
proportion of a hundredth part of the water: white crystals are formed,
and the lead loses about a fourth of what is lost in distilled water in
the same time. On the contrary, arseniate of soda is a complete
preservative when dissolved in the proportion of a 12,000th; and
phosphate of soda and hydriodate of potass are almost effectual
preservatives in the proportion of a 30,000th part only of the
water.[1240] Muriate of soda and sulphate of lime hold a middle place
between these extremes, and are both of them much more powerful than
Guyton-Morveau imagined: the former preserves in the proportion of a
2000th to the water, the latter in the proportion of nearly a 4000th.
Nitrate of potass is little superior to the acetate of soda: in the
proportion of a hundredth it prevents the action of the water almost
entirely; but if the proportion be diminished to a 160th, the loss
sustained by the lead is fully a third of the loss in distilled water.

When lead has been exposed for a few weeks to a solution of a protecting
salt and has acquired a thin film over its surface, it not only is not
acted on by the solution, but is even also rendered incapable of being
acted on by distilled water.

The preservative power depends on the acid, not on the base of the salt.
The acetate, muriate, arseniate, and phosphate of soda differ
exceedingly in power. On the other hand, the sulphates of soda,
magnesia, and lime, as well as the triple sulphate of alumina and
potass, preserve as nearly as can be determined in the same proportion.

When we attempt to ascertain the relative preserving power of the
neutral salts, it will appear that those whose acid forms with the lead
a soluble salt of lead are the least energetic; while those whose acid
forms an insoluble salt of lead are most energetic. The protecting
powers of acetate of soda, nitrate of potass, muriate of soda, sulphate
of lime, arseniate of soda, and phosphate of soda, are inversely as the
solubility of the acetate, nitrate, muriate, sulphate, arseniate, and
phosphate of lead. The existence of this ratio might naturally lead to
the inference that the protecting power depends simply on the salt in
solution being decomposed, so that there is formed on the surface of the
lead a thin crust consisting of the oxide of the metal in union with the
acid of the decomposed salt, and constituting an insoluble film which is
impermeable to aërated water: for example, that phosphate of soda acts
in the small proportion of a 30,000th part by forming on the surface of
the metal an impermeable film of phosphate of lead, which is known to be
one of the most insoluble of all the neutral salts. But this is not
altogether a correct statement of the fact.

When the protection afforded is complete, as for example by a 27,000th
of phosphate of soda, a 12,000th of arseniate of soda, or a 4000th of
sulphate of soda, the lead undergoes no change in appearance or in
weight for several hours, or even days. At length the surface becomes
dull, then white, and gradually a uniform film is formed over it. This
film, examined at an early period, is found to consist of carbonate of
lead,—being entirely soluble in diluted acetic acid, although the salts
in solution is a sulphate or phosphate. But after a few weeks the
carbonate is mixed with a salt of lead, containing the acid of a part of
the neutral salt dissolved in the water: if, after five or six weeks’
immersion in a preservative solution of phosphate or sulphate of soda,
the film on the lead be scraped off and immersed in diluted acetic acid,
effervescence and solution take place, but a part of the powder remains
undissolved; and if the protecting salt has been the muriate of soda,
the whole powder is dissolved, but muriatic acid will be found in
solution by its proper test, the nitrate of silver.—In all such
protecting solutions the lead gains weight for some weeks; but at length
it ceases to undergo farther change, and is not acted on even if removed
into distilled water. The crust, when formed thus slowly, adheres with
great firmness. The most careful analysis cannot detect any lead, either
dissolved in the water, or floating in it, or united with the insoluble
matter left on the side of the glass by evaporation. In short, the
preservation of the lead from corrosion, and of the water from
impregnation with lead, is complete.[1241]

When the protection afforded is not quite complete,—for example in
distilled water containing a 4000th of muriate of soda, a 6000th of
sulphate of soda, a 15,000th of arseniate of soda, or a 35,000th of
phosphate of soda,—besides a powdery crust, small crystals, with several
facettes, are sometimes formed on the lead, while, at the same time, a
minute white film will very slowly appear on the bottom of the glass, on
its side where it is left dry by the evaporation of the water, and
likewise on the surface of the water itself. These detached films are
composed of carbonate of lead, with a little of the muriate, sulphate,
arseniate, or phosphate of lead, according to the nature of the acid in
the alkaline salt which is dissolved in the water. In the course of the
changes now described, the lead in general no longer gains, but loses
weight. The loss, however, is exceedingly small.—No lead can be
discovered in solution, if the water before evaporation is carefully
filtered.

On progressively trying solutions of weaker and weaker preservative
power, it will be remarked, that the quantity of the detached powder,
and the proportion of carbonate in it, progressively increase; and
likewise, that what is formed on the lead adheres more and more loosely.
In distilled water and weak solutions of acetate of soda, or nitrate of
potass, the lead never becomes so firmly encrusted, but that gentle
agitation of the water will shake off the powder.

It is worthy of notice that, although a small quantity of lead is
dissolved by distilled water after it has remained some time in contact
with the metal, yet not a trace is found in solution where a protecting
salt is present. In solutions even weakly preservative I never could
detect any lead dissolved. Thus, in distilled water containing a 4000th
of muriate of soda, or a 160th of nitre, the lead lost weight, and loose
crystals of carbonate were formed; yet even after thirty days no lead
could be found in solution by the process with which I have always
detected it in pure distilled water. Free exposure to the air is
probably in part the cause of this. For it will be seen afterwards that
some natural waters in passing through a long course of lead pipes,
within which the action goes on without direct access of the atmosphere,
contract an impregnation, which is invisible when the water is newly
drawn, but after a few hours’ exposure to the air shows itself in the
form of a white film and milkiness.

The general result of these experiments appears to be, that neutral
salts in various, and for the most part minute, proportions, retard or
prevent the corrosive action of water on lead,—allowing the carbonate to
deposit itself slowly, and to adhere with such firmness to the lead as
not to be afterwards removable by moderate agitation, adding
subsequently to this crust other insoluble salts of lead, the acids of
which are derived from the neutral salts in solution,—and thus at length
forming a permanent impermeable skreen, through which the action of the
water cannot any longer be carried on.

An important subject of inquiry regards the natural causes by which the
preservative power of the neutral salts is impaired. This topic I have
not hitherto been able to examine with all the care which is desirable.

From the effect of the water of Edinburgh when highly charged with
carbonic acid, I was led to infer in former editions of this work that
an unusual quantity of carbonic acid is a counteracting agent. For if
Edinburgh water charged with it be corked up with some lead rods in a
phial half-filled with water, and half with atmospheric air, the lead,
which in common Edinburgh water, as will presently be mentioned, hardly
loses any of its brilliancy for six or seven days, becomes quite white
in twelve or sixteen hours. Subsequent experiments by Captain Yorke
seemed to him to render this conclusion doubtful; nor do I attach much
consequence to the observation just quoted. On the other hand it is said
Professor Daniell has found all waters dissolve lead, if they contain an
excess of carbonic acid.[1242] The point would be best settled by the
effect of a natural carbonated water passing through a long lead pipe.


               _On the Action of Natural Waters on Lead._

The preceding observations on the action of water on lead may be
resorted to for explaining many interesting facts, and correcting some
erroneous statements, which have been published by authors as to the
corrosion of lead by natural processes.

_Rain and Snow-Water._—It has been stated by Dr. Lambe that rain-water
does not corrode lead, that “its effect is so slight as not to be
discernible within a moderate compass of time.”[1243] But this
observation is far from being correct. Rain or snow-water, collected in
the country at a distance from houses, and before it touches the earth,
being nearly as pure as distilled water, ought to act with equal
rapidity on lead. I have accordingly found by a comparative experiment
with that mentioned in p. 401, that in twelve ounces of snow-water,
collected ten miles west from Edinburgh, and at some distance from any
house, twelve lead rods weighing 340 grains lost two grains in eight
days, and the usual crystals began to form in less than an hour. But
when collected in a great city, rain or snow-water is much impaired in
activity. Thus in an experiment made with eaves’-droppings collected
from the roof of my house in Edinburgh, after half an hour of gentle
rain from the south-east,—the first rain which had fallen for several
weeks,—there was no action at all. Yet even when collected in a great
city, and in circumstances which at first sight would appear not very
favourable to its action,—for example from eaves’-droppings a few hours
after the beginning of a shower,—it retains a little of its corroding
property; and when collected in like manner after twelve or twenty-four
hours’ rain, it corrodes almost as rapidly as distilled water. Thus with
four ounces of eaves’-droppings collected after the shower last alluded
to had continued four hours, the crystalline powder began to cover the
bottom of the glass in five hours, and in nine days three lead rods
weighing fifty-seven grains lost a fifth of a grain. And in another
experiment made with eaves’-droppings after a day’s steady rain from the
north-east, the powder began to form in half an hour, and the loss
sustained by the lead in thirty-three days was a grain and a third,
being very nearly what is lost in distilled water during the same time.

We must obviously be prepared to look for an explanation of these
differences in the relative purity of the different waters. Accordingly,
in the eaves’-droppings at the beginning of the shower the nitrates of
baryta and silver caused, the former a distinct, the latter a faint
precipitation, which, as oxalate of ammonia had no effect, arose from
the presence of alkaline sulphates and muriates: but after a four hours’
shower nitrate of baryta alone acted, and caused merely a faint haze:
and after a twenty-four hours’ shower, as well as in snow-water from the
country, none of the three tests had any effect whatever.

Hence, perhaps even in a town, but at all events certainly in the
country, it would be wrong to use for culinary purposes rain or
snow-water which has run from lead roofs or spouts recently erected.
When the roof or spout has been exposed for some time to the weather the
danger is of course much lessened, if not entirely removed; because
exposure to the weather encrusts it with a firmly adhering coat of
carbonate, through which, as already observed, even distilled water will
not act. But I believe it would be right to condemn the turning even old
leaden roofs to the purpose of collecting water for the kitchen.
Although the purest rain-water cannot act on them when it is once fairly
at repose, we do not know what may be the effect of the impetus of the
falling rain on the crust of carbonate; and if the crust should happen
to be thus worn considerably, or detached by more obvious accidents, the
corrosion would then go on with rapidity as long as the shower lasted.
Acid emanations too disengaged in the neighbourhood, and other more
obscure causes may enable rain-water actually to dissolve even the crust
of carbonate.

These remarks on the effect of rain-water on lead are pointedly
illustrated by what Tronchin has recorded of the circumstances connected
with the spreading of the lead colic at Amsterdam, about the time he
wrote his valuable essay on that disease. Till that period lead colic
was seldom met with in the Dutch capital. But soon after the citizens
began to substitute lead for tiles on the roofs of their
dwelling-houses, the disease broke out with violence and committed great
ravages. Tronchin very properly ascribed its increase to lead entering
the body insidiously along with the water, which for culinary purposes
was chiefly collected from the roofs during rain. He farther attempts to
account for the rain-water having acquired the power of corroding the
lead, by supposing that it was rendered acid in consequence of the roofs
having been covered with decaying leaves from trees which abounded in
the city; and without a doubt this explanation accords with the season
at which the lead colic was observed to be most frequent,—namely, the
autumn. But he does not seem to have been aware that rain-water itself
possesses the corroding property, independently of any extrinsic
ingredient except the gases it receives in its passage through the
atmosphere.[1244]—Mérat has referred to a Dutch author, Wanstroostwyk,
for an account of a similar incident which happened at Haarlem.[1245]

The co-operating effect of acid emanations in the atmosphere is well
exemplified by an interesting incident which occurred this year in
Manchester, as detailed in some documents put into my hands by Dr.
Hibbert Ware. A gentleman being seized with symptoms, which in the
opinion of his medical adviser were owing to the insidious introduction
of lead into the body, it was found by Mr. Davies that the rain-water
from a leaden roof, which had been used in the family for nine years,
contained a considerable impregnation of lead. At first this excited
some surprise, because the roof was an old one. But on farther inquiry
it was found, that the rain in descending contracted an impregnation of
hydrochloric acid from the vapours which escaped from an adjoining
manufactory. A portion of the water which was sent to me contained so
much lead dissolved that it became dark-brown on the addition of
hydrosulphuric acid, and a considerable black precipitate was slowly
deposited.

_Spring Water._—Most spring waters, unlike rain or snow-water, have
little or no action on lead, because they generally contain a
considerable proportion of muriates and sulphates.

As an example of a spring water which does not act on lead at all, the
mineral water of Airthrey, near Stirling, may be mentioned. In four
ounces of water from the strongest spring at Airthrey, I kept for
thirty-five days three bright rods of lead weighing 47·007 grains; and
at the end of that period the rods were very nearly as brilliant as when
they were first put in, and weighed 47·004 grains. This result is easily
explained on considering the nature of the water. It contains no less
than a seventy-seventh part of its weight of saline matters, which are
chiefly muriates, and partly sulphates.

Another good illustration occurred to me lately, which contrasts well
with some instances of an opposite description to be mentioned
presently. The house of Phantassie in East-Lothian was supplied with
water by a lead pipe from a distance of a mile. About a year afterwards,
when I had an opportunity of examining into the circumstances, I found
the cistern singularly clean and free of incrustation, and the water
quite free of lead. The composition of the water explained these facts.
It contains a 4,900th of salts, a large proportion of which consists of
carbonates of lime and magnesia.

The water of Edinburgh is another example of spring water nearly
destitute of action on lead. But it is not so completely inactive as the
water of Airthrey. In four ounces of water three bright rods weighing
fifty-seven grains lost in seven days a 250th of a grain, in twenty-one
days a 100th, in thirty-five days a 66th, and in sixty-three days a 59th
of a grain. In seven days the lead was hardly tarnished at all, and not
a speck of powder could be seen in the water, or on the glass. In
twenty-one days, but still more in thirty-five or sixty-three days, the
lead was uniformly dull; and on the surface of the water, as well as on
the bottom of the glass, and on the side where left dry by the
evaporation of the water, there were many white, filmy specks, which
became black with the hydrosulphate of ammonia. In another experiment
145 grains of lead kept for six months in six ounces of Edinburgh water,
which was filled up as it evaporated, lost a fifteenth of a grain; and
the white incrustation on the bottom and sides of the glass gave a large
proportion of black precipitate when scraped together and treated with
hydrosulphate of ammonia. These experiments are of some practical
importance. For they show that the impregnation which the water of
Edinburgh can receive in a few days from being kept in lead is so small
as to be barely perceptible by the nicest analysis; but that the
impregnation may be material if the same portion of water is kept in
lead for a considerable length of time. Hence the perfect safety of the
leaden cisterns and service-pipes used in this city. The same portion of
water rarely remains in them above a single day, and therefore cannot
become impregnated in a degree that is appreciable by the nicest
examination. Dr. Thomson of Glasgow, in an interesting inquiry made in
1815 into the purity of the water which supplies Tunbridge, has stated
that, when he lived in Edinburgh some years before, he could always
detect a minute trace of lead suspended in the water, which at that time
was brought six miles in leaden pipes.[1246] I presume it is owing to
the main pipes being now made of iron that this impregnation no longer
exists. For I have found that the residue of two gallons of water, very
carefully collected by gentle evaporation of successive portions in a
small vessel, did not furnish the slightest trace of lead, when strongly
heated with black flux and then acted on by nitric acid.[1247] The
feeble action of the Edinburgh water on lead arises from the salts it
holds in solution. It contains about a 12,000th part of its weight of
solid matter, of which about two-thirds are carbonate of lime, and
one-third consists of the sulphates and muriates of soda, lime, and
magnesia.

Many instances might be quoted of spring waters which act with
inconvenient or dangerous rapidity on lead. But it is hardly worth while
mentioning more than one or two of these, because the nature of the
waters has been seldom described.

A striking example was related by Dr. Wall of Worcester. A family in
that town, consisting of the parents and twenty-one children, were
constantly liable to stomach and bowel complaints; and eight of the
children and both parents died in consequence. Their house being sold
after their death, the purchaser found it necessary to repair the pump;
because the cylinder and cistern were riddled with holes and as thin as
a sieve. The plumber who renewed it informed Dr. Wall that he had
repaired it several times before, and in particular had done so not four
years before the former occupant died.[1248] The nature of the water was
not determined. Most of the water around Worcester is very hard; but
this will not account for its operation in the instance now described.

Another incident of the same kind, but hardly so unequivocal in its
circumstances, was related in 1823 by Dr. Yeats of Tunbridge. A plumber
undertook to supply that town with water for domestic purposes, and in
1814 laid a course of leaden pipes for a quarter of a mile. In the
subsequent year many cases of lead colic occurred among the inhabitants
who were supplied by those pipes; and one lady particularly, who was a
great water-drinker, lost the use of her limbs for some months. The
inhabitants naturally became alarmed; iron pipes were substituted; and
no case of colic appeared afterwards. Mr. Brande analyzed the water
which had passed through the pipes and detected lead in it, while at the
same time none could be detected at the source.[1249] Some uncertainty
was supposed to have been thrown over these statements by the analytic
researches of Drs. Thomson, Scudamore, and Prout, and Mr.
Children.[1250] But water like that in question can scarce fail to act
powerfully on lead in favourable circumstances; for according to the
analysis of Dr. Thomson it is extremely pure, as it contains only a
38,000th part of saline matter, three-fourths of which are a feebly
protecting salt, the muriate of soda.[1251] I am satisfied, therefore,
from my experiments, and the facts which follow, that no such water
could be safely conveyed through new lead pipes; and that it would be
dangerous even to keep it long in a lead cistern. It is difficult to
account for the failure of the gentlemen above mentioned to find lead in
the water, except by supposing that they had analyzed what had been
exposed for some time to the air, and deposited its oxide of lead in the
form of carbonate.

Since my attention was first turned to this subject, the three following
incidents have occurred to me, which show the danger of conveying very
pure water in long lead pipes. 1. A gentleman in Dumfries-shire resolved
to bring to his house in leaden pipes the water of a fine spring on his
estate, from a distance of three-quarters of a mile. As I happened to
visit him at the time, I took the opportunity of examining the action of
a tumbler of the water on fresh cut lead, and could not remark any
perceptible effect in fourteen days. It appeared to me, therefore, that
the water might be safely conveyed in lead pipes; and they were laid
accordingly. No sooner, however, did the water come into use in the
family, than it was observed to present a general white haze, and the
glass decanters in daily use acquired a manifest white, pearly
incrustation. On examining the cistern, the surface of the water, as
well as that of the cistern itself, where in contact with it, was found
completely white, as if coated with paint; and the water taken directly
from the pipe, though transparent at first, became hazy and white when
heated or left some hours exposed to the air. On afterwards analyzing
the water direct from the spring, I found it of very unusual purity; as
it contained scarcely a 22,000th of solid ingredients, which were
sulphates, muriates, and carbonates. The reader can be at no loss to
perceive why the experiment with a few sticks of lead in a tumbler was
not a correct representation of what was subsequently to go on in the
pipes: in fact, as the pipes were 4000 feet long, and three-fourths of
an inch in diameter, each portion of water may be considered as passing
successively over no less than 784 square feet of lead before being
discharged. The remedy employed in this case will be mentioned presently
[p. 415]. 2. A gentleman in Banffshire introduced a fine spring into his
house from a distance of three-quarters of a mile by means of a lead
pipe. Two years and a half afterwards he was attacked with stomach
complaints, obstinate constipation, and severe colic, for which he was
under medical treatment for three months, with only partial and
temporary relief. At last on leaving home and repairing to Edinburgh, he
soon got quite well. Two other members of his family were similarly, but
more slightly affected. On returning home some time afterwards, the same
symptoms began to show themselves; but he had not been many weeks there,
when his attention was accidentally drawn to a notice of my experiments,
and of the last case, in Chambers’s Journal. He then saw that a white
film lined the inside of the water-bottle in his dressing-room; and the
water was declared by a chemist to contain lead. I lately had an
opportunity of analyzing the water, and found it to contain only a
16,500th of solid matter, the principal salt being chloride of sodium,
and the others being sulphates of magnesia and lime, with very little
carbonate. This, therefore, was exactly a case in which action upon lead
might have been anticipated, as the principal proportion of the very
small quantity of saline matter present was a feebly protective salt. 3.
The third instance occurred at a country residence of Lord Aberdeen. Mr.
Johnston, surgeon at Peterhead, being called to visit the housekeeper,
found her affected with vomiting, constipation, acute pain at the pit of
the stomach, retraction of the navel, and great feebleness. Little
improvement was effected in three days, when Mr. Johnston, astonished at
this, and reflecting on the cause, suddenly was attracted by the
appearance of a silvery film on the inside of his patient’s
water-bottle, and recollected at the same time my narrative of the
Dumfries-shire case. He then perceived that the disease was lead-colic,
treated it accordingly, and slowly accomplished a cure. The
housekeeper’s niece, a young girl who had resided only a few weeks with
her, and who was the only other individual that had lived in the house
above a few days together for more than a year before, had begun also to
suffer from the premonitory symptoms. About twelve months before this
incident happened, a spring of water, which had been analyzed and
pronounced extremely pure, was brought to the house in a lead pipe; and
the housekeeper had used this water for eight months before she took
ill. Mr. Johnston found that the water issued from the pipe was quite
clear, but that a white silvery film formed on its surface under
exposure to the air; and he ascertained that the first-drawn water
contained lead in solution, and that the film was carbonate of lead. I
had an opportunity of analyzing the water, which proved to be by no
means very pure, as it contained a 4460th of solids. But as the solid
matter consisted almost entirely of chlorides, namely, in a great
measure of chloride of sodium and a very little of the chlorides of
magnesium and calcium, as there was no carbonate present, and the
sulphates constituted only a 32,000th of the water,—it is plain from the
principles formerly laid down that the action which took place was to be
anticipated from the nature of the spring.[1252]

For other instances of the corrosive action of spring water on lead the
reader may refer to Dr. Lambe’s treatise. Dr. Lambe was led by his
researches to imagine that no spring water whatever was destitute of
this property in a dangerous degree. This wide conclusion is not
supported by valid facts. Yet his work contains several accurative and
instructive examples of the action in question. Thus among other
instances he mentions that he had found the water of Warwick to act on
lead with great rapidity, and once saw holes and furrows in a cistern
there, which was the second that had been used in the course of ten
years.[1253] Sir G. Baker, in a letter to Dr. Heberden, has related
another striking instance of the same kind. Lord Ashburnham’s house in
Sussex was supplied from some distance with water, which was conveyed in
leaden pipes. The servants being often affected with colic, which had
even proved fatal to some of them, the water was carefully examined, and
found to contain lead. The solvent power of the water was ascribed to
its containing an unusual quantity of carbonic acid gas.[1254] This may
be doubted.

In the course of the preceding remarks, allusion has been made to the
danger of keeping the same portion of water for a length of time in
leaden cisterns, if it has the power of acting on lead even in a
trifling degree. The following illustrations deserve particular notice.

It was mentioned in p. 409, as the result of experiments on the small
scale, that although the water of Edinburgh does not contract a sensible
impregnation of lead on remaining a few days in contact with it, yet a
sufficient action ensues in the course of a few months, to show that it
might be dangerous to keep that water long in a lead cistern. After
coming to this conclusion, I had an opportunity of verifying it on a
large scale. A cistern in my laboratory in the University having been
left undisturbed for four or five months with about six inches of water
in it, I found so large a quantity of pearly crystals lying loose on the
cistern and diffused through the water, that when the whole was shaken
up and transferred to a glass vessel, the water appeared quite opaque.
Mérat observes that at the laboratory of the Medical Faculty of Paris
there was procured by evaporating six loads, or probably about 1000
pounds of water, which had been kept two months in a leaden pneumatic
trough, no less than two ounces of finely crystallized carbonate of
lead.[1255] Water in such circumstances has proved eminently poisonous.
Thus, the crew of an East India packet having been put on short
allowance of water, in consequence of being delayed by contrary winds,
the men got their share each in a bottle; but the officers united their
shares and kept it all in a lead cistern. In three weeks all the
officers began to suffer from stomach and bowel complaints, and had the
lead colic for six weeks; while the men continued to enjoy good health.
The surgeon detected lead in a tumbler of water without the process of
concentration, by adding to it the sulphuret of potass.[1256] A similar
accident has been briefly alluded to by Van Swieten. He mentions, that
he was acquainted with a family who were all attacked with colica
pictonum in consequence of using for culinary purposes water collected
in a large leaden cistern and kept there for a long time.[1257] The
composition of the water has not been mentioned in any of these
instances; but the water of Paris is so strongly impregnated with
calcareous salts, that in ordinary circumstances its action on lead must
be trifling.

It was probably from confounding the consequences of keeping the same
water long in a lead cistern with the action in ordinary circumstances,
that Dr. Lambe was led into the error of supposing that all spring
waters whatever act on lead so powerfully, as to render it in his
opinion advisable to abandon the use of this metal in the fabrication of
pipes and cisterns. It must be admitted, however, that in all likelihood
many waters will contain a trace of lead, without being kept more than
the usual time in the pipe or cistern. For Dr. Lambe’s results
correspond to a certain extent with the more recent and accurate
researches of Dr. Thomson, who mentions many instances where a faint
trace of lead was found in the residue of the evaporation of a large
quantity of spring water by himself, as well as by Dr. Dalton, Dr.
Wollaston, and Mr. Children.[1258] But, as Dr. Thomson properly adds,
when the quantity does not exceed a 600,000th or a millionth part of the
water, as in these instances, it is ridiculous to imagine that any harm
can result to man from the constant use of it for domestic purposes.

Another fact of some practical consequence, which flows from the
experimental conclusions stated above is, that although it may be
perfectly safe to keep some waters in leaden cisterns, it may be very
unsafe to use covers of this metal, because the water which condenses on
the covers must be considered as pure as distilled water. It has been
found that white lead forms in much larger quantity on the inside of the
covers of cisterns than on the cisterns themselves, where both are
constructed of lead. A remarkable illustration of this is mentioned in a
paper read before the Academy of Sciences at Paris in 1788 by the Comte
de Milly. About a year after getting two leaden cisterns erected in his
house, to keep the water of the Seine for general domestic purposes, he
was attacked with severe and obstinate colic; which led him to examine
his cisterns. He found that the sides, where they were occasionally left
exposed by the subsidence of the water, and more especially the leaden
cover, were lined with a white liquid, which was constantly dropping
from the lid into the cistern, like the drops in caverns where
stalactites are formed. The water was in consequence so strongly
impregnated with lead as to give a dark precipitate with liver of
sulphur.[1259] The reason of this occurrence is, that the water in the
cistern is a solution of preventive salts, but what reaches the lid is
in a manner distilled. In Edinburgh the lids of the cisterns are
invariably made of wood, whether on account of its superior cheapness
merely, or because a leaden cover had been found perishable, I have not
been able to discover.

It may be well to conclude these remarks on the action of spring waters
on lead with a general summary of the chief circumstances to be adverted
to in using lead for keeping or conveying water; to which may be added a
few hints for preventing action where it is found to have taken place.

The general results of the preceding inquiries are that rain or
snow-water for culinary use should not be collected from leaden roofs,
nor preserved nor conveyed in lead;—that the same rule applies to spring
waters of unusual purity, where for example the saline impregnation does
not exceed a 15,000th of the water;—that spring water which contains a
10,000th or 12,000th of salts may be safely conveyed in lead pipes, if
the salts in the water be chiefly carbonates and sulphates;—that lead
pipes cannot be safely used, even where the water contains a 4000th of
saline matter, if this consist chiefly of muriates;—that spring water,
even though it contain a large proportion of salts, should not be kept
for a long period in contact with lead;—and that cisterns should not be
covered with lids of this metal.

Where action is observed to take place in the instance of particular
waters, it may in some cases be impossible to prevent it by any
attainable means. But the inquiries detailed above suggest two modes by
which a remedy may be generally found. It appears that, where a crust of
carbonate is allowed to form slowly and quietly on the surface of lead,
even distilled water ceases to have any material action; and that the
action is reduced almost to nothing if a crust be thus formed in a
solution containing a minute quantity of some powerfully protecting
salt, such as phosphate of soda. It appears to me then that a remedy may
be often found in the instance of unusually pure spring waters—either by
leaving the new pipes filled with the water for a few months, care being
taken not draw any water from them in the interval,—or perhaps even more
effectually by filling the pipes for a similar period with a solution
containing about a 25,000th of phosphate of soda. I had determined to
try the latter plan with the pipes in the Dumfries-shire case mentioned
above, but recommended that in the first instance the pipes should be
left for a few months full of the water of the spring, and the
stop-cocks kept carefully shut; and on this being done for three or four
months, it was found that the water afterwards passed with scarcely any
impregnation of lead, and what little was contracted at first gradually
diminished in the course of time.—Probably neither of these methods will
be of more than temporary use, when the chief or only salt present is
chloride of sodium, even though the proportion be considerable. Both
plans seemed to answer for a time in the instance which occurred at Lord
Aberdeen’s (p. 411); but after a while the action recommenced, probably
owing to the deposited carbonate being slowly dissolved. At the time of
publication of my paper in the Transactions of the Royal Society of
Edinburgh, the cure appeared complete, and was there represented to be
so.

I should add that an effectual remedy has been lately introduced by a
patent invention for covering lead pipes both externally and internally
with a thin coating of tin.

In the remarks now made on the action of water on lead no account has
been taken of the effect of the galvanic fluid in promoting it. This,
however, is a most important co-operating agent, or rather perhaps it
ought to be considered a distinct power; for it acts with energy where
water alone acts least, namely, when there is saline matter in solution,
because then a galvanic current of greater force is excited. In general
it is necessary that two different metals be present in the water before
galvanic action be excited; but a very slight difference may be
sufficient. For example, it seems enough that the lead contain here and
there impurities, constituting alloys slightly different from the
general mass of the pipe or cistern. It is probable that galvanic action
may be thus excited by the joinings being soldered with the usual
mixture of lead and the more fusible metals. At least I have seen pipes
deeply corroded externally, when made of sheets of lead rolled and
soldered; and the action was deepest on each side of the solder, which
had itself entirely escaped corrosion. Even inequalities in the
composition of the lead may have the same effect. Sheet lead long
exposed to air or water is sometimes observed to be corroded in
particular spots; and these will always be found in the neighbourhood of
parts of the metal differing in colour, hardness or texture from the
general mass. I have not analyzed such spots; but I conceive the
supposition now made is exceedingly probable, and supplies a ready
explanation of the corrosion. Similar effects may arise simply from
fragments of other metals lying long in contact with the lead. They may
also arise from portions of mortar being allowed to lie on the lead; but
the action here is not galvanic.

I have no doubt that many of the instances of unusually rapid corrosion
of lead by water, such as that mentioned by Dr. Wall [p. 410] are really
owing, not to the simple action of water, but to an action excited
obscurely in one or other of the ways now mentioned.


       _Of the Action of Acidulous Fluids on Lead and its Oxide._

Water acidulated with various acids acts on lead with different degrees
of rapidity.

The effect of acidulation with _carbonic acid_ has not yet been
accurately ascertained. The effect of _sulphuric acid_ is peculiar.
Distilled water feebly acidulated with that acid acts much less rapidly
on lead than when quite pure. Thus I have found that, if it contained a
4000th or even only a 7000th of sulphuric acid, fifty grains of lead
kept in it for thirty-two days gained a seventh or a twelfth of a grain
in weight, and were covered with beautiful crystals of sulphate of lead.
A minute trace of lead could be detected in the water. _Hydrochloric
acid_ is somewhat more active as a solvent. Distilled water containing a
3000th of that acid acquired in thirty-two days a sweetish taste, and
yielded by evaporation a considerable quantity of muriate of lead, while
the lead rods lost weight, and were covered with acicular crystals of
the same salt.

It is much more important, however, to consider the effects of the
vegetable acids on lead and its oxide, because their solvent power is a
fruitful source of the accidental as well as intentional adulteration of
many articles of food and drink.

_Acetic acid_ in the form of common vinegar, even when much diluted,
attacks and dissolves metallic lead, if by exposing the surface of the
fluid to the air, a constant supply of oxygen be maintained to produce
oxidation. The _citric acid_ will attack it under the same
circumstances, but acts more slowly. In a solution of five grains of
citric acid in twenty-four parts or two drachms of water, three lead
rods lost two grains in weight in nine weeks. The greater part of the
citrate of lead separated slowly in white powdery crystals; but a small
portion was dissolved by the excess of acid, and imparted to the fluid a
pleasant sweetness. _Tartaric acid_ acts much less energetically. In a
comparative experiment with the last, the lead gained nearly half a
grain in weight by acquiring a crystalline coat of tartrate of lead. But
I could not detect any lead in solution; and there was no loose powder.
The tartrate of lead is very sparingly soluble in an excess of its acid,
so that a sweet taste cannot be communicated by it to a fluid acidulated
with tartaric acid. _Malic acid_, according to MM. Chevallier and
Ollivier, acts so quickly as a solvent, that if a solution be kept in a
lead vessel for three hours, the metal may be detected in the fluid by
any of its ordinary tests.[1260]

The acids act with greater rapidity on the protoxide of lead than on the
metal; and the presence of air is of course not required to enable them
to effect its solution.

The solvent power of the acids is liable to be counteracted by various
substances; the operation of which, however, has not been well
ascertained. It appears that substances containing gallic acid or tannin
throw down the lead; and on this account various adulterations which
would otherwise take place are either prevented or corrected. It has
been also ascertained by Proust, that the vegetable acids do not attack
lead when it is alloyed with tin. For as the latter metal has a stronger
attraction than the former for acids, no lead can be oxidated before the
tin undergoes that change.[1261]

From what has been said of the action of the vegetable acids, it follows
that the preparation or preservation of articles of food and drink in
leaden vessels is fraught with danger. For, if they contain a vegetable
acid, more particularly the acetic, as many of them do, and if they are
allowed to remain in the vessel for a moderate length of time, they will
be apt to be impregnated with the metal. In this way lead has been often
insidiously introduced into the food of man.

Thus milk has been poisoned by being kept in leaden troughs. An instance
of the kind has been related by Dr. Darwin. A farmer’s daughter used to
wipe the cream from the edge of the milk which was kept in leaden
cisterns, and being fond of cream, had a habit of licking it from her
finger. She was seized in consequence with the symptoms of lead colic,
afterwards with paralytic weakness of the hands, and she died of general
exhaustion.[1262] The circumstances under which the lead is acted on
have not been carefully examined. It appears to be sometimes used with
safety. It will of course be dissolved, if the milk should become sour.

Rum has been also supposed to be sometimes adulterated with lead by
being left in contact with the metal. The dry belly-ache of the West
Indies, which appears to be the same disease with the lead colic, has
been ascribed by some to the same cause. But on this subject precise
information is still wanted. Dr. J. Hunter has stated, that an epidemic
colic, which attacked three of our regiments in Jamaica during the years
1781 and 1782, and which seized almost every man of them, was traced by
him to the presence of lead in the rum; and he endeavours to show that
the spirit might dissolve the lead in passing through the leaden worms
of the distilling apparatus.[1263] He adds in another work, that,
according to information communicated by Dr. Franklin, the legislature
of Massachusetts passed an act in 1723, prohibiting the use of leaden
still-heads and worms in the distillation of spirituous liquors.[1264]
It is certain that rum has been often impregnated with lead; but it is
by no means clear that Dr. Hunter has successfully accounted for the
mode in which the adulteration is effected.

Wine has been accidentally impregnated in like manner, in consequence of
the bottles having been rinsed with shot, and some of the shot left
behind. An interesting example of this has been related in the
Philosophical Magazine. Severe abdominal symptoms were caused by a
bottle of wine; and the cause was discovered to be the action of the
wine on some shot in the bottom of the bottle. The shot had been so
completely dissolved, that it crumbled when squeezed between the
fingers.[1265] The illness in this instance must have been owing to the
arsenic contained in the shot, because the quantity of lead was hardly
sufficient to excite violent symptoms.—At one time home-made British
wines must have been frequently adulterated with lead, from the makers
being ignorant of the dangerous nature of the adulteration. Sir G. Baker
quotes the following receipt in a popular cookery book of his time: “_To
hinder wine from turning._—Put a pound of melted lead in fair water into
your cask, pretty warm, and stop it close.”[1266]

But by far the most remarkable adulteration of the kind now under review
is that of cider. At one time a disease in every respect the same as the
lead colic used to prevail in some of the south-west counties of England
at the cider season; and it was generally ascribed, in consequence
apparently of the opinion of Huxham, to the working people indulging too
freely in their favourite beverage during the season of plenty. The
subject, however, was carefully investigated in 1767 by Sir George
Baker, who succeeded in proving, that the disease arose from the cider
being impregnated with lead, sometimes designedly for the purpose of
correcting its acescency when spoiled, but chiefly by accident, in
consequence of the metal being used for various purposes in the
construction of the cider-house apparatus. The substance of his
researches is,—that a disease in all respects the same with the lead
colic was in his time so prevalent in Devonshire as to have supplied 289
cases to the Exeter Hospital in five years, and 80 to the Bath Infirmary
in a single season (1766); while, on the contrary, it was little, if at
all, known in the adjoining counties of Gloucester, Worcester, and
Hereford, although cider is there an equally common drink among all
ranks:—that in the latter counties lead was seldom or never used in
constructing the apparatus of the cider-houses, while in Devonshire it
was used sometimes for lining the presses, but more commonly for
fastening the iron cramps, and filling up the stone joinings of the
grinding troughs, and for conveying the liquor from vessel to
vessel:—that lead did not exist in the cider of Herefordshire, but might
be detected both in the ripe cider, and more especially in the must, of
Devonshire:—that from eighteen bottles of cider, a year in bottle, 4½
grains of metallic lead were procured.[1267] The accuracy of these
facts, and the soundness of the conclusions which Sir George Baker drew
from them have been universally admitted; and lead is now, I believe,
completely excluded from the cider apparatus.

Notwithstanding the notoriety of these facts, accidents from adulterated
cider seem still to occur occasionally in France. So recently as 1841 a
set of cases which presented the incipient symptoms of lead colic were
traced by MM. Chevallier and Ollivier to cider having been adulterated
with lead to the amount of nearly two grains and a half per quart, in
consequence of a publican having kept his cider for two days in a vessel
lined with lead.[1268]

If lead is previously oxidated, the presence of vegetable acids in
articles kept in contact with it is still more likely to give rise to a
poisonous impregnation, than in the case of lead itself.

Of accidental adulterations of this kind the most important is that
which arises from the action of vegetable acids on the glazing of
earthenware. This glaze is well known to contain generally a
considerable quantity of oxide of lead, and in consequence is more or
less easily dissolved by vegetable acids. A good example has been
noticed by Dr. Beck.[1269] A family in Massachusetts, consisting of
eight persons, were all seized with spasmodic colic, obstinate
costiveness, and vomiting; and the disease was satisfactorily traced to
a store of stewed apples, which had been kept some months in an
earthenware vessel and had corroded the lead glazing. Another
interesting example has been described by Dr. Hohnbaum of
Hildburghausen. A family of five persons were all violently affected for
a long time with spasmodic colic, and some with partial palsy. After
examining many articles of food, Dr. Hohnbaum at last found that the
vinegar for dressing their salads was kept in a large earthenware vessel
capable of holding eight or ten quarts, and glazed with lead; that an
ounce of vinegar remaining in the vessel contained no less than nine
grains of lead; and that the whole glazing of the vessel was completely
dissolved.[1270] Accidents like this appear from the statements of the
same author to have been common in Germany not long ago. Luzuriaga
attributes the great prevalence of colic in Madrid and the neighbourhood
to the general use in the kitchen of earthenware glazed with lead.[1271]
Jacob imputes it to the same cause.[1272] But others have doubted the
accuracy of this explanation.

The effect of acids on lead glazing appears to be variable. Sometimes
they hardly act on it at all.[1273] The difference probably depends on
differences in the composition of the glaze. Gmelin says, that if there
is little oxide of lead present, acids and fat do not corrode it; but
that potters often use too much, to render the glaze more fusible; and
that then it is easily corroded.[1274] Westrumb states, that, if the
lead glaze is thoroughly vitrified and not cracked, the strongest acids
do not attack it.[1275] Farther experiments are still required to
elucidate this subject.

It is not, however, by accident only that the food or drink of man is
subject to be poisoned with lead. Many articles are adulterated with it
designedly for a variety of purposes. These adulterations it is
necessary for the medical jurist to study.

No kind of adulteration with lead is more common than that of wine;
which, when too acid and harsh from the first, or rendered acescent by
decay, may be materially improved in taste by the addition of litharge.

The practice of correcting unsound wines in this way seems to have been
well known at an early period. Betwixt the years 1498 and 1577, various
decrees were passed against it by the German emperors; and in some
provinces the crime was even punished capitally.[1276] For some time
afterwards the dangerous effects of the practice appear to have been
lost sight of in Germany. But towards the close of the seventeenth
century, the attention of physicians and legislators in that country was
pointedly directed to the subject by various writers in the _Acta
Germanica_.[1277] The same practice has been long prevalent in France.
The famous endemic colic of Poitou, which appeared in 1572, and raged
for sixty or seventy years, has been with justice ascribed in modern
times to the adulteration of wine with lead, and has given to the lead
colic its scientific name of _colica pictonum_. More recently, the
practice became exceedingly prevalent in Paris. About the year 1750, the
farmers-general found that for some years before that, 30,000 hogsheads
of sour wine were annually brought into Paris for the alleged purpose of
making vinegar, while the previous yearly imports did not exceed 1200.
An inquiry was accordingly set on foot; which led to the discovery, that
the vinegar merchants corrected the sour wines with litharge, and thus
made them marketable.[1278] Notwithstanding the active system of medical
police in the French capital, the crime is not yet eradicated. Indeed
the small tart wines used so abundantly there by all ranks, hold out
great encouragement and facilities to its perpetration.

The process employed for correcting the acescency of wine is not
precisely known. Some wines are easily corrected; Mérat found that a
bottle of harsh wine, which had a sharp, bitterish, rather acrid taste,
took up in forty-eight hours twelve grains of litharge, and became
palatable.[1279] With other wines this simple method will not answer,
because the colour is destroyed, and a taste is substituted which has no
resemblance to that of the genuine wine. Thus Orfila remarked, that
Burgundy, neutralized with litharge, acquired a saccharine taste and
became pale-red, because the insoluble salts of lead which were formed,
combined with and removed the colouring matter.[1280] On the whole, it
is probable that the adulteration of wine with lead can only be
practised with success on the common tart kinds, such as those used by
the lower orders on the continent.

Some excellent observations have been published on this subject by
Fourcroy. In order to render what he has said intelligible, it is
necessary to premise, that in the course of the fermentation of wine,
the bitartrate of potass, which accelerates the conversion of the sugar
of the fruit into alcohol, is itself partly converted into malic acid;
that in sound wine, therefore, there is a mixture of tartaric and malic
acids; but that if the malic acid originally existed in the fruit in too
great abundance, the fermentation of the sugar is imperfect, and the
wine is consequently both too acid and too weak; and lastly, that all
wines, if neglected, are apt to ferment too much, in consequence of
which they pass the vinous stage of fermentation, and become impregnated
with acetic acid.[1281]

Now Fourcroy found that the oxide and other preparations of lead correct
acescency and harshness in wines, not so much by throwing down the
acids, as by combining with them in solution, and imparting to the
liquor the peculiar sweetness of lead. Hence tart wines, which owe their
acidity to too great a proportion of tartaric acid or bitartrate of
potass, cannot be improved by adulteration with oxide of lead. For the
bitartrate of potass cannot act at all as a solvent on the oxides or
carbonate of lead, and even pure tartaric acid takes up so little, that
wine containing it, could not acquire the sweet taste which is the
purpose of the adulteration. This statement I have confirmed. But the
case is very different when the wine contains acetic acid, the presence
of which is the general cause of spoiling or acidity. For Fourcroy
remarked, that acetic acid dissolves not only oxide and carbonate of
lead, but likewise the tartrate, notwithstanding its great insolubility
in water or in its own acid. Hence the presence of tartaric acid in a
wine spoiled by co-existence of the acetic, will not prevent the liquor
from taking up oxide of lead in sufficient quantity to acquire an
improved taste and flavour. Nay, an obvious mode of correcting excessive
acidity, produced by too much tartaric acid, is to add tartaric acid,
and then to treat the mixture with oxide of lead. Fourcroy farther
thinks, that the malic acid possesses the same solvent power as the
acetic over tartrate of lead, and that its presence may therefore be the
reason why some tart wines, which do not contain the acetic acid, become
nevertheless impregnated with the poison. The solvent power of acetic
acid is increased by the presence of other vegetable principles in the
wine.[1282] I may add, that I have found the citric acid to possess the
same property with the acetic and malic acids. It dissolves so much of
the tartrate of lead as to acquire a pleasant sweetness, unmixed with
metallic astringency.

The practice of adulterating wine with lead does not seem to have been
ever pursued to any material extent in Britain. Home-made wines may be
adulterated in this way, as may be inferred from the receipt formerly
quoted for preventing acescency. But I have never heard that any such
adulteration has been suspected in the foreign wines usually drunk in
this country. Considering, indeed, the nature of these wines, and the
class of people who alone make use of them, it is not likely that
adulteration with lead could be practised with success. If the foreign
wines used in Britain should become acescent, lead could hardly restore
their taste so thoroughly as to impose on the consumer.

Sometimes spirituous liquors and preserves have been adulterated with
lead, in consequence of sugar of lead having been used to clarify them,
or to render them colourless. Cadet de Gassicourt says it is a common
practice in France to clarify honey and sugar of grapes, and to make
brandy pale in this way; and M. Boudet has detected lead in many samples
of these articles in Paris.[1283] Hollands has likewise been poisoned in
the same manner. Dr. Shearman mentions his having detected an extensive
adulteration of smuggled Geneva by an excise officer, which had been
sold and dispersed over an extensive tract of country, and which
committed great ravages among the inhabitants.[1284]

The adulterations hitherto noticed take place through means of the
chemical action of the adulterated articles on lead or its oxide. Some
other substances are occasionally contaminated by its compounds being
merely mechanically mixed with them. There is no end to the number and
variety of adulterations of this kind. But the following will serve as
examples. Gaubius once detected an adulteration of butter with white
lead at a time when it was very scarce in Flanders, owing to a dreadful
mortality among cattle.[1285] An instance of poisoning with lead, in
consequence of cheese having been mixed with red lead, is mentioned in
the Repertory of Arts.[1286] This variety deserves to be remembered. Red
lead was at one time a good deal used to communicate the peculiar
reddish-yellow colour, which is supposed to characterize the finer
qualities of certain kinds of English cheese. In the Transactions of the
Medical Society of London, a singular instance has been related by Mr.
Deering, of lead colic attacking a whole family, and proving fatal to
two of them, in consequence of the insidious introduction of white lead
into the body. Although the nature of the symptoms in the several cases
left no doubt that lead was the cause of them, it was long before the
source of the poison was discovered. Every vessel and article used in
the kitchen was in vain examined; when at length it was discovered that
the sugar used by the family had been taken from a barrel which had
formerly contained white lead, and that, as the sugar from the centre of
the barrel had been dug out, and given away to various friends, the
outer part of it next the white lead was chiefly used by the family
themselves.[1287]


           _Process for detecting Lead in Organic Mixtures._

In the first place, a little nitric acid should be added to the
suspected matter before filtration; for nitric acid redissolves any
insoluble compound formed by the salts of lead with albumen and other
animal principles, as well as some of those formed with vegetable
principles; and consequently renders it more probable, that the poison
will be detected in the first part of the analysis, if present at
all.[1288] This being done, sulphuretted-hydrogen gas is to be
transmitted through the fluid part of the mixture; and if a
dark-coloured precipitate is formed, the whole is to be boiled and
filtered to collect the precipitate.

In order to ascertain that the precipitate positively contains lead,
those who are accustomed to use the blowpipe may put the sulphuret into
a little hole in a bit of charcoal, and reduce it by the fine point of a
blowpipe-flame; when a single globule is procured, which is easily
distinguished by its lustre and softness. A better process, for those
not accustomed to the blowpipe, and perhaps a better test of the
existence of lead in all circumstances, is to heat the sulphuret to
redness in a tube, and to treat it with strong nitric acid, without heat
or with the aid of a gentle heat only. The lead is thus dissolved
without the sulphur being acted on. The solution is then to be diluted
with water, filtered, evaporated to dryness, and gently heated to expel
the excess of nitric acid. If the residue be dissolved in water, it will
present the usual characters of a lead solution when subjected to the
proper liquid tests. Of these the hydriodate of potass is to be
preferred when the quantity is too small for trying more of them. But
for this purpose care must be taken to expel all the excess of nitric
acid, because an excess will strike a yellow colour with the test though
lead be not present.

If the preceding process should not detect lead in the filtered part of
the mixed fluid, then the insoluble matter left on the filter is to be
incinerated, and the residuum dissolved in nitric acid, and tested as
above. This branch, however, will be rarely required, if lead be
present, because the precaution of adding nitric acid, previous to
filtration, dissolves the lead from most of its compounds which are
insoluble in water. The process of incineration in medico-legal analysis
generally should be avoided if possible, as it is not easily managed by
unpractised persons.—The present branch of the process of analysis will
be particularly required for the contents of the stomach or vomited
matter, when any sulphate or phosphate has been given as an antidote.

A process different from the preceding, and analogous to those for
detecting copper and antimony in complex organic mixtures, has lately
been proposed by Professor Orfila, especially for those cases in which
lead is to be sought for in the textures of the body, where death is
supposed to have been occasioned by it. The subject of analysis, such as
the liver, spleen, or kidneys, being cut into small pieces, and boiled
in distilled water, and the filtered decoction being evaporated to
dryness, the extract is to be carbonized with nitric acid as directed
under the head of copper (p. 357); and care must be taken that the heat
be not raised to redness, so as to inflame the mass. The residuum is
then to be boiled with nitric acid; the solution being evaporated to
dryness to expel the excess of acid, the saline matter left is to be
redissolved and acted on by hydrosulphuric acid gas; and the sulphuret
thus formed may be recognized by the means mentioned above.[1289]

A question has been recently started, whether all the processes for
detecting lead in the tissues of the human body are not rendered
fallacious by the alleged existence of lead in the healthy animal
textures. In the first place, however, it is doubtful, as will be seen
presently, whether lead ever exists naturally in the animal organs. But
besides, the fallacy, if a real one, is obviated by the process of
Orfila; who states that lead, naturally combined in the animal tissues,
cannot be indicated by his method, if the animal matter be charred by
nitric acid without deflagration. And farther, in regard to the tissues
of the stomach in cases of acute poisoning with the preparations of
lead, it appears that in most instances there may be seen on the villous
coat little white points, which are blackened by hydrosulphuric acid, a
phenomenon never occasioned by lead naturally contained in the substance
of the membrane. [See p. 439.]


SECTION II.—_Of the Action of Lead and the Symptoms it excites in Man._

The effects of the preparations of lead on the body are very striking.
They differ according to the rapidity with which it enters the system.
Large doses of its soluble salts cause symptoms of irritant poisoning.
The gradual introduction of any of its oxidated preparations in minute
quantities brings on a peculiar and now well-known variety of colic,
which is often followed by partial palsy, and in violent cases by
apoplexy.

The physiological effects and mode of action of the soluble salts in
irritating doses have been examined experimentally by Professor Orfila,
M. Gaspard, Dr. Schloepfer, and Dr. Campbell. Their experiments agree in
showing that these poisons have a direct irritating action, and a remote
operation of an unknown kind; but the results obtained by different
experimentalists differ as to some of the details. The acetate may be
taken as a type of the whole genus.

Orfila found that it was hardly possible to bring dogs under the action
of the acetate if swallowed in solution, because they speedily
discharged it all by vomiting. But if the salt was given in powder in
the dose of half an ounce, or if the solution was retained in the
stomach by a ligature on the gullet, the symptoms produced were those of
violent irritation in the first instance, succeeded by extreme weakness
and death, sometimes in nine hours, more generally not till the second
day or later. The appearances in the body were unnatural whiteness of
the villous coat when death was rapid, and vascular redness when death
was slower. The whiteness in the former case Orfila ascribes to chemical
action. But as neither this appearance nor the redness in the latter
case was considerable, while at the same time the symptoms were not
those of continuous irritation, he was led to doubt whether the poison
causes death in consequence of its irritant properties. And the
phenomena observed by him when acetate of lead was injected into the
jugular vein prove that death is owing to certain remote effects.
Introduced through this channel thirteen grains killed a dog almost
immediately, death being preceded by no other symptom except convulsive
respiration; five grains killed another in five days, and the leading
symptoms were weariness, languor, staggering, and slight convulsions,
none of which symptoms appeared till the third day; and it is remarkable
that in neither animal could he find any morbid appearance on
dissection.[1290] Mr. Blake states that large doses, such as a drachm,
suddenly arrest the heart’s action; but that small doses of three
grains, injected into the jugular vein, cause diminished action of that
organ, and afterwards gorging and hepatization of the lungs; and that
when injected backwards into the aorta from the axillary artery, this
salt occasions obstruction of the capillary circulation, indicated by
increased arterial pressure,—and then an action on the nervous system,
producing insensibility, violent movements of the tail, and at last
arrestment of the respiration. It may be inferred from Mr. Blake’s
researches that lead obstructs both the systemic and pulmonary
capillaries, that it acts powerfully on the nervous centre, and that it
likewise depresses the heart’s action when the dose is large.[1291]

The experiments of Gaspard coincide with those of Orfila in assigning
considerable activity to the acetate of lead when it is directly
introduced into the blood,—the quantity of two or four grains generally
causing death in three or five days.[1292] The experiments of Campbell
farther show that death may be induced by applying it to a wound, and
that the symptoms antecedent to death resemble those remarked by Orfila
when it is injected into a vein.[1293] But the two last experimentalists
differ from Orfila in assigning to sugar of lead a property like that
possessed by arsenic, of acting on the alimentary canal, even when
applied to a wound, or directly introduced into the blood. For Campbell
found the stomach corrugated and red, and the small intestines also
vascular; while Gaspard not only observed analogous appearances after
death, but even also witnessed all the symptoms of violent dysentery
during life. In farther proof of the local irritating power of this
poison, it may be added, that when sugar of lead was injected into the
rectum Campbell found it to cause purging, tenesmus, itching of the
anus, and great debility.

I have found that the nitrate of lead is powerfully irritant and
corrosive in the dose of 400 grains. This quantity dissolved in four
ounces of water killed a strong dog in sixteen hours, producing violent
efforts to vomit and diarrhœa. And after death the whole inner membrane
of the gullet and stomach, and the villi of the upper half of the small
intestines, were uniformly white, brittle, and evidently disintegrated;
and the mucous coat of the great intestines was bright red in parallel
lines.

The only inquiries I have hitherto met with, which assign to lead in
continued small doses the power of producing in animals the peculiar
colic and palsy often produced by it in man are those of Schloepfer,
related in his thesis on the effects of poisons when injected into the
windpipe. He found that the acetate, introduced through this channel in
successive doses of ten grains, brought on all the symptoms of _colica
pictonum_, preceded by oppressed breathing, and ending fatally with
palsy and convulsions in the course of three weeks.[1294] More recently
Dr. Wibmer, in the course of some experiments on the long-continued use
of acetate and carbonate of lead, remarked weakness and stiffness of the
limbs in dogs; and in the rabbit I have observed in the like
circumstances gradually increasing weakness, ending in complete palsy of
the fore-legs.

The compounds of lead seem to produce their effects on the animal body
through the medium of absorption. At all events they are absorbed in the
course of their action, and are diffused throughout the animal textures.
Lead was long sought for with variable and dubious success in the fluids
and solids of men and animals killed by it or labouring under its
effects. But the late improvements in physiological science and chemical
analysis have demonstrated, that it may always be detected in favourable
circumstances in the liver and kidneys, often in the spleen and in the
urine, and sometimes even in the muscles. Wibmer was the first who
satisfactorily proved its presence. In dogs poisoned slowly by the
acetate or carbonate of lead in frequent small doses, and dying with
symptoms of lead-colic and palsy, he found the metal distinctly in the
liver, muscles, and spinal cord, and more obscurely in the blood, by
drying and deflagrating the animal matter with nitre, acting on the
residue with nitric acid, neutralizing the solution, and testing it with
hydrosulphuric acid, carbonate of potash, and iodide of potassium.[1295]
On repeating these experiments, I succeeded in detecting lead in very
minute quantity in the lumbar and dorsal muscles of rabbits, but not any
where else.[1296] Professor Orfila has since frequently found lead, by
means of his method of analysis described at page 424, in the kidneys,
liver, and urine of animals which had taken large doses of acetate of
lead, and once in the urine of a girl who had swallowed above an ounce
of the acetate twenty-five hours before the urine was passed.[1297]
About the same time M. Ausset, under the directions of Lassaigne,
detected lead largely in the blood and urine of a horse during life, and
in the liver and kidneys after death.[1298] Mr. Alfred Taylor found
traces of it in the milk of a cow accidentally poisoned by carbonate of
lead.[1299] M. Tanquerel Desplanches says it has been detected by M.
Devergie and himself in the palsied parts of persons who had died of
colica pictonum;[1300] and Dr. Budd observes, that Mr. Miller found lead
in abundance in the paralysed extensors of the hand in a man who died in
a London Hospital of the epileptic form of the effects of this
poison.[1301]

These facts seem to outweigh the negative results obtained by others.
Nor are they invalidated by the alleged existence of lead in the healthy
animal textures. For in the first place,—although M. Devergie says he
has always found traces of lead in the substance of the stomach and
intestines of men and women, who had not used preparations of lead or
been in any way exposed to it,[1302] and Professor Orfila confirmed
these observations by also finding traces of lead in the alimentary
canal under similar circumstances,[1303]—the conclusion flowing from
their researches is after all doubtful; for in a later inquiry MM.
Danger and Flandin could not find any lead, unless it had been purposely
introduced into the body.[1304] And secondly,—Devergie adds to his
remarks, that the quantity of lead he found in the textures and
secretions of those who had died of lead-colic was far greater than in
those who had not been exposed to lead preparations before death; and
Orfila ascertained that the process by which he detects adventitious
lead is incapable of indicating that which may be present naturally in
the body.[1305]

It is probable that all the preparations of lead are poisonous except
the metal, and perhaps also the sulphuret. The experimentalists at the
Veterinary School of Lyons found that nearly four ounces of the metal
might be given to a dog without even vomiting being excited; and Orfila
remarked that an ounce of carefully prepared sulphuret had as little
effect.[1306] The effects, which have been occasionally ascribed to
lead-shot, and which will be mentioned by and by [_see_ p. 435], seem at
variance with these experiments, but cannot outweigh such precise
negative results. It is probable that irritant poisoning can be produced
only by those compounds which are soluble, such as the acetate,
subacetate, and nitrate. It appears indeed from the experiments of
Orfila with the acetate and my own with the nitrate, that these
compounds are true corrosives, and of no mean energy when given in large
doses moderately diluted.

The insoluble compounds, such as the carbonate, red oxide and protoxide,
possess little irritant power. The experimentalists of Lyons found
litharge to be irritant in large doses of half an ounce.[1307] Orfila
gave dogs large doses of the red oxide and carbonate without observing
any signs of irritation in the stomach. A case has been published of a
young woman who swallowed accidentally an ounce and a half of the
carbonate without any bad effect whatever either at the time or
afterwards;[1308] and Dr. Ogston of Aberdeen has informed me he met with
a similar case, that of a girl who took an ounce with the view of
destroying herself, but without sustaining any harm whatever. In a
remarkable case, published by Mr. Cross of London, in which six drachms
were taken accidentally by a pregnant female instead of magnesia,
vomiting and violent colic were produced, and afterwards fainting,
paralysis of the extensor muscles, and contraction of the flexors; all
of which symptoms, however, after enduring without abatement till eight
hours after the poison was swallowed, gradually disappeared under
antidotes and laxatives. But such a case bears no great resemblance
either to the acute or chronic form of poisoning with lead, and was
probably hysterical.[1309] Orfila has found that an ounce and a quarter
of sulphate of lead had no effect whatever on a dog.[1310] Mr. Taylor
mentions a case where the chloride of lead caused vomiting, but no other
ill consequence.[1311] Dr. Cogswell found that three drachms of iodide
of lead caused in a dog merely depression and weakness for a few days;
but forty grains killed a rabbit in twelve days, with symptoms of
exhaustion and constipation; and doses frequently repeated, to the
amount of eleven drachms in eighteen days, killed a dog under symptoms
nearly the same.[1312]

It may be presumed that all the compounds of lead which are soluble in
water or in the animal fluids may produce in favourable circumstances
the lead colic and palsy. Dr. A. T. Thomson, indeed,[1313] has
endeavoured to show by some experiments, that the carbonate is the only
compound of lead which possesses this singular power; and that if the
acetate of lead produces similar effects, it is only because that salt
usually contains an excess of oxide which becomes carbonate from the
action of free carbonic acid in the stomach and other parts of animals,
or because the salt is decomposed by double decomposition from the
accidental presence of alkaline carbonates. It does not appear to me,
however, that the researches of Dr. Thomson, taken along with the prior
inquiries of other physiologists, will bear out this conclusion. The
experiments of Wibmer in particular would seem to show that the
carbonate is at least not more active than the acetate; nor does it
appear probable that the small doses of acetate given by him, seldom
exceeding two or three grains at a time, could yield any carbonate in
the alimentary canal of a dog, where there is commonly much free
muriatic acid. Farther, in many of the instances of lead colic related
above as produced by cider, wine, and other acid substances acting on
lead or its oxide, the acid must have been so greatly in excess, that it
was scarcely possible that carbonate of lead could have been formed
afterwards by any ordinary accident. And even supposing the carbonate to
be more active than other compounds in occasioning colic and palsy, as
Dr. Thomson’s inquiries would tend to show, the fact may be admitted
without necessarily leading to the inference, that it is the only active
compound of lead, or that other preparations must be converted into the
carbonate before they can act as slow poisons. For the superior activity
of the carbonate may be owing to the great obstinacy with which its
impalpable powder adheres to moist membranous surfaces, and the
consequent greater certainty of its ultimate absorption. It certainly
appears at least but consistent with a general law, to which hitherto no
undoubted exception has been found, that the carbonate must be dissolved
before it can act constitutionally.

The symptoms observed in man from the preparations of lead are of three
kinds. One class of symptoms indicate inflammation of the alimentary
canal: another spasm of its muscles: and a third injury of the nervous
system, sometimes apoplexy, more commonly palsy, and that almost always
partial and incomplete. Each of these classes of symptoms may exist
independently of the other two; but the last two are more commonly
combined.

The irritant effects of large doses of the soluble salts of lead come
first under consideration. Of these the acetate, or sugar of lead may be
taken as an example.

Here it will, in the first instance, be observed that, according to the
experiments mentioned above, the acetate of lead, though certainly an
irritant poison, is not very energetic,—being much less so than the
vulgar generally believe, and far inferior to most of the metallic
poisons hitherto treated of. This farther appears from the experience of
physicians as to its effects in medicinal doses. The acetate has been
often given in pretty large doses in medical practice; and although it
has sometimes excited colic when continued too long, ordinary irritation
of the stomach seems to have been rarely observed. Mr. Daniell, in a
paper on its effects as a remedy for mercurial salivation, states that
he gave it in doses of ten grains three times a day, and that he never
observed it to excite any other unpleasant symptom except slight colic,
which seldom came on till after the fourth dose.[1314] I have often
given it in divided doses to the amount of eighteen grains daily for
eight or ten days, without remarking any unpleasant symptom whatever,
except once or twice slight colic. Van Swieten even mentions a case in
which it was given to the amount of a drachm daily for ten days before
it caused any material symptom.[1315]

Yet facts are not wanting to prove that acetate of lead in an improper
dose will produce violent and immediate effects. The symptoms are then
either those of simple irritation, or more commonly those of
inflammation united with the peculiar spasmodic colic of lead, and
sometimes followed by convulsions and coma, or by local palsy.

In one of Sir George Baker’s essays there is an instance of immediate
and violent symptoms having been caused by a drachm taken twice with a
short interval between the doses. The subject was a soldier who took it
in milk to cure a diarrhœa. Five hours after the first dose he was
seized with pain in the bowels and a feeling of distension round the
navel. After the second these symptoms became much more acute; and he
was soon after seized with bilious vomiting, loss of speech, delirium,
and profuse sweating, while the pulse fell down to 40. He recovered,
however, with the aid of diluents and cathartics.[1316]

A case which proved rapidly fatal has been related in a French journal.
A drummer in a French regiment, who was much given to drinking, stole
some Goulard’s extract, and drank it for wine. Neither the first
symptoms nor the dose could be ascertained. On the second day he was
affected with loss of appetite, paleness, costiveness, and excessive
debility; on the third day he had severe and excessive colic, drawing in
of the belly, loss of voice, cold sweats, locked jaw, and violent
convulsions; and he expired before the evening of the same day. The
morbid appearances will be mentioned in their proper place. Sugar of
lead was detected in the stomach.[1317]

In both these instances the disorder excited partook very much of the
character of the spasmodic colic which is caused by the gradual
introduction of lead into the body; and in the last the whole course of
the man’s illness was very like that of the worst or most acute form of
_colica pictonum_. But in another example which came under my own
notice, the symptoms were more nearly those of ordinary
irritation,—namely, vomiting, burning, and pricking pain in the throat,
gullet, and stomach, with trifling colic subsequently; but the patient
recovered in two or three days. The quantity taken was supposed to
exceed a quarter of an ounce. So, too, in a case which occurred to M.
Villeneuve of Paris, the symptoms were chiefly vomiting and purging,
with faintness and some convulsions. His patient swallowed intentionally
above an ounce of acetate of lead in solution. Sulphate of soda and
sulphate of magnesia were given promptly as antidotes; in an hour the
symptoms had abated materially; and next day she was well.[1318] This
was the case in which Orfila found lead in the urine. Of the same
nature, also, are two cases briefly alluded to by Mr. Taylor, as having
been caused in London in 1840 by Goulard’s extract. The subjects, who
were children, were seized with vomiting, purging, and other symptoms
like those of Asiatic cholera; and both died within thirty-six
hours.[1319]

In another instance, related by Mr. Iliff of London, where an ounce of
the acetate was accidentally swallowed in solution, the symptoms were at
first colic pains and vomiting, in the course of a few hours vomiting
and tenderness, and, after these symptoms receded, a peculiar state of
rigidity and numbness, which was not entirely removed for several days.
In this case no remedies were used for three hours; and even two hours
later, when the stomach-pump was resorted to on account of the
slightness of the vomiting, lead was found in the first fluid
withdrawn,—a new proof of the feeble action of acetate of lead, compared
with some other metallic poisons.[1320]

So much for the operation of the acetate of lead in large doses.
Physicians, however, are much better acquainted with the effects of lead
when introduced in the body continuously and insidiously in minute
quantities. For all tradesmen who work much with its preparations are
apt to suffer in this way, and many other persons have been brought
under its action in consequence of articles of food and drink being
impregnated with it. The disease which is thus induced may be divided
into two distinct stages.

The first stage is an affection of the alimentary canal, the leading
feature of which is violent and obstinate colic. This symptom at times
begins abruptly during a state of sound health; but much more commonly
it is ushered in by a deranged state of the stomach, not unlike common
dyspepsia, seldom so severe as to excite alarm, and commonly imputed at
first to a wrong cause. There is general uneasiness and depression, a
dingy yellowish complexion, weakness and numbness in the limbs, a
sweetish styptic taste and fetid breath, a slaty tint of the teeth and
gums, with a blue line along the margin of the gums where they touch the
teeth, a slow hard pulse, great emaciation, loss of appetite and
tendency to indigestion. This state, which was first well characterized
by Mr. Wilson[1321] of Leadhills, and has lately been more fully
described by M. Tanquerel,[1322] is of great moment as apprizing the
workman of the necessity of taking active measures for preventing the
more formidable effects, which otherwise are sure to follow. Of the
warning symptoms none is so invariable or so characteristic as the blue
line along the edge of the gums, an appearance which was first noticed
by Dr. Burton of St. George’s, London,[1323] and has been since observed
in every case of lead colic, whether impending or present.—If alarm be
not taken in time, the obscure complaints hitherto mentioned become
attended by and by with uneasy sensations in the stomach, stretching ere
long throughout the whole belly. At the same time the stomach becomes
irritable, and the food is rejected by vomiting. Cramps in the pit of
the stomach then arise, and extend to the rest of the belly, till at
length the complete colic paroxysm is formed. The pain is sometimes
pretty constant; sometimes it ceases at intervals altogether; but much
more commonly there are remissions rather than intermissions; and it is
remarked that both the remissions and exacerbations are much longer than
those of common colic. The pain is very generally, yet not invariably,
relieved by pressure; even strong pressure seldom causes any uneasiness,
provided it be not made on the epigastrium; nay, some patients have been
known to bear, with relief to the paroxysms, the weight of two or three
people standing on the belly.[1324] The belly is almost always hard, the
abdominal muscles being contracted: sometimes it is rather full, more
commonly the reverse, and the navel is often drawn in so as almost to
touch the spine. The bowels all the while are obstinately costive.
Either there is no discharge from them at all; or scanty, knotty fæces
are passed with much straining and pain. This state, long supposed to
depend on spasm, is now known to arise on the contrary from paralysis,
of the intestinal muscular coat. In a few instances diarrhœa takes the
place of the opposite affection. The urine is commonly diminished. The
saliva has been described as greater than natural in quantity and bluish
in colour; but Dr. Burton says he did not observe a single instance of
this in forty cases which he carefully examined. From the beginning, or
more generally after a few hours or days, the limbs are racked with
diffuse cutting pains; which, according to Tanquerel, affect chiefly the
limbs, especially near the joints, are worst at night, are often
attended with cramps, and are relieved by pressure. The aspect of the
countenance is dull, anxious, and gloomy: in advanced cases the
expression of gloomy anxiety exceeds that of almost all other diseases.
It appears from the latest works on this disease published in France,
and particularly from the able treatise of Mérat, that the pulse is
rarely accelerated, but on the contrary often retarded.[1325] This does
not accord with the experience of some earlier writers;[1326] and in the
few cases I have seen in this city the pulse has been always frequent.
It cannot be questioned, however, that, as Mérat states, fever is not
essential. The skin has a dull, dirty, cadaverous appearance, is often,
though not always hot, and in either case is bedewed with irregular,
clammy, cold perspiration.

This, the first stage of colica pictonum, may end in three ways. In the
first place, the patient may recover at once from it as from an ordinary
colic; and it is consolatory to know, that a first attack, taken under
timely management, is for the most part easily made to terminate in that
favourable manner. In such circumstances it rarely endures beyond eight
days. But it is exceedingly apt to recur, if, for example, the patient
expose himself to what in ordinary circumstances would cause merely a
common colic or diarrhœa; and if he returns to a trade which exposes him
again to the poison of lead, the disease is sure to recur sooner or
later, and repeatedly, unless he observes the greatest precautions. In
one or other of these returns, sometimes even in the first attack, the
colic is not succeeded by complete recovery, but gives place to another
more obstinate and more alarming disease. This secondary affection is of
two sorts. One, which occurs chiefly in fatal cases, is a species of
apoplexy. The other, which does not of itself prove fatal, is partial
palsy.

In violent and neglected cases of colica pictonum, the colic becomes
attended in a few days with giddiness, great debility, torpor, and
sometimes delirium; as the torpor advances the pains in the belly and
limbs abate; at length the patient becomes convulsed and comatose, from
which state very few recover. Tanquerel, who is unnecessarily minute in
subdividing the various affections produced by the poison of lead,
distinguishes four kinds of affections of the head, coma, epilepsy,
delirium, and a combination of all these.[1327] A very rare termination
allied to that now described is sudden death during the colic stage,
without any symptom which would lead one to suspect its approach. A case
of this kind has been related by M. Louis. His patient, five minutes
after talking to the attendant of his ward, was found at his bedside in
the agony of death; and no cause for so sudden a death could be found on
dissection.[1328] Somewhat similar was a case which occurred in 1838 at
the hospital of La Charité at Paris. A man labouring for three days
severely under the colic stage of the disease, began to breathe
stertorously soon after straining at stool, and died in three
hours.[1329] In a case which occurred to Dr. Elliotson death was owing
to concomitant perforation of the stomach, a concurrence which was
probably accidental, but which was also once observed by Dr.
Copland.[1330]

In cases, on the other hand, which have not been neglected, and
particularly when the attack is not the first, the departure of the
colic often leaves the patient in a state of extreme debility, which by
and by is found to be a true partial palsy, more or less complete. This
affection is sometimes present before the colic departs, but is apt to
escape notice till the pain abates. Occasionally it supervenes on a
sudden, but more generally it is preceded by a sense of weariness,
numbness and tremor of the parts. The palsy is of a peculiar kind. It
affects chiefly the upper extremities, and is attended with excessive
muscular emaciation. The loss of power and substance is most remarkable
in the muscles which supply the thumb and fingers; and in every case
which I have seen the extensors suffered more than the flexors. The
paralysis is hardly ever complete, except perhaps in the extensors of
the fingers. When it is considerable, the position of the hands is
almost characteristic of the disease. The hands are constantly bent,
except when the arms hang straight down by the side; they dangle loosely
when the patient moves; he cannot extend them, and raises one arm with
the aid of the other. The palsy is attended, according to Tanquerel,
with diminished heat in the parts, and feeble pulsation in the arteries
which supply them. There is seldom any loss of sensation in the affected
parts. But the paralysis sometimes affects the nerves of the other
senses. Thus two cases of paralysis of the nerves of vision have been
related by Dr. Alderson of Hull;[1331] and Tanquerel says this affection
is not uncommon in Paris, and is attended with dilated and immovable
pupils. The latter author also once met with deafness in the same
circumstances.—Patients affected with lead palsy usually complain of
racking pains in the limbs and arms, digestion is feeble, and trivial
causes renew the colic. From this deplorable condition it is still
possible to restore the sufferer to health, chiefly by rigorous
attention to regimen. But he too often dies in consequence of a fresh
attack of colic as soon as he returns to his fatal trade.

The lead palsy, however, does not always come on in this regular manner.
Sometimes the primary stage of colic is wanting, so that the wasting of
the muscles and loss of power are the first symptoms. I have seen a
characteristic example of the kind in a sailor who had been employed for
a month in painting a vessel. He had great weakness and wasting of the
arms and hands, particularly of the ball of the thumb; but except a
tendency to indigestion, costiveness, and transient slight pain of the
belly, he had suffered no previous disorder of the intestines. I have
seen the paralytic affection confined to the extensors of one hand in a
compositor, and Dr. Chowne met with a similar affection of both hands in
a gas-fitter.[1332] Dr. Bright observed palsy without colic in the case
of a painter three times in the course of seven years.[1333]—In like
manner, according to Tanquerel, the neuralgic affection may occur
severely without any precursory colic; and the same author has witnessed
both coma and convulsions in the same circumstances.

Colica pictonum, with the collateral disorders specified above, is the
only disease which has been distinctly traced to the operation of lead
insidiously introduced into the body. But many other disorders have been
ascribed to its agency. Boerhaave seems to have imagined that
consumption might be so induced; and Dr. Lambe thought that to this
cause may be traced the increased prevalence of “scrofula, phthisis,
dropsy, chronic rheumatism, stomach complaints, hypochondriasis, and the
host of nervous complaints which infest modern life.”[1334] These
conjectures are wholly destitute of foundation in fact.

In whatever form lead is habitually applied to the body, it is apt to
bring on the train of symptoms mentioned above;—the inhalation of its
fumes, the habitual contact of any of its compounds with the skin, the
prolonged use of them internally as medicines, or externally as unguents
and lotions, and the accidental introduction of them for a length of
time with the food, may sooner or later equally induce colica pictonum.

Instances have occurred of colic being produced by the prolonged
employment of the compounds of lead inwardly in medical practice. Such
cases are so uncommon that it is evident some strong constitutional
tendency must co-operate. But it is in vain to deny, as some do, that
the medicinal employment of preparations of lead internally is
unattended with any risk whatever of slow poisoning. Dr. Billing of
Mulhausen relates a case of death, apparently from the comatose
affection succeeding the colic stage of poisoning with lead, in the
instance of a boy of fifteen, to whom he gave acetate of lead in
gradually increasing doses for six weeks, till he took two grains
daily.[1335] Tanquerel met with a case of colic produced by 130 grains
taken in fourteen days, and another occasioned by 149 grains in sixteen
days.[1336] Sir George Baker has mentioned similar instances.[1337] It
would even appear that metallic lead may have the same effect when taken
inwardly. Thus Dr. Ruva of Cilavegno has related the case of a man who
was violently attacked with the colic form of the effects of lead after
taking six ounces of shot by direction of a quack for the cure of
dyspepsia, and was seized again with the same symptoms six days
afterwards on taking four ounces more. On the second occasion he had
violent colic, great feebleness of the limbs, constant vomiting of any
thing he swallowed, severe headache, and other analogous symptoms, of
which he was not effectually cured for seven weeks.[1338] A case
somewhat similar, but less severe, has been described by Dr.
Bruce.[1339]—With regard to lead colic being excited by unguents and
lotions applied to the surface of the body, Sir George Baker mentions a
case of violent colic brought on by litharge ointment applied to the
vagina; he adds that children have been thrown into convulsions by the
same substance sprinkled on sores: and he quotes Zeller for a case where
symptoms of poisoning were occasioned by sprinkling the axilla with it,
as a cure for redness of the face.[1340] Dr. Wall, in a letter to the
preceding author, mentions his having seen the bowels affected by
Goulard’s extract applied to ulcers; in another paper he has given two
unequivocal cases, in one of which colic was brought on by saturnine
lotions applied to a pustular disease, and in the other by immersing the
legs twice a day for ten days in a bath of the solution of acetate of
lead:[1341] and lately Dr. Taufflieb of Barr observed lead colic to
arise from the continued use of diachylon plaster during eleven weeks
for dressing an extensive ulcer.[1342] Such accidents are exceedingly
rare, and some auxiliary cause must have favoured the operation of the
poison in the cases now noticed; for every one knows that free use is
made of lead unguents and lotions, yet we seldom hear of any bad
consequences.—These cases, however, will probably remove the doubts
which some entertain of the possibility of lead colic being induced by
the application of the compounds of lead to the sound skin in those
trades which compel the workmen to be constantly handling them. At the
same time it must be admitted, that in all these trades there exists a
more obvious and ready channel for the introduction of the poison;
because the workmen are either exposed to breathe its fumes, or are apt
to transfer its particles from the fingers into the stomach with their
food.—Of all exposures none is more rapid and certain than breathing the
vapours or dust of the preparations of lead. But for that very reason
workmen who are so exposed seldom suffer; because the greatness of the
risk has led to the discovery of means to avert it, and the openness of
the danger renders it easy for the workmen to apply them. Tanquerel
mentions a singular case of a woman who was attacked in consequence of
the fine dust of white lead ascending through chinks in the floor from a
room below, where a perfumer was in the practice of grinding and sifting
that substance.[1343]—It may be added that Dr. Otto of Copenhagen has
published an extraordinary instance of fatal lead-colic, originating in
the habitual use of Macuba snuff adulterated with twenty per cent. of
red lead.[1344]

To these observations on the various ways in which lead insidiously
enters the system a few remarks may be added on the trades which expose
workmen to its influence. The most accurate information on this subject
is contained in the work of Mérat.

He places foremost in the list miners of lead. In this country miners
are now rarely affected, because the frequency of colica pictonum among
them formerly led their masters to study the subject, and to employ
proper precautions for removing the danger. It has been stated by Dr.
Percival, and is generally thought, that the whole workmen in lead mines
are apt to be attacked with the colic,—those who dig the sulphuret as
well as those who roast the ore.[1345] If this idea were correct, it
would be in contradiction with the general principle in toxicology, that
the metals are not poisonous unless oxidated. But the opinion is in all
probability founded on error; for, according to information communicated
to me by Mr. Braid, and confirmed since by personal investigation, the
workmen at Leadhills who dig and pulverize the ore, although liable to
various diseases connected with their profession, and particularly to
pectoral complaints, never have lead colic till they also work at the
smelting furnaces. Next to miners may be ranked manufacturers of
litharge, red-lead and white-lead. The workmen at these manufactories
are exposed to inhale the fumes from the furnaces or the dust from the
pulverizing mills. It has been chiefly among the workmen of a former
white-lead manufactory in the neighbourhood of Edinburgh that I have had
an opportunity of witnessing the lead colic. By a simple change the
proprietor made in the process, and which will be mentioned presently,
the disease was almost extirpated some years before the manufactory was
given up.

Next in order, perhaps in the same class with colour-makers, are
house-painters. The causes of their liability is the great quantity of
the preparations of lead contained in the paints they use. It would
appear that lead colic is most frequent among people of that trade in
cities of the largest size. In Geneva, as I am informed by my friend Dr.
C. Coindet of that place, colica pictonum is now almost unknown and
never occurs among painters. In Edinburgh it is also little known among
painters. A journeyman painter, a patient of mine in the Infirmary, had
been seventeen years in the trade, and yet did not know what the
painters’ colic or lead palsy meant. In London, according to the
Dispensary reports, and in Paris, according to the tables of Mérat, many
workmen of that trade suffer. I have been informed by an intelligent
workman, once a patient of mine, who had been a journeyman painter both
in London and Edinburgh, that the number of his acquaintances who had
been affected with colic in the metropolis was incomparably greater than
here. This man ascribed the difference to the working hours being more
in the former place, so that the men had not leisure enough to make it
worth their while to clean themselves carefully in the intervals. This
appears a rational explanation. I do not know how the great prevalence
of colic among painters in Paris is to be accounted for.

Plumbers, sheet-lead manufacturers, and lead-pipe makers, are also for
obvious reasons apt to suffer; but as they are not necessarily exposed
to the vapours of lead, and suffer only in consequence of handling it in
the metallic form, it ought to be an easy matter to protect them. They
themselves conceive that a very hazardous part of their occupation is
the removing the melted lead from the melting pot, to make the sheets or
pipes; but this operation cannot be dangerous if the melting pots are
properly constructed.

A few cases of lead colic occur among glass-blowers, glaziers, and
potters, who use the oxide of lead in their respective trades.

There are a few also among lapidaries and others, who use it for
grinding and polishing, and among grocers and colourmen who sell its
various preparations. Printers seldom suffer from the colic, but are
generally thought liable to partial palsy of the hands, which is
ascribed to frequent handling of the types. I have met with one case
apparently of this nature.

Lead is not the only metal to which the power of inducing colica
pictonum has been ascribed. Mérat has mentioned several instances of the
disease occurring among brass-founders and other artizans who work with
copper.[1346] Tronchin quotes Scheuchzer for a set of well-marked cases
in a convent of monks, where the malady was supposed to have been traced
to all the utensils for preparing and keeping their food having been
made of untinned copper.[1347] The same author mentions two cases, one
of which came under his immediate notice, where the apparent cause was
the long-continued use of antimonial preparations internally.[1348]
Mérat likewise found a few iron-smiths and white-iron-smiths in the
lists kept at one of the Parisian hospitals.[1349] Chevallier alleges
that colic occurs at times among money-changers at Paris, and others who
constantly handle silver.[1350] Cases have even been noticed by Mérat
among varnishers, plasterers, quarrymen, stone-hewers, marble-workers,
statuaries, saltpetre-makers;[1351] and Tronchin enumerates among its
causes the immoderate use of acid wine or of cider, checked
perspiration, sea-scurvy, and melancholy. But the only substance besides
lead, whose operation in producing colica pictonum has been traced with
any degree of probability, is copper; and even among artizans who work
with copper the disease is very rare. As to the other tradesmen
mentioned by Mérat, it is so very uncommon among them, that we may
safely impute it, when it does occur, to some other agent besides what
the trade of the individual exposes him to; and in general the secret
introduction of lead into the body may be presumed to be the real cause.
Still, however, the connection of colica pictonum with other causes
besides the poison of lead is upheld by so many facts, and is believed
by so many authorities, that this disease cannot be safely assumed, even
in its most characteristic form, as supplying undoubted evidence of the
introduction of lead into the system. Dr. Burton thinks it will when the
blue line at the edge of the gums is seen.

The work of Mérat contains some interesting numerical documents,
illustrative of the trades which expose artisans to colica pictonum.
They are derived from the lists kept at the hospital of La Charité in
Paris, during the years 1776 and 1811. The total number of cases of
colica pictonum in both years was 279. Of these, 241 were artisans whose
trades exposed them to the poison of lead, namely, 148 painters, 28
plumbers, 16 potters, 15 porcelain-makers, 12 lapidaries, 9
colour-grinders, 3 glass-blowers, 2 glaziers, 2 toy-men, 2 shoemakers, a
printer, a lead-miner, a leaf-beater, a shot-manufacturer. Of the
remainder, 17 belonged to trades in which they were exposed to copper,
namely, 7 button-makers, 5 brass-founders, 4 braziers, and a
copper-turner. The remaining twenty-one were tradesmen, who worked
little, or not at all with either metal, namely, 4 varnishers, 2
gilders, 2 locksmiths, a hatter, a saltpetre-maker, a winegrocer, a
vine-dresser, a labourer, a distiller, a stone-cutter, a calciner,[1352]
a soldier, a house-servant, a waiter, and an attorney’s clerk.—Age or
youth seems not to afford any protection against the poison. Of the 279
cases, 24 were under twenty, and among these were several painter-boys
not above fifteen years old; 113 were between nineteen and thirty; 66
between twenty-nine and forty; 38 between thirty-nine and fifty; 28
between forty-nine and sixty; and 10 older than sixty. These proportions
correspond pretty nearly with the relative number of workmen of similar
ages.—Among the 279 cases fifteen died, or 5·4 per cent.

There seems to have lately been little or no diminution in the frequency
of the disease in Paris. In 1833–4–5–6, there were treated in the
hospitals 1541 cases, or 385 annually; of whom one in 39½ died. And in
1839–40–41 there were 761 cases, or 252 annually; of whom one in 24½
died. Of 302 cases in 1841 no fewer then 266 were from white-lead
manufactories.[1353]


        SECTION III.—_Of the Morbid Appearances caused by Lead._

The morbid appearances caused by poisoning with lead are in some
respects peculiar.

In acute poisoning, from the irritant action of its soluble salts, as in
the case of the drummer poisoned by Goulard’s extract, the lower end of
the gullet, the whole stomach and duodenum, part of the jejunum, and the
ascending and transverse colon, have been found much inflamed, and the
villous coat of the stomach as if macerated. In Mr. Taylor’s two cases
Dr. Bird found the villous coat of the stomach gray, but otherwise
natural; and the intestines were much contracted.

The stomach in the first of these cases contained a reddish-brown,
sweetish, styptic fluid, in which lead was detected by chemical
analysis,[1354]—an important medico-legal fact, since the man survived
nearly three days. Some valuable observations have been made by
Professor Orfila as to the presence of lead in the textures of the
stomach in such instances. When small doses of acetate or nitrate of
lead were administered to dogs and allowed to act for two hours only,
the villous coat presented numerous streaks of white points, which
contained lead, as hydrosulphuric acid blackened them. These points,
though less distinct, were still visible, when the animals were allowed
to live four days after the excess of salt had been removed; and even
after seventeen days, although no such appearance remained, lead could
still be detected in the tissues of the stomach.[1355]

The blood in animals is sometimes altered. Dr. Campbell found it fluid.
In a dog poisoned with litharge, the experimentalists of the Veterinary
School at Lyons found it of a vermilion colour in the veins, and
brighter than usual in the arteries.[1356] Mitscherlich also found it
unusually red and firmly coagulated.[1357]

The appearances in the bodies of those who have died of the various
forms of lead colic are different, and wholly unconnected with
inflammation.

The valuable work of Mérat contains four inspections after death from
the acute or comatose form of colica pictonum. The bodies were plump,
muscular and fat. The alimentary canal was quite empty, and the colon
much contracted,—in one to an extraordinary degree. The mucous coat of
the alimentary canal was everywhere healthy. He therefore infers that
the disease is an affection of the muscular coat only. It is a striking
circumstance, and conformable with what will be afterwards established
in regard to the true narcotics, that although both of the men died
convulsed and comatose, no morbid appearance was visible within the
head.[1358] Another case, which confirms the foregoing facts, has been
described by Mr. Deering. It was that of a lady who died convulsed after
suffering in the usual manner, and in whose body no trace of disease
could be detected any where.[1359] Senac informed Tronchin that he had
dissected above fifty cases of colica pictonum, and found no morbid
appearances.[1360] Schloepfer’s observations on animals are to the same
effect. In rabbits which died of colica pictonum the great intestines
were excessively contracted, but all the other organs of the body were
healthy except the liver, which was dark and brittle.[1361] Mitscherlich
observed in his animals extravasation of blood into the intestines, also
sometimes into the cavities of the pleura and peritoneum, and
occasionally under the peritoneal covering of the kidneys.[1362] The
only instance I have met with where morbid appearances were found within
the head, was in a case mentioned by Sir G. Baker, of a gentleman who
died apoplectic after many attacks of colica pictonum, and in whom the
brain was found unusually soft, and blood extravasated on its surface to
the amount of an ounce.[1363]

The appearances in those who have been long affected with the paralytic
form of colica pictonum have been rarely observed in modern times. I am
indebted to my late colleague, Dr. Duncan, Junior, for an account of the
appearances in the intestinal canal of a plumber, who had been long and
frequently afflicted with colica pictonum and its sequelæ. The
intestines were dark, tender, and far advanced in putrefaction. The
cardiac orifice of the stomach was so narrow that it would admit a
goose-quill. The mesenteric glands were enlarged and hardened. The
thoracic duct was surrounded by many large bodies like diseased glands,
exactly of the colour of lead, and composed of organized cysts
containing apparently an inorganic matter. The analysis of this matter
was unfortunately neglected. The muscles in similar circumstances are
much diseased. When the paralysis is not of long standing, it appears
from the experiments of Schloepfer (whose animals survived about three
weeks), that the whole muscular system becomes pale, bloodless, and
flaccid. When the palsy is of long standing, this change increases so
much, that the muscles in some parts, as in the arms and thumbs, acquire
the colour and general aspect of white fibrous tissue. Some observations
on the nature of these changes will be found in the essays of Sir G.
Baker.[1364] The facts are communicated by Mr. John Hunter. On examining
the muscles of the arm and hand of a house-painter who was killed by an
accident, Mr. Hunter found them all of a cream colour, and very opaque,
their fibres distinct, and their texture unusually dry and tough. These
alterations he at first imagined might have been the result merely of
the palsy and consequent inactivity of the muscles, but on finding the
same alterations produced by the direct action of sugar of lead on
muscle, he inferred that the poison gradually effected a change either
on the muscles directly, or on the blood which supplied them.

In a late elaborate inquiry into the pathology of lead-colic, M.
Tanquerel has arrived at the conclusion, that “the pathological
phenomena are not caused by anatomical changes cognisable by the
senses,” and that such appearances as may be found are the effects, not
the cause, of the disease.[1365]


         SECTION IV.—_Of the Treatment of Poisoning with Lead._

The treatment of poisoning with lead, and the mode of protecting workmen
from its influence, will now require a few remarks.

For the irritant form of poisoning, a safe and effectual antidote exists
in any of the soluble alkaline or earthy sulphates. If none of these be
at hand, then the alkaline carbonates may be given, particularly the
bicarbonates, which are not so irritating as the carbonates. The
phosphate of soda is also an excellent antidote. If the patient does not
vomit, it will be right also to give an emetic of the sulphate of zinc.
In other respects, the treatment does not differ from that of poisoning
with the irritants generally.

Colica pictonum is usually treated in this country with great success by
a practice much followed here in colic and diarrhœa of all kinds,—the
conjunction of purgatives with anodynes. A full dose of a neutral
laxative salt is given, and an hour afterwards a full dose of opium.
Sometimes alvine discharges take place before the opium acts, more
commonly not till its action is past, and occasionally not for a
considerable time afterwards. But the pain and vomiting subside, the
restlessness and irritability pass away, and the bowels return nearly or
entirely to their natural condition. Sometimes it is necessary to repeat
the practice. It is almost always successful. I have seldom seen the
second dose fail to remove the colic, leaving the bowels at worst in a
state of constipation. Dr. Alderson of Hull, who has had many
opportunities of treating the workmen of a white-lead manufactory there,
says powerful purgatives, such as croton-oil, are highly serviceable in
severe cases, and are borne well notwithstanding the extreme debility
often present.[1366] M. Tanquerel says he has found this treatment more
effectual in Paris than any other means.[1367] When the pulse is full
and strong, I have seen venesection premised with apparent advantage; in
some instances it appeared to me to be called for by the flushing of the
face and the violence of the spasms; and I have never seen it otherwise
than a safe remedy, notwithstanding the fears expressed by Dr. Warren
and others.[1368]

The hospital of La Charité in Paris has long enjoyed a high reputation
for the treatment of this disease. In the first place a decoction is
given of half an ounce of senna in a pound of water, mixed with half an
ounce of sulphate of magnesia and four ounces of the wine of antimony.
Next day an ounce of sulphate of magnesia and three grains of
tartar-emetic are administered in two pounds of infusion of cassia, to
keep up the operation of the first laxative. In the evening a clyster is
given, containing twelve ounces of wine and half as much oil. After this
the patient is made to vomit with tartar-emetic, then drenched with
_ptisanes_ for several days, and the treatment is wound up with another
dose of the first purgative succeeded by gentle anodynes. I am not aware
of any particular advantage possessed by this complicated and tormenting
method of cure, which is not equally possessed by the simpler plan
pursued in Britain.

In 1831 M. Gendrin announced to the French Institute that he had found
sulphuric acid to be at once the most effectual remedy, and the most
certain preventive, for the injurious effects of lead; and he has
subsequently spoken in strong terms of the utility of this
treatment.[1369] But the experience of others does not bear out his
conclusions.[1370]

Among the many other methods of cure that have been proposed for the
primary stage of this disease, salivation by mercury deserves to be
particularized. It appears to have been often used with success, the
colic yielding as soon as ptyalism sets in.[1371] If the case, however,
is severe, there is no time to lose in waiting for the action of the
mercury to commence.

The treatment in the advanced period of the disease, when palsy is the
chief symptom remaining, depends almost entirely on regimen. The patient
must for a time at least quit altogether his unlucky trade. He should be
allowed the most generous food he can digest. He ought to take frequent
gentle exercise in the open air, but never to fatigue. The hands being
the most severely injured of the affected parts, and at the same time
the most important to the workman, the practitioner’s attention should
be directed peculiarly to the restoration of their muscular power. This
appears to be most easily brought about by frictions, electricity, and
regulated exercise, the hands being also supported in the intervals by
splints extending from the elbows to the fingers. The dragging of the
emaciated muscles by the weight of the dangling hands certainly seems to
retard recovery.—Strychnia has also been repeatedly found of service in
restoring muscular action. Tanquerel states that electricity and
strychnia, but especially the latter, have appeared to him by far the
most efficacious remedies both for muscular paralysis and for
amaurosis.—In the head affections the best treatment consists in relying
on nature and merely combating symptoms; and blood-letting is of no use,
however much it may seem to be indicated by the coma and convulsions.

When a person has been once attacked with colica pictonum, he is more
easily attacked again. Hence if he is young enough, he should, if
possible, change his profession for one in which he is not brought into
proximity with lead. Few, however, have it in their power to do so. The
prophylaxis, therefore, or mode of preventing the influence of the
poison, becomes a subject of great importance; and more particularly
when we consider the vast number of workmen in different trades, whose
safety it is intended to secure.

On this subject many useful instructions are laid down in the work of
Mérat. He very properly sets out with insisting on the utmost regard
being paid to cleanliness,—a point too much neglected by most artizans,
and particularly by those to whom it is most necessary, the artizans who
work with the metals. In proof of the importance of this rule, he
observes he knew a potter, who contracted the lead colic early in life
when he was accustomed to go about very dirty, but for thirty years
after had not any return of it, in consequence simply of a scrupulous
attention to cleanliness. In order to secure due cleanliness three
points should be attended to. In the first place, the face and hands
should be washed once a day at least, the mouth well rinsed, and the
hair occasionally combed. Secondly, frequent bathing is of great
consequence, both with a view to cleanliness and as a general tonic; so
that masters should provide their workmen with sufficient means and
opportunities for practising it. Lastly, the working clothes should be
made, not of woollen, but of strong, compact linen, should be changed
and washed at least once and still better twice a week, and should be
worn as little as possible out of the workshop. While at work a cap of
some light impervious material should always be worn.

Next to cleanliness, the most important article of the prophylaxis
relates to the means for preventing the food being impregnated with
lead. For this end it is essential that the workmen never take their
meals in the workshop, and that before eating they wash their lips and
hands with soap and water, and brush out all particles of dirt from the
nails. It is also of moment that they breakfast before going to work in
the morning.

Derangements of the digestive organs should be watched with great care.
If they appear to arise from the poison of lead, the individual should
leave off work with the very first symptom, and take a laxative.
Habitual constipation should be provided against.

The nature of the diet of the workmen is of some consequence. It should
be as far as possible of a nutritive and digestible kind. Mérat condemns
in strong terms the small tart wines generally used by the lower ranks
of his countrymen. They constitute a very poor drink for all artizans;
and are peculiarly ill adapted for those who work with lead, because,
besides being at times themselves adulterated with that poison, they are
also apt to disorder the bowels by their acidity. Beer is infinitely
preferable. Various articles of diet have been recommended as tending to
impede the operation of the poison. Hoffmann recommends brandy, the
efficacy of which few workmen will dispute. There is some reason for
believing that the free use of fat and fatty articles of food is a
preservative. Dehaen was informed by the proprietor and the physician of
a lead mine in Styria, that the work-people were once very liable to
colic and palsy, but that, after being told by a quack doctor to eat a
good deal of fat, especially at breakfast, they were exempt for three
years.[1372] Another fact of the kind was communicated to Sir George
Baker by a physician at Osterhoüt, near Breda. The village contained a
great number of potters, among whom he did not witness a single case of
lead colic in the course of fifteen years; and he attributes their
immunity to their having lived much on cheese, butter, bacon, and other
fatty kinds of food.[1373] Mr. Wilson says, in his account of the colic
at Leadhills in Lanarkshire, that English workmen, who live much on fat
meat, suffer less than Scotchmen, who do not.[1374]

Professor Liebig says that lead colic is unknown in all white-lead
manufactories, where the workmen use as a beverage lemonade or
sugar-water acidulated with sulphuric acid; and it was stated above that
the same announcement has been made by Mr. Gendrin. This, however, is
doubtful. The prophylactic effects of sulphuric acid have been denied in
France by M. Tanquerel,[1375] and M. Grisolle;[1376] the latter of whom
in particular says that no advantage whatever was derived from it at the
white-lead manufactory of Clichy near Paris.

Some have likewise proposed as an additional preservative, that the
exposed parts of the body should be anointed with oily or fatty matters.
But Mérat maintains with some reason, that the lead will be thereby
enabled to penetrate the cuticle more easily by friction and pressure.

The observance of the preceding rules will depend of course in a great
measure on the intelligence and docility of the workmen. It would appear
that particular care should be taken in hot weather, statistical facts
having shown that three times as many workmen are attacked in Paris
during the month of January as in July.[1377]

Some other objects of much consequence are to be attained by the
humanity and skill of the masters.

The workshop should be spacious, and both thoroughly and systematically
ventilated, the external air being freely admitted when the weather will
allow, and particular currents being established, by which floating
particles are carried away in certain invariable and known courses.
Miners and others who work at furnaces in which lead is smelted, fused,
or oxidated, should be protected by a strong draught through the
furnaces. According to Mr. Braid, wherever furnaces of such a
construction were built at Leadhills, the colic disappeared; while it
continued to recur where the furnaces were of the old, low-chimneyed
form. Manufacturers of litharge and red-lead used formerly to suffer
much in consequence of the furnaces being so constructed as to compel
them to inhale the fine dust of the oxides. In drawing the furnaces the
hot material is raked out upon the floor, which is two or three feet
below the aperture in the furnace; and the finer particles are therefore
driven up and diffused through the apartment. But this obvious danger is
now completely averted by a subsidiary chimney, which rises in front of
the drawing aperture, and through which a strong current of air is
attracted from the apartment, the hot material on the ground performing
the part of a fire.

In white-lead manufactories a very important and simple improvement has
been effected of late in some places by abandoning the practice of
dry-grinding. In all manufactories of the kind, the ultimate pulverizing
of the white lead has been long performed under water. But in general
the preparatory process of rolling, by which the carbonate is separated
from the sheets of lead on which it is formed, continues to be executed
dry. This is a very dangerous operation, because the workmen must inhale
a great deal of the fine dust of the carbonate. In a white-lead
manufactory which formerly existed at Portobello, the process was
entirely performed under water or with damping; and to this precaution
in a great measure was imputed the improvement effected by the
proprietor in the health of the workmen, and their superior immunity
from disease over those of Hull and other places, where the same
precaution was not taken at that time. The only operation latterly
considered dangerous at the Portobello works was the emptying of the
drying stove, and the packing of the white lead in barrels; and the dust
diffused in that process was kept down as much as possible by the floor
being maintained constantly damp. By these precautions, by making the
workmen wash their hands and faces before leaving the works for their
meals, and by administering a brisk dose of castor oil on the first
appearance of any complaint of the stomach or bowels, the manufacturer
succeeded in extirpating colica pictonum entirely for several
years.—This trade continues to be a very pernicious one in France; for
no fewer than 266 cases of colic were admitted into the Parisian
hospitals in 1841 from the white-lead manufactories in and near the
capital. Yet facts are not wanting there to prove that with proper care
the disease may be all but extirpated. A French manufacturer, whose
workmen at one time suffered severely, had no case of colic among them
for nine years after breaking them in to the observance of due
precautions.[1378] Another says, from his own experience and information
obtained at other works, he is satisfied the risk is very much greater
among the intemperate than among sober workmen.[1379]




                              CHAPTER XIX.
                       OF POISONING WITH BARYTA.


Baryta and its salts, the last genus of the metallic irritants which
requires particular notice, are commonly arranged among earthy
substances, but on account of their chemical and physiological
properties, may be correctly considered in the present place. These
poisons are worthy of notice, because they are not only energetic, but
likewise easily procured, so that they may be more extensively used,
when more generally known.


   SECTION I.—_Of the Chemical Tests for the preparations of Baryta._

Three compounds of this substance may be mentioned, the pure earth or
oxide, the muriate, or chloride of barium, and the carbonate. The pure
earth, however, is so little seen, that it is unnecessary to describe
its chemical or physiological properties.

The _Carbonate of Baryta_ is met with in two states. Sometimes it is
native, and then commonly occurs in radiated crystalline masses, of
different degrees of coarseness of fibre, nearly colourless, very heavy,
and effervescing with diluted muriatic acid. It is also sold in the
shops in the form of a fine powder of a white colour, prepared
artificially by precipitating a soluble salt of baryta with an alkaline
carbonate. It is best known by its colour, insolubility in water,
solubility with effervescence in muriatic acid, and the properties of
the resulting muriate of baryta.

The _Muriate of Baryta_, or chloride of barium, is the most common of
the compounds of this earth, having been for some time used in medicine
for scrofulous and other constitutional disorders. It is procured either
by evaporating the solution of the carbonate in hydrochloric acid, or by
decomposing a more common mineral, the sulphate, by means of charcoal
aided by heat, dissolving in boiling water the sulphuret so formed, and
decomposing this sulphuret by hydrochloric acid.

It is commonly met with in the shops irregularly crystallized in tables.
It has an acrid, irritating taste, is permanent in the air, and
dissolves in two parts and a half of temperate water.

The solution is distinguished from other substances by the following
chemical characters. From all other metallic poisons hitherto mentioned,
it is easily distinguished by means of hydrosulphuric acid, which does
not cause any change in barytic solutions. From the alkaline and
magnesian salts it is distinguished by the effects of the alkaline
sulphates, which have no visible action except on the barytic solution,
and cause in it a heavy white precipitate, insoluble in nitric acid.
From the chlorides of calcium and strontium, it is to be distinguished
by evaporating the solution till it crystallizes. The crystals are known
not to be chloride of calcium, because they are not deliquescent. The
chloride of strontium (which resembles that of barium in many
properties, but which must be carefully distinguished, as it is not
poisonous), differs in the form of the crystals, which are delicate
six-sided prisms, while those of the barytic salt are four-sided tables,
often truncated on two opposite angles, sometimes on all four,—by its
solubility in alcohol, which does not take up the chloride of
barium,—and by its effect on the flame of alcohol, which it colours
rose-red, while the barytic salts colour it yellow. The chloride of
barium is known from other soluble barytic salts, by the action of
nitrate of silver, which throws down a white precipitate.

Vegetable and animal fluids do not decompose the solution of chloride of
barium, except by reason of the sulphates and carbonates which most of
them contain in small quantities. But the action of its tests may be
distinguished, although the salt has not undergone decomposition. In
that case the most convenient method of analysis is to add a little
nitric acid, which will dissolve any carbonate of baryta that may have
been formed,—to filter and then throw down the whole baryta in the form
of sulphate, by means of the sulphate of soda,—and to collect the
precipitate, and calcine it with charcoal for half an hour in a platinum
spoon or earthen crucible, according to the quantity. A sulphuret of
baryta will thus be procured, which is to be dissolved out by boiling
water, and decomposed after filtration by muriatic acid. A pure solution
is thus easily obtained. Orfila has lately proposed a process more
complex in its details, but the same in principle.[1380]


SECTION II.—_Of the Action of the Salts of Baryta, and the Symptoms they
                            excite in Man._

The action of the barytic salts on the body is energetic. Like most
metallic poisons, they seem to possess a twofold action,—one local and
irritating, the other remote and indicated by narcotic symptoms. This
narcotic action is more decided and invariable than in the instance of
any of the metallic poisons hitherto noticed. Such at least is the
result of the experiments of Sir B. Brodie,[1381] which have since been
amply confirmed by Professor Orfila[1382] and Professor Gmelin.[1383]
Orfila found that when the chloride was injected into the veins of a dog
in the dose of five grains only, death ensued in six minutes, and was
preceded by convulsions, at first partial, but afterwards affecting the
whole body. Sir B. Brodie found the same effects follow in twenty
minutes, when ten grains were applied to a wound in the back of a
rabbit,—the convulsions being preceded by palsy, and ending in coma.
Half an ounce when injected into the stomach excited the same symptoms
in a cat, and proved fatal in sixty-five minutes, though the animal
vomited. Schloepfer observed, that when a scruple, dissolved in two
drachms of water, was injected into the windpipe of a rabbit, it fell
down immediately, threw back its head, was convulsed in the fore-legs,
and died in twelve minutes.[1384] Gmelin observed in his experiments
that it caused slight inflammation of the stomach, and strong symptoms
of an action on the brain, spine, and voluntary muscles. He found the
voluntary muscles destitute of contractility immediately after death;
yet the heart continued to contract vigorously for some time, even
without the application of any stimulus. From some experiments made on
horses by Huzard and Biron, by order of the Société de Santé of Paris,
it appears that the hydrochlorate, when given to these animals in the
dose of two drachms daily, produced sudden death about the fifteenth
day, without previous symptoms of any consequence.[1385] In the
experiments now related, very little appearance of inflammation was
found in the parts to which the poison was directly applied. It is also
worthy of remark that the heart does not seem to have been particularly
affected; and yet according to the recent researches of Mr. Blake, the
barytic salts are the most powerful of all inorganic poisons in their
action on the heart, when they are injected into the veins. A quarter of
a grain of the chloride appreciably depresses arterial action; two
grains completely arrest the heart’s contractions in twelve seconds; and
when it is injected back into the aorta from the axillary artery, it
causes at first some obstruction to the capillary circulation, but soon
arrests the action of the heart, as when it is introduced into the
veins.[1386]

The pure earth appears to produce nearly the same effects in an inferior
dose. When swallowed, the symptoms of local irritation are more violent;
but death ensues in a very short space of time, and is preceded by
convulsions and insensibility. The stomach after death is found of a
reddish-black colour, and frequently with spots of extravasated blood in
its villous coat.

The carbonate in a state of minute division is scarcely less active than
the hydrochlorate, since it is dissolved by the acid juices of the
stomach. A drachm killed a dog in six hours; vomiting, expressions of
pain, and an approach to insensibility preceded death; and marks of
inflammation were found in the stomach.[1387] Pelletier made many
experiments on the poisonous properties of the carbonate. Fifteen grains
of the native carbonate killed one dog in eight hours, and another in
fifteen.[1388] Dr. Campbell found it to be a dangerous poison, even when
applied externally. Twelve grains introduced into a wound in the neck of
a cat, excited on the third day languor, slow respiration, and feeble
pulse; towards evening the animal became affected with convulsions of
the hind-legs and with dilated pupils; and death followed not long
afterwards.[1389] This substance, before its real nature was known, used
at one time to be employed in some parts of England as a variety of
arsenic for poisoning rats.

The salts of baryta are absorbed in the course of their action. The
chloride has been detected by Dr. Kramer both in the blood and urine by
incineration with carbonate of potash, washing the ashes with weak
solution of carbonate of potash, dissolving the residue in diluted
nitric acid, and testing the solution for baryta.[1390] Orfila has also
obtained baryta, by his process alluded to above, in the liver, kidneys,
and spleen of animals killed by the chloride.[1391]

The symptoms produced by the salts of baryta in man have seldom been
particularly described. An instance is shortly noticed in the Journal of
Science, where an ounce of the hydrochlorate was taken by mistake for
Glauber’s salt, and proved fatal. The patient immediately after
swallowing it felt a sense of burning in the stomach; vomiting,
convulsions, headache, and deafness ensued; and death took place within
an hour.[1392] A similar case, fatal in two hours, has been related by
Dr. Wach of Merseburg. A middle-aged woman who, though generally in good
health, had suffered for a day or two from pains in the stomach, took
one morning a solution of half an ounce of chloride of barium by mistake
for sulphate of soda. She was soon seized with sickness, retching,
convulsive twitches of the hands and feet, vomiting of clear mucus,
great anxiety, restlessness, and loss of voice; and she died under
constant efforts to vomit, and violent convulsive movements, but with
her faculties entire.[1393]

Unpleasant effects have been observed from too large doses of the
chloride administered medicinally. A case is mentioned in the Medical
Commentaries of a gentleman who was directed to take a solution as a
stomachic, but swallowed one evening by accident so much as seventy or
eighty drops. He had soon after profuse purging without tormina, then
vomiting, and half an hour after swallowing the salt excessive muscular
debility, amounting to absolute paraplegia of the limbs. This state
lasted about twenty-four hours, and then gradually went off.[1394] I
have known violent vomiting, gripes, and diarrhœa produced in like
manner by a quantity not much exceeding the usual medicinal doses.

Dr. Wilson of London has lately described a distinct case of poisoning
with the carbonate. The quantity taken was half a tea-cupful; but
emetics were given, and operated before any symptoms showed themselves.
In two hours the patient complained of dimness of sight, double vision,
headache, tinnitus, and a sense of distension in the stomach, and
subsequently of pains in the knees and cramps of the legs, with
occasional vomiting and purging next day; for some days afterwards the
head symptoms continued, though more mildly, and she was much subject to
severe palpitations; but she was in the way of recovery when the account
of her case was published.[1395] Mr. Parkes mentions that, according to
information communicated to him by the proprietor of an estate in
Lancashire, where carbonate of baryta abounds, many domestic animals on
his estate died in consequence of licking the dust of the carbonate, and
that it once proved fatal to two persons, a woman and her child, who
took each about a drachm.[1396] Dr. Johnstone says he once swallowed ten
grains of this compound, without experiencing any bad effect.[1397]


SECTION III.—_Of the Morbid Appearances caused by the Salts of Baryta._

In animals the mucous membrane of the stomach is usually found of a
deep-red colour, unless death take place with great rapidity, in which
case the alimentary canal is healthy. In all the animals, which in Dr.
Campbell’s experiments were killed by the application of the muriate to
wounds, the brain and its membranes were much injected with blood; and
in one of them the appearances were precisely those of congestive
apoplexy.

In Wach’s case the stomach was dark brownish-red externally, and the
small intestines brighter red. Internally the stomach presented uniform
deep redness, with clots of blood, and bloody mucus scattered over it;
and near the cardiac end there was a perforation, above half an inch in
diameter within, and half as wide at the outside, and surrounded with
swollen edges and extensive thickening of the villous coat. The small
intestines were internally very red and lined with red mucus
interspersed with clots of blood. The great intestines were extremely
contracted. The lungs were gorged, the heart full of dark liquid blood,
and the cerebral vessels distended. Chloride of barium was detected in
the stomach and intestines. The perforation in this case was evidently
an accidental concurrence.


                    SECTION IV.—_Of the Treatment._

The treatment of this variety of poisoning consists chiefly in the
speedy administration of some alkaline or earthy sulphate, such as the
sulphate of soda or sulphate of magnesia. The poison is thus immediately
converted into the insoluble sulphate of baryta, which is quite inert.
Two drachms of muriate of baryta were injected by Orfila into the
stomach of a dog, and eight minutes afterwards two drachms of sulphate
of soda. The gullet was then secured by a ligature. At first efforts
were made to vomit, and in an hour sulphate of baryta was discharged
with the alvine evacuations. There was neither insensibility nor
convulsions; and the next morning the animal evidently suffered only
from the ligature on the gullet. This fact not only proves the efficacy
of the sulphate, but likewise shows that in the kinds of poisoning where
diarrhœa occurs, the poison is very soon discharged, and ought therefore
to be looked for in the evacuations from the bowels.[1398]


A few observations may be here added on the effects of the salts of
_strontia_ on the animal frame. These compounds bear a close resemblance
to the salts of baryta, and the two earths were consequently long
confounded together till Dr. Hope pointed out their distinctions. One of
the most striking differences is, that the salts of the strontia are
very feebly poisonous. Some experiments of this purport were made by M.
Pelletier of Paris,[1399] and by Blumenbach; but the most accurate
researches are those of Professor Gmelin. He found that ten grains of
the chloride in solution had no effect when injected into the jugular
vein of a dog,—that two drachms had no effect when introduced into the
stomach of a rabbit,—that half an ounce was required to cause death in
that way,—that two drachms of the carbonate had no effect,—and that two
drachms of the nitrate, dissolved in six parts of water and given to a
rabbit, merely caused increase of the frequency and hardness of the
pulse and a brisk diarrhœa.[1400] Mr. Blake also found that small doses
of the salts of strontia have little effect when injected into the
veins; but that forty grains arrest the action of the heart in fifteen
seconds.[1401]




                              CHAPTER XX.


The fourth order of the irritant poisons contains a great number of
genera derived from the vegetable kingdom, and at one time commonly
arranged in a class by themselves under the title of Acrid Poisons. The
order includes many plants of the natural families _Ranunculaceæ_,
_Cucurbitaceæ_, and _Euphorbiaceæ_, and other plants scattered
throughout the botanical system. It likewise comprehends a second group
consisting of some acrid poisons from the animal kingdom, namely,
cantharides, poisonous fishes, poisonous serpents, and animal matters
become poisonous by disease or putrefaction.


                OF POISONING WITH THE VEGETABLE ACRIDS.

The vegetable acrids are the most characteristic poisons of this order.
They will not require many details, as they are seldom resorted to for
criminal purposes, and their mode of action, their symptoms, and their
morbid appearances are nearly the same in all.

We are chiefly indebted to Professor Orfila for our knowledge of their
_mode of action_. He has subjected them to two sets of experiments. In
the first place, he introduced the poison in various doses into the
stomach, sometimes tying the gullet, sometimes not: and, secondly, he
applied the poison to the subcutaneous cellular tissue by thrusting it
into a recent wound.

In the former way he found that, unless the gullet was tied, the animal
soon discharged the poison by vomiting, and generally recovered; but
that, if the gullet was tied, death might be caused in no long time by
moderate doses. The symptoms were seldom remarkable. Commonly efforts
were made to vomit; frequently diarrhœa followed; then languor and
listlessness; sometimes, though not always, expressions of pain; very
rarely convulsions; and death generally took place during the first day,
often within three, six, or eight hours. The appearances in the dead
body were redness over the whole mucous coat of the stomach, at times
remarkably vivid, often barely perceptible, and occasionally attended
with ulcers; very often a similar state of the whole intestines, more
especially of the rectum; and in some instances a slight increase of
density, with diminished crepitation, in patches of the lungs.

When the poison, on the other hand, was applied to a recent wound of the
leg, the animal commonly whined more or less; great languor soon
followed; and death took place on the first or second day, without
convulsions or any other symptom of note. It was seldom that any morbid
appearance could then be discovered in the bowels. But in every instance
active inflammation was found in the wound, extending to the limb above
it and even upwards on the trunk. Every part affected was gorged with
blood and serum; and an eschar was never formed. The appearances in
short were precisely those of diffuse inflammation of the cellular
tissue, when it proves fatal in its early stage.[1402]

Since these poisons do not appear to act more energetically through a
wound than through the stomach, it has been generally inferred that they
do not enter the blood, and consequently that the local impression they
produce is conveyed to distant organs through the nerves. This inference
is correct in regard to such species of the vegetable acrids as act in
small doses. But the validity of the conclusion may be questioned when
the poison acts only in large doses, as in the case with many of those
now under consideration. For they cannot be applied to a wound over a
surface equal to that of the stomach, and may therefore be more slowly
absorbed in the former than in the latter situation. And, in point of
fact, a few plants of the present order have been found to act through
the medium of absorption, as soon as chemistry discovered their active
principles, and thus enabled the physiologist to get rid of fallacy by
using the poison in small quantity. This principle has been proved to be
in some plants a peculiar resin, in others a peculiar extractive matter,
in others an oil, in others an alkaloid, and in others a neutral
crystalline matter. But in all there exists some principle or other in
which are concentrated the poisonous properties of the plant. Some of
these principles appear to act through the medium of the blood.

There is no doubt, however, but many plants of the present order, as
well as their active principles, have a totally different and very
peculiar action. They produce violent spreading inflammation of the
subcutaneous cellular tissue, and acute inflammation of the stomach and
intestines, without entering the blood; and death is the consequence of
a sympathy of remote organs with the parts directly injured.

As to their forming a natural order of poisons, it is evident, that if a
general view be taken of their properties, they are distinguished by
obvious phenomena from the three orders hitherto noticed. But if their
effects on man be alone taken into account, when of course their
influence on the external surface of the body must be left out of view,
nothing will be discovered to distinguish them from several of the
metallic irritants.

The _symptoms_ occasioned in man by the irritant poisons of the
vegetable kingdom, are chiefly those indicating inflammation of the
villous coat of the stomach and intestines. When taken in large doses,
they excite vomiting soon after they are swallowed; by which means the
patient’s life is often saved. But sometimes, like the mineral poisons
that possess emetic properties, the vegetable acrids present a singular
uncertainty in this respect: they may be retained without much
inconvenience for some length of time. If this should happen, or if the
dose be less, in which case vomiting may not be produced at all, or if
only part of a large dose be discharged at an early period by
vomiting,—the other phenomena they give rise to are sometimes fully
developed. The most conspicuous symptom then is diarrhœa, more or less
profuse. The diarrhœa and vomiting are commonly attended by twisting
pain of the belly, at first remittent, but gradually more constant, as
the inflammation becomes more and more strongly marked. Tension, fulness
and tenderness of the belly, are then not unfrequent. The stools may
assume all the characters of the discharges in natural inflammation of
the intestinal mucous membrane, but an additional character worthy of
notice is the appearance of fragments of leaves or flowers belonging to
the plant which has been swallowed. At the same time there is generally
excessive weakness. Sometimes, too, giddiness and a tendency to delirium
have been observed. But the latter symptoms are rare: if they occurred
frequently, it would be necessary to transfer any poison which produced
them to the class of narcotico-acrids.

The properties now mentioned have long ago attracted the attention of
physicians, and led them to introduce many vegetable irritants into the
materia medica. In fact they comprehended a great number of the most
active, or, as they are technically called, drastic purgatives. Among
others, elaterium, euphorbium, gamboge, colocynth, scammony, croton,
jalap, savin, stavesacre, are of this description. The effect of most of
them, however, is so violent and uncertain, that few are now much used
except when combined with other milder laxatives.

The _morbid appearances_ they leave in the dead body are the same with
those noticed under the head of their mode of action,—more or less
redness of the stomach, ulceration of its villous coat, redness of the
intestines, and especially of the rectum and colon, which are often
inflamed when the small intestines are not visibly affected.

In the following account of the particular poisons of this order, a very
cursory view will be taken of their physical and chemical properties. A
knowledge of these properties will be best acquired from any author on
the materia medica; and an account of them would be misplaced in a work
which professes to describe only the leading objects of the medical
jurist’s attention.

A great number of genera might be arranged under the present head. But
the following list comprehends all which require mention. _Euphorbia_,
or spurge, the _ricinus_, or castor-oil tree, the _jatropha_, or
cassava-plant, croton-oil, _elaterium_, or squirting cucumber,
_colocynth_, or bitter-apple, _bryony_, or wild cucumber, _ranunculus_,
or buttercup, _anemone_, _stavesacre_, _celandine_, _marsh marigold_,
_mezereon_, _spurge-laurel_, _savine_, _daffodil_, _jalap_,
_manchineel_, _cuckow-pint_.

The first plants to be noticed belong to the natural order
_Euphorbiaceæ_, namely, the euphorbia, ricinus, jatropha, and croton.


                    _Of Poisoning with Euphorbium._

_Euphorbium_ is the inspissated juice of various plants of the genus
euphorbia or spurge, but is principally procured from the _E.
officinarum_, a species that abounds in Northern Africa. It contains a
variety of principles; but its chief ingredient is a resin, in which its
active properties reside. It has been analysed by Braconnot, Pelletier,
Brandes,[1403] and Drs. Buchner and Herberger. According to Brandes the
resin forms above 44 per cent. of the crude drug, and is so very acrid,
that the eyelid is inflamed by rubbing it with the finger which has
touched the resin, even although it be subsequently washed with an
alkali.[1404] According to the most recent analysis, that of Drs.
Buchner and Herberger, this resin is a compound substance, which
consists of two resinous principles, one possessing in some degree the
properties of an acid, and the other the properties of a base. The
latter, which they have called euphorbin, is considered by them the true
active principle of euphorbium.[1405] It will be mentioned under the
head of Jalap, that they have taken the same view of the nature of other
resinous poisons.

Orfila found that a large dog was killed in twenty-six hours and a half
by half an ounce of powder of euphorbium introduced into the stomach,
and retained there by a ligature on the gullet.

The whole coats of the stomach, but especially the villous membrane,
were of a deep-red or almost black colour; the colon, and still more the
rectum, were of a lively red internally, and their inner membrane was
checkered with little ulcers. Two drachms of the powder thrust into a
wound in the thigh, and secured by covering it with the flaps of the
incision, killed a dog in twenty-seven hours; and death was preceded by
no remarkable symptom except great languor. The wounded limb was found
after death highly inflamed, and the redness and sanguinolent
infiltration, which were alluded to in the general observations on the
vegetable acrids, extended from the knee as high up the trunk as the
fifth rib,—a striking proof of the rapidity with which this variety of
inflammation diffuses itself.[1406] Mr. Blake concludes from his
experiments, that euphorbium, when injected in a state of solution in
the jugular vein, acts by obstructing both the pulmonary and systemic
capillaries, and so preventing the passage of the blood into the left
side of the heart; but that the heart is not primarily acted on.[1407]

The most common symptoms occasioned in man by euphorbium are violent
griping and purging, and excessive exhaustion; but it appears probable
that narcotic symptoms are also at times induced. A case of irritant
poisoning with it has been related in the Philosophical Transactions;
but it is not a pure one, as a large quantity of camphor was taken at
the same time. Much irritation was produced in the alimentary canal; but
by the prompt excitement of vomiting and the subsequent use of opium the
patient soon recovered.[1408] Mr. Furnival has related a fatal case
which arose from a farrier having given a man a tea-spoonful by mistake
for rhubarb. Burning heat in the throat and then in the stomach,
vomiting, irregular hurried pulse, and cold perspiration were the
leading symptoms; and the person died in three days. Several gangrenous
spots were found in the stomach, and its coats tore with the slightest
touch.[1409] The operation of this substance is so violent and
uncertain, that it has long ceased to be employed inwardly in the
regular practice of medicine, and has been even excluded from some
modern Pharmacopœias. It is still used by farriers as an external
application; and in the Infirmary of this city I met with a fatal case
of poisoning in the human subject, which was supposed to have been
produced by a mixture containing it, and intended to cure horses of the
grease. Pyl has related the proceedings in a prosecution against a man
for putting powder of euphorbium into his maid-servant’s bed; and from
this narrative it appears, that, when applied to the sound skin, it
causes violent heat, itching and smarting, succeeded by inflammation and
blisters.[1410] Dr. Veitch denies that the powder has any such
power;[1411] but the effects described by Pyl correspond with popular
belief.

Probably all the species of euphorbium possess the same properties as
_E. officinarum_. Orfila found that the juice of the leaves of E.
_cyparissias_ and _lathyris_ produces precisely the effects described
above. Sproegel applied the juice of the latter to his face, and was
attacked in consequence with an eruption like nettle-rash; and he found
that it caused warts and hair to drop out.[1412] Vicat mentions
analogous facts, and Lamotte notices the case of a patient who died in
consequence of a clyster having been prepared with this species instead
of the mercurialis.[1413] The seeds and root of the _E. lathyris_ or
caper-spurge are used by the inhabitants of the northern Alps in the
dose of fifteen grains as an emetic; and very lately the oil of the
seeds has been employed in Italy as an active purgative, which in the
dose of two or eight grains is said to possess all the efficacy of
croton oil.[1414] MM. Chevallier and Aubergier have also found the seeds
of the _E. hybeua_ and their expressed oil to be very energetic. The
seeds yield 44 per cent. of oil, which in the dose of ten drops produces
copious watery evacuations without pain, and resembles closely
croton-oil in its effects.[1415] The _E. esula_ appears to be a very
active species. Scopoli says that a woman who took thirty grains of the
root died in half an hour, and that he once knew it cause fatal gangrene
when imprudently applied to the skin of the belly.[1416] Withering
observes that all the indigenous species blister and ulcerate the skin,
and that many of them are used by country people for these
purposes.[1417]

I have no where seen any notice taken by authors of narcotic symptoms as
the effect of poisoning with euphorbium; and indeed this substance has
always been considered a pure irritant. I am informed, however, by the
Messrs. Herring, wholesale druggists in London, that their workmen are
subject to headache, giddiness and stupor, if they do not carefully
avoid the dust thrown up while it is ground in the mill; and that the
men themselves are familiarly acquainted with this risk. An analogous
fact has likewise been communicated to me by Dr. Hood of this city,
relative to the effects of the seeds of the _E. lathyris_. A child two
years of age ate some of the seeds, and soon after vomited severely,
which is the usual effect. Drowsiness, however, succeeded; and after a
few returns of vomiting, which were promoted by an emetic, deep sleep
gradually came on, broken by convulsions, stertorous breathing and
sighs. Sensibility was somewhat restored by blood-letting and the warm
bath; after which the tendency to sleep was interrupted by frequent
agitation and exercise in the open air. The vomiting then recurred for a
time; but the child eventually got well.


         _Of Poisoning with the Seeds of the Castor-Oil Tree._

_Castor-oil_ at present so extensively used as a mild and effectual
laxative, is nevertheless derived from a plant hardly inferior in
activity as a poison to that just considered. It is the expressed oil of
the seeds of the _Ricinus communis_ or Palma Christi. Much discussion
has taken place as to the source of the acrid properties of this seed,
some supposing that they reside in the embryo, others in the perisperm,
others in the cotyledon, others in a principle formed from the oil by
heat; and the question is scarcely yet settled. It is certain, however,
that, although castor oil owes its occasional acridity to changes
effected by the heat to which it is sometimes exposed in the process of
separation, nevertheless the cotyledons are in themselves acrid.[1418]

Two or three of the seeds will operate as a violent cathartic. Bergius,
as quoted by Orfila, says he knew a stout man who was attacked with
profuse vomiting and purging after having masticated a single seed.
Lanzoni met with an instance where three grains of the fresh seeds,
taken by a young woman, caused so violent vomiting, hiccup, pain in the
stomach, and faintness, that for some time her life was considered in
great danger.[1419] Mr. Alfred Taylor met with three cases of poisoning
with castor-oil seeds. Two sisters, who took each from two to four
seeds, suffered severely; and a third, who took twenty, died in five
days, with symptoms like those of malignant cholera.[1420] Climate
probably affects their activity; for I have known a person eat without
any effect several seeds ripened in the open air in this neighbourhood.
Dogs vomit so easily that they may take thirty seeds without material
inconvenience, if the gullet is not tied. But if the gullet is secured,
a much less quantity will occasion death in six hours. They produce
violent inflammation when applied to a wound.[1421]


                  _Of Poisoning with the Physic-nut._

The plants of the genus _Jatropha_, belonging to the same natural
family, have all of them the same acrid properties as the castor-oil
tree. The seeds of the _J. curcas_, the physic-nut of the West Indies,
when applied in the form of powder to a wound, produce violent spreading
inflammation of the subcutaneous cellular tissue; and when introduced
into the stomach they inflame that organ and the intestines.[1422] Four
seeds will act on man as a powerful cathartic.[1423] I have known
violent vomiting and purging occasioned by a few grains of the cake,
left after expression of the fixed oil from the bruised seeds; and in
some experiments performed a few years ago, I found that twelve or
fifteen drops of the oil produced exactly the same effects as an ounce
of castor-oil, though not with such certainty. In the last edition of
this work some observations were made, on the authority of MM. Pelletier
and Caventou, respecting the properties of a pure oil and a volatile
acid, supposed by them to exist in the physic-nut; but they analyzed the
croton seed by mistake for it.

Two other species have been also examined, but not with care, namely,
the _Jatropha multifida_, and the _Jatropha_ or _Janipha manihot_. It is
probable that the seeds of both are acrid, and also the oil which may be
extracted from them by pressure. But a much more interesting part of the
latter species in a toxicological point of view is the root; the juice
of which is a most energetic poison. The _Janipha manihot_, or
cassava-plant, has two varieties, one of which produces a small,
spindle-shaped, bland root, called, in the West Indies, sweet cassava,
while the other has a much larger, bitter, poisonous root, called bitter
cassava, and in universal use for obtaining the well-known amylaceous
substance, tapioca. The juice of the bitter variety is watery, and so
poisonous that, according to Dr. Clark of Dominica, negroes have been
killed in an hour by drinking half a pint of it.[1424] It has been
commonly, but erroneously, arranged among acrid poisons. It really
belongs to the narcotic class, for it occasions coma and convulsions.
And we now know the cause of this extraordinary anomaly in the natural
family to which the species belongs; because MM. Henry and Boutron
ascertained that the juice imported into France, as well as what they
expressed from fresh roots sent from the West Indies, contains
hydrocyanic acid, produces in animals all the usual effects of that
poison, and is rendered inert by such means as will remove the acid,—for
example, by the addition of nitrate of silver.[1425] I confirmed this
singular discovery in 1838 by examination of some well-preserved juice
from Demerara. It is easy to see how tapioca, which is obtained from the
poisonous root by careful elutriation, becomes quite bland during the
process.


                    _Of Poisoning with Manchineel._

The _manchineel_ [_Hippomane mancinella_], another plant of the same
natural family, contains a milky juice, which is possessed of very acrid
properties. Orfila and Ollivier have made some careful experiments with
it on animals,[1426] and M. Ricord has since added some observations on
its effects on man.[1427] From the former it appears that two drachms of
the juice applied to a wound in a dog will cause death in twenty-eight
hours, by exciting diffuse cellular inflammation; and that half that
quantity will prove fatal in nine hours when introduced into the
stomach. From the observations of M. Ricord it follows that inflammation
is excited wherever the juice is applied, even in the sound skin; but he
denies the generally received notion, that similar effects ensue from
sleeping under the branches of the tree, or receiving drops of moisture
from the leaves. This notion, however, it is right to add, has been
adopted by other recent authors. Descourtils, for example, states that
it is dangerous to sleep under the tree; that drops of rain from the
leaves will blister any part of the skin on which they fall; and that on
these accounts the police of St. Domingo were in the practice of
destroying the trees wherever they grew.[1428] Other species of
Hippomane are equally poisonous. The _H. biglandulosa_ and _H. spinosa_
are peculiarly so, especially the latter, which is known to the negroes
of St. Domingo by the name of Zombi apple, and is familiarly used by
them as a potent poison.[1429]


                      _Of Poisoning with Croton._

The oil of the _Croton Tiglium_ has been familiarly known for some years
as a very powerful hydragogue cathartic in the dose of a few drops; and
therefore little doubt could exist that both the oil and the seed which
yields it must be active irritant poisons in moderate doses. Accordingly
it has been lately found by experiments in Germany that forty seeds will
kill a horse in the course of seven hours;[1430] and Rumphius mentions
that it was a common poison in his time at Amboyna among the natives. I
have known most violent watery purging and great prostration caused by
four drops of the expressed oil. A fatal case of poisoning with it
occurred not long ago in France. A young man who swallowed two drachms
and a half of the oil by mistake, instead of using it as an embrocation,
was soon seized with tenderness of the belly, violent efforts to vomit,
cold sweating, laborious respiration, blueness of the lips and fingers,
and an almost imperceptible pulse,—then with profuse, involuntary
discharges by stool, burning along the throat and gullet, and
insensibility of the skin;—and in four hours he expired. The villous
coat of the stomach was soft, but not otherwise injured.[1431]

The activity of the seed and oil seems to depend on a peculiar volatile
acid, which was discovered by MM. Pelletier and Caventou when they
analysed the croton seed by mistake as the seed of the _Jatropha
curcas_, or physic-nut. When the oil was saponified by potash and then
freed of the acid by distillation, it became inert. On the other hand,
the acid was found by them to excite inflammation of the stomach, and
spreading inflammation of the cellular tissue, according as it was
administered internally or applied to a wound.[1432]

The next natural family in which plants are to be found that possess the
properties of the acrid poisons, is the _Cucurbitaceæ_, or gourds. This
family, it should be remarked, does not in general possess poisonous
properties. On the contrary, they are, with a few exceptions, remarkably
mild; and many of them supply articles of luxury for the table. The
melon, gourd, and cucumber belong to the order. The only poisons of the
order which have been examined with any care are elaterium, bryony, and
colocynth.


                      _Of Poisoning with Bryony._

The roots of the _Bryonia alba_ and _Dioica_ possesses properties
essentially the same with those of euphorbium. The _B. dioica_ is a
native of Britain, where it grows among hedges, and is usually known by
the name of wild vine, or bryony. The flowers are greenish, and are
succeeded by small, red berries. The root, which is the most active part
of the plant, is spindle-shaped, and varies in size from that of a man’s
thigh to that of a radish.

Orfila found that half an ounce of the root introduced into the stomach
of a dog, killed it in twenty-four hours, when the gullet was tied; and
that two drachms and a half applied to a wound brought on violent
inflammation and suppuration of the part, ending fatally in sixty
hours.[1433]

Bryony root owes its power to an extractive matter discovered in it by
Brandes and Firnhaber, to which the name of Bryonine has been given.
According to the experiments of Collard de Martigny, bryonine acts on
the stomach and on a wound exactly as the root itself, but more
energetically. When introduced into the cavity of the pleura it causes
rapid death by true pleurisy, ending in the effusion of fibrin.[1434]

Before bryony-root was expelled from medical practice, it was often
known to produce violent vomiting, tormina, profuse watery evacuations,
and fainting. Pyl mentions a fatal case of poisoning with it, which
happened at Cambray in France. The subject was a man who took two
glasses of an infusion of the root to cure ague, and was soon after
seized with violent tormina and purging, which nothing could arrest, and
which soon terminated fatally.[1435] Orfila quotes a similar case from
the Gazette de Santé, which proved fatal within four hours, in
consequence of a strong decoction of an ounce of the root having been
administered, partly by the mouth and partly in a clyster, to repel the
secretion of milk.[1436]


                     _Of Poisoning with Colocynth._

Colocynth, or bitter-apple, is another very active and more common acrid
derived from a plant of the same family, the Cucumis colocynthis. It is
imported into this country in the form of a roundish, dry, light fruit,
as big as an orange, of a yellowish-white colour, and excessively bitter
taste. Its active principle is probably a resinoid matter discovered by
Vauquelin, which is very soluble in alcohol and sparingly so in water,
but which imparts even to the latter an intensely bitter taste.[1437] It
is termed Colocynthin.

According to the experiments of Orfila, colocynth powder or its
decoction produces the usual effects of the acrid vegetables on the
stomach and on the subcutaneous cellular tissue. Three drachms proved
fatal in fifteen hours to a dog through the former channel when the
gullet was tied, and two drachms killed another when applied to a
wound.[1438]

A considerable number of severe cases of poisoning with this substance
have occurred in the human subject; and a few have proved fatal. Tulpius
notices the case of a man who was nearly carried off by profuse, bloody
diarrhœa, in consequence of taking a decoction of three colocynth
apples.[1439] Orfila relates that of a rag-picker, who, attempting to
cure himself of a gonorrhœa by taking three ounces of colocynth, was
seized with vomiting, acute pain in the stomach, profuse diarrhœa,
dimness of sight, and slight delirium; but he recovered under the use of
diluents and local blood-letting.[1440] In 1823 a coroner’s inquest was
held at London on the body of a woman who died in twenty-four hours,
with incessant vomiting and purging, in consequence of having swallowed
by mistake a tea-spoonful and a half of colocynth powder.[1441] M.
Carron d’Annecy has communicated to Orfila the details of an instructive
case, which also proved fatal. The subject was a locksmith, who took
from a quack two glasses of decoction of colocynth to cure hemorrhoids,
and was soon after attacked with colic, purging, heat in the belly, and
dryness of the throat. Afterwards the belly became tense and excessively
tender, and the stools were suppressed altogether. Next morning he had
also retention of urine, retraction of the testicles and priapism. On
the third day the retention ceased, but the other symptoms continued,
and the skin became covered with clammy sweat, which preceded his death
only a few hours. The intestines were red, studded with black spots, and
matted together by fibrinous matter; the usual fluid of peritonitis was
effused into the belly; the villous coat of the stomach was here and
there ulcerated; and the liver, kidneys, and bladder also exhibited
traces of inflammation.[1442]


                     _Of Poisoning with Elaterium._

Elaterium, which is procured from a third plant of the cucurbitaceæ, the
_Momordica elaterium_ or squirting cucumber, possesses precisely the
same properties with the two preceding substances. It appears, however,
to be more active; for a single grain has been known to act violently on
man. There can be no doubt that small doses will prove fatal; but its
strength and consequently its effects are uncertain. British elaterium,
which is the feculence that subsides in the juice of the fruit, is the
most powerful; French elaterium, which is the extract of the same juice,
is much weaker; and a still weaker preparation sometimes made is an
extract of the juice of the whole plant. The plant itself is probably
poisonous. But the only case in point with which I am acquainted is a
singular instance of poisoning, apparently produced in consequence of
the plant having been carried for some time betwixt the hat and head. A
medical gentleman in Paris, after carrying a specimen to his lodgings in
his hat, was seized in half an hour with acute pain and sense of
tightness in the head, succeeded by colic pains, fixed pain in the
stomach, frequent watery purging, bilious vomiting, and some fever.
These symptoms continued upwards of twelve hours.[1443]

The active properties of this substance reside in a peculiar crystalline
principle, discovered by Mr. Morries-Stirling, and named by him
_Elaterine_. It is procured by evaporating the alcoholic infusion of
elaterium to the consistence of thin oil, and throwing it into boiling
distilled water; upon which a white crystalline precipitate is formed,
and more falls down as the water cools. This precipitate when purified
by a second solution in alcohol and precipitation by water, is pure
elaterine. In mass it has a silky appearance. The crystals are
microscopic rhombic prisms, striated on the sides. It is intensely
bitter. It does not dissolve in the alkalis, or in water, is sparingly
soluble in diluted acids, but easily soluble in alcohol, ether, and
fixed oil. It has not any alkaline reaction on litmus.—It is a poison of
very great activity. A tenth of a grain, as I have myself witnessed,
will sometimes cause purging in man; and a fifth of a grain in two
doses, administered at an interval of twenty-four hours to a rabbit,
killed it seventeen hours after the second dose. The best British
elaterium contains 26 per cent. of it, the worst 15 per cent.; but
French elaterium does not contain above 5 or 6 per cent.[1444] These
facts account for the great irregularity in the effects of this drug as
a cathartic. The principle discovered by Mr. Morries-Stirling was also
discovered about the same time by Mr. Hennell[1445] of London.


                 _Of Poisoning with the Ranunculaceæ._

The natural family of the Ranunculaceæ abounds in acrid poisons. Indeed
few of the genera included in it are without more or less acrid
property.

The genus _Ranunculus_ is of some interest to the British toxicologist,
because many species grow in this country, and unpleasant accidents have
been occasioned by them. The most common are the _R. bulbosus_, _acris_,
_sceleratus_, _Flammula_, _Lingua_, _aquatilis_, _repens_, _Ficaria_,
which are all abundant in the neighbourhood of this city. The
_Ranunculus acris_ is the only species that has been particularly
examined. Five ounces of juice, extracted by triturating the leaves with
two ounces of water, killed a stout dog in twelve hours when taken
internally. Two drachms of the aqueous extract applied to a wound killed
another in twelve hours by inducing the usual inflammation.[1446]

Krapf, as quoted in Orfila’s Toxicology, found by experiments on
himself, that two drops of the expressed juice of the _Ranunculus acris_
produced burning pain and spasms in the gullet and griping in the lower
belly. A single flower had the same effect. When he chewed the thickest
and most succulent of the leaves, the salivary glands were strongly
stimulated, his tongue was excoriated and cracked, his teeth smarted,
and his gums became tender and bloody.[1447] Dr. Withering alleges that
it will blister the skin. A man at Bevay in the north of France, after
swallowing by mistake a glassful of the juice which had been kept for
some time as a remedy for vermin on the head, was seized in four hours
with violent vomiting and colic, and expired in two days.[1448] The
acridity of the genus ranunculus is entirely lost by drying, either with
or without artificial heat. The _R. acris_, however, is far from being
the most active species of the genus. The taste of the leaves of _R.
bulbosus_, _alpestris_, _gramineus_, and _Flammula_, and also of the
unripe germens of _R. sceleratus_, is much more pungent. The _R.
repens_, _Ficaria_, _auricomus_, _aquatilis_, and _Lingua_, I have found
to be bland.

The genus _Anemone_ produces similar effects on the animal economy. The
most pungent species I have examined are the _A. pulsatilla_, _A.
hortensis_, and _A. coronaria_; the _A. nemorosa_ and _A. patens_ are
less active; and the _A. hepatica_, as well as the _A. alpestris_, are
bland. The powder of the _A. pulsatilla_ causes itching of the eyes,
colic and vomiting, if in pulverizing it the operator do not avoid the
fine dust which is driven up; and Bulliard relates the case of a man
who, in applying the bruised root to his calf for rheumatism, was
attacked with inflammation and gangrene of the whole leg.[1449] The same
author mentions an instance where violent convulsions were produced by
an infusion of the _A. nemorosa_, and the person was for some time
thought to be in great danger.[1450] The acridity of the anemone is
retained under desiccation even in the vapour-bath; but is very slowly
lost under exposure to the air, not entirely, however, in two months.
The ripe fruit of the _A. hortensis_ is bland. The activity of the
anemones is owing to a volatile oil, which, when left for some time in
the water with which it passes over in distillation is converted into a
neutral crystalline body called anemonine, and a peculiar acid termed
anemonic acid.[1451]

The _Caltha palustris_, or marsh marigold, a plant closely allied in
external characters to the ranunculus, is considered by toxicologists a
powerful acrid poison. Wibmer observes that it has an acrid, burning
taste,[1452]—a remark which has been also made by Haller.[1453] On the
continent the flower buds are said to be sometimes pickled and used for
capers on account of their pungency. The following set of cases which
happened in 1817 near Solingen will show that in some localities it
possesses energetic and singular properties. The poison was taken
accidentally by a family of five persons, in consequence of their having
been compelled by the badness of the times to try to make food of
various herbs. They were all seized half an hour after eating with
sickness, pain in the abdomen, vomiting, headache, and ringing in the
ears, afterwards with dysuria and diarrhœa, next day with œdema of the
whole body, particularly of the face, and on the third day with an
eruption of pemphigous vesicles as large as almonds, which dried up in
forty-eight hours. They all recovered.[1454]

Notwithstanding these apparently pointed facts, however, I have no doubt
that the marsh marigold is in some circumstances bland, and is commonly
so in this country, or at least but feebly poisonous. Haller, in
speaking of its acrid taste, adds that when young it is eaten with
safety by goats. For my own part I have never been able to remark any
distinct acridity in tasting it either before inflorescence, or in the
young flower-buds, or in any part of the plant while in full flower. It
produces a peculiar, disagreeable impression on the back of the tongue,
when collected in dry situations; but never occasions that pungent
acridity which so remarkably characterizes many species of ranunculus,
anemone, and clematis.

The _stavesacre_, or _Delphinium staphysagria_, another plant of the
same natural family, is interesting in a scientific point of view,
because its properties have been distinctly traced to a peculiar
alkaloid. The seeds, which alone have been hitherto examined, were
analyzed by MM. Lassaigne and Feneulle, who, besides a number of inert
principles, discovered in them an alkaloid, possessing in an eminent
degree the poisonous qualities of the seeds. This alkaloid is solid,
white, pulverulent but crystalline, fusible like wax, very bitter and
acrid, almost insoluble in water, very soluble in ether and alcohol, and
capable of forming salts with most of the acids.[1455] It has been named
_delphinia_. It was also discovered about the same time by
Brandes.[1456]

Orfila found that six grains of it diffused through water, introduced
into the stomach of a dog and retained there with a ligature on the
gullet, brought on efforts to vomit, restlessness, giddiness,
immobility, slight convulsions, and death in two or three hours. The
same quantity, if previously dissolved in vinegar, will cause death in
forty minutes. In the former case, but not in the latter, the inner coat
of the stomach is found to be generally red.[1457]

An ounce of the bruised seeds themselves killed a dog in fifty-four
hours when introduced into the stomach, and two drachms applied to a
wound in the thigh killed another in two days. In the former animal a
part of the stomach was crimson-red; in the latter there was extensive
subcutaneous inflammation reaching as high as the fourth rib.[1458]

Besides these four genera of the ranunculaceæ many other genera of the
same natural order are equally energetic. The _Clematis vitalba_ or
traveller’s-joy is said to be acrid, but does not taste so: the _C.
flammula_, however, is pungently acrid to the taste; it reddens and
blisters the skin; and when swallowed excites inflammation in the
stomach. The _trollius_ or globe flower is also considered acrid; and
its root in appearance, smell, and taste, has been said to resemble
closely that of the black hellebore. The herb, however, in Scotland, has
certainly none of the peculiar acrid pungency of the ranunculus,
anemone, or clematis, but is on the contrary bland. Some other genera of
equal power have been usually arranged with the narcotico-acrid poisons
on account of their action on the nervous system; and probably some of
the present group of acrids might with equal propriety be removed to the
same class.

Of plants possessing acrid properties and interspersed throughout other
natural families, the only species I shall particularly notice are the
mezereon, cuckow-pint, gamboge, daffodil, jalap-plant, and savine.


                     _Of Poisoning with Mezereon._

The _mezereon_ and several other species of the genus Daphne to which it
belongs are powerfully acrid. They belong to the natural order Thymeleæ.
The active properties of the bark of mezereon have been traced to a very
acrid resin; and those of the allied species, _Daphne alpina_, to a
volatile, acrid acid.[1459]

The experiments of Orfila have been confined to a foreign species, the
_D. Gnidium_ or _garou_ of the French. Three drachms of the powder of
its bark retained in the stomach of a dog killed it in twelve hours; and
two drachms applied to a wound killed another in two days.[1460] The
action of the other species has not been so scientifically investigated;
but fatal accidents have arisen from them when taken by the human
species. Children have been tempted to eat the berries of the _D.
mezereon_ by their singular beauty; and some have died in consequence.
Three such cases, not fatal, have been related by Dr. Grieve of
Dumfries. Two of the children had violent vomiting and purging: in the
third narcotic symptoms came on in five hours, namely, great drowsiness,
dilatation of the pupils, extreme slowness of the pulse, retarded
respiration, and freedom from pain.[1461] Vicat relates the case of a
man who took the wood of it for dropsy, and was attacked with profuse
diarrhœa and obstinate vomiting, the last of which symptoms recurred
occasionally for six weeks.[1462] A fatal case, in a child about eight
years of age, occurred a few years ago in this city. Linnæus in his
_Flora Suecica_ says that six berries will kill a wolf, and that he once
saw a girl die of excessive vomiting and hæmoptysis, in consequence of
taking twelve of them to check an ague.[1463] The _D. laureola_ or
spurge-laurel, a common indigenous species, abounding in low woods, is
said by Withering to be very acrid, especially its root.[1464]


                    _Of Poisoning with Cuckow-pint._

The _Arum maculatum_, or cuckow-pint, one of our earliest spring
flowers, not uncommon in moist ground, under the shelter of woods, is
one of the most violent of all acrid vegetables inhabiting this country.
I have known acute burning pain of the mouth and throat, pain of the
stomach and vomiting, colic and some diarrhœa, occasioned by eating two
leaves. The genus possesses the same properties in other climates, the
several species being everywhere among the most potent acrid poisons in
their respective regions. The _Arum seguinum_, or dumb cane of the West
Indies, is so active that two drachms of the juice have been known to
prove fatal in a few hours.[1465] It is not a little remarkable that the
acridity of the arum is lost not merely by drying, but likewise by
distillation. I have observed that when the roots are distilled with a
little water, neither the distilled water nor the residuum possesses
acridity. Reinsch says he has eaten powder of arum root, which, though
not acrid to the taste, produced severe burning of the throat not long
after it was swallowed.[1466]


                      _Of Poisoning with Gamboge._

The familiar pigment and purgative _gamboge_ is one of the pure acrids,
and possesses considerable activity. It appears from the researches of
Orfila,[1467] some experiments by Schubarth,[1468] and various earlier
inquiries quoted by Wibmer,[1469] that two drachms will kill a sheep;
that a drachm and a half will kill a dog if retained by a ligature on
the gullet, while much larger doses have little effect without this
precaution, as the poison is soon vomited; that an ounce has little
effect on the horse; that eighteen grains will prove fatal to the rabbit
within twenty-four hours; and that the symptoms are such as chiefly
indicate an irritant action. Orfila farther found that it produces
intense spreading inflammation when applied to a recent wound, and in
this way may occasion death as quickly and with as great certainty as
when administered internally.

Gamboge in its action on man is well known to be one of the most certain
and active of the drastic cathartics, from three to seven grains being
sufficient to cause copious watery diarrhœa, commonly with smart colic.
Larger doses will induce hypercatharsis. A drachm has proved fatal, as
is exemplified by a case in the German Ephemerides where the symptoms
were excessive vomiting, purging, and faintness.[1470]

Under this head are probably to be arranged the repeated cases, which
have lately occurred in this country, of fatal poisoning with a noted
quack nostrum, Morison’s pills. Almost every physician in extensive
practice has met with cases of violent hypercatharsis occasioned by the
incautious use of these pills; and three instances are now on record
where death was clearly occasioned by them.[1471] No toxicologist will
feel any surprise at such results, when he learns that one sort
contains, besides aloes and colocynth, half a grain of gamboge, and
another three times as much, in each pill; and that ten, fifteen, or
even twenty pills are sometimes taken for a dose once or oftener in the
course of the day.[1472] The symptoms in the cases alluded to were
sickness, vomiting and watery purging, pain, tension, fulness,
tenderness, and heat in the abdomen, with cold extremities and sinking
pulse; and in the dead body the appearances were great redness of the
stomach with softening of its villous coat, in the intestines softening
and slate-gray coloration of the same coat, and in one instance
intestinal ulceration.

Gamboge is one of the poisons whose energy seems to be irregularly
modified by the co-existence of certain constitutional states in
disease. Physicians in Britain cannot but be startled to hear of the
practice, prevailing among the followers of Rasori in Italy, of
administering this purgative in doses of a drachm and upwards in
inflammatory diseases. But it is nevertheless undeniable, that it has
been given to that extent in such circumstances, with no further
consequence than brisk purging. Professor Linoli mentions two cases of
inflammatory dropsy, in which he gave gamboge-powder in gradually
increasing doses, till he reached in one instance an entire drachm, and
in the other 86 grains. In the course of a month one of his patients got
1044 grains, and the other took 850 grains in twelve days. Both
recovered from their dropsy, and the purging was never great.[1473]


                     _Of Poisoning with Daffodil._

The common _daffodil_, the _Narcissus pseudo-narcissus_ of botanists,
though commonly arranged with the vegetable acrids, seems not entitled
to a place among them. At least the experiments of Orfila rather tend to
show that it acts through absorption on the nervous system. Four drachms
of the aqueous extract of this plant secured in the stomach in the usual
way killed a dog in less than twenty-four hours; and one drachm applied
to a wound killed another in six hours. In both cases vomiting or
efforts to vomit seemed the only symptom of note; and in both the
stomach was found here and there cherry-red. The wound was not much
inflamed.[1474]


                       _Of Poisoning with Jalap._

_Jalap_, the powder of the root of the _Ipomæa purga_, and a common
purgative, is an active poison in large doses; and this every one should
know, as severe and even dangerous effects have followed its incautious
use in the hands of the practical joker. Its active properties reside in
a particular resinous principle. It contains a tenth of its weight of
mixed resin, which, like the resin of euphorbium, has been separated by
Drs. Buchner and Herberger into two, one possessing some of the
properties of acids, the other some of the properties of bases; and the
latter they consider the active principle, and have accordingly named
Jalapine.[1475] Mr. Hume of London some time ago procured from the crude
drug a powdery substance, to which he gave the same name, and which he
conceived to be the active principle. His analysis has not been
generally relied on by chemists; but it is not improbable that his
principle differs little from that of the German chemists.

The action of jalap has been examined scientifically by M. Felix Cadet
de Gassicourt, who found that it produced no particular symptom when
injected into the jugular vein of a dog in the dose of twenty-four
grains, or when applied to the cellular tissue in the dose of a drachm.
But when rubbed daily into the skin of the belly and thighs it excited
in a few days severe dysentery; when introduced into the pleura it
excited pleurisy, fatal in three days; when introduced into the
peritonæum it caused peritonitis and violent dysentery, fatal in six
days; and when introduced into the stomach or the anus, the animals died
of profuse purging in four or five days, and the stomach and intestines
were then found red and sometimes ulcerated. Two drachms administered by
the mouth proved fatal.[1476] _Scammony_, which is procured from another
species of the same family, the _Convolvulus scammonea_, has been found
by Orfila to be much less active. Four drachms given to dogs produced
only diarrhœa.[1477]


                       _Of Poisoning with Savin._

The leaves of the _Juniperus sabina_, or savin, have been long known to
be poisonous. They have a peculiar heavy, rather disagreeable odour, and
a bitter, acrid, aromatic, somewhat resinous taste. They yield an
essential oil, which possesses all their qualities in an eminent degree.

A dog was killed by six drachms of the powdered leaves confined in the
stomach. It appeared to suffer pain, died in sixteen hours, and
exhibited on dissection only trivial redness of the stomach. Two drachms
introduced into a wound of the thigh caused death after the manner of
the other vegetable acrids in two days; and besides inflammation of the
limb there was found redness of the rectum.[1478]

Savin is a good deal used in medicine for stimulating old ulcers and
keeping open blistered surfaces; which may be done without danger,
although it cannot be applied to a fresh wound without risk of diffuse
inflammation. Both the powder and the essential oil are of some
consequence in a medico-legal point of view, as they have been often
used with the intent of procuring abortion. The oil is generally
believed by the vulgar to possess this property in a peculiar degree.
Doubts, however, may be entertained whether any such property exists
independently of its operation as a violent acrid on the bowels. It has
certainly been taken to a considerable amount without the intended
effect; of which Foderé has noticed an unequivocal example. The woman
took daily for twenty days no less than a hundred drops of the oil, yet
carried her child to the full time.[1479] The powder has likewise been
taken to a large extent without avail. A female, whose case is noticed
by Foderé, took without her knowledge so much of the powder that she was
attacked with vomiting, hiccup, heat in the lower belly, and fever of a
fortnight’s duration; nevertheless she was not delivered till the
natural time.[1480] There is no doubt, however, that if given in such
quantity as to cause violent purging, abortion may ensue; but unless
there is naturally a predisposition to miscarriage, the constitutional
injury and intestinal irritation required to induce it are so great, as
to be always attended with extreme danger, independent of the uterine
disorder. Of this train of effects the following case, for which I am
indebted to Mr. Cockson of Macclesfield, is a good illustration. A
female applied to a pedlar to supply her with the means of getting rid
of her pregnancy: and under his direction appears to have taken a large
quantity of a strong infusion of savin-leaves on a Friday morning and
again next morning. A very imperfect account was obtained of the
symptoms, as no medical man witnessed them; but it was ascertained that
she had violent pain in the belly and distressing strangury. On the
Sunday afternoon she miscarried; and on the ensuing Thursday she died.
Mr. Cockson, who examined the body next day, found extensive peritonæal
inflammation unequivocally indicated by the effusion of fibrinous
flakes,—the uterus presenting all the signs of recent delivery,—the
inside of the stomach of a red tint, checkered with patches of florid
extravasation,—and its contents of a greenish colour, owing evidently to
the presence of a vegetable powder, as was proved by separating and
examining it with the microscope. My colleague Dr. Traill has
communicated to me the particulars of a similar case. A servant-girl,
after being for some time in low spirits, was seized with violent colic
pains, frequent vomiting, straining at stool, tenderness of the belly,
dysuria and general fever; under which symptoms she died after several
days of suffering. The stomach was inflamed, in parts black, and at the
lower curvature perforated. The uterus with its appendages was very red,
and contained a fine _membrana decidua_, but no ovum. The lower
intestines were inflamed. There was found in the stomach a greenish
powder, which, when washed and dried, had the taste of savin.

A singular case is quoted by Wibmer of a woman who died from taking an
infusion of the herb for the purpose of procuring miscarriage, and in
whom death seems to have been occasioned by the gall-bladder bursting in
consequence of the violent fits of vomiting.[1481]

In a charge of wilful abortion the mere possession of oil of savin would
be a suspicious circumstance, because the notion that it has the power
of causing miscarriage is very general among the vulgar; while it is
scarcely employed by them for any useful purpose. The leaves in the form
of infusion are in some parts of England a popular remedy for worms; and
the oil is used in regular medicine as an emmenagogue.

The following list includes all the other plants which have been either
ascertained experimentally to belong to the present order, or are
believed on good general evidence to possess the same or analogous
properties.

By careful experiment Orfila has ascertained that the Gratiola
officinalis, Rhus radicans and Rhus toxicodendron, Chelidonium majus and
Sedum acre, possess them; and the following species are also generally
considered acrid, namely, Rhododendron chrysanthum and ferrugineum,
Pedicularis palustris, Cyclamen Europæum, Plumbago Europæa, Pastinaca
sativa, Lobelia syphilitica and longiflora, Hydrocotyle vulgaris. To
these may be added the common elder or Sambucus nigra, the leaves and
flowers of which caused in a boy, once a patient of mine, dangerous
inflammation of the mucous membrane of the bowels lasting for eight
days.




                              CHAPTER XXI.
                     OF POISONING WITH CANTHARIDES.


The second group of the present Order of poisons comprehends most of
those derived from the animal kingdom. In action they resemble
considerably the vegetable acrids, their most characteristic effect
being local inflammation; but several of them also induce symptoms of an
injury of the nervous system.

This group includes cantharides, poisonous fishes, venomous serpents,
and decayed or diseased animal matter.

The first of these is familiarly known as a poison even to the common
people. I am not aware that it has ever been used for the purpose of
committing murder. But on account of its powerful effect on the organs
of generation it has often been given by way of joke, and sometimes
taken for the purpose of procuring abortion. Fatal accidents have been
the consequence.

The appearance of the fly is well known. When in powder, as generally
seen, it has a grayish-green colour, mingled with brilliant green
points. It has a nauseous odour and a very acrid burning taste. Alcohol
dissolves its active principle. This principle appears from a careful
analysis by M. Robiquet to be a white, crystalline, scaly substance,
insoluble in water, but soluble in alcohol as well as in oils, and
termed cantharidin.[1482]

In compound mixtures cantharides may generally be detected by the green
colour and metallic brilliancy even of its finest powder, if examined in
the sunshine—and sometimes by making an etherial extract of the
suspected matter, and producing with this extract the usual effects of a
blister on a tender part of the arm. By these two tests Barruel
discovered cantharides in chocolate cakes, part of which had been
wickedly administered to various individuals.

From the late important researches of M. Poumet[1483] it appears, that
cantharides cannot be detected by its chemical properties in the
contents, or on the inner surface, of the alimentary canal of animals
poisoned with it; and that in such circumstances it is seldom to be
discerned even by the shining green colour of its particles, unless the
matter to be examined be dried. The method he recommends for a
medico-legal investigation is to detach the stomach, small intestines,
and great intestines, each separately from the body,—to wash out their
contents with rectified spirit, and dry the pulpy fluid on sheets of
glass,—to dry the stomach and intestines by distending them, removing
their mesentery, and hanging them up vertically with a weight attached
to stretch them,—and then to examine both the surface of the glass, and
the inside of the stomach and intestines with the aid of sunshine or a
bright artificial light. In this way cantharides may be detected, by the
peculiar green hue of its powder, in most cases where this poison may
have proved fatal; for M. Poumet constantly found it in dogs. The same
author ascertained that the green particles generally abound most in the
contents of the great intestine or on its inner membrane, next in the
small intestines, and least of all in the stomach; and that they may be
seen in the bodies of animals at least seven months after interment.
Orfila had previously ascertained, that cantharides powder may be
recognized by its brilliancy in various organic mixtures after interment
for nine months.[1484] Poumet farther states that the green particles of
cantharides may be confounded with the particles of other coleopterous
insects, and also somewhat resemble particles of copper and tin. But he
with reason asks, what possible accident could introduce the powder of
any other coleopterous insect into the alimentary canal? And as to
particles of copper or tin, he ascertained, that, unlike cantharides,
these substances are visible in the contents, or on the tissues, of the
stomach and intestines only before desiccation, and never after it.


SECTION I.—_Of the Action of Cantharides and the Symptoms it excites in
                                 Man._

Cantharides, either in the form of powder, tincture, or oily solution,
is an active poison both to man and animals. As to its action on
animals, Orfila found that a drachm and a half of a strong oleaginous
solution, injected into the jugular vein of a dog, killed it in four
hours with symptoms of violent tetanus; that three drachms of the
tincture with eight grains of powder suspended in it caused death in
twenty-four hours, if retained in the stomach by a ligature on the
gullet,—insensibility being then the chief symptom; and that forty
grains of the powder killed another dog in four hours and a half,
although he was allowed to vomit. In all the instances in which it was
administered by the stomach, that organ was found much inflamed after
death; and generally fragments of the poison were discernible if it was
given in the form of powder. When applied to a wound the powder excites
surrounding inflammation; and a drachm will in this way prove fatal in
thirty-two hours without any particular constitutional symptom except
languor.[1485] M. Poumet has since obtained results not materially
different.

These experiments do not furnish any satisfactory proof of the
absorption of the poison, but rather tend to show that it does not enter
the blood. Such a conclusion, however, must not be too hastily drawn;
since its well-known effects on man when used in the form of a blister
lead to the conclusion that it is absorbed, and that it produces its
peculiar effect on the urinary system through the medium of the
circulation. On account of the magnitude of the dose required to produce
severe effects on animals, Orfila’s experiments on the stomach and
external surface of the body cannot, for reasons formerly assigned (452)
be properly compared together.

The effect of cantharides, when admitted directly into the blood, seems
much less than might be expected. Mr. Blake found that an infusion of
two drachms injected into the jugular vein of a dog, caused some
difficulty of breathing, irregularity of the pulse, and diminished
arterial pressure, but apparently no great inconvenience to the
animal.[1486] The greater effect observed in Orfila’s experiment was
probably owing to obstruction of the pulmonary capillaries by the oil.

Orfila has examined with care not only the preparations of cantharides
already mentioned, but likewise the various principles procured by M.
Robiquet during his analysis; and it appears to result, that the active
properties of the fly reside partly in the crystalline principle, and
partly in a volatile oil, which is the source of its nauseous odour.

The symptoms produced by cantharides in man are more remarkable than
those observed in animals. A great number of cases are on record; but
few have been minutely related. Sometimes it has been swallowed for the
purpose of self-destruction, sometimes for procuring miscarriage. But
most frequently, on account of a prevalent notion that it possesses
aphrodisiac properties, it has been both voluntarily swallowed and
secretly administered, to excite the venereal appetite. That it has this
effect in many instances cannot be doubted. But the old stories, which
have been the cause of its being so frequently used for the purpose, are
many of them fabulous, and all exaggerated. Often no venereal appetite
is excited, sometimes even no affection of the urinary or genital organs
at all; and the kidneys and bladder may be powerfully affected without
the genital organs participating. It is established, too, by frequent
observation, that the excitement of the genital organs can never be
induced, without other violent constitutional symptoms being also
brought on, to the great hazard of life.

The following abstract of a case by M. Biett of Paris gives a rational
and unexaggerated account of the symptoms as they commonly appear. A
young man, in consequence of a trick of his companions, took a drachm of
the powder. Soon afterwards he was seized with a sense of burning in the
throat and stomach; and in about an hour with violent pain in the lower
belly. When M. Biett saw him, his voice was feeble, breathing laborious,
and pulse contracted; and he had excessive thirst, but could not swallow
any liquid without unutterable anguish. He was likewise affected with
priapism. The pain then became more extensive and severe, tenesmus and
strangury were added to the symptoms, and after violent efforts he
succeeded in passing by the anus and urethra only a few drops of blood.
By the use of oily injections into the anus and bladder, together with a
variety of other remedies intended to allay the general irritation of
the mucous membranes, he was considerably relieved before the second
day; but even then he continued to complain of great heat along the
whole course of the alimentary canal, occasionally priapism, and
difficult micturition. For some months he laboured under difficulty of
swallowing.[1487]—Another case very similar in its circumstances has
been related by M. Rouquayrol. In addition to the symptoms observed in
Biett’s patient there was much salivation, and towards the close of the
second day a large cylindrical mass, apparently the inner membrane of
the gullet, was discharged by vomiting.[1488]—A case of the same kind,
but less severe, is related in the Medical Gazette. A woman, who had
taken an ounce of the tincture, was observed throughout the day to be
apparently intoxicated. Next morning, when she for the first time told
what she had done, she had excruciating pain, great tenderness and
distension of the belly, a flushed anxious countenance, a dry, pale
tongue, a natural pulse, and urine loaded with sediment and fibrinous
matter. In the evening there was extreme weakness, cold extremities, a
scarcely perceptible pulse, and retention of urine; and at night she was
delirious. After this she recovered progressively, the chief symptoms
then being pain in the kidneys and inability to pass urine.[1489]

Among the symptoms the affection of the throat, causing difficult
deglutition and even an aversion to liquids, appears to be pretty
constant. The sense of irritation along the gullet and in the stomach is
also generally considerable. Sometimes it is attended with bloody
vomiting, as in four cases related by Dr. Graaf of Langenburg;[1490] and
at other times, as in the instance of poisoning with the acids, there is
vomiting of membranous flakes. These have been mistaken for the lining
membrane of the alimentary canal, but are really in general a morbid
secretion.[1491] At the same time there is reason to believe that a
portion of the membrane of the gullet was discharged in Rouquayrol’s
case; for there were ramified vessels in it, and one so large that blood
issued on pricking it. A prominent symptom in general is distressing
strangury, and it commonly concurs with suppression of urine and the
discharge of blood.[1492] It would appear that, when the genital organs
are much affected, the inflammation may run on to gangrene of the
external parts. Ambrose Paré notices a fatal instance of the kind, which
was caused by a young woman seasoning comfits for her lover with
cantharides.[1493]

The preceding symptoms are occasionally united with signs of an
injury of the nervous system. Headache is common, and delirium is
sometimes associated with it.[1494] In a case communicated to Orfila
the leading symptoms at first were strangury and bloody urine; but
these were soon followed by violent convulsions and occasional loss
of recollection.[1495] The quantity in that instance was only eight
grains; and it was taken for the purpose of self-destruction. In one
of Graaf’s four cases the patient was attacked during convalescence
with violent phrensy of three days’ continuance.[1496] An instance
is also related in the Transactions of the Turin Academy, of tetanic
convulsions and hydrophobia appearing three days after a small
over-dose of the tincture of cantharides was taken, and continuing
for several days with extreme violence.[1497] The cause of the
symptoms, however, is here doubtful.

A rare occurrence is relapse after apparent convalescence. In a case
communicated to me by Dr. Osborne of Dundee, which there was every
reason to believe had arisen from cantharides administered to a girl by
an unprincipled scoundrel, the usual symptoms of violent irritation in
the bladder and rectum prevailed for 36 hours; and an interval of quiet
and apparent convalescence ensued for three days. But on the fifth day
the urinary symptoms returned, and were attended with great prostration,
a rapid feeble pulse, and severe diarrhœa for two days longer. She
eventually recovered. Another girl, poisoned at the same time, had most
distressing irritation in the bladder, and for some time passed nothing
but drops of blood; but she got well in two days, and had no relapse.

The following fatal cases deserve particular mention. Orfila quotes one
from the _Gazette de Santé_ for May, 1819, which was caused by two doses
of twenty-four grains taken with the interval of a day between them, for
the purpose of suicide. The ordinary symptoms of irritation in the
bowels and urinary organs ensued, miscarriage then took place, and the
patient died on the fourth day, with dilated pupils and convulsive
motions, but with unimpaired sensibility.[1498] Another instance related
by Dr. Ives of the United States, presented two stages, like that
related by Orfila, but with the remarkable difference that an interval
of several days intervened between the irritant and narcotic effects. A
man swallowed an ounce of the tincture and was seized in a short time
with hurried breathing, flushed face, redness of the eyes and
lacrymation, convulsive twitches, pain in the stomach and bladder,
suppression of urine and priapism; in the evening delirium set in, and
next morning there was loss of consciousness; but from this time under
the use of blood-letting, emetics, blisters, sinapisms, and castor-oil,
he got well and continued so for fourteen days. But after that interval
he was suddenly attacked with headache and shivering, then with
convulsions, and subsequently with coma; which, however, was removed for
a time by outward counter-irritants. Next day the coma returned at
intervals, and on the subsequent day the convulsions also, which
gradually increased in severity for three days more, and then proved
fatal.[1499] In this case it admits of question whether the affection
which proved the immediate cause of death really arose from the
cantharides, or was an independent disease.—A third case, fatal on the
fourth day, occurred in April, 1830, near Uxbridge in the south of
England. I have not been able to learn the particulars exactly; but it
appears to have been produced by cantharides powder, which was mixed
with beer by two scoundrels at a dancing party for the purpose of
exciting the venereal appetite of the females. A large party of young
men and women were in consequence taken severely ill; and one girl died,
who had been prevailed on to take the powder at the bottom of the
vessel, on being assured that it was ginger.

The quantity of the powder or tincture requisite to prove fatal or
dangerous has not been accurately settled. Indeed practitioners differ
much even as to the proper medicinal doses. The smallest dose of the
powder yet known was twenty-four grains (Orfila); and the smallest fatal
dose of the tincture was one ounce, which is equivalent to six grains of
powder.[1500] It is probable that this is one of the poisons whose
operation is liable to be materially affected by idiosyncrasy. The
medicinal dose is from half a grain to two grains of the powder, and
from ten drops to two drachms of the tincture. But Dr. Beck has quoted
an instance where six ounces of the tincture were taken without
injury.[1501] On the other hand Werlhoff has mentioned the case of a lad
who used to be attacked with erection and involuntary emission on merely
smelling the powder.[1502] This statement, though extraordinary, is not
without support from the parallel effects of other substances.

The familiar effects of cantharides on the external surface of the body
are not unattended with danger, if extensive, or induced in particular
states of the constitution. An ordinary blistered surface often
ulcerates in febrile diseases; and in the typhoid state which
characterizes certain fevers, this ulceration has been known to pass on
to fatal sloughing, especially when the blister has been applied to
parts on which the body rests. I have met with two such cases. On the
other hand if the blistered surface be very extensive, death may take
place in the primary stage of the local affection, in consequence of the
great constitutional disturbance excited. Thus in 1841 a girl, affected
with scabies, received cantharides ointment by mistake instead of
sulphur ointment from an hospital-serjeant at Windsor Barracks; and
having anointed nearly her whole body with it, was seized with violent
burning pain of the integuments, followed by vesication, general fever,
and the usual symptoms of the action of this poison on the urinary
organs. These effects were so severe that she died in five days.[1503]


     SECTION II.—_Of the Morbid Appearances caused by Cantharides._

The only precise account I have hitherto seen of the morbid appearances
caused by cantharides is contained in the history of the case from the
_Gazette de Santé_. The brain was gorged with blood. The omentum,
peritonæum, gullet, stomach, intestines, kidneys, ureters, and internal
parts of generation were inflamed; and the mouth and tongue were
stripped of their lining membrane.—In dogs Schubarth observed, besides
the usual signs of inflammation in the alimentary canal, great redness
of the tubular part of the kidneys, redness and extravasated patches on
the inside of the bladder, and redness of the ureters as well as of the
urethra.[1504] M. Poumet denies that any morbid appearance is ever found
in any part of the genito-urinary organs of animals; but he sometimes
found blood effused into the stomach and intestines.[1505] In Dr. Ives’s
case the blood-vessels of the brain and cerebellum were gorged, the
cerebellum spread over with lymph, the villous coat of the stomach
softened and brittle, and the kidneys inflamed and presenting blood in
their pelvis.

When the case has been rapid, the remains of the powder may be found in
the stomach or intestines by Poumet’s process. From the researches of
Orfila and Lesueur, confirmed by those of Poumet, it appears not to
undergo decomposition for a long time when mixed with decaying animal
matters. After nine months’ interment the resplendent green points
continue brilliant.[1506]


     SECTION III.—_Of the Treatment of Poisoning with Cantharides._

The treatment of poisoning with cantharides is not well established. No
antidote has yet been discovered. At one time fixed oil was believed to
be an excellent remedy. But the experiments of Robiquet on the active
principle of the poison, and those of Orfila on the effects of its
oleaginous solution, rather prove that oil is the reverse of an
antidote. The case mentioned in the Genoa Memoirs was evidently
exacerbated by the use of oil. When the accident is discovered early
enough, and vomiting has not already begun, emetics may be given; and if
vomiting has begun, it is to be encouraged. Oleaginous and demulcent
injections into the bladder generally relieve the strangury. The warm
bath is a useful auxiliary. Leeches and blood-letting are required,
according as the degree and stage of the inflammation may seem to
indicate.

Many other insects besides the _Cantharis vesicatoria_ possess similar
acrid properties. Two of them, however, may be briefly alluded to,
because they have caused fatal poisoning. The one is the _Meloë
proscarabæus_, the _Maiwurm_ of the Germans, a native of most European
countries. In Rust’s Magazin there is an account of four persons who
took the powder of this insect from a quack for spasms in the stomach.
The principal symptoms were stifling and vomiting; and two of the people
died within twenty-four hours.[1507] The other is the _Bombyx_, of which
at least two species are believed to possess powerful irritant
properties, the _B. pityocarpa_ and _B. processionea_. The following is
an instance of their effects. A child ten years old had a common blister
applied to the neck and spine as a remedy for deafness; and four days
afterwards her mother dressed the abraded skin with the leaves of
beet-root, from which she had previously shaken a great number of
caterpillars. The child soon complained of insupportable itching and
burning in the part, and endeavoured to tear off the dressings. The
mother persevered, however; and her child died in two days of gangrene
of the whole integuments of the back. The surgeon who saw the child on
the last day of her life, ascribed the gangrene to the insects mentioned
above, and states that they possess the power of exciting erysipelas
when applied even to the sound skin.[1508] It is probable that many
other insects in Europe have similar properties. The _Mylabris
cichorii_, which is partially used in Italy,[1509] and is in common use
in India and China for blistering, possesses active irritant properties.
The _Cantharis ruficollis_, another species used in the Nizam’s
Territories in India, is also energetic. Other species known to possess
activity are _Mylabris fusselini_, _Meloe majalis_, _M. trianthemum_,
_Coccinella bipunctata_, _C. septem-punctata_, and _Cantharis vittata_.




                             CHAPTER XXII.
             OF THE DELETERIOUS EFFECTS OF POISONOUS FISH.


The species of fish which act deleteriously, either always or in
particular circumstances, have also been commonly arranged in the
present order of poisons.

The subject of fish-poison is one of the most singular in the whole
range of toxicology, and none is at present veiled in so great
obscurity. It is well ascertained that some species of fish,
particularly in hot climates, are always poisonous,—that some, though
generally salubrious and nutritive, such as the oyster and still more
the muscle, will at times acquire properties which render them hurtful
to all who eat them,—and that others, such as the shell-fish now
mentioned, and even the richer sorts of vertebrated fishes, though
actually eaten with perfect safety by mankind in general, are
nevertheless poisonous, either at all times or only occasionally to
particular individuals. But hitherto the chemist and the physiologist
have in vain attempted to discover the cause of their deleterious
operation.

A good account of the poisonous fishes of the tropics has been given by
Dr. Chisholm[1510] and by Dr. Thomas;[1511] and some farther
observations on the same subject have been published by Dr.
Fergusson.[1512] These essays may be consulted with advantage. On the
effects of poisonous muscles several interesting notices and essays have
been written, among which may be particularized one by Dr. Burrows[1513]
of London, another by Dr. Combe of Leith,[1514] and the observations of
Professor Orfila, including some cases from the Gazette de Santé, and
from the private practice of Dr. Edwards.[1515] Of all the sources of
information now mentioned, that which appears to me the most
comprehensive and precise, is the essay of Dr. Combe, who has collected
many facts previously known, added others equal in number and importance
to all the rest put together, and weighed with impartiality the various
inferences which have been or may be drawn from them. The succeeding
remarks will be confined to a succinct statement of what appears well
established.

In this work, however, the poisonous fishes of the West Indies and other
tropical countries may be laid aside, because we are still too little
acquainted with the phenomena of their action to be entitled to
investigate its cause, and they are objects of much less interest to the
British medical jurist than the fish-poison of his own coast.

There is little doubt that some of the inhabitants of the sea on the
coast of Britain are always poisonous. Thus it is well known that some
of the molluscous species irritate and inflame the skin wherever they
touch it,—a fact which is familiar to every experienced swimmer. The
fishermen of the English coast are also aware that a small fish known by
the name of Weever (_Trachinus vipera_, Cuv.) possesses the power of
stinging with its dorsal fin so violently as to produce immediate
numbness of the arm or leg, succeeded rapidly by considerable swelling
and redness; and indeed an instance of this accident, which happened at
Portobello on the Firth of Forth, has been mentioned to me by Mr. Stark,
author of the Elements of Natural History, who witnessed the effects of
the poison. But our knowledge of the poisons of that class is too
imperfect to require more particular notice.

Of fishes which are commonly nutritive, but sometimes acquire poisonous
properties, by far the most remarkable is the common _Muscle_.
Opportunities have often occurred for observing its effects,—so often,
indeed, that its occasional poisonous qualities have become an important
topic of medical police, and in some parts, as in the neighbourhood of
Edinburgh and Leith, it has of late been abandoned by many people as an
article of food, although generally relished, and in most circumstances
undoubtedly safe. This result originated in an accident at Leith in
1827, by which no fewer than thirty people were severely affected and
two killed.


 _Of the Symptoms and Morbid Appearances caused by Poisonous Muscles._

The effects of poisonous muscles differ in different cases. Sometimes
they have produced symptoms of local irritation only. Thus Foderé
mentions the case of a sailor in Marseilles, who, in consequence of
eating a large dish of them, died in two days, after suffering from
vomiting, nausea, pain in the stomach, tenesmus, and quick contracted
pulse. The stomach and intestines were found after death red and lined
with an abundant tough mucus.[1516] One of the cases described by Dr.
Combe, which, however, terminated favourably, is of the same nature. The
patient had severe stomach symptoms from the commencement, attended with
cramps and ending in peritonitis, which required the frequent use of the
lancet.

But much more commonly the local effects have been trifling, and the
prominent symptoms have been almost entirely indirect and chiefly
nervous. Two affections of this kind have been noticed. One is an
eruptive disease resembling nettle-rash, and accompanied with violent
asthma; the other a comatose or paralytic disorder of a peculiar
description.

Of the former affection several good examples have been recorded in
different numbers of the Gazette de Santé.[1517] In these the number of
muscles eaten was generally small; in one instance ten, in another only
six. Nay, in a case related with several others by Möhring in the German
Ephemerides, the patient only chewed one muscle and swallowed the fluid
part, having spit out the muscle itself.[1518] The symptoms have usually
commenced between one and two hours after eating, and rapidly attained
their greatest intensity. In the patient who was affected by ten muscles
the first symptoms were like those of violent coryza; swelling and
itching of the eyelids, and general nettle-rash followed; and the
eruption afterwards gave place to symptoms of urgent asthma, which were
removed by ether. In other cases the symptoms of asthma preceded the
eruption. In one instance the eruption did not appear at all. The
swelling has not been always confined to the eyelids, but, on the
contrary, has usually extended over the whole face. All the patients
were quickly relieved by ether. The eruption, though generally called
nettle-rash, is sometimes papular, sometimes vesicular, but always
attended with tormenting heat and itchiness. Several cases of this kind
have been related by Möhring. The eruption was preceded by dyspnœa,
lividity of the face, insensibility, and convulsive movements of the
extremities. All recovered under the use of emetics.[1519] This
affection, however, may prove fatal. In the cases of two children
related by Dr. Burrows, the symptoms began, as in Möhring’s cases, with
dyspnœa, nettle-rash, and swelling of the face, combined with vomiting
and colic; but afterwards the leading symptoms were delirium,
convulsions, and coma; and death took place in three days.

In these children it is worthy of remark, that none of the symptoms
began till twenty-four hours after eating. In Möhring’s cases, on the
contrary, the symptoms began in a few minutes.

The other affection is well exemplified in the correct delineations of
Dr. Combe. The following is his general summary of the cases, which,
with the exception of the instance of peritonitis already alluded to,
were all singularly alike in their leading features.—“None, so far as I
know, complained of anything peculiar in the smell or taste of the
animals, and none suffered immediately after taking them. In general, an
hour or two elapsed, sometimes more; and then the bad effects consisted
rather in uneasy feelings and debility, than in any distress referable
to the stomach. Some children suffered from eating only two or three;
and it will be remembered that Robertson, a young and healthy man, only
took five or six. In two or three hours they complained of a slight
tension at the stomach. One or two had cardialgia, nausea, and vomiting;
but these were not general or lasting symptoms. They then complained of
a prickly feeling in their hands; heat and constriction of the mouth and
throat; difficulty of swallowing and speaking freely; numbness about the
mouth, gradually extending to the arms, with great debility of the
limbs. The degree of muscular debility varied a good deal, but was an
invariable symptom. In some it merely prevented them from walking
firmly, but in most of them it amounted to perfect inability to stand.
While in bed they could move their limbs with tolerable freedom; but on
being raised to the perpendicular posture, they felt their limbs sink
under them. Some complained of a bad coppery taste in the mouth, but in
general this was an answer to what lawyers call a leading question.
There was slight pain of the abdomen, increased on pressure,
particularly in the region of the bladder, which suffered variously in
its functions. In some the secretion of urine was suspended, in others
it was free, but passed with pain and great effort. The action of the
heart was feeble; the breathing unaffected; the face pale, expressive of
much anxiety; the surface rather cold; the mental faculties unimpaired.
Unluckily the two fatal cases were not seen by any medical person; and
we are therefore unable to state minutely the train of symptoms. We
ascertained that the woman, in whose house were five sufferers, went
away as in a gentle sleep; and that a few minutes before death, she had
spoken and swallowed.”[1520] She died in three hours. The other fatal
case was that of a dock-yard watchman, who was found dead in his box six
or seven hours after he ate the muscles.

The inspection of the bodies threw no light on the nature of these
singular effects. No appearance was found which could be called
decidedly morbid. The stomach contained a considerable quantity of the
fish half digested.

Dr. Combe’s narrative agrees with that of Vancouver, four of whose
sailors were violently affected, and one killed in five hours and a
half, after eating muscles which they had gathered on shore in the
course of his voyage of discovery.[1521]

In closing this account, allusion may be briefly made to a case related
by Dr. Edwards, which differs from all the preceding. The symptoms were
uneasiness at stomach, followed by epileptic convulsions, which did not
entirely cease for a fortnight. Dr. Edwards imputed the illness to
muscles; but it must be observed that this is a solitary instance of
simple convulsions arising from such a cause.[1522] The case deserves
particular attention, because a suspicion of intentional poison might
have been excited by the circumstances in which it occurred. The
individual, a young man, was attacked soon after eating in company with
another, who was about to marry his mother, and with whom on that
account he lived on bad terms.


                 _Of the Source of Poison of Muscles._

Various opinions have been formed as to the cause or causes of the
poisonous qualities of some muscles.

The vulgar idea that the poisonous principle is copper, with which the
fish becomes impregnated from the copper bottoms of vessels, is quite
untenable. Copper does not cause the symptoms described above. I
analyzed some of the muscles taken from the stomach of one of Dr.
Combe’s patients, without being able to detect a trace of copper. Others
have arrived at the same result in former cases. The only instance
indeed to the contrary is a late analysis by M. Bouchardat; who does not
mention the quantity of copper he detected, or what was the source of
the poisonous fish.[1523]

The theory which ascribes their effects to changes induced by decay is
equally untenable. In Dr. Burrows’s two cases the muscles appear to have
been decayed; yet he very properly refuses to admit this fact as
explanatory of their operation. And, indeed, it rather complicates than
facilitates the explanation; as it shows that the poison differs from
animal poison generally, in not being destroyed by putrefaction. Dr.
Combe’s inquiries must satisfy every one, that in the Leith cases decay
was out of the question, and I may add my testimony to the statement:
the muscles taken from the stomach of one of his fatal cases, and
likewise others obtained in the shell, and brought to me for analysis,
were perfectly fresh.

By some physicians, and especially by Dr. Edwards, their poisonous
effects have been referred to idiosyncrasy on the part of the persons
who suffer. It can hardly be doubted that this is the cause in some
instances. It was formerly mentioned that muscles, oysters, crabs, and
even the richer sorts of vertebrated fishes, such as trout, salmon,
turbot, holibut, herring, mackerel, are not only injurious to some
people, while salutary to mankind generally, but likewise that this
singular idiosyncrasy may be acquired. A relation of mine for many years
could not take a few mouthfuls of salmon, trout, herring, turbot,
holibut, crab, or lobster, without being attacked in a few minutes or
hours with violent vomiting; yet at an early period of life, he could
eat them all with impunity; and at all times he has eaten without injury
cod, ling, haddock, whiting, flounder, oysters, and muscles. Among the
cases which have come under Dr. Edwards’s notice in Paris, there is one
evidently of the same nature. In two others, the idiosyncrasy existed in
regard to the muscle, and although in both of these the affection
induced was slight, there is no doubt but idiosyncrasy will also account
even for some instances of the severe disorders specified above. In
particular, it appears sometimes to operate in the production of
nettle-rash and asthma; for in the instance quoted from the Gazette de
Santé, as arising from ten muscles, it happened that the father of the
patient partook very freely of the same dish without sustaining any harm
whatever; and in each of three distinct accidents mentioned by Möhring,
it appeared that other individuals had eaten of the same dish with equal
impunity.[1524]

But idiosyncrasy will not account for all the cases of poisoning with
muscles, oysters, and other fish. For, passing over other less
unequivocal objections, it appears that, when the accident related above
happened at Leith, every person who ate the muscles from a particular
spot was more or less severely affected; and an important circumstance
then observed for the first time was, that animals suffered as severely
as man, a cat and a dog having been killed by the suspected article.

Another theory ascribes the poisonous quality to disease in the fish;
but no one has hitherto pointed out what the disease is. The poisonous
muscles at Leith were large and plump, and seemed to have been chosen on
account of their size and good look. Dr. Coldstream, however, at the
time a pupil of this University, and a zealous naturalist, thought the
liver was larger, darker, and more brittle than in the wholesome fish,
and certainly satisfied me that there was a difference of the kind. But
whether this was really disease or merely a variety of natural
structure, our knowledge of the natural history of the fish hardly
entitles us to pronounce.

Considering the failure of all other attempts to account for the
injurious properties acquired by muscles, it is extraordinary that no
experiments have been hitherto made with the view of discovering in the
poisonous fish a peculiar animal principle. It certainly seems probable,
that the property resides in a particular part of the fish or in a
particular principle. In 1827, I made some experiments on those which
caused the fatal accident at Leith, but without success. My attention
was turned particularly to the liver; but neither there nor in the other
parts of the fish could I detect any principle which did not equally
exist in the wholesome muscle. This result, however, should not deter
others, any more than it would myself, from a fresh investigation; for
the want of a sufficient supply prevented me from making a thorough
analysis; and the reader will presently find an instance related, where
another singular poison, sometimes contained in sausages and in cheese,
was, after repeated failures, at length traced successfully to the real
cause by the hand of the analytic chemist.

M. Lamouroux, in a letter to Professor Orfila, conjectures that the
poison may be a particular species of Medusa, and enters into some
ingenious explanations of his opinion. But it is not supported by any
material fact, and seems to be surrounded by insuperable
difficulties.[1525] It is not a new conjecture; for Möhring mentions in
his paper formerly quoted, that several writers before him had conceived
such a cause might afford an explanation of the phenomena.[1526]

Little or no light is thrown on this singular subject by the nature of
the localities in which the poisonous muscle has been found. Even on
this point we possess little information. Both in Dr. Burrows’s and Dr.
Combe’s cases the fish was attached to wood. At Leith they were taken
from some Memel fir logs, which formed the bar of one of the wet-docks,
and had lain there at least fifteen years. From the stone-walls of the
dock in the immediate vicinity of this bar muscles were taken which
proved quite wholesome. It is impossible, however, to attach any
importance to these facts; for Dr. Coldstream informs me, that he
examined muscles which were attached to the fir piles of the Newhaven
Chain-pier, about a mile from Leith, and found them wholesome. In the
latter animals the liver was not large, as in the poisonous muscles of
Leith. Lamouroux states, but I know not on what authority, that muscles
never become poisonous unless they are exposed alternately to the air
and the sea in their place of attachment, and unless the sea flows in
gently over them without any surf,—these conditions being considered by
him requisite for the introduction of the poisonous Medusæ into the
shell.


                        _Of Poisonous Oysters._

_Oysters_ sometimes acquire deleterious properties analogous to those
acquired by muscles. But fewer facts have been collected regarding them.
M. Pasquier has mentioned some cases which occurred not long ago at
Havre, in consequence apparently of an artificial oyster-bed having been
established near the exit of the drain of a public necessary. But I have
not been able to consult his work.[1527] Another instance of their
deleterious operation occurred a few years ago at Dunkirk. At least an
unusual prevalence of colic, diarrhœa, and cholera was believed to have
been traced to an importation of unwholesome oysters from the Normandy
coast. Dr. Zandyk, the physician who was appointed to investigate the
matter, found that the suspected fish contained a slimy water, and that
the membranes were retracted from the shell towards the body of the
animal.[1528] Dr. Clarke believes that even wholesome oysters have a
tendency to act deleteriously on women immediately after delivery. He
asserts that he has repeatedly found them to induce apoplexy or
convulsions; that the symptoms generally came on the day after the
oysters were taken; and that two cases of the kind proved fatal.[1529] I
am not aware that these statements have been since confirmed by any
other observer.


                          _Of Poisonous Eels._

_Eels_ have also been at times found in temperate climates to acquire
poisonous properties. Virey mentions an instance where several
individuals were attacked with violent tormina and diarrhœa a few hours
after eating a paté made of eels from a stagnant castle-ditch near
Orleans; and in alluding to similar accidents having previously happened
in various parts of France, he adds that domestic animals have been
killed by eating the remains of the suspected dish.[1530]




                             CHAPTER XXIII.
                    OF POISONING BY VENOMOUS SNAKES.


Another entire group of poisons allied to the acrid vegetables in their
action, but infinitely more energetic, comprehends the poisons of the
venomous serpents. If we were to trust the impressions the vulgar
entertain of the effects of the bite of serpents, the poisons now
mentioned would be considered true septics or putrefiants; for they were
once universally believed, and are still thought by many, to cause
putrefaction of the living body. This property has been assigned them
probably on no other grounds, except that they are apt to bring on
diffuse subcutaneous inflammation, which frequently runs on to gangrene.
But there are some serpents, especially among those of hot climates,
which appear also to act remotely on the centre of the nervous system,
and to occasion death through means of that action.

The present group of poisons is of little consequence to the British
medical jurist, as an opportunity of witnessing their effects in this
country is seldom to be found. The viper is the only poisonous snake
known in Britain, where its poison is hardly ever so active as to
occasion death.[1531]

This serpent, like all the other poisonous species, is provided with a
peculiar apparatus by which the poison is secreted, preserved, and
introduced into the body of the animal it attacks. The apparatus
consists of a gland behind each eye, of a membranous sac at the lateral
and anterior part of the upper jaw, and of a hollow curved tooth
surrounded and supported by the sac. The cavity of the tooth
communicates with that of the sac, and terminates near the tip, in a
small aperture, by which the poison is expelled into the wound made by
the tooth.

The symptoms caused by the bite of the viper are lancinating pain, which
begins between three minutes and forty minutes after the bite, and
rapidly stretches up the limbs,—swelling, at first firm and pale,
afterwards red, livid and hard,—tendency to fainting, bilious vomiting,
sometimes convulsions, more rarely jaundice,—quick, small, irregular
pulse,—difficult breathing, cold perspiration, dimness of vision, and
injury of the mental faculties. Death may ensue. A case is related in
Rust’s Magazin of a child twelve years old, who died two days after
being bitten in the foot;[1532] another instance is briefly noticed in
the French Bulletins of Medicine, of a person forty years old, dying
also in two days;[1533] Dr. Wagner of Schlieben mentions his having met
with two instances where persons bit on the toes died before assistance
could be procured;[1534] and notice has been taken in Hufeland’s Journal
of a girl, eleven years old, having been killed in three hours at
Schlawe in Prussia.[1535] In the last case burning in the foot, which
was the part bitten, then severe pain in the belly, inextinguishable
thirst, and vomiting, preceded a fit of laborious breathing, which
ushered in death. The most remarkable instance, however, of death from
the bite of the European viper is one lately described by Dr. Braun, as
having been occasioned in the Dutchy of Gotha by the Coluber Chersea
[Kreuzotter of the Germans]. A man, who represented himself to be a
snake-charmer, insisted on showing his skill before Dr. Lenz, a
naturalist of Schnepfenthal; and putting the head of a viper belonging
to this gentleman’s collection into his mouth, he pretended to be about
to devour it. Suddenly he threw the snake from him, and it was found
that he had been bitten near the root of the tongue. In a few minutes he
became so faint that he could not stand, the tongue swelled a little,
the eyes became dim, saliva issued from the mouth, rattling respiration
succeeded, and he died within fifty minutes after being bitten.[1536] A
French writer observes that the common viper of France is not very
deadly; but that the bite of the red viper may occasion death in a few
hours.[1537]

The activity of the poison of the viper depends on a variety of
circumstances. When kept long confined, the animal loses its energy; and
after it has bitten repeatedly in rapid succession, its bite ceases for
some time to be poisonous, as the supply of poison is exhausted. It
appears also to be most active in hot and dry climates. Those cases are
always the most severe in which the symptoms begin soonest; and the
danger increases with the number of bites. An important observation made
by Dr. Wagner is that danger need not be dreaded except when the bite is
inflicted on small organs such as the fingers or toes, because larger
parts cannot be fully included between the animal’s jaws, and fairly
pierced by its fangs, but can only be scratched. The properties of the
fluid contained in the reservoir do not cease with the animal’s life;
nay they continue even when the fluid is dried and preserved for a
length of time. It may be swallowed in considerable quantity without
causing any injury whatever. In the course of some experiments lately
made in Italy, a pupil of Professor Mangili swallowed at once the whole
poison of four vipers without suffering any inconvenience; and that of
six vipers was given to a blackbird, that of ten to a pigeon, and that
of sixteen to a raven, with no other effect beyond slight and transient
stupor.[1538]

For the most recent account of the far more terrible effects of the
cobra di capello and rattlesnake, the reader may refer to the
authorities below.[1539]

It was stated above that the poison of the viper retains its activity
when dried. I have had an opportunity of observing this in regard to the
poison of the cobra di capello, which is said to be preserved in India
by simply squeezing out the contents of the poison-bag, and drying the
liquid in a silver dish exposed to the sun. The specimen in my
possession, for which I am indebted to Mr. Wardrop of London, has the
appearance of small fragments of gum-arabic. It had been kept for
fifteen years when I tried its effects on a strong rabbit. A grain and a
half dissolved in ten drops of water, having been introduced between the
skin and muscles of the back, the animal in eight minutes became very
feeble and averse to stir, so that it remained still even when placed in
irksome postures; occasional slight twitches of the limbs supervened; at
length it became extremely torpid, and breathed slowly by means of the
abdominal muscles and diaphragm alone; and in twenty-seven minutes it
died exhausted, without any precursory insensibility. The heart
contracted readily, when irritated nine minutes after death; so that the
poison seemed to operate by causing muscular paralysis, and consequently
arresting the respiration.

There might also be arranged in an appendix to the present group of
poisons those _insects_ whose sting is poisonous. The European insects
known to have a poisonous sting, are chiefly the scorpion, tarantula,
bee and wasp; of which the last two only are natives of Britain.

The poison of these insects occasions diffuse cellular inflammation,
which always ends in resolution. It is said, however,[1540] and it may
be readily believed, that death has been sometimes caused in consequence
of a whole hive attacking an intruder and covering his body with their
stings. In an old French journal is shortly noticed the case of a
peasant who died soon after being stung over the eye by a single
bee.[1541] A more probable story has been told in the Gazette de Santé
of a gardener who died of inflammation of the throat, in consequence of
being stung there by a wasp while he was eating an apple, in which it
had been concealed.[1542] But the same accident has often occurred
without any material danger.

The treatment of poisoning by venomous serpents need not be detailed
here. The subject is introduced merely to mention that the treatment of
poisoned wounds by the application of cupping-glasses has been lately
resorted to with success for curing the bite of the viper. A patient of
M. Piorry, two hours after being bitten, had all the constitutional
symptoms strongly developed, such as slow, very feeble pulse, nausea,
vomiting, and swelling of the face. When a cupping-glass was applied for
half an hour, the general symptoms ceased and did not return. Next day
diffuse inflammation began; but it was checked by leeches.[1543] An
equally successful case is related in the Calcutta Transactions by Mr.
Clarke.[1544]




                             CHAPTER XXIV.
          OF POISONING BY DISEASED AND DECAYED ANIMAL MATTER.


Another and much more important group of poisons, that may be arranged
in the present order, comprehends animal matter usually harmless or even
wholesome, but rendered deleterious by disease or decay. These poisons
are formed in three ways, by morbid action local or constitutional, by
ordinary putrefaction, and by modified putrefaction.


       _Of Animal Matter rendered Poisonous by Diseased Action._

Under the first variety might be included the latent poisons by means of
which natural diseases are communicated by infection, contact, and
inoculation. Such poisons, however, being usually excluded from a strict
toxicological system, the only varieties requiring notice are the animal
poisons engendered by disease, and which do not produce peculiar
diseases, but merely inflammation. Several species of this kind may be
mentioned, comprehending the solids and fluids in various unhealthy
states of the body.

One of these poisons, contained in the blood and perhaps in some of the
secretions of overdriven cattle, arises under circumstances in which the
body seems to deviate little from its natural condition. A good account
of the effects thus induced has been given in an essay on the subject by
Morand.[1545] From the cases he describes it follows, that the flesh of
such animals is wholesome enough when cooked and eaten; but that if the
blood or raw flesh be applied to a wound or scratch, nay even sometimes
to the unbroken skin, a dangerous and often fatal inflammation is
excited, which at times differs little from diffuse cellular
inflammation, and at other times consists of a general eruption of
gangrenous boils, the _pustules malignes_ of the French. The deleterious
effects occasionally observed to arise from offal are probably analogous
in their nature and their cause. On this subject Sir B. Brodie has made
some remarks which tend to show that the application of various kinds of
offal to wounds, and especially pricks of the fingers with spiculæ of
bone from the hare, may cause an obstinate chronic erysipelas of the
hand.[1546] I have met with a case of this nature, where the affection
was erratic erythema of the hand.

Another species of poison, allied to the preceding in its effects and
equally obscure in its nature, includes certain fluids of the human body
after natural death, which are probably modified, if not even formed
altogether, by morbid processes during life. Such poisons are the most
frequent source of the dreadful cellular inflammation, often witnessed
as the consequence of pricks received during dissection by the
anatomist. On this interesting but obscure subject, much minute
information will be found in the works quoted below.[1547]

It is still a matter of question among pathologists what these poisons
are, and in what circumstances they spring up. By some their baneful
properties have been suspected to arise from the operation of particular
diseases on natural or morbid secretions;[1548] and although the precise
diseases inducing these properties, and the precise fluids which acquire
them have by no means been satisfactorily ascertained, it appears well
established that no fluid possesses them more frequently or in a higher
degree than the serum effused into the cavities of the chest and belly
by recent inflammation of the serous membranes of these cavities. By
others the origin of the poison is suspected to be wholly independent of
diseased action in the living body and to lie merely in certain changes
effected in healthy secretions by decay. And as the accidents produced
by this poison have occurred chiefly during the dissection of bodies
recently dead, it is supposed to exist only for a short time at the
commencement of decay, and to disappear in the farther progress of
putrefaction.

But whatever may be its nature and origin, we are well enough acquainted
with its effects; which are diffuse inflammation and violent
constitutional excitement, quickly passing to a state resembling typhoid
fever. Sometimes the inflammation spreads steadily towards the trunk
from the part to which the poison was applied; sometimes the
inflammation around the injury is trifling and limited, but a similar
inflammation appears in or near the axilla, and subsequently on other
parts of the body; and the latter form of disease is always attended
with the highest constitutional derangement and with the greatest
danger.

Another singular poison, unequivocally the product of disease, and which
acts as a local irritant, is the flesh or fluids of animals affected at
the time of their death with a carbuncular disorder, denominated in
Germany _Milzbrand_, and analogous to the _pustule maligne_ of the
French. The disease, so far as I know, has not received a vulgar name in
the English language, being fortunately rare in Britain. It is a
constitutional and epidemic malady, which sometimes prevails among
cattle on the continent to an alarming extent, and is characterized by
the eruption of large gangrenous carbuncles on various parts of the
body. This distemper has the property of rendering the solids and fluids
poisonous to so great a degree, that not only persons who handle the
skin, entrails, blood, or other parts, but even also those who eat the
flesh, are apt to suffer severely. The affection thus produced in man is
sometimes ordinary inflammation of the alimentary canal, or
cholera;[1549] more commonly a disorder precisely the same as the
pustule maligne;[1550] but most frequently of all an eruption of one or
more large carbuncles resembling those of the original disease of
cattle.[1551] It is often fatal. The carbuncular form has been known to
cause death in forty-eight hours.[1552] It is an interesting fact, for
the knowledge of which we are indebted to M. Dupuy, that the carbuncle
of cattle may be caused by applying to a wound the blood or spleen of an
animal killed by gangrene of the lungs.[1553]

A poison analogous to the former in its nature, which has sometimes
occasioned severe and even fatal effects in man is the matter of
_glanders_, a contagious disease to which the horse is peculiarly
subject, and which is communicated probably by means of a morbid
secretion from the nostrils. This disease has been propagated to man by
infection; at least instances have been related where grooms attending
glandered horses, although they had no external injury through which
inoculation could take place, were attacked with profuse fetid discharge
from the nostrils, a pustular eruption on the face, and colliquative
diarrhœa, which has sometimes ended fatally in a few days.[1554] In
other instances inoculation of the hand with the blood of the glandered
horse has produced alarming diffuse inflammation, and a carbuncular
eruption.[1555]

It appears probable, that some peculiar circumstances with which we are
not yet acquainted must concur with the operation of the poisons now
under review, before they can take effect. At least unequivocal facts
have been published which show, that the fluids and solids, as well as
the emanations of animals infected and even killed by glanders or the
_pustule maligne_, may be often handled and breathed with impunity. Such
is the result of a careful inquiry made under the direction of the
Parisian Board of Health into the nuisance occasioned by the great
Nackery of Montfaucon.[1556] Parent-Duchatelet, the author of an
elaborate report on the subject, considers it clearly established that
neither the workmen nor the horses connected with the establishment, nor
the tanners who are supplied with hides from it, have ever presented a
single instance of disease referrible to the operation of diseased
animal matter. Yet upwards of twelve thousand horses are annually flayed
there, and among these it is calculated that at least three thousand six
hundred are affected with carbuncle, glanders, or farcy.[1557]


     _Of Animal Matter rendered Poisonous by common Putrefaction._

The second mode in which animal matters, naturally wholesome or
harmless, may acquire the properties of irritant poisons, is by their
undergoing ordinary putrefaction.

The tendency of putrefaction to impart deleterious qualities to animal
matters originally wholesome has been long known, and is quite
unequivocal. To those who are not accustomed to the use of tainted meat,
the mere commencement of decay is sufficient to render meat
insupportable and noxious. Game, only decayed enough to please the
palate of the epicure, has caused severe cholera in persons not
accustomed to eat it in that state. The power of habit, however, in
reconciling the stomach to the digestion of decayed meat is
inconceivable. Some epicures in civilized countries prefer a slight
taint even in their beef and mutton; and there are tribes of savages
still farther advanced in the cultivation of this department of
gastronomy, who eat with impunity rancid oil, putrid blubber, and
stinking offal. How far putrefaction may be allowed to advance without
overpowering the preservative tendency of habit, it is not easy to tell.
But with the present habits of this and other civilized nations, the
limit appears very confined.

Putrid animal matter when injected into the veins of healthy animals
proves quickly fatal; and from the experiments of Gaspard and
Magendie,[1558] together with the more recent researches of MM. Leuret
and Hamont,[1559] the disease induced seems to resemble closely the
typhoid fever of man.

Similar effects were observed by Magendie, when dogs were confined over
vessels in which animal matter was decaying, so that they were obliged
always to breathe the exhalations.[1560] These discoveries throw some
light on the question regarding the tendency of putrid effluvia to
engender fever in man; and notwithstanding many well ascertained facts
of an opposite import, they show that, probably in peculiar
circumstances, decaying animal matter may excite epidemic fevers. A
detailed investigation of this important topic would be misplaced here,
as it belongs more to medical police than to medical jurisprudence; but
the two works quoted below are referred to for examples, in my opinion,
of the unequivocal origin of continued fever in the cause now alluded
to;[1561] and other instances of the like kind will be found in the
Report of the Parliamentary Commission on the Health of Towns.

Another affection sometimes brought on by putrid exhalations is violent
diarrhœa or dysentery, of which a remarkable instance lately occurred in
the person of a well-known French physician, M. Ollivier. While visiting
a cellar where old bones were stored, he was seized with giddiness,
nausea, tendency to vomit and general uneasiness; and subsequently he
suffered from violent colic with profuse diarrhœa, which put on the
dysenteric character and lasted for three days.[1562] Chevallier, in
noticing this accident, mentions his having been affected somewhat in
the same way when exposed to the emanations of dead bodies; and it is a
familiar fact that medical men, who engage in anatomical researches
after long disuse, are apt to suffer at first from smart diarrhœa.

The same remark must be applied here as at the close of the observations
in the last section. Without peculiar concurring circumstances no bad
effect results. This will follow from many facts illustrative of the
innocuous nature of various trades where the workmen are perpetually
exposed to the most noisome putrid effluvia. But no facts of the kind
are so remarkable as those collected in regard to the establishment at
Montfaucon by Parent-Duchatelet, who makes it appear that this most
abominable concentration of the worst of all possible nuisances is not
merely not injurious to the health of the men and animals employed in
and around it, but actually even preserves them from epidemic or
epizootic diseases.[1563]

The effects of putrid animal matter when applied to wounds have been
investigated experimentally by Professor Orfila; who found that putrid
blood, bile, or brain, caused death in this way within twenty-four
hours,—producing extensive local inflammation of the diffuse kind, and
great constitutional fever. In man also several instances of diffuse
cellular inflammation have been observed as the consequence of pricks
received during the dissection of putrid bodies. The disease, as
formerly observed, certainly arises in general from pricks received in
dissecting recent bodies. At the same time, a few cases have been traced
quite unequivocally to inoculation with putrid matter;[1564] and if any
doubts existed on this point, the experiments of Orfila would remove
them.

M. Lassaigne has examined chemically the putrid matter formed by keeping
flesh long in close vessels, and has found it to consist of carbonate of
ammonia, much caseate of ammonia, and a stinking volatile oil,—the last
of which is probably the poisonous ingredient.


    _Of Animal Matter rendered Poisonous by Modified Putrefaction._

The third way in which animal matters naturally wholesome may become
irritant poisons, is by their undergoing a modified putrefaction.

It is probable that many common articles of food occasionally become
poisonous in this way; but none are so liable to acquire injurious
properties as certain articles much used in Germany, namely, a
particular kind of sausage, a particular kind of cheese, and bacon. The
last two species of poison have been occasionally observed in France,
and probably occur in Britain also. But the first has been hitherto met
with only in some districts of Germany.

The best account yet given of the _sausage-poison_ is contained in two
essays published by Dr. Kerner,[1565] in a Thesis by Dr. Dann,[1566] and
in a prize-essay by Dr. W. Horn.[1567] It has at various times committed
great ravages in Germany, especially in the Würtemberg territories,
where 234 cases of poisoning with it occurred between the years 1793 and
1827; and of that number no less than 110 proved fatal.[1568]

The symptoms of poisoning seldom begin till twenty-four, or even
forty-eight hours, after the noxious meal, and rather later than
earlier. The tardiness of their approach seems owing to the great
indigestibility of the fatty matter with which the active principle is
mixed. The first symptoms are pain in the stomach, vomiting, purging,
and dryness of the mouth and nose. The eyes, eyelids, and pupils then
become fixed and motionless; the voice is rendered hoarse, or is lost
altogether; the power of swallowing is much impaired; the pulse
gradually fails, frequent swoonings ensue, and the skin becomes cold and
insensible. The secretions and excretions, with the exception of the
urine, are then commonly suspended; but sometimes profuse diarrhœa
continues throughout. The appetite is not impaired; fever is rarely
present; and the mind continues to the last unclouded. Fatal cases end
with convulsions and oppressed breathing between the third and eighth
day. In cases of recovery the period of convalescence may be protracted
to several years. The chief appearances in the dead body are signs of
inflammation in the mucous membrane of the alimentary canal,—such as
whiteness and dryness of the throat, thickening of the gullet, redness
of the stomach and intestines; also croupy deposition in the windpipe;
great flaccidity of the heart; and a tendency in the whole body to
resist putrefaction. In a set of cases which occurred so lately as 1841,
there was found after death abscesses in the tonsils, dark bluish
redness of the membrane of the pharynx, windpipe and bronchial
ramifications, gorging of the pulmonary air-tubes and condensation of
the pulmonary tissue itself, dark redness of the fundus of the stomach,
with circumscribed softening, a dark gray, red, or black appearance of
the mucous coat of the intestines, accumulation of greenish-yellow fæces
in the colon, brittleness of the liver, and enlargement of the
spleen.[1569]

The article which is apt to occasion these baneful effects is of two
sorts, the white and the bloody sausage (_leberwürste_, _blut-würste_).
Both are of large size, the material being put into swine’s stomachs;
and they are cured by drying and smoking them in a chimney with
wood-smoke. Those which have been found to act as poisons possess an
acid reaction, are soft in consistence, have a nauseous, putrid taste,
and an unpleasant sweetish-sour smell, like that of purulent matter.
They are met with principally about the beginning of spring, when they
are liable to be often alternately frozen and thawed in the curing.
Those sausages only become poisonous which have been boiled before being
salted and hung up. They are poisonous only at a particular stage of
decay, and cease to be so when putrefaction has advanced so far that
sulphuretted-hydrogen is evolved. The central part is often poisonous
when the surface is wholesome.

Various opinions have been entertained of the cause of the deleterious
qualities thus contracted. In recent times the principle has been
supposed to be pyroligneous acetic acid, hydrocyanic acid, or cocculus
indicus. Dr. Kerner, however, has shown that none of these notions will
account for the phenomena; and at first conceived he had proved the
poisonous principle to be a fatty acid analogous to the sebacic acid of
Thenard, and originating in a modified process of putrefaction. From the
poisonous sausage he procured by double decomposition an acid similar in
chemical properties to that obtained from fat by destructive
distillation; and by experiments on animals he thought he observed, that
the acid procured in either way produced symptoms analogous to those of
poisoning with the deleterious sausage. Subsequently, however, he
changed his views in some measure; and he now considers that the poison
is a compound one, consisting of a fatty acid analogous to the sebacic,
and of a volatile principle.[1570] The results obtained by Dr. Dann
coincide with the last opinion. Dann infers from his researches that the
poisonous principle does not necessarily reside in an acid, but is an
acrid empyreumatic oil, which when pure is not active, but is rendered
so by uniting with various fatty acids.[1571]

The results lately obtained by Buchner after an elaborate and careful
analysis are somewhat different and probably nearer the truth. He first
ascertained that the product of the distillation of fat has no analogy
with the sausage-poison. He found it to consist of animalized acetic
acid, and a fetid empyreumatic oil, the former of which has no injurious
effect on animals, while the latter, though an active poison, is purely
narcotic in its operation. On next examining a sausage sent to him from
Würtemberg, which had violently affected four individuals and killed one
of them in six days, he remarked that the poisonous principle is not
soluble in water, or capable of being distilled over with it; and that
cold alcohol removes a granular fatty matter, which, when purified by
distilled water, has a yellowish colour, a peculiar nauseous smell, and
a disagreeable oleaginous taste, followed by extraordinary dryness of
the throat for several hours. Although it does not possess an acid
reaction on litmus, it forms a soap with alkalis, and is separated again
by acids unchanged; and consequently it may be considered a fatty acid,
to which Buchner proposes to give the name of Botulinic acid
[Würst-fett-saüre]. It concentrates in itself the poisonous properties
of the crude sausage. Thirty grains of it, which formed three-fourths of
the whole product of a single sausage, were given in two doses to a
puppy with an interval of a day between them. For some hours after the
second dose no apparent effect was produced. But gradually the animal
became dull, lay in the same spot, wasted rapidly away notwithstanding a
vigorous appetite, and died of exhaustion on the thirteenth day. Half a
grain causes insupportable dryness in the throat, which does not go off
for several hours.[1572] With these results the contemporaneous and
unconnected researches of Dr. Schumann accord very remarkably. Alcohol
boiled on the poison-sausage deposited on cooling a fatty matter, which,
when washed with distilled water, possessed all the properties specified
by Buchner, as characterizing his fatty acid, and acted on animals in
the same way as the sausage-poison.[1573]

The _poison of cheese_ has been for some time more generally known. Dr.
Henneman has published an interesting essay on several cases which
happened at Schwerin in 1823.[1574] Another account of a similar
accident which happened at Minden in 1825 has been published in Rust’s
Magazin.[1575] But by far the best information on the subject is to be
obtained from two papers in Horn’s Archiv,—the one by Professor Hünefeld
of Greifswald, describing the phenomena as he witnessed them in that
city in 1827, and containing an elaborate chemical analysis and
physiological experiments, by means of which he conceives he has
discovered the deleterious principles contained in the cheese,[1576]—the
other by Dr. Westrumb of Hameln, who investigated the particulars of
seven cases which came under his notice in 1826, and with the aid of
Sertürner, the chemist, traced the properties of the poison to almost
the same principles with those indicated by the researches of
Hünefeld.[1577] Besides the cases which have given origin to these
papers, others have occurred throughout Germany in the same period; and
during the third quarter of last century this kind of poisoning was so
common, that several of the German states investigated the subject, and
legislative enactments were passed in consequence.

For a long time the prevalent belief was that the cheese acquired an
impregnation from copper vessels used in the dairies; and accordingly
the Austrian, Wirtemberg and Ratesberg States prohibited the use of
copper for such purposes. This opinion, however, was proved by chemical
analysis to be untenable; and the inquiries of Hünefeld and Sertürner,
have now rendered it probable that the poisonous property of the cheese
resides in two animal acids, analogous, if not identical, with the
caseïc and sebacic acids.

The mode in which the formation of these acids is accounted for is as
follows. According to the researches of Proust the sharp peculiar taste
of old cheese is owing to the gradual conversion of the curd or casein
into the caseate of ammonia, which in sound cheeses is always united
with the excess of alkali. In the cheese in question (_barscher-käse_,
_quark-käse_, _hand-käse_) the curd, before being salted, is left for
some time in a heap to ferment, in consequence of which it becomes sour
and afterwards ripens faster. But if the milk has been curdled with
vinegar,—if the acid liquor formed while it ferments is not carefully
drained off,—if the fermentation is allowed to go too far,—if too little
salt is used in preserving the curd,—or if flour has been mixed with the
curd, the subsequent ripening or decaying of the cheese follows a
peculiar course, and a considerable excess of caseïc acid is formed, as
well as some sebacic acid.

The poisonous cheeses, according to Westrumb, present no peculiarity in
their appearance, taste or smell. But Hünefeld says that they are
yellowish-red, soft, and tough, with harder and darker lumps
interspersed, that they have a disagreeable taste, redden litmus, and
becomes flesh-red instead of yellow, under the action of nitric acid.

The symptoms they cause in man appear to be nearly the same with those
produced by the poisonous sausage, and usually commence, according to
Hünefeld, in five or six hours, according to Westrumb in half an hour.
They constitute various degrees and combinations of gastro-enteric
inflammation. In the most severe of Hünefeld’s cases the quantity taken
did not exceed four ounces, and was sometimes only an ounce.

The same author found that a drachm and a half of the caseïc acid, which
he procured from the cheese, killed a cat in eight minutes, and the same
quantity of the sebacic acid another in three hours. His experiments,
however, are not quite conclusive of the fact that these acids are
really the poisonous principles, as he has not extended his experimental
researches to the caseïc and sebacic acids prepared in the ordinary way.
His views will probably be altered and simplified, if future experiments
should confirm the late inquiries of Braconnot, who has stated that
Proust’s caseïc acid is a modification of the acetic, combined with an
acrid oil.[1578] Westrumb procured analogous results with those of
Hünefeld when he gave to animals the acid fat which he separated in the
course of his analysis.

The poisonous cheese has been hitherto met with chiefly in some parts of
Germany. From information communicated to me by Dr. Swanwick of
Macclesfield, there is some reason to think that a parallel poison is
occasionally met with in Cheshire, among the small hill-farms, where the
limited extent of the dairies obliges the farmer to keep the curd for
several days before a sufficient quantity is accumulated for the larger
cheeses.—I am indebted to Mr. Wilson of Lockerby for the particulars of
a set of cases, which seem to have been owing to some obscure poison in
cheese. A gentleman, an hour after eating the suspected cheese, was
seized with extreme weakness and severe vomiting for four hours, then
with general soreness and a mercurial taste in the mouth, and afterwards
with tenesmus, bloody stools, soreness of the gums, and cramps in the
limbs; from which symptoms he did not recover for four weeks. Five other
members of his household suffered similarly, but less severely, and also
the shop-boy who ate a little while selling it. None of the ordinary
mineral poisons could be detected in it.—It is hardly necessary to add,
that analogous properties may be imparted to cheese by the intentional
or accidental addition of other poisons of a mineral nature. This
subject has been already alluded to in the section upon lead.

As connected, though indeed but remotely, with the cheese-poison, some
notice may be here taken of a peculiar mode in which it has been
supposed that _milk_ may acquire the properties of an acrid poison. It
has been several times remarked on the continent, that the milk even of
the cow, but more particularly that of the ewe and goat, may act like a
violent poison, although no mineral or other deleterious impregnation
could be detected in it; and these effects have been variously and
vaguely ascribed to the animal having been diseased, or to its having
fed on acrid vegetables, which pass into the milk without injury to its
health, because though poisonous to most animals, they are not so to the
Ruminantia. This singular topic cannot be thoroughly investigated, as
precise facts are still wanting. But the two following examples of the
accident alluded to may be mentioned. One occurred at Aurillac, a
village in France. Fifteen or sixteen customers of a particular dealer
in goats’ milk were at one and the same time attacked with all the
symptoms of violent cholera; and about twenty-four hours afterwards the
goat too was taken ill with the same affection, and died in three
days.[1579] The other instance occurred at Hereford in Westphalia. Six
people of a family, after partaking of goat’s butter-milk, were
simultaneously attacked with violent vomiting, tension of the
epigastrium, and retraction of the lower belly; and several of them
suffered so severely as even to have been thought by their physician,
Dr. Bonorden, to be in danger.[1580] Dr. Westrumb has alluded to similar
cases in his memoir on the poison of cheese, and has proved that the
ordinary explanations of them are far from satisfactory. Among other
judicious observations he remarks, that the poison has been generally
believed to arise sometimes from the cattle having fed on the _Euphorbia
esula_, a species of spurge; that, according to Viridet in his
_Tractatus de Prima Coctione_, l. i. c. 15, certain fields in the
neighbourhood of Embrim were of necessity abandoned by the shepherds,
because the milk of their cows was rendered useless by the abundance of
that plant among the herbage; but that he himself has found cattle will
not touch it so long as grass and other wholesome vegetables are to be
found in the pasturage.[1581] Professors Orfila and Marc, who were
appointed by the Society of Medicine of Paris to report upon the
accident at Aurillac, state, that in parallel cases which had been
referred to them by the police at Paris they had been unable to detect
any mineral poison; that none of the received explanations are in their
opinion satisfactory; and that they are disposed to ascribe the
poisonous alteration of the milk to new principles formed by a vital
process.

Another common article of food, which has occasionally produced similar
effects with the poisonous sausages and cheese, is bacon. Dr. Geiseler
has related an accident which occurred in a family of eight persons, and
which he traced to this cause. The symptoms were almost exactly the same
with those described by Kerner, with the addition, however, of delirium
and loss of recollection; and in two they were so violent as seriously
to endanger life. The father of the family alone escaped, having stewed
his bacon, while the rest ate it raw.[1582] His escape might have arisen
from the fatty acid having been decomposed, or the acrid oil expelled,
by the heat. It is not improbable that other varieties of cured meat may
also become poisonous. Cadet de Gassicourt mentions, that he had been
frequently desired by the police to examine cured meat which had
produced symptoms of poisoning at Paris,[1583] and Orfila makes the same
remark in his Lectures on Medical Jurisprudence.[1584] As the meat
always came from the shops of meat-curers, and did not contain any
mineral poison, it probably owed its qualities to the same ingredient as
the bacon in Geiseler’s cases. A full and interesting account of an
accident of the kind has also been given by M. Ollivier, of which the
following is an analysis. Three members of a family at Paris, on the day
after eating a ham-pie, were seized with shivering, cold sweats, violent
pain in the stomach, frequent vomiting, burning thirst, excessive
tenderness of the belly, profuse purging, and colic; but they all
recovered under antiphlogistic treatment. On subsequent inquiry it
appeared that about the same period other customers of the pastry-cook
who supplied the pie had been similarly affected; and consequently an
investigation was made into the cause under the authority of the police.
After a very careful analysis, however, by MM. Barruel and Ollivier, it
was clearly made out, that the pie did not contain a trace of any of the
common mineral poisons; and therefore the only conclusion Ollivier
conceived it possible to draw was, that the ham had acquired the
properties of the poisonous sausage or cheese of Germany.[1585] Two
similar reports have been since published, one by MM. Lecanu,
Labarraque, and Delamorlière, another by Chevallier; and both agree in
ascribing the poisonous effects to the decay of the meat, the ordinary
poisons having been sought for in vain. In the cases examined by
Chevallier, the article was a sort of sausage, called in Paris “Italian
Cheese,” and made of scraps of various kinds of meat, especially
pork.[1586] M. Boutigny has published an account of a similar accident
which befel a great number of people at a festival in France. He could
not find any of the ordinary poisons in the meat, which had been taken
chiefly in the form of sausages; and being consequently persuaded that
the suspected articles were wholesome, he dined on stuffed turkey, sold
by the dealer who had supplied them. But he was seized with chilliness,
contracted pulse, cold sweating, lividity of the countenance, great
anxiety, and then with vomiting and purging; after which he slowly
recovered.[1587]

Other articles of food have been occasionally observed to act
injuriously on the health. Thus M. Ollivier has given an account of a
whole family having been apparently poisoned with mutton under the
influence of modified decay. Six individuals were attacked soon after
dinner with vomiting, purging, colic, tenderness of the belly, extreme
prostration, and a small hurried pulse. Four of them died within eight
days. General inflammatory redness, with some extravasation under the
mucous coat, was found throughout the whole course of the small
intestines. No trace could be detected of any of the ordinary poisons;
and Ollivier was therefore led to ascribe the accident to some
peculiar change produced in stewed mutton, which all the individuals
had partaken of at dinner.[1588] In 1839 a singular accident happened
at Zurich, which was ascribed to decayed _veal_ and _ham_. On a
fete-day 600 people, who had dined upon cold roast-veal and ham in a
wooden erection, were all taken ill with shivering, giddiness,
headache, burning fever, diarrhœa and vomiting; some had delirium,
others a fœtid salivation and even ill-conditioned ulcers of the
mouth; and in the worst cases collapse of the countenance, involuntary
stools, and extreme prostration preceded death. On dissection the
alimentary mucous membrane was found softened and the intestinal
follicles ulcerated. The cause was supposed to have been
satisfactorily traced to incipient putrefaction of the veal and ham,
which constituted the fundamental part of the repast.[1589] Effects
somewhat similar have been observed from spoiled _goose-grease_, used
in dressing food. Dr. Siedler has related four cases where violent
symptoms were thus induced. Two adults and two children, after eating
a dish seasoned with goose-grease, were seized with giddiness,
prostration of strength, anxiety, sweating,—burning pain in the lower
belly, aggravated by pressure,—violent vomiting, in one case
sanguinolent,—involuntary stools, and urine, and dilatation of the
pupil. In one of the adults there was also complete insensibility,
with imperceptible pulse for six minutes. No metallic poison could be
found. The grease was acid, and of a repulsive odour; and three ounces
given to a dog acted violently and in the same manner.[1590] Another
article of food which has appeared occasionally to produce parallel
effects is _smoked sprats_. An instance of their injurious operation
is briefly described in the work quoted below;[1591] and Dr.
O’Shaughnessey informed me some years ago, that, while in London, he
met with the case of a female, advanced in pregnancy, who after eating
smoked sprats, in which she remarked a disagreeable sharp taste, was
attacked with severe colic, sickness, vomiting of food mixed with
streaks and clots of blood, and some diarrhœa. Putrid _pickled salmon_
has occasioned death in this country;[1592] and I may mention that I
have known most violent diarrhœa occasioned in two instances by a very
small portion of the oily matter about the fins of _kipper_ or smoked
salmon, so that I have no doubt a moderate quantity would produce
serious effects.

Although these illustrations of the effects of modified putrefaction in
rendering wholesome meat noxious have been taken in a great measure from
continental experience, this has been done rather because the subject
has been more fully and accurately investigated there, than because
similar poisons are unknown in Britain. The defective system of medical
police in this country would allow such accidents as those mentioned
above to pass sometimes without notice, and almost always without
scientific examination; but it must not therefore be supposed that they
are wholly unknown.

The following incident, which happened a few years ago on the Galloway
coast, is an instance of poisoning not less alarming than any of those
which have occurred in Germany. In the autumn of 1826 four adults and
ten children ate at dinner a stew made with meat taken from a dead calf,
which was found by one of them on the sea shore, and of which no history
could be procured. For three hours no ill effect followed. But they were
then all seized with pain in the stomach, efforts to vomit, purging, and
lividity of the face, succeeded by a soporose state like the stupor
caused by opium, except that when roused the patient had a peculiar wild
expression. One person died comatose in the course of six hours. The
rest, being freely purged and made to vomit, eventually got well; but
for some days they required the most powerful stimulants to counteract
the exhaustion and collapse which followed the sopor. The meat, they
said, looked well enough at the time it was used. Yet the remains of the
fish which formed the noxious meal had a black colour and nauseous
smell; and the uncooked flesh had a white, glistening appearance, and
was so far decayed that its odour excited vomiting and fainting.[1593]
It is much to be regretted that this accident was not properly inquired
into. The only conjecture which the facts will warrant as to the cause
of the poisonous quality of the meat is, that in consequence of having
lain long in the water, the flesh had begun to undergo the adipocirous
putrefaction; and that in the course of the changes thus induced the
meat became impregnated with some poisonous principle, like that of the
German sausages, or cheese.

An accident of a similar nature, for the particulars of which I am
indebted to Dr. Swanwick of Macclesfield, occurred at Stockport in the
summer of 1830. A family of five persons took for dinner broth made of
beef, which, owing to its black colour, the master of the family had
previously said to his wife he thought bad and unfit for use. In the
course of some hours two boys were attacked with sickness and vomiting,
but appear to have got soon well, probably owing to the early discharge
of the poison. Next morning a washerwoman who had dined with the family
was seized with violent pain in the bowels, diarrhœa, racking pains and
weakness in the limbs; and she did not recover for ten days. On the
evening of the second day the master of the house was similarly
affected, and was ill for a fortnight. And a day later his wife was also
seized with a similar disorder, preceded by soreness of the throat and
tongue and difficulty of swallowing, and ending fatally in fourteen
days. The last person was previously in delicate health, and subject to
disorder in the stomach and bowels. The investigation made by the police
authorities into the circumstances of this accident was extremely
imperfect: but there seems little reason to doubt that unsound meat was
the cause.

I am not sure under what head to arrange the following observations,
communicated to me by Dr. M’Divitt of Canterbury, and of which he has
since published a detailed account.[1594] But they may be mentioned,
perhaps not inappropriately, in the present place; and at all events
they deserve careful attention, as referring to a description of cases
which may be mistaken for other kinds of poisoning.

It is well known that pork in all forms, but especially when fresh, is
apt to cause indigestion in many persons who are not accustomed to it.
But Dr. M’Divitt has shown by a number of interesting cases, that even
in those habituated to its use, it may, from unascertained causes,
excite symptoms closely allied to those of irritant poisoning. The
effects sometimes begin within three hours, the symptoms being those of
an affection of the stomach, such as sudden violent pain in the
epigastrium, difficult breathing, irregularity of the pulse, great
prostration and alarm, coldness of the extremities and vomiting. If a
longer period elapses,—and sometimes no injury accrues for many hours,
or even a whole day,—the symptoms indicate an affection of the abdomen,
namely, pain in the region of the duodenum, or of the sigmoid flexure of
the colon, with the other symptoms just enumerated, but which ere long
become attended with more pungent pain, tension and tenderness of the
belly, frequency of the pulse, and ineffectual straining to evacuate the
bowels. In the less urgent and slower cases of this nature there is
little or no vomiting. Sometimes nettle-rash appears. Stimulants,
opiates, and blood-letting are of no avail; and the only useful remedies
are emetics and cathartics, which speedily put an end to the symptoms by
removing their cause. In all the cases related by the author the pork
was either fresh or recently salted, fatter than usual, but not ill
preserved or otherwise faulty in any appreciable respect. In every
instance the individuals had eaten pork often before without injury; and
on several occasions others ate without harm the same pork which seemed
deleterious.




                              CHAPTER XXV.
                 OF POISONING BY MECHANICAL IRRITANTS.


The _fifth_ order of the irritant class of poisons includes mechanical
irritants.

These substances have not properly speaking any poisonous quality; but
occasion symptoms like those of poisoning, and even sometimes death
itself, in consequence of their mechanical qualities only. They have
therefore been excluded from every toxicological system proposed in
recent times; but in a medico-legal work on poisoning it would be wrong
to pass them without notice.

The most important of the mechanical irritants are those which cause
injury by reason of their roughness, sharpness, or size.

Many instances have occurred of persons having swallowed fragments of
steel, copper, iron, broken glass, or entire prune-stones,
cherry-stones, and the like,—who not long afterwards were attacked with
signs of inflammation, or some other abdominal disease, and were carried
off by it as by the administration of poison. The disorders thus induced
are almost always of a chronic or lingering kind, and commonly depend on
gradual perforation of the intestines by the foreign body pressing on
the coats. In general the illness ends in inflammation of the
peritonæum. Sometimes the irritating substance perforates the skin and
muscles as well as the intestines, and escapes outwardly; and a few
individuals have even recovered under these circumstances. An excellent
account of the ordinary course of such accidents is given in the London
Medical and Physical Journal. The person swallowed a chocolate bean, and
after experiencing many uneasy sensations throughout the belly for
several days, was attacked with peritonitis and died.[1595] Mr. Howship
has related the particulars of the case of a woman, died after two years
of constant suffering, in consequence of having swallowed a large
quantity of cherry-stones.[1596] Dr. Marcet has also described the case
of a sailor who died in a similar way after swallowing several large
clasp-knives.[1597] Thus too, although it is a familiar fact, that
needles and pins are in general swallowed with impunity, death
nevertheless sometimes arises from this cause. Guersent mentions the
case of a child who died in the course of two months of frequent
vomiting caused by swallowing a pin, which was found after death pinning
the stomach, as it were, to the liver.[1598] Dupuytren relates the case
of a woman, who, after swallowing an incredible number of needles and
pins, became very lean and was confined to bed by the excruciating pain
excited on motion by the needles and pins escaping through the skin.
There were seldom less than fifty tumours or abscesses on various parts
of the body; and Dupuytren, on opening about a hundred of these,
invariably found one or more needles or pins in each. She laboured under
general debility, irritative fever, and marasmus, and at length died
hectic. After death many hundred pins and needles were found among the
muscles and viscera.[1599] Many other examples might be referred to, but
these will suffice for information on the ordinary effects of mechanical
irritants of the kind under consideration.

From the case of Dr. Marcet and other similar facts, it appears that
large and even angular bodies do not always cause serious mischief, nay,
that they have been frequently swallowed without any material injury.
Dr. Marcet’s sailor in the course of his life had repeatedly swallowed
several clasp-knives in quick succession: and nevertheless recovered
perfectly after some days of slight illness. As to prune and
cherry-stones, buttons, coins, needles, pins, and the like, they have
been very often taken, and even sometimes in large quantities, without
any harm. It is indeed extraordinary, and almost incredible, if the
facts were not authenticated beyond the possibility of a doubt, how much
mechanical irritation the alimentary canal has been subjected to,
without sustaining any injury. Mr. Wakefield mentions that a man, who
was committed to the House of Correction, swallowed seven half-crowns,
to prevent the prison authorities from depriving him of them. He
suffered no inconvenience for twenty months; when, after an attack of
sickness, slight bowel-complaint, and general tenderness of the belly,
he discharged them all at one evacuation.[1600] Many singular instances
to the same effect have been related in the various medical journals of
Europe. At the head of the list, however, may be placed the following,
which is related by the late Professor Osiander of Göttingen, in his
work on Suicide.

A young German nobleman tried to kill himself in a fit of insanity by
swallowing different indigestible substances, but without success. He
never suffered any particular inconvenience except a single attack of
vomiting daily, though in the course of seven months after being
detected he passed the following articles by stool—150 pieces of sharp,
angular glass, some of them two inches long—102 brass pins—150 iron
nails—three large hair pins, and seven large chair-nails—a pair of
shirt-sleeve buttons—a collar-buckle, half of a shoe-buckle, and three
bridle-buckles—half a dozen sixpenny pieces—three hooks, and a lump of
lead—three large fragments of a currycomb, and fifteen bits of nameless
iron articles, many of them two inches in length.[1601]

Before such articles occasion serious harm, it is necessary that some
cause coincide, by means of which the foreign bodies are detained long
in the same part of the intestines; otherwise the irritation they
produce is too trivial to excite disease.

The only substance of this kind which it is necessary to particularize
is _pounded glass_. A common notion prevails that pounded glass is an
active poison. There is no doubt, indeed, that it does possess some
irritant properties even when finely pulverized; for it titillates and
smarts the nostrils, and inflames the eyes. There is also little doubt
that when swallowed in fragments of moderate size, especially if the
stomach is empty, it may wound the viscera. But it is in this way only
that it has any action when swallowed, and even then its effects are by
no means uniformly serious. It can have no chemical action on the
stomach; it cannot act through absorption, as it is quite insoluble: and
when finely pulverized, it cannot easily wound the villous coat of the
alimentary canal, on account of the abundance and viscidity of the
lubricating mucus.

Accordingly, M. Lesauvage ascertained that 2½ drachms of the powder may
be given to a cat at once without hurting the animal,—that in the course
of eight days seven ounces might be given to a dog without any bad
consequence, although the period chosen for administering it was always
some time before meals,—and that even when the glass was in fragments a
line in length, no symptoms of irritation were induced. Relying indeed
on these results he himself swallowed a considerable number of similar
fragments; and did not sustain any injury.[1602] Caldani likewise, an
Italian physician, after some experiments on animals, gave a boy fifteen
years old several drachms of pounded glass, without observing any bad
effects; and at his request Mandruzzato repeated his experiments on
animals, and himself swallowed on two successive days two drachms and a
half each day without sustaining any injury.[1603]

Similar observations have been made by others also. Dr. Turner of
Spanish Town, Jamaica, has informed me, that an attempt was made there
by a negro to poison a whole family by administering pounded glass; but,
although a large quantity was taken by seven persons, none of them
suffered any inconvenience. Not long ago the occurrence of a similar
case at Paris gave rise to a careful investigation of the whole subject
by Baudelocque and Chaussier. A young man, Lavalley, married a girl who
was pregnant by him; but it was agreed that she should live with her
father till her delivery was over. A month after the marriage Lavalley
invited his wife and father-in-law to dinner; and his wife ate heartily
boiled pork, bloody-sausages, and roast-veal, and subsequently drank
coffee with brandy in it. On returning home in the evening she became
unwell, continued so all night, next morning was seized with violent
pain in the stomach and vomiting, and died in convulsions. The period of
her death is not mentioned in the report I have seen. A suspicion of
poisoning having arisen after burial, the body was disinterred in
forty-two days; and, although it was much decayed, black points and
patches could be distinguished in many parts of the bowels, together
with a quantity of broken down glass. The medical inspectors accordingly
declared that she had died of poisoning with pounded glass; and the
husband was imprisoned. Baudelocque and Chaussier, who were consulted,
ascribed the black patches to putrefaction or venous congestion, and
declared that in whatever way the glass had got into the bowels, she had
not died of poisoning with the substance, as pounded glass is not
deleterious.[1604] A similar opinion as to the properties of pounded
glass was more lately given by Professor Marc, when consulted on a case
of attempted poisoning, in which the person against whom the attempt was
made felt the rough particles in his mouth while taking the second
spoonful of soup in which the glass was contained.[1605]

This opinion certainly appears to be in general true. At the same time
instances are not wanting to render it probable, that pounded or broken
glass is occasionally hurtful. Thus, passing over the more doubtful
examples recorded by the older authors, we have the two following cases
related by good authorities in the most modern times. One has been
published by Mr. Hebb of Worcester. A child, eleven months old, died of
a few days’ illness in very suspicious circumstances. On Mr. Hebb being
requested by the coroner to examine the body, he found the inside of the
stomach lined with a tough layer of mucus streaked with blood; the
villous coat was highly vascular, and covered with numberless particles
of glass of various sizes, some of which simply touched, while others
lacerated it; and no other morbid appearance could be detected in the
body.[1606] The other case is described by Portal. A man undertook for a
wager to eat his wine-glass, and actually swallowed a part of it. But he
was attacked with acute pain in the stomach, and subsequently with
convulsions. Portal made him eat a surfeit of cabbage; and having thus
enveloped the fragments, administered an emetic, which brought away the
glass and vegetables together.[1607] The same feat has undoubtedly been
sometimes accomplished with impunity. For example, in the Edinburgh
Medical and Surgical Journal, an instance is related of a man who
champed and swallowed three-fourths of a drinking-glass without
suffering any harm; and the person mentioned by Osiander swallowed many
pieces of glass, and sustained no inconvenience (p. 503). But these
facts will not altogether outweigh the equally pointed narratives of
Portal and Mr. Hebb. And, on the whole, the medical jurist must come to
the conclusion, that broken and pounded glass, though generally
harmless, may sometimes prove injurious or even fatal.[1608] Powdered
glass, however, is probably inert.

Another variety of injury from the mechanical irritants is inflammation
from hot liquids, such as _melted lead or boiling water_. These, when
swallowed, may unquestionably cause serious mischief, and even death;
and the symptoms they induce are exactly those of the irritant poisons
properly so called.

The effects of boiling water have been investigated experimentally by
Dr. Bretonneau of Tours; and the results illustrate forcibly the
observations which have been repeatedly made in the course of this work,
respecting the slight constitutional derangement caused by such poisons
as have merely a local irritating power. He found that when boiling
water was injected in the quantity of eight ounces into the stomach of
dogs, it excited inflammation, passing on to gangrene, both in the
villous and muscular coats. The symptoms, however, were trifling. For a
day or two the animals appeared languid; but in three days they
generally became lively and playful, one of them actually lined a bitch,
and it was only on strangling them and examining the bodies, that the
extent of the mischief was discovered.[1609]

I am not aware that any such case have hitherto occurred in man. Death
from drinking boiling water, indeed, is not an uncommon accident,
particularly in Ireland and some parts of England, where children, who
are in the habit of drinking cold water from the tea-kettle, have
swallowed boiling water by mistake. It appears, however, that in these
instances death is not owing to inflammation of the gullet and stomach,
but to inflammation of the upper part of the windpipe,—the water never
passing lower than the pharynx. The best information on this subject is
contained in an interesting paper by Dr. Hall.[1610] He has there given
the particulars of four cases which came under his notice; from which it
follows that the disease induced is always _cynanche laryngea_, proving
fatal by suffocation. Two of his patients died suffocated; another,
while in imminent danger, was relieved by tracheotomy, but died
afterwards of exhaustion; the fourth recovered suddenly during a fit of
screaming, when apparently about to be choked; and it was supposed that
the vesicles around the glottis had been burst by the cries.

Pouring melted lead down the throat was a frequent mode of despatching
criminals and prisoners in former ages. Only one authentic case is to be
found on record of death from this cause in modern times. It occurred at
the burning of the Eddistone light-house. A man, while gazing up at the
fire with his mouth open, received a shower of melted lead from the
building, and expired after twelve days of suffering. Seven ounces and a
half of lead had reached the stomach; and the stomach was severely
burnt, and ulcerated.[1611]


In concluding the Irritant Poisons, and before proceeding to the next
class, the Narcotics, it is necessary to observe, that besides the
substances which have been treated of, there are others not usually
considered poisons, and some that are even used daily for seasoning
food, which, nevertheless, when taken in large quantities, will prove
injurious and even occasion all the chief symptoms of the active
irritants. These substances connect the true poisons with substances
which are inert in regard to the animal economy.

It is impossible to particularize all the articles of the kind now
alluded to. But in illustration, I may refer in a few words to six
common substances, pepper, Epsom salt, alum, cream of tartar, sulphate
of potash, and common salt.

_Pepper_, which is daily used by all ranks with impunity, will
nevertheless cause even dangerous symptoms when taken in large quantity.
In Rust’s Journal is noticed the case of a man affected with a tertian
ague, who after taking between an ounce and a half and two ounces of
pepper in brandy, was attacked with convulsions, burning in the throat
and stomach, great thirst, and vomiting of every thing he swallowed. His
case was treated as one of simple gastritis, and he recovered.[1612]

A very striking instance, which may be arranged under the present head,
has also been related to me, of apparent poisoning with Epsom salt. A
boy ten years old took two ounces of this laxative partly dissolved,
partly mixed in a tea-cupful of water; and had hardly swallowed it
before he was observed to stagger and become unwell. When the surgeon
saw him half an hour after, the pulse was imperceptible, the breathing
slow and difficult, the whole frame in a state of extreme debility, and
in ten minutes more the child died without any other symptom of note,
and in particular without any vomiting. The circumstances having been
investigated judicially, it appeared that the substance taken was pure
Epsom salt; that the father, who was doatingly fond of the child, gave
the laxative on account of a trifling illness which he supposed might
arise from worms; and that on the most careful inspection of the body,
no morbid appearance whatever could be found in any part of it. For the
particulars of this singular case, I am indebted to Dr. Dewar of
Dunfermline, the medical inspector under the sheriff’s warrant. It shows
that in certain circumstances even the laxative neutral salts may be
irritating enough to cause speedy death.

Of the same nature probably are the cases which have lately led some to
ascribe poisonous properties to _sulphate of potash_, a purgative salt
at one time in common use. About three years ago several instances of
apparent poisoning with this substance occurred in Paris; and one of
them proved fatal. This was the case of a woman, recently delivered, who
got 100 grains every fifteen minutes till she had taken six doses.
Immediately after the first dose she was seized with severe pain in the
stomach, nausea, vomiting, numbness, and cramps in the arms and legs,
then with dyspnœa and severe purging, and in two hours she expired. The
stomach and intestines were emphysematous, but otherwise healthy; and
the stomach contained sulphate of potash, but not a trace of any of the
common poisons. The stock of this salt in the shop where it had been
purchased was found to be perfectly pure.[1613]—A remarkable case of the
same kind lately led to a criminal trial in London. A man Haynes was
charged with attempting to procure abortion by giving his wife sulphate
of potash. It was proved that on two successive evenings he gave her a
dose of two ounces of the salt; that she was seized after the first dose
with excessive and alarming sickness, from which, however, she soon
recovered without apparent harm; but that after the second dose she had
violent vomiting and profuse purging, of which she died in five hours,
without any alteration in the symptoms, except that she became
insensible for five minutes before death. The whole gastro-intestinal
mucous membrane was bright red, the vessels of the brain were much
congested, and between two and three ounces of blood had escaped from
the neighbourhood of the occipital sinus. The salt had been swallowed in
a single tumbler of water, so that part of it was undissolved. Mr.
Brande, who analyzed the sample which had been used, found it free of
all the ordinary irritant poisons. Mr. Coward of Hoxton, to whom I owe
the particulars of this singular case, was of opinion, along with other
medical gentlemen concerned in it, that death arose from apoplexy
brought on by the violent and unceasing vomiting.

Another cathartic, undoubtedly in general very mild in its action, the
_bitartrate of potash_, has also proved fatal, when taken in immoderate
quantity. Thus, a man, endeavouring to quench his thirst and cool his
stomach the morning after he had been drunk, ate a quarter of a pound of
this salt in lumps at once, and a good deal more throughout the day
afterwards. He was in consequence attacked with incessant vomiting,
frequent purging, and other signs of irritation in the alimentary canal.
He died on the third day; and the stomach and bowels were found much
inflamed.[1614]

Even _common salt_ has been known to act as a poison when taken in large
quantity. A striking instance of the kind occurred in London in
September, 1828. A man, who had been in the custom of exhibiting various
feats of gluttony, proposed to some of his comrades one afternoon to sup
a pound of _common salt_ in a pint of ale, and actually finished his
nauseous dish, but not without being warned of his imprudence by an
attack of vomiting in the middle of it. He was soon after seized with
all the symptoms of irritant poisoning, and died within twenty-four
hours. The stomach and intestines were found after death excessively
inflamed.[1615] This remarkable case is not without its parallel. In
1839, a girl in the North of England died in consequence of taking
upwards of half a pound of salt as a vermifuge.[1616] Not long ago I met
with an instance of somewhat similar, but less violent effects. A
student having taken upwards of two ounces of salt as an emetic,
dissolved in a small quantity of water, was seized with acute burning
pain in the stomach, tenderness in the epigastrium and great anxiety,
without any vomiting until he drank a large quantity of warm water as a
remedy. Before I saw him he had vomited freely, but still suffered
severe, intermitting pain, which was removed by a large dose of muriate
of morphia.

In France, though not hitherto, so far as I know, in Britain, several
instances have occurred of extensive sickness in particular districts,
which have been traced to the accidental adulteration of _common salt_
with certain deleterious articles. In an investigation conducted by M.
Guibourt, in consequence of several severe accidents having been
produced apparently by salt in Paris and at Meaux, oxide of arsenic was
detected;[1617] and this discovery was subsequently confirmed by MM.
Latour and Lefrançois, who ascertained that the proportion of arsenic
was sometimes a quarter of a grain per ounce.[1618] Another singular
adulteration which appears fully more frequent is with hydriodate of
soda. At a meeting of the Parisian Academy of Medicine in December,
1829, a report was read by MM. Boullay and Delens, subsequent to an
inquiry by M. Sérullas, into the nature of a sample of salt which
appears to have occasioned very extensive ravages. In 1829, various
epidemic sicknesses in certain parishes were suspected to have arisen
from salt of bad quality. In the month of July no less than 150 persons
in two parishes were attacked, some with pain in the stomach, nausea,
slimy and even bloody purging, others with tension of the belly,
puffiness of the face, inflammation of the eyes and swelling of the
legs; and in several parishes in the Department of the Marne a sixth
part of the population was similarly affected. The salt being suspected
to be the source of the mischief, as it had an unusual smell which some
compared to the effluvia of marshy ground, M. Sérullas analyzed it, and
after him MM. Boullay and Delens; and both analyses indicated the
presence of a hundredth of its weight of hydriodate of soda, besides a
little free iodine.[1619] Subsequently, in reference to the discovery of
arsenic by other chemists in different samples of suspected salt, M.
Sérullas repeated his analysis, but could detect none of that
poison.[1620] Still more lately the whole subject has been investigated
with great care by M. Chevallier.[1621] M. Barruel states that he
observed the occasional adulteration of salt with some hydriodate
accidentally in 1824, while preparing experiments for Professor Orfila’s
lectures. He found it in two samples from different grocers’ shops in
Paris.[1622] No satisfactory explanation has yet been given of the
source of the adulteration with arsenic; but the presence of hydriodate
of soda has been traced to the fraudulent use of impure salt from kelp
[see p. 160].

Some difference of opinion prevails among toxicologists in regard to the
alleged deleterious qualities of _alum_. On the whole it scarcely
appears so active as to deserve the name of a poison; yet, like other
salts, it may in large doses do serious injury. It merits particular
mention among the present description of substances, partly on account
of a trial at Paris, where dangerous effects were alleged to have been
produced by it, and partly for the physiological inquiries made on that
occasion. A druggist supplied a lady by mistake with powder of burnt
alum instead of gum-arabic; and the lady, who had long laboured under
chronic derangement of the stomach and bowels, took a single dose of a
solution containing between ten and twenty grains of the salt. She
immediately complained of acute pain in the stomach and gullet, burning
in the mouth, and nausea; the symptoms of a severe attack of
inflammation in the stomach and bowels ensued; and she was not
considered out of danger for several days. The druggist was accordingly
prosecuted, and heavy damages claimed. The attending physician ascribed
the symptoms to the alum. But Marc and Orfila, who were consulted,
declared that this was impossible except on the supposition that the
lady had a very unusual sensibility of the stomach to irritating
substances;—that it was a common thing to give three, four, and even
five times the quantity in the treatment of diseases, without any such
consequences resulting;—and that at the very time of the inquiry a
physician in Paris was using it to the amount of six or eight drachms in
a day. From an experimental inquiry conducted by Professor Orfila it
appears, that large doses of calcined alum, such as one or even two
ounces, excite in dogs little more than one or two attacks of vomiting,
even although retained between ten and thirty minutes,—that one ounce
will not excite any marked symptoms though secured in the stomach by a
ligature,—but that two ounces given in the same way prove fatal in five
hours, under symptoms of excessive exhaustion and insensibility.[1623] A
similar inquiry was instituted about the same time by M. Devergie, who
seems, however, to have remarked more activity in alum than is indicated
by Orfila’s experiments. He infers that two ounces may sometimes kill
dogs, even though they vomit freely; that half that quantity is fatal if
the gullet be tied; that calcined alum is more active than a solution of
the salt; that it is a corrosive or irritant; and that probably man is
more sensible to its operation than the lower animals.[1624] Whatever
may be thought of the effects of alum on the animal body when
administered in large doses, it is plain from its frequent medicinal use
as an internal astringent that it is not poisonous when given in small
doses, like that taken by the patient in the trial alluded to. I may add
that it appears very doubtful whether any injury accrues from the
long-continued use of very small doses. Bakers, it is well known, are in
the practice of using it in minute proportion for improving the
whiteness of bread; and it has been imagined that chronic disorders of
the stomach and bowels may consequently originate, by reason of its
constipating tendency. These fears, however, are not borne out by facts.
Either the quantity is insufficient to do harm in the way supposed; or
the constitution becomes accustomed to the continual operation of the
salt, and does not suffer.




                             CHAPTER XXIV.
                             CLASS SECOND.
                     OF NARCOTIC POISONS GENERALLY.


The term narcotism has been used by different writers with different
significations, but is now generally understood to denote the effects of
such poisons as bring on a state of the system like that caused by
apoplexy, epilepsy, tetanus, and other disorders commonly called
nervous. Narcotic poisons, therefore, are such as produce chiefly or
solely symptoms of a disorder of the nervous system.

The mode in which most narcotic poisons act has been well ascertained:
they act on the brain or spine or both by entering the blood-vessels.
Hence they are most active when most directly introduced into the blood,
that is, when injected into the veins; and when they are applied to an
entire membranous surface, their energy is in the ratio of its absorbing
power. Thus, when injected into the chest, they act more rapidly than
when swallowed. According to the generally received opinion, they are
conveyed with the blood to the brain and spine on which they act. But,
according to the views of Messrs. Morgan and Addison, they produce on
the inner coats of the blood-vessels a peculiar impression, which is
conveyed to the centre of the nervous system along the nerves.

The usual symptoms in man and the higher order of animals are giddiness,
headache, obscurity or deprivation of the sight, stupor or perfect
insensibility, palsy of the voluntary muscles or convulsions of various
kinds, and towards the close complete coma. The symptoms of each poison
are pretty uniform, when the dose is the same. But each has its own
peculiarities, either in the individual symptoms, or in the mode in
which they are combined together.

The morbid appearances they leave in the dead body are commonly
insignificant. In the brain, where chiefly the physician is led from the
symptoms to expect unnatural appearances, the organs are in general
quite healthy. Sometimes, however, the veins are gorged with blood, and
the ventricles and membranes contain serosity. The blood appears to be
sometimes altered in nature; but the alteration is by no means
invariable, and sometimes none is remarked at all. Many of the
statements to be found in authors on the morbid appearances caused by
narcotics are far from being accurate.

Before proceeding to notice the genera of this class in their order,
some remarks must be premised on the principal diseases which resemble
them in the symptoms and morbid appearances. Of these the only diseases
of much consequence are _apoplexy, epilepsy, inflammation of the brain,
hypertrophy of the brain, inflammation of the spinal cord, and syncopal
asphyxia_.


     _Of the Distinction between Apoplexy and Narcotic Poisoning._

_Of the Symptoms._—The symptoms of apoplexy are almost exactly the same
as those of the narcotic poisons, namely, more or less complete
abolition of sense and the power of motion, frequently combined with
convulsions. This disease commonly arises from congestion or effusion of
blood within the skull; but one variety of it, the nervous apoplexy of
older authors, or simple apoplexy of the moderns, is believed to be an
affection of the brain, unaccompanied by any recognizable derangement of
structure.

Apoplexy and narcotic poisoning may be often distinguished by the
following criterions:

1. Apoplexy is sometimes preceded at considerable intervals by warning
symptoms, such as giddiness, headache, ringing in the ears, depraved
vision, or partial palsy. But it is an error to suppose that warning
symptoms always occur; nay, if we may trust the experience of M.
Rochoux, they are by no means common: of sixty-three cases which came
under his notice nine only had distinct precursory symptoms.[1625]
Poisoning with narcotics of course has not any precursory symptom except
by fortuitous combination. And consequently, if warning symptoms have
occurred, the presumption is, that the cause of death is a natural one.

2. Apoplexy attacks chiefly the old. It is not, however, confined to the
old. On the trial of Captain Donnellan for poisoning Sir T. Boughton,
Mr. John Hunter mentioned that he had met with two instances of death
from apoplexy in young women; my colleague Dr. Alison has related to me
a similar case; Professor Bernt has described another of a young girl
who died apoplectic from extravasation of blood over the whole brain and
in the ventricles also;[1626] and Mr. Greenhow, a surgeon of London, has
even noticed a case of apoplexy from effusion of blood over the surface
of the brain in a child two years and a half old.[1627] On this subject
the treatise of Rochoux supplies excellent information: of his
sixty-three cases sixty-one were above thirty years of age, two less
than thirty, none younger than twenty.[1628] It is plain, therefore,
that apoplexy in young people is rare. On the other hand, a great
proportion of cases of poisoning with the narcotics when they have been
taken intentionally (and such cases are most likely to lead to
medico-legal questions), has occurred among the young, especially of the
female sex.

3. The next criterion is, that apoplexy occurs chiefly among fat people.
But it is here mentioned only that the medical jurist may be cautioned
against the belief that it is in all circumstances a correct criterion.
Upon this particular Rochoux has furnished some satisfactory data. Among
his sixty-three patients thirty were of an ordinary habit, twenty-three
were of a thin, meager habit, and ten only were large, plethoric and
fat.[1629] In receiving this statement, however, it is necessary to
consider, that although the vulgar idea, that most apoplectic people are
fat, does not apply to persons in the rank of Rochoux’s patients, who
were mostly hospital inmates, yet it may apply better to the upper
ranks. For the same circumstances which predispose to apoplexy, namely,
great strength, vigorous constitution and good digestive powers,
likewise predispose to corpulency, so that whenever the condition of
life permits the disposition to corpulency to be developed, the
connexion of apoplexy with it will appear.

4. A fourth criterion is drawn from the relation which the appearance of
the symptoms bears to the last article of food or drink that was taken.
I believe that the effects of the common narcotics, in the cases where
they prove fatal, begin not later than an hour, or at the utmost two
hours, after they are taken; and in a great majority of instances they
begin in a much shorter time, namely, in fifteen or thirty minutes.
Hence if it can be proved that the nervous symptoms, under which a
person died, did not begin till several hours after he took food, drink
or medicine, it appears almost, if not absolutely certain, that a
narcotic poison cannot have been the cause of death. To some narcotic,
or rather narcotico-acrid poisons this rule certainly will not apply,
such as the poisonous fungi and spurred rye; which seldom begin to act
for several hours, sometimes for not less than a day and a half. Neither
will the rule apply to poisoning with the deleterious gases, as their
action has no connexion at all with eating or drinking. But these facts
do not form a material objection to the rule laid down; because the
circumstances under which cases of the kind occur are generally so
apparent, as at once to point out their real nature to a careful
inquirer.

In regard to apoplexy as the disease which resembles most closely the
effects of the narcotics, it was formerly stated that this disease is
apt to occur soon or immediately after taking a meal (p. 95).[1630] In
the greater number of such cases, however, where the meal has been the
exciting cause of the disease, the symptoms have begun _immediately_
after, or even during a meal. This is very rarely the case with the
symptoms of narcotic poisoning, and never happens in respect to those of
the commonest of the narcotics, opium: An interval of 10, 15, 20 or 30
minutes always occurs. The deleterious gases and hydrocyanic acid, with
its compounds, are the only familiar narcotic poisons which act more
swiftly.

5. Another criterion relates to the progress of the symptoms. The
symptoms of narcotic poisoning advance for the most part gradually: but
those of apoplexy in general begin abruptly. Sometimes apoplexy
commences at once with deep sopor. Narcotic poisoning never begins in
that way, except in the instances of hydrocyanic acid and the narcotic
gases; the sopor is at first imperfect, and it increases gradually,
though sometimes very rapidly. Apoplexy, however, does not always begin
with deep sopor; occasionally the sopor begins and increases like that
of narcotism.

6. Although there is a great resemblance between the symptoms of
apoplexy and those of narcotism, so far as regards their general
features, there are particulars which are not indeed always present, but
which when present will help to distinguish the one from the other. When
the sopor of apoplexy is completely formed, it is rarely possible to
rouse the patient to consciousness, and never, I believe, where the risk
of confounding apoplexy with poisoning is greatest,—in the cases where
death happens neither instantly, nor after the interval of a day, but in
a few hours. On the other hand, in many cases of poisoning with the
narcotics, and particularly with the commonest variety, opium, the
person may be roused from the deepest lethargy, if he is spoken to in a
loud voice, or forcibly shaken for some time, or if water is injected
into his ear. Even in cases of poisoning with opium, however, the coma
may have continued too long to admit of this temporary restoration to
sense; the susceptibility of being roused is not so often remarked in
other varieties of narcotic poisoning; and in some, such as poisoning
with prussic acid, I am not aware that it has ever been remarked, at
least in fatal cases.

There are some other symptoms which in special cases may help to
distinguish narcotic poisoning from apoplexy. Thus in poisoning with
opium convulsions are rare; in apoplexy they are common enough. Bloating
of the countenance is likewise much more common in apoplexy than in
poisoning with opium. In apoplexy, too, the pupil is generally dilated,
while in poisoning with opium the pupil is almost always contracted. But
such distinctions do not apply either to the narcotics as a class, or to
all cases of any one kind of narcotic poisoning.

7. In the last place, a useful criterion may be derived from the
duration of the symptoms in fatal cases. I believe few people die of
pure narcotic poisoning who outlive twelve hours; and the greater number
die much sooner,—in eight, or six hours. Apoplexy often lasts a whole
day, or even longer. On the other hand, the narcotic poisons very rarely
prove so rapidly fatal as apoplexy sometimes does. Apoplexy, according
to the vulgar opinion, may prove fatal instantly or in a few minutes.
The only late author of repute who maintains that opinion is M.
Devergie. He mentions the case of an elderly man subject to somnolency,
who, after complaining for a short time of headache, became suddenly
pale, hung down his head, and expired immediately, and in whose body no
other morbid appearance was found, except great congestion of the
cerebral membranes.[1631] The best modern pathologists, however, deny
that apoplexy proves immediately fatal, and maintain with much apparent
reason that when death is so sudden, the cause is commonly disease of
the heart, and not apoplexy.[1632] However this may be, it is at all
events certain that apoplexy may occasion death in considerably less
than an hour. Now the only narcotics in common use which can prove fatal
so soon are the narcotic gases, and prussic acid. As to opium, the most
common of the narcotic poisons, and by far the most important to the
medical jurist, the shortest duration I have yet seen recorded is three
hours. Apoplexy often proves fatal in a much shorter time.

From this enumeration of the criterions between apoplexy and the
symptoms produced by narcotics, the toxicologist will conclude, that few
cases can occur in which he will not be able to give a presumptive
opinion of the real cause from the symptoms only,—that in many instances
a diagnosis may be drawn with an approach to certainty,—and that on all
occasions it will be possible to say without risk of error, whether
there are materials for forming a diagnosis at all,—a point which is of
great moment when the criterions are not universally applicable.

_Of the Morbid Appearances._—The next subject of inquiry is the
distinction between apoplexy and narcotic poisoning, as to the
appearances after death. It has been already stated, that the narcotic
poisons rarely produce very distinct morbid appearances,—that the
greatest extent of unnatural appearance they cause in the brain is
congestion of vessels,—and that the physical qualities of the blood
appear to be altered, though not invariably.

_Of Simple Apoplexy._—Apoplexy may, in the first place, occasion death
without leaving any sign at all in the dead body. Cases of this sort
were called nervous apoplexy by the older authors; but for the purpose
of avoiding a name that involves a theory as to their nature, they have
been more appropriately termed by Dr. Abercrombie simple apoplexy. At
one time they were believed to be common. The researches of modern
pathologists, however, have shown that they are rare, and that the
apparent absence of morbid appearances may be often with justice
ascribed to an insufficient examination; for it is not always easy to
detect, without minute attention, two disorders little known till in
recent times, and sometimes closely allied in their symptoms to
apoplexy,—hypertrophy of the brain, and inflammation of its substance.
On this account some have even gone so far as to deny altogether the
existence of simple or nervous apoplexy; and M. Rostan, who is of this
opinion, has supported it by the fact, that in the course of his
pathological researches he had examined no less than 4000 heads, and
never met with an instance of it.[1633] But although this statement,
made by so eminent a pathologist, is sufficient to prove the rarity of
the disease, it does not establish its non-existence in the face of
positive observations, made by others after the phenomena and effects of
cerebral inflammation were well known.

Among the modern authorities to whom reference may here be made for
examples of simple apoplexy, Dr. Abercrombie, M. Louis, my colleague Dr.
Alison, and M. Lobstein, may be particularized. Dr. Abercrombie has seen
four cases,[1634] M. Louis has recorded three,[1635] M. Lobstein
one,[1636] and Dr. Alison informs me, that he has seen one and got the
particulars of another from the late Dr. Gregory. In several of these
cases the individuals were at the time of the apoplectic seizure
affected with other diseases, such as asthma, anasarca, or slight
febrile symptoms; but in four of them the coma commenced during a state
of perfect health. I have myself seen two of the former class, one
occurring during convalescence from a slight pleurisy, the other
terminating a complicated case of pulmonary emphysema and catarrh,
diseased kidneys and anasarca. Reference may be also made under this
head to several cases of apoplexy described in Corvisart’s Journal, as
connected with the enormous accumulation of worms in the intestines.
Such a connexion is said to be common on the coast of Brittany; and one
striking instance is related of a young man, who, after an attack of
headache, vomiting, and loss of speech, died comatose in two days, and
in whose body no unnatural appearance could be seen except a prodigious
mass of worms in the small intestines.[1637]

In none of all the cases of apoplexy now under consideration was there
found within the head any appearance corresponding with the symptoms,
except occasionally a slight turgescence of vessels.

This form of apoplexy, then, is a very important affection in a
medico-legal point of view. The possibility of its occurrence is in fact
the chief obstacle, which, in many cases involving the question of
poisoning with narcotics, prevents the physician from coming to a
positive decision on a review merely of symptoms and appearances after
death. Instances will occur where it is impossible to draw a diagnosis
between the natural and the violent form of death. And indeed it might
even be a fair subject of inquiry, whether death from at least some
narcotic poisons, such as opium, is any thing else than death from
simple apoplexy.

It may be mentioned,—although too much importance ought not to be
attached to the fact, as forming the ground of a diagnosis in certain
rapid cases of narcotic poisoning,—that of the instances of simple
apoplexy referred to above none proved fatal in less than five hours.
This was Dr. Gregory’s case. Dr. Alison’s proved fatal in seven hours;
M. Louis’s cases in eight, nine, and ten hours; one of Dr. Abercrombie’s
in eight hours; the three others in about twenty-four hours; and M.
Lobstein’s in five days.

Another consideration is, that simple apoplexy is undoubtedly very rare,
more particularly in persons who enjoy perfect health. Hence, although
it is impossible to distinguish the effects of narcotics from this
disease by the appearances in the body after death, yet, when the
general evidence of poisoning is strong, and none of the medical
circumstances are at variance with the supposition of narcotic
poisoning, the evidence of poisoning, as judged of by the jury from the
whole facts, medical and general, will be commonly sufficient,—so far as
regards the possibility of death from simple apoplexy. For such a
concurrence of circumstances as is here supposed can scarcely be
outweighed by a mere possibility of death from so rare a natural
disease.

It is worthy of remark, in reference to charges and suspicions of
poisoning during a state of ill health, that simple apoplexy occurring
in the course of a considerable period of indifferent health is far from
uncommon. Such incidents, however, ought not to be confounded with
narcotic poisoning, because the coma comes on gradually. From what I
have myself frequently observed, cases of this nature are often
connected with the granular disintegration of the kidneys, which has
been brought under the notice of physicians by the able researches of
Dr. Bright. I have related two instances of the kind,[1638] and several
others have been since published by Dr. James Arthur Wilson.[1639] In
none of these could there have been any risk of mistaking the phenomena
for narcotic poisoning. But it may be well to advert to the subject here
for the sake of turning the attention of the profession to the propriety
of examining the state of the kidneys in all medico-legal cases of death
in a state of coma.

_Of Congestive Apoplexy._—Apoplexy may, in the second place, leave in
the dead body no other sign but congestion of vessels within the head.
This form or variety of apoplexy is so generally admitted, that it is
hardly necessary to mention special instances. But, for the sake of
those who may prefer special facts to general propositions, the two
following cases by M. Rostan are referred to. One of his patients,
without any precursory symptom, was suddenly deprived of sense, soon
became delirious and comatose, and expired in a day and a half. The
other, also without any previous symptom, became rapidly comatose, and
died in twenty-four hours. In both the whole membranes were minutely
injected with blood; and in one the whole brain had also a rose-red
colour.[1640] In regard to the diagnosis between such cases and
poisoning with narcotics, it must be remembered, that congestion of the
cerebral vessels is considered by many a common effect of such poisons,
and that therefore the diagnosis cannot be rested on the appearances in
the dead body. I have not perused a sufficient number of fatal cases of
congestive apoplexy to enable me to attempt a diagnosis; but, so far as
I have gone, it appears to me, that this form of the disease, which is
not often fatal without extravasation also being produced, does not
cause death till after an interval of nearly a day at least. Should this
prove a general fact, it would form the ground of a diagnosis between
congestive apoplexy and many forms of narcotic poisoning, which, if
death ensues, prove fatal much sooner.

_Of Serous Apoplexy._—Apoplexy may, in the third place, produce serous
effusion on the external surface, and in the ventricles of the brain.
This form of the disease, which has been named serous apoplexy, although
not very uncommon as an insulated affection, is for the most part united
with inflammation of the cerebral substance. Serous effusion is more
frequently the termination of an inflammatory disorder of the brain,
than of that deranged state which constitutes the apoplectic attack. But
nevertheless it does occur in connexion with pure apoplexy, as may be
seen, for example, on referring to Dr. Abercrombie’s work,[1641] or to
Bernt’s Contributions to Medical Jurisprudence,[1642] or to the Hospital
Reports of Dr. Bright.[1643] In such cases the only appearances have
been the effusion of an unusual quantity of serum on the surface of the
brain, in its ventricles, and in the base of the skull. Cases of this
sort agree very exactly as to the signs in the dead body with some cases
of narcotic poisoning. When serous effusion is preceded by decided
apoplectic symptoms, the disease, so far as I have been able to inquire,
is always of several days’ duration. But sometimes the symptoms are to
the very last obscure and different from those of apoplexy, as in an
instance related by Dr. Abercrombie.[1644]

_Of Apoplexy from extravasation._—The last variety of apoplexy is that
which leaves in the dead body extravasation of blood within the head.
This, the most common of all its forms, is very rarely imitated by
narcotic poisoning. A case, however, will be afterwards mentioned of
extravasation produced apparently by poisoning with opium, another of
extravasation caused by carbonic acid, another by poisonous fungus, and
several by spirits. The existence, therefore, of extravasated blood is
not absolutely certain proof, but supplies, in relation to most
narcotics, a strong presumption of natural death.

Here it will be necessary to add a word or two of caution regarding what
are called apoplectic cells or cavities, containing blood in the brain.
If an apoplectic cell be found, it must not be at once considered as the
cause of death. When blood is extravasated in the brain, the patient may
gradually recover altogether, and the cell nevertheless continue full.
Such persons often die of a subsequent attack of apoplexy, or of
inflammation around the cell. We can say with certainty, that an
apoplectic cell has been the occasion of death only when the blood is
recent, or when it is surrounded by signs of recent inflammation.

So much, then, as to the criterions derived from morbid appearances
within the skull, for distinguishing poisoning with narcotics from
apoplexy.

It has been proposed to derive other criterions from the state of the
blood. But on considering the effects of the individual poisons of the
class, it will appear that the state of the blood is by no means
characteristic.

It may be useful to conclude this view of the distinctions between
poisoning and apoplexy with the particulars of an interesting case, in
which the medical witnesses fell into an egregious error by disregarding
the most palpable criterions. In 1841, an elderly gentleman at Chambéry
in France, subject to apoplexy, one day after having made a hearty
dinner and afterwards supped on bread, cheese, and white wine, was
suddenly seized with staggering immediately after finishing his wine,
and soon lost all consciousness. Emetics and stimulants restored his
faculties so far as to enable him to say he felt better and had no pain;
but the tongue and mouth were drawn to the left side, and there was
great prostration. Four hours after his first seizure the countenance
became livid; he again became unconscious and insensible; the twisting
of the mouth increased; and the left arm presented spasmodic
contraction. Blood-letting and other remedies were resorted to without
avail; the pulse, previously strong and regular, became gradually
feeble; and in six hours after his first illness he expired, without
ever having had convulsions of any kind. On the body being examined
seven days after death, great congestion was found in the vessels on the
surface of the brain; on raising the brain, a dense dark clot of the
size of a large egg escaped from the lower part of the ventricles; and
an abundant extravasation of the same nature was found under the
_tentorium cerebelli_.

It appears scarcely possible to find a more characteristic case than
this of apoplexy from extravasation. The slight intermission in the
symptoms was the only unusual circumstance. Yet because the inspectors
remarked in various parts of the body a peculiar odour, which they could
not at the time characterise, but which they afterwards thought was the
odour of bitter almonds,—and misled by the sudden invasion of the
symptoms instantly after a meal,—they gave their opinion that death had
arisen from some narcotic poison; a chemical examination was made of
various textures of the body (not, however, of the contents of the
stomach), which yielded obscure and very doubtful indications of
hydrocyanic acid; poisoning with hydrocyanic acid was accordingly
declared to have been the cause of death; and, in defiance of an able
report by Professor Orfila, pointing out the error of the primary
witnesses, the nephew and heir of the deceased was condemned.[1645] It
is almost unnecessary to point out the impossibility of death having
arisen in this case from hydrocyanic acid. The length of time the
deceased survived, the want of convulsions, the presence of deflexion of
the mouth and tongue, the intermission of the symptoms, and the morbid
appearances, all clearly indicate that death in the way supposed was
impossible; and the chemical evidence, which it would require too much
space to analyze here, was proved by Orfila to be completely
unsatisfactory.


     _Of the Distinction between Epilepsy and Narcotic Poisoning._

_Of the Symptoms._—Epilepsy is distinguished from other diseases by the
abolition of sense and by convulsions. It resembles closely the symptoms
caused by prussic acid, and by some of the narcotic gases, such as
carbonic acid gas and the asphyxiating gas of privies. It also bears the
same resemblance to the effects of many narcotico-acrid poisons, such as
belladonna, stramonium, hemlock, and others of the first group of that
class, also camphor, cocculus indicus, and the poisonous fungi.

Epilepsy is in general a chronic disease, and for the most part ends
slowly in insanity. But sometimes it proves fatal during a paroxysm. The
circumstances by which an epileptic fit may be distinguished from
narcotic poisoning are the following:

1. The epileptic fit _is sometimes preceded by certain warnings_, such
as stupor, a sense of coldness, or creeping, or of a gentle breeze
proceeding from a particular part of the body towards the head.
Warnings, however, are by no means universal. M. Georget, indeed, has
even stated that they do not occur in more than five cases in the
hundred.[1646] But this estimate probably underrates their frequency.

2. The symptoms of the epileptic fit _almost always begin violently and
abruptly_. The individual is suddenly observed to cry out, often to
vomit, and instantly falls down in convulsions. The effects of the
narcotic poisons, if we except some cases of poisoning with hydrocyanic
acid, the narcotic gases, and a few rare alkaloids, never begin
otherwise than gradually, though their progress towards their extreme of
violence is often rapid. This distinction is generally an excellent one.
But it will not apply so well to some cases of epilepsy in which the
convulsions are trivial. Esquirol says an epileptic fit may consist of
nothing more than coma, with convulsive movements of the eyes, or lips,
or chest, or a single finger.[1647] Still even then the coma generally
begins abruptly, so that if the case is seen from the beginning, it can
hardly be mistaken for narcotic poisoning. Some forms of epilepsy, in
which the fit is constituted merely by giddiness, staring, wandering of
the mind, and imperfect loss of recollection,[1648] might be confounded
with the milder forms of narcotic poisoning. But collateral
circumstances will scarcely ever be wanting to distinguish such cases
from one another.

The varieties of narcotic poisoning which, in the violence and
abruptness of their commencement, bear the closest resemblance to an
epileptic attack, are some cases of poisoning with hydrocyanic acid or
with the deleterious gases. Both of these varieties, however, when they
begin so abruptly, are distinguished from a fatal paroxysm of epilepsy
by the fourth characteristic to be mentioned presently; and besides, in
abrupt cases of poisoning with hydrocyanic acid, the poison under
certain conditions will be found in the body; while in sudden poisoning
with the narcotic gases, the nature of the accident is rendered obvious
to a cautious inquirer by the collateral circumstances.

3. As in apoplexy, so in epilepsy the patient _in general cannot be
roused_ by external stimuli. This, as already observed, is often,
although certainly not always, practicable in cases of poisoning with
narcotics. Sometimes, too, in the epileptic fit a partial restoration of
consciousness may be effected by loud speaking, so that in reply to
questions the patient will roll his eyes or move his lips. It is
therefore to be understood in applying the present criterion, that it is
only a safe guide when, as in many cases of poisoning with opium, the
individual can be roused to a state of tolerably perfect consciousness.

4. When a person dies in a fit of epilepsy, _the paroxysm generally
lasts long_, sometimes more than a day. So far as I have been able to
ascertain (though on this point it must be confessed authors are
singularly silent), it never proves fatal in a shorter time than several
hours, unless there have been many previous fits; and even then it
rarely proves fatal more rapidly. I have met with a case which, after
many previous fits, proved fatal in little more than an hour.[1649] In
an instance mentioned by Mr. Clifton of irregularly recurring epilepsy,
the patient after being exempt for four months was attacked twice a day
for four days, and during an interval of ease fell down in the street
and died. General congestion and excessive softening of the brain were
found.[1650] I have met with a case very like this, where death was
owing to enormous extravasation of blood into the ventricles. So rapid a
termination never occurs except after several paroxysms; and probably
never without well-marked appearances in the dead body. The variety of
poisoning with which epilepsy is most apt to be confounded, poisoning
with hydrocyanic acid, has hitherto always proved fatal within
three-quarters of an hour, and can probably never prove fatal so late as
a whole hour after the symptoms begin, unless the dose has been small
and given repeatedly. Poisoning with the gas of privies,—another
variety, which sometimes imitates precisely a fit of epilepsy, appears
not to prove fatal in its convulsive form later than two hours after the
exposure.

5. M. Esquirol, a writer of high authority, says that epilepsy _very
rarely proves fatal in the first paroxysm_. I suspect it may be said
that the first paroxysm never proves fatal. For the cases considered and
described as such have been either inflammation of the brain or its
membranes, or hypertrophy of the brain, or inflammation of the spinal
cord, or effusion of serum or blood into the spinal canal, or worms in
the intestines,—all of which may be known by the morbid appearances. I
have also seen cases of continued fever with typhomania and convulsions,
which might have been considered by a careless observer examples of
epilepsy fatal in the first fit. On the present characteristic it would
be wrong to speak with confidence, as the question regarding the
possible fatality of epilepsy in the first fit must depend greatly on
the degree of extension given to the term epilepsy. I can only say, that
in the course of reading I have not hitherto met with an instance fatal
in the first paroxysm, which might not have been referred by the morbid
appearances to one or other of the diseases mentioned above.

_Of the Morbid Appearances._—With regard to the morbid appearances found
in the bodies of epileptics, much difference of opinion prevails among
pathologists. The most frequent are tumours within the cranium,
excrescences from the bone or dura mater, concretions in the brain
itself, or abscesses there, and effusion into the ventricles or on the
surface of the brain. Other appearances which have also been remarked
are probably little connected with the disease; and at all events have
been often seen when epilepsy did not precede death.[1651]

The morbid appearances connected with epilepsy are not always to be
looked for within the head. The cause which produces the fit is often
some irritation in distant organs.—The presence of worms in the
intestines of children may occasion fatal epilepsy. It is believed also
that they may cause fatal epilepsy even in adults; and whether their
presence has been the cause of death or not, it is certain that they
have been found enormously accumulated in the stomach or intestines of
adult epileptic subjects.[1652] The most recent information on this
subject is furnished by M. Gaultier de Claubry. In a girl seven years
old, who died of convulsions in six days, he found eleven _lumbrici_ in
the general cavity of the belly, and the coats of the stomach perforated
with holes, in some of which other worms were sticking. In another child
of the same age, who died in seven days of convulsions, he found
thirty-six worms in the peritoneal sac, a great mass of them in the
stomach, and twenty-seven making their way through holes in its
coats.[1653] In a singular case related by M. Lepelletier of a boy
twelve years old, who died of convulsions in four days, the only morbid
appearance found was a perforation of the gullet six lines in diameter,
through which two lumbrici had made their way into a cavity in the
middle right lobe of the lungs, while another was sticking in the hole,
six more occupied the lower part of the gullet, and three lay in the
stomach.[1654]—The irritation of teething may also excite epilepsy, and
in cases where it has proved fatal may be recognized by the redness and
swelling of the gum, by the tooth being on the point of piercing the
alveolar process, and by the turgescence of vessels around.[1655]—A
well-known but rather rare cause is the presence of some hard substance
in the course of a nerve. This variety, like those already mentioned,
may prove fatal in the fit, as appears from the following interesting
case. A stout young woman became suddenly liable to epilepsy, and, after
suffering repeated fits in the course of twenty months, died comatose in
a paroxysm of thirty-three hours’ duration. The fits having always begun
with acute pain in a particular part of the thigh, this part of the body
was carefully examined, and a bony tumour as big as a nut was found on a
branch of the sciatic nerve.[1656]—Other appearances might likewise be
here enumerated, which have been supposed the cause of symptomatic
epilepsy.[1657] But few of these have been so thoroughly ascertained as
to be allowed much influence on a medico-legal opinion.

It cannot, I apprehend, be denied, that in many cases of epilepsy no
decided morbid appearance is to be found in the body; and that in many
others the appearances are either so equivocal as not to be
satisfactorily recognized in any circumstances, or so hidden in their
situation that they may escape notice, unless the inspector’s attention
be drawn to the particular spot by a knowledge of the symptoms.

Hence in actual questions as to the occurrence of narcotic poisoning
when the symptoms resemble epilepsy, it will be seldom possible to found
on the absence of morbid appearances more than a presumptive opinion
that death did not proceed from the natural cause. It is right to
remember, however, that in considering the absence of morbid appearances
in reference to the diagnosis of narcotic poisoning and epilepsy, the
attention should be confined to cases of epilepsy which prove fatal
during the fit. Now I suspect no such case ever occurs, at least in
adults, without an adequate cause being discoverable in the dead body,
either in the head, or in the course of some nerve, or in the
accumulation of worms in the intestines. This statement must not be
considered as made with confidence; but it deserves investigation.

From all that has now been said on the subject of epilepsy as a disease
which imitates many varieties of narcotic poisoning, the medical jurist
will probably arrive at the conclusion, that, although a diagnosis
cannot always be drawn with certainty, yet in numerous cases the
consideration of the symptoms and appearances after death will enable
him to say positively that poisoning is out of the question, and in many
others that poisoning is highly probable.


    _Of the Distinction between Meningitis and Narcotic Poisoning._

Inflammation of the inner membranes of the brain, which constitutes the
_acute hydrocephalus_ or acute _meningitis_ of authors, is not in
general apt to cause much ambiguity; for its progress is commonly
gradual, well-marked and less rapid than most cases of narcotic
poisoning: and the appearances in the dead body, such as effusion of
serum, lymph or pus on the outer surface of the brain or in the
ventricles, are for the most part obvious.

Dr. Abercrombie, however, has described a form of it occurring among
children during the existence of other diseases, particularly of the
chest, which might be the cause of perplexity; for its course is
sometimes finished within a day, its symptoms are delirium, convulsions
and coma intermingled, and the only morbid appearance is congestion of
vessels on the surface and in the substance of the brain.[1658] The
affection now alluded to imitates closely, both in its progress and in
its signs after death, some varieties of poisoning with the vegetable
narcotico-acrids, such as belladonna, stramonium, and hemlock. But the
latter cases, when they prove fatal, seldom last nearly so long as a
day, while the instances of meningitis under consideration rarely cause
death within twenty-four hours. Dr. Abercrombie also notices a parallel
disease occurring among adults; but it is in them always marked by a
considerably longer, though often more obscure course.[1659]

Dr. Bright takes notice of a similar affection under the title of
“Arachnitis with excessive irritability” occurring chiefly among very
intemperate people, but independently of previous disease. In general
the disorder has a well-marked course of at least several days’
duration. But in two of the instances he has given the early stage was
very obscure, the only symptoms having been headache and sickness of no
great severity for four or five days; after which delirium came suddenly
on, and was followed by coma, and by death within thirty-six or forty
hours. The sole appearances found within the head were some serous
effusion and vascularity on the surface of the brain and in the
ventricles.[1660] To these illustrations may be added the heads of a
remarkable case which occurred here in the person of an eminent lawyer,
and for the particulars of which I am indebted to Dr. Maclagan. For
three days there had been occasional headache, not great enough to
prevent him pursuing his ordinary avocations, yet becoming so
troublesome on the morning of the third day as to induce him to have
leeches applied. But next morning he was seized rather suddenly with
quickly increasing coma, and in forty hours more he expired. In this
instance the whole surface of the arachnoid membrane, both over the
hemisphere and in the ventricles, was found lined with soft,
yellowish-green lymph.

In such cases it is apparent that an inspection after death will often
unfold their real nature, where the history of the symptoms may leave it
in doubt. But even without an inspection it is not likely that a careful
physician could mistake them for narcotic poisoning; for independently
of other considerations, the severe symptoms are ushered in by a
precursory stage of ill health, commonly indicating an obscure affection
of the head, and such as no one but a careless observer could fail to
discover and appreciate.

It is not improbable, however, that acute meningitis may seem to prove
suddenly fatal, in consequence of its course being in a great measure
latent. The following case reported by Mr. Davies of Somers Town, seems
of this nature. A woman, who had previously complained only of slight
headache, was attacked after breakfast with violent vomiting for half an
hour, when she fell down, and immediately expired. After death there was
found great gorging of the vessels of the cerebral membranes, with
opacity and thickening of the pia mater and arachnoid coats, and an
effusion of nearly five ounces of bloody serum under the dura
mater.[1661] Such a case might give rise to great perplexity in a charge
of poisoning, until the examination of the body unfolded its true
nature.

I should scarcely have thought it necessary to mention _chronic
meningitis_ among the diseases apt to imitate the effects of narcotic
poisons, because it is commonly marked by a long and distinct course.
But the following case, for which I am indebted to Dr. Arnoldi of
Montreal, will show that, like other diseases of the head, chronic
meningitis may be latent in its early stage, and may, after developing
itself, terminate in a day, and then in some measure imitate poisoning
with narcotics. A middle-aged female, subject for a twelvemonth to a
purulent discharge from the left ear, and occasional headache, which was
supposed to be rheumatic, was seized one morning with acute pain in the
head, followed in a few hours by convulsions and tendency to coma; under
which symptoms she died within twenty hours, although treated actively
from the commencement. On dissection, the brain and pia mater were found
healthy, except at the part corresponding with the petrous portion of
the left temporal bone, where the brain was a little softened. The
corresponding part of the temporal bone and the adjacent part of the
occipital were completely denuded and covered with pus, which had
established a passage for itself into the cavity of the ear.


   _Of the Distinction between Inflammation of the Brain and Narcotic
                              Poisoning._

Inflammation of the brain itself, the _ramollissement_ of French
writers, occasionally excites symptoms not unlike those produced by some
narcotic poisons; and in a few instances its course has appeared to be
equally short. It requires particular notice, because the appearances
left in the dead body are sometimes apt to escape observation.

This disease in its well-marked form has been noticed by various authors
from Morgagni downwards. But the first regular accounts of it were given
in 1818 by Dr. Abercrombie,[1662] and in 1819 by M. Rostan[1663] of
Paris, and Professor Lallemand[1664] of Montpellier. Its symptoms are
allied to those of apoplexy and epilepsy. But the comatose state is
generally preceded by delirium or imperfect palsy, and often by a
febrile state of the circulation. Contraction of the voluntary muscles,
once supposed to be a distinguishing sign of this disease, is neither
essential nor peculiar to it. In the dead body it is recognized by the
presence either of an abscess in the brain,—or more commonly of a
nucleus of disorganized cerebral tissue surrounded by unnatural redness
or softness,—or sometimes of a clot of blood surrounded by similar
softening. Occasionally, when the disease kills in its early stage,
nothing is found but redness of a part of the brain, and slight
softening of the tissue, recognizable only by scraping it with the edge
of the scalpel.

In the form in which it is commonly seen, and as described by Rostan and
Lallemand from a great number of cases, it can hardly be confounded with
the effects of narcotic poisons; for its course is much slower, being
seldom less than several days when it proves fatal.[1665] Yet in some
instances it may prove fatal instantly. Lancisi notices the case of an
Italian nobleman, who after an apoplectic fit became liable to frequent
attacks of lethargy,—who at length died quite suddenly more than a year
afterwards,—and in whose brain an organized clot was found, with
extensive suppuration of the brain around it.[1666] An unequivocal case
of the same kind has been related by Mr. Dickson, a navy-surgeon. An
elderly sailor, who for months before had done duty, eaten his rations,
and drunk his grog as usual, suddenly dropped down while in the act of
pulling his oar, and died at once; and after death there was found in
the middle lobes of the brain an extensive abscess, which had made its
way to the surface.[1667] Such cases might, in certain circumstances, be
mistaken for the effects of large doses of hydrocyanic acid; but the
morbid appearances are of course quite characteristic. M. Louis has
related an instance like the last two, but where the disease was
altogether latent. His patient after a long illness died of diseased
heart, the ventricles of which communicated together. He never had a
symptom of disorder of the head; yet on dissection an extensive recent
softening was found in the right _corpus striatum_ and another in the
right _thalamus_.[1668]

None of the treatises I have seen on the subject make mention of a
variety of this disease intermediate between suddenly fatal cases and
those which last several days,—a form in which the patient’s illness
endures for a few hours only, and which, both in the special symptoms
and in their course, imitates exactly the effects of some narcotics. Two
such cases have come under my notice, both of them judicial, poisoning
having been suspected. One of them proved fatal in an hour and a half,
the individual having previously been in excellent health; and the only
appearance of disease was softening of a considerable part of the
surface of the brain where it lies over the left orbit. The other was
more remarkable in its circumstances. In November, 1822, a man, who had
previously enjoyed excellent health, was found one morning in a low
lodging-house in the Lawnmarket comatose, and convulsed; and he died
seven hours afterwards. The neighbours spread a report, that the woman
of the house had poisoned him, with the view of selling the body; and by
an odd coincidence the police, when they went to apprehend the woman,
found an anatomist hid in a closet. The body was judicially examined by
Sir W. Newbigging and myself; and we found an ulcer on the forepart of
the left hemisphere of the brain, and a small patch of softening on each
middle lobe.

It is only in cases like the last two that the disease is likely to be
mistaken for the effects of poison; and the morbid appearances will at
once distinguish them. But it is requisite to remember that softening of
the brain when not far advanced is apt to escape notice, as it is not
necessarily attended with a change in the colour of the diseased part.
In the first of the two cases I have related, the cause of death was
very nearly assumed to have been simple apoplexy, when at length the
true disorder was unexpectedly noticed. I presume, indeed, that strictly
speaking, both of the cases which came under my notice ought to be
considered as simple apoplexy excited by pre-existing _ramollissement_.


   _Of the Distinction between Hypertrophy of the Brain and Narcotic
                              Poisoning._

This disease is not here mentioned, because its symptoms and progress
resemble very closely those of poisoning with the narcotics; for it
causes epileptic symptoms, which, besides that they are preceded for
some time by other head affections, very seldom prove fatal in less than
three days. But some notice of it is necessary, because the disease is
rare and of recent discovery, so that the appearances left by it in the
dead body may escape observation. Besides, the physician is at present
imperfectly acquainted with it, and therefore, when a more extensive
collection of cases shall have been made, it may be found to prove at
times fatal so rapidly as to admit of being confounded with narcotic
poisoning. Hypertrophy of the brain, it is true, is always a chronic or
slow disease, but, like other diseases of the brain, its early stages
may possibly be so completely latent that the patient may appear to die
of a few hours’ illness. This, however, must be left to the
determination of future experience. The most rapid case yet published
proved fatal twenty-four hours after the first appearance of symptoms.

The appearances left in the body are increased density and firmness of
the whole brain or a part of it,—flattening of the convolutions on their
outer surface, so that their grooves are almost obliterated and the
investing membrane uncommonly dry,—unusual emptiness of the
blood-vessels of the brain and its membranes,—and a protrusion of the
brain upwards on removal of the skull-cap, as if the organ were too
large for its containing cavity.[1669]

Some pathologists doubt the existence of hypertrophy of the brain as a
distinct disease, and conceive that the appearance of flattening of the
convolutions is produced by serum effused between the dura mater and
arachnoid membrane. But this explanation will not account for those
cases in which it is expressly stated that little or no fluid was to be
found in any part of the brain or in the base of the skull.


  _Of the Distinction between Diseases of the Spinal Cord and Narcotic
                              Poisoning._

It is not necessary to say much on the acute diseases of the spinal
cord, which are apt to be confounded with the effects of narcotic
poisons. The diseases are extravasation of blood into the spinal canal,
inflammation of the membranes, and inflammation [_ramollissement_] of
the cord itself. These disorders are commonly marked by obvious and
characteristic symptoms, as well as a much slower course than that of
the affections induced by narcotic poisons. But occasionally they
approach closely the characters of some of the slow cases of narcotic
poisoning,—palsy being absent, the leading symptoms consisting of
delirium, convulsions, and coma, and the fatal event occurring within
the third day. Dr. Abercrombie and M. Ollivier have related examples of
the kind arising from extravasation of blood,[1670] serous
effusion,[1671] and softening of the cord.[1672] Such cases are
exceedingly rare; but the possibility of their occurrence should impose
on the medical jurist the necessity of examining the spine with care in
all judicial cases of alleged narcotic poisoning, especially when death
has not been rapid.


 _Of the Distinction between syncopal Asphyxia, and Narcotic Poisons._

The only other natural disease requiring notice under the present head
is the _Asphyxia Idiopathica_ of the late Mr. Chevallier. It may be the
cause of embarrassment in questions regarding narcotic poisoning, when
the course of the symptoms to their fatal termination is rapid, and was
not witnessed by any person; for it causes death with equal rapidity,
and its signs in the dead body are very obscure. It has been observed
chiefly among women in the latter months of pregnancy, or soon after
delivery; but it has also been known to attack the male sex. It
generally commences during a state of perfect health, and is seldom
preceded by any warning of danger. The person suddenly complains of
slight sickness, giddiness, and excessive faintness, immediately seems
to sleep or swoon away, and expires gently without a struggle. The only
appearance of note found in the dead body is unusual flaccidity and
emptiness of the heart.[1673] But even these slight appearances are not
constant; for in a case related by Rochoux of a woman who, while in a
state of perfect health, suddenly grew pale, slipped off her chair, and
died on the spot, the auricles of the heart contained a great deal of
blood.[1674] This singular disorder appears to consist of nothing else
than a mortal tendency to fainting; and it may prove fatal either in the
first fit of syncope, or after an hour and a half.—Under the same head
are probably to be arranged the cases of sudden death described by M.
Devergie under the title of Death by Syncope. He has given scarcely any
account of the circumstances attending death; but it may be inferred
from his classification of the cases that fainting immediately preceded
it. In all of them he found blood in both sides of the heart; and the
blood, contrary to what happens in other kinds of sudden death, had
separated into clear serum, and fibrin free of colouring
matter.[1675]—Under the same head also may be noticed a denomination of
cases, which, though alluded to before by various pathologists, were
first distinctly characterized by M. Ollivier, where death is caused on
a sudden, apparently by the disengagement of a large quantity of
aëriform fluid from the blood in the heart and great vessels. Among the
instances described by Ollivier, it appears that death repeatedly
occurred quite suddenly while the individuals enjoyed sound health; and
the only appearances of any note found in the body were tympanitic
distension of the heart, absence of blood there and in the great
vessels, and the existence of a gaseous fluid in numerous globules
throughout the blood-vessels of the brain. The circumstances of death
and the appearances in the dead body are much the same with those
observed from the admission of air into the veins during surgical
operations. A case of this kind, owing to its suddenness, might be
confounded with the effects of the more active narcotic poisons, such as
hydrocyanic acid, especially as its characters in the dead body might
escape notice.[1676]

Death often takes place from sudden syncope in _organic diseases of the
heart_. Such cases may be confounded with the most rapid variety of
poisoning with hydrocyanic acid; and if the duration of the symptoms
preceding death is unknown, they may give rise to a suspicion of
poisoning generally. But they are at once distinguished by the morbid
appearances. A trivial organic derangement may be the occasion of
instant death.

The genera comprehended in the class of narcotics are opium, henbane,
lettuce-opium, solanum, hydrocyanic acid, and the deleterious gases. Of
these genera the last is by no means a pure one, for it includes many
gases which act as irritants only; but it is more convenient to consider
them together, than to distribute them into separate classes. Some other
vegetable substances besides henbane, lettuce-opium, and solanum,
possess nearly the same properties; but as they likewise cause
irritation, they are arranged more appropriately in the next class, the
narcotico-acrids.

Most narcotic vegetables owe their poisonous properties to a peculiar
principle, probably of an alkaline nature, and slightly different in
each. This discovery was made with regard to opium in 1812; and the
discovery of the active principle in that drug has been followed by the
detection of analogous principles in most narcotics, as well as in many
narcotico-acrids.

These principles are generally crystalline, soluble in alcohol and the
acids, little soluble in water, free from mineral admixture, and
entirely destructible by heat. When purified with the greatest care,
they still retain decided alkaline properties; but on account of their
number and the low power of neutralization their alkaline nature was
long denied; and they have been conventionally styled alkaloids.

In their natural state they exist in combination with various ternary
acids, some of which are peculiar; and they are likewise intimately
blended, or more probably united chemically, with other inert principles
of the vegetable kingdom, particularly resinous and extractive matters,
to which they adhere with great obstinacy.

They are all highly energetic, and generally concentrate in themselves
the leading properties of the substance from which they are obtained.

The experiments, which have led to the conclusion, that the narcotic
poisons act on the brain by entering the blood-vessels, have been
repeated with their alkaloids, and have yielded similar results. But the
alkaloids are in equal quantities much more energetic than the crude
poisons. Their effects indeed are truly formidable, and some well
authenticated instances of their action appear hardly less marvellous
than the most extravagant notions entertained in ancient times of the
operation of poisons. One of them, the principle of nux vomica, which,
however, does not belong to the present class, is so active that in all
probability a man might be killed with the third part of a grain in less
than fifteen minutes.

It is very difficult to detect some of the vegetable alkaloids; and it
is fortunate, therefore, that they are rare, and not to be procured but
by complex processes.

Chemical analysis does not by any means supply so good evidence of
poisoning with the narcotics as it does of poisoning with the irritants.
Their chemical properties are not very characteristic, and they are not
well developed unless with a larger quantity of the poison than will
usually be met with in medico-legal investigations. This remark,
however, does not apply universally; and it is probable, that, as
organic analysis goes on improving, better and more delicate processes
will be discovered.




                             CHAPTER XXVII.
                        OF POISONING WITH OPIUM.


To the medical jurist opium is one of the most important of poisons;
since there is hardly any other whose effects come more frequently under
his cognizance. It is the poison most generally resorted to by the timid
to accomplish self-destruction, for which purpose it is peculiarly well
adapted on account of the gentleness of its operation. It has also been
often the source of fatal accidents, which naturally arise from its
extensive employment in medicine. It has likewise been long very
improperly employed to create amusement. And in recent times it has been
made use of to commit murder, and to induce stupor previous to the
commission of robbery. Mr. Burnett, in his work on Criminal Law, has
mentioned a trial for murder in 1800, in which the prisoners were
accused of having committed the crime by poisoning with opium; and
although a verdict of _not proven_ was returned, there is little doubt
that the deceased, an adult, was poisoned in the way supposed. A few
years ago, a remarkable trial took place at Paris, where poisoning was
alleged to have been effected by means of the alkaloid principle of
opium; and the prisoner, a young physician of the name of Castaing, was
condemned and executed.

In several parts of Britain during the last fifteen years many persons
have been brought into great danger by opium having been administered as
a narcotic to facilitate robbery; and some have actually been killed. In
December, 1828, a conviction was obtained in the Judiciary Court of
Edinburgh for this crime, in which instance the persons who had taken
the opium recovered. A fatal case, which was strongly suspected to be of
the same nature, was submitted to me by the sheriff of this county in
1828; but sufficient evidence could not be procured. In July, 1829, a
man Stewart and his wife were condemned, and subsequently executed for
the same crime, the person to whom they gave the opium having been
killed by it. And about a year afterwards a similar instance occurred at
Glasgow, for which a man Byers and his wife were condemned at the Autumn
Circuit of 1831.


        SECTION I.—_Of the Chemical History and Tests of Opium._

Opium is the inspissated juice of the capsules of the _Papaver
somniferum_. It has a reddish-brown colour, and a glimmering lustre on a
fresh surface. It is soft and plastic when recent; but if pure, may be
dried so as to become brittle. Its smell is strong and quite peculiar.
It has a very bitter and most peculiar taste. In consequence of this
taste one would suppose it no easy matter to administer opium secretly.
The plan resorted to by thieves and robbers seems to be, to deaden the
sense of taste by strong spirits, and then to ply the person with porter
or ale drugged with laudanum, or the black drop, which possesses less
odour.

The following account of the chemical history of opium will be confined
in a great measure to the leading properties of the principles, in which
its active qualities are concentrated, or which are likely by their
chemical characters to supply proof of its presence.

The common solvents act readily on opium. Water dissolves its active
principles even at low temperatures. So does alcohol. So particularly do
the mineral and vegetable acids when much diluted. Ether removes from it
little else than one of its active principles, narcotine. By the action
of these agents are procured various preparations in common use.
_Laudanum_ is a spirituous infusion, and contains the active ingredients
of a twelfth part of its weight of opium. _Scotch Paregoric Elixir_, a
solution in ammoniated spirit, is only one-fifth of the strength of
laudanum; and _English Paregoric_, tincture of opium and camphor for its
chief ingredients, is four times weaker still. _Wine of opium_ contains
the soluble part of a sixteenth of its weight. The _black drop_ and
_Battley’s sedative liquor_ are believed to be solutions of opium in
vegetable acids, and to possess, the former four, the latter three times
the strength of laudanum. But their strength has been greatly
exaggerated; neither of them, according to my own experience, being
above half what is supposed. The juice and infusion of the garden poppy
are also powerfully narcotic, so as even to have caused death both when
given by the mouth and in the way of injection.[1677] Many other
pharmaceutic preparations contain opium.

If opium be infused in successive portions of cold water, the water
dissolves all its poisonous principles, and also a peculiar acid
possessing characteristic chemical properties. These principles are
separated by means of the alkalis, the alkaline carbonates, or the
alkaline earths. The most important of them are _morphia_, the chief
alkaloid of opium,—_narcotine_, a feeble poison, not an alkaloid,—a
peculiar acid, termed _meconic acid_,—and a _resinoid substance_. Other
crystalline principles also exist in opium, though apparently in too
small proportion either to affect its action or to be available in
medico-legal analysis as the means of detecting the drug. These are
codeïa, meconine, narceïne, paramorphia, and porphyroxine.

Of the various principles now indicated it is necessary to notice here
only morphia, narcotine, codeïa, porphyroxine and meconic acid. They
require mention either as being active poisons, or because a knowledge
of their leading characters may be useful in conducting a medico-legal
analysis in a case of poisoning with opium.

Meconic acid, as procured by evaporation, is usually in little scales of
a pale brown or yellowish tint, being rendered so by adhering resin or
extractive matter; but when nearly colourless, it forms long, extremely
delicate tabular crystals, which in mass have a fine silky appearance
like spermaceti. 1. When heated in a tube, it is partly decomposed, and
partly sublimed; and the sublimate condenses in filamentous, radiated
crystals. 2. When dissolved even in a very large quantity of water, the
solution acquires an intense cherry-red colour with the perchloride of
iron. The sublimed crystals have the same property. Only one other acid
is so affected, namely, the sulpho-cyanic, a very rare substance. It has
been repeatedly stated,[1678] that the redness produced by meconic acid
may be distinguished by the effect of an alkali, which is said to bleach
the colour produced by sulpho-cyanic acid, but to deepen the cherry-red
tint occasioned by the meconic. This is not correct; an alkali added to
the red solution of meconate of iron precipitates oxide of iron and
renders the liquid colourless. The best distinction yet proposed is the
following which has been suggested by Dr. Percy. Acidulate the red fluid
with sulphuric acid, drop in a bit of pure zinc, and suspend at the
mouth of the tube a bit of paper moistened with solution of acetate of
lead: If the redness be caused by sulpho-cyanic acid, hydrosulphuric
acid gas is evolved, and blackens the paper; but no such effect ensues,
it the redness be owing to meconic acid.[1679]—According to Dr. Pereira,
solutions of the acetates, an infusion of white mustard, decoctions of
Iceland moss, and of the _Gigantina helminthocorton_, besides other more
rare substances, are reddened, like solution of meconic acid, by the
salts of peroxide of iron.[1680] 3. The solution of meconic acid gives a
pale-green precipitate with the sulphate of copper, and, if the
precipitate is not too abundant, it is dissolved by boiling, but
reappears on cooling.

_Of the Tests for Morphia and its Salts._—Morphia, when pure, is in
small, beautiful, white crystals. Various forms have been ascribed to
it; but in the numerous crystallizations I have made, it has always
assumed when pure the form of a slightly flattened hexangular prism. It
has a bitter taste, but no smell.

A gentle heat melts it, and if the fluid mass is then allowed to cool, a
crystalline radiated substance is formed. A stronger heat reddens and
then chars the fused mass, white fumes of a peculiar odour are
disengaged, and at last the mass kindles and burns brightly.—Morphia is
very little soluble in water. It is more soluble, yet still sparingly
so, in ether. But its proper solvents are alcohol, or the diluted acids,
mineral as well as vegetable. All its solutions are intensely bitter,
and that in alcohol has an alkaline reaction.—From its solutions in the
acids crystallizable salts may be procured; and morphia may be separated
by the superior affinity of any of the inorganic alkalis; but it is
easily redissolved by an excess of potash.—Morphia when treated with
nitric acid is dissolved with effervescence, and becomes instantly
orange-red, which, if too much acid be used, changes quickly to yellow.
The coloration of morphia by nitric acid is a characteristic property;
which, however, it possesses in common with some other alkaloids, such
as brucia, and also strychnia when not quite pure. The change of colour
is said by some chemists to depend on adhering resinoid matter, and not
to be possessed by perfectly pure morphia; but this is a mistake. It is
probable that some other vegetable substances besides the three
alkaloids, morphia, brucia, and strychnia, may be turned orange-red by
nitric acid. Dr. Pereira says that oil of pimento undergoes the same
change.[1681]—When suspended in water, in the form of fine powder and
then treated with a drop or two of perchloride of iron containing little
or no free hydrochloric acid, it is dissolved and forms a deep blue
solution, the tint of which is more purely blue, the stronger the
solution, and the purer the morphia. This is a property even more
characteristic than the former, since no such effect is produced on any
other known alkaloid. Like the effect of nitric acid, it is said not to
be essential to morphia, but to depend on adhering resinoid matter; yet
the blue colour is always strongly produced with powdered morphia of
snowy-whiteness.—Another property by which morphia maybe also
distinguished is the decomposition of iodic acid. A solution of iodic
acid is turned brown either by morphia or its salts, owing to the
formation of iodine; and the test is so delicate that it affects a
solution containing a 7000th of morphia.[1682] So many other substances,
however, possess the property of disengaging iodine from iodic acid,
that little importance can be attached to this criterion.

_Acetate of Morphia_ is in some countries the common medicinal form for
administering morphia; but it has been almost entirely superseded in
this city by the hydrochlorate, since Dr. W. Gregory pointed out a cheap
mode of procuring that salt in a state of purity.[1683] The acetate is
in confused crystals, often of a brownish colour from impurities. The
stronger acids disengage acetic acid. The alkalis throw down morphia
from its solution in water. Nitric acid and perchloride of iron act on
it as on morphia itself.

_Hydrochlorate of Morphia._—The muriate or hydrochlorate must be
carefully attended to by the medical jurist, because it is extensively
used in medical practice instead of opium. As now prepared, it is
snowy-white and apparently pulverulent, but is in reality a congeries of
filiform crystals. It decrepitates slightly when heated, then melts, and
at the same time chars, exhaling a strong odour somewhat like that of
truffles. Nitric acid and perchloride of iron act on it as on morphia.
Boiling water dissolves fully its own weight, and very easily
three-fourths of its weight of hydrochlorate of morphia; and on cooling
down to 60° F. it retains seven parts per cent., and deposits the rest
in tufts of beautiful filiform crystals. The solution commonly employed
in medicine contains one per cent. of the salt. Nitric acid turns the
solution yellow, acting distinctly enough when the water contains a
hundredth, and perceptibly when it contains only a two-hundredth of its
weight. Perchloride of iron strikes a deep blue with a solution
containing a hundredth of its weight, very distinctly when the
proportion is a two-hundredth, and even perceptibly when it is only a
five-hundredth. A solution much more diluted than even the last has a
strong bitter taste. When moderately concentrated, morphia is
precipitated from it by the alkalis.

Of the preceding properties of morphia and its salts, those which
constitute the most characteristic tests are the effects of perchloride
of iron and of nitric acid on all of them, the effect of heat on
morphia, and the effect of an alkali on its solutions in acids.

_Of the Tests for Narcotine._—Narcotine is rather distinguished by
negative than by positive chemical properties. When pure, it is in
transparent colourless pearly crystals, which, as formed from alcohol,
may be either very flat, oblique, six-sided prisms, or oblong four-sided
tables obliquely bevelled on their sides. But when crystallized from
sulphuric ether the crystals are prisms with a rhombic base. They fuse
with heat, and concrete on cooling into a resinous-like mass. They are
soluble in ether, and fixed oil, less so in alcohol, insoluble in water
or the alkalis, very soluble in the diluted acids, but without effecting
neutralization; and if perfectly pure, they do not undergo the changes
produced on morphia by perchloride of iron or nitric acid. Few specimens
of narcotic, however, are so pure as not to render nitric acid yellow.
Care must be taken not to confound narcotine with morphia. When
crystallized together from alcohol and not quite pure, narcotine forms
tufts of pearly thin tabular crystals, while morphia is in short, thick,
sparkling prisms.

_Of Codeïa._—This substance is, like morphia, an alkaloid, capable of
combining with acids. It differs from morphia and narcotine in being
moderately soluble in water; and from this solution it may be
crystallized in large crystals affecting the octaedral form. It is
unnecessary to detail its chemical properties.

_Of the Tests for Porphyroxine._—This principle is a neutral crystalline
body, insoluble in water, soluble in alcohol and ether, and also soluble
in weak acids, which part with it unchanged on the addition of an
alkali. When heated with hydrochloric acid, a fine purple or rose-red
solution is produced; whence its name. It is supposed that this property
may be of use in medico-legal researches; and the following mode of
developing it has been proposed by Dr. Merck, its discoverer.[1684]
Decompose the suspected fluid with caustic potash; agitate the mixture
with sulphuric ether; dip a bit of white filtering paper repeatedly in
the etherial solution, drying it after each immersion; then wet the
paper with hydrochloric acid, and expose it to the vapour of boiling
water; upon which the paper will become more or less acid.


    _Of the Process for detecting Opium in mixed fluids and solids._

Having stated these particulars of the chemical history of opium and its
chief component ingredients, I shall now describe what has appeared to
me the most delicate and satisfactory method of detecting it in a mixed
state.

1. If there be any solid matter, it is to be cut into small fragments,
water is to be added if necessary, then a little acetic acid sufficient
to render the mixture acidulous, and when the whole mass has been well
stirred, and has stood a few minutes, it is to be filtered, and
evaporated at a temperature somewhat below ebullition to the consistence
of a moderately thick syrup. To this extract strong alcohol is to be
gradually added, care being taken to break down any coagulum which may
be formed: and after ebullition and cooling, the alcoholic solution is
to be filtered. The solution must then be evaporated to the consistence
of a thin syrup, and the residue dissolved in distilled water and
filtered anew.

2. Add now the solution of acetate of lead as long as it causes
precipitation, filter and wash. The filtered fluid contains acetate of
morphia, and the precipitate on the filter contains meconic acid united
with the oxide of lead.

3. The fluid part is to be treated with hydrosulphuric acid gas, to
throw down any lead which may remain in solution. It is then to be
filtered while _cold_, and evaporated sufficiently in a vapour-bath. The
solution in this state will sometimes be sufficiently pure for the
application of the tests for morphia; but in most cases it is necessary,
and in all advisable, to purify it still farther. For this purpose the
morphia is to be precipitated with carbonate of soda; and the
precipitate having been collected, washed, and drained on a filter, the
precipitate and portion of the filter to which it adheres are to be
boiled in a little pure alcohol. The alcoholic solution,—filtered, if
necessary,—will give by evaporation a crystalline residue of morphia,
which becomes orange-red with nitric acid, and blue with perchloride of
iron. The latter property I have sometimes been unable to develope when
the former was presented characteristically.

4. It is useful, however, to separate the meconic acid also; because, as
its properties are more delicate, I have repeatedly been able to detect
it satisfactorily, when I did not feel satisfied with the result of the
search for morphia. Dr. Ure made the same remark in his evidence on the
trial of Stewart and his wife. He detected the meconic acid, but could
not separate the morphia. It may be detected in one of two ways,—by
means of hydrosulphuric acid, or by sulphuric acid.

If the former method be chosen, suspend in a little water the
precipitate caused by the acetate of lead (par. 2); transmit
hydrosulphuric acid gas till the whole precipitate is blackened; filter
immediately without boiling; then boil, and if necessary filter a second
time. A great part of the impurities thrown down by the acetate of lead
will be separated with the sulphuret of lead; and the meconic acid is
dissolved. But it requires in general farther purification, which is
best attained by again throwing it down with acetate of lead, and
repeating the steps of the present paragraph. The fluid is now to be
concentrated by evaporation at a temperature not exceeding 180° F., and
subjected to the tests for meconic acid, more particularly to the action
of perchloride of iron, when the quantity is small. If there is
evidently a considerable quantity of acid, a portion should be
evaporated till it yields crystalline scales; and these are to be heated
in a tube to procure the arborescent crystalline sublimate formerly
described. About a sixth of a grain of meconic acid, however, is
required to try the latter test conveniently.

If the method of separating meconic acid by means of sulphuric acid be
preferred, the precipitate formed by acetate of lead is to be treated
with weak sulphuric acid, which forms insoluble sulphate of lead, and
disengages the meconic acid. The liquid obtained by filtration is then
to be evaporated as above, to obtain crystals, which are to be examined
by the tests for meconic acid. Orfila thinks this method more delicate
than the mode by hydrosulphuric acid gas. I am inclined from my own
experiments to doubt his statement.

5. If there be a sufficiency of the original material, Merck’s process
for detecting porphyroxin may be tried [see p. 534]. But I doubt whether
this process is sufficiently delicate for medico-legal purposes.

I wish I could add my testimony to the opinion, expressed on a
remarkable occasion by Professor Chaussier, in favour of the delicacy of
the tests for morphia and its compounds, that they might be detected
“jusqu’à une molécule.”[1685] In one sense this statement may be
correct. Morphia, separated from the complex mixture of principles with
which it is combined in opium, may be detected in extremely small
quantities. Accordingly, M. Lassaigne has supplied, for the discovery of
acetate of morphia in mixed fluids, an excellent process, whence the
chief part of the three first paragraphs of the preceding method for
opium are borrowed; and from the facts stated by him in his paper,[1686]
as well as from the experimental testimony of Professor Orfila,[1687] it
appears that Lassaigne’s process will furnish strong indications, if not
absolute proof of the presence of that salt, in the proportion of two
grains to eight ounces of the most complex mixtures. Hence the search
for acetate of morphia in a suspected case is by no means hopeless. But
the detection of acetate of morphia is an object of small moment,
compared with the detection of morphia in its natural state of
combination in opium. Now my own observations lead me to entertain
serious doubts, whether the best method of operating hitherto known
could be successfully applied to the detection of the equivalent opium
in complex mixtures. By the process I have recommended it is easy to
procure, from an infusion of ten grains of opium in four ounces of
water, satisfactory proof of the presence of morphia by the action of
ammonia, perchloride of iron and nitric acid, and equally distinct proof
of the presence of meconic acid by perchloride of iron, as well as
sulphate of copper. But on proceeding to apply the process to organic
mixtures, I have found that when the soluble part of ten grains of opium
was mixed with four ounces of porter or milk, I could develope no
property of morphia but its bitterness, and no indication of meconic
acid but the action of perchloride of iron. MM. Larocque and Thibierge,
it is right to add, have in similar circumstances found the process
somewhat more delicate.[1688]

It is of great consequence, however, to remark, that in cases of
poisoning with opium, the medical jurist will seldom have the good
fortune to operate even upon so large a proportion of the poison as in
my experiments; because the greater part of it disappears from the
stomach before death. This will not happen always, as may be seen from
various cases mentioned afterwards in the section on the morbid
appearances caused by opium. But, according to my own observations, the
poison will often disappear in a short time, so far as to render an
analysis abortive. Thus in the case of a young woman who died five hours
after taking not less than two ounces of laudanum, I could apply to the
fluid, procured from the contents of the stomach, by paragraphs 1, 2,
and 3 of my process, only the test of its taste, which had the
bitterness of morphia. In the case of another young woman, whose stomach
was emptied by the stomach-pump four hours after she took two ounces of
laudanum, I could obtain from the evacuated fluid, when properly
prepared, only the indications of the presence of morphia supplied by
its bitterness and the imperfect action of nitric acid,—and the
indication of the presence of meconic acid supplied by the imperfect
action of perchloride of iron. In a third case, where the stomach was
evacuated two hours after seven drachms of laudanum had been swallowed,
even the first portions of fluid withdrawn had not any opiate odour, and
did not yield any indication of the presence even of meconic acid. Now,
on the one hand, the quantity taken in these instances is rarely
exceeded in cases of poisoning with laudanum; and, on the other hand,
the interval during which it remained in the stomach subject to vital
operations is considerably less than the average in medico-legal, and
above all in fatal cases. It may be laid down, therefore, as a general
rule, that in poisoning with opium the medical jurist, by the best
methods of analysis yet known, will often fail in procuring satisfactory
evidence, and sometimes fail to obtain any evidence at all, of the
existence of the poison in the contents of the stomach. In a case
published by Dr. Bright from the experience of Mr. Walne of London, it
is stated that the matter removed from the stomach only half an hour
after an ounce and a half of laudanum had been taken, while the stomach
was empty, did not smell of opium.[1689] This case is quoted to put the
reader on his guard. But at the same time it does appear extremely
improbable that the whole opium had disappeared from the stomach in so
short a time, and much more likely that it might have been found by
analysis in the matter first withdrawn.

I have taken some pains to establish the proposition laid down above,
because in a matter of such importance it is always essential, that the
medical inspector know the real extent of his resources; and it has
appeared to me that, greatly as the hand of the chemist has been
strengthened by late discoveries in vegetable analysis, his power has
been overrated both by his scientific brethren, and by the medical
profession generally. I am happy to find, since the first publication of
these remarks, that they coincide with the experience and opinion of so
eminent an authority as Professor Buchner; who has observed that a
chemical analysis must often fail to detect opium where there could be
no doubt of its having been administered in large quantity.[1690]

It is of moment to add, that in two of the instances mentioned above the
odour of laudanum was perceived in the subject of analysis,—faintly,
however, and only for a few hours after it was removed from the stomach.
Although the peculiar odour of opium is a delicate criterion of its
presence, it does not follow that it should be preferred to an elaborate
chemical analysis. For it is a test of extreme uncertainty. There is in
the contents of the stomach such a complication of odours, that with a
rather delicate sense of smell, I have sometimes been unable to satisfy
myself of the presence of the opiate odour where others were sure it
existed. At the same time the medical jurist should not neglect it as a
subsidiary test. It is always strongest and most characteristic, first,
when the stomach is just opened, or the contents just withdrawn, and
again, when the fluid, in the course of preparation, as directed in
paragraph 1 (p. 535), is just reaching the point of ebullition. The
latter odour is somewhat different from the former, yet quite peculiar,
and such as every chemist must have remarked on boiling an infusion of
opium. It is further to be observed, that although the odour of opium is
a very delicate test of its presence even in complex organic mixtures,
chemical analysis may be successful, where this character fails. Dr.
Morehead of the Bombay service, in applying my process to the fluid
withdrawn by the stomach-pump, detected morphia both by nitric acid and
perchloride of iron, although he could not detect any odour of opium in
the fluid.[1691]

So much for the delicacy of the process. As to its precision,—from what
I have myself witnessed, as well as from the experience of Dr. Ure, it
will often happen in actual practice, that the only indication of opium
to be procured by the process consists in the deep red colour struck by
perchloride of iron with the meconic acid. Now, will this alone
constitute sufficient proof of the presence of opium? On the whole, I am
inclined to reply in the affirmative. Sulpho-cyanic acid, it is true,
has the same effect, and this acid has been proved by Professors Gmelin
and Tiedemann to exist in the human saliva,[1692]—a fact which was
called in question by Dr. Ure in his evidence on the trial of the
Stuarts, but which at the time I had verified, and which Dr. Ure has
since been compelled by experiments of his own to admit.[1693] But it
must be very seldom possible to procure a distinct blood-red coloration
from the saliva, after it has been mixed with the complex contents of
the stomach, and subjected to the process of analysis detailed
above;[1694] and the check proposed by Dr. Percy (p. 532) will
distinguish it.


  SECTION II.—_Of the Action of Opium, and the Symptoms it excites in
                                 Man._

The symptoms and mode of action of opium have been long made the subject
of dispute, both among physicians and toxicologists; and in some
particulars our knowledge is still vague and insufficient.

Under the head of general poisoning, some experiments were related, from
which it might be inferred that opium has the power of stupefying or
suspending the irritability of the parts to which it is immediately
applied. The most unequivocal of these facts, which occurred to Dr.
Wilson Philip, was instant paralysis of the intestines of a dog, when an
infusion of opium was applied to their mucous coat;[1695] another hardly
less decisive was palsy of the hind-legs of a frog, observed by Dr.
Monro Secundus, when opium was injected between the skin and the
muscles;[1696] and a third, which has been remarked by several
experimentalists, is immediate cessation of the contractions of the
frog’s heart when opium is applied to its inner surface.[1697]

The poison has also powerful constitutional or remote effects, which are
chiefly produced on the brain. Much discussion has arisen on the
question, whether these constitutional effects are owing to the
conveyance of the local torpor along the nerves to the brain, or to the
poison being absorbed, and so acting on the brain through the blood. The
question is not yet settled. It appears pretty certain, however, that
the poison cannot act constitutionally without entering the
blood-vessels; although it is not so clear, that after it has entered
them, it acts by being carried with the blood to the brain. The newest
doctrine supposes that it enters the blood-vessels, and produces on
their inner coat an impression which is conveyed along the nerves.

According to the experiments of Professor Orfila, it is more energetic
when applied to the surface of a wound than when introduced into the
stomach, and most energetic of all when injected into a vein.[1698] The
inference generally drawn from these and other analogous
experiments[1699] is, that the blood transmits the poison in substance
to the brain. They certainly, however, do not prove more than that the
poison must enter the blood before it acts.

The old doctrine, that the blood-vessels have no concern with its
action, and that it acts only by conveyance along the nerves of a
peculiar local torpor arising from its direct application to their
sentient extremities, has been long abandoned by most physiologists as
untenable. But some have adopted a late modification of this doctrine,
by supposing that opium may act both by being carried with the blood to
the brain, and by the transmission of local torpor along the nerves.
They believe, in fact, that opium possesses a double mode of
action,—through sympathy as well as through absorption. It would be
fruitless to inquire into the grounds that exist for adopting or
rejecting this doctrine, because sufficient facts are still wanting to
decide the controversy. So far as they go, however, they appear adverse
to the supposition of a conveyance of impressions along the nerves,
without the previous entrance of the poison within the blood-vessels.
The difficulties, in the way of the theory of the sympathetic action of
opium, would be removed by the doctrine of Messrs. Morgan and Addison.
According to their views, the experiments, which appear at first sight
to prove that this substance operates by being carried with the blood to
the part on which it acts, are easily explained by considering that the
opium makes a peculiar impression on the inside of the vessels, which
impression subsequently passes along the nerves to the brain.[1700] But,
as stated in the introductory chapter on the physiology of poisoning,
this theory requires support.

The effects of opium, through whatever channel it may produce them, are
exerted chiefly on the brain and nervous system. This appears from the
experiments of a crowd of physiologists, as well as from the symptoms
observed a thousand times in man. In animals the symptoms are different
from those remarked in man. Some experimentalists have indeed witnessed
in the higher orders of animals, as in the human subject, pure lethargy
and coma. But the latest researches, among the rest those of M. Orfila,
show that much more generally it causes in animals hurried pulse,
giddiness, palsy of the hind-legs, convulsions of various degrees of
intensity, from simple tremors to violent tetanus, and a peculiar
slumber, in the midst of which a slight excitement rouses the animal and
renews the convulsions. These symptoms are produced in whatever way the
poison enters the body, whether by the stomach, or by a wound, or by
direct injection into a vein, or by the rectum. In man, convulsions are
sometimes excited; but much more commonly simple sopor and coma.

According to the inquiries of M. Charret, which were extended to every
class of the lower animals, opium produces three leading effects. It
acts on the brain, causing congestion, and consequently sopor; on the
general nervous centre as an irritant, exciting convulsions; and on the
muscles as a direct sedative. It is poisonous to all animals,—man,
carnivorous quadrupeds, the _rodentia_, birds, reptiles, amphibious
animals, fishes, insects, and the _mollusca_. But of its three leading
effects some are not produced in certain classes or orders of animals.
In the _mammalia_, with the exception of man, there is no cerebral
congestion induced, and death takes place amidst convulsions. In birds
there is some cerebral congestion towards the close; but still the two
other phenomena are the most prominent.[1701]

It has been rendered probable, by what is stated above, that opium
enters the blood. The question, therefore, naturally arises, whether its
presence there can be proved by chemical analysis? But considering the
imperfection of the processes for detecting it when mixed with organic
substances, no disappointment ought to be felt if this proof should fail
in regard to so complex a fluid as the blood. The only person who has
represented himself successful in the search is M. Barruel of Paris. He
examined the urine and blood of a man under the influence of a poisonous
dose of laudanum, amounting to an ounce and a half; and procured
indications of morphia in both. When three ounces of urine were boiled
with magnesia, and the insoluble matter was collected, washed, dried,
and boiled, in alcohol, the residue of the alcoholic solution formed a
white stain, which became deep orange-red on the addition of nitric
acid. The blood was subjected to a more complex operation. One pound and
ten ounces of it were bruised in a mortar, diluted with two pounds of
water, strongly acidulated with sulphuric acid, boiled, filtered, and
washed. The filtered fluid was saturated with chalk, and the excess of
carbonic acid driven off by heat. The fluid was then filtered again, and
after being washed with water, was acted on by diluted acetic acid. The
acetic solution left on evaporation a residue which was repeatedly acted
on by alcohol; and the residue of the alcoholic solutions was treated
with pure alcohol and carbonate of lime. The new solution when filtered
and evaporated left several small white stains, which became orange-red
with nitric acid.[1702] These results have been since contradicted by M.
Dublanc. He in vain sought for morphia in the blood and urine of people
who were taking acetate medicinally, or of animals that were killed by
it.[1703] Barruel’s results are also at variance with some pointed
experiments of M. Lassaigne, who could not detect any acetate of morphia
even in blood drawn from a dog twelve hours after thirty-six grains were
injected into the crural vein;[1704] nor any in the liver or venous
blood of a dog poisoned with eight ounces of Sydenham’s laudanum.[1705]

In investigating the effects of opium and its principles on man, the
natural order of procedure is to consider in the first place those of
opium itself in its various forms.

The effect of a small dose seems to be generally in the first instance
stimulating: the action of the heart and arteries is increased, and a
slight sense of fulness is caused in the head. This stimulus differs
much in different individuals. In most persons it is quite
insignificant. In its highest degree it is well exemplified by Dr. Leigh
in his Experimental Inquiry, as they occurred to a friend of his who
repeatedly made the experiment. If in the evening when he felt sleepy,
he took thirty drops of laudanum, he was enlivened so that he could
resume his studies; and if, when the usual drowsiness approached, which
it did in two hours, he took a hundred drops more, he soon became so
much exhilarated, that he was compelled to laugh and sing and dance. The
pulse meanwhile was full and strong, and the temporal arteries throbbed
forcibly. In no long time the customary torpor ensued. The stimulant
effect of opium given during a state of exhaustion is also well
illustrated by Dr. Burnes in his account of Cutch. “On one occasion,”
says he, “I had made a very fatiguing night march with a Cutchee
horseman. In the morning, after having travelled above thirty miles, I
was obliged to assent to his proposal of haulting for a few minutes,
which he employed in sharing a quantity of about two drachms of opium
between himself and his jaded horse. The effect of the dose was soon
evident on both, for the horse finished a journey of forty miles with
great apparent facility, and the rider absolutely became more active and
intelligent.”[1706]

By repeating small doses frequently, the stimulus may be kept up for a
considerable time in some people. In this way are produced the
remarkable effects said to be experienced by opium-eaters in the east.
These effects seem to be in the first instance stimulant, the
imagination being rendered brilliant, the passions exalted, and the
muscular force increased; and this state endures for a considerable time
before the usual stage of collapse supervenes. A very poetical, but I
believe also a faithful, picture of the phenomena now alluded to is
given in the Confessions of an English Opium-eater,—a work well known to
be founded on the personal experience of the writer. It is singular that
our profession should have observed these phenomena so little, as to be
accused by him of having wholly misrepresented the action of the most
common drug in medical practice. In reply to this charge the physician
may simply observe, that he seldom administers opium in the way
practised by the opium-eater; that when given in the usual therapeutic
mode it rarely causes material excitement; that some professional people
prefer giving it in frequent small doses, with the view of procuring its
sedative effect, and undoubtedly do succeed in attaining their object;
that in both of these medicinal ways of administering it, excitement is
occasionally produced to a great degree and of a disagreeable kind; that
the latter phenomena have been clearly traced to idiosyncrasy; and
therefore that the effects on opium-eaters are probably owing either to
the same cause, or to the modifying power of habit. This much at all
events is certain,—that in persons unaccustomed to opium it seldom
produces material excitement in a single small dose, and does not always
cause continuous excitement when taken after the manner of the
opium-eater. The effect of a full medicinal dose of two or three grains
of solid opium, or forty or sixty grains of the tincture, is to produce
in general a transient excitement and fulness of the pulse, but in a
short time afterwards torpor and sleep, commonly succeeded in six,
eight, or ten hours by headache, nausea, and dry tongue.

The symptoms of poisoning with opium, administered at once in a
dangerous dose, begin with giddiness and stupor, generally without any
previous stimulus. The stupor rapidly increasing, the person soon
becomes motionless and insensible to external impressions; he breathes
slowly; generally lies still, with the eyes shut and the pupils
contracted; and the whole expression of the countenance is that of deep
and perfect repose. As the poisoning advances, the features become
ghastly, the pulse feeble and imperceptible, the muscles excessively
relaxed, and, unless assistance speedily arrive, death ensues. If
recovery take place, the sopor is succeeded by prolonged sleep, which
commonly ends in twenty-four or thirty-six hours, and is followed by
nausea, vomiting, giddiness, and loathing of food.

The period which elapses between the taking of the poison and the
commencement of the symptoms is various. A large quantity, taken in the
form of tincture, on an empty stomach, may begin to act in a few
minutes; but for obvious reasons it is not easy to learn the precise
fact as to this particular. Dr. Meyer, late medical inspector at Berlin,
has related a case of poisoning with six ounces of the saffron tincture
of opium, where the person was found in a hopeless state of coma in half
an hour,[1707] and M. Ollivier has described another instance of a man
who was found completely soporose at the same distance of time after
taking an ounce and a half of laudanum.[1708] In these cases, the
symptoms must have begun in ten or fifteen minutes at farthest. In a
case noticed by M. Desruelles the sopor was fairly formed in fifteen
minutes after two drachms of solid opium were taken.[1709] For the most
part, however, opium, taken in the solid form, does not begin to act for
half an hour or even almost a whole hour,—that period being required to
allow its poisonous principles to be separated and absorbed by the
bibulous vessels. It is singular that an interval of an hour was
remarked in a case where the largest quantity was taken which has yet
been recorded. The patient swallowed eight ounces of crude opium; but in
an hour her physician found her able to tell connectedly all she had
done; and she recovered.[1710] In some rare cases the sopor is put off
for a longer period: thus, in a case mentioned in Corvisart’s Journal,
there seems to have been no material stupor till considerably more than
an hour after the person took two ounces and a half of the tincture with
a drachm of the extract.[1711]

The result of almost universal observation, however, is, that in pure
poisoning with opium the commencement of the symptoms is not put off
much beyond an hour. Such being the fact, it is extremely difficult to
account for the following extraordinary case, which was communicated to
me by Dr. Heude, of the East India Company’s service. A man swallowed an
ounce and a half of laudanum, and in an hour half as much more, and then
lay down in bed. Some excitement followed, and also numbness of the arms
and legs. But he continued so sensible and lively seven hours after the
first dose was taken, that a medical gentleman, who saw him at that time
and got from him a confession of what he had done, very naturally did
not believe his story. It was not till at least the eighteenth hour that
stupor set in; but two hours later, when Dr. Heude first saw him, he
laboured under all the characteristic symptoms of poisoning with opium
in an aggravated degree. The stomach-pump brought away a fluid quite
free of the odour of opium. In seven hours more, under assiduous
treatment, after having been in an almost hopeless state of
insensibility, he had recovered so far as to be safely left in charge of
a friend; and eventually he got quite well. No particular cause could be
discovered for the long apparent suspension of the usual effects of
opium.

Although the symptoms are very rarely postponed beyond an hour in pure
poisoning with this substance, there is some reason for thinking that
the interval may be much longer, if at the time of taking the opium the
person be excited by intoxication from previously drinking spirits. Mr.
Shearmen has related a striking case of an habitual drunkard, who took
two ounces of laudanum while intoxicated to excitement with beer and
spirits, and had no material stupor for five hours, during which period
vomiting could not be induced. Five hours afterwards, he was found
insensible, and he eventually died under symptoms of poisoning with
opium.[1712]

The most remarkable symptom in the generality of cases of poisoning with
opium is the peculiar sopor. This state differs from coma, in as much as
the patient continues long capable of being roused. It may be difficult
to rouse him; but unless death is at hand, this may be commonly
accomplished by brisk agitation, tickling the nostrils, loud speaking,
or the injection of water into the ear. The state of restored
consciousness is always imperfect, and is speedily followed again by
lethargy when the exciting power is withheld.—It has been already
remarked, that the possibility of thus interrupting the lethargy caused
by opium is in general a good criterion for distinguishing the effects
of this poison from apoplexy and epilepsy.

It was observed, in describing the mode of action of opium, that
convulsions, although very frequently produced by it in animals, are
rarely caused in man. It is not easy to account for this difference.
Orfila has endeavoured to explain it, by supposing that convulsions are
produced only by very large doses; but there are many facts incompatible
with that supposition.

While convulsions are certainly not common in the human subject, yet
when they do occur they are sometimes violent. Tralles mentions that he
had himself several times seen convulsions excited in children by
moderate doses.[1713] The Journal Universel contains the case of a
soldier who took two drachms of solid opium, and died in six hours and a
half, after being affected with locked-jaw and dreadful spasms.[1714] A
case is related in the Medical and Physical Journal of a young man, who,
three hours after swallowing an ounce of laudanum, was found insensible,
with the mouth distorted, the jaws fixed, and the hands clenched; and
who, soon after the insensibility was lessened by proper remedies, was
seized with spasms of the back, neck, and extremities, so violent as to
resemble opisthotonos.[1715] Another good case of the kind is related by
Mr. M’Kechnie, where the voluntary muscles were violently convulsed in
frequent paroxysms, and affected in the intervals with subsultus, for
three hours before the sopor came on.[1716] Two instances of convulsions
alternating with sopor are shortly related by Dr. Bright.[1717] The
convulsions sometimes assume the form of permanent spasm, which may
affect the whole muscles of the body, as in a case related in
Corvisart’s Journal.[1718]—Another rare symptom of poisoning with opium
is delirium. It appears to occur occasionally along with convulsions, as
happened in Mr. M’Kechnie’s case, and in one related by M.
Ollivier.[1719]

The state of the pulse varies considerably. In an interesting case
described by Dr. Marcet it is mentioned that the pulse was 90, feeble
and irregular; and such appears to be its most common condition when the
dose has been so large as seriously to endanger life.[1720] Frequently,
however, it is much slower; and then it is rather full than feeble, just
as in apoplexy. In cases where convulsions occur, it is for the most
part hurried, and does not become slow till the coma becomes pure. In
Mr. M’Kechnie’s case the pulse was at first 126; but when the
convulsions ceased, and pure sopor supervened, it fell to 55. It always
becomes towards the close very feeble, and at length imperceptible.

The respiration is almost always slow. In Dr. Marcet’s case, as in some
others, it was stertorous; but this is not common. On the contrary, it
is more frequently soft and gentle, as it has been in all the cases I
have witnessed; and sometimes it can hardly be perceived at all, even in
persons who eventually recover, as in an instance of recovery recorded
by Dr. Kinnis.[1721]

The pupils are always at least sluggish in their contractions, often
quite insensible;—sometimes, it is said, dilated:[1722] but much more
commonly contracted, and occasionally to an extreme degree. In the case
last noticed, they were no bigger than a pin’s head. The pupils have
been so invariably found contracted in all recent cases of poisoning
with opium, that some doubt arises whether they are ever otherwise, and
whether the earlier accounts, which represent them to have been dilated,
may not be incorrect, and the result of hasty observation.

The expression of the countenance is for the most part remarkably
placid, like that of a person in sound natural sleep. Occasionally there
is an expression of anxiety mingled with the stupor. The face is
commonly pale. Sometimes, however, it is flushed;[1723] and in rare
cases the expression is furious.[1724]

In moderately large doses opium generally suspends the excretion of
urine and fæces; but it promotes perspiration. In dangerous cases the
lethargy is sometimes accompanied with copious sweating. In a fatal
case, which I examined judicially, the sheets were completely soaked to
a considerable distance around the body.

A remarkable circumstance, which has been noticed by a late author, is
the sudden death of leeches applied to the body. The patient was a child
who had been poisoned by too strong an injection of poppy-heads.[1725]

In some instances the symptoms proper to poisoning with opium become
complicated with those which belong rather to organic affections of the
brain, in consequence of such affections being suddenly developed
through means of the cerebral congestion occasioned by the poison. Thus,
in a case related in Corvisart’s Journal, there were convulsions and
somnolency on the third day, and palsy of one arm for four days; and for
nearly two months afterwards the patient complained of occasional
attacks of weakness and numbness, sometimes of one extremity, sometimes
of another.[1726] Here the brain must have sustained some more permanent
injury than usual.—A more remarkable illustration once occurred to Dr.
Elliotson. A young man, seven hours after swallowing two ounces of
laudanum, presented the usual effects of opium, such as contracted
pupils, redness of the features, a frequent feeble pulse, coldness of
the integuments, and stupor, from which he could be roused without
particular difficulty. The stomach-pump brought away a fluid which had
not any odour of opium; powerful stimulants were given, such as ether,
ammonia and brandy; and he was kept constantly walking between two men.
In an hour and a half, when sensibility had been materially restored,
his head suddenly dropped down upon his breast, and he fell down dead.
The sinuses and veins of the brain were turgid, and a moderately thick
layer of blood was effused over the arachnoid membrane.[1727]—Under the
same head must be arranged the following extraordinary case related by
Pyl. That author admits it as one of simple poisoning, with a complete
remission of the symptoms for several days. But the possibility of such
a remission must be received with great hesitation. It is well known
that most of the symptoms may be dispelled by vigorous treatment, and
the patient nevertheless relapse immediately if left to himself, and
even die. This is acknowledged on all hands. Pyl, however, admits the
possibility of a much more complete and longer interval. His case is
shortly as follows. A man who had taken a large quantity of opium, and
became very dangerously ill, was made to vomit in twelve hours, and
regained his senses completely. The bowels continued obstinately
costive; but he had for some days no other symptom referrible to the
poison; when at length the whole body became gradually palsied and
stiff, and he died on the tenth day. No importance can be attached to a
solitary case differing so widely from every other. The only way in
which opium could cause death in such a manner, must be by calling forth
some disposition to natural disease. Pyl’s case was probably one of
supervening _ramollissement_, or inflammation of the substance of the
brain.[1728]

Notwithstanding the purely narcotic or nervous symptoms, which opium
produces in a vast proportion of instances, there is no doubt that it
also excites in a few rare cases those of irritation. Thus, although it
generally constipates the bowels, it has been known to induce diarrhœa
or colic in particular constitutions. In the first volume of the Medical
Communications, it is observed by Michaëlis that both diarrhœa and
diuresis may be produced by it. The soldier, whose case was quoted as
having been accompanied with convulsions, had acute pain in the stomach
for some time after swallowing the poison; and in the case just quoted
from Corvisart’s Journal, the accession of somnolency was attended with
excruciating pain of two days’ duration.

Another and more singular anomaly is the spontaneous occurrence of
vomiting. Sometimes a little vomiting immediately succeeds the taking of
the poison. This may not interrupt, however, the progress of the
symptoms;[1729] but more commonly it is the means of saving the person’s
life, as in a striking case described by Petit of an English
officer,[1730] who, in consequence of vomiting immediately after taking
two ounces of laudanum, had only moderate somnolency. At other times
vomiting occurs at a much later period. Pyl, in his Essays and
Observations, gives a case in which, some hours after thirty grains were
swallowed, vomiting took place spontaneously, and recurred frequently
afterwards; in the same paper is an account of another case by the
individual himself, who attempted to commit suicide by taking a large
dose of laudanum, but was disappointed in consequence of the poison
being spontaneously vomited after the sopor had fairly set in;[1731] and
a similar case is related by M. Mascarel, where, after seven ounces of
Sydenham’s laudanum had been taken, vomiting occurred spontaneously, and
was followed only by inconsiderable stupor.[1732]—Vomiting is a common
enough symptom after the administration of emetics, or subsequent to the
departure of the somnolency.[1733]

The _ordinary duration_ of a fatal case of poisoning with opium is from
seven to twelve hours. Most people recover who outlive twelve hours. At
the same time fatal cases of longer duration are on record: Réaumur
mentions one which proved fatal in fifteen hours,[1734] Orfila another
fatal in seventeen hours,[1735] Leroux another fatal in the same
time,[1736] Alibert another fatal in nearly twenty-four hours.[1737] An
instance has even been related, which appeared to prove fatal not till
towards the close of the third day;[1738] but the whole course of the
symptoms was in that case so unusual, that some other cause must have
co-operated in occasioning death. Sometimes, too, death takes place in a
shorter time than seven hours; six hours is not an uncommon duration; I
once met with a judicial case, which could not have lasted above five
hours; an infirmary patient of my colleague, Dr. Home, died in four
hours; in the 31st volume of the Medical and Physical Journal, there is
one which proved fatal in three hours.[1739] This is the shortest I have
read of.

The dose of opium requisite to cause death has not been determined.
Indeed it must vary so much with circumstances, that it is almost vain
to attempt to fix it. Pyl relates a case, quickly fatal, where the
quantity taken was 60 grains;[1740] Lassus an instance of death from 36
grains;[1741] Wildberg has related a fatal case caused by little more
than half an ounce of the Berlin tincture,[1742] which contains the
soluble matter of forty grains; and Mr. Skae has mentioned a case fatal
in about thirteen hours, where the dose seems to have been well
ascertained not to have exceeded half an ounce of common laudanum, or
about twenty grains of opium.[1743] Dr. Paris, without quoting any
particular fact, says four grains may prove fatal.[1744] I should have
felt some difficulty in admitting this statement, as I have repeatedly
known persons, unaccustomed to opium, take three or four grains without
any other effect than sound sleep. But I have been favoured with the
particulars of a case by Mr. W. Brown of this city, where a dose of four
grains and a half, taken by an adult along with nine grains of camphor,
was followed by the usual signs of narcotism, and death in nine hours.
The man took the opium for a cough at seven in the morning; at nine his
wife found him in a deep sleep, from which she could not rouse him;
nothing was done for his relief till three in the afternoon, when Mr.
Brown found him labouring under all the usual symptoms of poisoning with
opium, contracted pupils among the rest; and death ensued in an hour,
notwithstanding the active employment of remedies. On examining the body
no morbid appearance was found of any note except fluidity of the
blood,—a common appearance in those who have died of the effects of this
drug.

It is more important than may at first sight be imagined to acquire an
approximative knowledge of the smallest fatal dose. For, in consequence
of the dread entertained of opium by many unprofessional persons, it is
currently believed to be much more active than it is in reality; and
instances of natural death have been consequently imputed to medicinal
doses taken fortuitously a short time before. The facts stated above
comprehend the only precise information I have been able to collect as
to the smallest fatal doses in adults. I may add some farther
observations, however, on the smallest fatal doses in children. Very
young children are often peculiarly sensible to the poisonous action of
opium, so that it is scarcely possible to use the most insignificant
doses with safety. Sundeling states in general terms that extremely
small doses are very dangerous to infants on account of the rapidity of
absorption. This opinion is amply supported by the following cases.—An
infant three days old got by mistake about the fourth part of a mixture
containing ten drops of laudanum. No medical man was called for eleven
hours. At that time there was great somnolency and feebleness, but the
child could be roused. The breathing being very slow, artificial
respiration was resorted to, but without advantage: the child died in
twenty-four hours, the character of the symptoms remaining unchanged to
the last. At the inspection of the body, which I witnessed, no morbid
appearance was found.—Of the same kind was a case communicated to me by
Dr. Simson of this city, where the administration of three drops of
laudanum in a chalk mixture, for diarrhœa, to a stout child fourteen
months old, was followed by coma, convulsions, and death in about six
hours. Dr. Simson satisfied himself, as far as that was possible, that
the apothecary who made up the mixture did not commit a mistake.—Dr.
Kelso of Lisburn met with a similar case in an infant of nine months,
who died in nine hours after taking four drops.[1745]—My colleague, Dr.
Alison, tells me he has met with a case where an infant a few weeks old
died with all the symptoms of poisoning with opium after receiving four
drops of laudanum, and that he has repeatedly seen unpleasant deep sleep
induced by only two drops.—These remarks being kept in view, it will, I
suspect, be difficult to go along with an opinion against poisoning
expressed by a German medico-legal physician in the following
circumstances. A child’s maid, pursuant to a common but dangerous custom
among nurses, gave a healthy infant, four weeks old, an anodyne draught
to quiet its screams. The infant soon fell fast asleep, but died
comatose in twelve hours. There was not any appearance of note in the
dead body; and the child was therefore universally thought to have been
killed by the draught. But the inspecting physician declared that to be
impossible, as the draught contained only an eighth of a grain of opium
and as much hyoscyamus.[1746] In the first edition of this work an
opinion was expressed to the same purport. But the facts stated above
throw doubt on its accuracy, and rather show that the dose was
sufficient in the circumstances to occasion death.

A very important circumstance to attend to in respect to the dose of
opium required to prove fatal is the influence of constitutional
circumstances in rendering this drug unusually energetic. In some
persons this peculiar anomaly exists always, even during a state of
health. Thus, I am acquainted with a gentleman on whom seven drops of
laudanum act with great certainty as a hypnotic. In such a one doses,
which are safely taken by many, might prove dangerous.

It is more usual, however, to meet with this anomaly in the course of
some diseases. These have not yet been satisfactorily indicated. I have
several times, however, met with unusually energetic action from
medicinal doses in elderly persons affected with severe habitual
catarrh; and in one instance death occurred after a dose of twenty-five
drops in the advanced stage of acute catarrh supervening on its chronic
form, the symptoms being those of poisoning with opium, succeeding
apparently a state of comfortable sleep.—A case seemingly of the same
nature, where the dose was fifteen drops of Battley’s Sedative Liquor,
occurred at Islington in 1841. An elderly lady, in delicate health, and
affected severely with asthma, which for ten days prevented her from
sleeping, got from a neighbouring druggist a draught of Battley’s
solution, syrup, and camphor-mixture. Next morning she was found
insensible and livid in the face, with cold extremities and contracted
pupils; and she died about twelve hours after taking the draught. There
was no sign of natural disease in the dead body to account for death.
The druggist was absurdly blamed for giving such a dose to a frail old
lady; for the dose was not more than would be generally given in such
circumstances. This case was communicated to me by the druggist in
question.—Another of the like kind has been communicated to me by Mr.
Garstang of Clitheroe. An elderly female, long subject to severe cough,
having enjoyed a comfortable night’s rest after a dose of a preparation
containing half a grain of opium, took in the morning the equivalent of
two grains and a half, or three grains at the utmost, and fell asleep
soon after. In no long time, her husband, alarmed because he could not
rouse her, sent for Mr. Garstang, who found her husband labouring under
all the symptoms of poisoning with opium; and, notwithstanding active
treatment, she died six hours after the second dose. Her husband took
half a grain with her the evening before, but experienced no effect from
it at all. Not the slightest ground could exist in this case for
suspecting either foul play or pharmaceutic error.—As a farther
illustration, the following incident deserves notice, which occurred
last year in London, and was communicated to me by Dr. G. Johnson, a
former pupil. A little girl, five years and a half old, affected with
violent cough, got a mixture containing opium, which was repeated six,
thirteen, and twenty-six hours afterwards. She slept soundly after each
dose, and awoke readily after the first three; but after the fourth she
had more stupor and much uneasiness; in which state, but with at least
one interval of sensibility, she died in nine hours more, or thirty-five
hours after the first dose. According to the prescriber’s intention, the
child ought to have taken only two minims of laudanum in all; but,
according to a rough analysis by Mr. Alfred Taylor, each dose contained
an eighth of a grain of opium, or a trifle more. In either view it is
impossible that doses so small, and so distant, could produce these
effects in ordinary circumstances.

Such cases are important in several respects, but especially because
they naturally give rise to suspicions of an over-dose of opium having
been incautiously given, and thus to misrepresentations injurious to the
druggist or medical attendant. In the last case a Coroner’s Jury brought
in the preposterous verdict, that death was caused by “too much opium
ordered without due instructions.”

It is scarcely necessary to add, that the dose required to prove fatal
is very much altered by habit. Those who have been accustomed to eat
opium are obliged gradually to increase the dose, otherwise its usual
effects are not produced. Some extraordinary, but I believe correct
information on this subject, is contained in the confessions of an
English opium-eater. The author took at one time 8000 drops daily, or
about nine ounces of laudanum.

An important topic relative to the effects of opium on man is its
operation on the body when used continuously in the manner practised by
opium-eaters. This subject was brought forcibly under my notice in 1831,
in consequence of a remarkable civil trial, in which I was concerned as
a medical witness,—that of Sir W. Forbes and company against the
Edinburgh Life Assurance Company. The late Earl of Mar effected
insurances on his life to a large amount while addicted to the vice of
opium-eating; which was not made known at the time to the insurance
company. He died two years afterwards of jaundice and dropsy. The
company refused payment, on the ground that his lordship had concealed
from them a habit which tends to shorten life; and Sir W. Forbes and
company, who held the policy of insurance as security for money lent to
the earl, raised an action to recover payment.

In consequence of inquiries made on this occasion, I became for the
first time aware of the frequency of the vice of opium-eating among both
the lower orders and the upper ranks of society; and at the same time
satisfied myself, that the habit is often easily concealed from the most
intimate friends,—that physicians even in extensive practice seldom
become acquainted with such cases,—that the effects of the habit on the
constitution are not always what either professional persons or the
unprofessional would expect,—and generally that practitioners and
toxicologists possess little or no precise information on the matter. In
what is about to be offered on the subject, some facts will be stated
which appear to me interesting, and may induce others to contribute
their knowledge towards filling up so important a blank in medico-legal
toxicology.

The general impression is, that the practice of opium-eating injures the
health and shortens life. But the scientific physician in modern times
has seen so many proofs of the inaccuracy of popular impressions
relative to the operation of various agents on health and
longevity,[1747] that he will not allow himself to be hastily carried
along in the present instance by vague popular belief. The general
conviction of the tendency of opium-eating to shorten life has obviously
been derived in part from the injurious effects which opium used
medicinally has on the nervous system and functions of the alimentary
canal,—and partly on the reports of travellers in Turkey and Persia, who
have enjoyed opportunities of watching the life and habits of
opium-eaters on a great scale. The statements of travellers, however,
are so vague that they cannot be turned to use with any confidence in a
scientific inquiry. Chardin, one of the earliest (1671) and best of
modern travellers in Turkey, merely says the opium-eater becomes
rheumatic at fifty, and “never reaches an extreme old age;”[1748] and
his successors have seldom been more precise,—no one having given
information as to the diseases which it tends to engender. By far the
greater number of authorities, however, agree in representing the
practice to be hurtful. Mr. Madden, a recent and professional authority,
even alleges that it is very rare for an opium-eater at Constantinople
to outlive his thirtieth year, if he began the practice early. On the
other hand, a few late observers deny altogether the accuracy of these
statements. To this number belongs Dr. Burnes of the Bombay army; whose
opinion is worthy of notice, because he had ample opportunities of
observation during his residence in Cutch and at the Court of Sinde for
several years prior to 1831. From what he there witnessed, Dr. Burnes is
inclined to think “it will be found in general that the natives do not
suffer much from the use of opium,”—that “this powerful narcotic does
not seem to destroy the powers of the body, nor to enervate the mind to
the degree that might be imagined.”[1749] Dr. Macpherson of the Madras
army, who had occasion to observe the effects of the parallel practice
of opium-smoking in China, coincides in opinion with Dr. Burnes. He
says, “were we to be led away by the popular opinion that the habitual
use of opium injures the health and shortens life, we should expect to
find the Chinese a shrivelled, emaciated, idiotic race. On the contrary,
although the habit of smoking opium is universal among rich and poor, we
find them to be a powerful, muscular, and athletic people, and the lower
orders more intelligent and far superior in mental acquirements to those
of corresponding rank in our own country.”[1750]

The familiar effects of the medicinal use of opium in disordering the
nervous system and the digestive functions constitute a better reason,
than the loose statements of eastern travellers, for the popular
impression of the danger of its habitual and long-continued use. Yet
this consideration ought not to be allowed too much weight; because the
functions of the nervous system and of digestion may be deranged by
other causes, for example by hysteria, without necessarily and
materially shortening life. It is desirable therefore to appeal if
possible to precise facts.

The following is a summary of twenty-five cases, the particulars of
which I have obtained from various quarters. The general result rather
tends to throw doubt over the popular opinion.—1. A lady about thirty,
in good health, has taken it largely for twenty years, having been
gradually habituated to it from childhood by the villany of her maid,
who gave it frequently to keep her quiet. 2. A female who died of
consumption at the age of forty-two, had taken about a drachm of solid
opium for ten years, but had given up the practice for three years
before her death, and led in other respects a licentious life from an
early age. 3. A well-known literary author, about sixty years of age,
has taken laudanum for thirty-five years, with occasional short
intermissions, and sometimes an enormous quantity, but enjoys tolerable
bodily health. 4. A lady, after being in the practice of drinking
laudanum for at least twenty years, died at the age of fifty,—of what
disease I have been unable to learn. 5. A lady about fifty-five, who
enjoys good health, has taken opium many years, and at present uses
three ounces of laudanum daily. 6. A lady about sixty gave it up after
using it constantly for twenty years, during which she enjoyed good
health; and subsequently she resumed it. 7. Lord Mar after using
laudanum for thirty years, at times to the amount of two or three ounces
daily, died at the age of fifty-seven of jaundice and dropsy; but he was
a martyr to rheumatism, and besides lived rather freely. 8. A woman, who
had been in the practice of taking about two ounces of laudanum daily
for very many years, died at the age of sixty or upwards. 9. An eminent
literary character, who died about the age of sixty-three, was in the
practice of drinking laudanum to excess from the age of fifteen; and his
daily allowance was sometimes a quart of a mixture consisting of three
parts of laudanum and one of alcohol. 10. A lady, who died lately at the
age of seventy-six, took laudanum in the quantity of half an ounce daily
for nearly forty years. 11. An old woman died not long ago at Leith at
the age of eighty, who had taken about half an ounce of laudanum daily
for nearly forty years, and enjoyed tolerable health all the time. 12.
Visrajee, a celebrated Cutchee chief, mentioned by Dr. Burnes, had taken
opium largely all his life, and was alive when Dr. Burnes drew up his
Narrative, at the age of eighty, “paralyzed by years, but his mind
unimpaired.”[1751]

For the particulars of the remaining cases I am indebted to Dr. Tait,
surgeon of police in this city. 13. M. C., a ruddy, healthy-looking
woman, sixty years of age, has taken laudanum for twenty-five years to
the extent of half an ounce daily in a single dose. 14. M. H., a flabby,
dissipated-looking woman of thirty-six, has taken for ten years thirty
grains of opium daily in three doses. 15. M. T., a widow, forty-eight
years of age, who takes twice daily a dose of one fluidrachm of
laudanum, and has done so for fourteen years, cannot observe any
permanent injury except diminution of appetite. 16. Mrs. G., aged
twenty-four, has taken a single dose of sixty drops regularly at
bed-time for five years, and has not suffered in health in any respect,
except that she is costive. 17. F. S., a thin, sallow woman of forty-six
years of age, has taken a fluidrachm of laudanum three times a day for
ten years, cannot take food without it, but is so well as to be able to
get up regularly at six in the morning. 18. H. S., a shrivelled
old-looking woman, who for thirty-eight years had taken daily towards a
drachm of opium in one dose, and who latterly was strong, lively, and of
good appetite, died recently at the age of sixty-nine. 19. Mrs. S., who
has taken about a scruple of opium for twenty-one years, is a tall,
active, old-looking woman of fifty-seven, enjoys good health when she
uses the opium, but suffers from an affection like delirium tremens,
when she cannot get her usual quantity. 20. M. A., aged thirty-one, has
taken half a drachm of opium daily in two doses for ten years, was a
thin, drunken, starved-looking prostitute some years ago, but, having
reformed her ways, is now “a fine-looking, bouncing woman,” younger in
appearance than formerly, and not liable to any suffering either before
or after her doses, except that she cannot take food without them. 21.
Miss M., who has taken ten grains of opium three times a day for five
years, is a healthy, florid young woman of twenty-seven, liable to
costiveness, and, when without her opium, to languor and want of
appetite, but otherwise free of complaint. 22. Mrs. ——, a plump,
hale-looking old lady of seventy, has taken opium for six and twenty
years, and for some years to the extent of a drachm daily in two doses.
She thinks her health improved by it, and has suffered no inconvenience
except merely costiveness, and always aversion to food till she gets her
dose. 23. J. B., aged 23, has taken laudanum since she was fourteen, and
some time past to the amount of an ounce or ten drachms in three or four
doses daily. She has only menstruated twice since first using the
laudanum, has bilious vomiting once a month, and looks older than her
years, but is otherwise quite healthy, and has two children. 24. Mrs.
M’C., a ruddy young-looking woman of forty-two, has taken opium during
two years for cough and pain in the stomach, latterly to the extent of
ten grains twice a day. She has never menstruated since, but has enjoyed
better health, and in particular has a good appetite after her dose, and
has got entirely quit of a former tendency to constipation. 25. An army
officer’s widow, fifty-five years old, healthy and young-looking,
although subject to costiveness and rather defective appetite, has taken
laudanum for eleven years, and latterly opium to the extent of fifteen
grains morning and evening.

These facts tend on the whole rather to show, that the practice of
eating opium is not so injurious, and an opium eater’s life not so
uninsurable, as is commonly thought; and that an insured person, who did
not make known this habit, could scarcely be considered guilty of
concealment to the effect of voiding his insurance. But I am far from
thinking,—as several represent who have quoted this work,—that what has
now been stated can with justice be held to establish such important
inferences; for there is an obvious reason, why in an inquiry of this
kind those instances chiefly should come under notice where the
constitution has escaped injury, cases fatal in early life being more
apt to be lost sight of, or more likely to be concealed.

Meanwhile, insurance companies and insurance physicians ought to be
aware, that not a few persons in the upper ranks of life are confirmed
opium-eaters without even their intimate friends knowing it. And the
reason is, that at the time the opium-eater is visible to his friends,
namely, during the period of excitement, there is frequently nothing in
his behaviour or appearance to attract particular attention. From the
information I have received, it appears that the British opium-eater is
by no means subject to the extraordinary excitement of mind and body
described by travellers as the effect of opium-eating in Turkey and
Persia; but that the common effect merely is to remove torpor and
sluggishness, and make him in the eyes of his friends an active and
conversible man. The prevailing notions of the nature of the excitement
from eating opium are therefore very much exaggerated. Another singular
circumstance I have ascertained is, that constipation is by no means a
general effect of the continued use of opium. In some of the cases
mentioned above no laxatives have been required; and in others a gentle
laxative once a week is sufficient.

In the civil suit regarding Lord Mar’s insurances, the insurance company
was at first found not entitled to refuse payment,—not, however, on the
ground that the habit of opium-eating is harmless to longevity,—but
chiefly on a technical ground, implying that they did not make inquiry
into his habits with the care usually observed by insurance companies,
and were therefore to be understood as accepting the life at a venture.
A new trial was granted by the court on the ground of the judge’s charge
having been not according to evidence; but on this occasion the parties
compromised the case.[1752]

The previous remarks on the symptoms of poisoning with opium in man have
been confined to its effects when swallowed. But it was mentioned under
the head of its mode of action, that this poison has been known to act
with energy upon animals through every channel by which it can be
introduced into the system. It is natural to expect that the same will
be the case with man also.

The only other modes in which poisoning with opium is reported to have
been produced in man, besides administration by the mouth, have been by
injections into the anus, by application to the skin deprived of its
cuticle, perhaps even also to the unbroken skin, and by its introduction
into the external opening of the ear.

In the Journal de Chimie Médicale, an instance is shortly noticed of a
lady who was poisoned by the administration of too strong an anodyne
injection prepared by herself from fresh poppy-heads. She
recovered.[1753]

It is generally believed in France that opium acts more energetically
through the medium of the rectum, than through the stomach. Orfila in
particular has endeavoured to establish this proposition by experiments
on animals, and quotations from cases recorded by some authors of its
action upon man.[1754] But neither the experiments nor the quotations
appear to me satisfactory; and the rule they go to support is completely
at variance with the practice pursued in the medicinal administration of
the drug in Britain. It is the custom to give at least twice as much in
an enema as in a draught. I have given by injection, without producing
more than the usual somnolency, one drachm and even two drachms by
measure of laudanum, a dose which, were Orfila’s statement correct,
would prove fatal.

As to the action of opium through the skin when deprived of its
cuticle, I am not acquainted with any fatal case of the kind, but have
no doubt that such may happen. One of my friends very nearly lost his
life in the way alluded to. He had applied an opium-poultice to the
scrotum to allay the violent irritation caused by a blister, and fell
into a state of profound sopor, which was luckily interrupted by a
visitor, so that the cause was discovered before it was too late. An
instance of the same kind has also been published by M. Pelletan. A
child two months old very nearly perished, in consequence of a cerate
containing fifteen drops of laudanum having been kept for twenty-four
hours on a slight excoriation produced by a fold of the skin. When the
cause of illness was discovered, the child had been for some hours
almost completely insensible, with a slow, obscure pulse, and
occasional convulsions.[1755]

But perhaps opium may in some circumstances act even through the
unbroken skin. It has certainly been often applied in this way to
relieve local pain without avail. Yet on the other hand its effect is at
times unequivocal; and the following incidents seem to show, that it may
even prove fatal, both when the skin is healthy, and in certain diseased
states of the integuments. A young dramatic writer in Paris was directed
by his father, a physician, to apply over the stomach a poultice
moistened with a few drops of laudanum. The patient, in order to relieve
his pain more quickly, poured the whole contents of the bottle over the
poultice, and soon fell into a deep sleep. Prompt assistance was
obtained, but proved of no avail, and death is said to have ensued with
great rapidity.[1756] A soldier affected with erysipelas of the leg, had
a linseed poultice applied, which his surgeon ordered to be sprinkled
with 15 drops of laudanum. Next morning the patient was found in a state
of deep sopor, accompanied with convulsive twitches of the muscles of
the face and limbs; and in no long time he expired. His soporose state
turned the surgeon’s attention to the poultice, which he found coloured
yellow and smelling strongly of opium; and on removing it he discovered
that it was completely soaked with laudanum, which the attendant had
carelessly poured on it to the extent of an ounce. The patient died
notwithstanding all the remedies which his state called for; and the
viscera were found quite healthy; but in many places the blood is said
to have had a strong odour of opium.[1757]

In an instance reported by M. Tournon of Bordeaux, death is supposed to
have arisen from the introduction of opium into the external opening of
the ear, as a remedy for ear-ache. It is possible that fatal poisoning
may thus be induced by laudanum too freely and frequently renewed: but
it seems very unlikely that death was owing to opium in the instance in
question, since it was used in the solid form, and in the quantity of
four grains; so that the dose was small, and absorption must have been
very slow. The account merely states that the patient fell asleep, but
his sleep was that of death.[1758]


    _Of the Action of Morphia, Narcotine, Codeïa, and Meconic Acid._

The action and symptoms caused by two active principles of opium,
morphia, and narcotine, have been examined by many experimentalists.

The action of _morphia_ is nearly the same as that of opium, but more
energetic. In its solid state it has little effect, being nearly
insoluble. But when dissolved in olive oil, or in alcohol, or in weak
acids, it excites in animals the same symptoms as opium.
Experimentalists are not yet agreed as to its power. The trial of
Castaing gave rise to a physiological inquiry by three French
physicians, Deguise, Dupuy, and Leuret, who assigned to it feeble
properties; but more reliance is usually placed in the experiments of
Orfila, who found that one part of morphia is equal in energy to two
parts of the watery extract, and to four parts of crude opium. The
observations I have made on the medicinal effects of morphia and its
muriate, lead me to believe that half a grain is fully equal in power to
three grains of the best Turkey-opium. Probably those who have observed
but slight effects from it have accidentally used narcotine instead of
it; for at one time they were often confounded together.

On man morphia acts like opium; it produces somnolency. It was at one
time thought that in medicinal doses it does not produce either the
disagreeable subsequent or idiosyncratic effects of opium; Magendie made
some observations to this purport;[1759] and Dr. Quadri of Naples was
led to the same conclusion.[1760] Others, however, have doubted the
accuracy of these authors, and opposite results appear to have been
procured by some. My own experience with the muriate of morphia inclines
me to concur in opinion with Magendie and Quadri.

The effects of morphia on man in fatal doses have hitherto been observed
in a few cases only. An instance, which was the occasion of a criminal
trial at Aberdeen in 1842, has been communicated to me by Dr. Traill,
who was consulted in the case on the part of the crown. A schoolmaster
gave ten grains of the muriate to a girl immediately after she came out
of an epileptic fit. In fifteen minutes she seemed to fall asleep; she
continued in this state for some hours before it was discovered that she
was in a state of stupor, from which she could not be roused; and she
expired twelve hours after the poison was administered. A similar case
occasioned by ten grains, and also fatal, occurred at Cheltenham in
1839.

Orfila relates the particulars of the case of a young Parisian graduate,
who swallowed twenty-two grains for the purpose of self-destruction. In
ten minutes he felt heat in the stomach and hindhead, with excessive
itchiness; in three hours and a half he had also a sense of pricking in
the eyes, with dimness of vision; and in an hour more he for the first
time felt approaching stupor. Half an hour afterwards, when the people
of the house entered his room he could not see them, though he was
sensible enough to be able to reply to their inquiries, that he lay in
bed because he had not slept the night before. Soon after this he fell
into a state of profound stupor and lost all consciousness. In thirteen
hours he was visited by Orfila, who found him cold, quite comatose, and
affected with locked-jaw; the pupils were feebly dilated, the pulse 120,
the breathing hurried and stertorous, the belly tense and tympanitic;
and there were occasional convulsions, with intense itching of the skin.
By means of copious venesection, sinapisms, ammoniated friction,
stimulant clysters, ice on the head, and acidulous drinks, he was
gradually roused, so that in six hours he recognised his physician. In
the subsequent night and following day he had difficult and scanty
micturition, with pain in the kidneys and bladder, and difficulty in
swallowing; but these symptoms went off during the second night; and on
the third morning he was quite well.[1761] The itching of the skin
remarked in this case is considered by M. Bally an invariable symptom of
the operation of morphia even in medicinal doses.[1762] It is not,
however, always produced.

Another case, which occurred at Lunéville, is very remarkable in its
circumstances. A young man addicted to opium-eating, but who had left
off the practice for a twelvemonth, took first ten grains, and in ten
minutes forty grains more of acetate of morphia. In five minutes he had
excessive general feebleness and a sense of impending dissolution, which
forced him to confess what he had done. In fifteen minutes more M.
Castara, who describes the particulars, found him motionless, almost
comatose, and breathing laboriously. The limbs were flaccid, the pupils
contracted, the face and lips livid, the skin warm and moist, the pulse
full and hard, and deglutition impossible. Tartar-emetic was ordered,
but could not be administered. He was then bled at the arm to eighteen
ounces; upon which he started as from sleep, rubbed his eyes, said every
thing turned round him, and that he could not see the people present.
When left to himself he quickly fell into a calm slumber; but if kept
awake, he told collectedly all that happened before he became comatose.
He complained chiefly of intense itching and a general sense of
bruising. In an hour, by keeping him constantly roused, consciousness
was almost restored, and this without vomiting having been produced,
though two grains of tartar-emetic had been swallowed and three
administered by the rectum. In four hours after he swallowed the poison
he vomited freely and had diarrhœa. He then steadily recovered, the
sleepiness continued all next day, and the itching of the skin even
longer.[1763]

M. Julia-Fontenelle met with a case of poisoning with this alkaloid, in
consequence of its having been administered with a clyster in the form
of sulphate. The subject was a child five years old, the dose five
grains, the symptoms those of apoplexy, and death supervened within
twenty-four hours.[1764]

Another case worthy of particular mention is that of the French
gentleman who was supposed to have been poisoned by Dr. Castaing. It is
not a pure one, for besides the symptoms of a consumptive complaint
under which he had laboured for some time, there were circumstances in
his last illness which indicated the administration of other deleterious
substances. About thirty-six hours before his death, however, they were
exactly such as might be expected from a large dose of morphia. About
five minutes after the administration of a draught by the prisoner, the
gentleman was attacked with convulsions, and not long afterwards his
physician found him quite insensible, unable to swallow, bathed in a
cold sweat, with a small pulse, a burning skin, the jaws locked, the
neck rigid, the belly tense, and the limbs affected with spasmodic
convulsions. In this state he seems to have continued till his death.
The only appearances found in the dead body, which bore any relation to
the poison suspected, were congestion of blood and serous effusion in
the vessels of the cerebral membranes. If morphia was the cause of
death, it is highly probable that, besides what was administered
thirty-six hours before he died, several doses were given subsequently;
otherwise, from what is known of the action of opium, the narcotism
could scarcely have lasted uninterruptedly for so long a period.[1765]

For the following extraordinary case I am indebted to one of my pupils,
Mr. Clark of Montrose: A woman took one morning by mistake ten grains of
pure muriate of morphia, which had been prepared not long before by Mr.
Clark in my laboratory, and was freed of codeïa. The mistake having been
discovered almost immediately, means were taken to prevent any ill
effects from the accident, and within half an hour after the poison was
swallowed, the stomach was completely cleared by the stomach-pump. At
this time she was quite sensible. But stupor quickly came on after the
poison was evacuated, and deep imperturbable coma gradually formed, so
that nothing could rouse her in the slightest degree except cold
affusion of the head and chest, which caused faint signs of returning
consciousness. Before night she expired, though all the usual remedies
were resorted to. An inspection of the body was not obtained, which is
much to be regretted, since without it the case is quite obscure. I do
not know a single instance of fatal coma from opium where the proper
remedies were resorted to before the stupor commenced; and death in such
circumstances is so inconceivable, that we must ascribe the result in
this case to apoplexy, either incidentally concurring, or brought on by
the operation of the poison.

Morphia, like opium, may occasion serous effects when too freely applied
to a blistered surface. In a case related by M. Dupont, four-tenths of a
grain of acetate of morphia, applied to a blister on the side, caused in
twenty minutes dimness of vision, vomiting, and delirium; and though it
was then removed, the patient had afterwards continued vomiting, dilated
pupils, and great feebleness of the pulse. Recovery took place, but the
patient was not quite free of incoherence next day.[1766] The dose here
was so small, and the symptoms were so unlike the usual effects of
morphia, that doubts arise whether the case was really one of poisoning.

The effects of _narcotine_ have been examined experimentally by Magendie
and Orfila; but their results do not coincide. According to Orfila it is
not easy to poison dogs with it, as it excites vomiting and is
discharged. But when the gullet is tied, the animal dies in two, three
or four days, without any remarkable symptom but languor and hard
breathing.[1767] In these experiments it was dissolved in olive oil; it
does not act at all in the solid state. Magendie found that it produces
in dogs a state like reverie, accompanied with convulsions. They lie
still except when convulsed, and they are apparently asleep or dreaming;
but they are really alive to external objects, and even in a state of
acute irritability. In short, he considers the symptoms to constitute an
aggravated form of the subsequent and idiosyncratic effects caused by
opium on man. Vinegar, he says, destroys altogether the poisonous
properties of narcotine. According to Orfila it only weakens them.
Muriatic acid would seem to annihilate them entirely; for Orfila found
no effect in dogs from forty grains dissolved in water with the aid of
muriatic acid; and Bally gave sixty grains in like manner to a patient
without injury.[1768] Forty grains dissolved by sulphuric acid, proved
fatal to a dog in twenty-four hours.[1769]

Narcotine, like other narcotic poisons, is more powerful when introduced
at once into the blood, but produces nearly the same effects as when it
is swallowed. Orfila found that a single grain was as powerful through
the former, as eight grains through the latter channel.[1770]
Dieffenbach observed that half a grain dissolved in water by means of a
drop or two of hydrochloric acid killed cats in five minutes when
injected into a vein, and always produced congestion within the head,
and extravasation on the surface of the cerebellum. A remarkable
circumstance observed in the course of his experiments was, that
leeches, applied to a rabbit under the influence of narcotine, died
immediately in convulsions; and that a portion of the blood of the same
rabbit when injected into the vein of another produced drowsiness,
languor, and pandiculation for nearly a day.[1771]

The effects of narcotine on man have not been much inquired into. From
the only researches on the subject I have yet seen, those of Dr. Wibmer
of Munich, it appears to be but a feeble poison. He found by experiment
on himself, that two grains dissolved in olive oil produced merely
slight transient headache; that eight grains dissolved by means of
muriatic acid had no effect at all; and that the same quantity of solid
narcotine occasioned temporary headache, and in twenty-eight hours a
singular state of excitement, with trembling of the hands, restlessness,
and inability to fix the thoughts on any object. These effects went off
in a few hours.[1772]

The effects of _codeïa_ have been examined by Dr. Kunkel. He found that
twelve grains, dissolved in water and introduced into the stomach,
killed a rabbit in three minutes; that six grains in solution when
injected into the cellular tissue occasioned death in little more than
two hours; that the same quantity administered by the mouth sometimes
had little effect; that when given in powder its action was very feeble;
and that the symptoms were excitement of the pulse, convulsions, and
tetanus, without any tendency to sopor or somnolency.[1773] Hence codeïa
is conceived to be a stimulant of the nervous system, and consequently
the cause of the excitant effects sometimes produced by opium. It may be
doubted, however, whether its proportion in opium is sufficient for
explaining these effects.

_Meconic acid_ is inert. Sertuerner, indeed, thought the meconate of
soda acted as a powerful poison in some experiments made on himself and
on dogs; but more careful researches have since proved that he was
misled by some error. Sömmering found that ten grains of meconic acid or
meconate of soda had no effect whatever on dogs.[1774] Subsequently, in
consequence of two people having died suddenly at Turin after taking
each a grain of the acid, some careful experiments were made by Drs.
Feneglio and Blengini, who gave eight grains to dogs, crows, and frogs,
and four grains to various men, without remarking any injurious effects
whatever.[1775]

The _distilled water_ of opium was formerly considered an active poison;
but Orfila found it nearly or altogether inert. Two pounds introduced
into the stomach of a dog, and two ounces and a half injected into a
vein, had no effect whatever.[1776]


       SECTION III.—_Of the Morbid Appearances caused by Opium._

In discussing this subject the appearances in the best marked cases will
be first noticed; and then some account; will be given of the variations
to which they are liable.

In Knape’s Annals there is a good example of the most aggravated state
of the appearances left by opium. It is the case of an infant who was
killed in the course of a night by a decoction of poppy-heads. There was
much lividity over the whole back part of the body. All the sinuses and
vessels of the brain were gorged with fluid blood; and a good deal of
serosity was found in the ventricles and base of the skull. The pharynx
was red. The lungs were distended, and so gorged with fluid blood, that
it ran out in a stream when they were cut. The cavities of the heart
contained the same fluid blood. There was some redness in the villous
coat of the stomach and intestines; and poppy-seeds were found in the
stomach. Although the body had been kept only two days in the month of
February, the belly emitted a putrid odour when it was laid open.[1777]

In commenting upon these appearances, it may be first remarked, that
turgescence of the vessels in the brain, and watery effusion into the
ventricles, and on the surface of the brain, are generally met with. Dr.
Bright mentions an instance where unusual turgescence was found, and on
the surface of the brain a spot of slight ecchymosis as big as a crown
piece.[1778] I have seen turgescence of vessels and serous effusion in
one instance to a considerable extent: each ventricle contained three
drachms of fluid, the arachnoid membrane on the surface of the brain was
much infiltered, and the vessels both in the substance and on the
surface of the brain were considerably gorged with blood. But congestion
and effusion are by no means universal: in a case I examined judicially
in November, 1822, which proved fatal in about seven hours, there was
neither unusual congestion nor effusion. In the remarks on the diseased
appearances caused by the narcotics generally, it was observed that
extravasation of blood is a very rare effect of opium. A good example of
the kind, however, is related by Mr. Jewel of London. It was the case of
a young married female, who died eight hours after taking two ounces of
laudanum. Several clots were found in the substance of the brain, one of
which, in the anterior right lobe, was an inch long.[1779] A similar
case, which occurred to Dr. Elliotson, has been mentioned already at p.
546. There is little doubt that poisoning with opium may cause
extravasation, by developing a disposition to apoplexy; but considering
the very great rarity of this appearance in persons killed by opium, it
may reasonably be questioned whether extravasation can be produced
without some predisposition co-operating.

The lungs are sometimes found gorged with blood, as in many cases of
apoplexy. They were so in the soldier mentioned in the Journal
Universel, who died in convulsions. They were in the same state in a
patient of Dr. Home, a man who died in the Infirmary here in 1825, four
hours after taking two ounces of laudanum in six ounces of whisky; and
likewise in the case quoted from Pyl, in which sixty grains of solid
opium were taken. But this appearance is not more constant than
congestion in the brain. Orfila never found it in dogs, and in three
cases I have examined the lungs were perfectly natural. Perhaps they are
more usually turgid when death is preceded by convulsions. They were
particularly so in the case of the soldier above mentioned, and likewise
in another case of the same nature recorded in Rust’s Magazin.[1780]

The stomach, as in Knape’s case, is occasionally red, and in the woman
mentioned by Lassus, who died after swallowing thirty-six grains, it is
said to have been inflamed. But even redness is rare, and decided
inflammation probably never occurs. In four cases I have examined, the
villous coat was quite healthy; and it was equally so in another related
in Knape and Hecker’s Register.[1781]

Lividity of the skin is almost always present more or less, and
sometimes it is excessive. In one of the cases I examined it was
universal over the depending surface of the body.

It has been said that the blood is always fluid. This certainly appears
to be very generally the case. For example, the blood was fluid in the
case of the soldier who died in convulsions, in Dr. Home’s patient, in
four adults I have examined, in Dr. Traill’s case of death from morphia,
and likewise in Pyl’s case. But at the same time this condition of the
blood is not invariable: In the case related in Knape and Hecker’s
Register, it was coagulated in the left cavities of the heart; in
another related by Petit in Corvisart’s Journal, there were clots in
both ventricles;[1782] and in the case of the first infant mentioned in
page 549, clots were also found in both ventricles. In Alibert’s case a
large fibrinous concretion was found in the heart, clearly showing that
the blood had coagulated after death as usual.

It appears that the body is often apt to pass rapidly into putrefaction.
In one of the cases I examined, although the body had been kept only
thirty hours in a cool place in the month of December, the cuticle was
easily peeled off, the joints were flaccid, and an acid smell was
exhaled. In Réaumur’s case, that of a young man who died in fifteen
hours, in consequence of his companions in a drunken frolic having mixed
a drachm of opium in his wine, the body soon became covered with large
blue stains, and gave out an insupportable odour. A French physician has
related in the Journal de Médecine a still more pointed case of a lady
who died seven hours after taking a large quantity of laudanum by
mistake, and whose body was so far gone in putrefaction fourteen hours
after death, that the dissection could not be delayed any longer. The
hair and cuticle separated on the slightest friction, and the stomach,
intestines, and large vessels were distended with air.[1783]

It is doubtful whether this is a constant appearance or not. In one case
I examined, the body was free from putrefaction forty-eight hours after
death.

Although opium is generally believed to suspend all the secretions and
excretions but the sweat, instances have been met with where a great
collection of urine was found in the bladder after death. In a paper on
the signs of death by opium, in Augustin’s Repertorium, it is stated
that Welper of Berlin always found the bladder full of urine, and the
kidneys gorged with blood, both in man and animals.[1784] I am not
prepared to say how far this is a common condition, as the state of the
urinary organs is seldom noticed in published cases.

In the examination of the dead body unequivocal evidence will sometimes
be procured by the discovery of a portion of the poison in the stomach.
But it must not always be concluded that opium has not been swallowed,
because the sense of smell, chemical analysis, and experiments on
animals fail to detect it. For, as previously remarked, the opium may
not remain in the stomach after death, though a large quantity was
swallowed, and not vomited. This may arise from two causes. It may be
all absorbed, as will often happen when it has been taken in the liquid
form: or it may be partly absorbed and partly decomposed by the process
of digestion. But in one or other of these ways it may certainly
disappear, and that in a very few hours only. Several instances to this
effect have been already mentioned (pp. 57, 537). These remarks are
important, because the fact is generally believed to be the reverse. Dr.
Paris, in his work on Medical Jurisprudence, has tended to propagate the
misconception, by asserting that in all fatal cases opium may be
detected in the stomach;[1785] and in the last edition of his
Toxicology, Orfila has overrated the facility and frequency with which
an analysis may be conducted successfully. [See p. 538.]

At the same time there is no doubt that the poison may sometimes be
found in the stomach. In Knape and Hecker’s Register there is the case
of a girl who died about eight hours after taking half an ounce of
laudanum; and the reporters found that an extract prepared from the
contents of the stomach caused deep sleep in frogs, chickens, and dogs,
and threw some of them into a comatose state, which proved fatal.[1786]
Wildberg has related a very interesting case of a young lady of Berlin,
who had been seduced, and finding herself pregnant, swallowed about half
an ounce of laudanum in the evening, and died during the night. In this
instance the contents of the stomach had a narcotic odour, and their
extract when given to a young dog caused excessive sleep, reeling, palsy
of the legs, convulsions, and death.[1787]

M. Petit has related another case fatal in about ten hours, where the
contents of the stomach had the smell of opium; and their alcoholic
extract had a bitter taste, and killed guinea-pigs, with symptoms of
narcotism.[1788] In a case related by Mayer in Rust’s Magazin, which
also proved fatal after an interval of ten hours, the poison, which in
this instance was the saffron-tincture, was distinctly detected in the
stomach by a strong odour of opium and saffron.[1789] In a case where
the patient lived between thirteen and fourteen hours, that of the
individual for whose murder Stewart and his wife were executed at
Edinburgh, Dr. Ure succeeded in detecting meconic acid in the contents
of the stomach, which had been removed by the pump about three hours
after the opium was swallowed.[1790] In another case published by Mr.
Skae of this city, where death was caused by half an ounce in thirteen
hours, without any attempt having been made to evacuate the stomach, the
contents of that organ, treated according to the process at p. 534,
yielded evident indications of morphia, and obscure evidence of meconic
acid.[1791] Lastly, it may be added that in Dr. Traill’s case of
poisoning with ten grains of muriate of morphia, when the contents of
the stomach were decomposed by magnesia, a solution was obtained from
the precipitate by rectified spirit, which, when concentrated, had the
strong bitter taste of morphia, and became yellow with nitric acid; and
yet the individual survived no less than twelve hours.

An important fact, ascertained by MM. Orfila and Lesueur, is that
neither opium nor the salts of morphia undergo decomposition by being
long in contact with decaying animal matter. Even after many months they
may be discovered; at least the putrefaction of the matter with which
they are mingled does not add any impediment in the way of their
discovery. It is only necessary to observe that the alkaloid may be
rendered insoluble by the evolution of ammonia, which separates it from
its state of combination.[1792]


        SECTION IV.—_Of the Treatment of Poisoning with Opium._

The treatment of poisoning with opium, owing partly to the numerous
cases that have been published, and partly to the experiments of Orfila
on the supposed antidotes,—is now well understood.

The primary object is to remove the poison from the stomach. This is
proper even in the rare cases in which vomiting occurs spontaneously. It
is by no means easy to remove all the opium by vomiting, especially if
it was taken in the solid state; for it becomes so intimately mixed with
the lining mucus of the villous coat, that it is never thoroughly
removed till the mucus is also removed, which is always effected with
difficulty.

The removal of the poison is to be accomplished in one of three ways, by
emetics administered in the usual manner, by the stomach-pump, or by the
injection of emetics into the veins.

By far the best emetic is the _sulphate of zinc_ in the dose of half a
drachm or two scruples, which may be repeated after a short interval, if
the first dose fails to act. In order to insure its action it is of
great use to keep the patient roused as much as possible,—a point which
is often forgotten.—The _sulphate of copper_ has been used by some as an
emetic; but it is not so certain as the sulphate of zinc. Besides, as it
is a much more virulent poison, it may prove injurious, if retained long
in the stomach. In Dr. Marcet’s case the patient, after recovering from
the lethargic symptoms, suffered much from pain in the throat and
stomach, occasioned probably by the sulphate of copper which he took
remaining some time undischarged. _Tartar emetic_, from the uncertainty
of its action when given in considerable doses, is even worse adapted
for such cases. This is illustrated by a case in the seventh volume of
the Medical and Surgical Journal, the same which has already been
referred to as exemplifying the occasional occurrence of convulsions and
delirium in poisoning with opium. A scruple of tartar emetic was
administered to cause vomiting, but to no purpose. When it had remained
fifteen minutes, sulphate of zinc was also given, and with immediate
effect. But the patient, after recovering from the sopor, was attacked
with pains in the stomach and bowels, and with tenesmus, which lasted
several days.

Emetics should be preferred for evacuating the stomach, provided the
case be not urgent. Even then, however, they sometimes fail
altogether. The best practice in that case is to endeavour to remove
the poison with the stomach-pump; and this in urgent cases should be
the first remedy employed. The treatment by the stomach-pump has now
become so generally known, that it is unnecessary to describe it
particularly. It was recommended in this country by the late Dr. Monro
in his lectures; but does not appear to have been tried by him. In
1803 it was first published by Renault in his treatise on the
counter-poisons of arsenic; and he had tried it on animals.[1793] But
the first person who used it in an actual case of poisoning with opium
was Dr. Physick of Philadelphia. He saved the life of a child with it
in 1812; and not long afterwards his countryman, Dr. Dorsey, cured two
other individuals.[1794] More lately it was again proposed in London
by Mr. Jukes, who does not appear to have been acquainted with these
prior trials and experiments. Although he cannot be considered in the
light of a discoverer, the profession is much indebted to him for
having recalled their attention to this treatment, and for having by
his success and activity fairly established its reputation. An account
will be seen of his apparatus and of several cases in the Medical and
Physical Journal for September and November, 1822. In using the
stomach-pump care must be taken not to injure the stomach by too
forcible suction.—When it is not at hand, Mr. Bryce of this city
recommended the substitution of a long tube with a bladder attached.
After the stomach has been filled with warm water from the bladder,
the tube is to be turned down so as to act upon the contents of the
stomach as a syphon. Dr. Alison cured a patient in this way.[1795]

Another method of removing opium from the stomach, which has been
practised successfully where the patient could not be made to submit to
the common treatment, is the injection of tartar-emetic into the rectum.
A case is related by Dr. Roe of New York where this treatment proved
successful. Fifteen grains in half a gallon of water excited free
vomiting, and ten grains more renewed it. Care was taken to insure the
discharge of the whole tartar-emetic by a subsequent purgative
injection.[1796]

The last method for removing opium from the stomach is a desperate one,
which can only be recommended when emetics by the mouth have utterly
failed, and when a stomach-pump or Mr. Bryce’s substitute, cannot be
procured. It is the injection of an emetic into the veins. Tartar-emetic
answers best for this purpose, and its effect is almost certain. A grain
is the dose. While injecting it, care must be taken by the operator not
to introduce air into the vein.

The next object in conducting the treatment of poisoning with opium is
to keep the patient constantly roused. This alone is sufficient when the
dose is not large, and the poison has been discharged by vomiting; and
in every case it forms, next to the evacuation of the stomach, the most
important of the treatment.

The best method of keeping the patient roused is to drag him up and down
between two men, who must be cautioned against yielding to his
importunate entreaties and occasional struggles to get free and rest
himself. For the sopor returns so rapidly, that I have known a patient
answer two or three short questions quite correctly on being allowed to
stand still, and suddenly drop the head in a state of insensibility
while standing. The duration of the exercise should vary according to
circumstances from three, to six, or twelve hours. When he is allowed at
length to take out his sleep, the attendants must ascertain that it is
safe to do so by rousing him from time to time; and if this should
become difficult, he must be turned out of bed again and exercised as
before.

It appears from some cases published not long ago by Mr. Wray[1797] and
Dr. Copland,[1798] and more lately also by Dr. Bright,[1799] that the
most insensible may be roused to a state of almost complete
consciousness for a short time, by dashing cold water over the head and
breast. This treatment can never supersede the use of emetics: and as
its effect is but temporary, it ought not to supersede the plan of
forced exercise. But it appears to be an excellent way to insure the
operation of emetics. If the emetic is about to fail in its effect, cold
water dashed over the head restores the patient for a few moments to
sensibility, during the continuance of which the emetic operates.
Dashing cold water over the head may perhaps be dangerous in the
advanced stage, when the body is cold and the breathing imperceptible;
but the most desperate remedies may be then tried, as the patient is
generally in almost a hopeless state. In one of the cases mentioned by
Dr. Bright from the experience of Mr. Walne, complete recovery was
accomplished, mainly by cold affusion of the head, where there appeared
reason to believe that more than an ounce and a half of laudanum had
disappeared from the stomach before evacuating remedies were used.—This
treatment seems to have been first proposed in 1767 by a German
physician, Dr. Gräter.[1800] A suggestion, which is probably an
improvement, has been recently made by Dr. Boisragon of Cheltenham, to
alternate the use of cold with that of warm water, applied to children
in the shape of warm bath, and to adults in the form of warm-sponging
and the foot-bath. The alternating impression of heat and cold may act
better as a stimulant than either agent singly; and the occasional
employment of heat prevents the risk of collapse from too continuous
exposure to cold. Dr. Boisragon saved in this way two cases in very
unpromising circumstances.[1801]

In some cases internal stimulants have been given with advantage, such
as assafœtida, ammonia, camphor, musk, &c. It is always useful to
stimulate the nostrils from time to time, by tickling them or holding
ammonia under the nose; but the application should be neither frequent
nor long continued, as the ammonia may cause deleterious effects when
too freely inhaled. Pulling the hair and injecting water into the ears
are also powerful modes of rousing the patient.

Venesection has been recommended and successfully used by some
physicians. If the stomach be emptied, and the patient kept roused, as
may almost always be done when means are resorted to in time,
venesection will be unnecessary. Sometimes, however, when the pulse is
full and strong, it may be prudent to withdraw blood; and it certainly
appears that in most cases where this remedy has been employed the
sensibility began to return almost immediately after. This is very well
shown in a case of poisoning with opium related by Mr. Ross[1802] in the
Edinburgh Medical Journal, in another described in the same journal by
Mr. Richardson,[1803] and also in two cases of poisoning with acetate of
morphia mentioned in a former page. Sometimes, on the contrary, it has
seemed injurious, probably because it was not had recourse to till the
patient was moribund. It is a sound general rule that blood-letting
ought not to be resorted to until the poison is thoroughly removed from
the stomach; for it favours absorption. And yet facts are not wanting to
show that this rule, now generally admitted since the researches of
Magendie on absorption, is not infallible. Dr. Young of the United
States has given the particulars of a case where imperturbable coma was
formed, together with puffing stertorous respiration, in consequence of
an ounce of laudanum having been swallowed,—and where recovery took
place, without the poison having been removed at all, simply under the
employment of three blood-lettings to the amount of twenty-eight ounces
altogether, of cold to the head, and of sinapisms to the legs.[1804]

Galvanism has been sometimes resorted to, but seldom with decided
advantage. I saw it tried, with dubious utility, a few years ago in an
urgent case which was treated in the Edinburgh Infirmary. Six ounces of
laudanum had been swallowed, but most of it was removed in
three-quarters of an hour by the stomach-pump. A stage of deep sopor
followed, after which sensibility was restored, and maintained for four
hours by forced exercise. A state of pure and extreme coma then ensued,
during which galvanism was for some time of great service, in rousing
the patient. Gradually, however, it ceased to have any effect of the
kind. Recovery took place eventually under the use of external and
internal stimuli. Mr. Erichsen of the University-College Hospital,
London, has related a case, in which electro-magnetism was of undoubted
service. The usual symptoms had been occasioned by an ounce of laudanum.
The poison had been withdrawn by the stomach-pump, when unavailing
attempts were made to restore sensibility by means of various
stimulants. At length several electro-magnetic shocks were passed from
the forehead to the upper part of the spine, with the effect of speedily
eliciting signs of consciousness; in twenty minutes the patient could
answer questions and walk a little; and eventually complete recovery
took place.[1805]

In desperate circumstances artificial respiration may be used with
propriety. After the breathing has been almost or entirely suspended the
heart continues to beat for some time; and so long as its contractions
continue, there is some hope that life may be preserved. But it is
essential for the continuance of the heart’s action, that the breathing
be speedily restored to a state of much greater perfection than that
which attends the close of poisoning with opium. It is not improbable
that the only ultimate cause of death from opium is suspension of the
respiration, and that if it could be maintained artificially so as to
resemble exactly natural breathing, the poison in the blood would be at
length decomposed and consciousness gradually restored. The following is
an interesting example by Mr. Whately, in which artificial respiration
proved successful. A middle-aged man swallowed half an ounce of crude
opium and soon became lethargic. He was roused from this state by
appropriate remedies, and his surgeon left him. But the poison not
having been sufficiently discharged, he fell again into a state of
stupor; and when the surgeon returned, he found the face pale, cold and
deadly, the lips black, the eyelids motionless, so as to remain in any
position in which they were placed, the pulse very small and irregular,
and the respiration quite extinct. The chest was immediately inflated by
artificial means, and when this had been persevered in for seven
minutes, expiration became accompanied with a croak, which gradually
increased in strength till natural breathing was established. Emetics
were then given, and the patient eventually recovered.[1806]—Dr. Ware of
Boston (U. S.) has more lately described another case, where artificial
respiration was employed with marked advantage, and would probably have
saved the patient’s life in very unfavourable circumstances, but for the
disease on account of which the opium was given.[1807]—Another has been
lately described by Mr. C. J. Smith of Madras. The patient was not seen
for four hours, and received no benefit from the ordinary remedies
during the next hour and a half. Artificial respiration was then
resorted to and maintained for nearly five hours with an hour of
interval; and this measure certainly seems to have brought the case to a
favourable termination under most unpromising circumstances.[1808]—Dr.
Watson of Glasgow has mentioned to me the particulars of an instructive
base in the person of an infant three weeks old, in whom, after the
breathing had stopped and the heart had nearly ceased to beat, the
occasional inflation of the chest with the breath at intervals of two or
three minutes restored for a time the action both of the heart and
lungs, and eventually accomplished recovery. On physiological principles
it appears probable, that this simple mode of procedure may prove more
frequently successful than might at first be thought.

It would be a fruitless task to examine into the merits of the numerous
antidotes which have from time to time been proposed for poisoning with
opium. Professor Orfila has examined many of them with great care, such
as vinegar, tartaric acid, lemonade, infusion of coffee, decoction of
galls, solution of chlorine, camphor, diluents; and he has found them
all useless before the poison is expelled from the stomach, with the
single exception of decoction of galls. As he remarked that this fluid
throws down the active principles of an infusion of opium, and
subsequently found that such a mixture acts more feebly on the animal
system than the opiate infusion itself, he thinks the decoction of galls
may with propriety be used as an imperfect antidote, till the poison can
be evacuated from the stomach.[1809] His experiments, however, do not
assign to it very material activity as a remedy; and certainly the whole
efforts of the physician ought in the first instance to be directed to
the removal of the opium, and to keeping the patient roused. When the
opium has been completely removed, the vegetable acids and infusion of
coffee have been found useful in reviving the patient, and subsequently
in subduing sickness, vomiting, and headache; but till the poison is
completely removed the administration of acids is worse than useless,
provided the opium was given in the solid state, because its solution in
the juices of the stomach is accelerated. It has been maintained that
iodine, chlorine, and bromine are all antidotes for poisoning with the
vegetable alkaloids.[1810] Some notice will be taken of this statement
in the chapter on Nux Vomica. It has also been lately alleged in the
United States that opium has no effect when given with acetate of lead;
and an hospital case is reported as having occurred at New York, where
the poison was swallowed in this way to the extent of thirty grains,
without any injurious effect.[1811] There must have been some mistake
here, however. When given with acetate of lead in medicinal doses, opium
exerts its usual sedative and anodyne action; and indeed there is no
chemical or physiological reason why it should not do so.




                            CHAPTER XXVIII.
          OF POISONING WITH HYOSCYAMUS, LACTUCA, AND SOLANUM.


_Of Poisoning with Hyoscyamus._—Of the narcotic poisons none bears so
close a resemblance to opium in its properties as the _hyoscyamus_ or
henbane. Several species are poisonous; but the only one that has been
examined with care is the _H. niger_, from which the extract of the
apothecary is prepared.

The hyoscyamus has been analyzed by various chemists, and found to
contain a peculiar alkaloid, in which the properties of the plant are
concentrated. It is named hyoscyamia. This substance in its pure state,
as first obtained by MM. Geiger and Hesse, is a solid body, in fine
silky crystals, without odour, of a strong acrid taste like tobacco,
partially volatilizable with boiling water, entirely volatilizable alone
at a somewhat higher heat, very soluble in alcohol and ether, but
sparingly so in water.[1812]

Farther, hyoscyamus, like many other narcotic vegetables, stramonium,
digitalis, opium, tobacco, and hemlock, has been found by Mr. Morries
Stirling to yield by destructive distillation an empyreumatic oil of
great activity. Its poisonous properties, however, are not essential to
the oil, but reside in a volatile principle which may be detached by
weak acetic acid. The relation of this principle to hyoscyamia has not
been ascertained; but it is an active poison, small doses producing in
rabbits, convulsions, coma, and speedy death.[1813]

Runge proposes as evidence of poisoning with hyoscyamus, in common,
however, with stramonium and belladonna, to concentrate a solution of
the contents of the stomach, and apply it to a cat’s eye to dilate the
pupil. Dilatation, he says, was even produced by an extract obtained
from the urine of a rabbit which had been fed some time on
hyoscyamus.[1814]

According to the experiments of Professor Orfila, the juice or extract
procured from the leaves, stems, and especially the root, produces in
animals a state of sopor much purer than that caused by opium. It is
most active when injected into the jugular vein, less so when applied to
the cellular tissue, and still less when introduced into the stomach.
Except occasional paralysis of the heart, indicated by florid blood in
its left cavities, no morbid appearance is to be found in the dead body.
Six drachms of the pharmaceutic extract of the leaves killed a dog in
two hours and a quarter when swallowed; and three drachms killed another
in four hours through a wound in the back. Its action appears to be
exerted through the medium of the blood-vessels, and is purely
narcotic.[1815]

It is probable that the activity of this plant is much affected by
season; and the energy of its preparations varies greatly with the
manner of obtaining them. The information, however, which is at present
possessed on these two points is vague, because the influence of the two
circumstances has seldom been viewed carefully apart.

The leaves, from which the pharmaceutic preparations of hyoscyamus are
obtained, are commonly held to be most active during the inflorescence
of the plant in the second summer of its existence. On general
principles this appears probable; but there are no satisfactory
experiments on the subject, even the late researches of Mr. Houlton
having left much still to be determined.[1816]

Orfila has made some important remarks as to the effect of season and
vegetation on the energy of the root as a poison. The root he maintains
is the most active part of the plant; but in the spring it is nearly
inert. Thus the juice of three pounds of the root collected near the end
of April, when the plant has hardly begun to shoot, killed a dog in
somewhat less than two days; while a decoction of an ounce and a half
collected on the last day of June, when the plant was in full
vegetation, proved fatal in two hours and a half.

The extract of the leaves, procured from different shops, was found by
Orfila to vary greatly in point of strength, some samples being
absolutely inert.[1817] The causes of these differences have been
ascertained experimentally by Brandes to be, that the herb loses its
active principle in part by decomposition in the process of simple
desiccation, and also when long kept; and that the greater part is also
similarly decomposed in preparing an extract, unless the process be
finished quickly, and at a low heat.

The seeds of hyoscyamus are poisonous, as well as the leaves and root.
Indeed the whole plant is so. The seeds contain much more hyoscyamia
than the leaves.

The effects of hyoscyamus on man differ somewhat from those on animals,
and vary greatly with the dose.

In medicinal doses it commonly induces pleasant sleep. This indeed has
been denied by M. Fouquier, who infers from his experiments that it
never causes sleep, but always headache, delirium, nausea, vomiting, and
feverishness.[1818] I have certainly seen it sometimes have these
effects; but much more generally it has acted as a pleasant hypnotic and
anodyne.

Its effect in large doses have been well described by M. Choquet as they
occurred in two soldiers who ate by mistake the young shoots dressed
with olive oil. They presently became giddy and stupid, lost their
speech, and had a dull, haggard look. The pupils were excessively
dilated, and the eyes so insensible that the eyelids did not wink when
the cornea was touched. The pulse was small and intermitting, the
breathing difficult, the jaw locked, and the mouth distorted by _risus
sardonicus_. Sensibility was extinct, the limbs were cold and palsied,
the arms convulsed, and there was that singular union of delirium and
coma which is usually termed typhomania. One of the men soon vomited
freely under the influence of emetics, and in a short time got quite
well. The other vomited little. As the palsy and somnolency abated, the
delirium became extravagant, and the patient quite unmanageable till the
evening of the subsequent day, when the operation of brisk purgatives
restored him to his senses. In two days both were fit for duty.[1819]

In a treatise on vegetable poisons, Mr. Wilmer has related the history
of six persons in a family, who were poisoned by eating at dinner the
roots of the hyoscyamus by mistake instead of parsneps. Several were
delirious and danced about the room like maniacs, one appeared as if he
had got drunk, and a woman became profoundly and irrecoverably comatose.
Emetics could not be introduced into the stomach, stimulant clysters had
no effect, external stimuli of every kind failed to rouse her, and she
expired next morning at six.[1820] The roots in this instance were
gathered in the winter time,—a fact, which does not quite coincide with
the conclusions of Orfila, that the plant must be in full vegetation
before the energy of the root is considerable.

From these and other cases, the abstracts of which are to be seen in
Orfila’s Toxicology, or in Wibmer’s Treatise on the Operation of
Medicines and Poisons, it follows that hyoscyamus in a poisonous dose
causes loss of speech, dilatation of the pupil, coma, and delirium,
commonly of the unmanageable, sometimes of the furious kind. In general
a stage of delirium precedes coma; and sometimes as the coma passes off,
delirium returns for a time. It has been known to act powerfully in the
form of clyster.[1821] It has also been known to act with considerable
energy even through the sound skin, as appears from a case which
occurred to Wibmer. He was called to a lady affected with great stupor,
dilated pupils, flushed face, loss of speech, full hard pulse, and
swelling of the abdomen; and he found that these symptoms were owing to
several ounces of henbane leaves having been applied to the belly in a
poultice, on account of strangury and tympanitis. She was still capable
of being roused by speaking loudly close to her ear; and under proper
treatment she recovered.[1822]

Henbane seldom causes any distinct symptoms of irritant poisoning. In
several, however, of the cases related by the older modern authors some
pain in the belly, a little vomiting, and more rarely diarrhœa, appear
to have occurred.[1823] Plenck quotes, from a Swedish authority, an
instance of its having produced burning in the stomach, intense thirst,
watching, delirium, depraved vision, and next day a crowded eruption of
dark spots and vesicles, which disappeared on the supervention of a
profuse diarrhœa.[1824] The same author alludes to cases where it proved
fatal; but this event is rare in the present day, obviously because the
precursory stage of delirium gives an opportunity of removing the
poison, before the stage of coma is formed. A fatal case, which occurred
to Mr. Wibmer, has been mentioned above; and another has been related in
Pyl’s Magazin. Two boys a few minutes after eating the seeds were
attacked with convulsions and heat in the throat; and one of them, who
could not be made to vomit, died in the course of the ensuing
night.[1825]

The accidents it has occasioned have commonly arisen from the
individuals confounding the root with that of the wild chicory or with
the parsnep, the latter of which it somewhat resembles.

Of the other species of the hyoscyamus, the _H. albus_ has been known to
cause symptoms precisely the same with those above described. Professor
Foderé has given a good example of its effects on man, as they occurred
in the crew of a French corvette in the Archipelago. The plant was
boiled and distributed among the whole ship’s company, as several of the
sailors said they knew it to be eatable and salubrious. But in no long
time they were all seized with giddiness, vomiting, convulsions, colic,
purging, and delirium of the active kind. They were all soon relieved by
emetics and purgatives.[1826]

Dr. Archibald Hamilton has described a case of the same nature, which
was caused by the seeds of this plant. A young medical student, who took
about twenty-five grains of the seeds, was seized in half an hour with
lassitude and somnolency, and successively with dryness of the throat,
impeding deglutition, convulsive movements of the arms, incoherency,
total insensibility of the skin, and loss of recollection. These
symptoms continued about twelve hours, and then slowly receded.[1827]

Three other species, the _H. aureus_, _physaloides_ and _scopolia_ are
represented by Orfila to be equally deleterious.

The alkaloid hyoscyamus possesses in an intense degree the active
properties of the plant. It has not been hitherto examined in this
respect with much care. But extremely minute quantities produce
excessive enlargement of the pupil, when put within the eyelids in the
form of neutral salt.

_Treatment._—The treatment of poisoning with hyoscyamus consists in
removing the poison, diminishing cerebral congestion, and restoring
sensibility. It is therefore substantially the same as in poisoning with
opium, except that general or local evacuation of blood is more
frequently required, in consequence of the greater tendency of
hyoscyamus to induce determination of blood towards the head and
congestion there. It has been lately alleged by an Italian author that a
large dose of lemon-juice is an immediate antidote for the effects of
too large a medicinal dose, even when the poison was administered in the
form of injection.[1828] This does not seem probable.


                      _Of Poisoning with Lactuca._

Allied in its effects, but greatly inferior in power to opium and
hyoscyamus, is the _Lactuca virosa_, together with the _Lettuce-opium_,
or inspissated juice of _L. sativa_, and _L. virosa_.

Orfila found that three drachms of the extract of _L. virosa_ introduced
into the stomach of a dog killed it in two days, without causing any
remarkable symptom; that two drachms applied to a wound in the back
induced giddiness, slight sopor, and death in three days; and that
thirty-six grains injected in a state of solution into the jugular vein
caused dulness, weakness, slight convulsions, and death in eighteen
minutes.[1829] This poison, therefore, like other narcotics, acts
through absorption. But it is far from being energetic. The extract is
very uncertain in strength,—as may indeed be inferred from the variable
nature of the processes by which it is prepared.

Lactucarium, the inspissated juice, especially that obtained from _L.
virosa_, is obviously a more active preparation than the extract. Doses
of no great magnitude kill small animals. But there is a want of good
observations on its effects and energy as a poison.


                      _Of Poisoning with Solanum._

Different species of _solanum_, a genus of the same natural order with
the hyoscyamus, have been considered by Orfila to possess the same
properties, though in a much feebler degree. The _S. dulcamara_ or
bittersweet has been erroneously believed by some to possess distinct
narcotic properties.[1830] M. Dunal found that a dog might take 180 of
the berries or four ounces of the extract without any inconvenience, and
quotes an experiment on the human subject where thirty-two drachms of
extract were taken in two doses also without injury.[1831] If it has any
power at all, therefore, it must possess too little to be entitled to
the name of a poison. Chevallier says he knew an instance of a
druggist’s apprentice being attacked with deep somnolency for ten hours
after carrying a large bundle of it on his head;[1832] but some other
cause may be justly suspected to have here been in operation. The _S.
nigrum_ or common nightshade has been made the subject of experiment by
Orfila, who found its extract to possess nearly the power and energy of
lettuce-opium.[1833] The following seems a genuine case of poisoning
with the berries of this species. Three children near Nantes in France
were seized with severe headache, giddiness, colic, nausea, and
vomiting. One of them then had excessive dilatation of the pupils,
sweating and urgent thirst; loss of voice, stertorous breathing, and
tetanic spasms ensued; and in twelve hours he died. Another had swelling
of the face, alternate contraction and dilatation of the pupils,
repeated vomiting, and eventually coma; but he recovered. The third was
similarly, but more slightly affected, and also recovered. The children
who recovered pointed out the berries they had eaten; which were found
to be those of _S. nigrum_.[1834] The _S. fuscatum_ is rather more
active, fifteen berries having caused hurried breathing and
vomiting.[1835] The _S. mammosum_ is also probably an active species,
the capsule of the berries having been known to excite vomiting,
giddiness, and confusion of mind.[1836] In the _S. nigrum_ and
_dulcamara_, M. Desfosses discovered in 1821 a peculiar alkaloid, which
induces somnolency in animals, but is not a very active poison.[1837]

It has been supposed by some that the tubers of _Solanum tuberosum_, the
common potato, may acquire in certain circumstances poisonous qualities
of no mean energy. Dr. Kabler of Prague has described the cases of four
individuals in a family who were seized with alarming narcotic symptoms
after eating potatoes which had begun to germinate and shrivel. The
father of the family, who had eaten least of them all, appeared as if
tipsy, and soon became insensible. The mother and two children became
comatose and convulsed. All had vomited before becoming insensible. They
recovered under the use of ether, frictions, and coffee; and in two
hours were out of danger.[1838]

An alkaloid has been indicated by several chemists in various species of
solanum. The most recent account, that of Otto, represents it to be a
pearly, white, pulverulent substance, alkaline in reaction, and capable
of uniting with acids. One grain of sulphate of solania killed a rabbit
in six hours, and three grains a stronger rabbit in nine hours,—the
symptoms being those of narcotic poisoning.[1839]

Violent effects have often been assigned to the genus Solanum, in
consequence of its similarity to a powerful poison, the _Atropa
belladonna_; which indeed is described by the older authors under the
name of _Solanum furiosum_. It will be noticed among the Narcotico-acrid
Poisons.




                             CHAPTER XXIX.
                  OF POISONING WITH HYDROCYANIC ACID.


The poisons, whose energy depends on the presence of the prussic or
hydrocyanic acid, are of great interest to the physiologist as well as
the medical jurist. Some of them are natural productions, derived from
the leaves, bark, fruit-kernels, and roots of certain plants; others are
formed artificially by complex chemical processes. The species to be
here noticed are the _hydrocyanic acid_ itself, and the essential oils
and distilled waters of the _bitter almond_, _cherry-laurel_,
_peach-blossom_, _cluster-cherry_, _mountain-ash_, and _bitter cassava_.
These poisons have for some time attracted great attention on account of
their extraordinary power. And indeed in rapidity of action, or the
minuteness of the quantity in which they operate, no poison surpasses
and very few equal them. They are exceedingly interesting to the medical
jurist, because, as they are now generally known, their effects often
become the subject of medico-legal investigation: they have been
repeatedly taken by accident; they have often been resorted to for
committing suicide; and they have likewise been employed as the
instruments of murder. A remarkable instance occurred in England towards
the close of last century, where murder was committed with the
cherry-laurel water; and two cases have been tried in England where
death arose from hydrocyanic acid, and the prisoners were charged with
administering it, but were found not guilty. These cases will be noticed
presently.


                       _Of the Hydrocyanic Acid._
            SECTION I.—_Of its Chemical History and Tests._

This singular substance was discovered some time ago by Scheele; but
Gay-Lussac was the first who obtained it in a state of purity. It is
familiarly known to chemists under two forms,—as a pure acid, and
diluted with water.

The pure acid is liquid, limpid, and colourless. It has an acrid,
pungent taste, and a very peculiar odour, which, when diffused through
the air, has a very distant resemblance to that of bitter almonds, but
is accompanied with a peculiar impression of acridity on the nostrils
and back of the throat. It is an error, however, to suppose, as is very
generally done, that the odour is the same with that of the almond. It
boils at 80°; freezes at 5°; and is very inflammable. I have kept it
unchanged for a fortnight in ice-cold water; but at ordinary
temperatures it decomposes spontaneously, and becomes brown, sometimes
in an hour, and commonly within twelve hours. On this account it is
extremely improbable that a case will ever happen, in which the medical
jurist will have to examine it in its concentrated form.

When united with water it forms the acid discovered by Scheele, and now
kept in the druggist’s shop. In this state it has the same appearance,
taste, and smell as the pure acid; but it is less volatile, does not
burn, and may be preserved long without change, if excluded from the
light. In consequence of its volatility, however, it becomes weak,
unless kept with great care; many samples of it also undergo
decomposition, and deposit brown flakes, if not excluded from the light;
and hence the acid of the shops is very variable in point of strength.
The acid prepared by decomposing the solution of the ferro-cyanate of
potass by sulphuric acid may be kept for years, even exposed to diffuse
light, without being decomposed at all. A French physician made some
experiments not long ago on the uncertainty of the strength of the
medicinal acid; and he found that he could swallow a whole ounce of one
sample, and a drachm of a stronger sample, without sustaining any
injury; but on trying some which had been recently prepared by
Vauquelin, he was immediately taken ill, as will be related presently,
and narrowly escaped with his life.[1840]—The acid of commerce differs
much in strength, according to the process by which it has been
prepared, and independently of decomposition by keeping. The medicinal
acid long used in this country is intended to be an imitation of that of
Vauquelin, which contains 3·3 per cent.;[1841] but the London College of
Physicians, in adopting it in their last Pharmacopœia, improperly
altered the strength to 2 per cent. That of Giese, which keeps well, is
of the same strength as the first; that of Schrader contains only one
per cent.; that of Göbel 2·5 per cent.; that of Ittner 10 per
cent.;[1842] that of Robiquet 50 per cent.[1843] Of the alcoholic
solutions the best known are that of Schrader, which contains about 1·5
per cent. of pure acid,—that of the Bavarian Pharmacopœia, which
contains 4 per cent.,—that of Duflos, 9 per cent.,—that of Pfaff, 10 per
cent.,—and that of Keller, 25 per cent.[1842] These statements are
necessary for understanding the cases of poisoning published in foreign
works.

The tests for hydrocyanic acid has been examined by M. Lassaigne of
Paris, by Dr. Turner of London, and by Professor Orfila. They are its
odour, the salts of copper, the salts of iron, and nitrate of silver.

The _peculiar odour_ of the acid is a very characteristic and delicate
test of its presence. According to Orfila, the smell is perceptible when
no chemical reagent is delicate enough to detect it.[1844] But I doubt
the accuracy of this statement, and may farther observe, that I have
known some persons nearly insensible of any smell, even in a specimen
which was tolerably strong. Hence, when the odour is resorted to as a
test, it ought to be tried by several persons.

_Sulphate of copper_ forms with hydrocyanic acid, when rendered alkaline
with a little potass, a greenish precipitate, which becomes nearly
white, on the addition of a little hydrochloric acid. The purpose of the
hydrochloric acid is to redissolve some oxide of copper thrown down by
the potass. The precipitate is then the cyanide of copper. This test,
according to Lassaigne, will act on the poison when dissolved in 20,000
parts of water. But as the precipitate is not coloured, the test is an
insignificant one compared with the next.

If the acid be rendered alkaline by potass, the _salts of the mixed
peroxide and protoxide of iron_ produce a grayish-green precipitate,
which, on the addition of a little sulphuric acid, becomes of a deep
prussian blue colour. Common green vitriol answers very well for this
purpose. The salts of the peroxide of iron will also often answer,
because, unless carefully prepared, they are never altogether free of
protoxide. But the salts of the pure peroxide of iron have no such
effect. They cause with the potass a brownish precipitate, which is
redissolved on the addition of sulphuric acid, leaving the solution
limpid. Mr. Ilott of Bromley has pointed out to me, that the iron test
does not act on a weak solution of hydrocyanic acid, if there be an
excess of ammonia present, either such from the first, or disengaged by
potash from muriate of ammonia; that the blue precipitate is produced by
driving off the ammonia with heat; but not by neutralizing it with an
acid.

The _nitrate of silver_ is a delicate and characteristic reagent for
hydrocyanic acid. A white precipitate, the cyanide of silver, is
produced in a very diluted solution; and this precipitate is
distinguished from the other white salts of silver, by being insoluble
in nitric acid at ordinary temperatures, but soluble in that acid at its
boiling temperature. In this action it is necessary to observe that
something more is accomplished than simple solution; the cyanide is
decomposed, nitrate of silver is formed, and hydrocyanic acid is
disengaged by the ebullition. A more characteristic property is, that
the precipitate when dried and heated emits cyanogen gas; which is
easily known by the beautiful rose-red colour of its flame.[1845]

Sometimes it is necessary to determine the strength of diluted
hydrocyanic acid; because, on account of its tendency to decomposition,
doubts may be entertained whether a mixture which contains it is strong
enough to be dangerously poisonous. According to Orfila, the best method
of ascertaining the strength either of a pure solution or of a mixture
in syrup, is to throw down the acid with the nitrate of silver and dry
the precipitate; a hundred parts of which correspond to 20·33 of pure
hydrocyanic acid.

_Process for Mixed Fluids._—Some important observations have been made
by MM. Leuret and Lassaigne on the effect of mixing animal matters with
hydrocyanic acid. The most material of their results are, that if the
body of an animal poisoned with the acid is left unburied for three
days, the poison can no longer be detected; and that if it is buried
within twenty-four hours the poison may be found after a longer
interval, but never after eight days. The reason is either that the acid
volatilizes, or that it is decomposed. The possibility thus indicated of
detecting the poison in the body some days after death has been since
confirmed by actual examination in a medico-legal case. In a case of
poisoning with hydrocyanic acid, followed by dismemberment of the body
for the purpose of concealment, distinct proof of the presence of the
poison seven days after death was obtained by the second of the
succeeding processes, although the trunk of the body had never been
buried, but had been for some time lying in a drain.[1846]

For detecting the poison in mixed fluids Orfila has lately advised the
following process. The fluid may be treated with animal charcoal without
heat. The colour being thus generally destroyed, the test will sometimes
act as usual. Or, without this preparation, a slip of bibulous paper
moistened with pure potass, may be immersed in the suspected fluid for a
few minutes, and then touched with a solution of sulphate of iron: upon
which the usual blue colour will be produced on the paper. If neither of
these methods should answer, the fluid is to be distilled.[1847]

Distillation of the fluid is on the whole the best mode of procedure. It
was proposed some time before by Lassaigne and Leuret for detecting the
poison in the stomach after death. The steps of their process, which
appears to me the best yet proposed, are as follows. The contents after
filtration are to be neutralized with sulphuric acid if they are
alkaline, in order to fix the ammonia which may have been disengaged by
putrefaction; the product is then to be distilled from a vapour-bath
till an eighth part has passed over into the receiver; and the distilled
fluid is to be tested with the sulphate of iron in the usual way.[1848]
Orfila maintains that from hydrocyanized syrup only two-thirds of the
acid can be distilled over; and cautions the analyst against estimating
quantity by such means.[1849] M. Ossian Henry has proposed to condense
the acid in distillation by a much more complex process, which consists
in obtaining it in the first instance in the form of cyanide of
silver.[1850] But with a good refrigeratory there is no difficulty in
condensing every particle of acid with no other aid than cold water.

By this process Lassaigne could detect the poison in a cat or dog killed
by twelve drops and examined twenty-four or forty-eight hours after
death.[1851] But Dr. Schubarth has objected to it,—and the same
objection will apply to every process in which heat is used,—that
hydrocyanic acid may be formed during distillation by the decomposition
of animal matter.[1852] His objection, however, appears only to rest on
conjecture or presumption at farthest; and I doubt whether, supposing
the distillation to go on slowly in the vapour-bath, the heat is
sufficient to bring about the requisite decomposition. The force of the
objection must be decided by future researches.

It is worthy of remark that hydrocyanic acid is apt to be formed in the
course of the changes produced by various agents in organic matters.
These are probably more numerous than the toxicologist is at present
exactly aware of. An instance of its formation in the course of the
decay of unsound cheese has been ascertained lately by Dr.
Witling;[1853] and another example will be mentioned under the head of
spurred rye.

_Cyanide of Potassium._—The only compound of hydrocyanic acid which
requires notice is the cyanide of potassium. This is, when pure, a white
salt, bitter, not decomposable by a red heat unless in contact with air,
very soluble in water, and sparingly so in rectified spirit. Its watery
solution restores the blue of reddened litmus, and does not precipitate
lime-water: the mixed sulphates of the two oxides of iron form with it
Prussian blue: nitrate of silver causes a white precipitate insoluble in
cold nitric acid, but disappearing when the acid is boiled: sulphate of
copper causes an apple-green precipitate, which becomes white on the
addition of hydrochloric acid: chloride of platinum or perchloric acid
will indicate the potash. In a complex organic mixture it is difficult
to detect the potash; but hydrocyanic acid may be obtained from it by
distilling the suspected fluid with tartaric acid.[1854]


   SECTION II.—_Of the Action of Hydrocyanic Acid and the Symptoms it
                            excites in Man._

The effects of hydrocyanic acid on the animal system have been examined
by several physiologists. The best experiments with the concentrated
acid are those of M. Magendie; who says that, if a single drop be put
into the throat of a dog, the animal makes two or three deep hurried
respirations, and instantly drops down dead; that it causes death almost
as instantaneously when dropped under the eyelid; and that when it is
injected into the jugular vein, the animal drops down dead at the very
instant, as if struck with a cannon ball or with lightning.[1855]

On repeating these experiments in order to determine less figuratively
the shortest period which elapses before the poison begins to operate,
as well as the shortest time in which it proves fatal,—two points it
will presently be found important to know,—I remarked that a single
drop, weighing scarcely a third of a grain, dropped into the mouth of a
rabbit, killed it in eighty-three seconds, and began to act in
sixty-three seconds,—that three drops weighing four-fifths of a grain,
in like manner killed a strong cat in thirty seconds, and began to act
in ten,—that another was affected by the same dose in five and died in
forty seconds,—that four drops weighing a grain and a fifth did not
affect a rabbit for twenty seconds, but killed it in ten seconds
more,—and that twenty-five grains, corresponding with an ounce and a
half of medicinal acid, began to act on a rabbit as soon as it was
poured into its mouth, and killed it outright in ten seconds at
farthest. Three drops injected into the eye acted on a cat in twenty
seconds, and killed it in twenty more; and the same quantity dropped on
a fresh wound in the loins acted in forty-five and proved fatal in 105
seconds. Dr. A. T. Thomson says he has seen the concentrated acid kill a
strong dog in two seconds.[1856] Mr. Blake on the other hand alleges
that all the accounts which represent the action of the poison to begin
in less than ten seconds are exaggerated, because he could never find it
to act more quickly, even when thirty minims of concentrated acid were
injected at once into the femoral vein.[1857] But it is impossible that
any negative results can outweigh positive observations, especially when
made, as mine were, expressly with the view of ascertaining the shortest
interval. In the slower cases enumerated above there were regular fits
of violent tetanus; but in the very rapid cases the animals perished
just as the fit was ushered in with retraction of the head. In rabbits
opisthotonos, in cats emprosthotonos, was the chief tetanic symptom.—The
practical application of these experiments will appear presently.

Of all the forms in which the pure acid can be administered, that of
vapour appears the most instantaneous in operation. M. Robert found,
that when a bird, a rabbit, a cat, and two dogs were made to breathe air
saturated with its vapour, the first died in one second, the second also
in a single second, the cat in two, one dog in five, and the other dog
in ten seconds.[1858]

The effects of the diluted acid are the same when the dose is large, but
somewhat different when inferior doses are given. These effects have
been observed by many physiologists; but the most accurate and extensive
experiments are those of Emmert published in 1805,[1859] those of
Coullon in 1819,[1860] and those of Krimer in 1827.[1861] They found
that when an animal is poisoned with a dose not quite sufficient to
cause death, it is seized in one or two minutes with giddiness, weakness
and salivation, then with tetanic convulsions, and at last with
gradually increasing insensibility; that after lying in this state for
some time, the insensibility goes off rapidly and is succeeded by a few
attacks of convulsions and transient giddiness; and that the whole
duration of such cases of poisoning sometimes does not exceed half an
hour, but may extend to a whole day or more.—When the dose is somewhat
larger the animal perishes either in tetanic convulsions or comatose;
and death for the most part takes place between the second and fifteenth
minute. I have seen the diluted acid, however, prove fatal with a
rapidity scarcely surpassed by the pure poison. Thus in an experiment
with Vauquelin’s acid, made on a strong cat at the same time with the
second and third of the experiments with the pure acid detailed above, I
found that thirty-two grains, which contain one of real acid, began to
act in fifteen seconds, and proved fatal in twenty-five more. According
to Schubarth’s experiments death may be sometimes delayed for thirty-two
minutes;[1862] but if the animal survives that interval, it recovers. He
farther states, that during the course of the symptoms the breath
exhales an odour of hydrocyanic acid.[1863] Coullon once saw a dog die
after nineteen hours of suffering; but cases of this duration are
exceedingly rare.[1864] When the dose is very large Mr. Macaulay, as
will afterwards be mentioned (p. 590), has found death take place in a
few seconds, exactly as when the pure acid is given.

The body presents few morbid appearances of note. The brain is generally
natural. Yet occasionally its vessels are turgid; and Schubarth once
found even an extravasation of blood between its external membranes in
the horse.[1865] The heart and great vessels are distended with black
blood, which is commonly fluid, but occasionally coagulated as usual.
The lungs, according to Schubarth, are sometimes pale, but much more
generally injected and gorged with blood.[1866] The pure acid, according
to Magendie, exhausts the irritability of the heart and voluntary
muscles so completely, that they are insensible even to the stimulus of
galvanism.[1867] The diluted acid has not always this effect. In the
experiments of Coullon the heart and intestines contracted, and the
voluntary muscles continued contractile, after death as usual.[1868] So
too Mr. Blake remarked both by inspection of the body after death, and
by means of the hæmadynamometer during life, that, when the poison is
introduced directly into a vein, so as to prove fatal in forty-five
seconds, the contractions of the heart, though irregular, are not
materially impaired in energy.[1869] On the other hand Schubarth states
that the heart is never contractile, although the intestines and
voluntary muscles retain their contractility.[1870] The reason of these
discrepant statements is that, as I have had occasion to observe, a
considerable difference really prevails in experiments conducted under
circumstances apparently the same. In eight experiments on cats and
rabbits with the pure acid the heart contracted spontaneously, as well
as under stimuli, for some time after death, except in the instance of
the rabbit killed with twenty-five grains, and one of the cats killed by
three drops applied to the tongue. In the last two the pulsations of the
heart ceased with the short fit of tetanus which preceded death; and in
the rabbit, whose chest was laid open instantly after death, the heart
was gorged and its irritability utterly extinct. The later researches of
Dr. Lonsdale likewise show great varieties in the condition of the
heart; and he has been led to conclude that the diluted acid does not
perceptibly influence the heart, while the pure acid enfeebles it, if
introduced into the stomach, but arrests it, if injected into the
windpipe.[1871]

The experiments of Emmert, Coullon, and Krimer show that the diluted
acid acts most energetically through the serous membranes, and next upon
the stomach; that it also acts with energy on the cellular tissue; that
it has no effect when applied to the trunks or cut extremities of
nerves, or to a fissure made in the brain or spinal marrow; that its
action is prevented when the vessels of any part are tied before the
part is touched with the poison; that its action is not prevented by
previously dividing the nerves; and that it may sometimes be discovered
in the blood after death by chemical analysis,[1872] and frequently by
the smell when analysis cannot succeed in separating it.[1873] These
results favour the supposition that hydrocyanic acid acts through the
medium of the blood-vessels. But the extreme rapidity of its operation
in large doses is usually considered incompatible with an action through
the blood, or any other channel except direct conveyance along the
nerves. The tremendous rapidity of action indicated by the experiments
of Magendie, or of Mr. Macaulay (p. 543), of M. Robert, as well as in
some of those performed by myself,—certainly appears rather inconsistent
with the notion, that the acid must enter the blood-vessels before
producing its effects.

This acid acts on the brain and also on the spine independently of its
action on the brain. Its action on both is clearly indicated by the
combination of coma with tetanus. The independent action on the spine is
well shown by the following experiment of Wedemeyer. In a dog the spinal
cord was divided at the top of the loins, so that no movement took place
when the hind-legs were pricked: hydrocyanic acid being then introduced
into a wound in the left hind-leg, symptoms of poisoning commenced in
one minute, and the hind-legs were affected with convulsions as well as
the fore-legs.[1874]

Hydrocyanic acid affects all animals indiscriminately. From the highest
to the lowest in the scale of creation all are killed by it; and all
perish nearly in the same manner. Such is the result of a very extensive
series of experiments by Coullon.

It is scarcely necessary to observe that hydrocyanic acid acts
energetically as a poison, through whatever channel it is introduced
into the body. Whether it be swallowed, or injected into the rectum, or
dropped into the eye, or applied to a fresh wound, or inhaled in the
form of vapour, its action is exerted with tremendous energy. Perhaps it
may even act through the sound skin. It has not, hitherto, indeed, been
found to affect animals in this way, evidently because their skin is too
thick and impermeable. But M. Robiquet informed me that once, while he
was making some experiments on the tension of its vapour, his fingers,
after being some time exposed to it, became affected with numbness,
which lasted several days; I have repeatedly remarked the same effect
when handling tubes which contained the concentrated acid; and Emmert
found that the essential oil of bitter almond, applied to the uninjured
skin of the back of a rabbit, produced the usual symptoms and death: and
that the peculiar odour of the poison was quite distinct after death in
the deep-seated muscles of the back.[1875]

This substance is poisonous in all its chemical combinations. Coullon
remarked that two drops of the hydrocyanate of ammonia killed a sparrow
in two minutes.[1876] Robiquet and Magendie found that a hundredth part
of a grain of the cyanide of potassium killed a linnet in thirty
seconds, and five grains a large pointer in fifteen minutes;[1877]
Orfila has related an instance of death in the human subject within an
hour after the administration of six grains of cyanide of potassium in
an injection;[1878] and in a recent experimental investigation the same
author found that this salt produces all the effects of hydrocyanic
acid.[1879] Schubarth killed a dog in twenty minutes with twenty drops
of the diluted acid neutralized by ammonia,[1880] and another in three
hours with twenty-five drops neutralized by potass. These facts are a
sufficient answer to a statement made by Mr. Murray of London, to the
effect, that a considerable dose of the acid may be given without injury
to a rabbit,[1881] if previously rendered alkaline by ammonia. But,
nevertheless, as will be seen under the head of the treatment, ammonia,
as Mr. Murray stated, is a good antidote when administered after the
poison as a stimulant.

The _ferro-cyanates_, or prussiates, do not possess deleterious
properties. These salts were at one time considered compounds of
hydrocyanic acid with a double oxidized base, oxide of iron being one.
Thus the prussiate of potass was considered a compound of hydrocyanic
acid with potass and oxide of iron. But since the investigations of Mr.
Porrett, it has been admitted that there is only one base, potash; and
that it is in union with a hydracid, called ferro-cyanic acid, the
radicle of which is a ternary body composed of carbon, azote, and iron.
The physiological effects of this substance, which have been examined by
many experimentalists, are favourable to Porrett’s opinion; for although
some have found it poisonous, all agree in assigning it very feeble
properties, and some have not been able to discover in it any
deleterious quality at all. Coullon observes that Gazan killed a dog
with two drachms, and Callies another with three drachms of the salt met
with in commerce.[1882] Schubarth found that half an ounce had not any
material effect on dogs, even when vomiting did not occur for half an
hour;[1883] and Callies, who found the salt of commerce somewhat
poisonous, also remarked, that when it was carefully prepared, several
ounces might be given without harm.[1884] D’Arcet once swallowed half a
pound of a solution without any injury.[1885] Similar results were
obtained previously with smaller doses by Wollaston, Marcet,[1886] and
Emmert,[1887] as well as afterwards by Dr. Macneven,[1888] and
Schubarth,[1889] who found that a drachm or even two drachms might be
taken with impunity by man and the lower animals.

The _sulpho-cyanic acid_, another substance analogous in chemical nature
to the ferro-cyanic, was once supposed like it to be a poison of great
activity, but this is doubtful. Professor Mayer of Bonn ascertained that
a drachm and a half of a moderately strong solution of the acid
sometimes killed a rabbit in ninety seconds when injected into the
windpipe, and that the same quantity of a solution of sulpho-cyanate of
potassa might occasion death in the course of four hours; but that some
rabbits took half an ounce of the former and three drachms of the latter
without material harm, both when administered through the windpipe, when
injected into the rectum, and when introduced into the stomach by a
gullet-tube. In the fatal cases death took place under symptoms of
oppressed breathing, rarely attended with convulsions; and extensive
traces of irritation were found in the alimentary canal.[1890] Dr.
Westrumb of Hameln, however, seems to have found it more active in the
form of sulpho-cyanate of potassa. Two scruples in an ounce of water
produced in a dog spasmodic breathing, convulsions, efforts to vomit,
and death in seven minutes; and forty grains killed another in less than
two hours. In the latter animal he detected the poison by the sulphate
of iron in the blood, lungs, liver, spleen and kidneys.[1891] Some
experiments by Soemering would even make it out to be a poison of very
great energy; for half a drachm of concentrated sulpho-cyanic acid given
to a dog occasioned immediate death; and the same quantity of
sulpho-cyanate of potassa killed another in one minute.[1892]

_Cyanic and cyanous acids_ are not poisonous, according to the
experiments of Hünefield;[1893] but _cyanogen_ is a powerful poison, as
will be mentioned under the head of the Narcotic Gases.

The symptoms of hydrocyanic acid observed in man are very similar to
those witnessed in animals.

Coullon has given a good account of the effects of small doses as
ascertained by experiment on himself. When he took from 20 to 86 drops
of a diluted acid, he was attacked for a few minutes with nausea,
salivation, hurried pulse, weight and pain in the head, succeeded by a
feeling of anxiety, which lasted about six hours.[1894] Such symptoms
are apt to be induced by too large medicinal doses. Another remarkable
symptom which has been sometimes observed during its medicinal use is
salivation with ulceration of the mouth. Dr. Macleod thrice had occasion
to remark this in patients who had been using the drug for about a
fortnight, and twice in one individual; and Dr. Granville says he had
also twice witnessed the same effect.[1895]

As to the effects of fatal doses, it is probable that in man, as in
animals, two varieties exist. When the dose is very large, death will in
general take place suddenly, without convulsions. But for obvious
reasons the symptoms in such cases have not been hitherto witnessed.

The most complete account of the symptoms from fatal doses when
convulsions occur, is given in a case reported by Hufeland of a man,
who, when apprehended for theft, swallowed an ounce of alcoholized acid,
containing about forty grains of the pure acid. He was observed
immediately to stagger a few steps, and then to sink down without a
groan, apparently lifeless. A physician, who instantly saw him, found
the pulse gone and the breathing for some time imperceptible. After a
short interval he made so forcible an expiration that the ribs seemed
drawn almost to the spine. The legs and arms then became cold, the eyes
prominent, glistening, and quite insensible; and after one or two more
convulsive expirations he died, five minutes after swallowing the
poison.[1896]

In Horn’s Journal is recorded another case which also proved fatal in
five minutes, with precisely the same symptoms.[1897] A short notice of
what appears to have been a similar case is given in the Annales de
Chimie. The person was a chemist’s servant, who swallowed a large
quantity of the alcoholic solution by mistake for a liqueur, the poison
having been accidentally left on the table by her master, who had been
showing it as a curiosity to some friends. No account is given of the
symptoms, farther than that she died apoplectic in two minutes.[1898] To
these cases may be also added a short notice of the French physician’s
case mentioned at the commencement of this chapter. It will convey a
good idea of the operation of the poison when not quite sufficient to
kill. Very soon after swallowing a tea-spoonful of the diluted acid he
felt confusion in the head, and soon fell down insensible, with
difficult breathing, a small pulse, a bloated countenance, dilated
insensible pupils, and locked jaw. Afterwards he had several fits of
tetanus, one of them extremely violent. In two hours and a half he began
to recover his intellects and rapidly became sensible; but for some days
he suffered much from ulceration of the mouth and violent pulmonary
catarrh, which had evidently been excited by the ammonia given for the
purpose of rousing him. This gentleman had eructations with the odour of
the acid three or four hours after he took it; and during the earlier
symptoms the same odour was exhaled by his breath.[1899] The hydrocyanic
odour of the breath is of course an important distinguishing character,
which would appear, from the observations of Dr. Lonsdale on
animals,[1900] to occur more frequently than might be supposed from the
silence observed on the subject by the reporters of cases.

Hydrocyanic acid is not considered a cumulative poison,—that is, the
continued use of frequent small doses is not believed to possess the
power recognised in iodine, mercury, and foxglove, of gradually and
silently accumulating in the body, and then suddenly breaking out with
dangerous or fatal violence. The frequent experience of practitioners in
this and other countries seems to prove that hydrocyanic acid possesses
no such property. It is right at the same time to mention, that a case
published by Dr. Baumgärtner of Freyburg has been thought by some[1901]
to establish the reverse. A man had taken for two months, on account of
chronic catarrh, ten drops of Ittner’s acid daily in doses of one grain,
without experiencing the slightest toxicological effect. At length he
was found one morning in bed apparently labouring under the poisonous
operation of the acid. He had headache, blindness, dilated insensible
pupil, feeble irregular pulse, occasional suspension of the breathing,
and rapidly increasing insensibility. The cold affusion and ammonia were
immediately resorted to, and at first with advantage. But in no long
time spasms commenced in the toes, and gradually affected the rest of
the body, till at length violent fits of general tetanus were formed,
lasting for six or ten minutes, and alternating in the intervals with
coma. Venesection was next resorted to; after which the spasms were
confined to the jaw and eyes. Delirium succeeded, but was removed by a
repetition of the blood-letting. At four in the afternoon he was
tolerably sensible; during the night delirium returned; at ten next
morning he recovered his sight; and on the subsequent morning he had no
complaint but headache and pain in the eyes.[1902] This case differs so
much from every other in the collateral circumstances, as well as in
duration, that, although the symptoms themselves correspond with those
of poisoning with hydrocyanic acid, we may justly suspect either some
other cause, or the accidental administration of too large a dose. It
ought, however, to turn the attention of practitioners to the
possibility of this poison acting by the accumulation of the effects of
small doses frequently repeated for a great length of time.

The period within which hydrocyanic acid usually proves fatal is fixed
with considerable accuracy, not only by the cases observed in the human
subject, but likewise by the experiments of many physiologists, and more
especially those of Schubarth (p. 583). It is probable that very large
doses occasion death in a few seconds; and at all events a few minutes
will suffice to extinguish life when the dose is considerable; but if
the individual survive forty minutes, he will generally recover. In the
course of a dreadful accident which happened a few years ago in one of
the Parisian hospitals, when seven epileptic patients were killed at one
time by too large doses of the medicinal acid, it was found that several
did not die for forty-five minutes.[1903] But the researches of
Schubarth would certainly justify the expectation that recovery will
take place under active treatment when the patient survives so
long.—These facts may be highly important in the practice of medical
jurisprudence.

The period within which it begins to operate ought also to be accurately
ascertained for the same reason. Indeed in a very interesting trial,
which took place a few years ago in this country, the fate of the
prisoner depended in a great measure on the question, within how short a
time the effects of this poison must show themselves?[1904] The nature
of the case was as follows: An apothecary’s maid-servant at Leicester
who was pregnant by her master’s apprentice, was found one morning dead
in bed; and she had obviously been poisoned with hydrocyanic acid.
Circumstances led to the suspicion that the apprentice was accessary to
the administration of the poison. On the other hand, it was distinctly
proved that the deceased had made arrangements for a miscarriage by
artificial means on the night of her death; and it was therefore
represented, on the part of the prisoner, that she had taken the poison
of her own accord. But the body was found stretched out in bed in a
composed posture, with the arms crossed over the trunk, and the
bed-clothes pulled smoothly up to the chin; and at her right side lay a
small narrow-necked phial, from which about five drachms of the
medicinal prussic acid had been taken, and which was corked and wrapped
in paper. There naturally arose a question, whether the deceased, after
drinking the poison out of such a vessel, could, before becoming
insensible, have time to cork up the phial, wrap it up, and adjust the
bed-clothes?[1905] To settle this point, experiments were made at the
request of the judge, by Mr. Macaulay, Mr. Paget, and several other
medical men of Leicester; and on the trial they, with the exception of
Mr. Paget, gave it as their opinion, founded on the experiments, that
the supposed acts of volition, although within the bounds of
possibility, were in the highest degree improbable. The chief
experiments were three in number, from which it appeared that one dog
was killed with four drachms in eight seconds, another with four drachms
in seven seconds, and another with four drachms and a half in three
seconds; but in other experiments the interval was greater.—For these
particulars I am indebted to Mr. Macaulay.

In the first edition of this work I expressed my concurrence with the
majority of the witnesses. But some facts, which came subsequently under
my notice, led me to think that this concurrence was given rather too
unreservedly. I still adhere so far to my original views as to think it
improbable that, if the deceased, after swallowing the poison, had time
to cork the phial, wrap it in paper, pull up the bed-clothes, and place
the bottle at her side, the progress of the symptoms could have been so
rapid and the convulsions so slight, as to occasion no disorder in the
appearance of the body and the bed-clothes,—and I still likewise think,
that after swallowing so large a dose it was improbable she could have
performed all the successive acts of volition mentioned above—with
ordinary deliberation. But I am informed on good authority, that some
gentlemen interested in the case found by actual trial, that all the
acts alluded to might be accomplished, if gone about with promptitude,
within the short period, which, in some of their experiments, the
witnesses found to elapse, before the action of the poison commenced.
And such being the fact, we ought not perhaps to attach too great
importance to the other argument I have employed,—the probability of
disorder in the body and bed-clothes from the convulsions; for if the
poisoning commenced very soon, the convulsions might have been slight.
The results of my own experiments related in p. 582, although on the
whole confirmatory of those of Mr. Macaulay and his colleagues, are
nevertheless sufficient to prove that large doses occasionally do not
begin to operate with such rapidity as was observed in their
experiments; for in one instance four drops of concentrated acid,
equivalent to two scruples of medicinal acid, did not begin to act on a
rabbit for twenty seconds; and certainly, for so small an animal, two
scruples are as large a dose as five drachms for a grown-up girl.

The two following cases will throw some farther light on the time within
which this poison begins to act on man when taken in large quantity. The
first case shows, that even when an enormous dose is taken, a few simple
voluntary acts may be executed before the symptoms begin. In this
instance which is related by Dr. Gierl of Lindau, the dose was no less
than four ounces of the acid of the Bavarian Pharmacopœia, which
contains four per cent. of pure acid, and is equivalent to five ounces
at least of that commonly used in Britain and France. The subject, an
apothecary’s assistant, was found dead in bed, with an empty two-ounce
phial on each side of the bed,—the mattrass, which is used in Germany
instead of blankets, pulled up as high as the breast,—the right arm
extended straight down beneath the mattrass,—and the left arm bent on
the elbow.[1906] The second case proves that, although one or two acts
of volition may be accomplished, the interval is so very brief that
these acts can only be of the simplest kind. An apothecary’s
apprentice-lad was sent from the shop to the cellar for some carbonate
of potass; but he had not been a few minutes away, when his companions
heard him cry in a voice of great alarm, “Hartshorn! Hartshorn!” On
instantly rushing down stairs, they found him reclining on the lower
steps and grasping the rail; and he had scarcely time to mutter “Prussic
acid!” when he expired,—not more than five minutes after leaving the
shop. On the floor of the cellar an ounce-phial was found, which had
been filled with the Bavarian hydrocyanic acid, but contained only a
drachm. It appeared that he had taken the acid ignorantly for an
experiment; and from the state of the articles in the cellar, it was
evident that, alarmed at its instantaneous operation, he had tried to
get at the ammonia, which he knew was the antidote, but had found the
tremendous activity of the poison would not allow him even to undo the
coverings of the bottle.[1907]

When the quantity of the poison is small, a much longer interval may
elapse before the commencement of its action. Thus, when the dose is
barely short of what is required to occasion death, the effects may be
postponed even for fifteen minutes, as in a case which occurred to Mr.
Garson of Stromness.[1908] This, so far as I am at present aware, is the
extreme limit of interval hitherto observed.

In the trial related above the prisoner Freeman was found _Not Guilty_.

It is important to fix, if possible, the smallest fatal dose of
hydrocyanic acid. This will vary with particular circumstances, such as
the strength of the individual, and the fulness or emptiness of the
stomach at the time. The cases of the Parisian epileptics, who were
killed each by a draught containing two-thirds of a grain of pure
acid,[1909] will supply pointed information. For, on the one hand,
considering the long time they survived, it is not probable that a dose
materially less would have a fatal effect on man. And on the other hand
repeated instances of recovery have been observed, where the dose was as
great or even greater. Thus Dr. Geoghegan had a patient who recovered
from a state of extreme danger after taking two-thirds of a grain;[1910]
and Mr. Banks of Lowth met with a case of recovery in similar
circumstances, where the dose was very nearly a whole grain.[1911]

It is almost unnecessary to add, that in man, as in animals, this poison
will act violently, through whatever channel it may be introduced into
the body. It has not been positively ascertained to act with force
through the unbroken skin. The chemist Scharinger indeed was supposed to
have been killed in consequence of accidentally spilling the acid on his
naked arm;[1912] but this was in all probability a mistake. Should the
skin be freely exposed to the air it seems reasonable to expect that the
poison will evaporate before it could act with energy; but if confined
by pledgets or otherwise, a different result might ensue. Through every
other surface, however, besides the unbroken skin, hydrocyanic acid acts
with very great power; and it is in particular important to remember
that its power is very great when inhaled, so that dangerous accidents
have ensued even from its vapour incautiously snuffed up the nostrils. I
have known a strong man suddenly struck down in this way; a French
physician, M. Damiron, has related the case of an apothecary who
remained insensible for half an hour subsequently to the same
accident;[1913] and cases of the kind are more apt to occur than might
at first view be thought, because, contrary to what is generally
believed and stated in chemical as well as medico-legal works, its smell
is for a few seconds barely perceptible, and never of the kind which
these accounts would lead one to anticipate. Accidental death may
readily arise from its action on a wound or an abraded surface.
Sobernheim mentions that Mr. Scharring, a druggist at Vienna, was
poisoned in consequence of a phial of the acid breaking in his hand and
wounding it; and he expired in an hour.[1914]

The only case with which I am acquainted of poisoning with the
artificial compounds of hydrocyanic acid is that formerly alluded to as
having been occasioned by the cyanide of potassium. Six grains dissolved
in a clyster amounting to six ounces, occasioned general convulsions,
palpitations, slow laboured breathing, coldness of the limbs, dilated
pupil, fixing of the eyeballs, and death in one hour,—phenomena much the
same with those produced by the acid itself.[1915]—Another case has been
published, in which a French physician, ignorant of the correct dose,
prescribed a potion with three grains of cyanide of potassium twice a
day. Immediately after the first dose the patient was seized with the
usual symptoms of poisoning with hydrocyanic acid; and expired in
three-quarters of an hour.[1916] In noticing the first of these cases,
Orfila draws the attention of practitioners particularly to the fact,
that not long before a similar dose of a sample of cyanide, which had
been moist for some time, was twice administered with impunity. The
reason is that the cyanide of potassium undergoes decomposition when
acted on by water, or when long kept.


 SECTION III.—_Of the Morbid Appearances produced by Hydrocyanic Acid._

Under this head the appearances in a special case will first be
mentioned, and then the varieties to which they are liable.

In _Hufeland’s_ case [p. 587] the inspection was made the day after
death. The eyes were still glistening, like those of a person alive; but
the countenance was pale and composed like one asleep. The spine and
neck were stiff, the belly drawn in, the back alone livid. The body
generally, the blood even within the head, and especially the serous
cavities, exhaled a hydrocyanic odour, so strong as to irritate the
nostrils. The blood was every where very fluid, so that two pounds
flowed from the incision in the scalp and twelve ounces from that of the
dura mater; and it had a glimmering bluish appearance, as if Prussian
blue had been mixed with it. The vessels of the brain were gorged, the
substance of the brain natural, and the left ventricle distended with
half an ounce of serum. The villous coat of the stomach was red, easily
removed with the nail, and gangrenous.[1917] The intestines were
reddish, and the liver gorged. The lungs were also turgid, and to such a
degree in the depending parts as to resemble the liver. The arteries and
left cavities of the heart were empty, the veins and right cavities
distended.

In commenting on this description it is first to be remarked, that the
blood, as in the preceding case, is generally altered in nature. Ittner,
who made some good experiments on the subject, found it in animals
black, viscid, and oily in consistence.[1918] Emmert found it fluid and
of a cochineal colour. In a case related by Mertzdorff of an
apothecary’s apprentice, who was found dead in bed after swallowing
three drachms and a half of diluted acid,[1919] in the case recorded in
Horn’s Archiv, and in that related by Dr. Gierl, it was fluid. It was
also perfectly fluid every where in the bodies of the seven epileptic
patients poisoned at Paris. Yet this state is not invariable. Coullon,
though his results tally in general with those of Ittner and Emmert, has
given some experiments in which the blood coagulated after flowing from
the body;[1920] and in the case of an apothecary related in Rust’s
Journal it was found coagulated in the heart.[1921]

In the next place, Magendie and other physiologists have observed that,
as in Hufeland’s case, the blood and cavities of the body in animals
exhale a hydrocyanic odour, even though the quantity taken was small.
The blood did so likewise in the heart of the apothecary just mentioned
as well as throughout the whole body in the case described in Horn’s
Journal. The odour, however, is not always present. For example, there
was none in the case of another German apothecary, who poisoned himself
with an ounce, as recorded in a later volume of Rust’s Journal;[1922]
neither was there any odour in the blood in Mertzdorff’s case, although
it was strong in the stomach; nor in the blood nor any other part of the
body in the Parisian epileptics. It also appears from an experiment by
Schubarth,[1923] and from a case by Leuret where life was prolonged
above fifteen minutes,[1924]—that the odour may be distinct in the
blood, brain, or chest, when hardly any is to be perceived in the
stomach. Schubarth has inquired with some care into the circumstances
under which the hydrocyanic odour may, or may not, be expected. He
states, as the result of his researches, that if the dose is sufficient
to cause death within ten minutes, the peculiar odour will always be
remarked in the blood of the heart, lungs, and great vessels, provided
the body have not been exposed to rain or to a current of air, and the
examination be made within a moderate interval,—for example, twenty-one
hours for so small an animal as a dog; but that, if the dose is so small
that life is prolonged for fifteen, twenty-seven, or thirty-two minutes,
then even immediately after death it may be impossible to remark any of
the peculiar odour, evidently because, as already mentioned, the acid is
rapidly discharged by the lungs; and that even when the dose is large
enough to cause death in four minutes, the smell may not be perceived if
the carcase has been left in a spacious apartment for two days, or
exposed to a shower for a few hours only. These facts explain
satisfactorily why no odour could be perceived in the bodies of the
Parisian epileptics; for they lived from half an hour to forty-five
minutes. The poison may exist in the stomach, though not appreciable by
the sense of smell. In Chevallier’s case mentioned above, the contents
of the stomach had not any odour of hydrocyanic acid; which, however,
was evident to the sense of smell, and plainly indicated by various
tests, in the fluid obtained by distilling the contents.

The presence of this odour in the blood may be accounted strong evidence
of poisoning with hydrocyanic acid, if it is unequivocal to the sense of
several individuals. An exhalation of the same kind is occasionally
formed by natural processes in the excrement. Itard once remarked in a
case of inflammation of the intestines, and again in a case of inflamed
liver, a strong smell of bitter almonds in the fæces, although no
medicine containing hydrocyanic acid had been given.[1925] Mr. Taylor
mentions that he once observed a sort of hydrocyanic odour in the brain
of a person who died of natural disease.[1926] These facts will render
the inspector cautious, but can scarcely throw a doubt over evidence
derived from an unequivocal hydrocyanic odour in the blood.

Few successful attempts have yet been made to detect the acid in the
blood by chemical analysis. The odour may be present, although chemical
analysis fails in eliciting any indication. This follows from the
observations of Dr. Lonsdale,[1927] as well as of various authors quoted
by him in his paper. The cyanide of potassium has been detected by Mayer
not merely in the blood, but likewise in the serous secretions and
sundry soft solids.[1928]

In most instances,—for example, in the Parisian epileptics, the state of
the brain, as to turgescence of vessels, has corresponded with the
description given by Hufeland. Venous turgescence and emptiness of the
arterial system are commonly remarked throughout the whole body. Thus in
the epileptic patients, the heart and great arteries were empty; the
great veins gorged; the spleen gorged, soft, and pultaceous; the veins
of the liver gorged; and the kidneys of a deep violet colour, much
softened, and their veins gorged with black blood.

It is impossible that hydrocyanic acid could cause gangrene of the
stomach, which is said to have been witnessed in Hufeland’s case. But
there are often signs of irritation in that organ. The villous coat has
been found red in animals; it was shrivelled, and its vessels were
turgid with black blood in the instance of the apothecary mentioned in
the fourteenth volume of Rust’s Journal; in Mertzdorff’s case it was red
and checkered with bloody streaks; and in the case related by Dr. Gierl,
where four ounces were swallowed, it was dark-red, as it were tanned or
steeped in spirits, and easily separated from the subjacent contents.
The contents of the stomach have in every instance had a strong
hydrocyanic odour, except in the cases of the Parisian epileptics, and
in those related by Leuret and by Chevallier. According to the
experiments of Lassaigne and Schubarth, formerly noticed, it is not to
be looked for when the body has been kept a few days, more especially if
the individual lived some time. Dr. Lonsdale generally found it eight or
nine days after death in animals, which had been either buried during
that time, or kept in an apartment at the temperature of 50° F.[1929] In
a case which occurred not long ago in London the poison was found in the
stomach five days after death. A coroner’s inquest had terminated in a
verdict of natural death. But suspicions having arisen, that the man had
poisoned himself in anticipation of a charge of forgery, another inquiry
was made; when the odour of hydrocyanic acid was evolved from the
contents of the stomach, and the distilled water obtained from them
yielded decisive chemical evidence of its being present.[1930] It is
important to observe, in reference to the evidence of hydrocyanic acid
in the stomach, that here, as in the instance of the blood, the odour
may be strong, and yet the poison may not be discoverable by analysis.
This fact rests on the united testimony of Coullon, Vauquelin, Leuret,
Turner, and Dr. Lonsdale; the last of whom mentions that he could not
detect it chemically after the fourth day in the bodies of some animals,
in which it was perceptible by its odour even four or five days
later.[1931] It is possible, however, that these failures to detect the
poison by analysis may have sometimes arisen from imperfections in the
method of analysis employed; for it was detected by the process formerly
mentioned in the stomach of the apothecary last alluded to, in
Chevallier’s case, though not perceptible to the smell, and frequently
by Lassaigne in animals.

Mertzdorff remarked both in his case of poisoning with hydrocyanic acid,
and likewise in a parallel instance of poisoning with the essential oil
of bitter almonds,[1932] a singular appearance in the bile, the colour
of which was altered to deep blue.

Coullon and Emmert say they have observed, that the bodies of animals
resist putrefaction. The latter in particular mentions, that he had left
them several days in a warm room without perceiving any sign of decay.
This certainly would not _à priori_ be expected, considering the state
of the blood. And it is not universal; for in one instance, the case of
Mertzdorff, putrefaction commenced within thirty hours after death. In
the Parisian epileptics, the bodies passed through the usual stage of
rigidity.

It appears that even long after death the eye, as in Hufeland’s case,
has a peculiar glistening and staring expression, so as to render it
difficult to believe that the individual is really dead; and this
appearance has been considered by Dr. Paris so remarkable, as even alone
to supply “decisive evidence of poisoning by hydrocyanic acid.”[1933]
But the accuracy of this opinion may be questioned. The appearance is
indeed very general in cases of poisoning with preparations containing
hydrocyanic acid. Besides occurring in the case of Hufeland, and in that
which gave occasion to Dr. Paris’s statement, it was witnessed by
Mertzdorff, and in the instance described in Horn’s Journal. But it is
not a constant appearance; for it was not observed in the seven Parisian
epileptics. Neither is it peculiar; for death from carbonic acid has the
same effect; I have remarked it six hours after death in a woman who
died of cholera; and it has been observed in cases of death during the
epileptic paroxysm.


   SECTION IV.—_Of the Treatment of Poisoning with Hydrocyanic Acid._

Much attention has been lately paid to the treatment of this variety of
poisoning; and the object of those who have studied it has naturally
been the discovery of an antidote.

An antidote to hydrocyanic acid must either be a substance which renders
it immediately insoluble, or one which exerts upon the body an action
contrary to that excited by the poison, that is, a powerful stimulant
action on the nervous system. Hence all such remedies as oil, milk,
soap, coffee, treacle, turpentine, at one time thought serviceable, are
quite inert.[1934]

Antidotes have hitherto been chiefly sought for among the powerful,
diffusible stimulants. And it is plain, that even although a chemical
antidote were known, a stimulant antidote is indispensable also, because
the mischief done, before the poison can be rendered inert, is generally
sufficient to cause death, unless counteracted by treatment.

Of the diffusible stimulants, _ammonia_ is considered by many the most
energetic antidote. The first who made careful experiments with it was
Mr. John Murray of London; and he was so convinced of its efficacy, that
he expressed himself ready to swallow a dose of the acid large enough to
prove fatal, provided a skilful person were beside him to administer the
antidote.[1935] The favourable results obtained by Murray were
afterwards confirmed by M. Dupuy.[1936] Afterwards, however, the
efficacy of ammonia was called in question. Orfila stated in the third
edition of his Toxicology that he had several times satisfied himself of
the complete inutility of this as well as many other antidotes.[1937]
And Dr. Herbst of Göttingen made some careful experiments, from which he
concludes that ammonia, though useful when the dose of poison is not
large enough to kill, and even capable of making an animal that has
taken a fatal dose jump up and run about for a little, yet will never
save its life.[1938] But farther experiments by Orfila have led him to
modify his former statement, and to admit, that, although liquid ammonia
is of no use when introduced into the stomach, yet if the vapour from it
is inhaled, life may sometimes be preserved, provided the dose of the
poison be not large enough to act with great rapidity. He remarked, that
when from eight to fourteen drops of the medicinal acid were given to
dogs of various sizes, they died in the course of fifteen minutes if
left without assistance, but were sometimes saved by being made to
inhale ammoniacal water, and recovered completely in little more than an
hour.[1939] As this is very nearly the conclusion to which Mr. Murray
was led by his experiments performed in 1822, it is rather
extraordinary, that his name, as the undoubted discoverer of the remedy,
has never been mentioned by the Parisian Professor. Buchner, it is right
to add, had found this remedy useful in the same year in which Mr.
Murray’s experiments were made.[1940] A gentleman who took an over-dose
of two drachms of hydrocyanic acid while using it medicinally, and who
seems to have been in great danger, owed his recovery to the assiduous
use of carbonate of ammonia held to the nostrils, and spirit of ammonia
internally. Relief was obtained immediately.[1941] Orfila suggests an
important caution,—not to use a strong ammoniacal liquor, otherwise the
mouth, air-passages, and even the alimentary canal may be attacked with
inflammation,—as indeed happened to the French physician whose case was
formerly mentioned. The strong _aqua ammoniæ_ should be diluted with
several parts of water.

Another remedy of the same kind with ammonia as to action is _chlorine_.
This substance was first proposed as a remedy in 1822 by Riauz, a
chemist of Ulm, who found that, when a pigeon, poisoned with hydrocyanic
acid, was on the point of expiring, it immediately began to revive, on
being made to breathe chlorine, and in fifteen minutes was able to fly
away.[1942] Buchner repeated Riauz’s experiments and arrived at the same
results. More lately M. Simeon, apothecary to the hospital of St. Louis
at Paris, apparently without being acquainted with the observations of
the German chemists, was likewise led to suppose, that this gas might
prove a useful antidote;[1943] and MM. Cottereau and Vallette have
formed the same conclusion.[1944] Orfila in his paper already quoted
expresses his conviction, that this remedy is the most powerful antidote
of all hitherto proposed. His experiments have convinced him, that
animals, which have taken a dose of poison sufficient to kill them in
fifteen or eighteen minutes, will be saved by inspiring water
impregnated with a fourth part of its volume of chlorine, even although
the application of the remedy be delayed till the poison has operated
for four or five minutes. In some of his experiments he waited till the
convulsive stage of the poisoning was passed, and the stage of
flaccidity and insensibility had supervened; yet the animals were
obviously out of danger ten minutes after the chlorine was first
applied, and recovered entirely in three-quarters of an hour.[1945]

The last remedy of this nature which deserves notice is the _cold
affusion_. This was first recommended by Dr. Herbst of Göttingen, who,
on account of the success he witnessed from it in animals, considers it
the best remedy yet proposed. When the dose of the poison was
insufficient to prove fatal in ordinary circumstances, two affusions he
found commonly sufficient to dispel every unpleasant symptom. When the
dose was larger, it was necessary to repeat the effusion more
frequently. Its efficacy was always most certain when resorted to before
the convulsive stage of the poisoning was over; yet even in the stage of
insensibility and paralysis it was sometimes employed with success. In
the latter instance the first sign of amendment was renewal of the
spasms of the muscles. Many experiments are related by the author in
support of these statements. But the most decisive is the following. Two
poodles of the same size being selected, hydrocyanic acid was given to
one of them in repeated small doses till it died. The whole quantity
administered being seven grains of Ittner’s acid, this dose was given at
once to the other dog. Immediately it fell down in convulsions, violent
opisthotonos ensued, and in half a minute the convulsive stage was
followed by flaccidity, imperceptible respiration, and failing pulse.
The cold affusion was immediately resorted to, but at first without any
amendment. After the second affusion, however, the opisthotonos
returned, and was accompanied by cries; and on the remedy being repeated
every fifteen minutes, the breathing gradually became easier and easier,
the spasms abated, and in a few hours the animal was quite well.[1946]
Professor Orfila repeated Dr. Herbst’s experiments, with analogous
results; but he considers the cold affusion inferior to
chlorine.[1947]—It is probably advantageous to apply the cold water
rather in the form of cold douche to the head and spine than to the body
at large. Dr. Robinson of Sunderland found that rabbits, which had taken
doses adequate to occasion death, might be saved by pouring on the
hindhead and along the spine cold water impregnated with common salt and
nitre.[1948] A case, which seems to have been cured in this way, has
been published by Mr. Banks of Lowth. A young woman took by mistake a
solution containing very nearly a grain of real acid, and immediately
became insensible and convulsed. Ordinary stimulants were of no use. But
in fifteen minutes, when the convulsions had ceased, and she lay in a
state of complete coma and general paralysis, the cold douche on the
head first renewed the convulsions, then strengthened the pulse and
restored some appearance of consciousness, and finally roused her, so
that in a few hours she was quite well.[1949]

It is probable, that _bleeding from the jugular vein_ deserves more
attention as a remedy than it has yet received. The right side of the
heart is almost invariably found much gorged with blood in animals
examined at the moment of death; and the contractions of the heart, in
such circumstances imperfect or arrested altogether, have often been
observed by experimentalists to be instantly restored on promptly
removing the state of turgescence. Accordingly Dr. Cormack found that a
dog, at the point of death after receiving a fatal dose of the acid, was
speedily roused and eventually saved by bleeding from the jugular
vein.[1950] And in a careful inquiry by Dr. Lonsdale, it was ascertained
that the turgescence of the heart might be effectually diminished in
this way, and that recovery might frequently be accomplished when the
poison was otherwise amply sufficient to have occasioned speedy
death.[1951] In a case treated by Magendie, that of a young lady
poisoned by too large a medicinal dose, the chief remedies were ammonia
and blood-letting from the jugular vein; and she recovered.[1952]

Few observations have hitherto been made on the chemical antidotes for
hydrocyanic acid, or those substances which render it innoxious by
converting it into an insoluble compound. It is plain that several
probable antidotes of this kind exist. But toxicologists have been
apparently deterred from trying them by the fearful rapidity with which
the poison acts, and the consequent improbability that in practice any
such antidote can be administered in time. It has lately been shown,
however, by Messrs. T. and H. Smith of this city, that the effects of a
fatal dose may be warded off by the timely administration of the
reagents necessary for converting the acid into Prussian blue. They
found that if a solution of carbonate of potash followed by a solution
of the mixed sulphates of iron be given to animals very soon after the
administration of a dose of thirty drops of the Edinburgh medicinal
acid, containing three per cent. of real acid, recovery in general takes
place, and sometimes little inconvenience seems to be sustained. The
solutions they used were one of 144 grains of carbonate of potash in two
ounces of water, and another composed of a drachm and a half of sulphate
of protoxide of iron, together with two drachms of the same salt
converted into sulphate of sesquioxide by means of sulphuric and nitric
acids in the usual way. About 52 minims of each of these solutions will
remove the whole acid contained in 100 grains of the Edinburgh medicinal
acid; but for certainty, three or four times as much should be
used,—which may be done with perfect safety.[1953]

On the whole, then, it appears that the proper treatment of a case of
poisoning with hydrocyanic acid consists in the cold affusion applied to
the head and spine, the inhalation of diluted ammonia or chlorine,
venesection at the jugular vein, and the administration of carbonate of
potash and the mixed sulphates of iron, if aid has been obtained in good
time.

It is right to remember, however, that on account of the dreadful
rapidity of this variety of poisoning, it will rarely be in the
physician’s power to resort to any treatment soon enough for
success;—and farther, that his chance of success must generally be
feeble even though the case be taken in time, because when hydrocyanic
acid is swallowed by man, the dose is commonly so large as not to be
counteracted by any remedies.


     _On the Vegetable Substances which contain Hydrocyanic Acid._

Hydrocyanic acid exists in several plants; which are consequently
poisonous. I have considered it advisable to describe their effects
separately from those of the pure acid.

The plants which have been thoroughly examined and found to yield it
belong chiefly to the division _Drupaceæ_, of Decandolle’s Natural
Family the _Rosaceæ_. These are the bitter almond, cherry-laurel,
bird-cherry, and peach. The leaves and seeds of the nectarine and
apricot, and the seeds of the plum and cherry, have the same taste with
these four, and therefore will certainly be found to contain the acid
also. The same inference may be drawn from the taste of some pomaceous
seeds; and accordingly I have obtained a hydrocyanated oil from the
seeds of the New York pippin, and those of the white-beam-tree, the
_Pyrus aria_. The poison procured from these sources exists in two
forms,—as a distilled water, and as an essential oil. Further, the acid
has been discovered to constitute the active poison of the juice of the
_Janipha manihot_, or bitter cassava [see p. 457].

The distilled waters yield hydrocyanic acid, as is shown by the blue
precipitate they give with potass and the mixed sulphates of iron. They
have a powerful, peculiar, grateful odour, which is usually likened to
that of pure hydrocyanic acid. But the smell really bears very little
resemblance to that of hydrocyanic acid, and is not owing to its
presence: the odour remains equally strong after the acid is thrown down
by the test now mentioned. The active part of the distilled water may be
separated in the form of a volatile oil. This is colourless at first,
afterwards yellowish or reddish, acrid, bitter, heavier than water, and
very volatile. The essential oil of the bitter almond has been carefully
examined by various chemists. Vogel, by subjecting it twice to
distillation from caustic potass, procured hydrocyanate of potass in the
residue; and a volatile oil was distilled over, which no longer
contained hydrocyanic acid, but nevertheless had the odour of the
original oil.[1954] This purified oil he considered equally poisonous
with that which contains hydrocyanic acid, a single drop of it having
killed a sparrow; and his opinion was confirmed by the experiments of
Professor Orfila. But according to some careful experiments by
Stange,[1955] which have been amply confirmed by Dr. Göppert of
Breslau,[1956] and also by MM. Robiquet and Boutron-Charlard,[1957]—if
the purified oil retains active poisonous properties, this must be owing
to the acid not having been entirely removed. Göppert in particular
remarked that twenty-five drops of the purified bitter-almond oil,
cherry-laurel oil, or bird-cherry oil had very little effect on rabbits,
not more indeed than the same quantity of the common essential oils. The
purified oil, according to all these chemists, possesses the odour of
the original oil, as Vogel first stated.


                        _Of the Bitter Almond._

The bitter almond was once extensively used in medicine, and is still
much employed by confectioners for flavouring puddings, sweetmeats, and
liqueurs. It is the kernel of the fruit of the _Amygdalus communis_.
This species has two varieties, the _dulcis_ and the _amara_; which
differ from one another in the fruit only. The fruit of the former
yields the sweet, and of the latter the bitter almond. The bitter almond
is the smaller of the two. The two plants, according to Murray, are
convertible into each other,—the sweet variety becoming bitter by
neglect,—the bitter becoming sweet by cultivation, or certain modes of
management not well known,—and the seed of either variety producing
plants of both.[1958] These statements as to the mutual convertibility
of the two varieties require confirmation.

The bitter almond depends for its activity on the essential oil, which
is common to all the vegetable poisons belonging to the present tribe.
According to the researches of Robiquet and Boutron-Charlard, followed
up by Liebig, the oil does not, like common essential oils, exist ready
formed in the almond, but is only produced when the almond-pulp comes in
contact with water. It cannot be separated by any process whatever from
the almond without the co-operation of water,—neither, for example, by
pressing out the fixed oil, nor by the action of ether, nor by the
action of absolute alcohol. After the almond is exhausted by ether, the
remaining pulp gives the essential oil as soon as it is moistened; but
if it is also exhausted by alcohol, the essential oil is entirely lost.
The reason is that alcohol dissolves out a peculiar crystalline
principle, named amygdalin, which, with the co-operation of water, forms
the essential oil by reacting on a variety of the albuminous principle
in the almond, called emulsion or synoptase.

In some respects, therefore, the essential oil of almonds is quite
peculiar in its nature, and quite different from the common essential or
volatile oils.—The presence of hydrocyanic acid in it is easily proved
by dissolving it with agitation in water, and treating the solution with
caustic potass, followed by the mixed sulphates of iron and sulphuric
acid.—The quantity of essential oil which may be procured from the
bitter almond amounts, according to Krüger of Rostock, to four drachms
from five pounds or a ninety-sixth part.[1959] The quantity of
hydrocyanic acid in the oil varies considerably: Schrader got from an
old sample 8·5 per cent., from a new sample 10·75;[1960] but Göppert got
from another specimen so much as 14·33 per cent.[1961]

_Effects on Animals._—The bitter almond is a powerful poison, which acts
in the same way as hydrocyanic acid, but likewise excites at times
vomiting and other signs of irritation. The first good experiments on it
are those related in Wepfer’s treatise on the Cicuta; but its properties
seem to have been known even to Dioscorides. The symptoms it induces in
animals are trembling, weakness, palsy, convulsions, often of the
tetanic kind, and finally coma. But frequently it occasions vomiting
before these symptoms begin, and the animal in that way may
escape.[1962] According to Orfila, twenty almonds will kill a dog in six
hours by the stomach if the gullet be tied; and six will kill it in four
days when applied to a wound.[1963]

The essential oil is not much inferior in activity to the pure
hydrocyanic acid. A single drop of it applied by Sir B. Brodie on the
tongue of a cat caused violent convulsions and death in five
minutes.[1964] But more generally a larger dose, or about seven drops,
has been found necessary to kill a middle-sized dog. Five drops,
according to Göppert, will kill a rabbit in six minutes. When entirely
freed of hydrocyanic acid, it becomes, as already mentioned, not more
poisonous than common volatile oils.

_Symptoms in Man._—The effects of the almond and of the oil upon man are
equally striking with those of hydrocyanic acid.

In small doses the bitter almond produces disorder of the digestive
organs, nausea, vomiting, and sometimes diarrhœa. These symptoms are
occasionally brought on by the small quantities used for flavouring
sweetmeats, if the confectioner has not been careful in compounding
them. Virey says that accidents occasionally happen to children at Paris
from their eating freely of macaroons, which are sometimes too strongly
flavoured with the bitter almond.[1965] In this country accidents from
the same cause may be with justice apprehended, as confectioners now
generally use, not the bitter almond, but its essential oil, which is
distilled for the purpose in London, and sold in the druggists shops
under the name of peach-nut oil. Göppert suggests that this oil ought to
be freed of its hydrocyanic acid by repeated distillation with caustic
potassa, because the flavour is not in the least injured by the process,
while its activity as a poison is greatly lessened.

In peculiar constitutions the minutest quantity, even a single almond,
will cause a state resembling intoxication, succeeded by an eruption
like nettle-rash. The late Dr. Gregory was subject to be affected in
this way. Other vegetable bitters had the same effect on him, but none
so remarkably as bitter almonds. They caused first sickness, generally
tremors, then vomiting, next a hot fit with an eruption of urticaria,
particularly on the upper part of the body. At the same time the face,
and head swelled very much, and there was generally a feeling like
intoxication. The symptoms lasted only for a few hours. The rash did not
alternately appear and disappear as in common nettle-rash.[1966] A lady
of my acquaintance is liable to be attacked with urticaria even from
eating the sweet almond.

The quantity of bitter almonds which may be eaten with impunity is
unknown; but Wibmer mentions an experimentalist who took half an ounce
without any other effect besides headache and sickness.[1967] Two cases
of death in the human subject from eating them have been quoted by
Coullon from the Journal de Médecine of Montpellier. One is a doubtful
case, but the other is unequivocal. A bath-woman gave her child the
“expressed juice” of a handful of bitter almonds to cure worms. The
child, who was four years old, was immediately attacked with colic,
swelling of the belly, giddiness, locked jaw, frothing at the mouth,
general convulsions, and insensibility, and died in two hours.[1968]
Murray, however, asserts in his Apparatus Medicaminum that the expressed
juice is sweet and not poisonous.[1969] But this apparent contradiction
is easily explained by referring to the chemical relations of the
almond,—the oil expressed without water being free from essential oil,
while the milky fluid expressed from the pulp beat up with water is
strongly impregnated with it.—Another case was published not long ago by
Mr. Kennedy of London; but the symptoms were imperfectly ascertained.
The person, a stout labourer, appeared to have eaten a great quantity of
bitter almonds, which were subsequently found in the stomach. He was
seen to drop down while standing near a wall; soon after which the
surgeon who was sent for found him quite insensible, with the pulse
imperceptible, and the breath exhaling the odour of bitter almonds; and
death took place in no long time.[1970]

Coullon has noticed many other instances where alarming symptoms were
produced by this poison, but were dissipated by the supervention of
spontaneous vomiting.

The effects of small doses of the oil have been tried by Sir B. Brodie
on himself; and a fatal case of poisoning with it has been recorded by
Mertzdorff. In the course of his experiments Sir B. Brodie once happened
to touch his tongue with the end of a glass rod which happened to be
dipped in the oil; and he says he had scarcely done so before he felt an
uneasy, indescribable feeling in the pit of the stomach, great
feebleness of his limbs, and loss of power to direct the muscles, so
that he could hardly keep himself from falling. These sensations were
quite momentary.[1971]

Mertzdorff’s case is interesting, not only as being accurately related,
but likewise on account of the exact resemblance of the symptoms to
those observed in the celebrated case of Sir Theodosius Boughton, which
will presently be mentioned. A hypochondriacal gentleman, 48 years old,
swallowed two drachms of the essential oil. A few minutes afterwards,
his servant, whom he sent for, found him lying in bed, with his features
spasmodically contracted, his eyes fixed, staring, and turned upwards,
and his chest heaving convulsively and hurriedly. A physician, who
entered the room twenty minutes after the draught had been taken, found
him quite insensible, the pupils immoveable, the breathing stertorous
and slow, the pulse feeble and only 30 in a minute, and the breath
strongly impregnated with the odour of bitter almonds, death ensued ten
minutes afterwards.[1972] A fatal case occurred lately in London, where
the individual, intending to compound a nostrum for worms with beech-nut
oil, got by mistake from the druggist peach-nut oil, which is nothing
else than the oil of bitter almond.—A singular case of recovery from a
very large dose of this poison has been lately published by M. Chevasse.
A shopkeeper, who swallowed half an ounce by mistake for spirit of
nitric ether, had an attack of spontaneous vomiting, which was forthwith
encouraged by sulphate of zinc. He nevertheless became pale and
convulsed; the pulse disappeared; and delirious muttering ensued, with
_risus sardonicus_, sparkling of the eyes, and panting respiration.
Recovery, however, took place under the use of brandy and ammonia.[1973]

The morbid appearances are the same as in poisoning with the pure acid.
In Mertzdorff’s case the whole blood and body emitted a smell of
almonds; putrefaction had begun, though the inspection was made
twenty-nine hours after death; the blood throughout was fluid, and
flowed from the nostrils and mouth; the veins were every where turgid;
the cerebral vessels gorged; the stomach and intestines very red.—In the
case from the Medical and Physical Journal of poisoning with the almond
itself, the vessels of the brain were much gorged, and the eyes
glistening and staring as if the person had been alive.


                        _Of the Cherry-Laurel._

The cherry-laurel, or _Cerasus lauro-cerasus_, was at one time much used
for flavouring liqueurs and sweetmeats. But it is now less employed than
formerly, as fatal accidents have happened from its having been used in
too large quantity. The custom, however, has not been altogether
abandoned; for there is an account in an English newspaper in 1823 of
two persons killed by ratifia’d brandy, which had been flavoured with
this plant; and Dr. Paris has mentioned an instance of several children
at an English boarding-school having been dangerously affected by a
custard flavoured with the leaves.[1974] Almost every part of the plant
is poisonous, especially the leaves and kernels; but the pulp of the
cherry is not. The flower has a totally different odour from the leaves.
The healthy vigorous shoots in the early part of summer, and the inner
bark, both then and in autumn, smell strongly of the bitter almond when
broken across. The kernels of the seeds have a strong taste of bitter
almonds.—The plant yields a distilled water and an essential oil, which
Robiquet found to have all the chemical properties of the oil of bitter
almond.[1975]—A very peculiar source of danger in using the leaves of
this plant, for imparting a ratafia flavour to sweetmeats and liqueurs,
is that the proportion of oil varies excessively according to the age of
the leaf. It abounds most in the young undeveloped leaves, and
diminishes gradually afterwards. Hence, the leaves being evergreen and
outliving more than two summers, the young leaves in May or June
contain, as I have found, nearly ten times as much oil as the old ones
at the same moment.

Cherry-laurel oil, according to Schrader, contains 7·66 per cent. of
hydrocyanic acid;[1976] but according to Göppert, a specimen supposed to
be genuine gave only 2·75 per cent.[1977] It is probably therefore a
weaker poison than the oil of bitter almond. The latest experiments made
with this oil are those of some Florentine physicians, performed at the
laboratory of the Marquess Rodolphi, and described by Professor
Taddei.[1978] Sixteen drops put on the tongue of rabbits killed them in
nine, fifteen, or twenty minutes; and ten or twelve drops injected in
oil into the anus killed them in four minutes. The symptoms were slow
breathing, palsy of the hind-legs, then general convulsions; and death
was preceded by complete coma. A very extraordinary appearance was found
in the dead body,—blood extravasated abundantly in the trachea and
lungs.

The cherry-laurel water, prepared by distillation from the leaves of
this plant, was long the most important of the poisons which contain the
hydrocyanic acid, as it was the most common before the introduction of
the acid itself into medical practice. Water dissolves by agitation 3·25
grains of oil per ounce; which may be considered the proportion in a
saturated distilled water. The water contains, according to Schubarth,
only 0·25 per cent. of hydrocyanic acid;[1979] according to
Schrader[1980] only half as much; and by long keeping even that small
proportion will gradually disappear, as I have ascertained by
experiment. Hence its strength must vary greatly,—a fact which will
explain the very different effects of the same dose in different
instances.

From experiments on animals by a great number of observers, it appears
that, whether it is introduced into the stomach, or into the anus, or
into the cellular tissue, or directly into a vein, it occasions
giddiness, palsy, insensibility, convulsions, coma, and speedy
death;—that the tetanic state brought on by the pure acid, is not always
so distinctly caused by cherry-laurel water;—and that tetanus is most
frequently induced by medium doses.

The attention of physicians was first called to this poison by an
account, published by Dr. Madden in the Philosophical Transactions for
1737, of several accidents which occurred at Dublin in consequence of
strong ratifia’d brandy having been prepared with it. Foderé has also
given an account of two cases, caused by servants having stolen and
drunk a bottle of it, which they mistook for a cordial.[1981] Being
afraid of detection, they swallowed it quickly, and in a few minutes
expired in convulsions. Murray has noticed several others in his
Apparatus Medicaminum.[1982] In most of these cases the individuals
suddenly lost their speech, fell down insensible, and died in a few
minutes. Convulsions do not appear to have been frequent. Coullon has
also related an instance where a child seems to have been killed by the
leaves applied to a large sore on the neck.[1983]

The dose required to occasion these effects, and more especially to
prove fatal, has not been determined with care. It must vary with the
age of the sample used. It will vary also according as the water has
been filtered or not; for what is not filtered often presents
undissolved oil suspended in it or floating on its surface. One ounce
has proved fatal;[1984] and half an ounce has caused only temporary
giddiness, loss of power over the limbs, stupor, and sense of pressure
in the stomach.[1985]

The appearances found in the dead body have varied. In general the blood
has been fluid. The smell of bitter almond has commonly been distinct in
the stomach.

The cherry-laurel water has attracted much attention in this country, in
consequence of being the poison used by Captain Donnellan for the murder
of Sir Theodosius Boughton. The trial of Donnellan, the most important
trial for poisoning which ever took place in Britain, has given rise to
some discrepance of opinion both among barristers and medical men, as to
the sufficiency of the evidence by which the prisoner was
condemned.[1986] For my part, taking into account the general, as well
as medical circumstances of the case, I do not entertain a doubt of his
guilt.

Leaving the general evidence out of view, however, as foreign to the
objects of the medical jurist’s regard, it must be admitted that the
medical evidence, taken by itself, was defective. It may be summed up
shortly in the following terms:—Sir Theodosius was a young man of the
age of twenty, and in perfect health, except that he had a slight
venereal complaint of old standing, for which he occasionally took a
laxative draught. On the morning of his death, his mother, Lady
Boughton, remarked, while giving him his draught, that it had a strong
smell of bitter almonds. Two minutes after he took it, she observed a
rattling or gurgling in his stomach; in ten minutes more he seemed
inclined to doze; and five minutes afterwards she found him quite
insensible, with the eyes fixed upwards, the teeth locked, froth running
out of his mouth, and a great heaving at his stomach and gurgling in his
throat. He died within half an hour after swallowing the draught. The
body was examined ten days after death, and the inspectors found great
congestion of the veins every where, gorging of the lungs, and redness
of the stomach. But the examination was unskilfully conducted. For the
head was not opened; the fæces were allowed to rush from the intestines
into the stomach; and, as a great quantity of fluid blood was found in
each cavity of the chest, the subclavian veins must have been divided
during the separation of the clavicles. Very little reliance, therefore,
can be placed in the evidence from the inspection of the body.[1987]

On comparing these particulars with what has been said above regarding
the effects of hydrocyanic acid and this whole genus of poisons, it will
be seen that every circumstance coincides precisely with the supposition
of poisoning with the cherry-laurel water. The symptoms were exactly the
same as in Mertzdoff’s case of poisoning with the essential oil of
almonds (p. 604). When to this are added, the smell of the draught,
which Lady Boughton could hardly mistake, the rarity of apoplexy in so
young and healthy a person as Sir Theodosius, and the improbability of
either that or any other disease of the head proving fatal so
quickly,—the conclusion at which, in my opinion, every sound medical
jurist must arrive is, that poisoning in the way supposed was very
probable. But I cannot go along with those who think that it was
certain; nor is it possible to see on what grounds such an opinion can
be founded, when the general or moral circumstances are excluded.

The medical evidence in Donnellan’s case has been much canvassed, and
especially that of Mr. John Hunter. It would be foreign to the plan
hitherto pursued in this work to analyze and review what was said by him
and his brethren. But I must frankly observe, that Mr. Hunter’s evidence
does him very little credit, and that his high professional eminence is
the reverse of a reason for palliating his errors, or treating them with
the lenity which they have experienced from his numerous critics.


           _Of the Peach, Cluster-Cherry, Mountain-Ash, &c._

Little need be said of the other plants formerly mentioned among those
which yield hydrocyanic acid, and act on the system in consequence of
containing that substance.

The _Amygdalus persica_ or peach is the most active of them. Most parts
of the plant exhale the odour of the bitter-almond, but particularly the
flowers and kernels. According to the chemical researches of M.
Gauthier, the fresh young shoots of the peach collected in July contain,
weight for weight, even more essential oil than the bitter almond, or
cherry-laurel leaves; for 250 grains yielded nearly five grains of it or
two per cent.; and he found the oil may be easily procured by distilling
the shoots without addition till the product begins to pass over
clear.[1988] The kernels of the peach, when distilled with water, yield
nearly one grain of hydrocyanic acid per ounce.[1989]

Coullon has collected two instances of poisoning with the peach-blossom.
One is the case of an elderly gentleman, who swallowed a sallad of the
flower to purge himself. Soon afterwards he was seized with giddiness,
violent purging, convulsions, and stupor; and he died in three days.
Here the poison must have proved fatal by inducing true apoplexy in a
predisposed habit; at least poisoning with hydrocyanic acid never lasts
nearly so long. The other, a child eighteen months old, after taking a
decoction of the flowers to destroy worms, perished with frightful
convulsions, efforts to vomit, and bloody diarrhœa.[1990] The
peach-blossom would therefore appear to be rather a narcotico-acrid,
than a narcotic.—Peach-leaves are represented to have produced even
purely irritant effects. A man, who took a decoction of a handful boiled
in a quart of water down to a third,—when of course no hydrocyanic acid
could remain,—was attacked with tightness in the chest, a sense of
suffocation, violent colic, pain in the stomach and frequent desire to
vomit, followed by a hard pulse, restlessness, and flushing of the face.
But he recovered slowly under the use of fomentations and opiates.[1991]

The bark of the _Prunus padus_, or cluster-cherry, a native of this
country, owes its poisonous qualities to the same substance as the
preceding plants. Heumann found that the distilled water obtained from
two ounces of bark in March contains two grains of acid, two ounces of
developed leaves half a grain, and two ounces of the seed a trifle
less.[1992] Its distilled water has the odour of bitter almonds,
contains the same essential oil with that of the bitter almond, and
yields more hydrocyanic acid than the cherry-laurel water.[1993] The
oil, according to Schrader, contains 9·25[1994] per cent. of hydrocyanic
acid, according to Göppert only 5·5 per cent.[1995] Bremer, who has
examined this plant with great care, found that both the distilled water
and the essential oil kill mice when put into the mouth, eye, nose, ear,
anus, or a wound; and that half an ounce of the water killed a dog in
twelve minutes.[1996] The fruit is also poisonous. It has a nauseous
taste, but communicates a pleasant flavour to spirituous liquors. The
kernels yield by expression a transparent, fixed oil, concrete at 41°
F., which contains a small quantity of the essential oil; and the cake
which is left yields so much of the latter, that, as we are informed by
M. Chancel of Briançon, a handful has proved fatal to cows in a short
time.[1997] In these kernels, as in the bitter almond, the essential oil
does not exist ready formed, but is developed only in consequence of the
contact of water; and hence, if the fixed oil by expression contains a
little of it, as Chancel says, this must arise from the kernels having
been moist when squeezed.

The _Sorbus aucuparia_, mountain-ash, or Rowan-tree as it is called in
Scotland, has been lately added to the list of plants which abound in
the same poisonous principle. M. Grassmann of St Petersburgh has found
that many parts of this tree, such as the flowers and the bark of the
trunk and branches, contain more or less of the peculiar essential oil;
and that the root in particular contains so much in the month of May as
to smell strongly of it when broken across, and to yield a distilled
water which holds fully as much hydrocyanic acid as that procured from
an equal weight of cherry-laurel leaves.[1998]

Several other plants of the same natural order possess similar though
weaker properties, such as the _Prunus avium_, or black-cherry, or
mazzard, the _Prunus insititia_, or bullace, the _Prunus spinosa_, or
sloe, the _Amygdalus nana_, or dwarf-almond, and even the leaves and
kernels of the common cherry, the _Cerasus communis_. Twelve ounces of
cherry kernels distilled with water, yield, according to Geiseler, seven
grains of hydrocyanic acid.[1999] I have no doubt, from my experiments,
that the seeds of _Pyrus malus_, the apple, _Pyrus aria_, the
white-beam, and also, if the taste may be taken for a criterion, the
whole seeds of the _Pomaceæ_, yield by distillation with water a large
quantity of hydrocyanic acid.




                              CHAPTER XXX.
                   OF POISONING WITH CARBAZOTIC ACID.


A substance long known to chemists by the name of indigo-bitter, which
is procured by the action of nitric acid on indigo, silk, and other
azotized substances, and which has been found to consist chiefly of a
peculiar acid, termed by Liebig, from its composition, the carbazotic
acid, appears to be a pure narcotic poison of considerable
activity.[2000] It is in the form of shining crystals, of an excessively
bitter taste, and of a yellow colour so singularly intense that it
imparts a perceptible tint to a million parts of water. The pure
crystals are composed of carbon, azote, and oxygen.

The only account I have seen of the physiological properties of this
substance is a full analysis by Buchner in his Toxicology, of some
interesting experiments by Professor Rapp of Tübingen.[2001] He found
that sixteen grains in solution, when introduced into the stomach,
killed a fox, ten grains a dog, and five grains a rabbit, in an hour and
a half; that the injection of a watery solution into the windpipe
occasioned death in a few minutes; that the introduction of it into the
cavity of the pleura or peritonæum occasioned death in several hours;
that a watery solution of ten grains injected into the jugular vein of a
fox killed it instantaneously, and in like manner five grains affected a
dog in three minutes and killed it in twenty-four hours; and that thirty
grains applied to a wound killed a rabbit. The symptoms remarked from
its introduction into the stomach of the fox were in half an hour
tremors, grinding of the teeth, constant contortion of the eyes and
convulsions, in an hour complete insensibility, and death in half an
hour more. In the dog there was also remarked an attack of vomiting and
feebleness of the pulse.

In the dead body no particular alteration of structure was remarked. The
heart, examined immediately after death from the introduction of the
poison into the stomach, was found much gorged and motionless; but the
irritability of the voluntary muscles remained. The stomach was not
inflamed, but dyed yellow. A very interesting appearance was dyeing of
various textures and fluids throughout the body. In the fox killed by
swallowing sixteen grains the conjunctiva of the eyes, the aqueous
humour, the capsule of the lens, the membranes of the arteries, in a
less degree those of the veins, the lungs, and in many places the
cellular tissue, had acquired a lemon-yellow colour. The dog killed in
the same manner presented similar appearances, also those killed by
injection of the poison into the pleura or peritonæum; and in the latter
animals the urine was tinged yellow. In a rabbit killed by the
application of the poison to a wound the same discoloration was also
every where remarked, together with yellowness of the fibrin of the
blood. But no yellowness could be seen any where in the dog, which died
in twenty-four hours after receiving five grains into the jugular vein.
In no instance was there any yellow tint perceptible in the brain or
spinal cord.

These facts form an interesting addition to the physiology of poisons.
They supply unequivocal proof that this substance is absorbed in the
course of its operation, and furnish strong presumption that other
poisons, which act on organs remote from the place where they are
applied, and which have been sought for without success in the blood, as
well as in other fluids and solids throughout the body, have not been
detected, merely because the physiologist does not possess such simple
and extremely delicate means of searching for them.

The researches of Professor Rapp have been arranged under the title of
carbazotic acid, because this acid forms the most prominent substance in
the matter with which his experiments appear to have been made. But it
is right to state, that the article actually used was, if I understand
correctly the abstract given by Buchner, not the pure crystals, but the
yellow fluid, from which the crystals are procured, and which contains
also a resinous matter and artificial tannin.—The bitter principle of
Welther produced by the action of nitric acid on silk, and that formed
by Braconnot by the action of the same acid on aloes, appear to be
impure carbazotic acid.




                             CHAPTER XXXI.
                        OF THE POISONOUS GASES.


The subject of the poisonous gases is one of great importance in
relation to medical police, as well as medical jurisprudence. They are
objects of interest to the medical jurist, because their effects may be
mistaken for those of criminal violence, and because they have even been
resorted to for committing suicide. They are interesting as a topic of
medical police, since some trades expose the workmen to their influence.

It has hitherto been chiefly on the continent that use has been made of
the deleterious gases for the purpose of self-destruction. Osiander
mentions, that Lebrun, a famous player on the horn, suffocated himself
at Paris in 1809 with the fumes of sulphur; and that an apothecary at
Pyrmont killed himself by going into the _Grotto del Cane_ there, which,
like that near Naples, is filled with carbonic acid gas.[2002] Many
instances have lately occurred in France of suicide caused by the
emanations from burning charcoal in a close chamber.

But these poisons come under the notice of the medical jurist chiefly
because their effects may be mistaken for those of other kinds of
violent death. Several mistakes of this nature are on record. Zacchias
mentions the case of a man, who was found dead in prison under
circumstances which led to the suspicion, that he had been privately
strangled by the governor. But Zacchias proved this to be impossible,
and ascribed death to the fumes from a choffer of burning charcoal left
in the room.[2003] A more striking instance of the kind occurred a few
years ago at London. A woman, who inhabited a room with other five
people, alarmed the neighbours one morning with the intelligence that
all her fellow-lodgers were dead. On entering the room they found two
men and two women actually dead, and another man quite insensible and
apparently dying. This man, however, recovered; and as it was said that
he was too intimate with the woman who gave the alarm, a report was
spread that she had poisoned the rest, to get rid of the man’s wife, one
of the sufferers. She was accordingly put in prison, various articles in
the house were carefully analysed for poison, and an account of the
supposed barbarous murder was hawked about the streets. At last the man
who recovered remembered having put a choffer of coals between the two
beds, which held the whole six people; and the chamber having no vent,
they had thus been all suffocated.[2004]—The following is a similar
accident not less remarkable in its circumstances. Four people in
_Gerolzhofen_ in Bavaria, were found one morning in bed, some dead,
others comatose; and only one recovered. A neighbour who had supped with
them, but slept at home, did not suffer. The stomach and intestines were
found very red and black; and the coats of the stomach brittle. The
contents of the stomach, the remains of their supper, and the wine were
analysed without any suspicious substance being found. A little smoke
having been noticed in the room by those who first entered it, the stove
and fuel were examined, but without furnishing any insight into the
cause of the accident. At last the cellar was examined, and then it was
found that one of the sufferers had heated a copper vessel there so
incautiously, that the fire communicated with the unplastered planks of
the floor above. The planks had burnt with a low smothered flame, and
the vapours passed through the crevices in the floor.[2005]


                _What Irrespirable Gases are Poisonous?_

Some gases act negatively on the animal system by preventing the access
of respirable air to the lungs; others are positively poisonous. The
first point, therefore, is to ascertain which are negatively, and which
positively hurtful.

M. Nysten, who has made the most connected train of experiments on this
subject, conceived that a gas will not act through any other channel
besides the lungs, if it exerts merely a negative action:—and that, on
the contrary, it certainly possesses a direct and positive power, if it
has nearly the same effects, in whatever way it is introduced into the
body.[2006] He therefore thought the best way to ascertain the action of
the gases would be, to inject them into the blood,—conceiving that,
after allowance is made for the mere mechanical effects of an aëriform
body, the phenomena would point out the true operation of each.

His first object then was to learn what phenomena are caused by the
mechanical action of atmospheric air. He found that four cubic inches
and a half, injected into the jugular vein of a dog, killed it
immediately amidst tetanic convulsions, by distending the heart with
frothy blood;—that a larger quantity introduced, gradually caused more
lingering death, with symptoms of oppressed breathing, which arose from
gorging of the lungs with frothy blood;—and that a small quantity,
injected into the carotid artery towards the brain, occasioned speedy
death by apoplexy, which arose from the brain being deprived by means of
the air of a due supply of its proper stimulus, the blood. Numerous
experimental inquiries have been since made on this subject, the latest
of which, those of Dr. Cormack, coincide with the first results of
Nysten, that air injected into the veins causes death by arrestment of
the action of the heart.[2007]

Proceeding with these data, Nysten found that _oxygen_ and _azote_ had
the same effect when apart, as when united in the form of atmospheric
air; that _carburetted hydrogen_, _hydrogen_, _carbonic oxide_, and
_phosphuretted hydrogen_ likewise seemed to act in the same way; and
that the _nitrous oxide_, or intoxicating gas, although it does not
cause so much mechanical injury as the others, on account of its
superior solubility in the blood, has the same effect when injected in
sufficient quantity, and produces little or none of the symptoms of
intoxication excited by it in man.[2008] As to _carbonic acid gas_, he
found that, on account of its great solubility in the blood, it is
difficult to produce mechanical injury with it; that sixty-four cubic
inches are absorbed, and do not excite any particular symptoms; but that
when injected into the carotid artery, it occasions death by apoplexy,
although it is rapidly absorbed by the blood.[2009]

The other gases he tried were hydrosulphuric acid, nitric oxide, ammonia
and chlorine; and all of these proved to be positively and highly
deleterious.

Two or three cubic inches of _hydrosulphuric acid gas_ caused tetanus
and immediate death, when injected into the veins, although the gas was
at once absorbed by the blood. The same quantity acted with almost equal
rapidity when injected into the cavity of the chest. Similar results
were obtained when it was injected into the cellular tissue, or even
when it was left for some time in contact with the sound skin.[2010] The
last important fact has been since confirmed by Lebküchner in his Thesis
on the permeability of the tissues;[2011] and it had previously been
observed also by the late Professor Chaussier, whose experiments will be
mentioned presently (p. 617). In none of Nysten’s experiments with this
gas was the blood changed in appearance.

_Nitric oxide gas_, according to Nysten, is the most energetic of all
the poisonous gases. A very small quantity causes death by tetanus, when
introduced into a vein, the cavity of the chest, or the cellular tissue;
and it always changes the state of the blood, giving it a
chocolate-brown colour, and preventing its coagulation. In one of
Nysten’s experiments a cubic inch and three-quarters injected into the
chest killed a little dog in 45 minutes.[2012] Dr. John Davy appears to
have found this gas not so active.[2013]

Nysten found the two other gases, _ammonia_ and _chlorine_, to be acrid
in their action. When injected into the veins they kill by
over-stimulating the heart; and when injected into the cavity of the
chest, they excite inflammation in the lining membrane.[2014] Hébréart
farther remarked in his experiments relative to the action of irritants
on the windpipe, that chlorine when inspired, produces violent
inflammation in the windpipe and its great branches, ending in the
secretion of a pseudo-membrane like that of croup;[2015] and that a very
small quantity of ammonia has the same effect.

From this abstract of Nysten’s researches, it appears to follow, that
ammonia and chlorine are irritants; hydrosulphuric acid and nitric
oxide, narcotics; oxygen, azote, hydrogen, carburetted hydrogen,
phosphuretted hydrogen, carbonic oxide, and nitrous oxide, negative
poisons; and carbonic acid, doubtful in its nature. Some of these
conclusions do not correspond with the effects observed in man; which
will presently be found to lead to the inference, that not only carbonic
acid, but likewise carbonic oxide, nitrous oxide, and carburetted
hydrogen are narcotics. The reason Nysten did not find these gases
injurious was probably, that, before they could pass from the vein into
which they were injected, to the brain on which they act, they were in a
great measure exhaled from the lungs. The experiments of physiologists
since Nysten’s time likewise tend to show that oxygen gas is a positive
poison when pure, and that even hydrogen possesses active properties.
The inquiries of Mr. Broughton led him to consider hydrogen a positive
poison, because animals die in it in half a minute, and the heart
immediately after death is found to have lost its contractility.
Previous experimentalists had also remarked hypnotic effects from the
inhalation of it diluted with oxygen.[2016] As to oxygen, the same
physiologist ascertained that when pure, it is a narcotic poison, though
a feeble one, as at least five hours of continuous respiration in the
pure gas are required to prove fatal.[2017]


            _Of the Effects of the Poisonous Gases on Man._

According to the effects of the poisonous gases on man, they may be
arranged in two groups, the first including the _irritants_, the second
the _narcotics_. It might have been therefore a more philosophical mode
of arrangement, if the former had been considered under the irritant
class of poisons; but it is more convenient to examine the whole
deleterious gases together.

The _irritant gases_ are nitric oxide gas and nitrous acid vapour,
hydrochloric acid gas, chlorine, ammonia, sulphurous acid, and some
others of little consequence.

_Of Nitric oxide gas and Nitrous acid vapour._—Before nitric oxide gas
can be breathed in ordinary circumstances, it is transformed by the
oxygen of the air into nitrous acid vapour, of a ruddy colour and
irritating odour. Hébréart found that in animals killed by inhaling it
the windpipe was much inflamed.[2018] Sir H. Davy tried to inhale it,
and with this view took the precaution of previously breathing the
nitrous oxide or intoxicating gas, in order to expel the atmospheric air
as much as possible from his lungs. But he found that the small quantity
of nitrous acid fumes formed with the remaining air was sufficient to
cause a sense of burning in the throat, and at once stimulated the
glottis to contract, so that none of the nitric oxide gas could pass
into the larynx. The subsequent entrance of the external air into the
mouth, which Sir Humphrey unluckily had not provided for, was of course
attended by the immediate formation of more acid fumes, by which his
tongue, cheeks, and gums, were irritated and inflamed; and there is no
doubt, as Sir Humphrey himself remarks, that if he had succeeded in
inhaling the nitric oxide gas, the same chemical change would have
happened in the lungs and excited pneumonia.[2019]

The following cases will prove that nitrous acid vapour, disengaged from
the fuming nitrous acid, is a very violent and dangerous poison when
inhaled. A chemical manufacturer, in endeavouring to remove from his
store-room a hamper in which some bottles of nitrous acid had burst,
breathed the fumes for some time, and was seized in four hours with
symptoms of inflammation in the throat and stomach. At night the urine
was suppressed; the skin then became blue; at last he was seized with
hiccup, acute pain in the diaphragm, convulsions, and delirium; and he
died twenty-seven hours after the accident.[2020] Another case has been
described in the Bulletins of the Medical Society of Emulation. It
proved fatal in two days, and the symptoms were those of violent
pneumonia. In this instance there was pneumonia of one side, and
pleurisy of the other; the uvula and throat were gangrenous, and the
windpipe and air-tubes dark-red; the veins throughout the whole body
were much congested, the skin very livid in many places, and the blood
fluid in the heart, but coagulated in the vessels.[2021] Dr. Reitz, a
writer in Henke’s Journal, met with two cases of death from the same
cause in hatters. They had incautiously exposed themselves too much to
the fumes, which are disengaged during the preparation of nitrate of
mercury for the operation of felting, and which are well known to be
nitric oxide gas converted into nitrous acid vapour by contact with the
air. Two men died of inflammation of the lungs excited in that manner;
and a third, a boy of fourteen, after sleeping all night in an apartment
where the mixture was effervescing, was attacked in the morning with
yellowness of the skin, giddiness, and colic, which ended fatally in six
days.[2022]

_Of Poisoning with Chlorine._—The experiments of Nysten and Hébréart
with chlorine, and its well-known irritating effects when inhaled in the
minutest quantities, show that it will produce inflammation of the lungs
and air-passages. The following is the only instance of poisoning with
it in man which has come under my notice. A young man, after breathing
diluted chlorine as an experiment, was instantly seized with violent
irritation in the epiglottis, windpipe, and bronchial branches, cough,
tightness, and sense of pressure in the chest, inability to swallow,
great difficulty in breathing or articulating, discharge of mucus from
the mouth and nostrils, severe sneezing, swelling of the face, and
protrusion of the eyes. Ammonia was of no use; but singular relief was
obtained from the inhalation of a little sulphuretted hydrogen, so that
in an hour and a half he was tolerably well.[2023]

Although this gas is very irritating to an unaccustomed person, yet by
the force of habit one may breathe with impunity an atmosphere much
loaded with it. I have been told by a chemical manufacturer at Belfast,
that his men can work in an atmosphere of chlorine, where he himself
could not remain above a few minutes. The chief consequences of habitual
exposure are acidity and other stomach complaints, which the men
generally correct by taking chalk. He has likewise observed that they
never become corpulent, and that corpulent men who become workmen are
soon reduced to an ordinary size. It is not probable, however, that the
trade is an unhealthy one; for several of this gentleman’s workmen have
lived to an advanced age; one man, who died not long ago at the age of
eighty, had been forty years in the manufactory; and I have seen in Mr.
Tenant’s manufactory at Glasgow a healthy-looking man who had been also
about forty years a workman there. It is an interesting fact, that
during the epidemic fever which raged over Ireland from 1816 to 1819,
the people at the manufactory at Belfast were exempt from it.

_Of Poisoning with Ammonia._—For an account of the effects of _ammonia_,
which, when in the state of gas, acts violently as an irritant on the
mouth, windpipe, and lungs, the reader is referred to the chapter on
ammonia and its salts in page 193. It appears to form one of the gases
disengaged from the soil of necessaries, as will be noticed presently,
and excites inflammation in the eyes of workmen who are incautiously
exposed to it.[2024]

_Of Poisoning with Hydrochloric Acid Gas._—I have not met with any
account of the effects of _hydrochloric acid gas_ on man. But no doubt
can be entertained that it will likewise act as a violent and pure
irritant.

It is exceedingly hurtful to vegetable life. In the course of some
experiments performed in 1827 by Dr. Turner and myself on the effects of
various gases on plants, we found that a tenth of a cubic inch diluted
with 20,000 times its volume of air, so as to be quite imperceptible to
the nostrils, shrivelled and killed all the leaves of various plants,
which were exposed to it for twenty-four hours.[2025] These experiments
were repeated in 1832 by Messrs. Rogerson, apparently in ignorance of
them. Their results are on the whole the same; and the slighter effect
obtained by them from minute proportions of the gas was evidently owing
to the small size of their glass-jars not allowing them to use a
sufficient quantity of it.[2026] They farther found that proportions of
hydrochloric acid gas, amounting to a twentieth of the air, kill small
animals in half an hour with symptoms of obstructed respiration. Their
experiments with less proportions are not precise, yet warrant the
inference that even a thousandth part of the gas will probably prove
fatal in no long time.[2027]

_Of Poisoning with Hydrosulphuric Acid Gas._—The _narcotic gases_
are of much greater importance than the irritants, on account of
the singularity of their effects, and the greater frequency of
accidents with them. This group includes hydrosulphuric acid,
carburetted-hydrogen, carbonic acid, carbonic oxide, nitrous
oxide, cyanogen, and oxygen.

Hydrosulphuric acid gas is probably the most deleterious of all the
gases. According to Thenard and Dupuytren, air containing only an 800th
of it will kill small birds in a few seconds; and a 290th is sufficient
to kill a dog; which, however, will sustain so much as a 400th.[2028]
Chaussier previously found, that a horse was killed by breathing
atmospheric air which contained a 250th of hydrosulphuric acid gas; and
that it acts with energy on animals, whether it be inhaled, or injected
into the stomach, anus, or cellular tissue, or even simply applied to
the skin. Nine quarts of the gas injected into the anus of a horse
killed it in one minute; and a rabbit, whose skin alone was exposed to
it, died in ten minutes.[2029] Ulterior inquiries by MM.
Parent-Duchâtelet and Gaultier de Claubry,—scarcely so precise however
as those of their predecessors,—appear to lead to the conclusion, that
its energy is in some circumstances not so great. While superintending
the clearing out of some of the choked drains of Paris, they found that
the workmen suffered no harm, though they habitually breathed an
atmosphere containing from 25 to 80 ten-thousandths of hydrosulphuric
acid gas, and on some occasions even so much as one per cent.; nay, on
one occasion Gaultier remained several minutes without injury,
collecting air for chemical analysis in an atmosphere, which proved to
be loaded with three per cent. of the gas.[2030] None of these
researches point out the precise manner of death. Dr. Percy of
Nottingham informs me he found in 1839, that dogs, which breathed air,
containing this gas, quickly died in convulsions like those caused by
hydrocyanic acid; that in some instances the heart’s action was observed
to have ceased, when the body was opened immediately after death; but
that in general it either continued to beat for some time, or could be
made to do so when its state of congestion was relieved by withdrawing a
little blood.

Dr. Turner and I found that hydrosulphuric acid gas is very injurious to
vegetables, and that it acts differently from muriatic acid gas, as it
appeared to exhaust the vitality of plants and to cause in them a state
analogous to narcotic poisoning in animals. Four cubic inches and a
half, diluted with eighty volumes of air, caused drooping of the leaves
of a mignonette plant in twenty-four hours; and the plant, though then
removed into the open air, continued to droop till it bent over
altogether and died.[2031]

The best description of the effects of this gas on man has been given by
M. Hallé,[2032] in his account of the nature and effects of the
exhalations from the pits of the Parisian necessaries; which exhalations
appear, from the experiments of Thenard and Dupuytren, to be mixtures
chiefly of ammonia and sulphuretted-hydrogen. The symptoms, in cases
where the vapours are breathed in a state of concentration, are sudden
weakness and all the signs of ordinary asphyxia. The individual becomes
suddenly weak and insensible; falls down; and either expires
immediately, or, if he is fortunate enough to be quickly extricated, he
may revive in no long time, the belly remaining tense and full for an
hour or upwards, and recovery being preceded by vomiting and hawking of
bloody froth.[2033] When the noxious emanations are less concentrated,
several affections have been noticed, which may be reduced to two
varieties, the one consisting of pure coma, the other of coma and
tetanic convulsions. In the comatose form, the workman seems to fall
gently asleep while at work, is roused with difficulty, and has no
recollection afterwards of what passed before the accident. The
convulsive form is sometimes preceded by noisy and restless delirium,
sometimes by sudden faintness, heaving or pain in the stomach, and pains
in the arms, and almost always by difficult breathing, from weakness in
the muscles of the chest. Insensibility, and a state resembling asphyxia
rapidly succeed, during which the pupil is fixed and dilated, the mouth
filled with white or bloody froth, the skin cold, and the pulse feeble
and irregular. At last convulsive efforts to breathe ensue; these are
followed by general tetanic spasms of the trunk and extremities; and if
the case is to prove fatal, which it may not do for two hours, a state
of calm and total insensibility precedes death for a short
interval.[2034] When the exposure has been too slight to cause serious
mischief, the individual is affected with sickness, colic, imperfectly
defined pains in the chest, and lethargy.[2035]

The appearances in the bodies of persons killed by these emanations are
fluidity and blackness of the blood, a dark tint of all the internal
vascular organs, annihilation of the contractility of the muscles, more
or less redness of the bronchial tubes, and secretion of brown mucus
there as well as in the nostrils, gorging of the lungs, an odour
throughout the whole viscera like that of decayed fish, and a tendency
to early putrefaction.[2036] Chaussier in his experiments also remarked
in animals, that when a plate of silver or bit of white lead was thrust
under the skin it was blackened.[2037] Dr. Percy could not detect the
gas in the brain of animals killed by inhaling it.

These extraordinary accidents may be occasioned not only by exposure to
the vapours from the _fosses_, but likewise by the incautious inhalation
of the vapours proceeding from the bodies of persons who have been
asphyxiated there. Sickness, colic, and pains in the chest, are often
caused in the latter mode; and Hallé has even given an instance of the
most violent form of the convulsive affection having originated in the
same manner.[2038]

In order that the reader may comprehend the exact cause of these
accidents,—as it is not easy for an Englishman to comprehend how
suffocation may arise from the fumes of a privy,—it may be necessary to
explain, that in Paris the pipe of the privy terminates under ground in
a pit, which is usually contained in a small covered vault, or is at the
bottom of a small square tower open at the roof of the house; and that
the pit is often several feet long, wide and deep. Here the filth is
sometimes allowed to accumulate for a great length of time, till the pit
is full; and it is in the process of clearing it out that the workmen
are liable to suffer. Hallé has given an interesting narrative of an
attempt made to empty one of these pits in presence of the Duc. de
Rochefoucault, the Abbé Tessier, himself, and other members of the
Academy of Sciences, who were appointed by the French government to
examine into the merits of a pretended discovery for destroying the
noxious vapours. The pit chosen was ten feet and a half long, six wide,
and at least seven deep; and repeated attempts had been previously made
without success to empty it. For some time the process went on
prosperously; when at last one of the workmen dropped his bucket into
the pit. A ladder being procured, he immediately proceeded to descend,
and would not wait to be tied with ropes. “But hardly,” says Hallé, “had
he descended a few steps of the ladder, when he tumbled down without a
cry, and was overwhelmed in the ordure below, without making the
slightest effort to save himself. It was at first thought he had slipped
his foot, and another workman promptly offered to descend for him. This
man was secured with ropes in case of accident. But scarcely had he
descended far enough to have his whole person in the pit except his
head, when he uttered a suppressed cry, made a violent effort with his
chest, slipped from the ladder, and ceased to move or breathe. His head
hung down on his breast, the pulse was gone; and his complete state of
asphyxia was the affair of a moment. Another workman, descending with
the same precautions, fainted away in like manner, but was so promptly
withdrawn that the asphyxia was not complete, and he soon revived. At
last a stout young man, secured in the same way as the rest, also went
down a few steps. Finding himself seized like his companions, he
re-ascended to recover himself for a moment; and still not discouraged,
he resolved to go down again, and descended backwards, keeping his face
uppermost, so that he was able to search for his companion with a hook
and withdraw the body.” It was impossible to go on with the operation of
clearing out; and the pit was shut up again. The first workman never
showed any sign of life; the second recovered after discharging much
bloody froth; all the persons in the vault were more or less affected;
and a gentleman who, in trying to resuscitate the dead workman,
incautiously breathed the exhalations from his mouth, was immediately
and violently seized with the convulsive form of the affection.[2039]

The same kind of accident has been observed at Paris in the vaults of
cemeteries, owing to the same cause,—the disengagement of hydrosulphuric
acid and hydrosulphate of ammonia during putrefaction. A remarkable
instance is related by Guérard.[2040] Analogous accidents have happened
in this country in clearing out drains.

In none of the French investigations on this singular subject has any
allusion been made to the question, whether the health sustains any
injury from long-continued exposure to the gas in very minute
proportion. It is probably injurious however. At one time, while in the
practice of not using any precautions against inhaling the gas in
chemical researches, I used to remark that daily exposure to it in
minute quantity caused in a few weeks an extraordinary lassitude,
languor of the pulse, and defective appetite. Strohmeyer in the like
circumstances was liable to severe headache. Mr. Taylor says that the
workmen in the Thames Tunnel suffered severely for some time from a
similar exposure. Many of them became affected with giddiness, sickness,
general debility and emaciation, then with a low fever attended with
delirium, and in the course of a few months several died. No cause could
be discovered for their illness except the frequent escape of
sulphuretted-hydrogen from the roof. The affection only disappeared,
when the communication from bank to bank was completed, so that the
tunnel could be thoroughly ventilated.[2041]

The presence of hydrosulphuric acid in all such emanations is best
proved by exposing to them a bit of filtering paper moistened with a
solution of lead. The smell alone must not be relied on, as putrescent
animal matter exhales an odour like that of hydrosulphuric acid, though
none be present. Workmen ought to be aware that hydrosulphuric acid may
be quickly fatal where lights burn with undiminished brilliancy; and
that in places where it is apt to accumulate, the degree of purity of
the air may vary so much in the course of working, as to be wholesome
only a few minutes before, as well as a few minutes after a fatal
accident.[2042]

In the present place, some notice may be taken of an extraordinary
accident, which happened in 1831 near London. Great doubts may be
entertained whether hydrosulphuric acid was the cause of it; and while
these exist, it is not possible to arrange it under a proper head. It is
too important, however, in relation to Medical Jurisprudence, to be
omitted in this work; and I take the opportunity of mentioning it here,
as the accident was ascribed to hydrosulphuric acid by those who
witnessed it.

In August, 1831, twenty-two boys living at a boarding-school at Clapham
were seized in the course of three or four hours with alarming symptoms
of violent irritation in the stomach and bowels, subsultus of the
muscles of the arms, and excessive prostration of strength. Another had
been similarly attacked three days before. This child died in
twenty-five, and one of the others in twenty-three hours. On examination
after death, the Peyerian glands of the intestines were found in the
former case enlarged, and as it were tuberculated; in the other there
were also ulcers of the mucous coat of the small intestines, and
softening of that coat in the colon. A suspicion of accidental poisoning
having naturally arisen, the various utensils and articles of food used
by the family were examined but without success. And the only
circumstance which appeared to explain the accident was, that two days
before the first child took ill, a foul cess-pool had been opened, and
the materials diffused over a garden adjoining to the children’s
play-ground. This was considered a sufficient cause of the disease by
Dr. Spurgin and Messrs. Angus and Saunders of Clapham, as well as by
Drs. Latham and Chambers, and Mr. Pearson of London, who personally
examined the whole particulars.[2043] Their explanation may be the only
rational account that can be given of the matter. But as no detail of
their chemical inquiries was ever published, their opinion cannot be
received with confidence by the medical jurist and the physician; since
it is not supported, so far as I am aware by any previous account of the
effects of hydrosulphuric acid gas.

_Of Poisoning with Carburetted Hydrogen._—Of the several species of
carburetted hydrogen gas it is probable that all are more or less
narcotic; but they are much inferior in energy to sulphuretted hydrogen.

Sir H. Davy found that when he breathed a mixture of two parts of air
and three of carburetted hydrogen, procured from the decomposition of
water by red-hot charcoal, he was attacked with giddiness, headache, and
transient weakness of the limbs. When he breathed it pure, the first
inspiration caused a sense of numbness in the muscles of the chest; the
second caused an overpowering sense of oppression in the breast, and
insensibility to external objects; during the third he seemed sinking
into annihilation, and the mouthpiece dropped out of his hand. On
becoming again sensible, which happened in less than a minute, he
continued for some time to suffer from a feeling of impending
suffocation, extreme exhaustion, and great feebleness of the pulse.
Throughout the rest of the day he was affected with weakness, giddiness
and rending headache.[2044] These experiments show that the gas is
deleterious. Yet Nysten found it inert when injected into the veins, and
what is more to the point, colliers breathe the air of coal mines
without apparent injury when strongly impregnated with it.

The mixed gases of coal-gas or oil-gas appear likewise to be inert when
considerably diluted; for gas-men breathe with impunity an atmosphere
considerably loaded with them; and in the course of some researches on
the illuminating power and best mode of burning these gases, Dr. Turner
and myself daily, for two months, breathed air strongly impregnated with
them, but never remarked any unpleasant effect whatever.

It would seem, however, from several accidents in France and England,
that when the impregnation is carried a certain length, poisonous
effects may ensue; and that the symptoms then induced are purely
narcotic. The first case, which occurred at Paris in 1830, has been
related by M. Devergie. In consequence of a leak in the service-pipe
which supplied a warehouse, five individuals who slept in the house were
attacked during the night with stupor; and if one of them had not been
awakened by the smell and alarmed the rest, it is probable that all
would have perished. As it was, one man was found completely comatose
and occasionally convulsed, with froth issuing from the mouth,
occasional vomiting, stertorous respiration, and dilated pupils. Some
temporary amendment was procured by blood-letting, but the breathing
continued laborious, and he expired about nine hours after the party
went to bed, and six hours after the alarm was given. On dissection the
vessels of the brain were found much gorged, the blood in the heart and
great vessels firmly coagulated, one of the lungs congested, and its
bronchial tube blocked up by a kidney bean. The immediate cause of death
in this case is therefore doubtful.[2045] A similar set of cases
happened at Leeds in 1838. An old woman and her grand-daughter were
found dead in bed one morning at nine o’clock, ten hours and a half
after they had been seen alive and well. The air of the apartment was
loaded with coal-gas from a leak in a street-pipe ten feet from the
bedroom. One body was cold and stiff when found, and the other became
rigid very soon. The attitude and expression were calm, the integuments
pale, the cerebral membranes natural, the brain itself turgid, and its
ventricles distended, in the case of the girl, with an ounce and a half
of serosity, the lungs congested, the alimentary mucous membrane red,
and the blood every where fluid, and unusually florid, even in the right
side of the heart.[2046] Another accident of the same kind, which proved
fatal to five individuals, occurred at Strasbourg in 1841. Four were
found dead, another survived twenty-four hours after the accident was
discovered, and a sixth recovered. It appears from the statement of this
person, that the first symptoms were headache and giddiness, then nausea
and vomiting, afterwards confusion of ideas, and at length
insensibility. General prostration, partial palsy, coma, and convulsions
were the leading symptoms after the accident was observed. In the four
people found dead the most remarkable appearances were cerebral
congestion, redness of the bronchial membrane, accumulation of bloody,
frothy mucus in the air tubes, scarlet redness of the lungs, coagulation
and darkness of the blood. In the person who was found alive, but did
not recover, there was no cerebral congestion, gorging of the air tubes,
or redness of the lungs. Professor Tourdes, who reports these cases,
ascertained that air containing a fiftieth of coal-gas kills rabbits in
twelve or fourteen minutes, and that even a thirtieth proves fatal,
though slowly. The gas which caused the accident, and which was prepared
from a mixture of water and slate coal, consisted of 22·5 per cent.
light carburetted hydrogen, 6·0 bicarburetted hydrogen, 21·9 carbonic
oxide, 31 hydrogen, 14 azote, and 4·6 carbonic acid; and by experiment
the author found that the most energetic of these gases as a poison is
the carbonic oxide, and that the action of the two carburetted-hydrogens
is quite feeble.[2047] It is somewhat remarkable that no such accident
has ever happened in Edinburgh, where nevertheless coal-gas is more used
for purposes of illumination in private houses than in any other city.
The fine quality of the gas,—for it contains a mere trace of carbonic
acid, and probably less than four per cent. of carbonic oxide,—may be
the reason why accidents are not occasioned by it. It is a singular
fact, however, that the powerful odour of the gas, when it accidentally
escapes in the night-time, generally awakes very soon those who are
exposed to inhale it.

_Of Poisoning with Carbonic Acid Gas._—Carbonic acid gas is the most
important of the deleterious gases; for it is the daily source of fatal
accidents. It is extricated in great quantity from burning fuel; it is
given out abundantly in the calcining of lime; it is disengaged in a
state of considerable purity in brew-houses by the fermentation of beer;
it is often met with in mines and caverns, particularly in coal-pits and
draw-wells; it may collect in apartments where fuel is burnt without a
proper outlet for the vitiated air, or where persons are crowded too
much for the capacity of the room. Hence many have been killed by
descending incautiously into draw-wells, by falling into beer-vats, and
by sleeping before the traps of lime-kilns, or in apartments without
vents and heated by choffers. Instances have even occurred of the same
accident from sleeping in greenhouses during the night, when plants
exhale much carbonic acid; and some dreadful cases have occurred of
suffocation from confinement in small crowded rooms.

Physiologists, as already remarked, are not quite agreed as to the
action of carbonic acid gas,—whether it is a positive poison, or simply
an asphyxiating gas. But in my opinion reasons enough exist for
believing that it is positively and energetically poisonous. This is
perhaps shown by its effects being much more rapidly produced, and much
more slowly and imperfectly removed, than asphyxia from immersion in
hydrogen or azote.[2048] Thus immersion for twenty-five seconds in an
atmosphere of carbonic acid gas has been found sufficient to kill an
animal outright; and fifteen seconds will kill a small bird.[2049] But
it is more unequivocally established by the three following facts:

In the first place, if, instead of the nitrogen contained in atmospheric
air, carbonic acid gas be mixed with oxygen in the same proportion,
animals cannot breathe this atmosphere for two minutes without being
seized with symptoms of poisoning.[2050] Even a much less proportion has
the same effect. Five per cent. in the air will affect small birds in
two minutes, and kill them in half an hour.[2051] Persons have become
apoplectic in an atmosphere of carbonic acid gas, which to those who
entered it appeared at first quite respirable.[2052]

Secondly, Professor Rolando of Turin having found that the land tortoise
sustained little injury when the great air-tube of one lung was tied,—he
contrived to make it breathe carbonic acid gas with one lung, while
atmospheric air was inhaled by the other; and he remarked that death
took place in a few hours.[2053]

Thirdly, the symptoms caused by inhaling the gas may be also produced by
applying it to the inner membrane of the stomach or to the skin. On the
one hand aërated water has been known to cause giddiness or even
intoxication when drunk too freely at first;[2054] and the sparkling
wines probably owe their rapid intoxicating power to the carbonic acid
they contain. And, on the other hand, M. Collard de Martigny has found
that, if the human body be enclosed in an atmosphere of the gas, due
precautions being taken to preserve the free access of common air to the
lungs, the usual symptoms of poisoning with carbonic acid are produced,
such as weight in the head, obscurity of sight, pain in the temples,
ringing in the ears, giddiness, and an undefinable feeling of terror;
and that if the same experiment be made on animals and continued long
enough, death will be the consequence.[2055]

When a man attempts to inhale pure carbonic acid gas, for example by
putting the face over the edge of a beer-vat, or the nose into a jar
containing chalk and weak muriatic acid, the nostrils and throat are
irritated so strongly, that the glottis closes and inspiration becomes
impossible. Sir H. Davy in making this experiment, farther remarked,
that the gas causes an acid taste in the mouth and throat, and a sense
of burning in the uvula.[2056] I have remarked the same effects from
very pure gas disengaged by tartaric acid from carbonate of soda. Hence,
when a person is immersed in the gas nearly or perfectly pure, as in a
beer-vat, or old well, he dies at once of suffocation.

The effects are very different when the gas is considerably diluted; for
the symptoms then resemble apoplexy. As they differ somewhat according
to the source from which the gas is derived, and the admixtures
consequently breathed along with it, it will be necessary to notice
separately the effects of the pure gas diluted with air,—of the
emanations from burning charcoal, tallow, and coal,—and finally of air
vitiated by the breath.

1. M. Chomel of Paris has related a case of poisoning with the gas
diluted with air, in the person of a labourer, who was suddenly immersed
in it at the bottom of a well, and remained there three-quarters of an
hour. He was first affected with violent and irregular convulsions of
the whole body and perfect insensibility, afterwards with fits of spasm
like tetanus; and during the second day, when these symptoms had gone
off, he continued to be affected with dumbness.[2057]—It is worthy of
particular remark that, contrary to general belief, these effects may be
produced in situations where the air is not sufficiently impure to
extinguish lights. Thus M. Collard de Martigny relates the case of a
servant, who, on entering a cellar where grape-juice was fermenting,
became suddenly giddy, and, under a vague impression of terror, fled
from the place, dropping her candle on the floor and shutting the door
behind her. She fell down insensible outside the door, and those who
went to her assistance found on opening the door that the light
continued to burn.[2058]—Mr. Taylor indeed has since ascertained that a
candle will burn in air, which contains ten, or even twelve per cent. of
carbonic acid,[2059]—a proportion more than sufficient to cause
poisoning in no long time. It is also important to observe, that,
contrary to what would be expected from the statements of Sir H. Davy
and other experimentalists on the effects of the pure gas, it will often
happen that no odour or taste is perceived. M. Bonami, in an account of
an accident which happened at Nantes to two workmen who descended an old
well, says that the first while descending uttered a piercing cry and
fell down; and that as soon as his comrade, who tried to rescue him, was
lowered ten or twelve feet, he felt as if he was about to be suffocated
for want of breath, but perceived no strong or disagreeable smell.[2060]
It should be remembered therefore by workmen, that there may be danger
in descending pits where none is indicated by the sense of smell, or by
the extinguishing of a light.

2. The fumes of burning charcoal have been long known to be deleterious.
The early symptoms caused by them have been little noticed; for, as this
variety of poisoning generally occurs during sleep, the patient is
seldom seen till the symptoms are fully formed. In an attempt at
self-destruction described in a French journal, the first effects were
slight oppression, then violent palpitation, next confusion of ideas,
and at last insensibility.[2061] Tightness in the temples, and an
undefinable sense of alarm have also been remarked;[2062] and others
have, on the contrary, experienced a pleasing sensation that seduced
them to remain on the fatal spot.[2063] The best account of the
incipient symptoms has been given by Mr. Coathupe of Wraxhall, in an
account of an experiment he made with Joyce’s stove,—a preposterous
invention, the fuel of which was supposed by the inventor to burn
without contaminating the air, although it was neither more nor less
than prepared charcoal. Having closed every aperture in a room of the
capacity of eighty cubic yards, Mr. Coathupe kindled the stove and
watched the results. In four hours he had slight giddiness, in five
hours and a half intense giddiness, the desire to vomit without the
power, excessive prostration and incapability of muscular effort, a
frequent full throbbing pulse, a sense of distention of the cerebral
arteries, agonizing headache, chiefly in the hindhead, but no sense of
suffocation. At this time he experienced great difficulty in opening the
window and removing the stove; and in seven hours, when his wife entered
the room, he was unable to tell what was the matter, although quite
conscious of all that was passing. He then slowly recovered.[2064] A
similar account has also been given by Mr. Chapman of Tooting of the
effects of this notorious stove. A young gentleman, after being only one
hour in a chamber heated by it, felt first slight giddiness and
headache, and afterwards violent pain in the head and tightness round
the forehead and temples; the pupils became excessively dilated and
nearly insensible; there was constant ringing in the ears, a feeble
frequent pulse, paleness of the features and lividity of the lips and
hands, coldness of the extremities, laborious irregular breathing, and
extreme prostration. A temporary relief, obtained by stimulants, was
succeeded by violence; which, however, was subdued by blood-letting; and
he recovered.[2065] A set of cases, 70 in number, similar to the last
two, but milder, occurred in January, 1836, in the church of Downham in
Norfolk, which was heated by two of these stoves.[2066]

The following abstract of a case by Dr. Babington will convey an
accurate idea of the advanced symptoms. The waiter of a tavern and a
little boy, on going to bed, left a choffer of charcoal burning beside
it; and next morning were found insensible. The boy died immediately
after they were discovered. The waiter had stertorous breathing, livid
lips, flushing of the face, and a full, strong pulse; for which
affections he was bled to ten ounces. When Dr. Babington first saw him,
however, the pulse had become feeble, the breathing imperfect, and the
limbs cold; the muscles were powerless but twitched with slight
convulsions, the sensibility gone, the face pale, the eyelids closed,
the eyes prominent and rolling, the tongue swollen and the jaw locked
upon it, and there was a great flow of saliva from the mouth. The
employment of galvanism at this time caused an evident amendment in
every symptom. But it was soon abandoned; because each time it was
applied, the excitement was rapidly followed by corresponding
depression. Cold water was then dashed upon him, ammonia rubbed on his
chest, and oxygen thrown into the lungs; through which means a warm
perspiration was brought out, and his state rapidly improved. He was
nearly lost, however, during the subsequent night by hemorrhage from the
divided vein; but next day he was so well that he could even speak a
little. For two days afterwards the left side of the face was paralyzed,
and his mental faculties were somewhat disordered.[2067]—In such cases
as this the stupor is generally very deep. There is a case in a French
Journal of a girl, who, after remaining some time in a small close
chamber heated by a charcoal choffer, fell down insensible, remained in
that state for three hours, and found, on recovering from her lethargy,
that the choffer had fallen, and burnt the skin and subjacent fat of the
thighs to a cinder.[2068]

Occasionally the stage of stupor is followed, as in some other varieties
of narcotic poisoning, by a stage of delirium, at times of the furious
kind, or by a state resembling somnambulism.[2069] It does not follow
that recovery is certain because coma has thus given place to
delirium,—an alteration, which in most varieties of narcotic poisoning
is considered a sure sign of recovery. Collard de Martigny has related a
case which eventually proved fatal, notwithstanding this sign of
improvement.[2070]

The narcotism induced by breathing charcoal fumes often lasts a
considerable length of time,—much longer indeed than the effects of
other narcotic poisons. This will appear sufficiently from the case
described by Dr. Babington. One of the people, mentioned at the
commencement of this chapter as having been suffocated at Gerolzhofen,
lingered five days in a state of coma before he expired.

Commonly in cases of recovery, there is found to have been no
consciousness of any thing going on around, or recollection of what
passed subsequently to the first impressions of poisoning. The reverse,
however, occurred in Mr. Coathupe’s experiment; and a similar instance
has been published, where the individual, though apparently insensible,
knew when the room was first entered by strangers, and heard them call
him by name and bid him put out his tongue, and stretch forth his
arm,—without, however, his having the power to answer, or in any way to
express the consciousness of understanding them.[2071]

Poisoning with charcoal vapour has become a subject of great importance
in French medical jurisprudence, partly on account of the frequency with
which it is resorted to for the purpose of committing suicide, and
partly because repeated attempts have been made to conceal murder by
arranging matters so as to present the appearances of suicide. M.
Devergie says, that in the years 1834 and 1835 no fewer than 360 cases
of poisoning with charcoal-vapour occurred in Paris, of which nearly
four-fifths proved fatal; and he has given the particulars of two
attempts to conceal murder under the appearance of death from this
cause.[2072]

The subject has therefore been carefully examined by various authors,
but by none so successfully as by M. Devergie; of whose important
researches the following is a brief analysis.

In stating the various sources whence charcoal-vapour may become
incidentally the cause of death, he dwells particularly on the risk of
its admission from adjoining vents, even in other houses from that where
the accidents happen,—because there may be currents in the apartment
which occasion back-draught. Three remarkable cases of this kind, very
obscure in their origin, have been related by M. d’Arcet.[2073]

The very discrepant effects of the poison on different individuals,
simultaneously and to appearance alike exposed to it, have usually been
explained by reference to the great density of the gas, which
consequently accumulates near the floor. Some, however, have doubted the
fact that the gas is unequally diffused. Mr. Taylor in particular says
he ascertained by analysis, that air collected above and below a choffer
of burning charcoal was equally contaminated, that what was collected a
foot above its level contained 4·65 per cent., and that another portion
taken the same distance below it contained 4·5 of carbonic acid.[2074]
M. Devergie has discovered the source of these discrepant opinions. He
has found,[2075] that, notwithstanding the high density of carbonic acid
gas, the currents caused by the heat, disengaged when charcoal is burnt
in a room, without an issue for the products of combustion, produce an
equable mixture of gases at all elevations in the apartment, provided
the air be examined while still warm, and not long after the charcoal
has burnt out; but that, at a later period, such as twelve hours, the
carbonic acid partly separates and sinks, so that, while the air at the
top contains only a 78th, that near the floor contains four times as
much, or a 19th of carbonic acid gas.

Disputes have also arisen as to the precise nature of the emanations
from burning charcoal,—some believing that carbonic acid is alone
discharged in such quantity as to prove injurious, and is singly
sufficient to account for the effects which have been observed,—while
others maintain that carbonic oxide, carburetted-hydrogen, or some
peculiar pyrogenous vapour, may be also formed, and prove the real cause
of the active properties of the vapour. According to the researches of
Orfila, charcoal in a state of vivid ignition emits carbonic acid only,
a hundred parts of the consumed air having been ascertained by him to be
composed of 42 azote, 46 common air, and 12 carbonic acid. But when the
combustion is low, a hundred parts consist of 52 azote, 20 common air,
14 carbonic acid, and 14 carburetted-hydrogen; so that not only is the
air more thoroughly consumed; but likewise an additional poisonous gas
is brought into action.[2076] The difference thus indicated has been
supposed to account for what is often observed in countries where
charcoal choffers are much in use for warming close apartments,—namely,
that the practice is attended with most danger when the combustion is
low, and that it is unsafe to close the doors of an apartment till the
fuel is in a state of vivid ignition. M. Guérard again maintains, that
when the supply of air is incomplete and combustion low, carbonic oxide
gas is formed in considerable quantity; and that this gas, confessedly a
much more powerful narcotic than carbonic acid, is probably the cause of
many cases of poisoning with charcoal fumes.[2077] M. Devergie doubts
the exactness of Orfila’s experiments on this head, but gives no new
analysis. He observes that charcoal-vapour gives the air of a room a
peculiar odour and bluish misty appearance, the latter of which slowly
diminishes, and in twelve hours disappears; and that possibly there may
be both a little carbonic oxide and carburetted-hydrogen in the air. But
nevertheless he is of opinion that the carbonic acid alone is adequate
to occasion all the effects observed in man or animals.[2078] Professor
Hünefeld is of a different opinion, and has supplied the most
satisfactory explanation of the important fact, that charcoal fumes are
most noxious when the fuel has been just kindled and burns low; for he
ascertained that at first it gives out a pyrogenous acid, which
occasions headache and tendency to sickness, and which is not a product
of combustion at the moment, but exists ready formed; and that when
charcoal is at a full red heat, this noxious substance is no longer
given off.[2079] Mr. Coathupe also thinks the cause of poisoning by
charcoal fumes is an unknown pyrogenous body, and not carbonic acid
gas.[2080]—This department of inquiry is obviously susceptible of more
precise information. But meanwhile, whatever may be the probability
that, besides carbonic acid, some other gases, or some peculiar
pyrogenous body, may occasionally exist in charcoal fumes, and increase
their poisonous property, little doubt can exist that the carbonic acid
is singly sufficient to account for all the leading phenomena.

M. Devergie has been led to the opinion that air, in which a fourth part
of its oxygen has been converted into carbonic acid, and which therefore
contains five per cent. of that gas, is amply enough impregnated to
occasion death.[2081] This corresponds with the observations of M.
Ollivier, who found that three per cent. was as much as could be
breathed with impunity even for a moderate length of time.[2082] Less,
however, will suffice to prove injurious or even fatal, if the air be
breathed long. Mr. Coathupe inferred from a rough estimate, that in the
dangerous experiment he made upon himself, the carbonic acid, if
uniformly diffused in the apartment, which was probably the case,
amounted to only two per cent.; but his data were inadequate.[2083]

Proceeding from the fact that five per cent. of carbonic acid is
sufficient to cause death, Devergie points out what quantity of charcoal
is required to form that proportion,—a question of no small moment in
respect to charges of murder, concealed under the semblance of suicide
by suffocation with charcoal fumes. And he shows, that a French bushel,
or decalitre, weighing 3000 grammes, is sufficient for a close apartment
of 1275 cubic mètres, that is 6·6 pounds avoirdupois for a space of 1666
English cubic yards, provided the gas be uniformly diffused.[2084] The
quantity of charcoal burnt in a given case may be arrived at pretty
nearly from the weight of ashes left, which is estimated in round
numbers at a twenty-fifth by himself,[2085] and at a twentieth by
Ollivier.[2086]

It is important to remark that complete closure of an apartment is by no
means essential for the action of carbonic acid, whether disengaged
within it or introduced from without. For poisoning has occurred, even
where a window was partially open.[2087]

3. It is probable that in some circumstances a very small quantity of
the mixed gases proceeding from the slow combustion of tallow and other
oily substances will produce dangerous symptoms. Dr. Blackadder remarked
in the course of his experiments on flame, that the vapour into which
oil is resolved, previous to its forming flame round the wick, excites
in minute quantities intense headache.[2088] The emanations from the
burning snuff of a candle, which are probably of the same nature, seem
to be very poisonous. An instance indeed has been recorded in which they
proved fatal. A party of iron-smiths, who were carousing on a festival
day at Leipzig, amused themselves with plaguing a boy, who was asleep in
a corner of the room, by holding under his nose the smoke of a candle
just extinguished. At first he was roused a little each time. But when
the amusement had been continued for half an hour he began to breathe
laboriously, was then attacked with incessant epileptic convulsions, and
died on the third day.[2089]—The effects of such emanations are probably
owing to empyreumatic volatile oil, which will be presently seen to be
an active poison.

4. The vapours from burning coal are the most noxious of all kinds of
emanations from fuel, and cause peculiar symptoms. But they are less apt
to lead to accidents than the vapour of charcoal, as they are much more
irritating to the lungs. This effect depends on the sulphurous acid gas
which is mingled with the carbonic acid.

Sulphurous acid gas is exceedingly deleterious to vegetable life, being
hardly inferior in that respect to hydrochloric acid. Dr. Turner and I
found that a fifth of a cubic inch diluted with ten thousand times its
volume of air destroyed all the leaves of various plants in forty-eight
hours.[2090] I am not acquainted with any experiments on animals or
observations on man regarding the effects of the pure gas. But it will
without a doubt prove a powerful irritant.

Some of the peculiarities in the cases now to be mentioned were possibly
owing to the admixture of sulphuric acid gas with the carbonic, both
being inhaled in a diluted state. The cases are described by Mr. Braid,
at the time surgeon at Leadhills. In March, 1817, several of the miners
there were violently affected, and some killed, in consequence, it was
supposed, of the smoke of one of the steam-engines having escaped into
the way-gates, and contaminated the air in the workings. Four men who
attempted to force their way through this air into the workings below
were unable to advance beyond, and seem to have died immediately. The
rest attempted to descend two hours after, but were suddenly stopped by
the contaminated air. As soon as they reached it, although their lights
burnt tolerably well, they felt difficulty in breathing, and were then
seized with violent pain and beating in the head, giddiness and ringing
in the ears, followed by vomiting, palpitation and anxiety, weakness of
the limbs and pains above the knees, and finally with loss of
recollection. Some of them made their escape, but others remained till
the air was so far purified that their companions could descend to their
aid. When Mr. Braid first saw them, some were running about frantic and
furious, striking all who came in their way,—some ran off terrified
whenever any one approached them,—some were singing,—some
praying,—others lying listless and insensible. Many of them retched and
vomited. In some the pulse was quick, in others slow, in many irregular,
and in all feeble. All who could describe their complaints had violent
headache, some of them tenesmus, and a few diarrhœa. In a few days all
recovered except the first four and three others who had descended to
the deeper parts of the mine.[2091]—Another accident of the same nature,
and followed by the same phenomena, happened more lately at
Leadhills.[2092] Similar accidents have been also witnessed by Mr. Bald,
civil engineer, among the coal-miners who work in the neighbourhood of a
burning mine belonging to the Devon Company. It is worthy of remark,
that the men sometimes worked for a considerable length of time before
they were taken ill. Such being the case, it will be readily conceived
that the burning of the lights was not a test of the wholesomeness of
the air. Here, as at Leadhills and in other instances already mentioned,
the lights continued to burn where the men were poisoned.[2093]

5. Somewhat analogous to the symptoms now described are the effects of
the gradual contamination of air in a confined apartment. Every one must
have read of the horrible death of the Englishmen who were locked up all
night in a close dungeon in Fort William at Calcutta. One hundred and
forty-six individuals were imprisoned in a room twenty feet square, with
only one small window; and before next morning all but 23 died under the
most dreadful of tortures,—that of slowly increasing suffocation. They
seem to have been affected nearly in the same way as the workmen at
Leadhills.[2094] A similar accident happened in London in 1742. The
keeper of the round-house of St. Martin’s, crammed 28 people into an
apartment six feet square and not quite six feet high; and four were
suffocated.[2095]

The morbid appearances left on the body after poisoning with carbonic
acid gas have been chiefly observed in persons killed by charcoal
vapour. According to Portal the vessels of the brain are congested, and
the ventricles contain serum; the lungs are distended, as if
emphysematous; the heart and great veins are gorged with black fluid
blood; the eyes are generally glistening and prominent, the face red,
and the tongue protruded and black.[2096]—Gorging of the cerebral
vessels seems to be very common. Yet sometimes it is inconsiderable, as
in two cases related by Dr. Bright, where, except in the sinuses and in
the greater veins of the ventricles and substance of the brain, no
particular gorging or vascularity seems to have been met with,—the
external membranes in particular having been very little injected.[2097]
This, however, is certainly a rare occurrence. Serous effusion in the
ventricles and under the arachnoid membrane is very general, yet not
invariable.—Dr. Schenck, medical inspector of Siegen, in reporting two
cases of death caused by the vapours of burning wood, notices paleness
of the countenance as a singular accompaniment of cerebral congestion;
and calls the attention of medical jurists to the extreme calmness of
the features as a general character of this variety of poisoning.[2098]
Although the same appearance has also been noticed by others,[2099] the
countenance nevertheless is often livid. But whether livid or pale, it
is always composed.—It appears from an account in Pyl’s Essays of
several cases of suffocation from the fumes of burning wood, that
besides the appearances mentioned by Portal, there is usually great
livor of the back, frothiness as well as fluidity of the blood, and more
or less gorging of the lungs with blood.[2100]—A common appearance where
the poisonous emanation has been charcoal vapour, is a lining of dark,
or sometimes actually black dust on the mucous membranes of the air
passages, thickest near the external opening of the nostrils, and
disappearing towards the glottis. There are obvious reasons why this
appearance cannot always be expected to occur; but when present, it may
be in doubtful circumstances a very important article of evidence.[2101]
In Wildberg’s collection of cases there is a report on two people who
were suffocated in bed, in consequence of the servant having neglected
to open the flue-trap when she kindled the stove in the bed-chamber; and
in each of them Wildberg found all the appearances now quoted from
Portal and Pyl. The tongue was black and swelled.[2102]—Mertzdorff has
related a case of death from the same cause, in which, together with the
preceding appearances, an effusion of blood was found between
the arachnoid and pia mater over the whole surface of both
hemispheres.[2103] In one of Dr. Bright’s cases there was a small
ecchymosis in the cortical substance on the outer side of the anterior
lobe, and not extending into the medullary matter. Fallot mentions an
instance of suffocation from charcoal vapour, where a little coagulated
blood was found between the layers of the arachnoid membrane of the
cerebellum in the region of the left occipital hollow.[2104] Three
instances of extravasation are enumerated in a list of German cases
analysed by Dr. Bird.[2105] Such appearances might be expected more
frequently, considering the manifest tendency of this kind of poisoning
to cause congestion in the head.—The blood is generally described as
being liquid and very dark. But M. Ollivier has lately called attention
to the fact, that the blood both before and after death is not unusually
more florid in the veins than natural.[2106] In a case mentioned by M.
Rayer globules of an oily-looking matter were found swimming on the
surface of the blood and urine.[2107] This is a solitary
observation.—The body usually remains flaccid, and the customary stage
of rigidity is imperfect. In some instances, however, as in those
related by Dr. Schenck, the stage of rigidity is passed through in the
usual manner. It is not uncommon to find vomited matter lying beside the
body, a circumstance which may naturally mislead the unpractised. This
is represented by Professor Wagner of Berlin to have occurred uniformly
in his experience;[2108] and it is also mentioned in many of the cases
reported by others;[2109] but it is not invariable.—A red appearance in
the stomach and intestines has been noticed in many cases,[2110] and
often ascribed to inflammation; but it is probably nothing more than the
result of the venous congestion, which pervades most of the membranous
surfaces of the body.

The least variable appearances according to Dr. Bird are general
lividity, protrusion of the tongue, a calm expression and attitude,
cerebral congestion, and serous effusion. This author’s paper in the
Medical Gazette, 1838–39, i., or in Guy’s Hospital Reports, iv., enters
very fully into the appearances after death, and may be consulted with
advantage for further details.

The treatment of poisoning with carbonic acid consists chiefly in the
occasional employment of the cold affusion, and in moderate
blood-letting either from the arm or from the head. In a case which
happened at Paris, where a lady tried to make away with herself by
breathing charcoal fumes, and was found in a state of almost hopeless
insensibility, various remedies were tried unsuccessfully, till cupping
from the nape of the neck was resorted to; and she then rapidly
recovered.[2111] Another instance where blood-letting was also
singularly successful deserves particular mention; because for three
hours the patient remained without pulsation in any artery, and without
the slightest perceptible respiration. At first neither by cupping nor
by venesection could any blood be obtained; and it was only after the
long interval just mentioned, and constant artificial inflation of the
lungs, that the blood at length trickled slowly from the arm. The pulse
and breathing were after this soon re-established; but it was not till
eight hours later that sensibility returned.[2112]

_Of Poisoning with Carbonic Oxide Gas._—Carbonic oxide gas, according to
Nysten, has not any effect on man when injected into the pleura; but
when thrown slowly into the veins, it gives the arterial blood a
brownish tint, and induces for a short time a state resembling
intoxication.[2113] The quantity injected into the veins was probably
too small to produce the full effect, or it was discharged in passing
through the lungs; for this gas certainly appears to be very deleterious
when breathed by man, or the lower animals. M. Leblanc found by
experiment that a sparrow was killed almost immediately in air
containing only a twentieth of it, and that so little even as a
hundredth part proved fatal in two minutes.[2114]

A set of interesting but hazardous experiments were made with it in 1814
by the assistants of Mr. Higgins of Dublin. One gentleman, after
inhaling it two or three times, was seized with giddiness, tremors, and
an approach to insensibility, succeeded by languor, weakness, and
headache of some hours’ duration. The other had almost paid dearly for
his curiosity. Having previously exhausted his lungs, he inhaled the
pure gas three or four times, upon which he was suddenly deprived of
sense and motion, fell down supine, and continued for half an hour
insensible, apparently lifeless, and with the pulse nearly extinct.
Various means were tried for rousing him, without success; till at last
oxygen gas was blown into the lungs. Animation then returned rapidly:
but he was affected for the rest of the day with convulsive agitation of
the body, stupor, violent headache, and quick irregular pulse; and after
his senses were quite restored, he suffered from giddiness, blindness,
nausea, alternate heats and chills, and then feverish, broken, but
irresistible sleep.[2115] A French aëronaut, who used for his balloon a
mixture of carbonic oxide and hydrogen, obtained by decomposing water
with red-hot charcoal, lately suffered from similar symptoms in a milder
degree, in consequence of the gas being disengaged upon him from the
safety-valve of his balloon.[2116]

_Of Poisoning with Nitrous Oxide Gas._—The nitrous oxide or intoxicating
gas is the last of the narcotic gases to be noticed. Nysten found, that,
when slowly injected in large quantity into the veins of animals, it
only caused slight staggering.[2117] Frequent observation, however, has
shown that it is by no means so inert when breathed by man. Sir H. Davy,
who first had the courage to inhale it, observed that it excited
giddiness, a delightful sense of thrilling in the chest and limbs,
acuteness of hearing, brilliancy of all surrounding objects, and an
unconquerable propensity to brisk muscular exertion. These feelings were
of short duration, but were generally succeeded by alertness of body and
mind, never by the exhaustion, depression, and nausea, which follow the
stage of excitement brought on by spirits or opium.[2118] Although many
have since experienced the same enticing effects, yet they are by no
means uniform. For others have been suddenly seized with great weakness,
tendency to faint, loss of voice, and sometimes convulsions; and two of
Thenard’s assistants, on making the experiment, fainted away, and
remained some seconds motionless and insensible.[2119] It is a
remarkable circumstance in the operation of this gas, that, unlike other
stimulants, it does not lose its virtues under the influence of habit.
Neither does the habitual use of it lead to any ill consequence. Sir H.
Davy, in the course of his researches, which were continued above two
months, breathed it occasionally three or four times a day for a week
together, at other periods four or five times a week only; yet at the
end his health was good, his mind clear, his digestion perfect, and his
strength only a little impaired.[2120]

Nitrous oxide gas is one of the few gases that are not injurious to
vegetables. Dr. Turner and I found that seventy-two cubic inches,
diluted with six times their volume of air, had no effect on a
mignionette plant in forty-eight hours.[2121]

_Of Poisoning with Cyanogen Gas._—_Cyanogen gas_ has been proved by the
experiments of M. Coullon to be an active poison to all animals,—the
guinea-pig, sparrow, leech, frog, wood-louse, fly, crab; and the
symptoms induced were coma, and more rarely convulsions.[2122] These
results are confirmed by the later experiments of Hünefeld, who found
that it produces in the rabbit anxious breathing, slight convulsions,
staring of the eyes, dilated pupils, coma, and death in five or six
minutes.[2123] Buchner likewise found that small birds, held for a few
seconds over the mouth of a jar containing cyanogen, died very speedily;
and on one occasion remarked, while preparing the gas, that the
fore-finger, which was exposed to the bubbles as they escaped, became
suddenly benumbed, and that this effect was attended with a singular
feeling of pressure and contraction in the joints of the thumb and
elbow.[2124] It would undoubtedly be most dangerous to breathe this gas,
except much diluted, and in very small quantity.

Of all narcotic gases it is the most noxious to vegetables. Dr. Turner
and I found that a third of a cubic inch, diluted with 1700 times its
volume of air, caused the leaves of a mignionette plant to droop in
twenty-four hours. As usual with the effects of narcotic gases on
vegetables, the drooping went on after the plant was removed into the
open air; and in a short time it was completely killed.[2125]

_Of Poisoning with Oxygen Gas._—Of all the narcotic gases, none is
more singular in its effects than oxygen. When breathed in a state of
purity by animals, they live much longer than in the same volume of
atmospheric air. But if the experiment be kept up for a sufficient
length of time, symptoms of narcotic poisoning begin to manifest
themselves. For an hour no inconvenience seems to be felt; but the
breathing and pulse then become accelerated; a state of debility next
ensues; at length insensibility gradually comes on, with glazing of
the eyes, slow respiration and gasping; coma is in the end completely
formed; and death ensues in the course of six, ten, or twelve hours.
If the animals are removed into the air before the insensibility is
considerable, they quickly recover. When the body is examined
immediately after death, the heart is seen beating strongly, but the
diaphragm motionless; the whole blood in the veins as well as the
arteries is of a bright scarlet colour; some of the membranous
surfaces, such as the pulmonary pleura, have the same tint, and the
blood coagulates with remarkable rapidity. The gas in which an animal
has died rekindles a blown out taper. These experiments, which
physiology owes to the researches of Mr. Broughton,[2126] furnish a
solitary example of death from stoppage of the respiration, although
the heart continues to pulsate, and the lungs to transmit florid
blood. Death is probably owing to hyper-arterialization of the blood.




                             CHAPTER XXXII.
                              CLASS THIRD.
                 OF NARCOTICO-ACRID POISONS GENERALLY.


The third class of poisons, the narcotico-acrids, includes those which
possess a double action, the one local and irritating like that of the
irritants, the other remote, and consisting of an impression on the
nervous system.

Sometimes they cause narcotism; which is generally of a comatose nature,
often attended with delirium; but in one very singular group there is
neither insensibility nor delirium, but merely violent tetanic spasms.

At other times they excite inflammation where they are applied. This
effect, however, is by no means constant. For Orfila justly observes,
that under the name of narcotico-acrids several poisons are usually
described which seldom excite inflammation. Those which inflame the
tissues where they are applied rarely occasion death in this manner.
Some of them may produce very violent local symptoms; but they generally
prove fatal through their operation on the nervous system.

For the most part, their narcotic and irritant effects appear
incompatible. That is, when they act narcotically, the body is
insensible to the local irritation; and when they irritate, the dose is
not large enough to act narcotically. In large doses, therefore, they
act chiefly as narcotics, in small doses as irritants. Sometimes,
however, the narcotic symptoms are preceded or followed by symptoms of
irritation; and more rarely both exist simultaneously.

Most, if not all, of them, to whatever part of the body they are
applied, act remotely by entering the blood-vessels; but it has not been
settled whether they operate by being carried with the blood to the part
on which they act, or by producing on the inner membrane of the vessels
a peculiar impression, which is conveyed along the nerves. Some of them
produce direct and obvious effects where they are applied. Thus
monkshood induces a peculiar numbness and tingling of the part with
which it is placed in contact. The organs on which they act remotely are
the brain and spine, and sometimes the heart also.

The appearances in the dead body are, for the most part, inconsiderable;
more or less inflammation in the stomach or intestines, and congestion
in the brain; but even these are not constant.

As a distinct class, they differ little from some poisons of the
previous classes. Several of the metallic irritants, and a few vegetable
acrids are, properly speaking, narcotico-acrids: they excite either
narcotism or irritation, according to circumstances. But still, the
poisons about to be considered form a good natural order when contrasted
with these irritants. For the irritants which possess a double action
are nevertheless characterized by the symptoms of inflammation being at
least their most prominent effects; while the most prominent feature in
the effects of the poisons now to be considered is injury of the nervous
system. It is more difficult to draw the line of separation between the
present class and the pure narcotics; for many narcotico-acrids rarely
cause any symptom but those of narcotism.

The narcotico-acrids are all derived from the vegetable kingdom. Many of
them owe their power to an alkaloid, consisting of oxygen, hydrogen,
carbon, and azote.

The characters which distinguish the symptoms and morbid appearances of
the narcotico-acrids from those of natural disease, do not require
special mention; for almost all the remarks made in the introduction to
the class of narcotics are applicable to the present class also. A few
of the characters, however, which have been laid down, do not apply so
well to the narcotico-acrids as to the narcotics. In particular, it
appears that what was said on the short duration of the effects of the
narcotics does not apply so well to the present class of poisons; some
of which, in a single dose, continue to cause symptoms even of narcotism
for two or three days. But the rule, that they seldom prove fatal if the
case lasts above twelve hours, is still applicable,—at all events they
rarely prove fatal after that interval by their narcotic action. The
poisonous fungi, however, have proved fatal as narcotics so late as
thirty-six hours, or even three days, after they were taken; and perhaps
digitalis has proved fatal narcotically at the remote period of three
weeks. But such cases are extremely rare.

Some narcotico-acids, such as the different species of _strychnos_, are
quite peculiar in their effects; so that their symptoms may be
distinguished at once from natural disease.

Orfila divides the narcotico-acrids into six groups, and this
arrangement will be followed in the present work; but they are not all
very well distinguished from one another.




                            CHAPTER XXXIII.
        OF POISONING WITH NIGHTSHADE, THORN-APPLE, AND TOBACCO.


The first group of the narcotico-acrids comprehends these whose
principal symptom in the early stage of their effects is delirium. All
the plants of the group belong to the natural order _Solanaceæ_, and
Linnæus’s class Pentandria Monogynia. Those which have been particularly
examined are deadly nightshade, thorn-apple, and tobacco.


                 _Of Poisoning with Deadly Nightshade._

The deadly nightshade, or _Atropa belladonna_, is allied in
physiological and botanical characters to the _hyoscyamus_ and _solanum_
formerly mentioned; and by the older writers, indeed, was confounded
with the latter. It is a native of Britain, growing in shady places,
particularly on the edge of woods. The berries, which ripen in
September, have a jet-black colour. Their beauty has frequently tempted
both children and adults to eat them, although they have a mawkish
taste; and many have suffered severely. It is not the berry alone which
is poisonous; the whole plant is so; and the root is probably the most
active part.[2127] From one to four grains of the dried powder of the
root will occasion dryness in the throat, giddiness, staggering, flushed
face, dilated pupils, and sometimes even delirium.[2128] The juice of
the leaves is very energetic, two grains of its extract being, when well
prepared, a large enough dose to cause disagreeable symptoms in man. It
is a very uncertain preparation, unless when procured by evaporation _in
vacuo_; for some samples from the Parisian shops have been found by
Orfila to be quite inert.

It contains a peculiar alkaloid, named _atropia_. In the belladonna
Brandes obtained a volatile, oily-like, alkaloidal fluid, of a
penetrating narcotic smell, and bitterish, acrid taste, which he
supposed to be the active principle of the plant.[2129] The ulterior
researches of Geiger and Hesse, however, as well as the simultaneous
analysis of Mein, have proved that this fluid is not the pure alkaloid
of belladonna, and that the real atropia is a solid substance, forming
colourless, silky crystals, soluble in ether and alcohol, sparingly so
in water, slightly bitter, liable to decomposition under contact with
air and moisture, volatilizable, but with some decomposition, a little
above 212°, and capable of forming definite crystallizable salts with
acids.[2130] The aqueous solutions of its salts exhale during
evaporation a narcotic vapour, which dilates the pupil, and causes
sickness, giddiness, and headache.[2131]

The ordinary extract of belladonna in the dose of half an ounce will
kill a dog in thirty hours when introduced into the stomach. Half that
quantity applied to a wound will kill it in twenty-four hours. And
forty grains injected into the jugular vein prove even more quickly
fatal. Convulsions are rarely produced, but only a state like
intoxication.[2132]

The oleaginous atropia of Brandes in a dose of two or three drops kill
small birds instantaneously like concentrated hydrocyanic acid; in less
doses it occasions staggering, gasping, and in a few minutes death
amidst convulsions; and the dead body presents throughout the internal
organs great venous turgescence and even extravasation of blood, but
more especially excessive congestion within the head.[2133] The pure
crystalline atropia of Mein, when dissolved in water and greatly
diluted, causes extreme and protracted dilatation of the pupils.

_Symptoms in Man._—On man the effects of belladonna are much more
remarkable. In small doses, whatever be the kind or surface to which it
is applied,—such as the skin round the eye, or the surface of a wound,
or the inner membrane of the stomach,—it causes dilatation of the pupil.
This effect may be excited without any constitutional derangement. When
the extract is rubbed on the skin round the eye, or a solution of it
dropped upon the eyeball, vision is not impaired; but when it is taken
internally so as to affect the pupils, the sight is commonly much
obscured. The effects of large or poisonous doses have been frequently
witnessed in consequence of children and adults being tempted to eat the
berries by their fine colour and bright lustre. From the cases that have
been published the leading symptoms appear in the first instance to be
dryness in the throat, then delirium with dilated pupils, and afterwards
coma. Convulsions are rare, and, when present, slight.

The dryness of the throat is not a constant symptom. It is often,
however, very distinct. It occurred, for example, in 150 soldiers who
were poisoned near Dresden, as related by M. Gaultier de Claubry,[2134]
and in six soldiers whose cases have been described by Mr.
Brumwell.[2135] The former had not only dryness of the throat, but
likewise difficulty in swallowing.

The delirium is generally extravagant, and also most commonly of the
pleasing kind, sometimes accompanied with immoderate uncontrollable
laughter, sometimes with constant talking, but occasionally with
complete loss of voice, as in the cases of the 150 soldiers. At other
times the state of mind resembles somnambulism, as in the instance of a
tailor who was poisoned with a belladonna injection, and who for fifteen
hours, though speechless and insensible to external objects, went
through all the customary operations of his trade with great vivacity,
and moved his lips as if in conversation.[2136] Sometimes frantic
delirium is almost the only symptom of consequence throughout the whole
duration of the poisoning. Thus a gentleman at Perigueux in France, who
took by mistake a mixture containing a drachm and a half of extract, was
attacked in half an hour with delirium, which soon became furious, and
continued till next day, when it gradually left him.[2137] In others the
delirium is attended with a singular and total loss of consciousness,
but without coma, as in the following case which occurred not long ago
at St. Omer. A young man having taken by mistake an infusion of two
drachms of dried leaves, was seized in an hour with great dryness of the
mouth and throat, afterwards slight delirium, loss of consciousness, and
dilatation of the pupil, next with retention of urine, convulsive
twitches of the face and extremities, and incessant tendency to walk up
and down. In three hours, after the action of an emetic and a clyster,
he lay down, but still in a state of total unconsciousness and muttering
delirium. Blood-letting being at last resorted to as a remedy, he
speedily recovered his senses, and eventually got well, after suffering
for some time from headache, fatigue, and much debility.[2138]

The pupil is not only dilated in all cases, but likewise for the most
part insensible;[2139] and, as in the soldiers at Dresden, the eyeball
is sometimes red and prominent. The vision also, as in these soldiers,
is generally obscure; sometimes it is lost for a time;[2140] and so
completely that even the brightest light cannot be distinguished.[2141]

The sopor or lethargy, which follows the delirium, occasionally does not
supervene for a considerable interval. In a case related by Munnik it
did not begin till twelve hours after the poison was taken.[2142]
Sometimes, as in the same case, the delirium returns when the stupor
goes off. A patient of my colleague Dr. Simpson, after using a
belladonna suppository consisting of two grains of extract, was attacked
with dryness of the throat and delirium, followed soon by drowsiness and
stupor; and in five or six hours more, as the stupor wore off, the
delirium returned, prompting to constant movements as if she was busy
with her toilette and various other ordinary occupations. Sometimes the
relation of the delirium to the coma is reversed, as in a case related
by Mr. Clayton, where sopor came on first, and delirium ensued in six
hours. The dose in this instance was forty grains of the extract.[2143]
Frequently the stupor is not distinct at any stage.—Even the delirium is
not always formed rapidly. A man whose case is described by Sir John
Hill did not become giddy for two hours after eating the berries, and
the delirium did not appear till five hours later.[2144] In Mr.
Brumwell’s cases, the delirium was not particularly noticed till the
morning after the berries were taken.

Convulsions, it has been already stated, are rare. In the case from the
24th volume of Sedillot’s Journal, the muscles of the face were somewhat
convulsed: there is also at times more or less locked-jaw,[2145] or
subsultus tendinum;[2146] and occasionally much abrupt agitation of the
extremities.[2147] But well-marked convulsions do not appear to be ever
present.

The effects now detailed are by no means so quickly dissipated as those
of opium. Almost every person who has taken a considerable dose has been
ill for a day at least. The case from Sedillot’s Journal lasted three
days, delirium having continued twelve hours, the succeeding stupor for
nearly two days, and the departure of the stupor being attended with a
return of delirium for some hours longer. One of Mr. Brumwell’s
patients, too, was delirious for three days; and Plenck has noticed
several instances where the delirium was equally tedious.[2148] Sage has
related a case in which the individual was comatose for thirty
hours.[2149] Blindness is also a very obstinate symptom, which sometimes
remains after the affection of the mind has disappeared. This happened
in Plenck’s cases. In two children whose cases have been described in a
late French journal, the eyes were insensible to the brightest light for
three days.[2150] In general, the dilated state of the pupils continues
long after the other symptoms have departed. It further appears from an
official narrative in Rust’s Journal, that dilated pupil is not the only
symptom which may thus continue, but that various nervous affections,
such as giddiness, disordered vision, and tremors, may prevail even for
three or four weeks.[2151]

Hitherto little or no mention has been made of symptoms of irritation
from this poison. They are in fact uncommon, and seldom violent. In the
cases related by Gaultier de Claubry and by Mr. Brumwell, dryness and
soreness of the throat and difficult deglutition were remarked, and
appear not unusual. These symptoms were especially noticed by Buchner,
who by way of curiosity took half a drachm of seeds digested in beer.
The sense of dryness and constriction of the throat were such as to
prevent him swallowing even the saliva.[2152] Sage’s patient passed
blood by stool; and after the symptoms of narcotic poisoning ceased, he
had aphthous inflammation in the throat, and swallowing was so difficult
as for some time to excite convulsive struggles. Aphthæ in the throat
and swelling of the belly also succeeded the delirium in Munnik’s case.
Mr. Wibmer alludes to the case of a man who, besides difficult
deglutition at the beginning, had violent strangury towards the
close.[2153] An instance of violent strangury with suppression of urine
and bloody micturition is also related by M. Jolly. In the early stage,
the patient had redness of the throat and burning along the whole
alimentary canal, combined with the customary delirium and loss of
consciousness. The symptoms were caused by forty-six grains of the
extract given by mistake instead of jalap.[2154] Nausea and efforts to
vomit are not infrequent at the commencement.

If the accident be taken in time, poisoning with belladonna is rarely
fatal; for, as the state first induced is delirium, not sopor, suspicion
is soon excited, and emetics may be made to act before a sufficient
quantity of the poison has been absorbed to prove fatal. Hence few fatal
instances have occurred in recent times. Mr. Wilmer, however, has
mentioned two fatal cases occurring in children, and terminating within
twenty-four hours.[2155] M. Boucher, a writer in the old French Journal
of Medicine, has referred to several cases of the same nature;[2156]
Gmelin has described the particulars of a good example;[2157] and many
others have been succinctly quoted by Wibmer, chiefly from the older
authors.[2158]

Cases of poisoning with this plant have occurred in man through other
channels besides the stomach. Allusion has already been made to the
instance of a tailor who was poisoned by an injection. A small quantity
will sometimes suffice when administered in that way. A woman, whose
case is mentioned in Rust’s Journal, was attacked with wild delirium,
flushed face and glistening eyes, in consequence of receiving, during
labour, a clyster, that contained six grains of the common
extract;[2159] and Dr. Simpson’s patient, who was severely affected, had
only two grains.

Perhaps the berry is in some circumstances not very active. A French
physician, M. Gigault of Pontcroix, says he has frequently had occasion
to treat cases of poisoning with it, as accidents of the kind are
extremely common in his neighbourhood; that he never knew it prove
fatal; and that in one instance a young man took a pound of the berries
before going to bed, and was not subjected to treatment till next
morning, when he was found in a state of delirium, but speedily
recovered after the free operation of emetics.[2160]

_Morbid Appearances._—I have hitherto seen but one good account of the
appearances after death from poisoning with belladonna. It is described
by Gmelin. The subject was a shepherd who died comatose twelve hours
after eating the berries. When the body was examined twelve hours after
death, putrefaction had begun, so that the belly was swelled, the
scrotum and penis distended with fetid serum, the skin covered with dark
vesicles, and the brain soft. The blood-vessels of the head were gorged,
and the blood every where fluid, and flowing profusely from the mouth,
nose, and eyes.[2161] In the only other fatal case I have read, where
the body was inspected, there appears to have been no unusual appearance
at all.[2162]

As the husks and seeds of the berries are very indigestible, some of
them will almost certainly be found in the stomach, as happened in the
instance last quoted. It should likewise be remembered that the best
possible evidence of the cause of the symptoms may be derived during
life from the presence of the seeds, husks, or even entire berries, in
the discharges. If vomiting has not been brought on at an early
period, we may expect to find these remains both in the vomited matter
and in the alvine evacuations. Mr. Wilmer mentions an instance in
which the black husks appeared in the stools brought away by laxatives
at least thirty hours after the poison was swallowed.[2163] One of Mr.
Brumwell’s patients vomited the seeds towards the close of the third
day.[2164] Several patients of M. Boucher vomited fragments of the
fruit on the second day, and passed more by stool and injections on
the third, although they had been treated with activity from the
commencement.[2165]

While most of the cases of poisoning with belladonna have originated in
accident, at the same time they have not been all of this description.
Gmelin has quoted an instance of intentional and fatal poisoning by the
juice of the berries being mixed with wine; and another singular case of
poisoning with the decoction of the buds, given by an old woman for the
purpose of committing theft during the stupor of the individual.[2166]

Other species of atropa are probably similar to belladonna in
properties. Wibmer quotes a single instance of frantic delirium
occurring among several shepherds, as well as their cattle, from eating
the herb of the _A. mandragora_.[2167] This is well known to have been
used anciently as a medicinal narcotic.


                    _Of Poisoning with Thorn-Apple._

The thorn-apple, or _Datura stramonium_, is another plant of the same
natural order, which it is proper to notice, because people have often
been poisoned with it, and it has become a common ornament of our
gardens. The cases of poisoning which have occurred in recent times in
this country have been all accidental. But not long ago the thorn-apple
appears to have been extensively used in Germany to cause loss of
consciousness and lethargy, preparatory to the commission of various
crimes.[2168] It was also proved to have been used lately in France for
this purpose. Some thieves made a man insensible with wine in which
stramonium seeds had been steeped, and robbed him of five hundred francs
while in this state. For twenty-four hours the victim knew nothing of
what became of him; he was met wandering in a wood, affected with
delirium, unconsciousness, staring of the eyes, and oppression of the
breathing; and for some time he was taken for a madman.[2169] In the
Eastern Archipelago, according to Mr. Crawford, this is a common mode of
committing theft and robbery.[2170]

It is chiefly the fruit and seeds that have hitherto been examined; but
the whole plant is probably poisonous. Brandes discovered in it a
volatile, oleaginous, alkaline substance, which he supposed to be its
active principle.[2171] But, though his observations were confirmed by
Bley,[2172] it now appears that the real principle is a colourless,
crystalline alkaloidal substance, of an acrid taste like tobacco, which
was discovered more lately by Geiger and Hesse; this is named daturine,
or daturia.[2173]

The physiological effects of the extract have been determined by Orfila.
He found that half an ounce killed a dog within twenty-four hours after
being swallowed, that a quarter of an ounce applied to a wound killed
another in six hours, and that thirty grains killed another when
injected into the jugular vein. The symptoms were purely nervous, and
not very prominent. Hence this poison, like the former, acts through the
blood-vessels, and probably on the brain.[2174] Bley’s daturia proves
quickly fatal to small animals in the dose of a few drops. The
crystalline daturia of Geiger and Hesse kills a sparrow in the dose of
an eighth of a grain, and occasions great and persistent dilatation of
the pupil when applied to the eye.

_Symptoms in Man._—The symptoms produced by a poisonous dose in man are
variable. The leading features are great delirium, dilatation of the
pupils, and stupor; but sometimes spasms occur, and occasionally palsy.

Dr. Fowler has related the case of a little girl who took a drachm and a
half of the seeds. In less than two hours she was attacked with maniacal
delirium, accompanied with spectral illusions; and she remained in this
state most of the following night, but had some intervals of lethargic
sleep. Next morning, after the operation of a laxative, she fell fast
asleep, and after some hours she awoke quite well.[2175] In a case
somewhat like this, related in Henke’s Journal, the child had general
redness of the skin, swelling of the belly, locked jaw, tremors of the
extremities, and an attitude and expression as if about to tumble into a
pit. Recovery took place after the action of an emetic.[2176]

In two instances, one related by Vicat in his treatise on the poisonous
plants of Switzerland,[2177] the other by Dr. Swaine[2178] in the Edin.
Phys. and Lit. Essays, the leading symptoms were furious delirium and
palsy of the whole extremities. In the instances of three children
related by Alibert there were delirium, restlessness, constant
incoherent talking, dancing and singing, with fever and flushed
face.[2179] In another recorded by Dr. Young, there were some
convulsions, and livid suffusion of the countenance.[2180] In an
instance communicated to me by my colleague Dr. Traill, where eighteen
or twenty grains of extract of stramonium were taken by mistake for
sarsaparilla, the symptoms were dryness of the throat immediately
afterwards, then giddiness, dilated pupils, flushed face, glancing of
the eyes, and incoherence, so that he seemed to his friends to be
intoxicated: and subsequently there was incessant unconnected talking,
like that of demency. Emetics were given without effect, and little
amendment was obtained from blood-letting, leeches on the temples, cold
to the head, or purgatives. But after a glass of strong lemonade
vomiting took place, the symptoms began to recede, in ten hours he
recognized those around him, and next day he was pretty well. Kaauw
Boerhaave has related with great minuteness the case of a girl who very
nearly lost her life in consequence of a man having given her the powder
in coffee with the view of seducing her. The symptoms were redness of
the features, delirium, nymphomania, loss of speech; then fixing of the
eyes, tremors, convulsions, and coma; afterwards tetanic spasm and slow
respiration with the coma. She was with much difficulty roused for a
time by the operation of emetics, and eventually got well after her
lethargy had lasted nearly a day.[2181] In another related in Rust’s
Magazin, and caused by a decoction of the fruit, which was mistaken for
thistle-heads, the leading symptoms were spasmodic closing of the
eyelids and jaws, spasms also of the back, complete coma, and excessive
dilatation and insensibility of the pupil.[2182] This case, which seems
to have been a very dangerous one, was rapidly cured by free
blood-letting. Blood-letting, indeed, seems peculiarly called for in
poisoning with thorn-apple, on account of the strong signs of
determination of blood to the head.—Gmelin has quoted several fatal
cases, one of which endured for six hours only;[2183] and Dr. Young
says, that a child has been killed by a single apple.[2184] The most
complete account yet published of the phenomena of poisoning with
stramonium when fatal is given by Mr. Duffin of London. A child of his
own, two years old, swallowed about 100 seeds without chewing them. Soon
after she became fretful and like a person intoxicated; in the course of
an hour efforts to vomit ensued, together with flushed face, dilated
pupils, incoherent talking, and afterwards wild spectral illusions and
furious delirium. In two hours and a half she lost her voice and the
power of swallowing, evidently owing to spasms of the throat. Then
croupy breathing and complete coma set in, with violent spasmodic
agitation of the limbs, occasional tetanic convulsions, warm
perspiration, and yet an imperceptible pulse. Subsequently the pulse
became extremely rapid, the belly tympanitic, and the bladder paralyzed,
but with frequent involuntary stools, probably owing to the
administration of cathartics; and death took place in twenty-four hours.
At an early period twenty seeds were discharged by an emetic: the stools
contained eighty; and none were found in the alimentary canal after
death. There was never any marked sign of congestion of blood in the
head, except flushed face at the beginning.[2185] Dr. Droste of Osnaburg
has related a fatal case occasioned by a decoction of 125 seeds given to
remove colic. In fifteen minutes the patient became delirious, but soon
fell apparently fast asleep, and died in seven hours without again
awaking.[2186]

Dangerous effects may result from the application of the thorn-apple to
the skin when deprived of the cuticle. An instance has been lately
published of alarming narcotism from the application of the leaves to an
extensive burn.[2187]

_Morbid Appearances._—As to the _morbid appearances_, Droste found in
his case redness of the cardiac end of the stomach, which contained two
table-spoonfuls of a pulpy matter mixed with black and white grains, the
remains of the teguments of the seeds; and there was also lividity of
the back, lividity of the lungs, emptiness of the cavities of the heart,
and gorging of the vessels of the brain. Haller says he once found
general congestion of the brain and sinuses,[2188]—an appearance which
may naturally be expected, considering the signs of strong determination
of blood towards the head, which often prevail during life. In Mr.
Duffin’s case, however, the brain was healthy, not congested; the
stomach and intestines presented no morbid appearance; and the only
unusual appearances observed were a slight blush over the pharynx,
larynx, and upper third of the gullet, thickening and swelling of the
rima glottidis, and a semi-coagulated state of the blood.


                      _Of Poisoning with Tobacco._

A plant of the same natural order with the two former, tobacco, the
_Nicotiana tabacum_ of botanists, is familiarly known to be in certain
circumstances a virulent poison. Every part of the plant possesses
active properties. It has been used as a poison in this country for
criminal purposes.

_Vauquelin_ analyzed it some time ago, and procured an acrid volatile
principle which he called nicotine.[2189] This substance, which was
afterwards obtained in a purer state as a crystalline body by
Hermbstädt, has been more recently ascertained by MM. Posselt and
Reimarus to be nothing else than essential oil of tobacco, which is sold
at ordinary temperatures; and they succeeded in procuring another
principle which they consider the true nicotina. This is fluid at 29°
F., volatile, extremely acrid, alkaline, and capable of forming
crystallizable salts with some of the acids.[2190] Tobacco then appears
to contain an acrid alkaline principle, and an essential oil to which
the alkaloid adheres with great obstinacy. The relation of the
empyreumatic oil of tobacco to these principles has not been accurately
ascertained, though it probably contains one or other of them. It is
well known to be an active poison, which produces convulsions, coma and
death. Mr. Morries-Stirling found that its active part is removed from
the oil by washing with weak acetic acid, as he also observed in the
instance of similar oils obtained from various narcotic
vegetables.[2191]

_Process for detecting Tobacco in Organic mixtures._—In a medico-legal
case which happened at Aberdeen in 1834, and of which some notice is
taken at page 651, Dr. Ogston of that city successfully employed the
following process for detecting tobacco in the contents of the stomach.
The contents, consisting of a pulpy fluid, were acidulated with acetic
acid, digested, and filtered; the liquid was treated with diacetate of
lead, filtered again, freed of lead by hydrosulphuric acid, filtered a
third time, treated with caustic potash, and then allowed to settle. The
supernatant liquid, which had the taste of tobacco-juice, was separated
and distilled to half its volume. The distilled liquor had a strong
tobacco odour and taste, and some acridity, and gave a precipitate with
infusion of galls. The residuum in the retort presented oily particles
on its surface, and when heated in an open basin filled the apartment
with a vapour which had a strong odour of tobacco smoke, and caused in
several persons present a sense of acridity of the throat, watering of
the eyes, and tendency to sneeze. Various additional experiments
confirmatory of these results were also performed; and a simultaneous
examination of tobacco-powder gave precisely the same indications. I am
indebted to Dr. Ogston for these particulars and a detailed narrative of
his investigation; which appears to supply a convenient and conclusive
process for the detection of tobacco.—Perhaps the ordinary process for
obtaining nicotina may also be employed with advantage. This consists in
distilling the suspected substance with caustic potash, neutralizing the
distilled liquor with sulphuric acid, concentrating the product to a
thin syrup, exhausting this with etherized alcohol, evaporating off the
solvent, and distilling the extract with strong solution of potash.
Nicotina passes over, and may be recognized by its sensible and chemical
qualities.

The effects of tobacco are somewhat different from those of belladonna
and thorn-apple; but it is here arranged with them, as it belongs to the
same natural family. Orfila remarked that 5½ drachms of common rappee,
introduced into the stomach of a dog and secured by a ligature, caused
nausea, giddiness, stupor, twitches in the muscles of the neck, and
death in nine hours; and that two drachms and a quarter applied to a
wound proved fatal in a single hour. Mr. Blake thinks tobacco has no
direct action on the heart, even when admitted directly into the blood
by the jugular vein;—that it acts primarily on the capillary circulation
of the lungs, by obstructing which it prevents the blood from reaching
the left cavities of the heart, and thus acts on that organ indirectly.
For he observed, that laboured respiration always preceded any sign of
depressed action of the heart, that forcible action of the heart often
returned after its first cessation, and that its contractility continued
after death.[2192] An infusion of ten grains caused laborious breathing
in ten seconds, and in twenty seconds temporary arrestment of the
heart’s action, which then returned, and was attended for a time with
increased arterial pressure. Soon afterwards the animal recovered,
without any convulsions or loss of sensibility. Two scruples had the
same effect. But when three drachms were used, convulsions succeeded
similar phenomena, and death ensued in two minutes, the heart continuing
to act for some time after respiration had ceased, until at length it
was stopped by the usual consequences of asphyxia.[2193] On the other
hand, Sir B. Brodie found that the effects are very different, according
to the form in which the poison is used. Thus four ounces of a strong
infusion, when injected into the anus of a dog, killed it in ten minutes
by paralyzing the heart; for after death the blood in the aortal
cavities was arterial. But the empyreumatic essential oil does not act
in that manner: it excites convulsions and coma, without affecting the
heart. It may prove fatal in two minutes.[2194] Like other violent
poisons, tobacco has no effect when applied directly to the brain or
nerves.[2195] Two drops of the alkaloid, nicotina, injected into the
jugular vein of a dog, begin to act in ten seconds, and will prove fatal
in a minute and a half.[2196]

_Symptoms in Man._—The effects observed in man are allied to those
produced in dogs by the infusion. In a slight degree they are frequently
witnessed in young men, while making their first efforts to acquire the
absurd practice of smoking. The first symptoms are acceleration and
strengthening of the pulse, with very transient excitement, then sudden
giddiness, fainting and great sickness, accompanied with a weak,
quivering pulse. These effects are for the most part transient and
trifling, but not always. Some degree of somnolency is not uncommon. Dr.
Marshall Hall has given an interesting account of a young man who smoked
two pipes for his first debauch, and in consequence was seized with
nausea, vomiting, and syncope, then stupor, stertorous breathing,
general spasms and insensible pupils. Next day the tendency to faint
continued, and in the evening the stupor, stertor and spasms returned;
but from that time he recovered steadily.[2197] Gmelin has quoted two
cases of death from excessive smoking,—caused in one by seventeen, in
the other by eighteen pipes, smoked at a sitting.[2198] It is likewise
mentioned by Lanzoni that an individual fell into a state of somnolency
and died lethargic on the twelfth day in consequence of taking too much
snuff;[2199] Dr. Cheyne says, “he is convinced apoplexy is one of the
evils in the train of that disgusting practice;”[2200] and I have met
with an instance where the excessive use of snuff, occasioned twice, at
distant intervals, an attack resembling imperfect apoplexy, united with
delirium. Such cases, however, must be admitted to be rare; and the
practice of taking snuff is in general unattended with injury.

Serious consequences have resulted from the application of tobacco to
the abraded skin. In the Ephemerides an account is given of three
children who were seized with giddiness, vomiting, and fainting from the
application of tobacco-leaves to the head for the cure of
ring-worm.[2201] Dr. Merriman has also alluded to an instance of death
in a child from the incautious employment of a strong decoction of
tobacco as a lotion for ring-worm of the scalp.[2202] And in Leroux’s
Journal there is an account of a man, who, after using a tobacco
decoction for the cure of an eruptive disease, was seized with symptoms
of poisoning, and died in three hours.[2203]

In recent times poisoning with tobacco has been often produced by the
employment of too large doses in the way of injection. Richard has
mentioned a case, not fatal, which arose from an infusion of five leaves
in a choppin of water, used as an injection by a lady for costiveness.
She was immediately seized with colic, giddiness, buzzing in the ears,
headache, nausea, and then syncope of seven hours’ duration. During this
period the breathing was difficult, the pulse very slow, the pupils
dilated, the skin cold and moist, the urine suppressed, the efforts to
vomit constant, and the belly depressed, contracted, and affected with
constant borborygmus. She recovered under the use of emollient
injections and fomentations.[2204] Dr. Grahl of Hamburg has related
minutely a fatal case, which arose from an ounce of rather more, boiled
for fifteen minutes in water, and administered by advice of a female
quack. The individual, who laboured merely under dyspepsia and obstinate
costiveness, was seized in two minutes with vomiting, violent
convulsions, and stertorous breathing, and died in three-quarters of an
hour.[2205] Another accident of the same kind is noticed in the Journal
de Chimie Médicale, where the person became as it were intoxicated, and
died immediately. Instead of an infusion of two drachms she had used a
decoction of two ounces.[2206]—M. Tavignot describes the following
remarkable case occasioned by a similar dose. An infusion prepared by
mistake with two ounces and one drachm, instead of a drachm and a half,
was used as an injection for a stout man affected with ascarides. In
seven minutes he was seized with stupor, headache, paleness of the skin,
pain in the belly, indistinct articulation, and slight convulsive
tremors, at first confined to the arms, but afterwards general. Extreme
prostration and slow laborious breathing soon ensued, and then coma,
which ended fatally in eighteen minutes.[2207]—Even two drachms,
however, or a drachm and a half, are by no means a safe dose. An
anonymous writer in the Medical and Surgical Journal says a patient of
his died in convulsions an hour or two after receiving a clyster
composed of two drachms infused in eight ounces.[2208] Nay, in the Acta
Helvetica there is an account by an anonymous writer of the case of a
woman, who, after an injection made with one drachm only, was seized
with pain in the belly, anxiety and faintings, proving fatal in a few
hours.[2209] And a case, fatal in thirty-five minutes, which was
occasioned by the same dose, occurred not long ago in Guy’s Hospital,
London.[2210]

Tobacco is an equally deadly poison when swallowed in large quantity. M.
Caillard has related the particulars of the case of a lunatic, who,
having swallowed half an ounce of snuff during a lucid interval, was
seized with vomiting, and afterwards with oppression, incoherence, cold
sweats, a slow full pulse, and dilated pupils; but he slowly
recovered.[2211] The French poet Santeuil was killed in this way by a
practical joker at the Prince of Condé’s table. When the bottle had
circulated rather freely, a boxful of Spanish snuff was emptied into a
large glass of wine, and thus administered to the unlucky victim, who
was in consequence “attacked with vomiting and fever, and expired in two
days amidst the tortures of the damned.”[2212] The following important
case has been communicated to me by Dr. Ogston of Aberdeen, who was
employed in the judicial investigations connected with it. An elderly
man, a pensioner, was seen to enter a brothel, while in perfect health;
and in an hour he was carried out insensible and put down in a passage,
where he was found by the police unable to speak or move. While carrying
him to the watch-house hard by, the officers observed him attempt to
vomit; but he was scarcely laid down before the fire, when he expired.
It was ascertained, that he had drunk both rum and whisky in the
brothel, and that something had been given him “to stupefy him or set
him asleep.” On dissection the blood was found every where very fluid,
and four ounces of serosity were collected from the lateral ventricles
and base of the skull. But there was no other unusual appearance, except
that the stomach contained about four ounces of a thick brownish pulp,
in which were seen several pellets of a powder resembling snuff. In
these contents Dr. Ogston could not detect any opium; but he detected
tobacco by the process mentioned above. No doubt could exist that the
man died of poisoning with tobacco; but as no evidence could be obtained
to inculpate any one in particular of many individuals who were in the
brothel with him, the case was not made the subject of trial.

Evidence is not wanting, therefore, to prove that this plant is a very
active poison; yet every one knows that under the influence of habit it
is used in immense quantities over the whole world as an article of
luxury, without any bad effect having ever been clearly traced to it.
Its poisonous qualities were known in Europe as soon as it was brought
from America; and the belief that such properties could not fail to be
attended, as in the case of spirits and opium, with evil consequences
from its habitual use, led to much opposition on the part of various
governments to its introduction. Soon after it was brought to England by
Sir W. Raleigh, King James wrote a philippic against it, entitled “The
Counter-blaste to Tobacco.” Some countries even prohibited it by severe
edicts. Amurath the 4th in particular made the smoking of tobacco
capital; several of the Popes excommunicated those who smoked in the
church of St. Peter’s; in Russia it was punished with amputation of the
nose; and in the Canton of Bern it ranked in the tables next to
adultery, and even so lately as the middle of last century a particular
court was held there for trying delinquents.[2213] Like every other
persecuted novelty, however, smoking and snuff-taking passed from place
to place with rapidity; and now there appear to be only two luxuries
which yield to it in prevalence, spirituous liquors and tea.

The only accounts I have seen of the morbid appearances after poisoning
with tobacco are contained in the cases of Dr. Grahl and Dr. Ogston. In
the former there was great lividity of the back, paleness of the lips,
flexibility of the joints (two days after death), diffuse redness of the
omentum without gorging of vessels, similar redness with gorging of
vessels both on the outer and inner coats of the intestines, in some
parts of the mucous coat patches of extravasation, unusual emptiness of
the vessels of the abdomen; while the stomach was natural, the lungs
pale, the heart empty in all its cavities, and the brain natural. The
appearances in Dr. Ogston’s case have been already stated.

Writers on the diseases of artisans have made many vague statements on
the supposed baneful effects of the manufacture of snuff on the
workmen.[2214] It is said they are liable to bronchitis, dysentery,
ophthalmia, carbuncles and furuncles. At a meeting of the Royal Medical
Society of Paris, however, before which a memoir to this purport was
read, the facts were contradicted by reference to the state of the
workmen at the Royal Snuff Manufactory of Gros-Caillou, where 1000
people are constantly employed without detriment to their health.[2215]
This subject was afterwards investigated with care by MM.
Parent-Duchatelet and D’Arcet, who inquired minutely into the state of
the workmen employed at all the great tobacco-manufactories of France,
comprising a population of above 4000 persons; and the results at which
they arrived are,—that the workmen very easily become habituated to the
atmosphere of the manufactory,—that they are not particularly subject
either to special diseases, or to disease generally,—and that they live
on an average quite as long as other tradesmen.[2216] These facts are
derived from accurate statistical returns, showing the number of days
each person was annually off work from sickness, the ages at which
superannuated allowances were granted, the period of death, and the
prevalent diseases.




                             CHAPTER XXXIV.
            OF POISONS OF THE UMBELLIFEROUS ORDER OF PLANTS.


The Natural Order _Umbelliferæ_ contains a variety of plants, to which
narcotico-acrid properties have been at different times ascribed. But
these properties have been satisfactorily traced in the instance of four
species only, the _Conium maculatum_, _Œnanthe crocata_, _Cicuta
virosa_, and _Æthusa cynapium_. It is supposed that others may be
poisonous. But the facts on the subject are equivocal; for the several
species of the family are very apt to be confounded with one another,
and there is reason to think that other species have repeatedly been
mistaken for one of the four already mentioned.

The symptoms caused by the umbelliferous narcotics comprehend chiefly
coma, convulsions, paralysis, and delirium. But the knowledge possessed
on this head is rather vague, and the phenomena are not unfrequently
complex and difficult to observe with accuracy; so that their nature has
been sometimes misunderstood. The irritant properties of the poisons of
this tribe of narcotico-acrids are seldom well defined.


                      _Of Poisoning with Hemlock._

The first to be mentioned is the common hemlock, or _Conium maculatum_,
one of the most abundantly diffused of umbelliferous vegetables. It is
distinguished from all those which it resembles by its tall, smooth,
spotted stem,—its smooth leaves,—the rugged edge of the five ribs of its
fruit,—its singular mousy odour,—and the very peculiar odour of conia,
emitted when the pulp or juice of the leaves is mixed with caustic
potash. The only other umbelliferous native which has a spotted stem,
the _Myrrhis temulenta_, is easily distinguished from hemlock by the
whole plant being very hairy.

Cases of poisoning with hemlock are not infrequent on the continent, the
root having been mistaken for fennel, asparagus, parsley, but
particularly parsnep.[2217] It is generally believed to have furnished
the poison which was used in ancient times, and especially among the
Greeks, for despatching criminals; but we have not any precise
information on the subject.

A peculiar alkaloid was indicated in hemlock not long ago by Brandes,
half a grain of which killed a rabbit with symptoms like those of
tetanus.[2218] Other chemists were unable to obtain his results. But the
subject was afterwards taken up with success by Geiger, who obtained
from the plant a volatile, oleaginous alkaloid, which possesses great
energy as a poison.[2219] Mr. Morries-Stirling procured from hemlock by
destructive distillation an empyreumatic oil similar in properties to
those of hyoscyamus, stramonium and tobacco, but producing in animals a
state of pure coma.[2220]

The effects of hemlock on the animal system have been variously
described by different observers. Sometimes they have appeared to be
purely soporific like those of opium; at other times they have resembled
the effects of belladonna and thorn-apple; and in the lower animals they
are quite different, as I have witnessed them, from what they have been
described to be in man,—the phenomena being simply those of asphyxia
from paralysis of the muscles, without material convulsions and without
insensibility. Its irritant action is not well established.

Orfila observed that an ounce of the extract of the leaves killed a dog
in forty-five minutes when swallowed, ninety grains killed another
through a wound in an hour and a half, and twenty-eight grains another
through a vein in two minutes. It therefore acts by entering the
blood-vessels. The extract is a very uncertain preparation; the reason
of which is, that the alkaloid conia is very easily decomposed in its
natural state of mixture by heat or age, being converted into an inert
resinoid matter,—that the dried leaves of hemlock contain scarcely any
of it,—and that even an extract of the fresh leaves contains little,
unless prepared with a gentle heat, yet speedily.[2221] The symptoms
remarked by Orfila were convulsions and insensibility; and in the dead
body the blood of the left cavities of the heart was sometimes found
arterial.—The result of my observations is quite at variance with this
statement. In various experiments with a strong extract prepared from
the green seeds with absolute alcohol, the only effect I could remark
were palsy, first of the voluntary muscles, next of the chest, lastly of
the diaphragm,—asphyxia in short from paralysis, without insensibility,
and with slight occasional twitches only of the limbs, and the heart was
always found contracting vigorously for a long time after death. Thirty
grains of a soft extract introduced between the skin and muscles of the
back killed a rabbit in five minutes, and a five months’ puppy in twenty
minutes.[2222]

The root is much less energetic than is represented by some authors, and
probably varies in this respect at different seasons. I have found that
four ounces and a half of juice, the produce of twelve ounces of roots
collected in November, had no effect on a dog when secured in its
stomach by a ligature on the gullet; and that four ounces obtained from
ten ounces of roots in the middle of June, when the plant was coming
into flower, merely caused diarrhœa and languor. Orfila had previously
observed that three pounds of roots had no effect in the month of April;
but that two pounds in the end of May, when the plant was in full
vegetation, killed a dog in six hours.[2223] The alcoholic extract of
the juice obtained from six ounces of roots on the last day of May, I
have found to kill a rabbit in thirty-seven minutes, when introduced in
a state of emulsion between the skin and muscles of the back; and the
effects were analogous to those obtained with the extract of the leaves.
The differences depending on season will probably account for various
persons having found the juice of the root harmless. Gmelin quotes an
instance where four ounces of the juice were taken without injury. He
adds another where three ounces of the juice of the herb were swallowed
daily for eight days with as little effect. But, as he judiciously
observes, other less active plants have probably been sometimes mistaken
for hemlock.[2224]

The alkaloid, conia, seems to be the active principle of hemlock, and is
a poison of extraordinary virulence. On investigating this subject in
1835,[2225] I found that it is a local irritant, possessing an acrid
taste, and capable of exciting redness or vascularity in any membrane to
which it is applied; but that these topical effects are readily
overwhelmed by its swift and intense narcotic action. This action
consists of swiftly spreading palsy of the muscles, which affects first
those of voluntary motion, then the respiratory muscles of the chest and
abdomen, and lastly the diaphragm, so as to terminate by causing
asphyxia. The paralytic state is usually interrupted from time to time
by slight convulsive twitches of the limbs and trunk at the beginning.
The muscular contractility is impaired or annihilated by the topical
action of the poison, but not by its indirect action through absorption.
The heart is not appreciably affected; for it contracts vigorously long
after all motion, respiration, and other signs of life are extinct; and
it contains after death, not florid but dark blood in its left cavities.
The blood undergoes no alteration. The external senses are little, if at
all impaired, until the breathing is almost arrested; and volition too
is retained. But a contrary inference may be drawn by a careless
observer, in consequence of the paralytic state taking away the means,
by which in animals sensation is expressed and volition exercised. The
action of conia, in short, is confined to the spinal cord; and it acts
as a sedative, by exhausting the nervous energy.

Conia is probably a deadly poison to all orders of animals: at least I
found it to be so to the dog, cat, rabbit, mouse, frog, fly, and flea;
and Geiger killed the kite, pigeon, sparrow, slow-worm, and earth-worm
with it. It acts through every texture where absorption is carried on
readily, through the stomach, eye, lungs, cellular tissue, peritonæum,
or veins; and its activity is in proportion to the speed with which
absorption is carried on in the part. It acts therefore through
absorption. Its activity is increased by neutralization with an acid, by
which it is rendered much more soluble in water. Few poisons equal it in
subtility and swiftness. A single drop, applied to the eye of a rabbit,
will kill it in nine minutes; and three drops in the same way will kill
a strong cat in a minute and a half. Five drops, introduced into the
throat of a little dog, began to act in thirty seconds, and proved fatal
in one minute. And when two grains, neutralized with thirty drops of
weak hydrochloric acid, were injected into the femoral vein of a young
dog, it died before there was time to note the interval, so that only
two or three seconds at most had elapsed, before all internal signs of
life were extinct. This extraordinary rapidity of action seems
incompatible with its operation taking place by conveyance of the poison
with the blood to the spinal cord. Mr. Blake, as formerly mentioned (p.
15), denies that its action in this way was ever so swift in his hands,
and alleges that he could never observe the interval to be shorter than
fifteen seconds. If the reader, however, will consult the original
account of my experiment,[2226] which was made along with Dr. Sharpey,
he will see that we could scarcely be mistaken as to the interval in
that instance.

_Symptoms in Man._—M. Haaf, a French army-surgeon, has described a fatal
case of poisoning with hemlock, which closely resembled poisoning with
opium. The subject of it, a soldier, had partaken along with several
comrades of a soup containing hemlock leaves, and appeared to them to
drop asleep not long after, while they were conversing. In the course of
an hour and a half they became alarmed on being all taken ill with
giddiness and headache; and the surgeon of the regiment was sent for. He
found the soldier, who had fallen asleep, in a state of insensibility,
from which, however, he could be roused for a few moments. His
countenance was bloated, the pulse only 30, and the extremities cold.
The insensibility became rapidly deeper and deeper, till he died, three
hours after taking the soup.[2227] His companions recovered.

Dr. Watson has briefly described two cases which were fatal in the same
short space of time. The subjects were two Dutch soldiers, who, in
common with several of their comrades, took broth made with hemlock
leaves and various other herbs. Giddiness, coma, and convulsions were
the principal symptoms. The men who recovered were affected exactly as
if they had taken opium.[2228]

When the dose is not sufficient to prove fatal, there is sometimes
paralysis, attended with slight convulsions, as in a case noticed by
Orfila.[2229] More commonly there is frantic delirium. Matthiol has
related an instance of this last description, occurring in the cases of
a vine-dresser and his wife, who mistook the roots for parsneps Both of
them became in the course of the night so delirious that they ran about
the house, knocking themselves against every object which came in their
way.[2230] Kircher, as quoted by Wibmer, tells a parallel story of two
monks who became so raving mad after eating the roots, that they plunged
into water, imagining that they were turned into geese, and they were
affected for three years with incomplete palsy and neuralgic
pains.[2231] These and some other cases of the like kind, recorded by
the older medical authors, must be received with reserve. Independently
of other considerations, there is often no certainty that the poison was
really the hemlock of modern botanists, and not some other umbelliferous
vegetable.

_Morbid Appearances._—In Haaf’s case the vessels of the head were much
congested; and the blood must have been very fluid, for on the head
being opened a quantity flowed out, which twice filled an ordinary
chamber-pot. This state of the blood likewise occurred in a case which I
examined here some years ago along with Dr. C. Coindet of Geneva. A
hypochondriacal old woman took by advice of a neighbour two ounces of a
strong infusion of hemlock leaves with the same quantity of whisky,
which she swallowed in the morning fasting. She died in an hour,
comatose and slightly convulsed. The vessels within the head were not
particularly turgid; but the blood was everywhere remarkably fluid. Dr.
Coindet subsequently found that a small portion of the infusion prevents
fresh drawn blood from coagulating; but I suspect there must have been
some mistake here, for a carefully prepared alcoholic extract of very
great power, which was used in my experiments alluded to above, had no
such effect on blood fresh drawn from rabbits and dogs. On account of
this extreme fluidity of the blood, it often flows from the nose, but
the skin is much marked with lividity.[2232] The fluidity of the blood
is nothing more than the result of the proximate cause of death,—slowly
formed asphyxia.


                   _Of Poisoning with Water-Hemlock._

Another plant of the order Umbelliferæ, the water-hemlock or _Cicuta
virosa_, possesses also great energy as a poison; and in its effects it
appears to resemble considerably the hydrocyanic acid. The plant is
indigenous. It is easily known from other umbelliferous species
inhabiting watery places by the peculiar structure of its root-stock,
which is not fleshy, but hollow, and composed of a number of large cells
with transverse plates.

From a numerous set of experiments with the root of the cicuta performed
by Wepfer, it appears to cause true tetanic convulsions in frequent
paroxysms, and death on the third day.[2233] Simeon ascertained that the
alcoholic extract of the root is very poisonous.[2234] Schubarth found
that an ounce of the juice of the stems and leaves, collected after the
flowers had begun to blow, produced no effect on the dog.[2235] It is
probably inert, or at all events feebly poisonous in this climate,
although it grows luxuriantly in many localities. I have found that
twelve ounces of juice, expressed from sixteen ounces of roots in the
beginning of August, merely caused some efforts to vomit, when secured
in the stomach of a dog by a ligature on the gullet; that the alcoholic
extract of twelve ounces of leaves gathered at the same time had no
effect when introduced in the form of emulsion between the skin and
muscles of the back of a rabbit; and that the alcoholic extract of two
ounces of unripe seeds proved equally inert when imployed in the same
way.

_Symptoms in Man._—Wepfer has likewise related several instances which
occurred in the human subject. Among the rest he has described the cases
of eight children who ate the roots instead of parsneps. Of those who
were seriously affected, one, a girl six years old, who ultimately
recovered, had tetanic fits, followed by deep coma, from which it was
impossible to rouse her for twenty-four hours. Two of them died. The
first symptoms in these two were swelling in the pit of the stomach,
vomiting or efforts to vomit, then total insensibility, with involuntary
discharge of urine, and finally severe convulsions, during which the
jaws were locked, the eyes rolled, and the head and spine were bent
backwards, so that a child might have crept between the body and the
bed-clothes. One of them died half an hour after being taken ill, and
the other not long after.[2236] Mayer of Creutsburg mentions four cases,
which were occasioned by the roots. One of the individuals, a child
three years old, was attacked with colic, vomiting, and convulsions, and
died in a few hours. The three others, the eldest of whom was six years
of age, had coldness, paleness of the features, dilated immoveable
pupils, violent colic, general spasms, and insensibility. The action of
the heart was intermitting and the breathing oppressed. After the
remains of the roots were brought up by emetics, and infusion of gall
was administered, they gradually recovered. They had eaten between them
no more than a single root weighing about two ounces, as they had in
their possession another of that weight, which they said was not so
large. This accident happened in the middle of March.[2237]

According to Guersent, poisoning with the cicuta commences with dimness
of sight, giddiness, acute headache, anxiety, pain in the stomach,
dryness in the throat, and vomiting.[2238]

Mertzdorff has related the particulars of the inspection of three cases
which proved quickly fatal with convulsions and vomiting. Nothing
remarkable seems to have been found except great gorging of the cerebral
vessels.[2239]


                 _Of Poisoning with Hemlock Dropwort._

The _Œnanthe crocata_ of botanists, the hemlock dropwort,
five-finger-root, or dead-tongue of vernacular speech in England, a
species of the same family with the last two, and an abundant plant in
some localities throughout this country, has usually been held one of
the most virulent of European vegetables. It seems well entitled to this
character in general; but climate, or some other more obscure cause,
renders it inert in some situations.

It is said to be liable to be confounded with common hemlock, or _Conium
maculatum_,—a mistake which can happen only in very ignorant hands. It
has smooth, dark-green leaves, more fleshy, and much less minutely
divided, than those of hemlock; it presents a purplish appearance at the
joints only of the stem, and no diffused purple spots; its fruit is
oblong and black, not round, rough, and light brown; and its root,
instead of being single, long, tapering, and little branched, consists
of from two to ten tubers, like fingers, which are white, and terminate
in a few rootlets. These tubers are formed annually in summer from the
flowering stem of the season, and send out flowering stems the
subsequent year. During the first autumn, winter, and spring they are
firm, white, and amylaceous; but in their second summer they become more
pulpy, less amylaceous, and grayer. At all times they emit, when broken
across, an oleo-resinous juice, which quickly becomes yellow; this juice
abounds most when the plant, which is growing at their expense, is about
to flower; and it abounds much more at this period in localities in the
south of England, than in Scotland, especially in the neighbourhood of
Edinburgh.

Brotero and some others have attempted to subdivide the species into
two, the _Œnanthe crocata_ proper, and the _Œ. apiifolia_. But the best
authorities deny that these can be distinguished; and from what I have
now seen in sundry localities, it appears to me that the distinctions
pointed out by Brotero, confessedly obscure enough in themselves, are
the result of differences in climate, soil, and situation.

The only analysis of this plant with which I am acquainted is one
executed in 1830 by MM. Cormerais and Pihan-Dufeillay, who found in the
root a resinoid matter, which adheres obstinately to the solid portion
of it, and which seems to be the active ingredient.[2240] I have
subjected the roots to various processes, and among the rest to that by
which Geiger detected conia in hemlock, but without discovering any
indication of the existence of an alkaloid. My materials, however, were
not well fitted for a chemical analysis; because the œnanthe root of
this neighbourhood is inert or nearly so. The whole plant contains a
heavy-smelling volatile oil, which may be obtained by distillation in
the usual way, and most abundantly from the ripe seeds. This oil is
yellowish, viscid, and inert.

It is strange that a plant, so universally considered a potent poison,
and so frequently the cause of fatal accidents, has not yet been made
the subject of physiological investigation. A few imperfect experiments
by M. Cormerais and his companion, made with the resinoid matter of the
roots, show that this substance produces in animals dulness, convulsions
of the voluntary muscles, a semi-paralytic state of the hind legs, and
sometimes shortness of breath, vomiting, and fluid evacuations by stool.
All the animals experimented on recovered. On repeating these
experiments with larger quantities I found the resin of the root, grown
near Woolwich, and kindly sent to me by Dr. Pereira, to be a poison of
great energy and singular properties. Twenty-four grains obtained from
eight ounces of roots in the middle of December, when introduced in the
form of emulsion between the skin and muscles of the rabbit, caused in
half an hour depression, uneasiness, and hurried breathing,—then
twitches of the ears, neck, and fore-legs,—next combined spasm and
convulsive starting of the head and limbs,—then, after a quiet interval,
a more violent fit of the same kind, affecting the whole body with a
singular combination of tetanus and convulsive starting,—finally, after
several such fits, a paroxysm more violent than before, ending in
immoveable tetanic rigidity, which speedily proved fatal, 78 minutes
after the application of the poison. No morbid appearance could be
detected in the body. The heart contracted vigorously for some time
after death. These phenomena correspond in the main with what has been
recorded of the symptoms caused by the roots in man.—Dr. Pereira informs
me he had found the juice both of the root and leaves to act as a
poison, either when introduced into the peritonæum, or when injected
into the veins; and in the latter way it was so energetic as to prove
fatal in one minute.

_Symptoms in Man._—Since Lobel first took notice of the poisonous
properties of the œnanthe root in 1570, an uninterrupted series of
observations has been published, down to the present day, showing that
in France, Germany, Holland, Spain, and various parts of England as far
north as Liverpool, it is at all seasons of the year, even in October
and in the beginning of January, a poison of great activity. In several
of the cases death has been occasioned by a single handful of the roots,
in one instance by a piece no bigger than the finger, or even in
consequence of the individuals merely tasting them. A girl seems to have
had a narrow escape after eating, with an interval of three hours, two
pieces of the size of a walnut. Very seldom has death been delayed
beyond four hours, and on some occasions a single hour has been
sufficient. Sometimes the symptoms have been slow in making their
appearance, an hour and a half having occasionally elapsed before the
effects were evident; but in every instance their progress was rapid,
once the symptoms had fairly set in; and some died in convulsions almost
immediately after being taken ill.

The particular effects have been variable. Most generally the first
symptoms have been giddiness and staggering, as if from ordinary
intoxication, occasionally headache, and often extreme feebleness of the
limbs. Stupor has then generally succeeded, sometimes with the
intervention of efforts to vomit, sometimes too with an interval of
delirium. Convulsions have also commonly made their appearance in the
next place; and ere long a state of insensibility has ensued attended in
every instance with occasional violent convulsive fits like epilepsy,
and with permanent locked-jaw; which symptoms have continued till near
death. In one or two cases the individual has suddenly, without any
premonitory symptoms, fallen down convulsed, and died almost
immediately. In one or two instances again, the effects have rather been
those of irritant poisoning, namely, inflammation of the mouth and
throat, spasms of the muscles of the throat, vomiting, and excessive
weakness and faintness, without any convulsions or insensibility.—It
appears then that this plant is a true narcotico-acrid poison. The
emanations from the plant are said on some occasions to have proved
injurious; but the effect here was probably the work of the imagination.

Aware of these singular properties being generally ascribed to the
_Œnanthe crocata_, I was anxious to make a methodical examination of the
subject, physiologically as well as chemically,—especially as the plant
grows in great abundance and very luxuriantly in a locality not far from
Edinburgh. But I have found it in that situation, to all appearance,
quite inert. The juice of fourteen ounces of the root in the end of
October had no effect on a little dog when secured in the stomach by a
ligature on the gullet. The juice of sixteen ounces in the middle of
June was also without effect. An alcoholic extract of four ounces of the
full grown leaves in the end of June, introduced into the cellular
tissue in the form of emulsion, had no effect on a rabbit. An alcoholic
extract of three ounces of the ripe seeds was administered in the same
way with the same result. Finally, the resinoid extract of eight ounces
of the root, analogous to that which had proved so deadly in my hands
when obtained from Woolwich plants, had also no effect whatever, when
prepared from those growing in the neighbourhood of Edinburgh. Relying
upon these results, I ate a whole tuber weighing an ounce, without
observing any effect, except its disagreeable taste; which was the only
circumstance that prevented me from trying a larger quantity.—It may be
well to add, that, amidst the numerous cases of poisoning with œnanthe
now on record, there is not one that has occurred in Scotland. At the
same time, the common people in Scotland are not at all given to rash
experiments in cookery, or to make use of vegetables not produced by the
care of the gardener or farmer.[2241]

The only other locality from which I have been hitherto able to obtain
plants for examination is the neighbourhood of Liverpool, where a fatal
case of poisoning with it occurred near the close of last century. When
the juice of sixteen ounces of this root in the beginning of September
was secured in the stomach of a dog, efforts to vomit were produced,
followed by several fits of violent convulsions and spasm of the
voluntary muscles, a paralytic state of the fore-legs, and a constant
tendency to fall backwards; but the animal recovered.

No morbid appearances of any note have been observed after death in any
of the fatal cases which are recorded.—The most appropriate treatment
consists in the prompt employment of emetics, and diffusible stimulants.


                  _Of Poisoning with Fool’s Parsley._

Another umbelliferous plant of great activity is fool’s parsley, or
_Æthusa cynapium_. It has occasioned several accidents by reason of its
resemblance to parsley,—from which, however, it is at once distinguished
by the leaves being dark and glistening on their lower surface, and by
the nauseous smell they emit when rubbed. It contains an alkaloid, which
crystallizes in rhombic prisms, and is soluble in water and alcohol, but
not in ether. It was discovered by Professor Ficinus of Dresden.[2242]

Orfila found that six ounces of the juice, when retained in the stomach
of a dog, by a ligature, caused convulsions and stupor, and death in an
hour.[2243]

_Symptoms in Man._—Some interesting information on the characters and
properties of this plant is contained in the Medical and Physical
Journal. Among other cases the writer relates those of two ladies who
ate a little of it in a sallad instead of parsley, and who were soon
seized with nausea, vomiting, headache, giddiness, somnolency, pungent
heat in the mouth, throat, and stomach, difficulty in swallowing and
numbness of the limbs.[2244] Gmelin has related the case of a child, who
died in eight hours in consequence of having eaten the æthusa. The
symptoms were spasmodic pain in the stomach, swelling of the belly,
lividity of the skin, and difficult breathing.[2245] In two children who
recovered, the chief symptoms at the height of the poisoning were
complete insensibility, dilated, insensible pupil, and staring of the
eyes. In one of them there was also frequent vomiting, in the other
convulsions. The treatment consisted in the administration of milk,
sinapisms to the legs, and cold spunging with vinegar.[2246]




                             CHAPTER XXXV.
                     OF THE NARCOTIC RANUNCULACEÆ.


The greater part of the poisons belonging to the Natural Family
_Ranunculaceæ_ are acrid only in their action, and have been already
taken notice of among the irritants. Two only are yet known to possess
narcotic properties, namely, _monkshood_, and _black hellebore_. The
latter is a true narcotico-acrid. The former has till lately been always
considered so; but its acrid properties seem doubtful or feeble, while
its action on the nervous system is most intense.


                     _Of Poisoning with Monkshood._

Monkshood, the _Aconitum napellus_ of botanists, is an active poison,
and has commonly been considered a true narcotico-acrid. But its effects
have been hitherto much misunderstood. It has been used for criminal
purposes in Ireland; and in 1841, a woman, M’Conkey, who was executed
there for poisoning her husband, was proved to have administered this
substance [see p. 61]. The root of another species, the _A. ferox_, is
well known to be in common use as a poison, under the name of Bikh, in
Bengal, and Nabee, in the Madras Presidency.

The toxicological history of the genus, and of this species in
particular, has been rendered complex and obscure, by the extreme
difficulty of distinguishing accurately the several species from one
another. The whole genus, now a numerous one, is generally conceived to
be eminently poisonous. But from some observations of my own, as well as
an elaborate inquiry, not yet made public, by Dr. Alexander
Fleming,[2247] a recent graduate of this university, I am inclined to
think that this is a mistake, that the poisonous species are not
numerous, and that many aconites are inert, at least in this climate.

The _A. napellus_, a doubtful native of Britain, and the most common
species in our gardens, shoots up annually a leafy stem from a black,
tapering, spindle-shaped root. The stem, which is from two to five feet
high, ends in a long dense spike of fine blue flowers; and when the
seeds ripen in autumn, it dies down, and the root also shrivels and
perishes. But in the spring, while the stem is rising, one or more
tubers form near the crown of the root; each tuber quickly assumes the
spindle-shaped form of its parent, but has a light brown, instead of a
brownish-black tegument; and when the plant is in flower, the new tuber,
destined for the root of next year’s plant, is as large as the parent
one, firmer, more amylaceous, and not so apt to shrivel in drying. This
mode of propagation has led some to describe the root erroneously as
sometimes palmated. Dr. Fleming considers the young, full-grown tuber to
be the most active part of the plant; but the root of the existing
plant, the leaves, and also the seeds, are highly energetic; and every
part is more or less so.

Every part of the _A. napellus_, but especially the root, affects
remarkably the organs of taste, producing a very singular sense of heat,
numbness, and tingling of those parts of the mouth to which it is
applied. Dr. Fleming has ascertained, that this peculiar taste, or
rather sensation, is a property belonging to the narcotic principle of
monkshood, and that in all probability it is a measure of the activity
of the plant as a poison. It is most intense in the root, next in the
seeds, and next in the leaves before the flowers blow. Geiger first
ascertained, and I have since observed, that the sensation thus
occasioned by the leaves diminishes in intensity as the flowers expand,
and almost disappears when the seeds ripen. Contrary to what has been
often stated, it is not diminished by drying the leaves, even with the
heat of the vapour-bath. Nor is it materially lessened by time, if the
dried leaves be preserved with care; for I have found it intense after
six years. Geiger observed some years ago, that several species or
varieties do not possess it. I have ascertained that _A. napellus_,
_sinense_, _tauricum_, _uncinatum_, and _ferox_, possess it intensely,
_A. schleicheri_ and _nasutum_ feebly, _A. neomontanum_ very feebly; all
of which are therefore probably poisonous, in proportion to the
intensity of their taste. _A. ferox_, well known as a deadly poison in
the East, and undoubtedly the most virulent of all the species, produces
by far the most intense and persistent effect on the mouth of all the
species I have had an opportunity of examining. Those which do not
produce it at all, at least in this climate, are _A. paniculatum_,
_lasiostomum_, _vulparia_, _variegatum_, _nitidum_, _pyrenaïcum_, and
_ochroleucum_. It would be premature to say that all these species are
inert; but I suspect they are: and, at all events, I have ascertained
that the leaves of _A. paniculatum_, although the officinal species
recognised in the London Pharmacopœia, are quite inactive in this
climate; and Dr. Fleming has found the root inert in medicinal doses of
considerable magnitude.

The properties of monkshood have been traced by Geiger and Hesse to a
peculiar alkaloid, named aconitina: which is white, pulverulent,
fusible, not volatile, soluble in ether and alcohol, sparingly so in
water, and capable of forming crystallizable salts with acids. It
produces most intensely the peculiar impression caused by the plant on
the mouth, tongue, and lips; and it is a poison of tremendous activity,
probably indeed the most subtle of all known poisons. Although not a
volatile principle, it has been supposed peculiarly liable to
decomposition by heat, at least in its natural state of combination in
the plant or its pharmaceutic preparations. This opinion is founded on
the uncertainty of the medicinal action of the common extract of the
shops, and on the results of experiments on animals by Orfila.[2248] In
one experiment he found that half an ounce of the extract of the
Parisian shops had no effect at all on a dog, while a quarter of an
ounce killed another within two hours. Careless preparation may account
for such differences; but at the same time an error in choosing the
species of plant is an equally probable explanation. The properties of
monkshood appear to me to resist a heat of 212°, either in drying the
plant or in preparing an extract from it.

The medico-legal chemistry of monkshood has not been studied. If any of
the suspected matter be obtained in a pure state, its best character is
its remarkable taste; to which I have found nothing exactly similar in
the numerous trials I have made with other narcotic and acrid plants. A
complex substance, such as the contents of the stomach, or vomited
matter, should be evaporated over the vapour-bath to the consistence of
thin syrup, and agitated with absolute alcohol. The filtered alcoholic
solution being then evaporated, the extract may be subjected to the
sense of taste.

_Action._—The action of monkshood is a subject of great interest, but
has hitherto been much misunderstood. Sir B. Brodie, who was the first
to examine it in recent times, found that the leading phenomena in
animals, were staggering, excessive weakness, slow laborious
respiration, and slight convulsive twitches before death.[2249] Had
these observations been followed up by his successors with a
discriminating eye, toxicologists would not have been so much misled as
they have been. Orfila, who was the next to examine the subject
experimentally, failed to appreciate the phenomena with exactness.[2250]
He thinks monkshood acts peculiarly upon the brain, causing delirium,
and that it is a local irritant, capable of developing more or less
intense inflammation. A single experiment made in 1836 convinced me that
the former statement is incorrect, and led me to consider that the
symptoms depend in a great measure on gradually-increasing paralysis of
the muscles, which terminates in immobility of the chest and diaphragm,
and consequent asphyxia. Dr. Pereira, in some experiments with an
alcoholic extract, published in 1842, took notice of two remarkable
phenomena,—an extraordinary diminution of common sensation, evidenced by
the animal being insensible to pinching and pricking,—and the total
absence of stupor, as shown by the animal following its owner, and
recognizing him when called.[2251] Similar observations have been made
in poisoning with monkshood in man. The ablest investigation yet
undertaken into the actions of this substance is contained in the
unpublished Inaugural Dissertation of Dr. Fleming.

He found that the most remarkable symptoms are weakness and staggering,
gradually increasing paralysis of the voluntary muscles, slowly
increasing insensibility of the surface, more or less blindness, great
languor of the pulse, and convulsive twitches before death. He farther
observed that the pupil becomes much contracted; that the irritability
of the voluntary muscles is impaired; that the veins are congested after
death, the blood unaltered, and the heart capable of contracting for
some time after respiration has ceased. Lastly, he maintains that this
poison has not, as is generally thought, any irritant properties, that
neither the plant, nor its extract, nor its alkaloid occasions
vascularity in any membrane to which it is applied, even, for example,
in the lips or tongue while burning and tingling from its topical
action; that this peculiar effect is therefore merely a nervous
phenomenon; and that he never could observe either the diffuse cellular
inflammation described by Orfila to arise from the application of
monkshood to a wound, or the inflammatory redness of the alimentary
canal noticed by others as one of its effects when swallowed.

Orfila ascertained that monkshood exerts its action through the medium
of the blood; for its effects are greater when it is introduced into a
wound, than when it is swallowed, and they are still greater when it is
injected directly into a vein. It is a poison of very great activity. I
have found that thirty grains of an alcoholic extract, the produce of
three-quarters of an ounce of fresh leaves, will kill a rabbit in two
hours and a quarter, if introduced between the skin and muscles of the
back. Five drachms of the root in one of Orfila’s experiments with the
dog, occasioned death in twenty-one minutes, when swallowed.

The alkaloid, aconitina, seems to produce in animals precisely the same
effects as the plant or its extract. Orfila and Dr. Pereira agree in
this; and my own observation, limited to a single experiment, is to the
same effect. It is probably the most subtile of all known poisons. Dr.
Pereira mentions that the fiftieth part of a grain has endangered life
when used medicinally.[2252] In my experiment the tenth of a grain,
introduced in the form of hydrochlorate into the cellular tissue of a
rabbit, killed it in twelve minutes.

_Symptoms in Man._—A perplexing discrepance exists in the accounts that
have been published of the effects of monkshood on man; which seems to
have arisen, less from any actual contrariety in the phenomena, than
from loose observation, or a misunderstanding of the facts; for most of
the recent statements of competent observers are consistent with one
another.

Dr. Fleming says that in medicinal doses it occasions warmth in the
stomach, nausea, numbness and tingling in the lips and cheeks, extending
more or less over the rest of the body, diminution in the force and
frequency of the pulse, which sometimes sinks to 40 in the minute, great
muscular weakness, confusion of sight or absolute blindness; and if the
dose be unduly large, there is a sense of impending death, sometimes
slight delirium, and a want of power to execute what the will directs,
but without any loss of consciousness. The warmth which is excited is
unattended with any elevation of temperature, vascularity of the skin,
or acceleration of the pulse. No true hypnotic effect is produced; but
by inducing serenity, or deadening pain, it may predispose to sleep. The
highest degree of these effects is not unattended with danger.

When it is administered in doses adequate to occasion death, it seems in
general to operate by inducing extreme depression of the circulation.
Dr. Fleming recognizes two other modes of death in animals,—first, by an
overwhelming depression of the nervous system, proving fatal in a few
seconds, without arresting the action of the heart,—and secondly, by
asphyxia, or arrestment of the respiration, the result of paralysis
gradually pervading the whole muscular system, respiratory, as well as
voluntary. But these effects, he thinks, cannot be recognized in the
cases which have been published of poisoning in man, because the dose
required to produce either of them is very large. The least variable
symptoms in the human subject are, first, numbness, burning, and
tingling in the mouth, throat, and stomach,—then sickness, vomiting, and
pain in the epigastrium,—next, general numbness, prickling, and impaired
sensibility of the skin, impaired or annihilated vision, deafness, and
vertigo,—also frothing at the mouth, constriction at the throat, false
sensations of weight or enlargement in various parts of the body,—great
muscular feebleness and tremor, loss of voice, and laborious
breathing,—distressing sense of sinking and impending death,—a small,
feeble, irregular, gradually-vanishing pulse,—cold, clammy sweat and
pale bloodless features,—together with perfect possession of the mental
faculties, and no tendency to stupor or drowsiness,—finally, sudden
death at last, as from hemorrhage, and generally in a period varying
from an hour and a half to eight hours. The symptoms may begin in a few
minutes, as in a case observed by Dr. Fleming, which was occasioned by
the tincture of the root; or they may be postponed for three-quarters of
an hour, as in an instance recorded by Dr. Pereira,[2253] which arose
from the root being used by mistake for horse-radish. Two or three
drachms of the root are sufficient to kill a man; and Dr. Fleming
mentions one instance where two grains of the alcoholic extract
occasioned alarming effects, and another where four grains proved fatal.
I may observe, however, that I have given six grains of a carefully
prepared alcoholic extract (the same of which thirty grains killed a
rabbit in little more than two hours), to a female suffering from
rheumatism, without being able to observe any effect whatsoever.

If all the reports of cases now on record are to be trusted, the
following anomalies have occurred. Some persons are said to have
presented convulsions. Slight spasmodic twitches of the muscles are not
uncommon, and probably depend, as Dr. Fleming suggests, on venous
congestion, the result of incomplete asphyxia. Stupor and even
apoplectic insensibility are also sometimes represented to have been
observed. If really ever present, they must depend on the same cause;
but there is reason to apprehend, that extreme nervous depression and
faintness have been mistaken for stupor and coma. Delirium of the
frantic kind, mentioned by some of the older authors, is justly
considered by Dr. Fleming to be of doubtful occurrence, as it has never
been observed in recent times. Irritation in the alimentary canal is
distinctly mentioned as indicated by prominent symptoms, even in some
cases observed but a few years ago, and apparently with care. Dr.
Fleming properly objects to nausea, vomiting, or pain in the epigastrium
as evidence of irritation in the stomach; for these symptoms may all
depend on the same local nervous impression which is produced on the
organs of taste. And he denies that purging is ever produced in any
genuine case of poisoning with monkshood. The following, however, seem
unequivocal examples of irritation in the alimentary canal. M.
Pallas[2254] mentions, that three out of five persons, who took a
spirituous infusion of the root by mistake for lovage [_Ligusticum
levisticum_], died in two hours with burning in the throat, vomiting,
colic, swelling of the belly and purging. A similar set of cases is
described by M. Degland.[2255] Four persons took the tincture of the
root by mistake for tincture of lovage; and three of them were seized
with burning pain from the throat to the stomach, a sense of enlargement
of the tongue and face, colic, tenderness of the belly, vomiting, and
purging. One of these, who ultimately recovered, had frantic delirium
for some time after the other symptoms went off. The two others died,
one in two hours, the other half an hour later. Dr. Pereira[2256] and
Dr. Fleming doubt the authenticity of these cases; and it may be, that
such unusual symptoms may have arisen either from some other root
mistaken by the narrators for monkshood, or from irritant substances
given along with or after it. At the same time I may mention, that in
the first trials I made with monkshood as a medicine, using a carefully
prepared extract of the root, I was deterred from proceeding by two
patients being attacked with severe vomiting, griping, and diarrhœa.

It may be well to conclude these general statements by the particulars
of a few well authenticated cases. Dr. Pereira describes two that were
occasioned by the root having been dug up in February by mistake for
horse-radish.[2257] The parties, a gentleman and his wife, ate, the
former about a root and a half, the latter not much more than half a
root. Both of them in three-quarters of an hour had burning, and
numbness in the lips, mouth, and throat, extending to the stomach and
followed by vomiting. The husband had subsequently violent and frequent
vomiting, partly owing to an emetic. His extremities became cold, the
lips blue, the eyes glaring, and the head covered with cold sweat. There
was no spasm or convulsion, but some tremor. He had no delirium, or
stupor, or loss of consciousness, but complained of violent headache.
The respiration was not affected; and although he felt very weak, he was
able to walk with a little assistance only a few minutes before death;
which took place, as if from fainting, about four hours after the poison
was swallowed.—His wife, in addition to the early symptoms already
mentioned, had such weakness and stiffness of the limbs that she was
unable to stand; and she could utter only unintelligible sounds; but she
had no spasms or convulsions. She experienced a strange sensation of
numbness in the hands, arms, and legs, diminution of sensibility over
the whole integuments, especially of the face and throat, where the
sense of touch was almost extinguished. She had also some dimness of
vision, giddiness, and at times an approach to loss of consciousness,
but no delirium, sleepiness, or deafness. She recovered, under the use
of emetics, laxatives, and stimulants. In neither of these cases was
there any diarrhœa.—A patient of Mr. Sherwen,[2258] five minutes after
taking a tincture of the root, suffered from the same incipient symptoms
as above, but without actual vomiting. The face seemed to her to swell,
and the throat to contract; she became nearly blind, and excessively
feeble, but did not lose her consciousness. The eyes were fixed and
protruded, and the pupils contracted, the jaws stiff, the face livid,
the whole body cold, the pulse imperceptible, the heart’s action feeble
and fluttering, and the breathing short and laborious. An emetic was
followed first by violent convulsions, and then by vomiting; after which
she slowly recovered. At all times she was so sensible as to be able to
tell how the accident happened.—Dr. Ballardini of Brescia met with
twelve simultaneous cases of poisoning with the juice of the leaves,
used by mistake for scurvy-grass [_Cochlearia officinalis_]. Each person
had three ounces of juice. Three of them died in two hours; but the rest
were saved. The chief symptoms were extreme weakness and anxiety,
paleness and distortion of the features, dilatation of the pupils,
dulness of the eyes, giddiness, headache, chiefly occipital, some
distension and pain of the belly, vomiting of a green matter, and in
some diarrhœa. The whole body was cold, the nails livid, the limbs
cramped, the pulse small and scarcely perceptible. In the fatal cases
there were convulsions.[2259]—MM. Pereyra and Perrin mention, that,
while using the alcoholic extract in the Hospital of St. André at
Bordeaux, the sample of the drug happened to be changed when the dose
had been raised so high as ten grains; and that the patients who were
taking it were then all seized with burning in the mouth and throat,
vomiting, pungent pains in the extremities, cold sweating, anxiety,
extreme general prostration, great slowness and irregularity of the
pulse, convulsions, and congestion in the venous system. One patient
died; the others recovered under no other treatment than stimulant
friction along the spine.[2260] An infant at Suippe, in the French
Department of the Marne, ate a few leaves and flowers of monkshood,
while walking in a garden. Soon afterwards he began to stagger as if
tipsy, and to complain of pain in the belly. In two hours an emetic was
given; but a few minutes afterwards, the eyes became convulsed, the jaws
locked, the trunk bent rigidly backward, and the limbs convulsed; and
death ensued in five minutes more.[2261]

_Morbid Appearances._—In Ballardini’s fatal cases the pia mater and
arachnoid were much injected; there was much serosity under the
arachnoid and in the base of the cranium; the lungs were considerably
gorged with blood; the heart and great vessels contained but a little
black fluid blood: the villous coat of the stomach was spotted with red
points; and the small intestines presented inwardly red patches and much
mucus. In the Bordeaux case there was venous congestion in the head and
chest, the lungs particularly being much gorged with blood. The right
side of the heart was full of blood, of gelatinous consistence. In
Pallas’s cases the gullet, stomach, small intestines and rectum were
very red, the lungs dense, dark, and gorged, and the cerebral vessels
turgid.

Few trustworthy observations have been made on the effects of the other
species of aconite. Dr. Pereira found the A. ferox of the East Indies to
be a much more deadly poison to animals than common monkshood; but its
effects were otherwise identical.[2262] Three grains of the root put
into the throat of a rabbit, killed it in nineteen minutes; one grain of
the alcoholic extract, introduced into the peritonæum, proved equally
deadly. Nine grains will kill a cat in four hours.[2263]——Of the other
aconites the A. cammarum, and A. lycoctonum are said to have proved
fatal frequently in Germany; but no accurate facts on the subject are on
record.—It was stated above that the A. paniculatum, supposed by De
Candolle to have been the true aconite of Baron Störck, is inert in this
country. I introduced the alcoholic extract of three ounces of the fresh
leaves collected near the end of June, into the cellular tissue between
the skin and muscles of a young rabbit, having previously converted the
extract into an emulsion with mucilage and water. This was four times
the dose of A. napellus, which I had found sufficient to kill a strong
adult rabbit in two hours and a quarter; but no effect whatever was
produced.—Mr. Ramsay of Broughty Ferry has described a case of fatal
poisoning with a handful of aconite leaves which were mistaken for
parsley, and which he supposes to have been those of A. neomontanum. The
subject, a boy of fourteen, was attacked with a sense of burning in the
mouth, throat, and stomach, afterwards with vomiting and convulsions,
and died considerably within five hours.[2264] The very feeble taste of
this species—which besides is little cultivated in Scotland,—inclines me
to doubt whether it was the species that produced such violent effects.


                  _Of Poisoning with Black Hellebore._

Black hellebore, or Christmas-rose, the _Helleborus niger_ of botanists,
is a true narcotico-acrid poison. It is a doubtful native of this
country. It produces a large white ranunculus-like flower about
midwinter. The root, the only part used in medicine, or to be found in
the shops, consists of a short root-stock and numerous, long, black
undivided rootlets. The fresh root in January is not acrid to the taste.
Its active principle appears from the researches of MM. Feneulle and
Capron, to be an oily matter containing an acid.[2265]

Its action has not yet been examined with particular care. Two or three
drachms of the root killed a dog in eighteen hours, when swallowed; two
drachms killed another in two hours, when applied to a wound; and six
grains in a wound caused death in twenty-three hours. In all cases the
leading symptoms are efforts to vomit, giddiness, palsy of the
hind-legs, and insensibility.[2266] Ten grains of the extract introduced
into the windpipe killed a rabbit in six minutes.[2267] Orfila found
redness of the rectum, when the animals survived a few hours. But none
of these experiments show the powerful irritant action exerted by the
root upon man.

The Bulletins of the Medical Society of Emulation mention two cases of
poisoning with hellebore, which arose from the ignorance of a quack
doctor. Both persons, after taking a decoction of the root, were seized
in forty-five minutes with vomiting, then with delirium, and afterwards
with violent convulsions. One died in two hours and a half, the other in
less than two hours.[2268] Morgagni has related a case which proved
fatal in about sixteen hours, the leading symptoms of which were pain in
the stomach, and vomiting. The dose in this instance was only half a
drachm of the extract.[2269] In a case not fatal, related by Dr.
Fahrenhorst, the symptoms were those of irritant poisoning generally,
that is, burning pain in the stomach and throat, violent vomiting, to
the extent of sixty times in the first two hours, cramps of the limbs,
and cold sweating. The most material symptoms were at this time quickly
subdued by sinapisms to the belly and anodyne demulcents given
internally; and in four days the patient was well. The dose here was a
table-spoonful of the root in fine powder.[2270] In small doses of ten
or twenty grains, it is well known to be a powerful purgative to man. I
have known severe griping produced by merely tasting the fresh root in
January.

The morbid appearances in Morgagni’s case were the signs of inflammation
in the digestive canal, particularly in the great intestines. In the
case described in the French Bulletins, there was gorging of the lungs,
and the stomach had a brownish-black colour as if gangrenous.

The other species of hellebore have not been carefully examined; but it
is probable that they all possess similar properties. The _H. hyemalis_
and _viridis_ are said by Buchner to be weaker than the _H. niger_; and
the _H. fœtidus_ is the most poisonous of all.[2271]




                             CHAPTER XXXVI.
OF POISONING WITH SQUILL, MEADOW-SAFFRON, WHITE HELLEBORE, AND FOXGLOVE.


The natural family _Liliaceæ_, and the allied family, _Melanthaceæ_,
contain many species which possess narcotico-acrid properties. Those
which are best known in Europe are squill, meadow-saffron, cevadilla,
and white hellebore. To these may be added foxglove, as possessing
properties in some measure analogous, and also rue and ipecacuan.


                      _Of Poisoning with Squill._

The root of the squill, or _Squilla maritima_, possesses the properties
of the narcotico-acrids. Orfila’s experiments on animals, indeed, assign
to it only an action on the nervous system. He found that two ounces and
a half of the fresh root, when secured in the stomach of a dog by a
ligature on the gullet, excited efforts to vomit, dilated pupil, and
lethargy; and in two hours the animal suddenly fell down in a violent
fit of tetanus, and expired. From thirty-six grains injected into the
jugular vein no effect followed for sixteen hours; when at last, as in
the former case, the animal dropped down convulsed and died
immediately.[2272]

The effects, however, caused by squill on man leave no doubt that it is
also an active irritant; for it causes sickness, vomiting, diarrhœa,
gripes, and bloody urine, when given in over-doses. It has likewise
produced narcotic symptoms in man. Lange mentions an instance of a
woman, who died from taking a spoonful of the root in powder to cure
tympanitis. She was immediately seized with violent pain in the stomach;
and in a short time expired in convulsions. The stomach was found every
where inflamed, and in some parts eroded.[2273]—A woman, whose case is
mentioned in a French journal, after taking from a female quack a vinous
tincture made with seventy-five grains of extract of squill, was seized
with nausea and severe colic, to which were added in twenty-four hours a
small contracted pulse, extreme tenderness of the belly, and cold
extremities; and she died in the course of the second day.[2274]
Twenty-four grains of the powder have proved fatal.[2275] I have seen a
quarter of an ounce of the syrup of squills, which is a common medicinal
dose, cause severe vomiting, purging, and pain.

An acrid principle, named scillitin, has been discovered in the squill.
A difference of opinion prevails as to its nature. Some chemists
consider it to be a resin; but Landerer has obtained it in the
crystalline form, with alkaline properties. A grain of it will kill a
dog.


           _Of Poisoning with White Hellebore and Cevadilla._

White hellebore, the root-stock of _Veratrum album_, and cevadilla, the
seed and capsules of _Asagræa officinalis_, and possibly of _Veratrum
sabadilla_, seem to be characteristic examples of the narcotico-acrid
poisons. They both possess a strong bitter taste, followed by acridity.
The cevadilla-seed in particular has an intensely disagreeable and
persistent bitter taste, and produces at the same time a combination of
acridity and numbness of the lips, tongue, and cheeks. They owe their
active properties chiefly to an alkaloid of great energy, termed
veratria.

White hellebore root is familiarly known to be a virulent poison. The
best account of its effects is contained in a Thesis by Dr. Schabel,
published at Tübingen in 1817. Collecting together the experiments
previously made by Wepfer, Courten, Viborg, and Orfila, and adding a
number of excellent experiments of his own, he infers that it is
poisonous to animals of all classes,—horses, dogs, cats, rabbits,
jackdaws, starlings, frogs, snails, and flies;—that it acts in whatever
way it is introduced into the system,—by the stomach, rectum, windpipe,
nostrils, pleural membrane of the chest, an external wound, or the
veins;—that it produces in every instance symptoms of irritation in the
alimentary canal, and injury of the nervous system;—and that it is very
active, three grains of the extract applied to the nostrils of a cat
having killed it in sixteen hours.[2276]

_Symptoms in Man._—Its effects on man are similar. A singular account of
several cases of poisoning with the root is contained in Rust’s Journal.
A family of eight people, in consequence of eating bread for a whole
week, in which the powder of the root had been introduced by mistake
instead of cumin seeds, were attacked with pains in the belly, a
sensation as if the whole intestines were wound up into a clue, swelling
of the tongue, soreness of the mouth, and giddiness; but they all
recovered by changing the bread and taking gentle laxatives.[2277]

Another set of cases of a more aggravated nature, though still not
fatal, is given in Horn’s Archives.[2278] Three people took the root by
mistake for galanga. The symptoms that ensued were characteristic of its
double action. In an hour they all had burning in the throat, gullet,
and stomach, followed by nausea, dysuria, and vomiting; weakness and
stiffness of the limbs; giddiness, blindness, and dilated pupil; great
faintness, convulsive breathing, and small pulse. One of them, an
elderly woman, who took the largest share, had an imperceptible pulse,
stertorous breathing, and total insensibility even to ammonia held under
the nose. Next day she continued lethargic, complained of headache, and
had an eruption like flea-bites. A fatal case is quoted by Bernt from
Schuster’s Medical Journal. A man took twice as much as could be held on
the point of a knife, was attacked with violent and incessant vomiting,
and lived only from morning till night. The gullet, stomach, and colon
were here and there inflamed.[2279]

No detailed inquiry has yet been made respecting the properties of
cevadilla; but there can be no doubt that it will prove an energetic
poison, similar in its effects to white hellebore, and probably more
active. Wibmer quotes Villemet for the fact, that half a drachm of the
seeds excites vomiting and convulsions in the cat and dog, and Lentin
for the case of a child, who died in convulsions in consequence of the
powder having been used inwardly and outwardly.[2280]

The alkaloid, veratria, has been made the subject of experiment by
various physiologists. The most complete investigation yet undertaken is
that of Dr. Esche;[2281] who found that it causes in a few minutes
restlessness, anxiety, salivation, slowness and irregularity of the
pulse, slow respiration, nausea, violent vomiting, borborygmus, spasms
of the abdominal muscles and brisk purging of watery mucus, often tinged
with blood;—that by and by the muscles become extremely feeble, so that
the animal cannot support itself;—that coldness of the surface succeeds,
together with spasmodic contractions of the throat, face, and
extremities, but without any stupor;—and that finally the respiration
and pulse gradually become extinguished, extreme prostration ensues, and
death takes place in a fit of tetanic spasm. No particular morbid
appearance was found in the dead body, and especially no sign of
inflammation. Magendie found, that one grain in the form of acetate
killed a dog in a few seconds when injected into the jugular vein, and
in nine minutes when injected into the peritonæum; and that the
principal symptom in such rapid cases was tetanic spasm.


                  _Of Poisoning with Meadow-Saffron._

The _Colchicum autumnale_, meadow-saffron, or autumn-crocus, is a more
familiar poison in this country than white hellebore, and seems to
possess very similar properties. Two parts of the plant are met with in
the shops, the _cormus_ or bulb, and the seeds; both of which are
poisonous. Both have a strong, disagreeable, persistent, bitter taste.
The seeds, and probably the bulb also, contain a bitter crystalline
principle, called colchicina, which is soluble in water, neutralizes
acids, and possesses intense activity as a poison.

A good physiological investigation into the action of colchicum as a
poison is still wanting. Baron Störck found that two drachms of the
dried bulb caused in dogs violent diarrhœa and diuresis, ending
fatally.[2282] Sir Everard Home observed that the active part of about
two drachms dissolved in sherry, caused in a dog, when injected into the
jugular vein, slow respiration, languor of the pulse, vomiting,
diarrhœa, extreme prostration, and death in five hours.[2283]—Geiger and
Hesse, the discoverers of colchicina, gave a cat a tenth of a grain,
which occasioned salivation, vomiting, purging, staggering, extreme
languor, colic, and death in twelve hours.[2284]

The effects of colchicum on man, like those observed in animals, rather
associate it with the acrid than with the narcotic poisons.

In the Edinburgh Journal a case is briefly noticed of a man who took by
mistake an ounce and a half of the wine of the bulb, and died in
forty-eight hours, after suffering much from vomiting, acute pain in the
stomach, colic, purging, and delirium.[2285]—Chevallier has described a
similar case arising from the wine of the bulb having been given
intentionally as a poison. In a few minutes burning pain, urgent thirst,
and frequent vomiting of mucus ensued; and death took place in three
days.[2286]—Three American soldiers, who drank by mistake a large
quantity of colchicum wine prepared from the bulb, died with similar
symptoms. One of them, who took eighteen ounces, and died in two days,
presented the leading symptoms of malignant cholera, namely, frequent
vomiting, copious rice-water stools, cramps of the abdominal muscles and
flexion of the extremities, coldness of the skin, tongue, and breath,
blueness of the nails, dull, sunken eyes, contracted pupils, and
collapse of the features. The two others had at first similar symptoms,
which passed into those of chronic dysentery, and proved fatal in a few
weeks.[2287]—M. Caffe has related the case of a young lady who destroyed
herself by taking five ounces of the wine containing the active matter
of rather more than the fourth part of one bulb. She was soon seized
with acute pain in the stomach, then with frequent vomiting, general
coldness and paleness, a sense of tightness in the chest and oppression
of the breathing, a slow thready pulse, and extreme prostration,—and
subsequently with severe and constant cramps in the soles of the feet.
In eleven hours she had less frequent efforts to vomit, but was
excessively exhausted; in twenty hours the pulse was imperceptible; and
in two hours more she died. There was no suppression of urine, no
purging, no diminution of sensibility, delirium, convulsions, or change
in the state of the pupils.[2288] About a twelvemonth afterwards the
sister of this patient put an end to herself with the same preparation,
of which she took the same quantity; and she died, with precisely the
same symptoms, in twenty-eight hours.[2289] M. Ollivier met with two
cases of death within twenty-four hours, in consequence of a tincture
being taken which contained the active part of forty-eight grains of the
dry bulb; and a third case of death in three days caused by three doses
of a watery decoction made each time with 46 grains of the bruised bulb
collected in July. Severe purging and prostration followed each dose.
There was no symptom of any affection of the brain.[2290]—Mr. Henderson
describes a case occasioned by an ounce of the tincture. No injury
accrued for three hours. The patient then had gnawing pain in the
stomach followed by vomiting, and then by purging, at first bilious,
afterwards watery, and attended with numbness in the feet, and
subsequently a sense of prickling. In the course of the second day there
was intense gnawing pain in all the joints of the extremities, profuse
acid sweating, tightness in the head, and pain in the hindhead and nape
of the neck. Blood-letting, laxatives, and hyoscyamus were employed with
success; but the case seems very nearly to have proved fatal.[2291]

The seeds produce similar effects. Bernt has noticed the cases of two
children who were poisoned by a handful of colchicum seeds, and who
died in a day, affected with violent vomiting and purging.[2292] Mr.
Fereday of Dudley relates a carefully detailed case of a man who died
in forty-seven hours after swallowing by mistake two ounces of the
wine of the seeds, and in whom the symptoms were acute pain, coming on
in an hour and a half, then retching, vomiting, and tenesmus, feeble
pulse, anxious expression, afterwards incessant coffee-coloured
vomiting, suppression of urine, excessive weakness of the limbs and
feeble respiration, and, for a short period before death, profuse,
dark, watery purging. There was neither insensibility nor
convulsions.[2293]—Blumhardt relates a similar case caused by an
infusion of a large table-spoonful of the seeds. In three-quarters of
an hour the man was seized with griping, and then profuse diarrhœa and
vomiting. Next morning, twelve hours after the poison was taken, his
physician found him still affected with vomiting and purging, but not
with pain. He seemed, indeed, to suffer so little, and to improve so
much under the use of emollients, that he was thought to be fairly
recovering. But next day the pulse was almost imperceptible, the
countenance and extremities were cold, the voice hoarse, the breathing
hurried, the eyes sunk, the pupils dilated, the epigastrium tender,
and the forehead affected with pain; and he died at twelve the same
day.[2294]

The leaves, too, are poisonous. Dr. Bleifus has related a case in proof
of this. A man gathered the leaves in the middle of May, and, after
cooking them, ate about two ounces for supper. In six hours he was
seized with violent colic, vomiting, and purging. In fifteen hours, when
his physician first saw him, the countenance was ghastly as in malignant
cholera, the pupils dilated and scarcely contractile, but the mind
entire. He complained of rheumatic pains in the neck, and burning pain
in the pit of the stomach. He had frequent vomiting and purging, spasms
of the muscles of the belly, coldness of the skin, a slow, small, wiry
pulse, and cramps of the fingers and the calves of the legs. Coffee and
lemon-juice allayed the vomiting, and a temporary amendment ensued. But
early on the third morning he became worse, and soon afterwards the
narrator of the case found him dying.[2295]

The flowers are not less poisonous than the bulbs, leaves, and seeds. A
case is noticed in Geiger’s Journal of poisoning with a decoction of
some handfuls of the flowers, where death occurred within twenty-four
hours, under incessant colic, vomiting and purging.[2296]

Doubts exist as to the degree of activity of colchicum. Some
practitioners direct half an ounce of the tincture of the seeds to be
given as a medicinal dose,[2297] even four times a day.[2298] Others
administer from one to two drachms night and morning. According to more
general experience, these are dangerous doses. Dr. Lewins, junior, has
seen dangerous symptoms from a drachm given thrice a day for a
week;[2299] a fatal case occurred a few years ago in the Edinburgh
Infirmary, from this amount having been given for a few days only; I
have known very violent effects produced by half an ounce taken by
mistake, although most of it was brought away by emetics in an hour;
and, in medical practice, I have seldom seen the dose of a sound
preparation gradually raised to a drachm thrice a day, without such
severe purging and sickness ensuing as rendered it prudent to diminish
or discontinue the remedy. There is no doubt, however, that larger doses
have occasionally been taken without any ill effect. Constitutional
peculiarity can alone account for such differences in the instance of
the tincture of the seeds. As to the preparations of the bulb, an
additional source of diversity of effect is a difference in the activity
of the bulb according to season. On this point no accurate facts have
yet been brought forward. The bulb is usually directed to be gathered in
July, when it is most plump and firm, and most charged with starch.
Orfila, however, says that three bulbs, collected at this time, had no
effect whatever on a dog;[2300] and Buchner maintains that it is most
energetic in the autumn, when the flowering stem is rising.[2301] I
suspect, on the other hand, that it is very energetic in the spring,
when it is watery, more membranous, and shrivels much in drying; for it
is then very bitter.

The morbid appearances are chiefly those of inflammation of the
alimentary canal.

In the bodies of the children mentioned by Bernt there was considerable
redness of the stomach and small intestines; in Geiger’s case
inflammation of the stomach and duodenum only; in the case mentioned in
the Edinburgh Journal, and in that related by Chevallier, there was no
morbid appearance at all to be found. In Mr. Fereday’s case the omentum
was curled and folded up between the stomach on the one hand, and the
liver and diaphragm on the other; the stomach and intestines were coated
with much mucus; there was no appearances of inflammation there but on
two points, one in the stomach, the other in the jejunum, where a red
patch appeared, owing to blood effused between the muscular and
peritoneal coats; the bladder was empty, the pleura red, the lungs much
gorged, their surface, as well as that of the diaphragm and heart,
covered with ecchymosed spots; and the skin over most of the body
presented patches of a purple efflorescence.—In Blumhardt’s case the
muscles were rigid twenty-three hours after death; the heart and great
vessels contained coagulated blood; the cardiac end of the gullet was
internally dark-violet; the stomach externally of a clear violet hue,
and its veins turgid; the gall-bladder turgid with greenish-yellow bile;
and the inner membrane of the whole small intestines chequered here and
there with red, inflamed-like spots.[2302]—In one of M. Caffe’s cases
there was congestion of the cerebral vessels, coagulated blood in the
heart, uniform grayness, softness, and brittleness of the mucous coat of
the stomach, and enlargement of the muciparous follicles of the small
intestines, as well as unusual distinctness and lividity of the Peyerian
glands. In the other case putrefaction was so far advanced in
forty-eight hours as to make the appearances equivocal.

The treatment consists in evacuation of the stomach and bowels by
emetics and oleaginous laxatives in the early stage, and afterwards in
the employment of opium, stimulants, the warm bath, and occasionally
blood-letting.


                     _Of Poisoning with Foxglove._

Foxglove, or _Digitalis purpura_, a plant which is common in this
country both as a native and in gardens, possesses powerful and peculiar
properties. The leaves are considered its most active part. They contain
an alkaloid; but chemists have not fixed its nature with precision. M.
Le Royer of Geneva procured a pitchy, deliquescent, uncrystallizable
substance;[2303] but more lately M. Pauguy obtained a principle in fine
acicular crystals, soluble in alcohol and ether, but insoluble in water,
alkaline in its reaction, and of a very acrid taste. This principle is
called digitalin.[2304] It seems to be the same substance, which has
also been detected by Radig, as quoted by Dr. Pereira.[2305] The leaves,
like those of other narcotic vegetables, yield by destructive
distillation an empyreumatic oil similar in chemical qualities and
physiological effects to the empyreumatic oil of hyoscyamus.[2306]

From an extensive series of experiments on animals by Orfila with the
powder, extract and tincture of the leaves, foxglove appears to cause in
moderate doses vomiting, giddiness, languor, and death in twenty-four
hours, without any other symptoms of note; but in larger doses, it
likewise produces tremors, convulsions, stupor and coma. It acts
energetically both when applied to a wound, and when injected into a
vein.[2307] Mr. Blake has inferred from his researches, that when
injected into the jugular vein, it occasions both obstruction of the
pulmonary capillaries, and direct depression of the heart’s action. In
the dog an infusion of three drachms of leaves arrested in five seconds
the action of the heart; which was motionless after death, turgid,
inirritable, and full of florid blood in its left cavities. An infusion
of an ounce, injected back into the aorta from the axillary artery,
caused in ten seconds great obstruction of the systemic capillaries,
indicated by sudden increase of arterial pressure in the
hæmadynamometer; the heart was unaffected for forty-five seconds, when
it became slow in its pulsations, and the arterial pressure diminished;
and in four minutes the heart ceased to beat, although for a little
longer it continued excitable by stimulation. As no affection of the
brain or spine was apparent before the heart became affected, the author
infers that the action depends on the poisoned blood being circulated
through the substance of the heart, and not on any intermediate
influence upon the nervous centre.[2308]

_Symptoms in Man._—Upon man its effects as a poison have been frequently
noticed, partly in consequence of its being given by mistake in too
large a dose as a medicine, partly on account of the singular property
it possesses, in common with mercury, of accumulating silently in the
system, when given long in moderate doses, and at length producing
constitutional effects even after it has been discontinued. The effects
of a dose somewhat larger than is usually given, are great nausea,
frontal headache, sense of disagreeable dryness in the gums and pharynx,
some salivation, giddiness, weakness of the limbs, feebleness and
increased frequency of the pulse, in a few hours an appearance of sparks
before the eyes, and subsequently dimness of vision, and a feeling of
pressure on the eyeballs. These effects may be occasioned by so small a
dose as two or three grains of good foxglove.[2309] The symptoms arising
from its gradual accumulation are in the slighter cases nausea,
vomiting, giddiness, want of sleep, sense of heat throughout the body,
and of pulsation in the head, general depression, great languor and
commonly retardation of the pulse, sometimes diarrhœa, sometimes
salivation, and for the most part profuse sweating. A good instance of
this form of the effects of foxglove is mentioned in the Medical
Gazette. A man took it at his own hand for dropsy during twenty days,
when the pulse sank to half its previous frequency, he was seized with
restless, want of sleep, incoherent talking with imaginary persons,
dilated pupils, nausea, thirst, and increase of urine; and these
complaints did not materially subside for six days.[2310] The depressed
action of the heart may be the occasion of death in particular
circumstances. Mr. Brande mentions from the experience of Dr. Pemberton
the case of an elderly woman, who, while under the full influence of
foxglove, fell in a fainting fit on walking across the floor; after
which, although she at first got better, there were frequent attacks of
fainting and vomiting till she died.[2311] In other instances
convulsions also occur; and it appears from a case mentioned by Dr.
Blackall, that the disorder thus induced may prove fatal. One of his
patients, while taking two drachms of the infusion of the leaves daily,
was attacked with pain over the eyes and confusion, followed in
twenty-four hours by profuse watery diarrhœa, delirium, general
convulsions, insensibility, and an almost complete stoppage of the
pulse. Although some relief was derived from an opiate clyster, the
convulsions continued to recur in frequent paroxysms for three weeks; in
the intervals he was forgetful and delirious; and at length he died in
one of the convulsive fits.[2312]

A case which exemplifies the effects of a single large dose is related
in the Edinburgh Journal. An old woman drank ten ounces of a decoction
made from a handful of the leaves in a quart of water. She grew sick in
the course of an hour, and for two days she had incessant retching and
vomiting, with great faintness and cold sweats in the intervals, some
salivation and swelling of the lips, and a pulse feeble, irregular,
intermitting, and not above 40. She had also suppression of urine for
three days.[2313]

A somewhat similar instance may be found in the Journal de Médecine. A
man, fifty-five years old took by mistake a drachm instead of a grain
for asthma, and was attacked in an hour with vomiting, giddiness,
excessive debility, so that he could not stand, loss of sight, colic,
and slow pulse. These effects continued more or less for four days, when
the vomiting ceased; and the other symptoms then successively
disappeared, the vision, however, remaining depraved for nearly a
fortnight.[2314]

A very interesting fatal case, which arose from an over-dose
administered by a quack doctor, and which became the ground of a
criminal trial at London in 1826, is shortly noticed in the same
Journal. Six ounces of a strong decoction when taken as a laxative early
in the morning. Vomiting, colic, and purging, were the first symptoms;
towards the afternoon lethargy supervened; about midnight the colic and
purging returned; afterwards general convulsions made their appearance;
and a surgeon, who saw the patient at an early hour of the succeeding
morning, found him violently convulsed, with the pupils dilated and
insensible, and the pulse, slow, feeble, and irregular. Coma gradually
succeeded, and death took place in twenty-two hours after the poison was
swallowed.[2315]

This is the only case in which I have seen an account of the appearances
in the dead body, and they are related imperfectly. It is merely said
that the external membranes of the brain were much injected with blood,
and the inner coat of the stomach red in some parts.

The affections induced by poisoning with digitalis are often much more
lasting than the effects of most other vegetable narcotics. Dr.
Blackall’s case is one instance in point, and another no less remarkable
in its details is described in Corvisart’s Journal. The usual local and
constitutional symptoms were produced by a drachm of the powder being
taken by mistake; and the slowness of the pulse did not begin to go off
for seven days, the affection of the sight not for five days more.[2316]

The preparations of foxglove are very uncertain in strength. From what I
have observed in the course of their medicinal employment, I conceive
few powders retain the active properties of the leaves, and even not
many tinctures. Two ounces of the tincture of the London College have
been taken in two doses with a short interval between them, yet without
causing any inconvenience.[2317] This assuredly could not happen with a
sound preparation.


                        _Of Poisoning with Rue._

The _Ruta graveolens_, or rue, although its wild variety is expressly
declared by Dioscorides to be mortal when taken too largely, has
attracted little attention as a poison in recent times, and is indeed
scarcely considered deleterious. Orfila seems to have found it by no
means active; for the juice of two pounds of leaves, secured in the
stomach of a dog by tying the gullet, did not prove fatal till the
second day, the symptoms were not well marked, and the only appearances
in the dead body were the signs of slight inflammation in the stomach.
Even when the distilled water was injected into a vein, the only effects
were a temporary nervous disorder similar to intoxication.[2318]

According to the late experimental inquiry, however, by M. Hélie,[2319]
rue is possessed of peculiar and energetic properties. All parts of its
organization, especially the roots and leaves, produce the effects of
the narcotico-acrid poisons; and although he never met with any instance
of a fatal result, its activity is such as to render this event not
improbable, even when the dose is by no means very large. His attention
was drawn to the subject in consequence of finding, that it was often
employed in his neighbourhood for producing abortion,—a property
ascribed to it immemorially by the country people of France; and all the
instances he has seen of its poisonous action were cases in which it had
been given with this object. Sometimes the juice of the leaves is given,
sometimes an infusion of them, sometimes a decoction of the root; and in
one instance a woman took a decoction of two roots, each about as thick
as the finger. The effects were, severe pain in the stomach, followed by
violent and obstinate vomiting, drowsiness, giddiness, confusion,
dimness of sight, difficult articulation, staggering, contracted pupils,
convulsive movements of the head and arms, like those of chorea,
retention of urine, slowness of the pulse, and great prostration. There
was never any purging. In the course of two days or a little more
miscarriage took place, preceded by the usual precursors, and followed
by abatement of the symptoms of poisoning. At the period of the
milk-fever, however, these symptoms again increased, and the patient was
also attacked with swelling and pain in the tongue and copious
salivation. In about ten days the pulse began to increase in frequency;
and a mild typhoid fever commonly succeeded, from which recovery took
place slowly. In another case the symptoms throughout their whole course
were so mild, that, although miscarriage occurred, the subject of it was
not confined to bed, and in fifteen days recovered her health
completely. M. Hélie adds, that with full knowledge of the doubts
entertained by eminent authorities, whether any substance whatever
possesses a peculiar property of inducing miscarriage, he is strongly
persuaded that rue is really a substance of the kind, and that it will
take effect even when there is no natural tendency to miscarriage, or
any particular weakness of constitution.

Notwithstanding these statements, it may be suspected that M. Hélie has
overrated both its poisonous properties and its virtues as a drug
capable of inducing miscarriage.


                     _Of Poisoning with Ipecacuan._

Ipecacuan is well known as an emetic. It is procured from a plant of the
natural family Rubiaceæ, the _Cephaëlis ipecacuanha_. It contains a
peculiar principle, not yet crystallized, which is white, permanent in
the air, sparingly soluble in water, easily soluble in alcohol and
ether, fusible about 122° F., capable of forming crystallizable salts
with acids, and possessing an alkaline reaction on litmus. It was
discovered by M. Pelletier.[2320]

Ipecacuan itself is not known to be a poison; because in consequence of
its emetic properties it is quickly discharged from the stomach. But in
doses of considerable magnitude it would probably be dangerous. In some
constitutions the odoriferous effluvia from the powder induce difficult
breathing, anxiety, and imperfect convulsions. I have met with several
instances of this singular idiosyncrasy, and one in particular where the
subject of it, a surgeon’s apprentice, suffered so often and so severely
as to be induced to abandon the medical profession. A German physician,
Dr. Prieger, has published a remarkable case of a druggist’s servant,
who, in consequence of incautiously inhaling the dust of ipecacuan
powder, was attacked with a sense of tightness in the chest, vomiting,
and soon after an alarming sense of suffocation from tightness of the
throat. When these symptoms had continued several hours the uneasiness
in the throat was removed after the use of a decoction of uva-ursi and
rhatany-root; but the dyspnœa remained several days.[2321]

Its active principle, emeta, is a powerful poison. Two grains of the
pure alkaloid will kill a dog; and the symptoms are frequent vomiting,
followed by sopor and coma, and death in fifteen or twenty-four hours.
In the dead body the lungs and stomach are found inflamed. The same
effects result from injecting it into a vein, or applying it to a
wound.[2322] It appears, then, to be a narcotico-acrid. But its irritant
properties are so prominent that it might be properly arranged with the
vegetable acrids.




                            CHAPTER XXXVII.
     OF POISONING WITH STRYCHNIA, NUX VOMICA, AND FALSE ANGUSTURA.


The next group of the narcotico-acrids includes a few vegetable poisons
that act in a very peculiar manner. They induce violent spasms, exactly
like tetanus, and cause death during a fit, probably by suspending the
respiration. But they do not impair the sensibility. During the
intervals of the fits the sensibility is on the contrary heightened, and
the faculties are acute.

Death, however, does not always take place by tetanus. In some cases the
departure of the convulsions has been followed by a fatal state of
general and indescribable exhaustion.

Besides thus acting violently on the nervous system, they also possess
local irritant properties; but these are seldom observed on account of
the deadliness and quickness of their remote operation on the spine and
nerves.

They exert their action by entering the blood-vessels. The dose required
to prove fatal is exceedingly small. The organ acted on is chiefly the
spinal cord; but sometimes they seem also to act on the heart.

They seldom leave any morbid appearances in the dead body. Like the
other causes of death by obstructed respiration, such as drowning and
strangling, they produce venous congestion; but this is frequently
inconsiderable. Sometimes, however, they leave signs of inflammation in
the alimentary canal.

Their energy resides in peculiar alkaloids. The only poisons included in
this group, are derived from the genus _Strychnos_. The bark of _Brucea
antidysenterica_ was long supposed also to possess similar properties;
but it is now known that the bark of _Strychnos nux-vomica_ was mistaken
for the bark of that tree.

Several species of _Strychnos_ have been examined, namely, the _S.
Nux-vomica_, the _S. Sancti Ignatii_ or St. Ignatius bean, the _S.
colubrina_, or snake-wood, the _S. tieuté_, which yields an Indian
poison the Upas tieuté, the _S. Guianensis_, and likewise the _S.
potatorum_ and _Pseudo-kina_; and all have been found to possess the
same remarkable properties, except the last two, which are inert.

All of them, except the _S. pseudo-kina_, and probably the _S.
potatorum_,[2323] contain an alkaloid to which their poisonous
properties are owing. This is _strychnia_ or strychnin, a substance
which has lately been made the subject of many experiments by chemists
and physiologists.


                     _Of Poisoning with Strychnia._

Strychnia was discovered by Pelletier and Caventou soon after the
discovery of morphia.[2324] For an account of the best process for
preparing it, the reader may consult a paper by M. Henry in the journal
quoted below.[2325]

Its leading properties are the following. Its crystals when pure are
elongated octaedres. It has a most intensely bitter taste, perceptible,
it is said, when a grain is dissolved in 80 pounds of water.[2326] It is
very sparingly soluble in water, but easily soluble in alcohol and the
volatile oils. Its alcoholic solution has an alkaline reaction. It forms
neutral and crystallizable salts with the acids. In its ordinary form it
is turned orange-red by the action of nitric acid; which tint becomes
violet-blue on the gradual addition of hydrosulphate of ammonia. The
action of nitric acid is owing to the presence of a yellow colouring
matter, or of another alkaloid, brucia, which is also contained in nux
vomica, but exists in larger quantity in the false angustura bark. Pure
strychnia is not turned orange-red by nitric acid.[2327]

No poison is endowed with more destructive energy than strychnia. I have
killed a dog in two minutes with a sixth part of a grain injected in the
form of alcoholic solution into the chest; I have seen a wild-boar
killed in the same manner with the third of a grain in ten minutes; and
there is little doubt that half a grain thrust into a wound might kill a
man in less than a quarter of an hour. It acts in whatever way it is
introduced into the system, but most energetically when injected into a
vein. The symptoms produced are very uniform and striking. The animal
becomes agitated and trembles, and is then seized with stiffness and
starting of the limbs. These symptoms increase till at length it is
attacked with a fit of violent general spasm, in which the head is bent
back, the spine stiffened, the limbs extended and rigid, and the
respiration checked by the fixing of the chest. The fit is then
succeeded by an interval of calm, during which the senses are quite
entire or unnaturally acute. But another paroxysm soon sets in, and then
another and another, till at length a fit takes place more violent than
any before it; and the animal perishes suffocated. The first symptoms
appear in 60 or 90 seconds, when the poison is applied to a wound. When
it is injected into the pleura, I have known them begin in 45 seconds,
and Pelletier and Caventou have seen them begin in 15 seconds.[2328] M.
Bouillaud has recently found that it has no effect when directly applied
to the nerves.[2329] The experiments of Mr. Blake tend to show, that its
action is exerted solely on the nervous system, and that it has no
direct action on the heart, even when directly admitted into the blood
by the jugular vein.[2330] It appears to act peculiarly by irritating
the spinal cord.

Dangerous effects have often been occasioned by an accidental over-dose
in ordinary medical practice. These are well exemplified by a case
communicated to Dr. Bardsley by Dr. Booth of Birmingham. A man of 46,
affected with hemiplegia for nearly four weeks, began to use strychnia,
and had been affected by it for eleven days without particular
inconvenience. During this period he took twice a day gradually
increasing doses, till the amount of one grain was attained; when the
usual physiological effect having ceased to occur, the quantity was
increased to a grain and a half. But the first dose caused anxiety and
excitability, in three hours stupor and loss of speech, and at length
violent tetanic convulsions, which proved fatal in three hours and
three-quarters.[2331] A fatal case, occasioned by the large dose of two
scruples, has been recorded by a German physician, Dr. Blumhardt. In
fifteen minutes, imperfect vomiting was brought on by emetics. At this
time, the patient, a lad of seventeen, lay on his back, quite stiff, and
with incipient fits of locked-jaw. The spasms gradually extended to the
rest of the body, till at last violent fits of general tetanus were
established, under which the whole body became as stiff as a board, the
arms spasmodically crossed over the chest, the legs extended, the feet
bent, so that the soles were concave, the breathing arrested, the
eyeballs prominent, the pupils dilated and not contractile, and the
pulse hurried and irregular. In the second severe fit he died, one hour
and a half after taking the poison.[2332] I have known very dangerous
tetanic spasm induced by so small a dose as two-thirds of a grain of the
ordinary impure strychnia of the shops; and Dr. Pereira describes a
case, communicated by a friend, where death was occasioned by a dose of
half a grain administered three times a day.[2333] As each fit of spasm
went off, respiration, which was found to have ceased, was maintained
artificially; but no sooner did natural breathing return, than the
paroxysm of tetanus returned also; and at length artificial inflation of
the lungs failed to restore life.

The only accounts I have seen of the morbid appearances after death from
strychnia are in the cases of Dr. Booth and Dr. Blumhardt. In the
former, the muscles were in a rigid state, the fingers contracted, the
vessels of the brain gorged, the membranes of the spinal cord highly
injected; and four patches of extravasated blood were found between the
spinal arachnoid and the external membrane. In the latter, twenty-four
hours after death, there was general lividity of the skin, and
extraordinary rigidity of the muscles. Fluid blood flowed in abundance
from the spinal cavity, where the veins were gorged, the pia mater
injected, the spinal column softened at its upper part, and here and
there almost pulpy. There was also congestion and softening of the
brain. The head and great vessels were flaccid, and contained scarcely
any blood. The inner membrane of the stomach and intestines presented
some redness, but not more than is often seen independently of
irritation there.

Strychnia has been found by Pelletier and Caventou in four species of
_Strychnos_, the _S. nux vomica_, _Sancti Ignatii_, _Colubrina_, and
_Tieuté_; and from the researches of MM. Martius and Herberger on the
composition and properties of the American poison Wourali, it is also
probably contained in the _S. guianensis_.[2334] Vauquelin could not
find it in the _S. pseudo-kina_, which is destitute of bitterness.


                    _Of Poisoning with Nux Vomica._

_Tests of Nux Vomica._—Nux vomica, the most common of these poisons, is
a flat, roundish seed, hardly an inch in diameter, of a yellowish or
greenish-brown colour, covered with short silky hair, and presenting a
little prominence on the middle of one of its surfaces. In powder it has
a dirty greenish-gray colour, an intensely bitter taste, and an odour
like powder of liquorice. It inflames on burning charcoal, and when
treated with nitric acid acquires an orange-red colour, which is
destroyed by the addition of protochloride of tin. Its infusion also is
turned orange-red by nitric acid, and precipitated grayish-white with
tincture of galls.

Orfila and Barruel have made some experiments on the mode of detecting
it in the stomach, and the following is the plan recommended by them.
The contents of the stomach, or the powder, if it can be separated, must
be boiled in water acidulated with sulphuric acid. The liquid after
filtration is neutralized with carbonate of lime, and then evaporated to
dryness. The dry mass is then acted on with successive portions of
alcohol, and evaporated to the consistence of a thin syrup. The product
has an intensely bitter taste, yields a precipitate with ammonia,
becomes deep orange-red with nitric acid, and will sometimes deposit
crystals of strychnia on standing two or three days.[2335] By this
process Dr. R. D. Thomson, in a case which proved fatal in three hours,
detected nux-vomica, although vomiting had been induced by
emetics.[2336]

These experiments it is important to remember, because, contrary to what
takes place in regard to vegetable poisons generally, nux vomica is
often found in the stomachs of those poisoned with it.

_Its Mode of Action and Symptoms in Man._—The poisonous properties of
nux vomica are now well known to the vulgar; and in consequence it is
occasionally made the instrument of voluntary death, although no poison
causes such torture. It is difficult to conceive, considering its
intensely bitter taste, how any one could make it the instrument of
murder. But a fact is stated in Rust’s Journal, which shows that it may
be used for that purpose. At a drinking party one man wagered with
another, that if he took a little _Cocculus indicus_ in beer, he would
be compelled to walk home on his head. The wager was taken and the
potion drunk; but nux vomica was substituted for the Cocculus indicus,
itself too a virulent poison; and the man went home and died in
convulsions fifteen minutes afterwards.[2337]

Many experiments have been made on animals with nux vomica; but the
first accurate inquiry was that of Magendie and Delille read before the
French Institute in 1809. The symptoms they remarked were precisely the
same with those produced by strychnia. Half a drachm of the powder
killed a dog in forty-five minutes, and a grain and a half of the
alcoholic extract thrust into a wound killed another in seven minutes.
The animals uniformly experienced dreadful fits of tetanic spasm, with
intervals of relaxation and sensibility, and were carried off during a
paroxysm.

The cause of death appears to be prolonged spasm of the thoracic muscles
of respiration. The spasm of these muscles is apparent in the unavailing
efforts which the animals make to inspire. The external muscles of the
chest may be felt during the fits as hard almost as bone; and, according
to an experiment of Wepfer, the diaphragm partakes in the spasm of the
external muscles.[2338]

On account of the singular symptoms of irritation of the spinal cord,
uncombined with any injury of the brain, this poison is believed to act
on the spinal marrow alone. This is farther shown by the experiments of
Mr. Blake with strychnia alluded to above. But from some experiments by
Segalas it appears also to exhaust the irritability of the heart: for in
animals he found that organ could not be stimulated to contract after
death, and life could not be prolonged by artificial breathing.[2339] A
similar observation was made long ago by Wepfer, who found the heart
motionless and distended with arterial blood in its left cavities;[2340]
and a case of poisoning in the human subject to the same effect will be
presently related. The pulse is always very weak, often wholly
suppressed during a paroxysm; and in the case alluded to it was found on
dissection pale, flaccid and empty, having been apparently affected with
spasm. The action exerted through the medium of the spinal cord on the
muscles is wholly independent of the brain; for Stannius found that in
frogs the removal of the brain does not interfere with the
effects.[2341]

Of late poisoning with nux vomica has been common. The most
characteristic example yet published is a case related by Mr. Ollier, of
a young woman, who in a fit of melancholy, took between two and three
drachms of the powder in water. When the surgeon first saw her, half an
hour afterwards, she was quite well. But going away in search of an
emetic, and returning in ten minutes, he found her in a state of great
alarm, with the limbs extended and separated, and the pulse faint and
quick. She then had a slight and transient convulsion succeeded by much
agitation and anxiety. In a few minutes she had another, and not long
afterwards a third, each about two minutes in duration. During these
fits, “the whole body was stiffened and straightened, the legs pushed
out and forced wide apart; no pulse or breathing could be perceived; the
face and hands were livid, and the muscles of the former violently
convulsed.” In the short intervals between the fits she was quite
sensible, had a feeble rapid pulse, complained of sickness with great
thirst, and perspired freely. “A fourth and most violent fit soon
succeeded, in which the whole body was extended to the utmost from head
to foot. From this she never recovered: she seemed to fall into a state
of asphyxia, relaxed her grasp, and dropped her hands on her knees. Her
brows, however, remained contracted, her lips drawn apart, salivary foam
issued from the corners of the mouth, and the expression of the
countenance was altogether most horrific.” She died an hour after
swallowing the poison.[2342]—A case precisely similar, produced by three
pence worth of the powder, and fatal in little more than an hour, is
related by Mr. Watt of Glasgow.[2343]—Another apparently also similar
but fatal in three hours, is related by Dr. R. D. Thomson.[2344] There
is in fact very little variety of symptoms in different cases, where
death occurs in the primary stage.—Occasionally even in such rapid cases
there is a little vomiting in the first instance. This was remarked in
Mr. Watt’s case, and also in another described by MM. Orfila and
Ollivier.[2345]

When death does not take place thus suddenly in a fit of spasm, the
person continues to be affected for twelve or sixteen hours with
similar, but milder paroxysms; and afterwards he may either recover
without farther symptoms, or expire in a short time apparently from
exhaustion, or suffer an attack of inflammation of the stomach and
intestines, which may or may not prove fatal.

M. Jules Cloquet has described a case, where the patient seemed to die
of the excessive exhaustion produced by the violent, long continued
spasms. The tetanic fits lasted about twenty-four hours, the sensibility
in the intervals being acute. Slight signs of irritation in the stomach
succeeded; and death ensued on the fourth morning.[2346]

In the Bulletins of the Medical Society of Emulation another case is
related, which arose from an over-dose of the alcoholic extract being
taken by an old woman who was using it for palsy. She took three grains
at once. Violent tetanus was soon produced; and afterwards she had a
regular attack of inflammation of the stomach and intestines, which
proved fatal in three days.

The last instance to be noticed exemplifies very well the effects of the
poison when the quantity is insufficient to cause death. A young woman
swallowed purposely a drachm mixed in a glass of wine. In fifteen
minutes she was seized with pain and heat in the stomach, burning in the
gullet, a sense of rending and weariness in the limbs succeeded by
stiffness of the joints, convulsive tremors, tottering in her gait, and
at length violent and frequent fits of tetanus. Milk given after the
tetanus began excited vomiting. She was farther affected with redness of
the gums, inflammation of the tongue, burning thirst, and pain in the
stomach. The pulse also became quick, and the skin hot. Next day, though
the fits had ceased, the muscles were very sore, especially on motion.
The tongue and palate were inflamed, and there was thirst, pain in the
stomach, vomiting, colic and diarrhœa. These symptoms, however, abated,
and on the fourth day disappeared, leaving her exceedingly weak.[2347]

This and the previous case show clearly the double narcotico-acrid
properties of the poison.

With regard to the dose requisite to prove fatal, the smallest fatal
dose of the alcoholic extract yet recorded is three grains, which was
the quantity taken in the case from the Parisian bulletins: Hoffmann
mentions a fatal case caused by two fifteen grain doses of the
powder;[2348] and in Hufeland’s Journal there is another caused by two
drachms, which was fatal in two hours.[2349]—A dog has been killed by
eight grains of the powder, and a cat by five.[2350] It is even said
that a dog has been killed by two grains.[2351]

It has been thought, from some observations by Mr. Baker on the
medicinal use of nux vomica in Hindostan that, by the force of habit,
the constitution may become to a certain extent accustomed to large
doses of this poison, in the same manner as it acquires the power of
enduring large doses of opium. The natives of Hindostan, often take it
morning and evening for many months continuously, beginning with an
eighth part of a nut, and gradually increasing the dose to an entire
nut, or about twenty grains. If it is taken either immediately before or
after meals, it never occasions any unpleasant effects; but if this
precaution be neglected, spasms are apt to ensue.[2352] As it is found
unsafe, however, to increase the dose beyond one nut, and the poison is
taken in the form of coarse powder, in which state it must be slowly
acted on by the fluid in the stomach, it is probable that the modifying
influence of habit is inconsiderable. Habit certainly does not
familiarize the system to strychnia used medicinally. The same dose,
which has once excited its peculiar physiological action, will for the
most part suffice to excite it again, however frequently the dose may be
repeated.—The facts mentioned by Mr. Baker show that nux vomica is not a
cumulative poison; and European experience, in the instance of
strychnia, is to the same effect.

_Morbid Appearances._—The morbid appearances differ according to the
period at which death occurs. In Mr. Ollier’s case, where death took
place in an hour, the appearances were insignificant. The stomach was
almost natural, the vessels of the brain somewhat congested, the heart
flaccid, empty, and pale. In the case in Hufeland’s Journal there was
general inflammation of the stomach, duodenum and part of the jejunum.
In Cloquet’s case, a slower one, there was very little appearance of
inflammation. In that from the Parisian bulletins, on the contrary, the
stomach was highly inflamed, the intestines violet-coloured, in many
places easily lacerated and apparently gangrenous. In an interesting
dissection of a case, which was quickly fatal,—that related by Orfila
and Ollivier, there was found much serous effusion on the surface of the
cerebellum, and softening of the whole cortical substance of the brain,
but especially of the cerebellum. Blumhardt too, found softening of the
cerebellum and congestion of the cerebral vessels, together with
softening of the spinal cord and general gorging of the spinal veins.
This is some confirmation of an opinion advanced not long ago in France
by Flourence and others, that nux vomica acts particularly on the
cerebellum.[2353] In Dr. R. D. Thomson’s case, which was examined by Mr.
Taylor, there was found much congestion of the whole membranes and
substance of the brain and cerebellum, and even some extravasation of
blood within the cavity of the arachnoid over the upper surface of the
former. Mr. Watt remarked in his case (sixty hours, however, after death
in summer) softening of the substance of the brain and the lumbar part
of the spinal cord.—In Orfila and Ollivier’s case the lungs were found
much gorged with black fluid blood.—In Blumhardt’s case the heart and
great vessels were entirely destitute of blood.—There is sometimes seen,
as in Dr. R. D. Thomson’s case, a brown powder lining the stomach, even
although vomiting may have occurred.

The body appears sometimes to retain for a certain period after death
the attitude and expression impressed on it by the convulsions during
life. In the instance mentioned by Orfila and Ollivier the muscles
immediately after death remained contracted, the head bent back, the
arms bent, and the jaws locked. This state may even continue for some
hours, so that the body appears to pass into the state of rigidity which
precedes decay, without also passing through the preliminary stage of
flaccidity immediately after death. In the case related by Mr. Ollier,
the body five hours after death “was still as stiff and straight as a
statue, so that if one of the hands was moved the whole body moved along
with it;” and in Blumhardt’s case the rigidity twenty hours after death
was unusually great. This state of rigidity, however, does not
invariably occur. On the contrary, in animals the limbs become very
flaccid immediately after death; but the usual rigidity supervenes at an
early period.[2354] In Dr. R. D. Thomson’s case flaccidity immediately
followed death.

_Treatment._—Little is known of the treatment in this kind of poisoning.
But it is of the greatest moment to evacuate the stomach thoroughly, and
without loss of time. Hence emetics are useful; but if the stomach-pump
is at hand it ought to be resorted to without waiting for the operation
of emetics. Torosiewicz describes the case of a young woman who, after
the usual symptoms had begun to appear in consequence of the
administration of a tea-spoonful of powder, recovered under the action
of an emetic followed by rhatany-root.[2355] When nux vomica is taken in
powder,—the most frequent form in which it has been used,—it adheres
with great obstinacy to the inside of the stomach. Consequently whatever
means are employed for evacuating the stomach, they must be continued
assiduously for a considerable time. If the patient is not attacked with
spasms in two hours, he will generally be safe.

M. Donné of Paris has stated that he has found iodine, bromine, and
chlorine to be antidotes for poisoning with the alkaloid of nux vomica,
as well as for the other vegetable alkaloids. Iodine, chlorine, and
bromine, he says, form with the alkaloid compounds which are not
deleterious,—two grains and a half of the iodide, bromide, and chloride
of strychnia, having produced no effect on a dog. Animals which had
taken one grain of strychnia or two grains of veratria, did not sustain
any harm, when tincture of iodine was administered immediately
afterwards. But the delay of ten minutes in the administration of the
antidote rendered it useless. In the compounds formed by these antidotes
with the alkaloids, the latter are in a state of chemical union, and not
decomposed. Sulphuric acid separates strychnia, for example, from its
state of combination with chlorine, iodine, or bromine, and forms
sulphate of strychnia, with its usual poisonous qualities.[2356] It
remains to be proved that the same advantages will be derived from the
administration of these antidotes in the instance of poisoning with the
crude drug, nux vomica, as in poisoning with its alkaloid.

In general little difficulty will be encountered in recognizing a case
of poisoning with nux vomica. _Tetanus_ or locked-jaw is the only
disease which produces similar effects. But that disease never proves so
quickly fatal as the rapid cases of poisoning with nux vomica; and it
never produces the symptoms of irritation observed in the slower cases.
Besides, the fits of natural tetanus are almost always slow in being
formed; while nux vomica brings on perfect fits in an hour or less. It
is right to remember, however, that nux vomica may be given in small
doses, frequently repeated, and gradually increased, so as to imitate
exactly the phenomena of tetanus from natural causes. Medical men will
be at no loss to discover, on reflection, how the preparations of this
drug may be rendered formidable secret poisons.


       _Of Poisoning with the St. Ignatius Bean and Upas Tieuté._

The _Strychnos Sancti Ignatii_, or St. Ignatius bean, contains about
three times as much strychnia as nux vomica, namely, from twelve to
eighteen parts in the 1000. It is very energetic. Dr. Hopf has mentioned
an instance of a man, who was attacked with tetanus of several hours’
duration after taking the powder of half a bean in brandy, and who seems
to have made a narrow escape.[2357]

The _Strychnos tieuté_ is the plant which yields the Upas tieuté, one of
the Javanese poisons. This substance has been analyzed by Pelletier and
Caventou, and found to contain strychnia.[2358] From the experiments of
Magendie and Delille, the Upas tieuté appears to be almost as energetic
as strychnia itself.[2359] Mayer found that the bark of the plant which
yields it, when applied in the dose of fifty grains to a wound, killed a
rabbit in two hours and a half.[2360] Dr. Darwin has given an account of
its effects on the Javanese criminals, who used formerly to be executed
by darts poisoned with the tieuté. The account quoted by him is not very
authentic; yet it accords precisely with what would be expected from the
known properties of the poison. He says, that a few minutes after the
criminals are wounded with the instrument of the executioner, they
tremble violently, utter piercing cries, and perish amidst frightful
convulsions in ten or fifteen minutes.[2361]


               _Of Poisoning with False Angustura Bark._

Besides these poisons of the genus Strychnos, the present group
comprehends another, of the same properties, which was once supposed to
be derived from a plant of a different family, the _Brucea
antidysenterica_.

A species of bark, commonly called the false angustura bark, was
introduced by mistake into Europe instead of the true angustura,
cusparia, or bark of the _Galipea officinalis_. It was long supposed to
be the bark of the _Brucea antidysenterica_; but it is now known to be
the bark of _S. nux vomica_.[2362] It is a poison of great energy. It
gave rise to so many fatal accidents soon after its introduction, that
in some countries on the continent all the stores of angustura were
ordered to be burnt. It contains a less proportion of strychnia, but
more of the alkaloid brucia than nux vomica, the seed of the plant.

According to Andral, brucia is twenty-four times less powerful than
strychnia;[2363] but the bark itself is as strong nearly as nux-vomica,
for Orfila found that eight grains killed a dog in less than two
hours.[2364]

The symptoms it induces are the same as those caused by nux vomica. They
are minutely detailed in a paper by Professor Emmert of Bern.[2365] It
appears that during the intervals of the fits the sensibility is
remarkably acute: a boy who fell a victim to it implored his physician
not to touch him, as he was immediately thrown into a fit. Professor
Marc of Paris was once violently affected by this poison, which he took
by mistake for the true angustura to cure ague. He took it in the form
of infusion, and the dose was only three-quarters of a liqueur-glassful;
yet he was seized with nausea, pain in the stomach, a sense of fulness
in the head, giddiness, ringing in the ears, and obscurity of vision,
followed by stiffness of the limbs, great pain on every attempt at
motion, locked-jaw, and impossibility of articulating. These symptoms
continued two hours; and abated under the use of ether and
laudanum.[2366]

Some interesting experiments were made by Emmert with this poison to
show that it acts on the spine directly, and not on that organ through
the medium of the brain. If an animal be poisoned by inserting the
extract of false angustura bark into its hind-legs after the spinal cord
has been severed at the loins, the hind-legs as well as the fore-legs
are thrown into a state of spasm; or if the medulla oblongata be cut
across and respiration maintained artificially, the usual symptoms are
produced over the whole body by the administration of it internally or
externally,—the only material difference being that they commence more
slowly, and that a larger dose is required to produce them, than when
the medulla is not injured. On the other hand, when the spinal cord is
suddenly destroyed after the symptoms have begun, they cease
instantaneously, although the circulation goes on for some
minutes.[2367]

The true angustura bark has a finer texture than the other, and is
darker coloured, aromatic, pungent, and less bitter. The ferro-cyanate
of potass causes in a muriatic infusion of the false bark a precipitate,
which is first green and then becomes blue; and the same reagent
converts into blue the reddish powder which lines the bark. No such
effects are produced on the true angustura bark. Nitric acid renders the
rusty efflorescence of the spurious bark deep dirty blue, but has no
such effect on the true bark; which, besides, never exhibits a yellow
efflorescence.

With the preceding poisons Orfila has arranged also some poisons used by
the American Indians; but, as in Europe they are mere objects of
curiosity, it is scarcely necessary to treat of them particularly here.

The most interesting and best known of them is the _wourali poison_ of
Guiana, variously called woorara, urari, or curare, by different
authors. It is believed to have been traced by Martius to a new species
of strychnos, the _S. guianensis_, and more recently by Dr. Schomburg to
a different species, the _S. toxicaria_ of that traveller. But the
action it exerts does not correspond exactly with what would be expected
of a plant belonging to that genus.

The effects of wourali have been investigated by Sir B. Brodie in the
Philosophical Transactions for 1811–12, in Orfila’s Toxicology, in
Magendie’s Memoir on Absorption, and in Fontana’s Traité des Poisons.
But the most detailed inquiry is that by Emmert, published in 1818. It
produces, not convulsions or spasm of the muscles, but on the contrary
paralysis, and probably occasions death in this way by suspending the
respiration, in the same way as hemlock and conia. According to Emmert’s
experiments the spine only is acted on, and not the brain also.[2368]
Some remarkable experiments were made in 1839 by Mr. Waterton, to show
the power of artificial respiration in accomplishing recovery from its
effects. After the animals had fallen down motionless from the action of
the poison introduced through a wound, and when the action of the heart
had become so feeble as not to affect the pulse, artificial respiration,
continued in one instance for seven hours and a half, and in another for
two hours, had the effect of restoring the animals to health.[2369]




                            CHAPTER XXXVIII.
           OF POISONING WITH CAMPHOR, COCCULUS INDICUS, ETC.


The third group of the narcotico-acrids resemble strychnia in their
action so far, that they occasion in large doses convulsions of the
tetanic kind. But they differ considerably by producing at the same time
impaired sensibility or sopor. They are camphor, Cocculus indicus, its
active principle picrotoxin, the Coriara myrtifolia, the Upas antiar, a
Java poison, and perhaps also the yew-tree.


                      _Of Poisoning with Camphor._

Camphor dissolved in oil soon causes in dogs paroxysms of tetanic spasm.
At first the senses are entire in the intervals; but by degrees they
become duller, till at length a state of deep sopor is established, with
noisy laborious breathing, and expiration of camphorous fumes; and in
this state the animal soon perishes. A solution of twenty grains in
olive oil will kill a dog in less than ten minutes when injected into
the jugular vein. When camphor is given to dogs in fragments, it does
not excite convulsions, but kills them more slowly by inducing
inflammation of the alimentary canal. These are the results of numerous
experiments by Orfila.[2370]

They are confirmed by others performed more lately by Scudery of
Messina; but this experimentalist likewise remarked, that the
convulsions were attended with a singular kind of delirium, which made
the animals run up and down without apparent cause, as if they were
maniacal. He also found the urinary organs generally affected, and for
the most part with strangury.[2371] Lebküchner discovered camphor in the
blood of animals poisoned with it.[2372]

_Symptoms in Man._—The symptoms caused by camphor in man may not have
been observed; but so far as they have been witnessed, they establish
its claim to be considered a narcotic and acrid poison. Its effects
appear to be singularly uncertain: at least they are very discrepant;
and the reason for this is not apparent.

Its narcotic effects are well exemplified in an account given by Mr.
Alexander from personal experience, and by Dr. Edwards of Paris, as they
occurred in a patient of his who received a camphor clyster.

Mr. Alexander, in the course of his experiments on his own person with
various drugs, was nearly killed by this poison, and has left the best
account yet published of its effects in dangerous doses on man. After
having found, by a previous experiment, that a scruple did not cause any
particular symptom, he swallowed in one dose two scruples mixed with
syrup of roses. In the course of twenty minutes he became languid and
listless, and in an hour giddy, confused, and forgetful. All objects
quivered before his eyes, and a tumult of undigested ideas floated
through his mind. At length he lost all consciousness, during which he
was attacked with strong convulsive fits and maniacal frenzy. These
alarming symptoms were dispelled, on Dr. Monro, who had been sent for,
accidentally discovering the subject of his patient’s experimental
researches, and administering an emetic. But a variety of singular
mental affections continued for some time after. The emetic brought away
almost the whole camphor which had been swallowed three hours
before.[2373]

In Dr. Edwards’s patient, the symptoms were excited by an injection
containing half a drachm of camphor. In a few minutes he felt a
camphrous taste, which was followed by indescribable uneasiness. On then
going down stairs for assistance, he was astonished to feel his body so
light, that he seemed to himself to skim along the floor almost without
touching it. He afterwards began to stagger, his face became pale, he
felt chilly, and was attacked with a sense of numbness in the scalp. On
then taking a glass of wine, which he asked for, he became gradually
better; but for some time his mind was singularly affected. He felt
anxious, without thinking himself in danger; he shed tears, but could
not tell why; they flowed in fact involuntarily. For twenty-four hours
his breath exhaled a camphrous odour.[2374]

Hoffmann has related a case analogous to those of Alexander and Edwards.
The dose was two scruples taken in oil; the symptoms vertigo,
chilliness, anxiety, delirium, and somnolency.[2375]

These cases would seem to indicate very considerable activity; yet there
can be little doubt that even larger doses have been at times taken with
much less effect. Thus, from an account given by Dr. Eickhorn of New
Orleans, of its operation on himself, when incautiously swallowed to the
amount of two drachms in frequent small doses within three hours, it
would appear that the only result was great heat, palpitation, hurried
pulse, and pleasant intoxication, then moisture of the skin, next
profound sleep for some hours, attended with excessive sweating, and
finally no ultimate ill consequence except great debility.[2376] I am
assured by a correspondent, Dr. Jennison of Cambridge, U. S., that a
medical friend of his has given 90 grains of camphor four times a day in
phrenitis, with safety and advantage.

Professor Wendt of Breslau has related an instance, which proves the
irritant action of camphor on man, and likewise the uncertainty of the
dose required to act deleteriously. In the case of Mr. Alexander, two
scruples would in all probability have proved fatal, had they not been
discharged in time by vomiting. In the case now to be noticed, 160
grains were taken in a state of solution in alcohol, and were not
vomited; yet the individual recovered. He was a drunkard, who took four
ounces of camphorated spirit, prescribed for him as an embrocation. Soon
afterwards he was attacked with fever, burning heat of the skin,
anxiety, burning pain in the stomach, giddiness, flushed face, dimness
of sight, sparks before the eyes, and some delirium. He soon got well
under the use of almond oil and vinegar, but did not vomit.[2377]

_Morbid Appearances._—The morbid appearances caused by camphor have not,
so far as I know, been witnessed in man. In dogs examined immediately
after death, the heart is no longer contractile, and its left cavities
contain arterial blood of a reddish-brown colour. When the poison has
been given in fragments, it leaves marks of inflammation in the stomach
and intestines. Orfila found these organs much inflamed in such
circumstances.[2378] Scudery found the membranes of the brain much
injected, and the brain itself sometimes softened; the inner membrane of
the stomach either very red, or checkered with black, gangrenous-like
spots of the size of millet-seeds; the duodenum in the same state; the
ureters, urethra, and spermatic cords inflamed; and every organ in the
body, even the brain, impregnated with the odour of camphor.[2379]


                 _Of Poisoning with Cocculus Indicus._

The _Menispermum cocculus_, _Cocculus suberosus_, or _Anamirta cocculus_
of botanists, is a creeping plant which grows in the island of Ceylon,
on the Malabar coast, and in other parts of the East Indies. Its fruit,
which is the only part of the plant hitherto particularly examined, is
like a large, rough, grayish-black pea, and is known in the shops by the
name of Cocculus indicus. It has a rough, ligneous pericarp, enclosing a
pale grayish-yellow, brittle kernel, of a very strong lasting bitter
taste. The medical jurist should make himself well acquainted with its
external characters, because, besides being occasionally used in
medicine, it is a familiar poison for destroying fish, and has also been
extensively used by brewers as a substitute for hops,—an adulteration
which is prohibited in Britain by severe statutes. It has been analyzed
by M. Boullay of Paris,[2380] who found in it besides other matters, a
peculiar principle termed picrotoxin. This principle constitutes,
according to Boullay, about a fifth part of the kernel; according to
Nees von Esenbeck, only a hundreth part:[2381] and my own experiments
agree with the results of the latter. It is moderately soluble in water,
and crystallizes readily from a hot acidulous watery solution. It is
more soluble in hot alcohol, from which it crystallizes in granular
masses. Ten grains of it killed a dog in twenty-five minutes in the
second paroxysm of tetanus.

The seeds themselves occasion vomiting soon after they are swallowed; so
that animals may often swallow them, if not without injury, at all
events without danger. But if the gullet be tied, the animal soon begins
to stagger; the eye acquires a peculiar haggard expression, which is the
sure forerunner of a tetanic paroxysm; and the second, third, or fourth
fit commonly proves fatal. Three or four drachms will kill a dog when
introduced into the stomach; less will suffice when it is applied to a
wound; and still less when it is injected into a vein.[2382] Wepfer has
related a good experiment, from which he infers that Cocculus indicus
acts by exhausting the irritability of the heart. In the intervals of
the fits the pulse could not be felt; and on opening the chest
immediately after death, he found the heart motionless and all its
cavities distended.[2383] Orfila also sometimes found the heart
motionless, and its left cavities filled with reddish-brown blood.[2384]

This poison does not seem to possess distinct acrid properties in regard
to animals. M. Goupil indeed found that it produced vomiting and
purging,[2385] but Orfila could not observe any such effect. According
to Goupil it possesses the singular property of communicating to the
flesh of animals, more particularly of fish, that have been killed with
it, some of the poisonous qualities with which it is itself endowed. The
accuracy of this statement may be doubted, the alleged fact being
contrary to analogy. Besides, this poison has been used immemorially in
the East for taking fish; and it is familiarly used for the same purpose
in some parts of France, though prohibited by statute. Chevallier
mentions that in a particular parish the inhabitants live half the year
on fish caught with this poison; and that a friend of his made trial of
fish so caught, without the slightest injury.[2386]

_Symptoms in Man._—Although it is well known that malt liquors have
often been adulterated with Cocculus indicus for the purpose of
economizing hops, cases of poisoning in the human subject are rare,
because the quantity required to communicate the due degree of
bitterness is small. Professor Bernt has shortly noticed a set of cases,
which arose in consequence of an idiot having seasoned soup with it by
mistake. Nine people were taken ill with sickness, vomiting, pain in the
stomach and bowels; and one died in twelve days.[2387] The symptoms
under which this person died are not stated; but the account of the
accident sent to Bernt imputed death to the poison,—which is improbable,
considering the length of the interval before death.

In the same group with camphor and Cocculus indicus Orfila has arranged
_Upas antiar_, a Javanese poison. This poison is a very bitter milky
juice or extract, which is known in Europe only as an article of
curiosity. It has been sometimes confounded with the Upas tieuté. It
owes its properties to a neutral principle called antiarin.[2388] From
the experiments of MM. Magendie and Delille,[2389] as well as from those
of Sir B. Brodie[2390] and of Emmert[2391] it appears to act in the same
manner, and to produce the same effects, as camphor and Cocculus
indicus. In small doses it acts as an irritant; in large doses it causes
convulsions and coma.

It is here noticed principally because it is one of the poisons which
act violently on the heart. If the body of an animal be examined
immediately after death from the Upas antiar, the heart is found to have
lost its irritability, and the left ventricle to contain florid blood:
Schnell found, that, like many other active poisons, it has no effect
when applied to the divided end of a nerve.[2392]

The _Coriaria myrtifolia_ is also supposed by some to possess the
properties of the present group, and is sufficiently important from its
energy, and its occasional injurious effects on man, to claim some
notice here.

Its toxicological action has been investigated by Professor Mayer of
Bonn, who found that it excites in most animals violent fits of tetanus,
giving place to apoplectic coma; and that in the dead body the brain is
seen gorged with blood, the blood in the heart and great vessels fluid,
the heart not irritable immediately after death, and the inner membrane
of the stomach yellowish and shrivelled. A drachm of the extract of the
juice killed a cat in two hours when swallowed; half a drachm applied to
a wound killed another in eighty-five minutes; and six grains in the
same way killed a kitten in three hours and a half. A drachm swallowed
by a young dog killed it in two hours and a half. Ten grains of the
extract of the infusion applied to a wound killed a kitten in six hours;
and three grains another in three hours. A buzzard was killed in
three-quarters of an hour by half a drachm of the extract of the juice.
Frogs are also soon killed by it. Rabbits, it is remarkable, are
scarcely affected by this poison, either administered internally, or
applied to a wound,—a drachm in the former way, and half as much in the
latter, having produced no effect at all. A grain, however, injected
into the jugular vein occasioned in about five hours a single convulsive
paroxysm, which proved immediately fatal.[2393]

Instances of poisoning with this substance have occurred in the human
subject,—generally in consequence of its having been taken in various
parts of the continent with senna, which it is employed to adulterate.
Sauvages has recorded two cases of death occasioned by the berries. In
one, a child, death took place within a day under symptoms like
epileptic convulsions; and in the other, an adult, who swallowed only
fifteen berries, convulsions, coma, and lividity of the face were
produced, ending fatally the same evening, though the greater part of
the berries were discharged by emetics.[2394] In recent French journals
various similar cases are recorded. M. Fée describes five cases, one of
them fatal. In this instance, a male adult, death occurred within four
hours after he took an infusion of senna adulterated with the coriaria;
and the symptoms were violent convulsions, locked-jaw and colic.[2395]
M. Roux has noticed a great number of cases in the fullest paper yet
published on its effects on man, and gives the details of three which
came under his own notice, and of which one proved fatal. In the fatal
case, that of a child three years and a half old, who took between
eighty and a hundred berries, the symptoms were heat and pricking of the
tongue, sparking and rolling of the eyes, loss of voice, locked-jaw, and
convulsions recurring in occasional fits of eight or ten minutes in
duration. Death ensued in sixteen hours and a half.[2396] Roux refers
also among other instances to those of no fewer than ten soldiers, who
were attacked at the same time in consequence of eating the berries, and
of whom two died. In Roux’s fatal case there was injection of the
membranes of the brain, and no other particular appearance; in that
mentioned by Fée, there was inflammation of the stomach and bowels; and
in one of Sauvages’s cases no morbid appearance at all was discovered.

Considering these very pointed proofs of the poisonous qualities of the
coriaria, it is not a little singular that doubts have lately arisen
whether it is a poison at all. Peschier of Geneva says he has
ascertained that tanners, who use it in their trade on account of the
powerful astringency of the leaves, also take it internally for gleet,
and that he gave a decoction of an ounce to chickens, dogs, and men,
without witnessing any ill effect.[2397]


                        _Of Poisoning with Yew._

The leaves and berries of the _Taxus baccata_, or yew, are known to be
poisonous; but their effects have not been investigated with care. I
have arranged it in the meantime with the present group.

M. Grognier, as quoted by Orfila, ascertained that a decoction of eight
ounces of berries without seeds had no effect on a dog; that a pound and
a half of seeds had no effect on a horse; that three ounces of the juice
of the leaves given to a large dog merely caused vomiting; and that a
decoction of twelve ounces of leaves, confined in the stomach of a dog
by a ligature on the gullet, had also no effect. But two ounces of the
juice of the leaves killed a small dog; and Orfila himself ascertained,
that thirty-six grains of extract of the leaves, injected into the
jugular vein, caused giddiness, stupor, and death.[2398]

Accidents have repeatedly happened to children in this country from
yew-berries. Mr. Hurt of Mansfield has given the particulars of an
interesting case. A child, three years and a half old, two hours after
eating the berries, was observed to look ill at dinner, and became
affected with lividity and heaviness of the eyes, as if he was about to
fall asleep. Vomiting followed, without any pain; and he died before a
medical man, who was sent for, could arrive. Four other children,
somewhat older, who had eaten the seeds, were made to vomit by emetics,
and got well. The dead body of the first child presented many livid
spots, redness of the villous coat of the stomach, and gorging of the
brain and membranes with blood. A mass of berries, seeds, and potatoes
was found in the stomach.[2399]—Dr. Hartmann of Frankfort mentions that
a girl, who took a decoction of the leaves to produce abortion, died in
consequence, but without having miscarried.[2400]—Dr. Percival has
related other cases in his essays.[2401]




                             CHAPTER XXXIX.
                        OF THE POISONOUS FUNGI.


A fourth group of poisons possessing narcotico-acrid proper ties,
includes the poisonous _fungi_ or mushrooms.

Accidents arising from the deadly fungi being mistaken for eatable
mushrooms are common on the continent, and especially in France. They
are not uncommon, too, in Britain; but they are less frequent than
abroad, because the epicure’s catalogue of mushrooms in this country
contains only three species, whose characters are too distinct to be
mistaken by a person of ordinary skill; while abroad a great variety of
them have found their way to the table, many of which are not only
liable to be confounded with poisonous species, but are even also
themselves of doubtful quality.

The present subject cannot be thoroughly studied without a knowledge of
the appearance and characters of all the fungi which have been
ascertained to be esculent, as well as of those which are known to be
deleterious. This information, however, I cannot pretend to communicate,
as it would lead to great details. In what follows, therefore, a simple
list will be given of the two classes, with references to the proper
source for minute descriptions of them, and some general observations on
the effects of the poisonous species.

_List of the wholesome and poisonous Fungi._—The only good account yet
published of the innocent or eatable fungi of Great Britain is contained
in an elaborate essay on the subject by Dr. Greville of this place. He
enumerates no fewer than twenty-six different species, which grow
abundantly in our woods and fields, and which, although most of them
utterly neglected in this country, are all considered abroad to be
eatable, and many of them delicate. They are the following: _Tuber
cibarium_, or common truffle; _T. moschatum_ and _T. album_, two species
of analogous qualities; _Amanita cæsarea_ or _aurantiaca_, the Oronge of
the French, a species which is often confounded by the ignorant with a
very poisonous one, the _A. muscaria_, or _pseudo-aurantiaca_; _Agaricus
procerus_; _A. campestris_, the common mushroom of meadows; _A. edulis_,
or white caps; _A. oreades_, or Scotch bonnets; _A. odorus_; _A.
uburneus_; _A. ulmarius_; _A. ostreatus_; _A. violaceus_; _A.
deliciosus_; _A. piperatus_; and _A. acris_; _Boletus edulis_; and _B.
scaber_; _Fistulina hepatica_; _Hydnum repandum_; _Morchella esculenta_,
the common morelle; _Helvella mitra_, and _H. leucophæa_. Of these the
_Agaricus acris_, _procerus_, and _piperatus_ are probably unwholesome;
and the _Amanita cæsarea_ is very rare in this country, if indeed it is
indigenous at all. The _A. muscaria_, with which it is apt to be
confounded, is common enough. The species to which our cooks confine
their attention are the _Tuber cibarium_ or truffle, the _Agaricus
campestris_, or common mushroom, and the _Morchella esculenta_, or
morelle. The _Agaricus edulis_ is also to be met with in some markets,
but is not in general use.[2402]

The best description of the poisonous species is to be found in Orfila’s
Toxicology. He enumerates the _Amanita muscaria_, _alba_, _citrina_, and
_viridis_; the _Hypophyllum maculatum_, _albocitrinum_, _tricuspidatum_,
_sanguineum_, _crux-melitense_, _pudibundum_ and _pellitum_; the
_Agaricus necator_, _acris_, _piperatus_, _pyrogalus_, _stypticus_,
_annularis_, and _urens_.[2403] To these may be added the _Agaricus
semiglobatus_, on the authority of Messrs. Brande and Sowerby,[2404] the
_A. campanulatus_,[2405] the _A. procerus_, on the authority of a case
by Dr. Peddie of this city,[2406] the _A. myomica_, on the authority of
Ghiglini,[2407] the _A. panterinus_ on that of Dr. Paolini of
Bologna,[2408] the _A. bulbosus_ of Bulliard, or _Amanita venenata_, on
that of Pouchet,[2409] the _Agaricus vernus_, _insidiosus_,
_globocephalus_, _sanguineus_, _torminosus_ and _rimosus_, on that of
Letellier,[2410] and the _Hypophyllum niveum_ on the authority of
Paulet.

_Circumstances which modify their qualities._—The qualities of the fungi
as articles of food are liable to considerable variety. Some, which are
in general eaten in safety, occasionally become hurtful; and some of the
poisonous kinds may under certain circumstances become inert, or even
esculent. But the causes which regulate these variations are not well
ascertained.

It has been thought by some that most fungi become safe when they have
been dried;[2411] and there may be some truth in this remark, as their
poisonous qualities appear to depend in part on a volatile principle.
But it is by no means universally true. Foderé mentions that the
_Agaricus piperatus_ continues acrid after having been dried.[2412]

Climate certainly alters their properties. The _Agaricus piperatus_ is
eaten in Prussia and Russia;[2413] but is poisonous in France. The
_Agaricus acris_ and _A. necator_, also enumerated above as meriting
their names, are used freely in Russia.[2414] The _Amanita muscaria_ in
France and Britain is a violent poison, and is considered so even in
Russia;[2415] but in Kamschatka it yields a beverage which is used as a
substitute for intoxicating liquors.[2416]

There is some reason to believe also that the weather or period of the
season influences some of the esculent species. Thus Foderé has
mentioned instances of the common morelle having appeared injurious
after long-continued rain.[2417]

Even the _Agaricus campestris_ or common mushroom is generally believed
to become somewhat unsafe towards the close of the season, or as it
turns old. Its external characters at that time are sensibly altered;
the margin of the cap is more acute, its white colour less lively, and
the fleshy hue of its lamellæ is changed to brown or black. In this
state, however, I have often eaten it freely and with impunity.

Cooking produces some difference on their effects. The very best of them
are indigestible when raw; and some of the poisonous species may lose in
part their deleterious qualities when cooked, because heat expels the
volatile principle; but, on the whole, I believe the effect of cooking
has not been satisfactorily shown to be considerable. Dr. Pouchet of
Rouen seems to have clearly proved, that the poisonous properties of two
of the most deadly fungi, the _Amanita muscaria_ and _A. venenata_, may
be entirely removed by boiling them in water. A quart of water, in which
five plants had been boiled for fifteen minutes, killed a dog in eight
hours, and again another in a day; but the boiled fungi themselves had
no effect at all on two other dogs; and a third, which had been fed for
two months on little else than boiled amanitas, not only sustained no
harm, but actually got fat on this fare.[2418] Pouchet is inclined to
think that the whole poisonous plants of the family are similarly
circumstanced.—On the other hand some cryptogamous botanists have
maintained that the qualities of the esculent mushrooms are injured by
cooking, and that when used in the raw state they may be taken for a
long time as a principal article of food without injury. This statement,
as to the effect of mushrooms when used for a length of time as food,
will be more fully considered presently. It is easy to understand how
boiling may remove their active properties, although other modes of
cookery may not do so. Roasting had no effect in impairing the activity
of _Agaricus procerus_ in the case observed by Dr. Peddie.

On certain persons all mushrooms, even the very best of the eatable
kinds, act more or less injuriously. They cause vomiting, diarrhœa, and
colic. In this respect they are on the same footing with the richer
sorts of fish, which by idiosyncrasy act as poisons on particular
constitutions. It is probably under this head that we must arrange an
extraordinary case mentioned by Sage of a man who died soon after eating
a pound of truffles. He was seized with headache, a sense of weight in
the stomach, and faintness; and he lived only a few hours.[2419]

Lastly, it is not improbable from a singular set of cases to be related
presently, that, contrary to what some botanists have alleged, the best
mushrooms when taken in large quantity, and for a considerable length of
time, are deleterious to every one.

Foderé,[2420] Orfila,[2421] Decandolle,[2422] and Greville,[2423] have
laid down general directions for distinguishing the esculent from the
poisonous varieties; but it is extremely questionable whether their
rules are always safe; and certainly they are not always accurate, as
they would exclude many species in common use on the continent. It
appears that most fungi which have a warty cap, more especially
fragments of membrane adhering to their upper surface, are poisonous.
Heavy fungi, which have an unpleasant odour, especially if they emerge
from a _vulva_ or bag, are also generally hurtful. Of those which grow
in woods and shady places a few are esculent, but most are unwholesome;
and if moist on the surface they should be avoided. All those which grow
in tufts or clusters from the trunks or stumps of trees ought likewise
to be shunned. A sure test of a poisonous fungus is an astringent,
styptic taste, and perhaps also a disagreeable, but certainly a pungent,
odour. Some fungi possessing these properties have indeed found their
way to the epicure’s table; but they are of very questionable quality.
Those whose substance becomes blue soon after being cut are invariably
poisonous. Agarics of an orange or rose-red colour, and boleti which are
coriaceous or corky, or which have a membranous collar round the stem,
are also unsafe; but these rules are not universally applicable in other
genera. Even the esculent mushrooms, if partially devoured and abandoned
by insects, are avoided by some as having in all probability acquired
injurious qualities which they do not usually possess; but this test I
have often disregarded.—These rules for knowing deleterious fungi seem
to rest on fact and experience; but they will not enable the collector
to recognise every poisonous species. The general rules laid down for
distinguishing wholesome fungi are not so well founded, and therefore it
appears necessary to specify them.

_On the Poisonous Principle of the Fungi._—Few attempts have been
hitherto made to discover by chemical analysis the principles on which
the effects of the poisonous mushrooms depend. M. Braconnot analyzed a
considerable number both of the esculent and poisonous species, and
found in some a saccharine matter, in others an acrid resin, in others
an acrid volatile principle, and in all a spongy substance, which forms
the basis of them, and which he has denominated fungin.[2424] The last
ingredient is innocuous, and it does not appear that M. Braconnot could
trace the peculiar powers of the fungi to any of the acrid principles.
The subject was afterwards resumed by M. Letellier, who says he found in
some of them one, in others two poisonous principles. One of these is an
acrid matter so fugacious, that it disappears when the plant is either
dried, or boiled, or macerated in weak acids, alkalis, or alcohol. To
this principle he says are owing the irritant properties of some fungi.
The other principle is more fixed, as it resists drying, boiling, and
the action of weak alkalis and acids. It is soluble in water, has
neither smell nor taste, and forms crystallizable salts with acids; but
he did not succeed in separating it in a state of purity. To this
principle he attributes the narcotic properties of the fungi. He found
it in the _Amanita bulbosa_, _muscaria_, and _verna_; and he therefore
proposed to call it amanitine. Its effects on animals appear to resemble
considerably those of opium.[2425]—Chansarel found that the poisonous
principle resides in the juice, and not in the fleshy part after it is
well washed.[2426]

_Of the Symptoms produced in Man by the Poisonous Fungi._—The mode of
action of the poisonous fungi has not been particularly examined; but
the experiments of Paulet long ago established that they are poisonous
to animals as well as to man.[2427]

The symptoms produced by them in man are endless in variety, and fully
substantiate the propriety of arranging them in the class of
narcotico-acrid poisons. Sometimes they produce narcotic symptoms alone,
sometimes only symptoms of irritation, but much more commonly both
together. It is likewise not improbable, that fungi, even though not
belonging to the varieties commonly acknowledged as poisons, induce,
when taken for a considerable length of time, a peculiar depraved state
of the constitution, leading to external suppuration and gangrene. Each
of these statements will now be illustrated by a few examples.

The following is a good instance of pure narcotism. A man gathered in
Hyde Park a considerable number of the _Agaricus campanulatus_ by
mistake for the _A. campestris_, stewed them, and proceeded to eat them;
but before ending his repast, and not above ten minutes after he began
it, he was suddenly attacked with dimness of vision, giddiness,
debility, trembling, and loss of recollection. In a short time he
recovered so far as to be able to go in search of assistance. But he had
hardly walked 250 yards when his memory again failed him, and he lost
his way. His countenance expressed anxiety, he reeled about, and could
hardly articulate. The pulse was slow and feeble. He soon became so
drowsy that he could be kept awake only by constant dragging. Vomiting
was then produced by means of sulphate of zinc; the drowsiness gradually
went off; and next day he complained merely of languor and
weakness.[2428]—An equally remarkable set of cases of pure narcotism,
which occurred a few years ago in this city, has been related by Dr.
Peddie. Half an hour after eating the _Agaricus procerus_, an elderly
man and a boy of thirteen were attacked with giddiness and staggering,
as if they were intoxicated; and in an hour they became insensible, the
man indeed so much so that for some time he could not be roused by any
means. Emetics having little effect, the stomach was cleared out by the
pump, and powerful stimulants were employed both inwardly and outwardly,
by means of which sensibility was in some degree restored. Occasional
convulsive spasms ensued, and afterwards furious delirium, attended with
frantic cries and vehement resistance to remedies, and followed by a
state like delirium tremens. The pupils were at first much contracted,
afterwards considerably dilated as sensibility returned, and in the boy
contracted while he lay torpid, but dilated when he was roused. In
neither instance was there any pain felt at any time; nor were the
bowels affected. Another boy who took a small quantity only had no other
symptom but giddiness, drowsiness, and debility.[2429]—A singular form
of the narcotic effects of the fungi occurred in the case of a boy of
fourteen, who had eaten the _Agaricus panterinus_ near Bologna. In the
course of two hours he was seized with delirium, a maniacal disposition
to rove, and some convulsive movements. Ere long these symptoms were
succeeded by a state resembling coma in every way, except that he looked
as if he understood what was going on: and in point of fact really did
so. He recovered speedily under the use of emetics.[2430]

In the next set of cases the symptoms were those of almost pure
irritation. Several French soldiers in Russia ate a large quantity of
the _Amanita muscaria_, which they had mistaken for the _Amanita
cæsarea_. Some were not taken ill for six hours and upwards. Four of
them, who were very powerful men, thought themselves safe, because while
their companions were already suffering, they themselves felt perfectly
well; and they refused to take emetics. In the evening, however, they
began to complain of anxiety, a sense of suffocation, frequent fainting,
burning thirst, and violent gripes. The pulse became small and
irregular, and the body bedewed with cold sweat; the lineaments of the
countenance were singularly changed, the nose and lips acquiring a
violet tint; they trembled much; the belly swelled, and a profuse fetid
diarrhœa supervened. The extremities soon became livid, and the pain of
the abdomen intense; delirium ensued; and all four died.[2431]

Such cases, however, do not appear to be very common; and much more
generally the symptoms of poisoning with the fungi present a well-marked
conjunction of deep narcotism and violent irritation, as the instances
now to be mentioned will show.

Besides the four soldiers whose cases have just been described, several
of their comrades were severely affected, but recovered. Two of these
had weak pulse, tense and painful belly, partial cold sweats, fetid
breath and stools. In the afternoon they became delirious, then
comatose, and the coma lasted twenty-four hours.

A man, his wife, and three children, ate to dinner carp stewed by
mistake with the _Amanita citrina_. The wife, the servant, and one of
the children had vomiting, followed by deep sopor; but they recovered.
The husband had true and violent cholera, but recovered also. The two
other children became profoundly lethargic and comatose, emetics had no
effect, and death soon ensued without any other remarkable symptom. The
individuals who recovered were not completely well till three weeks
after the fatal repast.[2432] This set of cases shows the tendency of
the poisonous fungi to cause in one person pure irritation, and in
another pure narcotism.

The last set of cases to be mentioned were produced by the _Hypophyllum
sanguineum_, a small conical fungus of a mouse colour, well known to
children in Scotland by the name of _puddock-stool_. This species seems
to cause convulsions as well as sopor. A family of six persons, four of
whom were children, ate about two pounds of it dressed with butter. The
incipient symptoms were pain in the pit of the stomach, a sense of
impending suffocation, and violent efforts to vomit; which symptoms did
not commence in any of them till about twelve hours after the poisonous
meal, in one not till twenty hours, and in another not till nearly
thirty hours. One of the children, seven years of age, had acute pain of
the belly, which soon swelled enormously; afterwards he fell into a
state of lethargic sleep, but continued to cry; about twenty-four hours
after eating the fungi the limbs became affected with permanent spasms
and convulsive fits; and in no long time he expired in a tetanic
paroxysm. Another of the children, ten years old, perished nearly in the
same manner, but with convulsions of greater violence. The mother had
frequent bloody stools and vomiting; the skin became yellow; the muscles
of the abdomen were contracted spasmodically, so that the navel was
drawn towards the spine; profound lethargy and general coldness
supervened; and she too died about thirty-six hours after eating the
fungus. A third child, after slight symptoms of amendment had shown
themselves, became worse again, and died on the third day with
trembling, delirium, and convulsions. This patient, who had taken very
little of the poison, was not attacked till about thirty hours after the
meal. The fourth child, after precursory symptoms like those of the
rest, became delirious, and had an attack of colic and inflammation of
the bowels, without diarrhœa; but he eventually recovered. The father
had a severe attack of dysentery for three days, and remained five days
speechless. For a long time afterwards he had occasional bloody
diarrhœa; and, although he eventually recovered, his health continued to
suffer for an entire year.[2433] The cases now mentioned illustrate
clearly the simultaneous occurrence of narcotic and irritant symptoms in
the same individuals.

A striking circumstance in respect to the symptoms of poisoning with the
fungi, is the great difference in the interval which elapses before they
begin. In the first case the symptoms appear to have commenced in a few
minutes; but, on the contrary, an interval of twelve hours is common;
and Gmelin has quoted a set of cases, seventeen in number, in which, as
in one of those related by Picco, the interval is said to have been a
day and a half.[2434] The tardiness of the approach of the symptoms is
owing to the indigestibility of most of the fungi. Their indigestibility
is in fact so great, that portions of them have been discharged by
vomiting so late as fifty-two hours after they were swallowed.[2435]

Another circumstance, worthy of particular notice, is the great
durability of the symptoms. Even the purely narcotic effects of some
fungi have been known to last above two days. In the instance just
alluded to, the vomiting of the poison was the first thing that
interrupted a state of deep lethargy, which had prevailed for fifty-two
hours. The symptoms of irritation, after their violence has been
mitigated, might continue, as in the instance quoted from Orfila, for
about three weeks.

It was stated above, that some people are apt to suffer unpleasant
effects from eating even the best and safest of the esculent mushrooms.
These effects, which depend on idiosyncrasy, are confined chiefly to an
attack of vomiting and purging, followed by more or less indigestion.
Some persons have been similarly affected, even by the small portion of
mushroom-juice which is contained in an ordinary ketchup seasoning. This
accident, however, may very well be often unconnected with idiosyncrasy;
as I have seen those who gather mushrooms near Edinburgh, for the
purpose of making ketchup, picking up every fungus that came in their
way.

There is some reason for suspecting that even the best mushrooms, when
taken as a principal article of food for a considerable length of time,
will prove injurious, and that they then induce a peculiar depraved
habit, which leads to external suppuration and gangrene. The only cases
which have hitherto appeared in support of this statement, were lately
published in Rust’s Journal. A family, consisting of the mother and four
children, were seized with a kind of tertian fever, and the formation of
abscesses, which discharged a thin, ill-conditioned pus, passed rapidly
into spreading gangrene, and proved fatal to the mother and one of the
children. No other cause could be discovered to account for so
extraordinary a conjunction of symptoms in so many individuals, except
that for two months they had lived almost entirely on mushrooms; and the
probability of this being really the cause, was strengthened by the
fact, that the father who slept always with his family, and who alone
escaped, lived on ordinary food at a place where he worked not far
off.[2436] In opposition, however, to the natural inference from this
narrative, some have believed, that mushrooms may be safely eaten to a
large amount and for a long time, provided they be used raw. A botanist
of Persoon’s acquaintance, while studying the cryptogamous plants in the
vicinity of Nuremberg, says he found that the peasants ate them in large
quantities as their daily food; and, in imitation of their custom, he
ate for several weeks nothing but bread and raw mushrooms; yet at the
end he experienced an increase rather than a diminution of strength, and
enjoyed perfect health. He adds that they lose their good qualities by
cooking; but he has supplied no facts in support of that
statement.[2437] It is said that eatable fungi, used for a considerable
time as a principal article of food, as in Russia, cause greenness of
the skin.[2438] There is no reason for supposing, as some have
done,[2439] that wholesome mushrooms may produce the effects of the
poisonous kinds, if eaten in large quantity.

_Of the Morbid Appearances._—The morbid appearances left in the bodies
of persons poisoned by this deleterious fungi have been but imperfectly
collected.

The body is in general very livid, and the blood fluid; so much so
sometimes, that it flows from the natural openings in the dead
body.[2440] In general, the abdomen is distended with fetid air, which,
indeed, is usually present during life. The stomach and small intestines
of the four French soldiers (p. 705), presented the appearance of
inflammation passing in some places to gangrene. In two of them
especially, the stomach was gangrenous in many places, and far advanced
in putrefaction. The same appearances were found in Picco’s cases. In
these there was also an excessive enlargement of the liver. The lungs
have sometimes been found gorged or even inflamed. The vessels of the
brain are also sometimes very turgid. They were particularly so in a
case related by Dr. Beck, where death was occasioned in seven hours by
an infusion of the _Amanita muscaria_ in milk. The whole sinuses of the
dura mater, as well as the arteries were enormously distended with
blood; the arachnoid and pia mater were of a scarlet colour; the vessels
of the membrane between the convolutions, together with the plexus
choroides, were also excessively gorged; and the substance of the brain
was red. Lastly, a clot of blood, as big as a bean, was found in the
cerebellum.[2441]—The stomach, unless there had been vomiting or
diarrhœa, will usually contain fragments of the poison, if it has not
been taken in a state of minute division; and this evidence of the cause
of death may be obtained, even although the individual survived two days
or upwards. Sometimes fragments are found in the intestines. In one of
Picco’s patients who lived twenty-four hours, there was found in the
neighbourhood of the ileo-cæcal valve, which was much inflamed.[2442]

_Of the Treatment._—The treatment of poisoning with the fungi does not
call for any special observations. Emetics are of primary importance;
and after the poison has been by their means dislodged, the sopor and
inflammation of the bowels are to be treated in the usual way. No
antidote is known. Several have at different times been a good deal
confided in; but none are of any material service. Chansarel found acids
useless, but thought infusion of galls advantageous.[2443]

In concluding the present chapter it is necessary to take notice of a
variety of poisoning, not altogether unimportant in a medico-legal point
of view. A person may seem to die of poisoning with the deleterious
fungi, from eating esculent mushrooms intentionally drugged with some
other vegetable or mineral poison. It must be confessed, that if the
murderer is dexterous in the choice and mode of administering the
poison, such cases might readily escape suspicion, and even when
suspected might not be cleared up without difficulty. The ascertaining
the species of mushroom, by finding others where it has been gathered,
will not supply more than presumptive proof of the wholesomeness of that
which has been eaten; because the esculent and poisonous species
sometimes grow near one another, and have a mutual resemblance, so that
a mistake may easily occur. The presumption may be somewhat strengthened
by evidence derived from the interval which elapses before the symptoms
begin, from the nature and progress of the symptoms themselves, and from
the morbid appearances. Some one or other of these circumstances may
establish the fact of poisoning with a deleterious fungi. It is
impossible, however, that they shall ever establish satisfactorily that
the fungus was naturally wholesome; and, on the whole, the only decided
evidence of poisoning by some other means will be the actual discovery
of another poison.

The case now under consideration is not a mere hypothetical one. Ernest
Platner has related a very interesting example, which proves how easily
poisoning of the kind supposed may be accomplished without suspicion. A
servant-girl poisoned her mistress by mixing oxide of arsenic with a
dish of mushrooms. She died in twenty hours, after suffering severely
from vomiting and colic pains. On dissection there were found
inflammation of the stomach, gangrenous spots in it, clots of blood in
its contents, and redness of the intestines. Her death, however, was
ascribed to the mushrooms having been unwholesome; and the real cause
was not discovered till thirteen years after, when the girl was
convicted of murdering a fellow-servant in a somewhat similar way by
mixing arsenic with her chocolate, and then confessed both crimes.[2444]

_Poisonous Mosses._—It is not improbable that some of the mosses possess
poisonous properties similar to those of the deleterious fungi. Dr.
Winkler of Innsbruch mentions that the _Lycopodium selago_ is used in
the Tyrol in the way of infusion for killing vermin on animals; and that
unpleasant accidents have been produced in man by its accidental use.
Its effects appear to be sometimes irritant, but more generally narcotic
in their nature.[2445]




                              CHAPTER XL.
              OF THE EFFECTS OF POISONOUS GRAIN AND PULSE.


The different sorts of grain are subject to certain diseases, in
consequence of which meal or flour made from them is apt to be
impregnated with substances more or less injurious to animal life. It is
likewise believed, that unripe grain possesses properties which render
it to a certain extent unfit for the food of man.

It is for the most part difficult to trace satisfactorily the operation
of the poisons now alluded to, because they are seen acting only in
times of famine and general distress, when it is not always easy to make
due allowance for the effect of collateral circumstances. There is one
poison of the kind, however, whose baneful influence has been so
frequently and unequivocally witnessed, that no doubt now exists
regarding its properties, I mean _spurred rye_, or _ergot_. It is a
poison of no great consequence, perhaps, to the English toxicologist;
for indeed I am not aware that a single instance of its operation has
hitherto been observed in Britain.[2446] But its effects are so
singular, and the ravages it has often committed on the continent have
been so dreadful, that a short account of it cannot fail to interest
even the English reader. Besides, it has lately been introduced into the
materia medica, as possessing very extraordinary medicinal qualities;
and since its use is gaining ground, every medical jurist ought to be
conversant with its properties as a poison. I have also met with an
instance where it was administered for the purpose of procuring
miscarriage.


                    _Of Poisoning with Spurred Rye._

_Spurred Rye_, or _Secale cornutum_, the _Seigle ergoté_, or _Ergot_ of
the French, and _Mutterkorn_, or _Roggenmutter_, of the Germans, is a
disease common to various grains, in consequence of which the place of
the pickle is supplied by a long, black substance, like a little horn or
spur. It has been known to attack many plants of the order
Graminaceæ;[2447] and among those used as food by man, it has been
observed on barley, oats, spring-wheat, winter-wheat, and rye. But the
rye seems peculiarly subject to it, almost all the poison which has
caused epidemics, as well as what is now used in medicine, being
produced by that grain.

_Of the Cause and Nature of the Spur in Rye._—The spur attacks rye
chiefly in damp seasons, and in moist clay soils, particularly those
recently redeemed from waste lands in the neighbourhood of forests. Of
all the places where the spur has been hitherto observed none combines
these conditions so perfectly, and none has been so much infested with
the disease, as the district of Sologne, situated between the rivers
Loire and Cher, in France. According to the statistical researches of
the _Abbé Tessier_, who in 1777 was deputed by the Parisian Society of
Medicine to investigate the causes of the extraordinary prevalence of
the ergot in that district, the country was then so much intersected by
belts of wood around the fields, that the traveller in passing along
might imagine he was constantly approaching an immense forest; the
arable land was so poor, that, although it lay fallow every third
season, it was exhausted in nine or twelve years at farthest, and then
remained a long time in pasture before it could again bear white crops;
the surface was so level, and consequently so wet, that crops were
obtained only when the seed was sown on the tops of furrows a foot high;
and the climate is so moist, that from the month of September till late
in spring the whole country is overhung by dense fogs.[2448] Here the
rye, the common food of the peasantry, appears to have been in Tessier’s
time more liable to be attacked by the spur than in any other part of
the continent. Tessier found, that after being thrashed it contained on
an average about a forty-eighth part of ergot, even in good seasons; but
in bad seasons, and taking into account a considerable proportion which
is shaken out of the ears and sheaves before they reach the barn, the
proportion of ergot in the whole crop has been estimated so high as a
fourth or even a third. In Sologne the disease was farther observed by
Tessier to be always most prevalent in the dampest parts of a field, and
to affect above all the first crop of fields redeemed from waste land,
or from land which had previously been for some time in pasture.[2449]
The same connexion between moisture and the development of the ergot has
been repeatedly traced in other parts of France, as well as in
Germany.[2450] And according to the experiments of Wildenow, it may be
brought on at any time, by sowing the rye in a rich damp soil, and
watering the plants exuberantly in warm weather.[2451]

Opinions are much divided as to the cause and nature of the spur. It had
been conceived by some that nothing else is required for its production
but undue moisture combined with warmth; and that under these
circumstances the spur is formed simply by a diseased process from the
juices of the plant.[2452] By others, such as Tillet, Fontana, and Réad,
who also consider it to be simply a diseased formation, it has been held
to arise from the germen being punctured when young by an insect;[2453]
and in support of this statement, General Field says he saw flies
puncture the glumes in their milky state where spurs afterwards formed,
and imitating the operation with a needle obtained the same
result.[2454] On the other hand, Decandolle, reviving a previous
doctrine that the spur is a kind of fungus, conceived he had given
strong grounds for believing this excrescence to be a species of
_sclerotium_, which he terms _S. clavus_. Wiggers supports this doctrine
by chemical analysis; for he endeavours to show that the basis of the
structure of the spur is almost identical in chemical properties with
the principle fungin.[2455] Lastly, the most recent researches, those of
Smith,[2456] Queckett,[2457] and Bauer,[2458] founded chiefly on
microscopical observations, tend to a union and modification of these
two views,—namely, that the great mass of the spur is a peculiar morbid
formation, and that the whitish bloom which covers fresh specimens
consists of a multitude of microscopic fungi in the form of _sporidia_,
which thickly envelope and impregnate the parts of fructification in the
nascent state of the embryo, and are in all probability the exciting
cause of the morbid degeneration of the pickle.[2459]

Various opinions have been formed as to the mode of propagation of the
spur. Fontana has alleged that one variety of it may spread from plant
to plant over a field; and that he has expressly transmitted it by
contact from one ear to another.[2460] His opinion and statement of
facts are at variance with experiments lately made by Hertwig, a German
physician, who found that even when the ear while in flower was
surrounded for twelve days with powder of spurred rye, the healthiness
of the future grain was not in the slightest degree affected.[2461] The
same results have also been obtained by Wiggers, and more recently by
Dr. Samuel Wright.[2462] Wiggers, however, although he could not produce
spurs in the way indicated by Fontana, observed that the white dust on
the surface of the spurs will produce the disease in any plant, if
sprinkled in the soil at its roots, appearing therefore to be analogous
to the sporules or spawn of the admitted fungi. Mr. Queckett has made
the most precise experiments on the mode of reproduction of the disease.
He succeeded in infecting rye repeatedly with ergot by means of the
sporidia developed on the spurs; but it is remarkable that he could not
in the same way infect wheat or barley.[2463]

_Description and analysis of Spurred Rye._—The spur varies in length
from a few lines to two inches, and is from two to four lines in
thickness. If it is long, there is seldom more than one or two on a
single ear, and the remaining pickles of the ear are healthy. But the
ears which have small spurs have generally several, sometimes even
twenty; and when there are many, few of the remaining pickles are
altogether without blackness at the tips.[2464] The substance of the
spur is of a pale grayish-red tint; and externally it is bluish-black or
violet, with two, sometimes three, streaks of dotted gray. It is
specifically lighter than water, while sound rye is specifically
heavier, so that they are easily separated from one another.[2465] It is
tough and flexible when fresh, brittle and easily pulverized when dry.
The powder is disposed to attract moisture. It has a disagreeable heavy
smell, a nauseous, slightly acrid taste, and imparts its taste and smell
both to water and alcohol. Bread which contains it is defective in
firmness, liable to become moist, and cracks and crumbles soon after
being taken from the oven.[2466]—It is easily known, when entire, by its
external characters. Its powder, which is of an obscure grayish-red hue,
is best known by the action of solution of potash, which immediately
disengages a powerful odour of ergot, and forms a lake-red pulp; and
this pulp yields by filtration a splendid lake-red solution, which gives
a beautiful lake-red flaky precipitate, when either neutralized by
nitric acid, or treated with an excess of solution of alum.

Spurred rye has been repeatedly subjected to analysis. The earlier
researches of Vauquelin[2467] and of Pettenkofer[2468] do not lead to
any pointed results. The presence of hydrocyanic acid indicated by
Robert,[2469] would not account for the very peculiar effects of ergot,
and has besides been denied by Wiggers. Winkler obtained various
principles from it, and among the rest a thick, rancid, slightly acrid
oil, and a nauseous, sweetish, acrid fluid; but he did not determine,
any more than his predecessors, in which of these principles the active
properties of the spur reside.[2470] Wiggers supplied more definite
information on the subject. He denies the presence of hydrocyanic acid,
and says he found ergot to consist chiefly of a heavy-smelling fixed
oil, fungin, albumen, osmazome, waxy matter, and an extractive substance
of a strong, peculiar taste and smell, in which, from experiments on
animals, he was led to infer that its active properties reside. I have
obtained all his chief results, except the most important of them; for
the substance which ought to have been his ergotin was destitute of
marked taste or smell of any kind.[2471] Dr. Wright too could not obtain
the ergotin of Wiggers, and concludes from his own experiments, that the
spur consists of fungin, modified starch, mucilage, gluten, osmazome,
colouring matter, various salts, and thirty-one per cent. of fixed oil,
in which the active properties of the poison seemed to him to
reside.[2472] Buchner, however, thinks that the oil is not itself
active, but owes its apparent energy to an acrid principle which alcohol
removes from it, and which is not removed from the crude substance in
separating the oil in the usual way by sulphuric ether, unless the ether
be somewhat alcoholized.[2473] However this may be, it seems ascertained
by the experiments of Dr. Wright, that the fixed oil, obtained by means
of common ether, concentrates in itself the peculiar properties
possessed by ergot, either in small doses as a medicine, or in a single
large dose as a poison.

_Effects of Spurred Rye on Man and Animals._—Before proceeding to relate
the effects of this poison on man, it should be mentioned, that at
different times doubts have been entertained, whether the baneful
effects ascribed to it might not really arise from some other cause. But
independently of the connexion which has been frequently traced between
the poison and the diseases imputed to it in the human subject, the
question has been set at rest by the experiments which have been tried
on animals, and which indeed were instituted with a view to settle the
point in dispute.

The experiments hitherto made on animals are variable in their results,
yet sufficient to show that spurred rye is an active poison of a very
peculiar kind. According to the observations collected by Dr. Robert
from a variety of authors, it follows that it is injurious and even
fatal to all animals which are fed for a sufficient length of time with
a moderate proportion of it, unless they escape its action by early
vomiting; that dogs and cats, in consequence of discharging it by
vomiting, suffer only slight symptoms of irritant poisoning;—but that
swine, moles, geese, ducks, fowls, quails, sparrows, as well as leeches
and flies, are sooner or later killed by it;—and that the symptoms it
causes in beasts and birds are in the first instance giddiness, dilated
pupil, and palsy, and afterwards diarrhœa, suppurating tumours,
scattered gangrene throughout the body, and sometimes dropping off of
the toes. Wiggers ascertained that nine grains of the substance he has
considered its active principle occasioned in a fowl dulness, apparent
suffering, gradually increasing feebleness, coldness and insensibility
of the extremities, and in three days a fit of convulsions, ending in
death.[2474] Taddei lately found, that sparrows were killed by six
grains of it in six or seven hours, with symptoms merely of great
weakness, torpor, and indisposition to stir.[2475]

Dr. Wright, whose experiments are the most extensive and precise yet
made on this subject, found that a single dose, consisting of a strong
infusion of between two drachms and a half and six drachms of ergot, if
introduced into the jugular vein of a dog, occasions death, sometimes in
a few minutes, sometimes not for more than two hours, with symptoms of
alternating spasm and paralysis, occasionally a tendency to coma, and
often depressed or irregular action of the heart, or even complete
arrestment of its function;—that, when introduced into the cellular
tissue, it produces inflammation and suppuration, sometimes
circumscribed, sometimes diffuse, and always attended with an unhealthy
discharge and great exhaustion;—and that, when admitted into the
stomach, it excites irritation of the alimentary canal, excessive
muscular prostration, at first excitability, but afterwards singular
dulness or even complete obliteration of the senses, and occasional
slight spasms; but that it is not a very active poison through this
channel, as above three ounces are required to prove fatal to a dog.
When it was administered in frequent small doses, he could not observe
the effects remarked by Robert, but found that it induced a peculiar
cachectic state, indicated by extreme muscular emaciation and weakness,
loss of appetite, frequency of the pulse, repulsive fetor of the
secretions and excretions, congestion of the alimentary mucous membrane,
excessive contraction of the spleen, enlargement of the liver and
absorbent glands, and non-formation of callus at the ends of fractured
bones.[2476]

With regard to its effects on man, it has been found by express
experiment, that a single dose of two drachms excites giddiness,
headache, flushed face, pain and spasms in the stomach, nausea, and
vomiting, colic, purging, and a sense of weariness and weight in the
limbs.[2477] But it is not in this way that it has been usually
introduced into the system; nor are these precisely the symptoms already
hinted at as particular in its action. The effects now to be mentioned
form a peculiar disease, which has often prevailed epidemically in
different territories on the continent, and which arises from the spur
being allowed to mix with the grain in the meal, and being taken as food
for a continuance of time in rye-bread. The affection produced differs
much in different epidemics and even in different cases of the same
epidemic. Two distinct disorders have been noticed; the one a nervous
disease, characterized by violent spasmodic convulsions; the other a
depraved state of the constitution, which ends in that remarkable
disorder, dry gangrene; and it does not appear that the two affections
are apt to be blended together in the same case.

The first form of disease, the _convulsive ergotism_ of the French
writers, has been very well described by Taube, a German physician, as
it occurred in the north of Germany in 1770–1. In its most acute form,
it commenced suddenly with dimness of sight, giddiness and loss of
sensibility, followed soon by dreadful cramps and convulsions of the
whole body, _risus sardonicus_, yellowness of the countenance, excessive
thirst, excruciating pains in the limbs and chest, and a small, often
imperceptible pulse. Such cases usually proved fatal in twenty-four or
forty-eight hours. In the milder cases the convulsions came on in
paroxysms, were preceded for some days by weakness and weight of the
limbs, and a strange feeling as of insects crawling over the legs, arms,
and face; in the intervals between the fits the appetite was voracious,
the pulse natural, the excretions regular; and the disease either
terminated in recovery, with scattered suppurations, cutaneous
eruptions, anasarca or diarrhœa, or it proved in the end fatal amidst
prolonged sopor and convulsions.[2478] Another more recent and very
clear account of this form of the disease has been given by Dr. Wagner
of Schlieben from his experience of an epidemic which prevailed in the
neighbourhood of that place so lately as the years 1831 and 1832. In
consequence of unusual moisture and late frosts in the summer of 1831,
the rye was so much spurred in many fields that a fifth at least of the
pickles was diseased. As soon as the country people proceeded to use the
new rye, convulsive ergotism began to show itself, and it recurred more
or less till next midsummer, when the diseased grain was all consumed.
The usual symptoms were at first periodic weariness, afterwards an
uneasy sense of contraction in the hands and feet, and at length violent
and permanent contraction of the flexor muscles of the arms, legs, feet,
hands, fingers and toes, with frequent attacks of a sense of burning or
creeping on the skin. These were the essential symptoms; but a great
variety of accessory nervous affections occasionally presented
themselves. There was seldom any disturbance of the mind, except in some
of the fatal cases, where epileptic convulsions and coma preceded death.
Every case was cured by emetics, laxatives, and frequent small doses of
opium, provided it was taken in reasonable time, and the unwholesome
food was completely withdrawn.[2479]

The other form of disease, which has been named _gangrenous ergotism_,
by the French writers, and is known in Germany by the vulgar name of
creeping-sickness (_kriebelkrankheit_), has been minutely described by
various authors. In the most severe form, as it appeared in Switzerland
in 1709 and 1716, it commenced, according to Lang, a physician of
Lucerne, with general weakness, weariness, and a feeling as of insects
creeping over the skin; when these symptoms had lasted some days or
weeks, the extremities became cold, white, stiff, benumbed, and at
length so insensible that deep incisions were not felt; then
excruciating pains in the limbs supervened, along with fever, headache,
and sometimes bleeding from the nose; finally the affected parts, and in
the first instance the fingers and arms, afterwards the toes and legs,
shrivelled, dried up, and dropped off by the joints. A healthy
granulation succeeded; but the powers of life were frequently exhausted
before that stage was reached. The appetite, as in the convulsive form
of the disease, continued voracious throughout.[2480] In milder cases,
as it prevailed at different times in France, nausea and vomiting
attended the precursory symptoms, and the gangrenous affection was
accompanied with dark vesications.[2481] In another variety, which has
been witnessed in various parts of Germany, the chief symptoms were
spasmodic contraction of the limbs at first, and afterwards weakness of
mind, voracity and dyspepsia, which, if not followed by recovery, as
generally happened, either terminated in fatuity or in fatal
gangrene.[2482]

These extraordinary and formidable distempers were first referred to the
operation of spurred rye in 1597 by the Marburg Medical Faculty, who
witnessed the ravages of the poison in Hessia during the preceding year.
Since then repeated epidemics have broken out in Germany, Bohemia,
Holstein, Denmark, Sweden, Lombardy, Switzerland, and France.[2483]
About the close of last century, partly in consequence of the attention
of the respective governments being turned to the subject, partly by
reason of the improved condition of the peasantry in these countries,
and the greater rarity of seasons of famine, the epidemics became much
less common or extensive. Nevertheless the creeping-sickness has been
several times noticed in Germany since the present century began.[2484]

Spurred rye is now generally believed to possess another singular
quality, in consequence of which it has been lately introduced into the
materia medica of this and other countries,—a power of promoting the
contractions of the gravid uterus. This property seems to have been long
familiar to the quacks and midwives of Germany; and towards the close of
last century it rendered ergot so favourite a remedy with them, that
several of the German states prohibited the use of it by severe
statutes.[2485] It was first fairly brought under the notice of regular
accoucheurs by the physicians of the United States between the years
1807 and 1814.[2486] There appears little reason for doubting that it
possesses the power of increasing the contractions of the uterus when
unnaturally languid; and consequently it has been employed, apparently
with frequent good effect, to hasten languid natural labour, to promote
the separation of the placenta, and to quicken the contraction of the
womb after delivery. These facts, however, are mentioned chiefly as
preparatory to the statement, that it has been also supposed to possess
the power of producing abortion, and has been actually employed for that
purpose in some foreign countries, and even in this city. Accurate
information is still much wanted on this subject. No other poison seems
so likely to possess a peculiar property of the kind. Nevertheless it is
the opinion of the best authorities, that spurred rye has no such power,
except in connexion with violent constitutional injury produced by
dangerous doses; and that it is endowed with the property only of
accelerating natural labour, not of inducing it, particularly in the
early months of pregnancy.

It seems from the experiments of Dr. Wright to have no power whatever of
inducing miscarriage in the lower animals.[2487] Notwithstanding the
improbability, however, of its possessing the property of bringing on
abortion, it is one of the substances at present occasionally employed
with the view of feloniously causing this accident. In a case of attempt
to procure abortion, which occurred not long ago in this city, one of
the articles repeatedly employed, but without success, was powder of
spurred rye,—as I had occasion to ascertain by chemical analysis.

_Of Spurred Maize._—It has been already observed, that many other plants
of the Natural Family of Grasses are subject to the ergot besides rye.
But the only other species in which the disease has been particularly
examined is Indian corn or maize [_Zea Mays_]. It appears from the
inquiries of M. Roullin that maize is very subject to the spur in the
provinces of Neyba and Maraquita in Colombia; that the spur forms a
black, pear-shaped body on the ear in place of the pickle; and that in
this state the grain, which is known by the name of _maïs peladero_,
possesses properties injurious to animal life. Its effects, however, are
somewhat different from those of spurred rye. Men who eat the ergotted
maize lose their hair and sometimes their teeth, but are never attacked
with dry gangrene or convulsions. When swine eat it, which after a time
they do with avidity, the bristles drop off, and the hind-legs become
feeble and wasted. Mules likewise lose their hair, and the hoofs swell.
Fowls lay their eggs without the shell. Apes and parrots, which frequent
the fields of spurred maize, fall down as if drunk; and the native dogs
and deer experience similar effects.[2488]


                        _Of the Rust of Wheat._

There are several other diseases to which grain is liable, and which are
much more common in this country than the ergot. But very little is
known of their effects on the animal body; which circumstance, since the
wheat of this and other countries often suffers from them, is probably
sufficient to show that their influence must be trifling, or at all
events very seldom called forth. Wheat is liable to three diseases. One
is a disease of the stalk and leaf rather than of the ear, and has the
effect of preventing the development of the ear or its pickles, and of
covering the plant with a brown powder. Of the two other diseases, which
both attack the pickles of the ear, one consists in the substitution of
a brown dry powder for the farina of the pickle, and the other of a
deposition of black moist matter in the fissure of the pickle, the
substance of which it also invades and partially destroys. One of these
is called in Scotland _brown rust_, the other _black rust_.

Of the three diseases the only one which is apt to infect the flour is
the black rust. The others, as they consist of a light dry powder, are
almost entirely separated in thrashing and winnowing the grain. But the
black rust being damp and adhesive, it is carried along with the
pickles. Such pickles are almost invariably separated by the farmer if
they are abundant; for otherwise, on account of the dark colour and
disagreeable odour of the matter deposited on them, the flour possesses
external qualities which would be at once recognized by a dealer of
ordinary experience.

It is not improbable, that a moderate impregnation of bread with the
powder formed by the diseases in question may take place, without
leading to any unpleasant effect on the human body. Experiments to this
effect were made by Parmentier with one of them, termed in France
_carie_, or caries of wheat, which from his description appears to be
the black rust of Scottish farmers. He gave two dogs each two drachms
daily of the powder for fifteen days, without remarking any sign of ill
health. Bread made with wheat flour containing a 64th of the powder,
when eaten by various people, and Parmentier among the rest, to the
amount of a pound daily for several days, caused slight headache and
pain in the stomach the first day only; and in larger proportion it had
as little effect.[2489]

It appears, then, that the introduction of any deleterious ingredient
into wheat bread is hardly to be dreaded from the common diseases to
which wheat is liable in this country.


                           _Of Unripe Grain._

Wheat and other grains have been supposed to acquire qualities
detrimental to health, from being cut down while unripe, or used
immediately after being cut down, although ripe. I am not aware that
accidents have ever been traced or even imputed to such causes in this
country; and, on the whole, I believe it is generally considered here,
that imperfect ripening of the pickle rather lessens the quantity, than
impairs the quality, of the flour. But several times epidemics have been
ascribed in France to unripe wheat. In 1801 M. Bouvier read a memoir to
the Society of Medicine at Paris, ascribing to new and unripe wheat an
epidemic dysentery, which laid waste several districts of the department
of the Oise in the autumn of 1793. These districts abound in small farms
of a few acres, on the produce of which the cultivators depend in great
measure for their subsistence. Hence in unfavourable seasons the corn
was commonly cut down before it was ripe, and made into bread soon after
being reaped. It was accordingly among the peasantry of these farms
only, and not among the agriculturists in large farms, which were under
better management, that the epidemic prevailed. Bouvier remarks, that at
all times when the long continuance of wet weather has compelled the
inhabitants of a district to cut down the wheat before it is ripe, or a
previous dearth has forced them to use it when newly cut, epidemic
disorders of the bowels have been observed to rage in the latter months
of autumn. And as an instance of this he refers to the year 1783, when
the crops around Paris were believed to have been injured by the
extraordinary prevalence of fogs, and were cut down unripe and used
immediately. Various epidemics broke out in the metropolis, and still
more in the surrounding country.[2490] This is an important subject for
farther inquiry; but at present I cannot help thinking that M. Bouvier
exaggerates the effects of the immaturity of the grain. At all events,
the grain is often cut down in an unripe state in various districts of
this country; and I have never heard that any epidemic diseases were
produced. When M. Bouvier witnessed the epidemic of 1793 in the
department of the Oise, he instructed the inhabitants of his own parish
to dry the unripe corn before thrashing it, to repeat the process before
the grain was converted into flour, and to mix with the flour a larger
quantity than usual of yeast in making it into bread; and he states that
in the succeeding year, which was even more unfavourable to the crops,
they were enabled, by following these directions, to use unripe corn
with safety.


                          _Of Spoiled Bread._

This is the fittest opportunity for noticing certain injurious effects
sometimes observed from the use of spoiled or mouldy bread. On the
continent repeated instances have occurred of severe and even dangerous
poisoning from spoiled rye-bread, barley-bread, and even wheat bread.
Several instances have been observed of horses having been killed in a
short space of time with symptoms of irritant poisoning after eating
such bread with their ordinary food.[2491] And Ur. Westerhoff has given
an account of its effects on two children and several adults. In
children the symptoms were redness of the features, dry tongue, frequent
weak pulse, violent colic pains, urgent thirst and headache, and
subsequently vomiting and diarrhœa, alternating with great exhaustion
and sleepiness. The bread in these instances was made of rye.[2492] It
appears that in bread so spoiled a variety of mucedinous vegetables are
developed, especially the _Penicillium glaucum_ and _P. roseum_; and it
is imagined by some, that this circumstance may account for the
deleterious effect of the bread.[2493]


                   _Of the Effects of Darnel-Grass._

Grain is also rendered more or less injurious by the accidental or
intentional admixture of a variety of foreign substances, by which, in
common speech, it is said to be adulterated. The subject of the
adulteration of grain is a very important topic in medical police. But
as this practice seldom imparts to the grain qualities decidedly
poisonous, the consideration of it would be misplaced here. One variety,
however, the accidental adulteration of flour with the seeds of the
_Lolium temulentum_ or darnel-grass calls for some notice; for it may
occasion not only symptoms of poisoning, but even also death itself.

This is the only poisonous species of the natural order of the grasses.
The seeds appear to be powerfully narcotic, and at the same time to
possess acrid properties. Seeger gave a dog three ounces of a decoction
of the flour, and observed that it was seized in five hours with violent
trembling and great feebleness, which were succeeded in four hours by
sopor and insensibility; but it recovered next day.[2494]

When mixed with bread and taken habitually by man, darnel-grass has been
known to cause headache, giddiness, somnolency, delirium, convulsions,
paralysis, and even death. M. Cordier found by experiment on himself,
that very soon after eating bread containing darnel-grass flour, he felt
confusion of sight and ideas, languor, heaviness, and alternate attacks
of somnolency and vomiting. The bread was commonly vomited soon after he
ate it.[2495] Seeger has related some cases in which the somnolency was
much more deep; and states that general tremors are almost always
present.[2496] A few years ago almost the whole inmates of the Poor’s
House at Sheffield, to the amount of eighty, were attacked with
analogous symptoms after breakfasting on oatmeal porridge; and it was
supposed that the meal had been accidentally adulterated with the
lolium. The chief symptoms were a piercing stare, violent agitation of
the limbs, quivering of the lips, frontal headache, confusion of sight,
dilated pupil, small tremulous pulse, twitches of the muscles, and
palpitation. In twelve hours all of the persons attacked were well but
two, who had strong convulsions in the subsequent night, but also
eventually recovered.[2497] A similar accident is mentioned by Perleb,
as having happened at Freyburg in the House of Correction. The inmates,
soon after eating bread made with new flour, were attacked to the number
of forty, with loss of speech and somnolency; and for some days
afterwards they complained of sickness.[2498] The accident was ascribed
to darnel-grass. In a recent instance which happened in the workhouse of
Beninghausen, and which was traced to the lolium, seventy-four people
were attacked with giddiness, tremor, convulsions, and vomiting. Those
who had led a dissipated life suffered most, and children least of
all.[2499]

Sometimes this poison appears to excite symptoms of intestinal
irritation, without acting as a narcotic. A small farmer near Poicters
in France saved five bushels of the seed from a field of wheat,—had it
ground with a single bushel of wheat, and afterwards made bread with the
mixture for his own family. He himself, with his wife and a servant,
began to eat the bread on a Thursday; but the two last were so violently
affected with vomiting and purging, that they refused to continue taking
it. He persevered himself, however, till on the Sunday evening he became
so ill that his wife wished to send for medical aid. This he refused to
allow, and next day he expired after suffering severely from fits of
colic.[2500]

Bley of Bemburg has examined chemically the grain of lolium. He obtained
from it a bitter extractive matter, without any characteristic chemical
properties, but which killed a pigeon. The seed has a very feeble
bitterish taste. Bley maintains that its poisonous properties are
essential to it, and not incidental, as some think.[2501]


        _Of the Effects of certain Poisonous Leguminous Seeds._

Among the injurious substances with which various grains are apt to be
accidentally mixed from their growing together, two leguminous plants
may be here shortly mentioned, as they have often been the source of
disagreeable accidents on the continent.

In the department of the Cher and Loire in France, severe effects have
been traced to bread made partly with flour of the _Lathyrus cicera_. M.
Desparanches, in a report to the Prefect of the Department, says this
flour occasionally forms one-half of that of which bread is made in some
parishes; that it produces sometimes sudden incapability of walking,
sometimes imperfect paraplegia and pain, with a draggling gait and
turning in of the toes, and sometimes also slight convulsive movements
of the thighs and legs.[2502] Similar effects have been traced to this
substance formerly. Virey says it has been known to produce in
particular a singular stiffness and state of semiflexion of the
knee-joint, compelling the individual to move the limbs in one rigid
mass.[2503]

The _Ervum ervilia_, or Bitter-vetch, which is not a native of this
country, has also been found in France to possess analogous properties.
In 1815, according to Virey, a great variety of herbs grew up with the
grain, in consequence of the wetness of the summer; and their seeds were
thus subsequently mixed with the wheat and rye. Among these he
particularizes the bitter-vetch as peculiarly noxious, because it
produces so great weakness of the extremities, but especially of the
limbs, that the individual trembles while standing, and totters when he
walks, or even requires the help of stilts; and he adds, that horses are
similarly affected, so as to become almost paralytic.[2504]

The _Cytisus laburnum_, or laburnum tree, is another plant of the same
family, which yields poisonous seeds. The whole plant is more or less
deleterious. But it is chiefly the seed that has attracted attention
hitherto.

I am not acquainted with any experiments relative to the action of the
seeds on animals.—Its effects on man present considerable variety, and
show that it is a true narcotico-acrid. In some instances they seem to
have been purely narcotic. My colleague Dr. Traill has communicated to
me two cases of this nature. In one of these, that of a child two years
old, the first evident effects were sudden paleness and a fit of
screaming, followed immediately by insensibility, and then by coldness
of the whole body and lividity of the face; but vomiting having been
induced by warm water and mustard, the seeds were discharged, the
symptoms abated, and next day he was quite well. The other case was that
of a boy who was left by his companions at Dr. Traill’s door in a state
of complete insensibility, with froth at the mouth and a feeble pulse.
An emetic, administered immediately, brought up a large quantity of
laburnum seeds; after which the pulse became firmer, and sensibility
quickly returned.—Mr. North has briefly noticed a similar case of a
child, who after eating laburnum flowers, was seized with paleness and
twitches of the face, coldness of the skin, laborious breathing, efforts
to vomit, and great feebleness of the pulse. But recovery took place
after the flowers were vomited.[2505]—In other instances the effects
have been chiefly limited to an irritant action on the stomach and
bowels. Dr. Bigsby of Newark informs me that a few years ago a little
girl in his neighbourhood, in consequence of eating the seeds, was
attacked with violent vomiting and purging, and became in other respects
very ill, but recovered in forty-eight hours.—Most generally, however,
the effects are partly irritant, partly narcotic. In 1839 Dr. Annan of
Kinross communicated to me the case of a little boy, who in an hour
after swallowing a small quantity of unripe seeds, was attacked with
violent vomiting and ghastly expression of countenance, and then fell
into a very drowsy state, from which he was constantly roused by shaking
him and dashing cold water on his body. But for a month afterwards he
continued subject to vomiting and diarrhœa.—Mr. Bonney of Brentford has
related the particulars of eleven cases, which presented all the
varieties of poisoning with the seeds. The subjects were children from
seven to nine years of age; and they took, some of them one seed, and
none more than five. Three scarcely suffered at all. One vomited the
poison and got well at once. Of the others, some had only nausea and
feebleness of the pulse, another had also dilatation of the pupils, some
had vomiting and purging, others great drowsiness, others again both
sets of symptoms. In all the pulse was weak and generally rapid.
Emetics, laxatives and ammonia were administered with success.[2506]

The leaves of this plant are stated by Vicat, a good authority, to
possess the property of acting violently as an emetic and
purgative;[2507] and Cadet says the unripe pods have been known to
produce in small quantities severe vomiting, and profuse, protracted
diarrhœa.[2508]

My attention was lately turned by a criminal trial in this country to
the effects of the bark, which is not alluded to as a poison by any
author, although its properties seem well known to the peasantry in the
north of Scotland. A lad Gordon was tried lately at Inverness for
administering poison to a fellow-servant, and it was proved that he gave
her laburnum-bark in broth. She immediately became very sick, and was
soon attacked with incessant vomiting and purging, pain in the belly,
rigor, and extreme feebleness; and several days elapsed before she could
return to her work. The sickness, vomiting, purging and pain continued
afterwards to recur more or less; great emaciation ensued; in six weeks
she was so much reduced as to be compelled to quit service; and even six
months afterwards, she continued so ill with a chronic dysenteric
affection, that fears were entertained for her life, although eventually
she did recover. Being consulted in the case, I was inclined to rely in
the general properties of the plant and the peculiar, intense, nauseous
bitterness of the bark, even more intense there than in the seeds, as
adequate proof that the bark was capable of producing the effects
observed in this case. I was scarcely prepared, however, to find it so
deadly a narcotic poison, as it proved to be on careful experiment. Dr.
Ross of Dornoch, who saw the woman and was also consulted on the part of
the crown in the case, found that from twenty to seventy grains of dried
laburnum-bark caused speedy and violent vomiting when administered to
dogs, but no other marked effect. I found that when an infusion of a
drachm of dried bark was injected into the stomach of a strong rabbit,
the animal in two minutes began to look quickly from side to side, as if
alarmed and uncertain in which direction to go, then twitched back its
head two or three times, and instantly fell on its side in violent
tetanic convulsions, with alternating opisthotonos and emprosthotonos so
energetic that its body bounded with great force upon the side up and
down the room. Suddenly in half a minute more all motion ceased,
respiration was at an end, and, excepting that the heart continued for a
little to contract with some force, life was extinct. No morbid
appearance was visible anywhere. The heart was gorged, but irritable.
Dr. Ross subsequently repeated this experiment, and obtained analogous
results; but the animals he operated on did not die for half an hour or
upwards.[2509]

MM. Chevallier and Lassaigne have discovered in the seeds an active
principle called cytisin, a nauseous, bitter, brownish-yellow, neutral,
uncrystallizable substance, of which small doses killed various animals
amidst vomiting and convulsions, and eight grains taken by man in four
doses brought on giddiness, violent spasms, and frequency of the pulse,
lasting for two hours, and followed by exhaustion.[2510]

A great number of Brown’s division Papilionaceæ of the present natural
family probably possess similar properties.




                              CHAPTER XLI.
        OF POISONING WITH ALCOHOL, ETHER, AND EMPYREUMATIC OILS.


The last group of the narcotico-acrids comprehends _alcohol_, _ether_,
and the _oleaginous products of combustion_.


                      _Of Poisoning with Alcohol._

_Of its Action on Animals, and Symptoms in Man._—Alcohol has been
generally believed, since the experiments of Sir B. Brodie,[2511] to act
on the brain through the medium of the nerves, and to do so without
entering the blood. This may be doubted. At least in some experiments
performed several years ago by Dr. C. Coindet and myself it appeared not
to act so swiftly, but that absorption might easily have taken place
before its operation began. At all events, through whatever channel it
may operate, there is no doubt that it enters the blood; for in man the
breath has a strong smell of spirit for a considerable time after it is
swallowed; and it has been found in the tissues and secretions after
death from large doses. Professor Orfila found that alcohol is a violent
poison when injected into the cellular tissue; and that it produces
through that channel the same effects as when taken into the
stomach.[2512] In the course of our experiments Dr. C. Coindet and I
found that it acted with great rapidity when injected into the cavity of
the chest.

Authors who have treated of the action of alcohol and spirituous liquors
on man, have distinguished three degrees in its immediate effects.

1. When the dose is small, much excitement and little subsequent
depression are produced.

2. When the effect is sufficiently great to receive the designation of
poisoning, the symptoms are more violent excitement, flushed face,
giddiness, confusion of thought, delirium, and various mental
affections, varying with individual character, and too familiar to
require description here. These symptoms are soon followed by dozing and
gradually increasing somnolency, which may at length become so deep as
not to be always easily broken. After the state of somnolency has
continued several hours, it ceases gradually, but is followed by
giddiness, weakness stupidity, headache, sickness, and vomiting.

This degree of injury from alcohol may prove fatal, either in itself, by
the coma becoming deeper and deeper,—or from the previous excited state
of the circulation causing diseases of the brain in a predisposed
habit,—or more frequently from the occurrence of some trifling accident,
which in his torpid state the individual cannot avoid or remedy, such as
exposure to cold, falling with the face in mud or water, suffocation
from vomited matters getting into the windpipe, and the like.

Of simple poisoning by the gradual increase of coma the following
judicial case in which I was consulted is a characteristic example. Two
brothers drank in half an hour three bottles of porter, with which three
half-mutchkins (24 ounces) of whisky had been secretly mixed by a
companion, whose object was to fill them drunk by way of joke. In the
course of drinking both became confused. In fifteen minutes after
finishing the last bottle one of them fell down insensible, and had no
recollection of what happened for twelve hours; but he recovered. The
other staggered a considerable distance for an hour, and then became
quite insensible and unable to stand. In four hours more consciousness
and sensibility were quite extinct, the breathing stertorous and
irregular, the pulse 80 and feeble, the pupils dilated and not
contractile, and deglutition impossible. In this state he remained
without any material change till his death, which took place in fifteen
hours after he finished his debauch. A surgeon saw him when he had been
five hours ill, but did little for his relief, as the case appeared
hopeless.

There is a singular variety in the principal symptoms of this form of
poisoning, even when completely formed. From a careful tabular analysis
of no fewer than twenty-six cases, chiefly of the present denomination,
collected by Dr. Ogston of Aberdeen from the experience of the
police-office there, it appears that when the stage of stupor is fully
formed, the person is sometimes capable of being roused, sometimes
immovably comatose for a long time,—that the pulse is sometimes
imperceptible or very feeble, sometimes distinct or even full, generally
slow or natural, seldom frequent, very seldom firm,—that the pupils are
occasionally contracted, much more generally dilated, and in a few
instances alternating between one state and the other,—that the
countenance is commonly pale, sometimes turgid and flushed,—and that the
breathing is for the most part slow, and also soft, yet not unfrequently
laborious, but very rarely stertorous. Convulsions are rare, having been
observed twice only, and on both occasions in young people of the age of
twelve or fourteen.[2513] Dr. Ogston has tried to group these several
symptoms together in classified cases; but the general conclusions at
which he arrives are subject to important exceptions. Neither do any of
the special symptoms seem to bear a marked relation to the ultimate
event. It is peculiarly worthy of remark, that very many cases got well
where the pupils were much dilated, the coma profound, and the pulse
imperceptible.

In the present form of poisoning with alcoholic fluids, it usually
happens that if the stage of stupor be completely overcome, recovery
speedily ensues, without any particular symptom except headache,
giddiness, sickness, and the customary consequences of a debauch. Hut on
some occasions the comatose stage is succeeded by one which indicates
much cerebral excitement,—by flushed face, injected eyes, restlessness,
a febrile state of the pulse, and delirium, even of the violent kind. In
other cases this affection puts on very much the characters of a slight
attack of typhoid fever.

In the second variety of the second degree of intoxication, an
apoplectic disposition is called into action by the excited state of the
circulating system; and death ensues from apoplexy or some other disease
of the brain, rather than from simple poisoning. Thus in some instances,
as will be more fully mentioned under the head of the morbid
appearances, extravasation of blood is found within the head after
death, preceded by the usual phenomena of ordinary intoxication. Since
this is a rare effect of intoxication, it must be considered as the
result of poisoning with spirits, exciting sanguineous apoplexy in a
predisposed constitution. In other cases the stupor of intoxication,
after putting on all the characters of apoplexy for two days and
upwards, terminates fatally without extravasation. Here the poison
operates by developing a constitutional tendency to congestive apoplexy.
Again, this mode of action is still more clearly shown in some cases,
where an interval of returning health occurs between the immediate
narcotic effects of the poison and the ultimate apoplectic coma which is
the occasion of death. Such a course of events, which, however, is of
rare occurrence, is well exemplified in the following cases. A man drank
32 ounces of rum one afternoon, and was comatose most of the ensuing
night. Next morning, though very drowsy, he was sensible when roused;
and in the evening he was considered convalescent. But two days
afterwards he became delirious; in two days more he died comatose; and
congestion was the only appearance found in the brain.[2514] Another
instance, most remarkable in its circumstances, is the following, which
has been related by Dr. Golding Bird. A workman in a distillery, after
drinking eight ounces of rectified spirit by mistake for water, suddenly
fell down senseless and motionless, and remained so for eleven hours. He
then began to recover, and came round so far that he returned to his
work next morning. After this he continued to pass dark, pitch-like
evacuations. In three weeks he became drowsy, mistook one thing for
another, answered questions sluggishly, and had a frequent pulse, and
dilated sluggish pupils; in which state he continued three weeks later
when the account was published.[2515] The following case, related by Dr.
Chowne, also seems to belong to the same category, although it presents
anomalies. A boy, eight years of age, soon after swallowing about eight
ounces of gin, said he felt like a drunk man, and suddenly became
motionless and insensible. In no long time he vomited a fluid of the
odour of gin; and in seven hours from the commencement a fluid was
withdrawn from the stomach, possessing no longer any such odour. He was
now motionless, insensible, pale, and cold; the pupils were contracted,
the pulse feeble and hurried, the breathing stertorous and slow; and he
made ineffectual efforts to vomit. Stimulants of all kind had little
effect on him for a day and a half, when the breathing became more
natural, and his look quite intelligent. Yet he could not answer
questions, exhibited no sign of volition, and had a pulse so frequent as
160. In twenty-four hours more the breathing became laborious and
rattling, and the lips livid; and death took place near the close of the
third day. The only appearances of any note in the dead body were
general injection of the arachnoid membrane of the brain, and effusion
of frothy mucus into the bronchial ramifications.[2516] Similar to these
is the following extraordinary case which has been communicated to me by
Dr. Traill. A boy seven years of age, who was persuaded by two
miscreants to take nearly five ounces of undiluted whisky, suffered for
two days from the ordinary symptoms of excessive intoxication, which
were then immediately followed by epileptic convulsions. These continued
to recur with more or less violence, but always frequently, for two
months down to the date of the judicial investigation to which the case
gave rise. All these forms of the effects of drinking ardent spirits can
scarcely be considered as simple poisoning, but as the result of
poisoning developing a tendency to diseases of the head.

The third variety of poisoning with spirits in the second degree proves
fatal, not in itself, but by some trivial accident happening, from which
the individual cannot escape on account of his powerless insensibility.
Thus, it is no uncommon thing for persons in a state of deep
intoxication to fall down in an exposed place, where they perish from
cold, or to tumble with the face in a puddle, and so be suffocated, or
to be choked by inhaling the contents of the stomach imperfectly
vomited, or by lying in such a posture that their neck-cloth produces
strangulation. These statements are so familiar, that it is unnecessary
to illustrate them by special facts. The reader’s attention was called
to such accidents in the previous editions of this work. Two well-marked
cases of the kind have been since published by Mr. Skae.[2517]

In cases of simple poisoning in the second degree the progress of the
symptoms is on the whole remarkably uniform, gradual and uninterrupted.
But there are likewise some anomalies which it may be well to notice.
Thus, occasionally after the phenomena of ordinary intoxication have
gone on gradually increasing without having attained a very great
height, sudden lethargy supervenes at once, and may prove fatal with
singular rapidity. My colleague, Dr. Alison, has communicated to me the
particulars of a case of the kind where death took place from simple
intoxication, twenty minutes after the state of lethargy began. The
individual reached his home in a state of reeling drunkenness, but able
to speak and give an indistinct account of himself. He then became
lethargic, and died in the course of twenty minutes. On examining the
body, Dr. Alison could not discover any morbid appearance, except some
watery effusion on the surface of the brain and in the ventricles; but
the contents of the stomach had a strong smell of spirits. Instances of
such excessive rapidity, however, are rare, unless from the third form
of poisoning.—An anomaly of a different kind, of which a remarkable
example was brought judicially under my notice, is sudden supervention
of deep insurmountable stupor, without the usual precursory symptoms,
yet not till after a considerable interval subsequently to drinking. In
May, 1830, a lad of sixteen, in consequence of a bet with a
spirit-dealer, swallowed sixteen ounces of whisky in the course of ten
minutes, and, pursuant to the terms of the wager, walked up and down the
room for half an hour. He then went into the open air, apparently not at
all the worse for his feat; but in a very few minutes, while in the act
of putting his hand into his pocket to take out some money, he became so
suddenly senseless as to forget to withdraw his hand, and so insensible
that his companions could not rouse him. A surgeon, who was immediately
procured, contented himself with giving several clysters and a dose of
tartar-emetic, which did not operate; and the young man died in the
course of sixteen hours. The cause of the retardation of the symptoms
was partly perhaps that he had taken supper only an hour before drinking
the spirits, but chiefly, I presume, because the stupor was kept off for
a time by the stimulus of determination to win his bet.—Several cases
somewhat similar have been described by Dr. Ogston. In these sudden
insensibility came on while the individuals had been drinking freely for
some time, without showing any marked sign of approaching
intoxication.[2518] The cause of the postponement and sudden invasion of
the stupor does not exactly appear; but a familiar cause of its abrupt
invasion in ordinary cases of drunkenness is sudden exposure to cold.

It is impossible to fix the extremes of duration of the present form of
poisoning in fatal cases. For, on the one hand, one or other of the
accidents mentioned above may bring the case to a speedy close; and, on
the other hand, the supervention of apoplexy may protract it to several
days. The ordinary duration in fatal cases seems to be from twelve to
eighteen hours.

3. The third degree of poisoning is not so often witnessed, because, in
order to produce it, a greater quantity of spirits must be swallowed
pure and at once, than is usually taken by those among whom poisoning in
the second degree chiefly occurs. When swallowed in large quantity, as
by persons who have taken foolish wagers on their prowess in drinking,
there is seldom much preliminary excitement; coma approaches in a few
minutes and soon becomes profound, as in apoplexy. The face is then
sometimes livid, more generally ghastly pale; the breathing stertorous,
and of a spirituous odour; the pupils sometimes much contracted, more
commonly dilated and insensible; and if relief is not speedily procured,
death takes place,—generally in a few hours, and sometimes immediately.
According to Mr. Bedingfield, who witnessed many cases of poisoning with
rum at Liverpool, which always follow the arrival of the West India
vessels, the patient will recover if the iris remains contractile; but
if it is dilated and motionless on the approach of a light, recovery is
very improbable.[2519]

A case is briefly alluded to by Orfila of a soldier, who drank eight
pints of brandy for a wager, and died instantly.[2520] A case of the
same kind is quoted by Professor Marx.[2521] Another, which happened in
the person of a London cabman, is noticed in a French Journal. The man,
for a bribe of five shillings, drank at a draught a whole bottle of gin;
and in a few minutes he dropped down dead.[2522] Similar accidents occur
not infrequently in this country; but I have not met with any fully
described by authors. A case of the less rapid variety of the present
form occurred at the Infirmary here in 1820. A man stole a bottle of
whiskey; and, being in danger of detection, took what he thought the
surest way of concealing it, by drinking it all. He died in four hours
with symptoms of pure coma.

Convulsions are not common in such cases. I have seen a remarkable
example, however, in which the coma was accompanied with constant
alternating _opisthotonos_ and _emprosthotonos_. The subject was a boy
who had been induced to drink raw whisky by an acquaintance, and had
been two hours insensible before I saw him. The stomach-pump, which was
immediately applied, brought away a large quantity of fluid with a
strong spirituous odour; and he recovered his senses in fifteen minutes,
but remained very drowsy for the rest of the day.

Such are the forms of poisoning with spirits usually admitted by
authors. But it also appears to act sometimes as an irritant. After its
ordinary narcotic action passes off, another set of symptoms
occasionally appear, which indicate inflammation of the alimentary
canal. Cases of this kind are exceedingly rare; yet they have been met
with, as the following extract shows. “A young man at Paris had been
drinking brandy immoderately for several successive days, when at length
he was attacked with shivering, nausea, feverishness, pain in the
stomach, vomiting of everything he swallowed except cold water, thirst,
and at last hiccup, delirium, jaundice, and convulsions; and death took
place on the ninth day. On examining the body the stomach was found
gangrenous over the whole villous coat; the colon too was much inflamed;
and all the small intestines were red.”[2523]

A case of great complexity, but probably of the same nature, has been
related by Opitz in Pyl’s Memoirs. The subject was a woman liable to
epilepsy, and addicted to excessive drinking. After one of her
drinking-bouts she was seized with vomiting and severe pain of the
bowels, afterwards with delirium, then with convulsions, and she died in
twenty-four hours after the first attack. The stomach and intestines
were greatly inflamed, a table-spoonful of blood was effused into the
ventricles of the brain, and the left lung was purulent.[2524]

Besides the immediately fatal effects of spirituous liquors now
described, there is still another variety of poisoning more common than
any yet mentioned, and constituting a peculiar disease. People who fall
into the unhappy vice of habitual intoxication, after remaining in a
state of drunkenness for several days together, are often attacked with
a singular maniacal affection, which is accompanied with tremors,
particularly of the hands, and after enduring for several days, ends at
last in coma. When the delirium is not so violent, the disease by proper
treatment may be cured. But frequently, after the delirium and tremor
have continued mildly for some time, they increase, and the delirium
becomes furious, or coma rapidly supervenes; in either of which cases
the disorder commonly proves fatal in two or three days more. This
disease, which is now familiar to the physician, is called _delirium
tremens_. It is supposed by some to depend on inflammation of the
membranes of the brain, followed by effusion.

Other diseases, besides _delirium tremens_, are also slowly induced by
the habitual and excessive use of spirituous liquors; but in general
the habit of intoxication acts in inducing these diseases only as a
predisposing cause. A particular variety of tuberculated liver
probably arises from the habitual use of spirits without the
co-operation of other causes. That variety of disease of the kidney,
which was first brought under the notice of the profession by Dr.
Bright,[2525] is also obviously often connected with the habit of
drinking spirits. The following have been enumerated among the
diseases where the same habit acts powerfully as a predisposing
cause—indurated pancreas,—indurated mesenteric glands,—scirrhous
pylorus,—catarrh of the bladder,—inflammation, suppuration and
induration of the kidneys,—incontinence of urine,—aneurism of the
heart and great vessels,—apoplexy of the lungs,—varicose
veins,—mania,—epilepsy,—tendency to gangrene of wounds,—spontaneous
combustion.[2526]

_Of the Morbid Appearances._—Some doubts exist as to the morbid
appearances in the bodies of those poisoned by spirituous liquors.

In animals killed by alcohol, Orfila says he found the villous coat of
the stomach constantly of a cherry-red odour. I have several times
remarked the same appearance. When the stomach was empty before the
alcohol was introduced, I have always found the prominent part of its
rugæ of a deep cherry-red tint, the margin of the patches being more
florid, and evidently consisting of a minute network of vessels.

In man these signs of irritation have not been always observed. In the
patient who died in the Infirmary here, the stomach was quite natural to
appearance. Dr. Ogston notices injection of the small intestines and
thickening of the mucous membrane of the stomach and intestines as
common appearances in the cases he has examined; but he seems to
consider these the effects not of the last fatal dose, but of the habit
of frequent excessive drinking.[2527]

The blood in the heart and great vessels is commonly fluid and very
dark, and the lungs are sometimes more or less gorged with the same
fluid.

The state of the brain differs much according to the mode of death.
Sometimes great congestion and even actual extravasation of blood are
found in the heads of persons who have died of excessive continuous
drinking,—the excitement of such a debauch being apt, as already
mentioned, to induce apoplexy in a predisposed habit. Accordingly
extravasation was found by Professor Bernt of Vienna in no less than
four cases of the kind, two of which happened in the persons of young
men not above twenty-two years of age;[2528] and Dr. Cooke quotes
another in his work on nervous diseases.[2529] I have myself met with
another remarkable instance. A female out-pensioner of Trinity Hospital
here, who was much addicted to drinking, and for fourteen days after the
New-year of 1830 had been very little in her sober senses, soon after
arriving at home one evening much intoxicated, fell down comatose, and
died in ten or twelve hours. An enormous extravasation of clotted blood
was found in the ventricles, producing extensive laceration of the right
middle and anterior lobes of the brain.—In such cases it is natural to
suppose that a predisposition to apoplexy must concur with the
intoxication; otherwise it is not easy to see why death from
extravasation is not more frequently produced by excessive drinking.

Extravasation is not apt to occur in the cases of rapid death brought on
by a very large quantity swallowed at once. The circulation, indeed, is
during life in a state quite the reverse of excitement; and accordingly
the brain and its membranes are found quite healthy. They were
particularly so in the man who died in the hospital here. It is right to
mention, however, that one of Bernt’s cases, although the symptoms and
other particulars are not mentioned, possibly belongs to the present
variety, as the man swallowed for a wager a quart of brandy at a
draught.[2530] According to Dr. Ogston, who has given the best account
of the appearances within the head in the ordinary cases of this kind,
there is usually serous effusion under the arachnoid membrane,
occasionally minute injection of vessels, commonly more or less general
gorging of the larger veins, and especially effusion of serosity to the
amount of two or even four ounces in the ventricles.[2531]

When delirium tremens proves fatal, effusion is commonly found among the
membranes of the brain; and occasionally to a great extent. In one
instance, which proved fatal in two or three days, I have seen minute
vascularity of the membranes, with effusion of fibrin, and without
effusion of serosity; but such cases are rare. There is also, according
to Andral, very extensive softening of the mucous coat of the
stomach.[2532] In an instance mentioned in Rust’s Journal, besides
effusion into the cerebral membranes, there was found an enormous
accumulation of fat in all the cavities, a conversion of the muscular
substance into fat, and a nauseous sweet smell from the whole
body.[2533]

In all cases of rapid poisoning with spirituous liquors some of the
poison will be found in the stomach. For when the case is one of pure
narcotic poisoning, unaided by the effects of blows, exposure to cold,
or the like, and the person dies in a few hours, the poison cannot be
all absorbed before death.—Although the spirituous liquors used in
Britain have all very powerful odours, the inspector in a case of
importance ought not to confine himself to this test alone. He must
subject the suspected matter to distillation; and then remove the water
from what distils over by repeated agitation with dry carbonate of
potass, till he procures the alcohol of the spirit in such a state of
purity as to be inflammable.

Alcohol may also be in some circumstances detected in the tissues and
secretions of the body. A spirituous odour has been remarked not
infrequently in various parts, and especially in the brain. Dr. Cooke
mentions a case in which the fluid in the ventricles of the brain had
the smell and taste of gin, the liquor which had been taken;[2534] Dr.
Ogston adverts to an instance, in which after death by drowning during
intoxication, he found in the ventricles nearly four ounces of fluid,
having a strong odour of whisky;[2535] in the case which occurred in the
hospital here the odour of whisky was said to have been perceived in the
pericardium; and in a man who died of long-continued intoxication from
immoderate drinking Dr. Wolffe found that the surface, and still more
the ventricles, of the brain had a strong smell of brandy, although the
contents of the stomach had not.[2536]

The presumption afforded by such facts as these, in favour of the
absorption of alcohol and the possibility of detecting it throughout the
animal system, has been turned to certainty by the late experimental
researches of Dr. Percy; who found that in animals poisoned with
alcoholic fluids, as well as in the case of a man who died during the
night after drinking a bottle of rum, alcohol could be detected,
generally in the urine, and also in the brain, by cautious distillation,
and removing the water from the distilled fluid by means of dry
carbonate of potass.[2537] Dr. Percy gave me an opportunity of verifying
his results with the brain of the man; and I had no difficulty in
obtaining from a few ounces of brain a sufficiency of spirit to exhibit
its combustion on asbestus repeatedly.

It is hardly necessary to add, that when the individual has survived the
taking of the poison a considerable length of time, an odour of spirits
will not be perceived either in the stomach or elsewhere. In the
out-pensioner of Trinity Hospital, for example, who survived about
twelve hours, no spirituous odour could any where be perceived. In such
cases the poison disappears during life by absorption.—A question may
even be entertained, whether the odour may not sometimes be
imperceptible at the inspection of the body, although the poison was
really present immediately after death. It is probable that, as in the
instance of hydrocyanic acid, the alcohol, on account of its volatility
or fluidity, will evaporate or percolate away in a few days. In this
manner only can be explained the occasional absence of the odour in
persons who have been killed in the early stage of drunkenness. I could
not perceive any odour of whisky in the stomach of the woman Campbell,
who was murdered by the notorious resurrectionist Burke, although she
had drunk spirits to intoxication half an hour before her death. The
body was not examined till thirty-eight hours after.[2538] It must be
observed, however, that alcohol may exist in the contents of the stomach
and be detected by chemical analysis, although it is not indicated by
its odour. I have twice had occasion to observe this, where the bodies
were disinterred some time after death.

From all that has been said, there ought seldom to be much difficulty in
recognizing a case of poisoning with spirituous liquors.

But, before quitting the subject, a form of it must be noticed which may
be extremely difficult to distinguish. It was formerly remarked that the
eatable mushrooms have been sometimes poisoned with substances
possessing effects on the system analogous to those caused by the
deleterious fungi. In the same manner spirituous liquors may be poisoned
with narcotics allied to them in action. Thus, in former parts of this
work, it has been stated that a young man was killed during a debauch in
consequence of his companions having mingled opium with his wine; that
many persons have been poisoned and some killed by fermented liquors
drugged in the same manner; that murder has been accomplished by
poisoning wine with nightshade; and that several fatal accidents have
occurred in consequence of liqueurs having been too strongly impregnated
with hydrocyanic acid, to give them a ratafia flavour. Cases of this
nature may be embarrassing. In general, they may be made out by
attending strictly to the symptoms, the quantity of liquor taken, and
the contents of the stomach. But, it must be admitted, that if a
murderer, who chooses such a method, should season his guest’s drink
judiciously, and ply him well with it, a medical jurist might be puzzled
to determine whether the liquor was to blame in point of quality or
quantity.

_Of the Treatment._—The treatment of poisoning with alcoholic fluids
does not differ essentially from that of poisoning with opium. In the
former, as in the latter, the chief objects must be to remove the poison
from the stomach, and to rouse the patient from his state of stupor; but
in poisoning with alcoholic fluids it is also frequently necessary to
treat a secondary stage of reaction by local and even general
antiphlogistic measures. As to the primary object, the removal of the
poison from the stomach, it appears that in the present form of
poisoning emetics are more seldom effectual than in the case of other
narcotics, and that the stomach-pump should be promptly resorted to. It
is remarkable that the operation of clearing out the stomach is likewise
often a sufficient stimulus to dispel stupor immediately and even
permanently. I have seen almost complete consciousness permanently
restored with the discharge of the alcoholic fluid; and the same remark
has been made by others. Where the senses are not thus restored, one of
the most effectual stimulants, according to the practice of the
police-office of this city, is the injection of water into the ears.
Great advantage has been derived, as in poisoning with opium, from the
cold affusion applied to the head. Dr. Ogston, who has appended to his
paper formerly quoted a very useful summary of the treatment of
poisoning with spirits, has found this a safe and effectual remedy where
the heat of the head was unnaturally great and that of the body not too
low.[2539] Cases have been published where it proved successful although
the pulse was gone at the wrist, the breathing scarcely perceptible, and
the temperature of the whole body greatly reduced.[2540] It is doubtless
a powerful remedy: but where the general temperature of the surface is
much lowered, I conceive it should be restricted to the head and neck,
and conjoined with the application of warmth to the body. Dr. Ogston
objects to the general use of blood-letting in cases of poisoning with
spirits, as being often apt to be followed by sudden sinking. Where
other remedies are judiciously used, it is probably seldom called for;
and the purpose it is intended to serve, namely, the relief of cerebral
congestion and determination, is better fulfilled by the local
employment of cold, and local blood-letting. Ammonia and its acetate
have been found useful as internal stimulants where the stupor is deep.
The treatment of the secondary affections adverted to above does not
require specific mention.


            _Of Poisoning with Sulphuric and Nitric Ether._

Sulphuric ether and nitric ether are poisons of the same nature with
alcohol. But the effects produced by them when taken in considerable
doses are not very well known.

Orfila found that half an ounce of sulphuric ether introduced into the
stomach of a dog and secured there by a ligature on the gullet, excited
efforts to vomit, in ten minutes inability to stand, and in six minutes
more, insensibility. In fifteen minutes more the animal revived a
little, but soon became again comatose; and it died in three hours after
the commencement of the experiment. The villous coat of the stomach was
reddish-black, the other coats of a lively red colour.[2541]

The effects of the ethers on man have not been accurately ascertained.
From some observations published in the Journal of Science, sulphuric
ether appears to act energetically even in small doses. In moderate
quantity it produces a strong sense of irritation in the throat, a
feeling of fulness in the head, and other symptoms like those excited by
nitrous-oxide gas. A gentleman, in consequence of inhaling it too long,
was attacked with intermitting lethargy for thirty-six hours, depression
of spirits and lowness of pulse.[2542] When long and habitually used, as
by persons afflicted with asthma, its dose must be gradually increased;
and it appears that considerable quantities may then be taken for a
great length of time without material injury. I have been informed of an
instance of an asthmatic gentleman about sixty years of age who consumed
sixteen ounces every eight or ten days, and had been in the habit of
doing so for many years. Yet, with the exception of his asthma, he
enjoyed tolerable health.

An interesting case has been published which proves that nitric ether in
vapour is a dangerous poison when too freely and too long inhaled. A
druggist’s maid-servant was found one morning dead in bed, and death had
evidently arisen from the air of her apartment having been accidentally
loaded with vapour of nitric ether, from the breaking of a three-gallon
jar of the _spiritus etheris nitrici_. She was found lying on her side,
with her arms folded across the chest, the countenance and posture
composed, and the whole appearance like a person in deep sleep. The
stomach was red internally, and the lungs were gorged.[2543] The editor
of the journal, where this case is related, says he is acquainted with a
similar instance where a young man became completely insensible from
breathing air loaded with sulphuric ether, remained apoplectic for some
hours, and would undoubtedly have perished had he not been discovered
and removed in time.


       _Of Poisoning with the Oleaginous products of Combustion._

The physiological effects of these substances have not yet been
extensively investigated. It has been already mentioned, that the
empyreumatic oils of tobacco and other narcotic vegetables are active
poisons; and that the emanations from candle snuffings and imperfectly
consumed tallow probably owe their injurious properties to a peculiar
oil. Many empyreumatic oils are known, and some are used in medicine,
which act powerfully on the animal system as stimulants and
antispasmodics. Among these may be enumerated naphtha, oil of galbanum,
oil of guiaiac, oil of amber, oil of wax, and Dippel’s oil. The last in
particular, which is the rectified empyreumatic oil of hartshorn, but is
prepared also from blood and various animal matters,[2544] has been a
good deal used of late on the continent for medical purposes, and has
even been resorted to as a poison for the purpose of self-destruction.

The only one of these substances whose physiological properties have
been examined with particular care, is the empyreumatic oil procured by
the destructive distillation of lard. When freed of adhering acid by
rectification from quicklime, this oil is limpid and very volatile, has
an insupportable smell, and when diffused in the air, irritates the eyes
and nostrils, and even excites giddiness. Buchner found it to possess
simple narcotic properties. When a mouse was confined under a jar, into
which a little of its vapour was introduced, it suddenly tried to
escape, immediately fell down exhausted, and, although soon afterwards
removed into the open air, expired in about fifteen minutes, without
convulsions. It is much less powerful when introduced into the stomach,
yet is still a dangerous poison through that channel; for five drops
projected into the throat of a chaffinch very nearly proved fatal; and
the only symptoms were excessive exhaustion, slow respiration, and
insensibility.[2545]

Similar effects have been occasionally observed in man. The late
Professor Chaussier has related a case of poisoning in the human subject
from the _oil of Dippel_, or rectified empyreumatic oil of hartshorn. It
is merely mentioned, however, that the individual, on taking a spoonful
by mistake, died immediately; and that no morbid appearance could be
discovered in the dead body.[2546] Another case has been more recently
related, where the poison was the impure oil of commerce, from which the
oil of Dippel is prepared by rectification. The subject was a woman, who
took it intentionally in the dose of an ounce and a half. The symptoms
induced could not be ascertained; but it appeared, that she had been
attacked with vomiting, and, finding the action of the poison either
less speedy, or less supportable than she expected, had thrown herself
into a well and been drowned. The appearances in the body clearly showed
that in this instance the poison had not acted as a pure narcotic. The
whole body exhaled the peculiar fetid odour of the oil. The palate,
tongue, throat, and gullet, were white and shrivelled. The stomach had
outwardly a diffuse rose tint, crossed by gorged black veins, which here
and there had burst and formed patches of extravasation. The contents of
the stomach consisted of remains of food, a good deal of the oil, some
water, and likewise some extravasated blood. Its villous coat was thick,
covered with red points, corrugated into prominent rugæ, but not eroded.
The intestines also presented signs of irritation, but in an inferior
degree.[2547] Dr. Kurtze, a German author, mentions that the impure oil
[Oleum Animale Fœtidum] was given with malicious intention in repeated
doses to an infant eighteen days old, whom he attended, and that it
caused crying and vomiting; and he quotes Froriep’s Notizen, for the
case of a woman of thirty, who swallowed nearly two ounces, and, after
repeated attacks of vomiting, threw herself into a well and was
drowned.[2548]

These facts seem to establish sufficiently the propriety of arranging
the empyreumatic oils among the narcotico-acrids.

_Oil of turpentine_ possesses somewhat similar properties; but is much
less active. It was found by Professor Schubarth, that two drachms of
this oil administered to a dog produced immediate staggering, cries,
tetanus, failure of the pulse and breathing, and death in three minutes;
and in the dead body he remarked flaccidity of the heart, gorging of the
lungs, and redness of the stomach.[2549] It is likewise well known to be
a powerful poison for vermin, such as lice, fleas, and worms.—On man its
effects are capricious. It is frequently used along with other laxatives
against obstinate constipation of the bowels, and either in the same
manner or alone as a remedy for intestinal worms. For these purposes it
has been at times administered in very large doses, for example in the
quantity of two, three, or four ounces, without any other effect than
brisk purging. But on the other hand it has sometimes, in much inferior
doses, induced violent hypercatharsis, or acted severely on the urinary
organs, producing strangury and bloody micturition, or affected the
brain, producing a state like intoxication, followed by trance for many
hours.[2550] I am not aware that it has ever proved fatal.

_Oil of tar_, a composite substance obtained by the distillation of
wood-tar, is another pyrogenous fluid of poisonous properties. Messrs.
Slight of Portsmouth have related the case of a seaman, who, after
taking nearly four ounces by mistake for spirits, was attacked with
frequent vomiting of a matter having a strong odour of tar, attended
with excessive pain in the bowels and loins. Nothing was done for his
relief till about seven hours afterwards, when he was freely bled and
purged, with immediate relief; and next morning he was so better as to
be able to resume his work. The urine had a strong tarry odour, and for
some time he suffered from heat in passing it.[2551] A case occurred in
the London Hospital, in which the symptoms were very different. A lad of
eighteen, while intoxicated, took two or three draughts of oil of tar,
although aware of its being poisonous. Not long afterwards he became
insensible, and had laborious, rattling respiration, coldness of the
extremities, suffusion of the conjunctiva, contraction of the pupils,
and an exceedingly feeble pulse. The stomach-pump brought away a liquid
with an overpowering smell of tar. Stimulants, external as well as
internal, venesection, and turpentine clysters were of little avail; the
insensibility continued, with only a short and imperfect interval; and
he died about twenty-four hours after swallowing the poison. The
pulmonary mucous membrane was highly injected, the lungs gorged with
blood and of a tarry odour, the stomach and intestines natural, except
that the whole _valvulæ conniventes_ were yellow,—the brain and its
membranes also natural.[2552] It is mentioned in the paper of Messrs.
Slight that a gentleman at Brighton died in consequence of a druggist
using oil of tar by mistake for something else in making up a
prescription.

_Creasote_ is another pyrogenous substance possessing considerable
activity as a poison. It is now extensively used in small doses as a
medicine for a variety of purposes.

It has been made the subject of physiological experiment by various
inquirers, and especially by Dr. Cormach; who found that doses of
twenty-five or forty drops caused death in a few seconds when injected
into the jugular vein of a dog, by arresting the heart’s action, and
without visibly altering the condition of the blood; that a quantity
somewhat larger caused only sopor and spasmodic twitches of the muscles,
if injected into the carotid artery, and without proving fatal; that
thirty drops introduced into the stomach of a rabbit excited
convulsions, acute cries, and death in one minute, apparently from
arrestment of the action of the heart; and that the same dose given to a
dog brought on salivation, giddiness, tetanic spasm, a feeble,
fluttering, almost imperceptible pulse, and general insensibility, with
dilated immovable pupils; but recovery took place under the employment
of blood-letting.[2553]—The effects of too large a medicinal dose in man
are pain in the stomach and vomiting, and also, according to Dr.
Elliotson, giddiness, headache, and stupor.[2554] Dr. Pereira alludes to
a case, mentioned in the Times newspaper, of death caused in 36 hours by
two drachms taken at once; and in this instance acute pain in the
abdomen was a prominent symptom.[2555] I presume this is the same case
which is mentioned in the Edinburgh Medical and Surgical Journal as
having occurred at Liverpool.[2556]—The results of Dr. Cormack’s
experiments on animals lead to the conclusion, that in poisoning with
creasote, this substance may always be detected in the body, if it has
not been removed by artificial means a considerable time before death.




                             CHAPTER XLII.
                         OF COMPOUND POISONING.


Having now investigated the three great classes of poisons in their
relations to physiology, practice of physic, and medical jurisprudence,
it will be necessary to offer a few observations on a subject of
considerable medico-legal importance, which has been almost overlooked
in systems of Toxicology,—Compound Poisoning.

When two poisons of different or opposite properties are administered
about the same time in poisonous doses, the effects of the one may
overpower and prevent the operation of the other, or they may merely
modify the action of one another. In this manner the usual symptoms
produced by one or by both may be entirely or in a great measure
wanting; and even in the dead body the usual appearances occasioned by
one or both may be modified or perhaps altogether absent.

Although in the course of reading I have met with a sufficient number of
cases of the kind to show that compound poisoning is an object of some
consequence to the medical jurist, the facts hitherto made public are
not so numerous as to render a systematic arrangement of them
practicable. The most advisable course, therefore, seems to be merely to
describe for the present the cases which have been brought under my
notice. These are as follows:

1. _Poisoning with Arsenic and Alcohol._—A man, after taking twelve
ounces of whisky at a debauch, swallowed, an hour afterwards, while in a
state of excitement, but not particularly drunk, a quantity of arsenic,
the dose of which could not be ascertained. Fifteen minutes after the
arsenic was taken medical aid was procured, upon which repeated attempts
were made to produce vomiting by means of ipecacuan and sulphate of
zinc, but to no purpose. The stomach-pump was therefore resorted to;
and, after at least an hour had been spent in previous attempts by
emetics, the stomach was cleared of a fluid in which arsenic was
unequivocally detected. No symptom of poisoning with arsenic followed.
As the man took the arsenic seven hours after a meal, when of course the
powder would at once be brought freely in contact with the villous coat
of the stomach, it must, I think, be inferred, that the operation of the
arsenic was impeded or prevented by the narcotism previously induced by
the ardent spirits. For this case I am indebted to a former pupil, Mr.
King.

_Poisoning with Arsenic and Alcohol._—A case of the same description
with the last, but which proved fatal in consequence of the large
quantity of arsenic taken, has been related by Dr. Wood of Dumfries. A
lad of seventeen, after a night’s debauch, swallowed half an ounce of
arsenic early in the morning. In two hours and a half, when Dr. Wood
first saw him, there was no symptom of poisoning with arsenic,—no
symptom at all indeed but languor and drowsiness. A few minutes
afterwards he had slight vomiting, which was repeatedly renewed by
artificial means. For some hours the pulse was but little elevated. In
eighteen hours he began to sink, and presented the usual constitutional
symptoms of poisoning with arsenic; and in forty-one hours he expired.
But from first to last he had scarcely any local symptom except
vomiting, even although the stomach presented after death signs of
violent irritation.[2557]

3. _Poisoning with Tartar-Emetic and Charcoal Fumes._—Under the head of
poisoning with antimony, notice has already been taken of the case of a
man who, after swallowing seventeen grains of tartar-emetic, attempted
to commit suicide by suffocating himself with the fumes of burning
charcoal. He recovered from both attempts, suffered severely from the
usual narcotic effects of carbonic acid gas, but showed scarcely any
symptom of the irritant action of tartar-emetic.[2558]

4. _Poisoning with Alcohol and with Laudanum._—Under the head of
poisoning with opium, allusion has already been made to a remarkable
case related by Mr. Shearman, where the usual effects of opium were much
retarded in an individual who, at the time of swallowing the opium, was
in a state of excitement from intoxication. For five hours there was no
material stupor. But after that the usual narcotic symptoms supervened
and eventually proved fatal.[2559] The excitement of intoxication,
however, has not always the effect of suspending the action of opium;
for in a case which came under my notice in the Infirmary of this
city,—that of a woman, who swallowed an ounce and a half of laudanum
while much intoxicated,—the usual narcotic symptoms were fully formed in
an hour: and although the stomach-pump was applied soon afterwards, she
expired in less than five hours from the time the laudanum was
swallowed,—those who had charge of her before she was brought into the
hospital having neglected to use the proper means for keeping her
roused.

5. _Poisoning with Laudanum and Corrosive Sublimate._—Of all the cases
of compound poisoning I have met with, the most remarkable is an
instance which occurred in Edinburgh Castle, a few years ago, of
poisoning with laudanum and corrosive sublimate. In this case, the
individual, a young soldier, swallowed about the same time two drachms
of the latter and half an ounce of the former. He had at first no
violent symptoms whatever, indicating the operation of corrosive
sublimate; which is an extremely rare occurrence. Afterwards he had
frequent purging and tenesmus, with bloody stools and all the usual
phenomena of violent dysentery, but no pain of belly, no tenderness even
on firm pressure, no vomiting except under the use of emetics. On the
fourth day a violent salivation set in; and under this and the
dysenteric affection he became quickly exhausted, yet not so much, but
that on the day of his death, the ninth after he took the poison, he was
able to walk a little in his room without assistance. He died on the
close-stool rather unexpectedly. I have unfortunately lost the original
notes I had of this case, and have forgotten whether any narcotic
symptoms were present at first; but my impression is that they were
present, though in a slight degree only. Most of the previous
particulars were communicated to me by the late Dr. Mackintosh. The
stomach, duodenum, ileum, colon, and rectum were found after death
enormously inflamed, ulcerated, and here and there almost gangrenous.—In
this instance some of the corrosive sublimate must have been decomposed
by the laudanum, and an insoluble meconate of mercury formed. But the
quantity thus decomposed could have been but a small proportion of the
whole,—as was indeed proved by the extensive ravages actually committed
in the whole alimentary canal. I conceive, therefore, that there is no
other way of accounting for the slight apparent effects of the corrosive
sublimate, at the commencement particularly, than by supposing that the
narcotic operation of the opium veiled or actually retarded the irritant
action of the corrosive sublimate.

6. _Poisoning with Opium and Belladonna._—A lady, who used a compound
infusion of opium and belladonna as a wash for an eruption in the vulva,
took it into her head one day to use the wash as an injection; and
actually received three successive injections, containing each the
active matter of a scruple of opium and half an ounce of belladonna
leaves. Fortunately none of the three was retained above a few minutes,
except the last, which was not discharged for ten minutes. In less than
an hour, she was found in bed in a deep sleep, but the true cause was
not suspected till three hours later. She was then completely insensible
and motionless, with the face pale, the pupils excessively dilated and
not contractile, the pulse frequent and small, and the breathing
hurried. After the use of purgative injections, blood-letting, leeches
to the head, and sinapisms to the legs, she began in five hours to show
some sign of returning consciousness, which improved after a fit of
vomiting. When thoroughly roused, her vision continued dim, the pupils
excessively dilated, and the ideas somewhat confused. For three days the
pulse continued frequent, and the pupils somewhat dilated.[2560] Here
the opium seems to have prevented the delirium usually induced by
belladonna in the early stage, while on the other hand the belladonna
prevented the usual effect of opium on the pupils, and actually produced
the opposite action.

7. In the following cases, the active poisons to which the individuals
were exposed were so numerous, that it is impossible to say which or how
many of them occasioned the symptoms. A colour-maker was superintending
a process in which cobalt, arsenic, mercury, sal-ammoniac, and nitric
acid were subjected to heat in a mattrass, when the mattrass suddenly
gave way, and a dense vapour was instantly discharged. The manufacturer,
before he could escape, fell down insensible; and though speedily
removed, he died in no long time, affected with enormous swelling of the
abdomen. A workman who was also present, escaped by a window; but was
nevertheless immediately attacked with swelling of the belly, which
speedily became very great, and was attended with pain in the jaws, and
dimness of sight. These symptoms were very slowly dissipated under the
use of cold bathing and purgatives, which brought away an enormous
quantity of fetid gas.[2561]

These are not the only examples of compound poisoning which have come
under my attention. But others I have noticed are not detailed with
sufficient exactness to make it worth while to quote them. The instances
given, however, are sufficient to show that poisons of opposite
qualities given about the same time in large doses will disguise one
another’s effects, or impede, or perhaps even prevent them, in a manner
which renders such a combination of circumstances an important subject
of inquiry for the medico-legal toxicologist.

It is probable that the modifying influence is established in one of two
ways,—either by one poison producing a state of venous plethora or
distension, which impedes, or for a time prevents, the absorption of the
other,—or by one poison producing an insensibility of the membrane with
which the other is in contact; so that not only the local injury
actually done has not the usual remote effect on the constitution, or on
distant organs, but likewise is at times substantially less extensive
than in ordinary circumstances. These reflexions arise naturally from a
review of the preceding cases; but of course further facts are necessary
to give them weight.




                                 INDEX.


 Absorption, its extreme rapidity, 15

 — action of poisons through, 17

 — effect of in removing poisons beyond the reach of analysis, 57

 Acetatæ of lead, tests of, in its pure state, 398

 — — — process for detecting it in organic mixtures, 423

 — — — effects on the animal body. See _Lead_.

 Acetates of copper, their tests, 350

 — — morphia, its tests, 533

 Acid, acetic, its tests in the pure and mixed state, 164

 — — effects on man and animals, 165

 Acid, arsenious, its chemical properties, 200

 — — its taste, 200

 — — its solubility in various menstrua, 201

 — — its tests when in the solid state, 203

 — — its tests when in solution, 206

 — — its liquid tests give complete evidence conjunctly, not separately,
    209

 — — its tests when mixed with organic substances, 215

 — — Marsh’s process for, 211, 217

 — — Reinsch’s process for, 214, 216

 — — process for by hydrosulphuric acid, 217

 — — process for by Fresenius and Von Bab, 218

 — — fallacies in the process for detecting, 219

 — — its effects on the body. See _Arsenic_.

 Acid, carbonic. See _Gas_.

 — carbazotic, a poison, 610

 — citric, not poisonous, 180

 Acid, hydrochloric, tests for, in its pure and mixed state, 146

 Acid, hydrocyanic, its action on the body, 582

 — — rapidity of its action, 582, 590

 — — acts in all its chemical combinations, 585

 — — acts through every animal tissue, 584, 592

 — — enters the blood and communicates its odour, 594

 Acid, hydrocyanic, why its odour is not always perceptible in the
    blood, 594

 — — contained in many plants, renders them poisonous, 600

 — — its tests when pure, 578

 — — process for detecting it in organic mixtures, 580

 — — symptoms it induces in man, 587

 — — may cause instant death, 582, 590

 — — morbid appearances caused by it, 593

 — — treatment of poisoning with, 596

 Acid, meconic, its tests, 532

 Acid, nitric, its tests in the pure and mixed state, 142, 143

 — — process for stains produced by, 143

 Acid, oxalic, its action on the animal body, 173

 — — its morbid appearances, 177

 — — symptoms caused by it in man, 173

 — — its symptoms are occasionally of themselves complete proof of
    poisoning, 179

 — — its tests when pure, 168

 — — process for, in organic mixtures, 170

 — — treatment of poisoning with, 178

 Acid, phosphorous, a feeble poison, 152

 — — sulpho-cyanic, not a poison, 587

 Acid, sulphuric, its tests in the pure state, 123

 — — process for it in the mixed state, 126

 — — process for stains occasioned by, 125

 — — action on animals, 128

 — — morbid appearances, 135

 — — the morbid appearances are at times of themselves complete proof of
    poisoning, 139

 Acid, sulphuric, symptoms in man classified, 129

 — — the symptoms are at times alone complete proof of poisoning, 135

 — — throwing of, to disfigure or disable, is a capital crime, 122

 — — treatment of poisoning with, 140

 Acid, sulphuric, effects of on the intestines after death, 139

 Aconitina, the alkaloid of monkshood, 662

 _Aconitum_, poisoning with, 662

 Acrid poisons of the vegetable and animal kingdoms, 451

 Action of poisons, 9

 — — — by absorption, 17

 — — — causes which modify the, 27

 — — — local, 9

 — — — remote, 11

 — — — organs acted on by the remote, 22

 — — — rapidity of the, 14, 582

 — — — through sympathy, 12

 — — — applied to the discovery of antidotes, 37

 Administration of poison by prisoner, necessity of the proof of, on
    trials, 72

 — — — by prisoner, may be proved by pure medical evidence, 73

 _Æthusa_, poisoning with, 662

 Aggregation, state of, its effects on the action of poisons, 28

 Alcohol, poisoning with, 725

 — morbid appearances induced by, 731

 — poisoning of with other poisons, 734

 — symptoms of poisoning with, in its several degrees, 725

 — treatment of poisoning with, 735

 Alkalies and Alkaline salts, fixed, 180

 — — — — their mode of action, 183

 — — — — morbid appearances caused by them, 186

 — — — — symptoms caused in man, several varieties of, 183

 — — — — tests for, 181

 — — — — treatment of poisoning with, 187

 Alkaline sulphurets. See _Sulphurets_.

 Almond. See _Bitter-Almond_.

 Alum, effects of on man and animals, 509

 Ammonia and its salts, tests of, 193

 — — — — their effects on man and animals, 193

 Ammoniacal gas, effects of, on man, 194

 Amygdalus. See _Bitter Almond_.

 Anemone, its effects as a poison, 463

 Angustura bark, false, its effects on man and animals, 692

 Animal acrids, general observations on their effects, 470

 Animal matter poisoned by disease, 487

 — — poisonous from ordinary putrefaction, 490

 — — poisonous from modified putrefaction, 492

 Animals, evidence of poisoning from experiments on, 62

 Animals, effects of suspected articles of food on, 63

 — effects of suspected matters of vomiting or contents of stomach on,
    67

 — experiments on, may illustrate physiological points disputed on
    trials, 71

 — various effects of poisons on different, 63

 Antidotes, by what principles the search for them must be regulated, 37

 Antimony, tests for its compounds, 367

 — tartrate of. See _Tartar-emetic_.

 Apoplexy, distinction between it and narcotic poisoning, drawn from
    symptoms, 511

 — distinction between it and narcotic poisoning, drawn from morbid
    appearances, 514

 — congestive appearances of, 517

 — from extravasation, 517

 — serous, 517

 — simple, 515

 Arseniate of potass, its tests, 224

 Arsenic, tests for its compounds, 198

 — action of, illustrated by experiments on animals, 227

 — acts through all the animal tissues, 229

 — acts in all its chemical forms, except in the metallic state, 230

 — action of, is a little impaired by the effects of mixture—not by
    habit, 233

 — acts when applied to ulcers and eruptions, 251

 — acts when applied to the sound skin, 257

 — acts when introduced into the rectum, 253

 — acts when thrust into the vagina, 254

 — acts powerfully when inhaled, 254

 — does it exist in the blood of those poisoned with it?, 228

 Arsenic, dose required to cause death, 232

 — morbid appearances caused by it, 262

 — morbid appearances sometimes not caused by it at all, 262

 — morbid appearances caused by it after death, 282

 — does it prevent the bodies of those poisoned with it from
    putrefying?, 273 273

 — symptoms it causes in man classified according to three varieties,
    234

 — symptoms of, at times supply alone complete evidence of poisoning,
    259

 Arsenic, symptoms of, occasionally very trifling, even where fatal, 286

 — symptoms of, how soon may they begin, and how long may they be
    delayed?, 234

 — symptoms of, how soon may they kill?, 239

 — symptoms of, how long may they last?, 248

 — treatment of poisoning with, 283

 — treatment of, no antidotes known, 285

 — changes it undergoes in the stomach after death, 268

 — metallic, not a poison, 230

 — oxide of. See _Acid, arsenious_.

 — sulphurets of. See _Sulphurets_.

 Arsenite of copper, its tests, 223

 — — — seldom contained in mineral green, 223, 346

 — of potass, its tests, 223

 Arseniuretted-hydrogen, 227

 — — its effects, 256

 _Arum maculatum_, poisoning with, 465

 _Asagræa officinalis_, 672

 _Atropa_, poisoning with, 639

 — symptoms induced by it in man, 640

 — morbid appearances caused by it, 643

 Atropia, alkaloid of belladonna, 639


 Bacon, poisonous at times, 497

 Baryta, poisoning with its compounds, 446

 — muriate of, tests for, 446

 — — — and carbonate, their effects on man and animals, 448

 — morbid appearances caused by, 450

 — treatment of poisoning with, 450

 Bee, its poisonous sting, 487

 Belladonna. See _Atropa_.

 Bichloride of mercury. See _Corrosive Sublimate_.

 Bicyanide of mercury, 303

 Biliary ducts, rupture of, imitates irritant poisoning, 97

 Bilious vomiting, imitates irritant poisoning, 100

 Bismuth, poisoning with its compounds, 383

 Bitartrate of potash, a poison in large doses, 507

 Bitter-almond, its poisonous effects, 602

 — may cause death, 603

 — essential oil of, its effects as a poison, 604

 — essential oil of, its composition, 601

 — essential oil of, its formation, 602

 Bitter-apple, poisoning with, 460

 Bitter cassava, poisoning with, 457

 Bitter-sweet, a feeble poison, 576

 Blood, discovery of poisons in the, 21

 Boiling water, effects of, when swallowed, 505

 — — causes cynanche laryngea, 506

 _Bombyx processionaria_, its poisonous effects, 477

 Brain, inflammation of its membranes, distinguished from narcotic
    poisoning, 523

 — inflammation of its substance, distinguished from narcotic poisoning,
    524

 — hypertrophy of, distinguished from narcotic poisoning, 526

 Bread, adulteration of, with the sulphate of copper, 354

 — effects of spoiled, 720

 Bromine, tests for, 161

 — its effects on animals, 162

 _Brucea antidysenterica_, not the False Angustura tree, 692

 Brucia, alkaloid of false angustura bark, 692

 Bryony-root, effects of, on man and animals, 459


 Calomel, its tests, 292

 — can it be considered an irritant poison?, 332

 _Calthapalustris_, its effects as a poison, 463

 Camphor, its effects on animals, 694

 — morbid appearances caused by, 696

 — symptoms excited by, in man, 694

 Cantharides, physical characters of, 471

 — action of, on animals, 471

 — morbid appearances caused by, 476

 — symptoms it excites in man, 472

 — treatment of poisoning with, 476

 Carbonate of ammonia, 193

 — of baryta, tests of, 446

 — of lead, tests of, 398

 — of lead is formed on lead by the action of air and water,—and see
    _Lead_, 399

 Carbonates of potass and soda, tests of, 181

 Carbonic acid. See _Gas_.

 Carbonic oxide gas, effects of, on man, 624

 Carburetted-hydrogen gas, its effects on man, 622

 Cassada, bitter, its effects, 457

 Castor-oil-seeds, effects of, on man and animals, 456

 Cerasus Lauro-cerasus. See _Cherry-laurel_.

 Cevadilla, a poison, 672

 Cheese, occasionally poisonous without intentional adulteration, 494

 Chemical analysis, evidence of general poisoning from, 54

 — — may be rendered unavailing by vomiting and purging, 55

 — — may be rendered useless by absorption, 57

 — — may be fruitless, because the poison has been decomposed, 58

 — — is often successful after long interment, 58

 Chemical combination, its influence in modifying the operation of
    poisons, 28

 Chemical decomposition, its effects in removing poisons beyond the
    reach of analysis, 58

 Chemical evidence not always indispensable to the proof of poisoning,
    59

 Cherry-laurel water, a deadly poison, 605

 — essential oil of, is the same as the oil of bitter-almond, 605

 — effects of the distilled water and oil on animals and man, 605, 606

 Chlorine, its effects on man and animals, 152, 616

 Chloride of barium, 446

 — of iron, poisoning with, 392

 Chlorides of soda, potassa and lime, their action as poisons, 191

 Cholera imitates irritant poisons, and how to be distinguished, 100

 — its shortest duration, 101

 — supposed to have been caused by emanations from a cess-pool, 621

 — impairs the activity of some poisons, 35

 — malignant, how distinguished from irritant poisoning, 102

 Chrome, poisoning with the compounds of, 385

 _Cicuta_, its effects on man and animals, 662

 Cinnabar, its tests, 290

 Citric acid, not a poison, 180

 Classification of poisons, 90

 Cluster-cherry, its distilled water and essential oil are active
    poisons, 608

 Cocculus indicus, its effects on man and animals, 696

 _Colchicum autumnale_, effects of, on man, 674

 Colchina, alkaloid of colchicum, 674

 Cold water, death from drinking it, imitating irritant poisoning, 98

 Colic, how it is distinguished from irritant poisoning, 109

 Colica pictonum, causes of, 426, 431, 437

 — — trades which are subject to suffer, 436

 Colica pictonum, precautions for preventing it in workmen, 443

 Colocynth, effects of, on man and animals, 460

 Common salt, a poison in very large doses, 508

 Compound poisoning, 740

 Conduct of prisoner, illustrated by medical evidence, may prove his
    guilt, 73

 Conia, alkaloid of hemlock, 653

 _Conium_, effects of, on man and animals, 654

 Copper, poisoning with, 345

 — action of its compounds, 358

 — adulteration of bread with, 354

 — corrosion of, by articles of food and drink, 350, 353

 — corroded by saline solutions, 350

 — corroded by wine and vegetable acids, 352

 — corroded by fatty matters, 352

 — metallic, not poisonous, 360

 — morbid appearances caused by, 364

 — process for detecting its salts when pure, 346

 — process for detecting it in organic mixtures, 355

 — sulphuret not poisonous, unless long exposed to the air, 361

 — symptoms of poisoning with in man, 361

 — treatment of poisoning with, 365

 — contained in most vegetable substances, 355

 — is it contained in the blood of animals poisoned with it?, 360

 _Coriaria myrtifolia_, poisoning with, 698

 Corrosion caused by poisons, examples of, 9

 Corrosive sublimate, action on animals. See _Mercury_.

 — — action on dead intestine, 341

 — — chemical properties of, 291

 — — is decomposed by organic principles, 297

 — — process for, in the solid state, 292

 — — process by reduction when it is dissolved, 292

 — — process by liquid tests when it is dissolved, 293

 — — process for it in organic mixtures, 296

 — — additional tests for it in the pure state, 294

 — — symptoms caused by it in man. See _Mercury_.

 Cream of tartar, a poison in large doses, 507

 Creasote, a poison, 739

 Croton-oil and seed, effects of, 459

 Cuckow-pint, poisoning with, 465

 Cupping-glasses, in the treatment of external poisoning, 38

 Cyanide of mercury, tests for, 303

 — its effects on man, 332

 Cyanogen gas, its effects on animals, 636

 Cyanous acid, a feeble poison, 587

 _Cytisus Laburnum_, its poisonous effects, 723


 Daffodil, its effects as a poison, 467

 _Daphne_, effects of its different species on man and animals, 465

 Darnel-grass, its effects on man, 721

 _Datura_, poisoning with, 644

 Daturia, alkaloid of thorn-apple, 645

 Dead-tongue, poisoning with, 658

 Death-bed, evidence in cases of poisoning, its importance, and hints
    for collecting it, 84

 Delirium tremens, impair the activity of some poisons, 35

 — — the effect of alcohol, 731

 Delphinia, alkaloid of stavesacre, 464

 _Delphinium_, poisoning with, 464

 Digestion of poisons, tends to remove them beyond the reach of
    analysis, 58

 _Digitalis_, poisoning with, 678

 Dippel’s oil, a poison, 737

 Diseases, their influence on the operation of poisons, 35

 Distension of stomach, death from, how distinguished from irritant
    poisoning, 95

 Dysentery impairs the activity of opium as a poison, 35


 Eels sometimes poisonous, 484

 Elaterium and elaterin, their poisonous properties, 461

 Emeta, its poisonous properties, 682

 Empyreumatic oils are active poisons, 737

 Epilepsy, distinction between it and narcotic poisoning from the
    symptoms, 519

 — distinction of, from narcotic poisoning by morbid appearances, 521

 Epsom salt, a poison in large doses, 506

 Ergot. See _Spurred rye_.

 _Ervum Ervilia_ is a poison, 722

 Ether, effects of, on man and animals, 736

 Euphorbium, its effects on man and animals, 454

 Evidence of poisoning. See _Symptoms. Morbid Appearances. Chemical
    Evidence. Animals._

 — of general poisoning from symptoms, 43

 — — — — from morbid appearances, 51

 — — — — from chemical analysis, 54

 Evidence of general poisoning from experiments on animals, 62

 — — — — from moral circumstances, 71

 Evidence, medical, of the administration in charges of poisoning, 72

 — — may prove the prisoner’s intent, 78

 — — on death-bed, 83


 Fainting, mortal, distinction between it and narcotic poisoning, 527

 Feigned poisoning, 86

 Ferro-cyanate of potass not poisonous, 586

 Fever impairs the activity of some poisons, 35

 Fish-poison, 477

 Fly-powder, tests for, 199

 Fool’s parsley, effects on man and animals, 661

 Foxglove, its effects on man and animals, 678

 Fowler’s solution, tests of, 223

 Fungi, list of the wholesome, 700

 — list of the deleterious, 701

 — circumstances which modify their qualities, 702

 — rules for knowing poisonous, 703

 — active principles of, 704

 — symptoms of poisoning with, 704

 — morbid appearances caused by, 708

 — treatment of poisoning with, 709

 — poisoning of wholesome kinds with other poisons, 709


 Gamboge, poisoning with, 466

 Gas, carbonic acid, morbid appearances caused by, 632

 — — — is poisonous positively, not negatively, 614, 624

 — — — symptoms caused by, when pure, 625

 — — — symptoms it causes when diluted with air, 625

 — — — symptoms, when from burning charcoal, 626

 — — — symptoms, when from burning coal, 631

 — — — symptoms, when from burning tallow, 630

 — — — symptoms when formed by respiration, 632

 — — — treatment of poisoning with, 634

 Gas, carbonic oxide, its effects on man, 634

 — carbureted-hydrogen, effects on man, 622

 — coal and oil, effects on man, 622

 — chlorine, its effects on man, 616

 — cyanogen, its effects on animals and plants, 636

 — hydrosulphuric acid, effects when injected into the veins, 613

 — — — effects when breathed by man, 618

 — — — effects on vegetables, 618

 Gas, hydrosulphuric acid, morbid appearances caused by, 619

 — — — proves fatal though applied to the skin only, 614, 617

 — muriatic acid, very poisonous to plants, 617

 — nitric oxide and nitrous acid, effects when injected into the veins,
    614

 — nitrous acid, effects on man, 615

 — nitrous oxide, its effects on man and plants, 635

 — oxygen, a positive poison, 636

 — sulphurous acid, extremely poisonous to plants, 631

 Gases, poisonous, medico-legal importance of, 611

 — which of them are negatively, and which positively poisonous, 612

 Gastritis. See _Stomach_.

 General poisoning, evidence of, 39
   and see _Evidence_.

 Glass-powder, is it a poison?, 503

 Gold, poisoning with its compounds, 383

 Goulard’s extract, tests for, 399

 Grain, sometimes poisonous, 710

 — unripe, its supposed effects on man, 719

 Green vitriol. See _Sulphate of Iron_.

 Gullet, perforation of, how distinguished from irritant poisoning, 108,
    119


 Habit, its effect in modifying the action of poisons, 34

 Hæmatemesis, how distinguished from irritant poisoning, 109

 Heart, organic diseases of, may imitate narcotic poisoning, 528

 Hellebore, effects of its different species on man and animals, 672

 Hellebore, white. See _Veratrum_.

 Hemlock, its effects on man and animals, 653

 — dropwort, its effects as a poison, 660

 Henbane. See _Hyoscyamus_.

 _Hippomane Mancinella_, its poisonous effects, 458

 Hot liquids cause symptoms of irritant poisoning, 505

 Hydrochlorate of ammonia. See _Ammonia_.
   Also, 193

 Hydrochlorates. See _Muriates_.

 Hydrochloric acid. See _Acids_.

 Hydrocyanic acid. See _Acid_.

 Hyoscyamus, its effects on man and animals, 573

 Hydrophobia impairs the activity of some poisons, 35

 Hypertrophy of brain. See _Brain_.

 Hysteria lessens the effect of opium, 35


 Idiosyncrasy, its influence in modifying the action of poisons, 32

 — sometimes renders wholesome articles deleterious to individuals, 33,
    68

 Iliac passion imitates irritant poisoning, 109

 Imaginary poisoning, 85

 Imputed poisoning, 88

 Inflammation of brain. See _Brain_.

 — of intestine. See _Intestines_.

 — of stomach. See _Stomach_.

 Insects, poisonous, 486

 Intent in the administration of poison may be sometimes proved by
    medical evidence, 78

 Interment for years may not prevent the detection of poisons, 58

 Intestines, inflammation of, how distinguished from irritant poisoning,
    99

 — obstruction of, may imitate irritant poisoning, 109

 — perforation of, how distinguished from irritant poisoning, 108, 119

 Iodide of potassium, effects, 157

 — — — tests of, 158

 Iodine, its effects on man and animals, 154

 — its tests in the pure and mixed state, 152

 Ipecacuan, poisoning with, 682

 Ipomæa Purga, a poison, 467

 Iron, poisoning with the salts of, 391

 Irritant poisons, general observations on, 92

 — — distribution of into orders, 121

 — — morbid appearances of, contrasted with those of various natural
    diseases, 110

 — — symptoms of, contrasted with those of various natural diseases, 93

 Irritation, examples of, caused by poisons, 9


 Jalap, its effects as a poison, 467

 _Jatropha_, its effects on man and animals, 457

 _Juniperus Sabina_, its poisonous effects, 468


 King’s yellow, its tests and composition, 225


 Laburnum seeds poisonous, 723

 _Lacluca_, poisoning with, 575

 _Lathyrus Cicera_ is a poison, 722

 Lead, tests for its compounds, 396

 — action of air and water on, 399

 — adulteration of wines with, 420

 — adulteration of spirits with, 422

 — adulteration of a mechanical nature, 422

 — corrosion of, by distilled water, 401

 — corrosion of, by water prevented by salts in solution, 403

 — corrosion of, prevented by excessively minute proportions of some
    salts, 403

 — corrosion of, by natural waters, 406

 — corrosion of, by rain and snow-water, 406

 Lead, corrosion of, by spring waters, how prevented, 414

 — corrosion of, not caused by some spring waters, 408

 — dissolved by many acidulous fluids, 415

 — dissolved by these fluids much more rapidly if it is oxidated, 419

 — metallic, is not poisonous, 427

 — mode of action on the animal body, 424

 — does it exist in the blood or organs of animals poisoned with it?,
    426

 — morbid appearances caused by, 439

 — process for detecting its compounds, 396

 — process for detecting it in organic mixtures, 422

 — sulphuret of, not poisonous, 427

 — symptoms caused by, in man, classified according to two varieties,
    429

 — symptoms caused by, as an irritant, 429

 — symptoms of, constituting the disease colica pictonum, 431

 — tradesmen who are subject to suffer from poisoning with, 436

 Lead, treatment of poisoning with, 441

 Lead glazing is rapidly acted on by acidulous fluids in some
    circumstances, not in others, 419

 Lettuce-opium, effect of, on animals, 575

 Lime, poisoning with, 192

 Liver of sulphur. See _Sulphurets_.

 Litharge, tests for, 396

 Lividity is no evidence of poisoning, 51

 Local action of poisons, 9

 _Lolium temulentum_, its effects on man, 721


 Maize, spurred, 718

 Manchineel, its effects on man and animals, 458

 Mania impairs the activity of some poisons, 35

 Marsh marigold, its effects on man and animals, 464

 Meadow-saffron, its effects on man, 674

 Mechanical irritants produce the same effects as irritant poisons, 501

 Meconic acid, its tests, 53

 — — is not poisonous, 562

 _Meloe proscarabæus_, its poisonous effects, 477

 Melanosis of stomach imitates the effects of irritant poisons, 112

 Melæna, how distinguished from irritant poisoning, 109

 Meningitis, how distinguished from narcotic poisoning, 523

 _Menispermum Cocculus_, poisoning with, 696

 Mercurial salivation in cases of poisoning, when does it begin?, 314

 Mercurial salivation, phenomena of, 316

 — — can it be confounded with any other disorder?, 319

 — — may it return after a long intermission?, 322

 — — its duration, 322

 — — in what modes it may prove fatal, 324

 Mercurial tremor, 324

 Mercury, action of its soluble compounds on the animal body, 303

 — acts through all animal tissues, 327

 — acts in all soluble chemical compounds, 329

 — acts not, when in the metallic state, 330

 — acts not, in the form of sulphuret, 331

 — acts not, when its soluble compounds are decomposed by organic
    principles, 336

 — existence in the blood of those who have taken it is extremely
    probable, 306

 — morbid appearances caused by, 337

 Mercury, processes for its compounds when pure, 289

 — process for detecting it in organic mixtures, 299

 — symptoms of poisoning with, classified according to three varieties,
    310

 — symptoms of corrosive poisoning with, their longest duration, 312

 — symptoms of, their shortest duration in fatal cases, 313

 — symptoms of, sometimes furnish of themselves decisive evidence of
    poisoning, 337

 — treatment of poisoning with an antidote, 342

 Metals, not poisonous unless oxidated, 230, 329, 360, 427

 Mezereon, its effects on man and animals, 465

 Milk at times poisonous without intentional adulteration, 496

 Mineral-green, tests of, 347

 — See _Arsenite of Copper_.

 Mixture, its effect in modifying the action of poisons, 29

 _Momordica Elaterium_, its poisonous properties, 461

 Monkshood, its effects on man and animals, 662

 Moral evidence of poisoning, 71

 Morbid appearances, evidence of general poisoning from, 51

 — — sometimes supply alone full proof of poisoning, 139

 Morphia, its tests, 532

 — its effects on man and animals, 557

 Mosses, poisonous, 710

 Mountain-ash is poisonous, as containing hydrocyanic acid, 609

 Muriate of baryta. See _Baryta_.

 Muriate of morphia, its tests, 533

 Muriate of mercury. See _Calomel_—_Corrosive Sublimate_.

 Muriate of soda, a poison in large quantity, 508

 Muriatic acid, 146

 Muriatic acid gas, 617

 Muscles are occasionally poisonous, 479

 — causes why they become poisonous, 481

 — copper cannot account for their effects, 481

 — decay, does it render them poisonous?, 481

 — disease, will this explain their effects?, 482

 — idiosyncrasy sometimes makes them poisonous, 482

 — insects of a poisonous nature entering their shell, will this explain
    their effects?, 483

 Muscles, principle of a poisonous nature not yet discovered in them,
    482

 — symptoms and morbid appearances caused by the poisonous, 479

 Mushrooms. See _Fungi_.


 _Narcissus Pseudo-narcissus_, a poison, 467

 Narcotico-acrid poisons, general remarks on, 637

 Narcotic poisoning, its symptoms and morbid appearances, contrasted
    with those of natural disease, 510

 Narcotics, their active principles, 529

 Narcotine, its tests, 534

 — its effects on animals, 560

 Nervous local impressions, examples of, caused by poisons, 10

 _Nicotiana Tabacum._ See _Tobacco_.

 Nicotianin, poisonous principle of tobacco, 647

 Nightshade. See _Solanum_—_Atropa_.

 Nitrates of mercury, their tests, 303

 Nitre, its tests, 187

 — its action and symptoms in man, 188

 — morbid appearances caused by, 191

 Nitric acid. See _Acids, Mineral_.

 Nitric oxide gas, its effects on animals, 614

 Nitrous acid vapour, its effects on man, 615

 Nitrous oxide gas, its effects on man, 635

 Nux-vomica, action of, on animals, 688

 — morbid appearances caused by, 689

 — symptoms it excites in man, 686

 Nux-vomica, symptoms of, sometimes alone are complete evidence of
    poisoning, 690

 — its tests, 686

 — treatment, 690


 _Œnanthe_, poisoning with, 653

 Oil of Dippel, 737

 Oil of tar, 738

 Oil of turpentine, 738

 Oils, empyreumatic, are poisonous, 737

 Opium, frequently used for the purpose of poisoning, 530

 — action of, illustrated by experiments, 539

 — acts as a poison through every animal tissue, even the skin, 556

 — chemical history of, 530

 — chemical analysis cannot detect it in the blood, 541

 — morbid appearances caused by, 562

 — process for detecting it in organic mixtures, 534

 — may cause death and not be discoverable in the stomach why?, 537

 Opium, symptoms of, in man, 539

 — symptoms of, how soon may they begin, and how long may they be
    delayed?, 543

 Opium, ordinary, shortest, and longest duration of fatal poisoning
    with, 547

 — smallest fatal dose of, in adults, 549

 — fatal dose in infants extremely small, 549

 — principles contained in, 531

 — tests for the principles of, when pure, 532

 — treatment of poisoning with, 566

 Opium-eaters, are they short lived?, 551

 Orpiment, 224, 230

 Osmium, 395

 Oxygen, a poison, 636

 Oysters, sometimes poisonous, 483


 Peach flowers may cause fatal poisoning, 608

 Pepper, a poison in very large doses, 506

 Perforation. See _Stomach_—_Intestines_—_Gullet_.

 Peritonæum, inflammation of, how distinguished from irritant poisoning,
    105

 Phosphorus, its effects on man and animals, 149

 Phosphorous acid, a feeble poison, 152

 Picrotoxin, active principle of Cocculus Indicus, 696

 Pretended poisoning, 85

 Protochloride of Mercury, See _Calomel_.

 _Prunus Lauro-cerasus._ See _Cherry-Laurel_.

 _Prunus Padus._ See _Cluster-Cherry_.

 Prussiate. See _Ferro-cyanate_.

 Prussic acid. See _Hydrocyanic_.

 Putrefaction of the body, not a proof of poisoning when premature, 51

 — does not always prevent the detection of poisons, 59

 — does arsenic preserve the body from?, 273

 Putrefied animal matter, its effects as a poison on man and animals,
    492


 Quantity or dose, its influence in modifying the action of poisons, 27


 _Ramollissement._ See _Brain_.

 Ranunculaceæ, their effects on man and animals, 462, 662

 Ranunculus, its poisonous effects, 462

 Realgar, its tests, 224

 Remote action of poisons, through what channel is it carried on?, 12

 Red-lead, tests for, 397

 Red precipitate, tests for, 290

 Redness of Stomach. See _Stomach_.

 Ricinus. See _Castor oil_.

 Rue, poisoning with, 681

 Rupture of stomach, death from, how distinguished from irritant
    poisoning, 97

 Rupture of duodenum, death from, how distinguished from irritant
    poitant poisoning, 97

 Rupture of biliary ducts, 97

 — of uterus, 98

 Rust of wheat is not poisonous, 719

 Rye. See _Spurred rye_.


 Sal-ammoniac, its tests, 193

 — its action on animals, 196

 Salivation may be caused by various poisons, 319

 — may be caused by ulcerated sore throat, 319

 — sometimes an idiopathic disease, 319

 — sometimes arises from the influence of the imagination, 321

 Salivation, mercurial. See _Mercurial_.

 Salmon, pickled or kippered, sometimes injurious, 499

 Salt, common, a poison in very large quantity, 508

 Savin, its effects on man and animals, 468

 Sausages, occasionally poisonous, 492

 _Scilla maritima_, effects on man and animals, 671

 _Secale cornutum._ See _Spur_.

 Secret poisoning, 39, 249

 Serpents, venomous, 484

 Silver, poisoning with its compounds, 380

 Simultaneous illness of several persons, important proof of general
    poisoning, 80

 Skin, poisons act slowly or not at all through the sound, 30

 Skin, poisons act through it sometimes when long applied or rubbed in,
    or in the gaseous state, 257, 328, 435, 556, 614, 618, 625

 Snakes, venomous, 484

 _Solanum_, effects of its species on man and animals, 576

 _Sorbus aucuparia._ See _Mountain-ash_.

 Spinal cord, diseases of, distinguished from narcotic poisoning, 527

 Spirituous liquors. See _Alcohol_.

 Sprats smoked, sometimes poisonous, 499

 Spur, what kinds of grain are attacked by, 711

 Spurred maize, 718

 Spurred rye, its causes, 711

 — chemical analysis of, 713

 — effects on man and animals, 714

 — miscarriage supposed to be induced by, 717

 Squill, poisoning with, 670

 Stavesacre, its effects on man and animals, 464

 St. Ignatius’ bean, effects of, on man and animals, 691

 Stomach, distension of, death from, contrasted with irritant poisoning,
    95

 — fibrinous and mucous effusion in, imitates the effects of irritant
    poisoning, 113

 — gelatinization of, a cause of perforation, 107

 — inflammation of, how distinguished from irritant poisoning, 102

 — inflammation of, is it in its acute state ever a natural disease?,
    102

 — partial laceration of, contrasted with irritant poisoning, 97

 — redness of, from natural causes, imitates the effects of irritant
    poisons, 110

 — rupture of, contrasted with the effects of irritant poisons, 96

 — spontaneous perforation of, distinguished from irritant poisoning,
    105

 — spontaneous perforation of, its symptoms and varieties, 105

 — spontaneous perforation of, its morbid appearances, nature and
    causes, 113

 — ulceration of, how distinguished from the effects of irritant
    poisons, 113

 Stomach-pump, discovery of, 567

 Stramonium, its effects on man and animals, 645

 Strontia, its salts not poisonous, 451

 Strychnia, alkaloid of the _Strychni_, effects of, on animals, 683

 _Strychnos_, which of its species are poisonous, 683

 Sugar of Lead. See _Acetate_.

 Sulphate of copper, tests for, 348

 — — — adulteration of bread with, 354

 — — iron occasionally poisonous, 392

 — — magnesia, poisonous in very large doses, 506

 — — mercury, its tests, 290

 — — potash, poisonous in large doses, 507

 — — zinc, tests of when pure, 386

 — — — effects on animals, 387

 — — — effects on man, 388

 — — — morbid appearances by, 391

 — — — process for detecting it in organic mixtures, 386

 Sulpho-cyanic acid a feeble poison, 586

 Sulphur, its effects on man and animals, 152

 Sulphurets of the alkalis, effects on man, morbid appearances, and
    treatment of poisoning with, 196

 Sulphurets of antimony, tests of, 367

 — — arsenic, tests of, 224

 — — arsenic, its effects as a poison, 230

 Sulphuret of copper, not poisonous unless long exposed to the air, 360

 — — lead not poisonous, 428

 — — mercury its tests, 290

 — — mercury, not poisonous, 331

 Sulphuretted hydrogen. See _Gas_.

 Sulphuric acid. See _Acids, Mineral_.

 Sympathetic effects of poisons, 12

 Symptoms of poisoning, evidence from, 42

 — — — general character of, contrasted with those of the symptoms of
    natural disease, 42, 46

 — — — suddenness of the invasion of, 43, 46

 — — — commence after a meal, 45, 47

 — — — commence during health, 49

 — — — regularity of their increase, 44, 47

 — — — uniformity of their nature, 45, 47

 — — — may sometimes of themselves be complete evidence of poisoning,
    179, 259, 337, 691

 Syncopal asphyxia, how distinguished from narcotic poisoning, 527


 Tartar-emetic, action of, on animals, 371

 — action on the skin, 375

 — morbid appearances caused by, 376

 — process for detecting it in a pure solution, 368

 — process for detecting it in organic mixtures, 369

 — symptoms excited in man by, 372

 — sometimes not poisonous in large doses, 373

 Tartar-emetic, treatment of poisoning with, 377

 Tartaric acid, not a poison, 180

 Tetanus lessens the activity of some poisons, 35

 Thorn-apple effects on man and animals, 645

 Ticunas, an American poison, 693

 Tin, poisoning with its compounds, 378

 Tissues, influence of different, in modifying the action of poisons, 30

 Tobacco, effects on man and animals, 649

 — effects of, by the way of injection, 650

 — not injurious to workmen who manufacture it, 652

 Toffana, alleged effects of the _Aqua Toffana_, 249

 _Trachinus_ has poisonous spines, 478

 _Tremblement metallique_, its nature and causes, 325

 Treatment of poisoning, general inferences as to, drawn from the
    physiological action of poisons, 36

 Turbith-mineral, its tests, 290


 Unripe grain, its supposed deleterious effects, 719

 Upas antiar, 698

 — tieuté, 691

 Uterus, rupture of, imitates irritant poisoning, 97


 Vegetable acrids, general remarks on their effects, 451

 Venomous insects, 486

 Venomous serpents, 484

 Veratria, alkaloid of _veratrum_, 673

 _Veratrum_, poisoning with the different species of, 672

 Verdigris, artificial, tests of, 349

 Verdigris, natural, tests of, 348

 Verditer, tests of, 347

 Vermilion, tests of, 290

 Vitriol, blue. See _Sulphate of Copper_.

 Vomiting, effects of, in removing poisons beyond the reach of analysis,
    55


 Wasp, its poisonous effects, 480

 Water-hemlock, effects of, on man and animals, 658

 Weever, poisonous spines of, 478

 Wheat, rust of, is hardly poisonous,

 White-lead, tests for, 397

 White vitriol. See _Sulphate of Zinc_.

 White precipitate, 332

 Worms perforating the intestines may imitate irritant poisoning, 108

 — producing epilepsy may imitate narcotic poisoning, 521

 Woorara, an American poison, 693


 Yew, poisoning with, 699


 Zinc, poisoning with its compounds, 386

 — sulphate of. See _Sulphate_.




                       DESCRIPTION OF THE PLATE.


  1. Small funnel-shaped tube for testing minute portions of liquids.

  2. Apparatus for the distillation of fluids suspected to contain
    acids, one-seventh the natural size.

  3. Tube for reducing very small portions of arsenic or mercury. The
    figure is of half the natural size. The ball may be blown larger, if
    the material to be reduced is bulky.

  4. A small glass funnel for introducing the material into the tube
    Fig. 1, without soiling its inside.

  5. The ordinary apparatus for disengaging sulphuretted-hydrogen. The
    funnel must be a little longer than the emerging tube. The fluid
    should not be at any time much higher than in the figure, in order
    to secure the operator against its effervescing up into the emerging
    tube. The figure is a fourth of the natural size.

  6. Instrument for washing down scanty precipitates on filters. It is a
    thin bottle capable of standing heat—half-filled with water, which
    may be boiled on occasion,—and having its cork pierced with a small
    tube drawn at its outer end to a very fine bore. The breath is
    impelled into the bottle, and, the bottle being then reversed, a
    very fine stream issues with great force.

[Illustration: Fig. 1.]

[Illustration: Fig. 2.]

[Illustration: Fig. 3.]

[Illustration: Fig. 4.]

[Illustration: Fig. 5.]

[Illustration: Fig. 6.]

  7. Tubes of natural size for collecting small portions of mercury by
    the process, p. 300.

  8. Pipette, one-fourth the natural size, for removing by suction
    fluids lying over precipitates. Some have a rectangular bend in the
    upper part, by means of which the operator sees better the point of
    the instrument when in action; but such pipettes are difficult to
    clean. That represented in the figure is easily cleaned with a
    feather.

  9. Apparatus for reducing the sulphurets of some metals by a stream of
    hydrogen. A, the vessel with zinc and diluted sulphuric acid, the
    latter of which may be renewed by the funnel B. C, a ball on the
    emerging tube to prevent the liquid thrown up by the effervescence
    from passing forward. D, E, corks by which C and G are fitted into
    F, the tube which contains the sulphuret at F. G, the exit-tube for
    the sulphuretted-hydrogen, plying into a vessel containing acetate
    of lead. When the hydrogen has passed long enough to expel all the
    air, the spirit-lamp flame is applied at F; and when
    sulphuretted-hydrogen is formed, the lead solution is blackened. The
    figure is one-third the size of the apparatus.

  For Description of Figures 10 and 11, see p. 212.

[Illustration: Fig. 7.]

[Illustration: Fig. 8.]

[Illustration: Fig. 9.]

[Illustration: Fig. 10.]

[Illustration: Fig. 11.]

-----

Footnote 1:

  Orfila and Ollivier, Archives Générales de Médecine, x. 360.

Footnote 2:

  Philosophical Transactions, 1811, 186.

Footnote 3:

  Experiments on Opium, 1795, reprinted in his Treatise on Fevers, iv.
  697.

Footnote 4:

  Essay on the Operation of poisonous agents on the living body, 1829,
  p. 63.

Footnote 5:

  Edin. Phys. and Lit. Essays, iii. 311.

Footnote 6:

  Researches sur l’Acide Hydrocyanique, 1819, p. 179.

Footnote 7:

  Experimental Inquiry on poisoning with oxalic acid. By Dr. Coindet and
  myself.—Edin. Med. and Surg. Journal, xix. _passim_.

Footnote 8:

  Philosophical Transactions, 1811, p. 184.

Footnote 9:

  Annales de Chimie et de Physique, vi. 349.

Footnote 10:

  Report of the Trial of Freeman for the murder of Judith Buswell,
  London Medical Gazette, viii. 796–8.

Footnote 11:

  See subsequently the chapter on Hydrocyanic acid.

Footnote 12:

  Taylor’s Medical Jurisprudence, p. 18.

Footnote 13:

  Annales de Chim. et de Phys. xxvi. 54.

Footnote 14:

  Philosophical Transactions, 1811, p. 182.

Footnote 15:

  Trans. Royal Soc. of Edinburgh, xiii. 393.

Footnote 16:

  Zeitschrift für die Physiologie, iii. i. 81.

Footnote 17:

  Edin. Med. and Surg. Journal, liii. 35, and lvi. 412.

Footnote 18:

  Archiv. für Anatomie und Physiologie, iv. 192.

Footnote 19:

  Ed. Med. and Surg. Journ. liii. 46.

Footnote 20:

  Ed. Med. and Surg. Journ. xix. 335.

Footnote 21:

  Bull. de l’Acad. Roy. de Méd. iii. 426, _et passim_.

Footnote 22:

  Edin. Phys. and Lit. Essays, iii. 334.

Footnote 23:

  Philosophical Transactions, 1811, 198; and Archiv. für Anatomie und
  Physiologie, iv. 192.

Footnote 24:

  Sur le Mechanisme de l’Absorption, 1809; republished, in Journ. de
  Physiol. i. 26.

Footnote 25:

  Recherches sur l’Acide Hydrocyanique, 180.

Footnote 26:

  Revue Médicale, 1827, i. 515.

Footnote 27:

  Edin. Med. and Surg. Journal, xix. 173.

Footnote 28:

  Diss. Inaug. de Venenatis acidi Borussici effectibus. Tubingæ, 1805.

Footnote 29:

  Edin. Med. and Surg. Journal, liii. 45.

Footnote 30:

  Journal des Progrès des Sciences Méd. 1827, iii. 121.

Footnote 31:

  Essay on the Operation of Poisonous Agents on the Living Body.

Footnote 32:

  Essay, &c. pp. 75, 76.

Footnote 33:

  Essay, &c. pp. 69, 71.

Footnote 34:

  Ibidem, pp. 81, 87.

Footnote 35:

  Edin. Med. and Surg. Journal, liii. 35.

Footnote 36:

  Ed. Med. and Surg. Journal, lvi. 412.

Footnote 37:

  Philosophical Transactions, 1841, p. 186. When death begins with any
  other organ but the heart, the heart remains irritable for some time
  after, and contains black blood in all its cavities.

Footnote 38:

  Ib. p. 196.

Footnote 39:

  Diss. Inaug. de Venenis Mineralibus. Edinburgi, 1813.

Footnote 40:

  Edin. Med. and Surg. Journal, xix. _passim_.

Footnote 41:

  Edin. Med. and Surg. Journal, li. 330; liv. 339; lvi. 104. The
  Hæmadynamometer is an instrument invented by M. Poiseulle, which, when
  communicating with the interior of a blood-vessel, indicates the force
  of the circulation by the pressure of the blood on a column of
  mercury.

Footnote 42:

  Mémoire sur l’Emétique—Bulletins de la Société Philomatique, 1812–13,
  p. 361.

Footnote 43:

  Orfila, Toxicologie Générale, i. 258.

Footnote 44:

  Edin. Med. and Surg. Journal, lvi. 104, and other papers there quoted
  above.

Footnote 45:

  Ibid. liv. 121.

Footnote 46:

  Ibid. li. 344.

Footnote 47:

  Emmert, Archiv. für Anatomie und Physiologie, i. l. 180. See also the
  Article False Angustura.

Footnote 48:

  Transactions of the Roy. Soc. of Edinburgh, xiii.

Footnote 49:

  Edin. Med. and Surg. Journal, li. 330, liv. 339, lvi. 104.

Footnote 50:

  Archives Gén. de Med. Nov. 1839, and Edin. Med. and Surg. Journal,
  lvi. 106.

Footnote 51:

  Ibidem, lvi. 123 and 422.

Footnote 52:

  Ibid. xix. 326, 327.

Footnote 53:

  Die Wirkung der Arzneimittel und Gifte, i. 278.

Footnote 54:

  London Med. Gazette, xiv. 63.

Footnote 55:

  Recherches sur l’Acide Hydrocyanique, 140.

Footnote 56:

  Edin. Med. and Surg. Journal, xix. 330.

Footnote 57:

  Journal de Physiologie, iv. 285.

Footnote 58:

  Giornale di Fisica, ix. 458.

Footnote 59:

  These views regarding the decomposition of poisons, were suggested to
  me in 1823 by my friend Dr. Coindet, Junior, of Geneva.

Footnote 60:

  It is not any part of the object of this work to enter into the
  history of toxicology, more especially in early times. But it may be
  well here to state, that the claim which has been made by some for Dr.
  Barry, of having discovered this mode of treatment, is groundless. It
  is distinctly laid down by Nicander, Celsus, Dioscarides, Galen, and
  others who lived in their times; and among the moderns who have
  mentioned it, Gräter, in 1767, notices it in his thesis, “de venenis
  in genere,” printed at Frankfort. On the ancient history of toxicology
  the reader will find an excellent summary by Mr. Adams in the
  Edinburgh Medical and Surgical Journal, xxxiii. 315, and a full
  exposition in Professor Marx’s elaborate work, “die Lehre von den
  Giften.”

Footnote 61:

  Archives Générales de Médecine, Nov. 1826.

Footnote 62:

  Journal des Progrès des Sciences Médicales, 1827, iii. 121.

Footnote 63:

  See the Chapter on Arsenic for some remarks on this subject.—Also
  Beckman’s History of Inventions.

Footnote 64:

  See subsequently the cases of the Crown Prince of Sweden, in the first
  section of the present chapter, and that of General Hoche, Part II.
  Chap. ii. Sect. 2.

Footnote 65:

  I allude to the case of Castaing. See Opium.

Footnote 66:

  Feuerbach. Actenmässige Darstellung Merkwürdiger Verbrechen, i. 1. For
  some observations on the three fatal cases, see the Chapter on
  Arsenic, under the head of the effects of that poison as an
  antiseptic.

Footnote 67:

  See an opinion of the Berlin College in Pyl’s Repertorium für die
  gerichtliche Arzneikunde, i. 244.

Footnote 68:

  Orfila. Médecine-Légale, ii. 360.
  Henke. Lehrbuch der gerichtlichen Medizin, 448.
  Tortosa. Istituzioni di Medicina Forense, ii. 86.
  Beck’s Medical Jurisprudence, 419.

Footnote 69:

  Hume on Crimes, i. 178.

Footnote 70:

  Howell’s State Trials, xviii. 1135.

Footnote 71:

  Hünefeld in Horn’s Archiv, 1827, i. 203.

Footnote 72:

  Weiss in Revue Médicale, Janv. 1826.

Footnote 73:

  See subsequently the Chapter on Arsenic, Section ii.

Footnote 74:

  Archives Générales de Médecine, i. 17; also Abercrombie on Diseases of
  the Stomach, &c. 273.

Footnote 75:

  See Oxalic Acid and Nux Vomica.

Footnote 76:

  Rossi. Ueber die Art und Ursache des Todes des hochseligen Kronprinzen
  von Schweden. Berlin, 1812.

Footnote 77:

  Edinburgh Medico-Chirurgical Transactions, ii. 309.

Footnote 78:

  Alberti, Systema Jurispr. Medic, i. c. 13. § 4.

Footnote 79:

  See Arsenic—Morbid appearances.

Footnote 80:

  Magazin für die gesammte Heilkunde, xiv. 104.

Footnote 81:

  Journal de Médecine, xxix. 107.

Footnote 82:

  Aufsätze und Beobachtungen aus der gerichtlichen Arzneiwissenschaft,
  v. 103.

Footnote 83:

  Wildberg. Praktisches Handbuch für Physiker, iii. 227.

Footnote 84:

  Aufsätze und Beobachtungen, &c. ii. 122.

Footnote 85:

  Edinburgh Medical and Surgical Journal, xviii. 171.

Footnote 86:

  London Medico-Chirurgical Transactions, ii. 158.

Footnote 87:

  Archiv für Medizinische Erfahrung, 1834, p. 754.

Footnote 88:

  Edinburgh Medico-Chirurgical Transactions, ii. 303.

Footnote 89:

  New York Medical and Philosophical Journal, iii. No. 1.

Footnote 90:

  De Veneficio caute dijudicando in Schlegel’s Collectio opusculorum,
  &c. iv. 22.

Footnote 91:

  Edinburgh Medico-Chirurgical Transactions, ii. 291, Edinburgh Medical
  and Surgical Journal, xxvii. 457, and xxix. 26.

Footnote 92:

  Archives Générales de Médecine, ii. 58.

Footnote 93:

  Materialien für die Staatsarzneikunde, 130.

Footnote 94:

  Ueber die gerichtlich-medizinische Beurtheilung der Vergiftungen.
  Kopp’s Jahrbuch, vii. 159.

Footnote 95:

  Rust’s Magazin für die gesammte Heilkunde, iii. 24.

Footnote 96:

  Aufsätze und Beobachtungen, viii. 92.

Footnote 97:

  Morning Chronicle, Jan. 8, 1823.

Footnote 98:

  Journal Universel des Sciences Médicales, xix. 340.

Footnote 99:

  Horn’s Archiv für Medizinische Erfahrung, 1823, i. 451.

Footnote 100:

  Bachmann. Einige auserlesene gerichtlich-medizinische Abhandlungen,
  von Schmitt, Bachmann, &c. p. 21.

Footnote 101:

  Revue Médicale, 1828, ii. 469.

Footnote 102:

  Orfila, in Journ. de Chim. Med. 1842, p. 77.

Footnote 103:

  Probably black extravasation.

Footnote 104:

  Marx, die Lehre von den Giften, i. ii. 429, from Hitzig’s Zeitschrift
  für die Criminal-Rechts-Pflege, I. i. 1.

Footnote 105:

  Charret, in Revue Médicale, 1827, i. 514.

Footnote 106:

  As a specimen of the vague, desultory, and erroneous nature of the
  investigations which have been made by authors on this subject, I may
  quote some remarks published by Virey in the Journal Universel (vi.
  26), and drawn, he says, from a comparison of statements in various
  works. He states that arsenic, which is so fatal to animals in
  general, merely purges dogs and wolves more or less; that nux vomica
  is less fatal to man than to dogs; that pepper is fatal to hogs,
  parsley to parrots, the agrostis arundinacea to goats, elder-berries
  to poultry, chenopodium vulvaria to swine; that on the contrary the
  goat eats with impunity hemlock, daphne gnidium, and some species of
  euphorbia; that the camel eats all species of euphorbia, the hedgehog
  cantharides, the horse monkshood, ranunculus flammula, and buckthorn;
  asses and mules white hellebore, swine yew-berries; all which are
  poisonous to animals in general. He does not state special authorities
  for these facts; but they are taken from authors not of the most
  modern times, and must be received, in my opinion, with great reserve,
  notwithstanding the respect which he claims for the older writers.
  Some of the statements are plainly false.

  In a more recent paper Virey lays it down as a general principle, that
  poisons from the inorganic kingdom act more or less on the whole
  animated creation, but that vegetable and animal poisons are such only
  in respect to particular animals; that carnivorous animals are more
  sensible to the action of vegetable poisons, but less so to that of
  animal poisons, than herbivorous or graminivorous animals; and that
  the activity of poisons on different animals bears a ratio in the
  first place to their relative sensibility, and secondly, to the
  digestive power of their stomach. I question whether these views will
  be generally admitted by toxicologists, without much more extensive
  and more careful inquiries than any hitherto made. [Journ. de Chim.
  Méd. vii. 214.]

  Another singular illustration of the facility with which facts are
  admitted in proof of the varying effects of poisons on different
  animals, is a statement by a German naturalist, Dr. Lenz, to the
  effect that the hedgehog altogether resists the most powerful poisons.
  He states that he has seen one receive ten or twelve wounds from a
  viper on the ears, muzzle, and tongue, without sustaining any harm;
  and that ultimately it kills and devours the snake. He quotes Palias
  for the fact that it has taken 100 cantharides flies without injury,
  and says a medical friend who wished to dissect a hedgehog, gave it
  successively hydrocyanic acid, arsenic, opium, and corrosive
  sublimate, without being able to kill it [L’Institut. ii. 84]. His
  countryman Reich, however, contradicts these statements, observing
  that he has poisoned the hedgehog with hydrocyanic acid, arsenic, and
  corrosive sublimate, but that doses considerably larger are required
  for a dog or cat. Ninety grains of medicinal hydrocyanic acid, thirty
  of arsenic, and twenty of corrosive sublimate, occasioned death.
  [Annalen der Pharmacie, i. 358.] One of my colleagues having lately
  quoted Lenz’s assertion in his lectures, some of his pupils brought me
  two hedgehogs to be subjected to experiment. A drop of the pure acid
  put upon the tongue killed each within a minute.

  The following experiments by Professor Gohier of the veterinary school
  of Lyons are worth mentioning; but in order to be satisfactory would
  require to be performed in a more consecutive train. Muriate of soda
  in the dose of two or three pounds causes in the horse great disorder
  and even death. Calomel has no effect. The juice of rhus toxicodendron
  has no effect on the _solipedes_ either internally or applied to the
  skin. Ten drachms of opium cause in the horse tympanitis and stupor,
  not somnolency. Thirty-six grains of opium had no effect on a dog.
  Cantharides does not injure the horse in the dose of a drachm, or the
  dog in that of nine grains. When the sheep swallows yew-leaves it is
  soon seized with locked-jaw and convulsive movements of the lips and
  flanks: in the horse they cause dilated pupil, convulsive movements of
  the eyes, and restlessness: the goat and dog eat them with impunity
  [Corvisart’s Journal de Médecine, xix. 156]: man is severely affected
  by them. Hyoscyamus, stramonium, hemlock, and other narcotic
  vegetables, though powerfully narcotic to man, will not affect the
  domestic animals unless given in doses 100 times as great as those
  given to man. [Ibid. 154.]

  The most important researches I have yet seen in this line of inquiry
  are those of Professor Viborg of Copenhagen, read in the Royal Danish
  Society of Sciences in 1792. He instituted a connected series of
  experiments, expressly to determine how far the effects of poisons on
  man correspond with those on the lower animals. The results were, that
  mineral poisons appeared to act nearly in the same manner on all
  orders of animals, antimonial and barytic salts alone excepted, the
  former of which acted powerfully on man, the carnivorous animals, and
  swine, but scarcely at all on ruminating and herbivorous animals,
  while the latter in doses of a drachm had no effect on horses: That
  animal poisons resemble mineral poisons in their leading effects on
  most animals: That the vegetable acrids also act pretty uniformly on
  most animals: and that of the vegetable narcotics there are few which
  possess poisonous properties in regard to certain animals only.
  Yew-leaves kill all ruminating animals, and, notwithstanding Virey’s
  statement, swine, mules, and horses, also chickens; and they produce
  violent symptoms in geese, ducks, cats and dogs, although Gohier says
  dogs eat them with impunity. An ape ate a large quantity of the Æthusa
  cynapium without injury. Dogs took from an ounce and a half to three
  ounces of belladonna without dangerous symptoms. [Marx, die Lehre von
  den Giften,—from Viborg’s Sammlung von Abhandlungen für Thierärzte, i.
  277.]

  Professor Mayer of Bonn, in an inquiry into the effects of the
  Coriaria myrtifolia, found that rabbits are not affected at all by a
  drachm of the extract of the juice given internally, or applied to a
  wound; while half a drachm swallowed by a cat kills it in a few hours,
  and three grains will have the same effect when introduced into a
  wound. He likewise found that it is a deadly poison to the dog, the
  hawk, and the frog. [Journal der Praktischen Heilkunde, lxviii. 4,
  43.]

  Professor Giacomini of Padua says, that “in many experiments performed
  by him on dogs and rabbits, he has constantly observed, that the
  former, as being carnivorous by nature, sustain stimulating substances
  tolerably well; while rabbits, being herbivorous, stand stimulants
  ill, but sedatives well.” “Hence many herbivorous animals eat with
  impunity large quantities of vegetable poisons of the sedative kind
  which prove fatal to carnivorous animals.” [Annali Univ. di Med. 1841,
  i. 372.] This may be true as a general rule. But it is not universally
  applicable; for alcoholic fluids kill dogs with great swiftness in no
  great dose.

  An extraordinary statement was lately brought before the French
  Institute, to the effect that 120 sheep, affected with an epidemic
  pleurisy, got each about 500 grains of arsenic without sustaining the
  slightest harm; and that it was also ascertained to have no poisonous
  action upon sheep even in a state of health. A commission of the
  Institute, however, which was appointed to test this assertion, found
  that healthy sheep were killed by a dose of 155 grains, if they had
  fasted for some time before [Annales d’Hyg. Publ. &c. 1843, xxix.
  468.] It is reasonable to suppose, that ruminating animals, whose
  alimentary canal is scarcely ever empty should suffer less than
  carnivorous animals from such poisons as arsenic.

  Lassaigne, in some experiments with arsenic, incidentally remarked,
  that 246 grains of solid arsenic given daily for four days had no
  effect whatever on a horse; but that this result seemed to depend on
  the difficulty which the stomach must experience in appropriating it
  among the bulky materials of its food; for 154 grains in solution
  killed the same animal in six hours [Journ. de Chim. Méd. 1841,
  82].—Gianelli of Lucca found that a horse was killed in eight hours by
  185 grains of powder of arsenic given in the form of bolus [Annales
  d’Hyg. Publ. &c. 1842, xxviii. 88].

  I might easily extend these extracts. But the result would be merely a
  mass of contradiction, from which no sound conclusion could be drawn,
  otherwise the subject would have been discussed in the text.

Footnote 107:

  Pyl’s Aufsätze und Beobachtungen, i. 29.

Footnote 108:

  Celebrated Trials, vi. 55.

Footnote 109:

  Toxicologie Générale, ii. 676.

Footnote 110:

  Journal des Progrès des Sciences Médicales, 1827, iv. 124. See
  subsequently the articles Oxalic Acid and Narcotine.

Footnote 111:

  Journal de Chimie Méd. vii. 131.

Footnote 112:

  Journal de Physiologie, ii. 1, and iii. 81.

Footnote 113:

  Ibidem, iii. 84.

Footnote 114:

  De Sedibus et Causis Morborum, T. ii. Ep. lix. 18.

Footnote 115:

  Knape und Hecker’s Kritische Jahrbücher der Staatsarzneikunde, ii.
  100.

Footnote 116:

  L’Examinateur Médical, 1 Juin, 1842, from Bulletino delle Scien. Med.
  Jan. 1842.

Footnote 117:

  Annales d’Hyg. Publ. et de Méd. Lég. 1842, xxviii. 84.

Footnote 118:

  Ibid. 1843, xxix. 471.

Footnote 119:

  Trial.—This is a good illustration. Nevertheless, it will be seen
  under the head of morbid appearances caused by the irritant class of
  poisons, that Dr. Bostock’s experiments, though conclusive as to the
  statement in the text, did not affect the real questions in the case.

Footnote 120:

  See trial of Freeman—_article_ Hydrocyanic Acid.

Footnote 121:

  I have unfortunately mislaid the reference to this interesting fact,
  which was taken, I think, from a French periodical. In this country
  arsenic is never employed for the purpose mentioned in the text.

Footnote 122:

  Edinburgh Med. and Surg. Journal, xxxiii. 67.

Footnote 123:

  Archives Générales de Médecine, xxi. 364.

Footnote 124:

  Journal de Chimie Médicale, vi. 149.

Footnote 125:

  Edin. Med. and Surg. Journal, xxix. 23.

Footnote 126:

  Ibid., xxvii. 441. On considering, however, this and other instances
  of the kind which have since come under my notice, I suspect the case
  is rendered intelligible by the effect of sleep in suspending or
  delaying for a time the action of arsenic and other simply irritating
  poisons. See above—_evidence from symptoms beginning soon after a
  meal_, p. 46.—also _article_ Arsenic.

Footnote 127:

  Howell’s State Trials, xviii.

Footnote 128:

  Edinburgh Med. and Surg. Journal, xxxv. 298.

Footnote 129:

  Edinburgh Medical and Surgical Journal, xxii. 438.

Footnote 130:

  For a very striking example of the latter description see Hufeland’s
  Journal der Praktischen Heilkunde, xii. i. 110. Fourteen people were
  seized about the same time in a charity workhouse.

Footnote 131:

  Having mislaid the copy I possessed of this trial, I am unable to give
  here the reference.

Footnote 132:

  De Sedibus et Causis Morborum, T. ii. Ep. lix. 7.

Footnote 133:

  Edin. Med. and Surg. Journal, xxxiii. 67.

Footnote 134:

  Howell’s State Trials, xviii.

Footnote 135:

  Edin. Med. and Surg. Journal, xxvii. 441. The reader will remember
  that what was considered defective in the proof in this trial, the
  connection between the administration of a suspicious article and the
  first invasion of the symptoms, would now appear less so, for the
  reason assigned in note [126] p. 77.

Footnote 136:

  Sur l’Empoisonnement par l’acide nitrique, p. 243.

Footnote 137:

  Edinburgh Medical and Surgical Journal, xxix. 19.

Footnote 138:

  MM. Chevallier et Boys de Loury, in Annales d’Hyg. Publ. et Méd. Lég.
  xivv. 400.

Footnote 139:

  MM. Lecanu and Chevallier in Annales d’Hyg. Publ. 1840, xxiv. 282.

Footnote 140:

  London Medical Gazette, 1839–40, i. 575.

Footnote 141:

  Dictionnaire des Sciences Médicales, Art. Indigestion, xxiv. p. 374.

Footnote 142:

  Praktisches Handbuch für Physiker, iii. 292.

Footnote 143:

  See also Dictionnaire des Sciences Médicales, _Art._ Rupture, xlix.
  225.

Footnote 144:

  Médicina Légale, ii. 22.

Footnote 145:

  Archives Générales de Médecine, xx. 433.

Footnote 146:

  Mr. Weekes, in London Medico-Chirurgical Transactions, xiv. 447.

Footnote 147:

  London Medical and Physical Journal, June, 1831, vol. lxvi.

Footnote 148:

  London Medico-Chirurgical Transactions, v. 93.

Footnote 149:

  London Medical Repository, xvii. 108.

Footnote 150:

  Bulletins des Sciences Médicales, x. 64.

Footnote 151:

  Journal des Progrès des Sciences Médicales, xiv.

Footnote 152:

  For an instance, see Bulletins des Sciences Médicales, ix. 249.

Footnote 153:

  Aufsätze und Beobachtungen aus der gerichtlichen Arzneiwissenschaft,
  v. 89.

Footnote 154:

  Med. Rep. on the Effects of Cold Water, 1798, p. 96.

Footnote 155:

  New York Medical Register.

Footnote 156:

  Ann. d’Hyg. Publ. et de Méd. Lég. xxvii. 57.

Footnote 157:

  Abercrombie on Diseases of the Stomach, &c. 14.

Footnote 158:

  Ann. d’Hyg. Publ. xxvii. 60.

Footnote 159:

  Bulletins des Sciences Médicales, vi. 34.

Footnote 160:

  De cauta et circumspecta veneni dati accusatione, § 12.

Footnote 161:

  Edinburgh Medical and Surgical Journal, xxviii. 88.

Footnote 162:

  Ibid. xxix. 70.

Footnote 163:

  London Medical Gazette, viii. 496.

Footnote 164:

  Edinburgh Medical and Surgical Journal, xxviii. 99.

Footnote 165:

  Trial of Donnal.—See Paris and Fonblanque’s Medical Jurisprudence,
  iii. Appendix, 277, _et seq._

Footnote 166:

  Edinburgh Medical and Surgical Journal, xxviii. 87.

Footnote 167:

  On Diseases of the Stomach and other Abdominal Viscera, p. 15.

Footnote 168:

  Recherches sur la Gastro-entérite, ii. 51.

Footnote 169:

  Laisné sur les Perforations Spontanées, p. 206, from Recueil des
  observations des Hopitaux Militaires, i. 375.—This case is also given
  by MM. Petit and Serres in their treatise entitled “de la Fièvre
  Entéro-Mésenterique,” p. 197, and is considered by them an instance of
  that particular disease.

Footnote 170:

  Trans. of Provinc. Med. and Surg. Association, vol. i.

Footnote 171:

  Louis in Archives Générales de Médecine, i. 17, or Edin. Med. and
  Surg. Journal, xxi. 239, also Abercrombie on Diseases of the Stomach,
  &c. 273, and Louis Recherches sur la Gastro-entérite, _passim_.

Footnote 172:

  Abercrombie on Diseases of the Stomach, &c. pp. 156 and 243.

Footnote 173:

  Abercrombie on Diseases of the Stomach, &c., p. 52.

Footnote 174:

  For cases of this disease, see Abercrombie on Diseases of the Stomach,
  &c., p. 156 and 181.

Footnote 175:

  Considérations Medico-légales sur les perforations spontanées de
  l’estomac, 1819. This thesis, published with three others on
  medico-legal subjects, is understood to have been in a great measure
  the work of the late Professor Chaussier.

Footnote 176:

  Trans. of the Dublin College of Physicians, i. 2, and London
  Medico-Chirurgical Transactions, viii. 228.

Footnote 177:

  Guy’s Hospital Reports, 1839, iv. 20.

Footnote 178:

  Abercrombie on Diseases of the Stomach, 41.

Footnote 179:

  London Medico-Chirurg. Transactions, viii. 233.

Footnote 180:

  Archives Générales de Médecine, xxvi. 123.

Footnote 181:

  On Diseases of the Stomach, pp. 35, 37.

Footnote 182:

  Guy’s Hospital Reports, 1839, iv. 16.

Footnote 183:

  Guy’s Hosp. Rep. 1839, 52.

Footnote 184:

  Edinb. Med-Chirurgical Transactions, i. 311.

Footnote 185:

  Rust’s Magazin für die gesammte Heilkunde, xxi. 199. This paper is
  analysed in Edinburgh Med. and Surg. Journal, xxvi. 451.

Footnote 186:

  Philosophical Transactions, lxii. 447.

Footnote 187:

  Gastellier in Leroux’s Journal de Médecine, xxxiii. 24.

Footnote 188:

  Archives Générales de Médecine, xi. 463.

Footnote 189:

  Mr. Kell in London Medical Gazette, ii. 649.

Footnote 190:

  Magazin für die gesammte Heilkunde, xviii. 107.

Footnote 191:

  Revue Médicale, 1826, i. 100.

Footnote 192:

  Jahrbuch des Oesterreiches Staates, xxii. 54, or Arch. Gén. de Méd.
  xlvi. 480.

Footnote 193:

  Journal de Médecine, xxxiv. 25.

Footnote 194:

  Affaire Hullin. Archives Générales de Médecine, xix. 332.

Footnote 195:

  London Medico-Chirurgical Transactions, iv. 371.

Footnote 196:

  Archives Générales de Médecine, Oct. and Nov. 1826; also Edin. Medical
  and Surgical Journal, xxviii. 149.

Footnote 197:

  De la Membranes Muqueuse Gastro-intestinale, 1825.

Footnote 198:

  Ibid. p. 220.

Footnote 199:

  For a case of this rare and singular disease, see Edin. Medical and
  Surgical Journal, xxvi. 214.

Footnote 200:

  Kopp’s Jahrbuch der Staatsarzneikunde, ii. 169.

Footnote 201:

  Journal de Médecine, vii. 333. Also Foderé, Traité de Médecine-Légale,
  iv. 282.

Footnote 202:

  Nouvelle Bibliothèque Médicale, 1828, iii. 141.

Footnote 203:

  Philos. Trans. lxii. 450.

Footnote 204:

  See Analysis of his Essay by Dr. Gumprecht, Lond. Med. Repos. x. 416.

Footnote 205:

  Laisné, Sur les Perforations Spontanées, 149.

Footnote 206:

  The last cases were observed by Hunter. See Philos. Transactions,
  lxii. 452.

Footnote 207:

  Fisica Animale e Vegetabile. Dissertazione quinta, § ccxxiii.-ccxxxi.
  T. ii. 86–89, Edit. Venezia, 1782.

Footnote 208:

  De Alimentorum Concoctione. Diss. Inaug. Edinburgh 1777.

Footnote 209:

  Experiments on Digestion. Appendix to Spallanzani’s Dissertations
  relative to the Natural History of Animals and Vegetables. London
  Edition, 1784, i. 317.

Footnote 210:

  Expériences sur la Digestion dans l’homme. Paris, 1814, pp. 20, _et
  seq._

Footnote 211:

  Die Verdauung nach Versuchen, &c. Heidelberg, 1825, or the French
  Edition, Recherches Expérimentales Physiologiques et Chimiques sur la
  Digestion, 1826, _passim_.

Footnote 212:

  Inquiry into the Chemical Solution of the stomach after death.
  Edinburgh Med. and Surg. Journal, xxxiv. 282.

Footnote 213:

  Medizinisch-Chirurgische Zeitung, 1828, ii. 57, 77, 93, and 107.

Footnote 214:

  Edinb. Med. and Surg. Journal, vi. 135.

Footnote 215:

  Journal Complémentaire du Dict. des Scien. Med. xxxvii. 194.

Footnote 216:

  Horn’s Archiv für Medizinische Erfahrung, 1823, i. 45.

Footnote 217:

  Trial of Angus for the murder of Margaret Burns, 1808.

Footnote 218:

  Laisné sur les Perforations de l’Estomac, p. 190, and Bìllìard,
  Considérations sur l’Empoisonnement par les Irritans, _passim_.

Footnote 219:

  Edin. Med. and Surg. Journal, vi. 137.

Footnote 220:

  London Medical Gazette, ii. 619.

Footnote 221:

  Laisné. &c. p. 564.

Footnote 222:

  Edin. Med. and Surg. Journal, xxxii. 38.

Footnote 223:

  London Med. Gazette, xiv. 30.

Footnote 224:

  Traité de l’Empoisonnement par l’acide Nitrique, 1802, p. 87.

Footnote 225:

  Novellæ Medico-legales, Cas. xxix. p. 211.

Footnote 226:

  Bulletins ties Sciences Médicales, Janvier, 1830.

Footnote 227:

  Edinburgh Medical and Surgical Journal, xxxv. 298.

Footnote 228:

  Burnett on Criminal Law, 544. _Note._

Footnote 229:

  Edinburgh Med. and Surg. Journal, xxxvi. 102.

Footnote 230:

  Ibidem, xxii. 222.

Footnote 231:

  Report of the Committee of the House of Commons on the Combination
  Laws, June, 1825, pp. 323–328. Evidence of Mr. Campbell and Mr.
  Robinson.

Footnote 232:

  Cases and Observations in Medical Jurisprudence, Case iii. Edin. Med.
  and Surg. Journal, xxxi. 229.

Footnote 233:

  London Med. Gazette, 1839–40, i. 944.

Footnote 234:

  A Manual of Medical Jurisprudence, 1844, p. 94.

Footnote 235:

  Toxicologie Générale, 1843, i.

Footnote 236:

  Archiv für Medizinische Erfahrung, 1823, i. 456.

Footnote 237:

  Revue Médicale, 1824, ii. 469.

Footnote 238:

  Toxicologie Gén. 4ème edition, 1843, i. 112.

Footnote 239:

  Poggendort’s Annalen der Physik und Chemie, xli. 643. Buchner’s
  Repertorium, 1838, lxiv. 20.

Footnote 240:

  Buchner’s Repertorium, lxiv. 32.

Footnote 241:

  Journal de Chimie Médicale, 1841, 474.

Footnote 242:

  Toxicologie Gén. i. 77.

Footnote 243:

  Ibidem, 78.

Footnote 244:

  Journal de Chimie Médicale, 1842, 266.

Footnote 245:

  London Medical Gazette, 1841–42, ii. 254.

Footnote 246:

  Traité de l’Empoisonnement par l’acide nitrique, 1802.

Footnote 247:

  Lebidois, Arch. Gén. de Med. xiii. 367.

Footnote 248:

  Martini in Rust’s Magazin für die gesammte Heilkunde, xviii. 159.

Footnote 249:

  Correa de Serra in Journal de Chimie Médicale, ii. 209, on the third
  day.

Footnote 250:

  Edinburgh Med. and Surg. Journal, xxxvi. 103.

Footnote 251:

  Archives Générales de Médecine, xiii. 367.

Footnote 252:

  Tartra, iii. 87.

Footnote 253:

  Desgranges, Recueil Périodique de la Société de Médecine, vi. 22.
  Tulpius, Observationes Medicinales, iii. 43.

Footnote 254:

  Annales d’Hygiène Publique, xvii. 362.

Footnote 255:

  Journal der Praktischen Heilkunde, vii. ii. 18.

Footnote 256:

  Archives Générales, xiii. 367.

Footnote 257:

  Tartra, p. 160.

Footnote 258:

  Edinburgh Med. and Surg. Journal, xxxvi. 102.

Footnote 259:

  Journal der Praktischen Heilkunde, xlix. iii. 60.

Footnote 260:

  Journal der Praktischen Heilkunde, vii. ii. 18.

Footnote 261:

  Mr. J. B. Thomson in London Med. Gazette, 1841–42, i. 146.

Footnote 262:

  Martini’s case.

Footnote 263:

  London Med. Gazette, 1834, xiv. 489.

Footnote 264:

  Tendering in Horn’s Archiv für Medizinische Erfahrung, 1825, i. 458.

Footnote 265:

  Journal de Médecine par Corvisart, xix. 263.

Footnote 266:

  Rust’s Magazin für die gesammte Heilkunde, xxiii. 156.

Footnote 267:

  Lancet, 1836–37, ii. 835.

Footnote 268:

  Lancet, 1836–37, i. 195.

Footnote 269:

  London Medical Gazette, xii. 219.

Footnote 270:

  Augustin’s Repertorium, i. ii. 15.

Footnote 271:

  Archives Gén. de Méd., xxi. 372, _note_.

Footnote 272:

  Journal Hebdomadaire.

Footnote 273:

  Tartra, p. 124.

Footnote 274:

  Dr. Bartley, iv. 289, and Mr. Diamond, v. 110.

Footnote 275:

  Mr. Bevan, i. 756.

Footnote 276:

  Journal de Chimie Médicale, 1835, 426.

Footnote 277:

  Dublin Journal of Med. and Chem. Science, No. 25.

Footnote 278:

  Horn’s Archiv für Medizinische Erfahrung, 1823, i. 465.

Footnote 279:

  Ibid. 452.

Footnote 280:

  Edin. Med. and Surg. Journal, xxxvi. 101. Lond. Med. Gazette, xii.
  221.

Footnote 281:

  Horn’s Archiv, &c. 453.

Footnote 282:

  London Medical Gazette, xiv. 489, and 1837–8, ii. 76.

Footnote 283:

  Louis, ibidem, xiv. 30.

Footnote 284:

  Philadelphia Journal of Med. and Phys. Sciences, iv. 410.

Footnote 285:

  London Medical Gazette, viii. 76.

Footnote 286:

  Edinburgh Med. and Surg. Journal, liii. 406.

Footnote 287:

  Aufsätze und Beobachtungen, ii. 122.

Footnote 288:

  Archives Générales de Médecine, xiii. 368.

Footnote 289:

  Horn’s Archiv, &c. 1823, i. 456.

Footnote 290:

  Edin. Med. and Surg. Journal, liii. 401.

Footnote 291:

  Edin. Med and Surg. Journ. xxii. 222, and xxxvi. 103.

Footnote 292:

  Kerkringii opera omnia, p. 146.

Footnote 293:

  Annales d’Hygiène Publique, &c. xvii. 362.

Footnote 294:

  Robert in Nouvelle Bibliothèque Médicale, 1827, iv. 415.

Footnote 295:

  Henke’s Zeitschrift für die Staatsarzneikunde, xxxii. 161.

Footnote 296:

  Toxicologie Générale, ii. 689.

Footnote 297:

  Edinburgh Med. and Surg. Journal, xxii. 222.

Footnote 298:

  Ibidem, xxxv. 302.

Footnote 299:

  Journal de Chimie Médicale, 1840, 30.

Footnote 300:

  Medizinisch-Chirurgische Zeitung, 1824, iv. 276.

Footnote 301:

  Rust’s Magazin für die gesammte Heilkunde, 1837, l. 501.

Footnote 302:

  Dr. Sinclair. Edin. Med. and Surg. Journal, xxxvi. 99; and case of
  Humphrey. Ibidem, xxxv. 301.

Footnote 303:

  London Medical Gazette, xii. 219. Mr. Arnott’s Case.

Footnote 304:

  Lancet, 1829–30, ii. 330 and 432.

Footnote 305:

  Orfila. Journal de Chimie Médicale, 1842, p. 5.

Footnote 306:

  Peligot. Journal de Pharmacie, 1833, p. 644.

Footnote 307:

  Barthemot. Journal de Pharmacie, 1841, 560.

Footnote 308:

  Archives Générales de Médecine, xxi. 365.

Footnote 309:

  Lancet, 1829–30, ii. 840.

Footnote 310:

  Annales d’Hygiène Publique, &c. xxviii. 200. Also Toxicologie
  Générale. 1843, i. 142.

Footnote 311:

  Journal de Chim. Médicale, 1842, 266.

Footnote 312:

  Annales d’Hygiène Publique, 1842, xxviii. 317.

Footnote 313:

  Prout, Philosophical Transactions, 1824, p. 45.—Tiedemann and Gmelin,
  Die Verdauung nach Versuchen, _passim_.—_Children_, Annals of
  Philosophy, 1824, viii. 68.

Footnote 314:

  Philosophical Transactions, 1824, p. 49.

Footnote 315:

  London Medical Gazette, 1839–40, i. 285.

Footnote 316:

  Lancet, 1839–40, i. 899.

Footnote 317:

  Toxicologie Générale, i. 155.

Footnote 318:

  Lins in Buchner’s Repertorium, lxviii. 389.

Footnote 319:

  Toxicologie Générale, i. 56.

Footnote 320:

  Worbe in Mémoires de la Société Médicale d’Emulation, ix. 507.

Footnote 321:

  Annales de Chimie, xxvii. 87.

Footnote 322:

  Worbe, &c. and Edin. Med. and Surg. Journal, xxviii. 228.

Footnote 323:

  Revue Médicale, 1829, iii. 429.

Footnote 324:

  Buchner’s Repertorium für die Pharmacie, lxxi. 341.

Footnote 325:

  Diction. de Méd. et de Chir. Pratiques, xii. 707.

Footnote 326:

  Medizinisch-Chirurgische Zeitung, 1826, iv. 183.

Footnote 327:

  Horn’s Archiv für Medizinische Erfahrung, 1830, ii. 861.

Footnote 328:

  Corvisart’s Journal de Médecine, xxi. 70.

Footnote 329:

  Toxicologie Générale, i. 141.

Footnote 330:

  Dr. O’Shaughnessey, in Lancet, 1829–30, ii. 632.

Footnote 331:

  Experimental Essay on Iodine, &c. 1837, p. 21.

Footnote 332:

  Journal de Chimie Médicale, ii. 291.

Footnote 333:

  Ibid. iv. 388.

Footnote 334:

  Lancet, 1830–31, vol. i. 613.

Footnote 335:

  Ibidem, 612.

Footnote 336:

  Annales d’Hygiène Publique, xxviii. 431.

Footnote 337:

  Annali Universali di Med. 1833.

Footnote 338:

  Essay on the Effects of Iodine, 1824, p. 20.

Footnote 339:

  Horn’s Archiv für Medizinische Erfahrung, 1829, i. 340.

Footnote 340:

  Dessaigne in Journal de Chim. Médicale, iv. 65.

Footnote 341:

  Moncourrier, Ibidem, iv. 216.

Footnote 342:

  Formulaire pour les Nouveaux Médicaments, 1825, p. 161.

Footnote 343:

  Quoted in Dr. Cogswell’s Experimental Essay, p. 23.

Footnote 344:

  Quoted in Dr. Cogswell’s Experimental Essay, p. 27.

Footnote 345:

  Gairdner on the Effects of Iodine, p. 9.

Footnote 346:

  Journal Complémentaire, xviii. 126.

Footnote 347:

  Magazin für die gesammte Heilkunde, xvi. 111.

Footnote 348:

  Gairdner, &c. p. 12.

Footnote 349:

  Magazin für die gesammte Heilkunde, xxii. 291.

Footnote 350:

  American Journal of Medical Science, viii. 546.

Footnote 351:

  Archiv für Medizinische Erfahrung, 1829, i. 342.

Footnote 352:

  Johnson’s Preface to his Translation of Coindet on Iodine, p. ix.

Footnote 353:

  Gairdner, p. 20.

Footnote 354:

  Coindet on Iodine, p. 17.

Footnote 355:

  London Medical Gazette, 1839–40, ii. 588.

Footnote 356:

  Cogswell’s Essay, p. 42.

Footnote 357:

  Lancet, 1829–30, ii. 635.

Footnote 358:

  Toxicologie Générale, 1843, i. 74.

Footnote 359:

  Lancet, 1829–30, ii. 638.

Footnote 360:

  Archives Générales de Médecine, x. 255.

Footnote 361:

  Lancet, 1831–32.

Footnote 362:

  Manual of Medical Jurisprudence, 128.

Footnote 363:

  London Medical Gazette, 1841.

Footnote 364:

  Ibidem, 1839–40, i. 588.

Footnote 365:

  This adulteration and its effects have been indicated by various
  chemists. For the best account, see Chevallier, sur les falsifications
  qu’on fait subir au sel marin, Annales d’Hyg. Publ. et de Méd. Lég.
  viii. 250. At one time he found about a third of the salt in Paris
  thus sophisticated.

Footnote 366:

  Cours de Médecine-Légale, 1840, iii. 183.

Footnote 367:

  Manual of Medical Jurisprudence, p. 38.

Footnote 368:

  Zeitschrift für Physiologie, ii.

Footnote 369:

  Ibidem.

Footnote 370:

  Lancet, 1830–31, i. 613.

Footnote 371:

  Experimental Essay on Iodine, &c. 1837, p. 91.

Footnote 372:

  De l’Action du Brôme et de ses combinaisons sur l’économie animale.
  Thèse Inaug. à Paris, 1828.

Footnote 373:

  Hufeland’s Bibliothek der Praktischen Heilkunde, Sept. 1829; or
  Archives Gén. de Méd. xxiv. 289.

Footnote 374:

  Meckel’s Archiv für Anatomie und Physiologie, xiv. 222.

Footnote 375:

  Edin. Med. and Surg. Journal, lviii. 120.

Footnote 376:

  Bulletins de Thérapeutique, Février, 1830.

Footnote 377:

  Journal de Chimie Médicale, 1837, 227.

Footnote 378:

  Annales d’Hygiène Publ. et de Méd. Lég. vi. 169.

Footnote 379:

  Beiträge zur Kentniss der Wirkungen der Arzneimittel und Gifte. Horn’s
  Archiv. 1824, i. 59.

Footnote 380:

  Medizinische Zeitung, 1828, ii. 256.

Footnote 381:

  Ann. d’Hyg. Publ. et de Méd. Lég. vi. 160.

Footnote 382:

  Beiträge, &c. Horn’s Archiv, 1824, i. 56.

Footnote 383:

  Corvisart’s Journal de Médecine, xxiv. 215.

Footnote 384:

  Annales d’Hyg. Publ. et de Méd. Lég. vi. 159.

Footnote 385:

  See Trousseau and Blanc, Arch. Gén. de Méd. Sept. 1830.

Footnote 386:

  London Courier, September 22, 1827.

Footnote 387:

  Manual of Medical Jurisprudence, 116.

Footnote 388:

  London Medical Repository, i. 382.

Footnote 389:

  Lond. Med. Rep. iii. 382.

Footnote 390:

  Dissertatio Inauguralis de Acidi Oxalici vi venenata, Edin. 1821.

Footnote 391:

  Edinburgh Med. and Surg. Journal, xix. 163.

Footnote 392:

  Medizinisch-Chirurgische Zeitung, 1828, ii. 203, _et seq._

Footnote 393:

  Lancet, 1830–31, i. 96.

Footnote 394:

  Mr. A. Taylor. Manual of Medical Jurisprudence, p. 120.

Footnote 395:

  Edin. Med. and Surg. Journal, xix. 168.

Footnote 396:

  Mr. Davies in Lancet, 1838–39, i. 30.

Footnote 397:

  Lancet, 1830–31, i. 187.

Footnote 398:

  Toxicologie Gén. 1843, i. 190.

Footnote 399:

  Bulletins de Pharmacie, vi. 87.

Footnote 400:

  Edin. Med. and Surg. Journal, xix. 166.

Footnote 401:

  Ibid. 169.

Footnote 402:

  Edin. Med. and Surg. Journal, xix. _passim_.

Footnote 403:

  Medizinisch-Chirurgische Zeitung, 1828, ii. 203, 219, 235, 254.

Footnote 404:

  Toxicologie Gén., 1843, i. 187.

Footnote 405:

  London Courier, Feb. 1, 1823.

Footnote 406:

  St. James’s Chronicle, August 17, 1826.

Footnote 407:

  London Medical Repository, xxii. 476.

Footnote 408:

  Edin. Med. and Surg. Journal, xiv. 606.

Footnote 409:

  London Medical Gazette, 1842–43, i. 490.

Footnote 410:

  Edin. Med. and Surg. Journal, xix. 187.

Footnote 411:

  London. Med. Gaz. i. 737.

Footnote 412:

  Dr. Scott, in Edin. Med. and Surg. Journal, xxiv. 67.

Footnote 413:

  London Medical Gazette, 1842–43, i. 490. The quantity could scarcely
  have been two ounces, 1, because a penny-worth, which was what the
  person bought, amounts only to two drachms, and 2, because it could
  not have been dissolved, as the patient said was done, in four ounces
  of water. The word _ounces_ is probably a misprint for drachms.

Footnote 414:

  Guy’s Hospital Reports, 1838, iii, 353.

Footnote 415:

  London Med. Repository, xi. 20.

Footnote 416:

  Ibid. vi. 474.

Footnote 417:

  Guy’s Hospital Reports, 1838, iii. 353.

Footnote 418:

  London Med. Repository, iii. 380.

Footnote 419:

  Lancet, 1838–39, ii. 748.

Footnote 420:

  London Medical Repository, xii. 18. London Medical Gazette, i. 737.
  Edinburgh Medical and Surgical Journal, xxiv. 67.

Footnote 421:

  Edin. Med. and Surg. Journal, xiv. 607.

Footnote 422:

  London Medical Gazette, i. 737.

Footnote 423:

  Edinburgh Med. and Surg. Journal, xix. 190.

Footnote 424:

  Journal de Chim. Med. 1842, 211, and Orfila, Toxicologie Gén. 1843, i.
  195.

Footnote 425:

  Annales d’Hyg. Publique, 1842, xxvii. 422.

Footnote 426:

  Lond. Med. Gazette, 1840–41, i. 480.

Footnote 427:

  Edin. Med. and Surg. Journal, xix. 185.

Footnote 428:

  Medizinisch-Chirurgische Zeitung, 1828, ii. 255.

Footnote 429:

  Orfila, in Journal de Chimie Médicale, 1842, 145.

Footnote 430:

  Annales d’Hygiène, Publique, 1842, xxviii. 206.

Footnote 431:

  Journal de Chimie Médicale, 1842, 197.

Footnote 432:

  Toxicol. Gén. i. 164, 3me Edition.

Footnote 433:

  Ibid. 166, and also Archives Gén. de Méd. xiii. 373.

Footnote 434:

  Edin. Med. and Surg. Journal, li. 335, lvi. 345, lvi. 123.

Footnote 435:

  Annales d’Hyg. Publique, xxviii. 212.

Footnote 436:

  Edin. Med. and Surg. Journal, liv. 341.

Footnote 437:

  London Medical Gazette, 1842–43, i. 188.

Footnote 438:

  Edin Med. and Surg. Journal, xxx. 310.

Footnote 439:

  Toxicologia, p. 225.

Footnote 440:

  London Med. Repository, vii. 118.

Footnote 441:

  Orfila, Toxic. Gén. i. 167.

Footnote 442:

  Edin. Med. and Surg. Journ. xxx. 310.

Footnote 443:

  Surgical Observations, Part i. 82.

Footnote 444:

  Toxic. Gén. i. 169.

Footnote 445:

  Bulletin de l’Acad. Roy. de Méd. 1836, i. 151.

Footnote 446:

  Journal de Pharmacie, ix. 355, or Med. Repos. xx. 441.

Footnote 447:

  Annales d’Hygiène Publique, xxix. 417.

Footnote 448:

  Toxic. Gén. i. 193.

Footnote 449:

  Edinburgh Med. and Surg. Journal, li. 334, liv. 346.

Footnote 450:

  Annales d’Hygiène Publique, xxix. 415.

Footnote 451:

  Experimental Essays, p. 113.

Footnote 452:

  Journal de Médecine, lxxiii. 22.

Footnote 453:

  Tartra sur l’empoisonnement par l’acide nitrique, 136.

Footnote 454:

  London Med. Repository, xxiii. 523.

Footnote 455:

  Experimental Essays, pp. 114, 115.

Footnote 456:

  Souville in Journal de Médecine, lxxiii. 19.

Footnote 457:

  Laflize in Journ. de Méd. lxxi. 401.

Footnote 458:

  Manual of Medical Jurisprudence, 1844, 130.

Footnote 459:

  Alexander, Experimental Essays, p. 109.

Footnote 460:

  Memoirs of London Med. Society, iii. 527.

Footnote 461:

  Edin. Med. and Surg. Journ. xiv. 34.

Footnote 462:

  Annali Univers. di Medicina, 1836, iii. 333.

Footnote 463:

  Journal der Praktischen Heilkunde, lvii. i. 124.

Footnote 464:

  Journal de Physiologie, iii. 243.

Footnote 465:

  Toxicol. Gén. i. 174.

Footnote 466:

  Gmelin’s Geschichte der Mineralischen Gifte, s. 252.7

Footnote 467:

  Timæi Casus Medicinales, lvii. c. 12.

Footnote 468:

  Orfila, Toxic. Gén. i. 220.

Footnote 469:

  Edinburgh Med. and Surg. Journal, li. 336, lvi. 422, liii. 38.

Footnote 470:

  Toxicol. _ut supra_.

Footnote 471:

  Plenck, Toxicologia, 226.

Footnote 472:

  Essay on Fevers, p. 308.

Footnote 473:

  Bulletins de la Soc. de Méd. 1815, No. viii. T. iv. 352.

Footnote 474:

  Edinburgh Medical and Surgical Journal, xiv. 642.

Footnote 475:

  Revue Médicale, xvii. 265.

Footnote 476:

  Journal de Chimie Médicale, 1840, 499.

Footnote 477:

  London Medical Gazette, 1837, xxi. 529.

Footnote 478:

  Orfila, Toxicol Gén. i. 229.

Footnote 479:

  De salis ammoniaci, vi, &c. Heidelberg, 1826. Analysed in Revue Med.
  1827, i. 284.

Footnote 480:

  Orfila, i. 228.

Footnote 481:

  Orfila, Annales d’Hygiène Publique, xxviii. 431.

Footnote 482:

  Toxic. Gén. i. 177.

Footnote 483:

  Annales, _ut supra_.

Footnote 484:

  Toxicologie Gén. 1843, i. 269. Two from an Essay by M. Chantourelle,
  read before the Acad. de Médecine,; and one from M. Lafranque in Ann.
  de la Méd. Physiolog. Février, 1825.

Footnote 485:

  Journ. Universel, xviii. 265.

Footnote 486:

  See _Poisonous Gases_.

Footnote 487:

  Journal de Chimie Médicale, 1842, p. 656.

Footnote 488:

  It appears that arsenic does not always undergo this change. Berzelius
  once kept some fragments in an open phial for three years without
  observing any change in appearance or weight. [Annales de Chimie et de
  Physique, xi. 240.] Buchner once made a similar observation, and is
  inclined to think that oxidation does not occur, if the metal is quite
  pure. [Repertorium für die Pharmacie, xxi. 29.]

Footnote 489:

  American Journ. of Med. Science, x. 122.

Footnote 490:

  Hahnemann, Uber die Arsenic-vergiftung, 13.

Footnote 491:

  Edin. Medico-Chirurgical Transactions, ii. 292.

Footnote 492:

  Journal de Chimie Médicale, ii. 61.

Footnote 493:

  As far back at least as the time of Zacchias. See his Quæstiones
  Medico-legales, iii. 37, 11.

Footnote 494:

  Edin. Med. and Surg. Journal, 1827, xxviii. 96.

Footnote 495:

  Consult among others, Taylor’s Manual of Medical Jurisprudence, p.
  135.

Footnote 496:

  Toxicologie Gén. 1843, i. 376.

Footnote 497:

  Magazin für die gesammte Heilkunde, v. 66.

Footnote 498:

  Mr. Blandy, for example, who said he “perceived an extraordinary
  grittiness in his mouth, attended with a very painful pricking and
  burning pain in his tongue, throat, stomach, and bowels.” [Howell’s
  State Trials, xviii. 1135.]

Footnote 499:

  American Journal of Medical Science, x. 122.

Footnote 500:

  Schweigger’s Journal der Chemie. vi. 232.

Footnote 501:

  Journal de Chimie Médicale, ii. 61.

Footnote 502:

  London Philosophical Journal, 1837, ii. 482.

Footnote 503:

  Ueber die Arsenic-vergiftung, 10.

Footnote 504:

  Contrepoisons de l’Arsenic du sublimé corrosif, &c. i. 20.

Footnote 505:

  Neues Nordisches Archiv. i.

Footnote 506:

  Journal de Chimie Médicale, ii. 61.

Footnote 507:

  Ueber die Arsenic-vergiftung, 223.

Footnote 508:

  Lectures on Chemistry, ii. 430.

Footnote 509:

  Edin. Med. and Surg. Journal, xxii. 82, and Edin. Medico-Chirurgical
  Transactions, ii. 293.

Footnote 510:

  Paris and Fonblanque’s Medical Jurisprudence, ii. 251.

Footnote 511:

  Donovan in Dublin Phil. Journal, ii. 402.

Footnote 512:

  Ibid.

Footnote 513:

  American Journal of Medical Science, x. 126.

Footnote 514:

  Annales d’Hyg. Pub. et de Med. Lég. xi. 224.

Footnote 515:

  The only probable source of such impregnation is pyritic sulphur,
  which is frequently used abroad, and has of late been occasionally
  employed in this country, for making sulphuric acid. As pyrites
  commonly contains arsenic, the acid becomes adulterated with oxide of
  arsenic, and may communicate the same impregnation to various other
  reagents which are prepared by means of sulphuric acid. The oxide may
  easily be detected in that acid by a stream of hydrosulphuric acid
  gas, after moderate dilution with water; for pure acid is rendered
  milky; but an arsenical acid yields a yellow precipitate of sulphuret
  of arsenic.

Footnote 516:

  Journal de Chim. Méd. viii. 449.

Footnote 517:

  Reinsch, in Repertorium für die Pharmacie, lvi. 183.

Footnote 518:

  This has been occasionally observed by Chevallier [Journal de Chim.
  Méd. 1840, 434], and once by M. Roturier [Ibidem, 627]. The former met
  with a medico-legal case where from this circumstance an erroneous
  opinion was at first formed in favour of poisoning.

Footnote 519:

  London Med. Chirurgical Transactions, iii. 342.

Footnote 520:

  See a paper by myself in Edin. Med. and Surg. Journal, xxii. 60, where
  the fallacies to which the liquid tests are liable are investigated at
  great length.

Footnote 521:

  Horn’s Archiv für Medizinische Erfahrung, 1827, i. 230.

Footnote 522:

  Edin. Med. and Surg. Journal, xxii. 74.

Footnote 523:

  Edinburgh Med. and Surg. Journal, July, 1824.

Footnote 524:

  Edinburgh New Philosophical Journal, 1836, xxi. 229.

Footnote 525:

  Mr. L. Thomson in Lond. Phil. Journal, 1837, i. 353.—Orfila, Journal
  de Chimie Médicale, 1841, p. 212.—Bischoff, Repertorium für die
  Pharmacie, lxxv. 411.—Mr. H. H. Watson, Manchester Memoirs, vi.
  603.—Pettenkoffer, Repertorium für die Pharmacie, lxxvi.
  289.—Berzelius, and a Committee of the French Institute, Journal de
  Chimie Médicale, 1841, 393.—Flandin and Danger, Ibidem, 1841,
  435.—Malapert, Ibidem, 1841, 295.—Lassaigne, Ibidem, 1840, 638,—Mr.
  Ellis, Lancet, 1843.—A paper of my own, Edinburgh Monthly Journal of
  Med. Science, iii. 257.

Footnote 526:

  Journal de Chimie Médicale, 1841, 393. Rapport de l’Institut.

Footnote 527:

  Edinburgh Monthly Journal of Medical Science, 1843, iii. 257.

Footnote 528:

  Journal für Praktischen Chemie, 1842, xxiv. 242.

Footnote 529:

  See Edinburgh Monthly Journ. of Med. Science, 1843, iii. 774.

Footnote 530:

  Annalen der Chimie und Pharmacie, 1844, xlix. 291.

Footnote 531:

  Edinburgh Medical and Surgical Journal, 1824, xxii. 78.

Footnote 532:

  Annalen der Chemie und Pharmacie, xlix. 308.

Footnote 533:

  Journal de Chimie Médicale, 1841, p. 413.

Footnote 534:

  Annalen der Chemie und Pharmacie, 1844, Mär 3, xlix. 308.

Footnote 535:

  London Medical Gazette, 1840–41, i. 723.

Footnote 536:

  Annales de Hygiène Publique, 1839, xxii. 404.

Footnote 537:

  Ibidem, p. 418.

Footnote 538:

  Journal de Chimie Médicale, 1839, 452.

Footnote 539:

  Ibidem, 1841, 534.

Footnote 540:

  Ibidem, 1842, 650.

Footnote 541:

  London Philosophical Journal, 1842, ii. 403.

Footnote 542:

  Wohler, Journal de Chim. Médicale, 1840, 96.

Footnote 543:

  Bulletins de l’Acad. Roy. de Médecine, 1839, iii. 1073.

Footnote 544:

  Journal de Chimie Médicale, 1840, 645, and 1841, 242.

Footnote 545:

  Journ. de Chim. Méd. 1839, 346.

Footnote 546:

  Annales d’Hygiène Publique, 1839, xxii.

Footnote 547:

  Ibidem, 404.

Footnote 548:

  Journal de Chimie Médicale, 1841, 223.

Footnote 549:

  Repertorium für die Pharmacie, lxxv. 107.

Footnote 550:

  Guy’s Hospital Reports, 1841, vi. 163.

Footnote 551:

  Journal de Chimie Médicale, 1841, 17, 421, 431.

Footnote 552:

  Annales d’Hygiène Publique, xxii. 450.

Footnote 553:

  Journal de Chimie Médicale, 1841, 223.

Footnote 554:

  Ibidem, 1840, 690.

Footnote 555:

  Annales, &c. _ut supra_.

Footnote 556:

  Revue Médicale. 1827, i. 365.

Footnote 557:

  Beiträge zur gerichtlichen Arzneikunde, iv. 221.

Footnote 558:

  January, 1819.

Footnote 559:

  Annales d’Hygiène Publ. et de Med. Légale, xii. 393.

Footnote 560:

  Ueber die Arsenic-vergiftung, pp. 14, 45.

Footnote 561:

  Journal de Pharmacie, xiii. 207.

Footnote 562:

  Journal de Chim. Med. ii. 113.

Footnote 563:

  Trans. of Provincial Med. and Surg. Association, iii. 465.

Footnote 564:

  See subsequently _Morbid Appearances_.

Footnote 565:

  Dublin Journal of the Med. Sciences, xx. 422.

Footnote 566:

  Repertorium für die Pharmacie, lxix. 271.

Footnote 567:

  Buchner’s Toxicologie, 476.

Footnote 568:

  Treatise on Poisons, third edition, pp. 270, 271.

Footnote 569:

  Bulletins de l’Acad. Roy. de Médecine, 1839, iii. 426.

Footnote 570:

  Journal de Chimie Médicale, 1840, p. 690.

Footnote 571:

  Gazette Médicale, 1839, No. 20.

Footnote 572:

  In a rabbit killed by arsenic applied to a wound Sir B. Brodie found
  the heart contracting feebly after death; and in a dog there were
  tremulous contractions incapable of supporting circulation. Sproegel
  found the peristaltic motion of the intestines and gullet vigorous in
  a dog an hour after death. [Diss. Inaug. in Halleri Disput. Med. Prac.
  vi. Exp. 31] Orfila in some experiments found the heart apparently
  inflamed and its irritability destroyed. [Arch. Gén. de Med. i. 147.]

Footnote 573:

  Haller’s Disput. Med. Pract. vi. Exp. 35.

Footnote 574:

  Diss. Inaug. Tubing. 1808. De effectibus Arsenici in var. organismos.

Footnote 575:

  Phil. Trans. cii. 211.

Footnote 576:

  Jaeger, p. 28.

Footnote 577:

  Halleri Disput., &c., Exp. 36.

Footnote 578:

  Renault sur les Contrepoisons de l’Arsénic, p. 42.

Footnote 579:

  Ibidem, 45.

Footnote 580:

  Journal de Chim. Méd. ii. 153.

Footnote 581:

  Acta Germanica, v. Observ. 102.

Footnote 582:

  Sur les Contrepoisons de l’Arsénic, p. 57.

Footnote 583:

  Sur les Contrepoisons de l’Arsénic, p. 48.

Footnote 584:

  Nov. Bibliothèque Méd. 1827, ii 59.

Footnote 585:

  Acta Germanica, v. Observ. 102

Footnote 586:

  For the references to these cases, see p. 227.

Footnote 587:

  Ueber Arsenic-Vergiftung, p. 53–4.

Footnote 588:

  Journal Complémentaire, i. 107.

Footnote 589:

  Edin. Med. and Surg. Journal, xxxiii. 67.

Footnote 590:

  Guy’s Hospital Reports, 1841, vi. 29.

Footnote 591:

  Annales d’Hygiène Publique, 1837, xvi. 336, 345.

Footnote 592:

  Rust’s Magazin für die gesammte Heilkunde, xx. 492.

Footnote 593:

  Wibmer. Die Wirkung der Arzneimittel und Gifte, i. 257. From Alberti,
  Jurisp. Med. v. 619, cas. 24.

Footnote 594:

  Bulletins de l’Académie Roy. de Médecine, 1841, v. 145.

Footnote 595:

  Valentini Pandectæ Med.-legales, 1. iii. c. 24.

Footnote 596:

  Sur les Contrepoisons de l’Arsénic, p. 62.

Footnote 597:

  Foderé, in Journal Complémentaire, i. 107, from Bertrand, Manuel
  Medico-legal des Poisons, p. 185.

Footnote 598:

  Toxicologie Gén. i. 429.

Footnote 599:

  American Journal of Med. Science, xi. 61.

Footnote 600:

  Mr. Hume, London Medical and Physical Journal, xlvi. 467.

Footnote 601:

  Edinburgh Med. and Surg. Journal, xxxvi. 94.

Footnote 602:

  Beiträge zur gerichtlichen Arzneikunde, iv. 221.

Footnote 603:

  Praktisches Handbuch für Physiker, iii. 298.

Footnote 604:

  London Med. and Phys. Journal, xlix 117.

Footnote 605:

  Annales d’Hygiène Publique, xvii. 338.

Footnote 606:

  Pandectæ Medico-legales, P. i. s. iii. cas. xxvi. pp. 134, 135.

Footnote 607:

  Diction. de Méd. et de Chir. Pratique, Art. Arsenic, iii. 340.

Footnote 608:

  Archives Gén. de Médecine, vii 14.—Another case somewhat analogous has
  been related by Tonnelier in Corvisart’s Journal de Médecine (iv. 15).
  The person, a girl nineteen years of age, took the poison at eleven,
  dined pretty heartily at two, and concealed her sufferings till seven.
  Even before dinner, however, she had been observed occasionally to
  change countenance, as if uneasy.

Footnote 609:

  Edin. Med. and Surg. Journal, xxvii. 450.

Footnote 610:

  London Med. Chir. Trans. ii. 134.

Footnote 611:

  Edin. Med. and Surg. Journal, xxix. 23. See also above, p. 77.

Footnote 612:

  Mr. Page, Lancet, 1836–37, ii. 626.

Footnote 613:

  Wendland in Augustin’s Archiv der Staatsarzneikunde, ii. 34.

Footnote 614:

  Pyl’s Aufsätze und Beob. i. 55.

Footnote 615:

  Bachmann. See subsequently, p. 260. State Trials, xviii. Case of Miss
  Blandy.

Footnote 616:

  Wepfer, Historia Cicutæ, 276.

Footnote 617:

  In a case by Schlegel. See Henke’s Zeitschrift für die
  Staatsarzneikunde, i. 81.

Footnote 618:

  Buchmann, p. 40.

Footnote 619:

  Journal de Médecine, iv. 383.

Footnote 620:

  Journal de Chimie Med. 1842, p. 580.

Footnote 621:

  Pyl’s Aufsätze und Beob. i. 55.

Footnote 622:

  Metzger’s Materialien für die Staatsarzneikunde, ii. 96.—Lond. Med.
  Phys. Journ. xxviii. 345—and Wildberg’s Praktisches Handbuch, iii.
  235–390.

Footnote 623:

  Edinburgh Med. and Surg. Journal, lix. 350.

Footnote 624:

  Henke’s Zeitschrift für die Staatsarzneikunde, i. 29.

Footnote 625:

  Tonnelier’s case. Corvisart’s Journal de Médecine, iv.—Roget’s case.
  Med. Chir. Transactions, ii.

Footnote 626:

  Med. and Phys. Journal, xxviii. 347.

Footnote 627:

  Henke’s Zeitschrift, i. 31.

Footnote 628:

  De Veneficio caute dijudicando. Schlegel’s Opusc. iv. 22.

Footnote 629:

  Praktisches Handbuch für Physiker, iii. 298.

Footnote 630:

  Zeitschrift für die Staatsarzneikunde, ii. 307.

Footnote 631:

  Aufsätze und Beobachtungen, v. 106.

Footnote 632:

  Edinburgh Med. and Surg. Journal, 1843, lix. 350.

Footnote 633:

  Elements of Juridical Medicine, 68.

Footnote 634:

  Historia Cicutæ, p. 282.

Footnote 635:

  Essay on Mineral Poisons, 1795, p. 30.

Footnote 636:

  These facts are important, because they will enable the medical jurist
  in some circumstances to decide a question which may be started as to
  the possibility of arsenic having been the cause of death when it is
  very rapid. I have dwelt on them more particularly than may appear
  necessary, because some loose statements on the subject were made in a
  controversy on the occasion of a trial of some note, that of Hannah
  Russell and Daniel Leny, at Lewes Summer Assizes 1826, for the murder
  of the husband of the former. Arsenic was decidedly detected in the
  stomach, and it was proved that the deceased did not live above three
  hours after the only meal at which the prisoners could have
  administered the poison. Now during the controversy which arose after
  the execution of one of the prisoners, it was alleged by one of the
  parties, among other reasons for believing arsenic not to have been
  the cause of death, that this poison never proves fatal so soon as in
  three hours,—that Sir Astley Cooper and Mr. Stanley of London had
  never known a case prove fatal in less than seven hours—and that Dr.
  Male’s case mentioned above is the shortest on record. The instances
  quoted above overthrow this whole line of statement. It was mentioned
  by Mr. Evans, the chief crown witness, but I know not on what
  authority, that, on the trial of Samuel Smith for poisoning, held at
  Warwick Summer Assizes 1826, the deceased was proved to have expired
  in two hours after taking a quarter of an ounce of arsenic. I have
  examined with some care the documents in the Lewes case, which were
  obligingly communicated to me by Mr. Evans; and I have been quite
  unable to discover any reason for questioning the reality of
  poisoning, or for the ferment which it seems the subsequent
  controversy excited. The case seems to have been satisfactorily made
  out by Mr. Evans in the first instance; and no sound medical jurist
  would for a moment suffer a shadow of doubt to be thrown over his mind
  by the criticisms of Mr. Evans’s antagonist.

Footnote 637:

  Die Wirkung der Arzneimittel und Gifte, i. 271.

Footnote 638:

  London Medical Repository, ii. 270.

Footnote 639:

  Edinburgh Med. and Surg. Journal, xxxii. 305.

Footnote 640:

  Ibidem, v. 389.

Footnote 641:

  Philos. Transactions, 1812, p. 212.

Footnote 642:

  Henke’s Zeitschrift für die Staatsarzneikunde, v. 410.

Footnote 643:

  Magazin für die gesammte Heilkunde, xxii. 483.

Footnote 644:

  This statement might be excellently illustrated by the particulars of
  an English trial in 1842, where the prisoner escaped, though arsenic
  was found in the stomach of the deceased, because the judge, resting
  on the medical evidence, urged that arsenic caused so much pain in the
  stomach as generally to make the person shriek with agony, while in
  this case there was no uneasiness except pain in the head. As the
  case, however, was by no means creditable to the parties concerned in
  it, I shall rest satisfied with the present allusion.

Footnote 645:

  Vol. iii. quoted in Kopp’s Jahrbuch, vii. 401.

Footnote 646:

  Materialien für die Staatsarzneikunde, ii. 95.

Footnote 647:

  Edin. Med. Chir. Transactions, ii. 298.

Footnote 648:

  Lond. Med. Phys. Journal, xxxiv.

Footnote 649:

  Revue Médicale, 1822, vii. 105.

Footnote 650:

  Archives Gén. de Médecine, vii. 14.

Footnote 651:

  London Medical Gazette, xv. 828.

Footnote 652:

  Orfila, Toxicologie Gén. i. 397.

Footnote 653:

  Lancet, xvi. 612.

Footnote 654:

  Epist. Anat. lix. 3.

Footnote 655:

  Journal de Médecine, lxx. 89.

Footnote 656:

  Annali Universali di Medicina, 1836, ii. 43.

Footnote 657:

  Zeitschrift für die Staatsarzneikunde, xlii. 402.

Footnote 658:

  Journal Hebdomadaire, 1832, viii. 476.

Footnote 659:

  London Med. Chir. Transactions, ii. 134.

Footnote 660:

  See also a full abstract in Edin. Med. and Surg. Journal, xiii. 507.

Footnote 661:

  Edin. Med. and Surg. Journal, xv. 553.

Footnote 662:

  Traitement des Asphyxiés, 135.

Footnote 663:

  Ratio Medendi, iii. 113.

Footnote 664:

  Edin. Med. and Surg. Journal, xviii. 167.

Footnote 665:

  Annales d’Hygiène Publique, xvii. 336.

Footnote 666:

  Beiträge zur gerichtlichen Arzneikunde, iv. 221.

Footnote 667:

  Mem. of London Medical Society, ii. 224.

Footnote 668:

  Nova Acta Naturæ Curiosorum, iii. 532.

Footnote 669:

  Hahnemann über die Arsenic-Vergiftung, 59.

Footnote 670:

  Curationes Medicinales. Cent. ii. Obs. 33.

Footnote 671:

  Cicutæ Aquaticæ Historia et Noxæ, 280.

Footnote 672:

  Ueber die Arsenic-Vergiftung, 61.

Footnote 673:

  Die Wirkung der Arzneimittel und Gifte, i. 266.

Footnote 674:

  Diet. des Sciences Méd. ii. 307.

Footnote 675:

  Edin. Med. and Surg. Journal, xv. 415.

Footnote 676:

  Cadet de Gassicourt. Article Arsenic in Dict. des Sc. Méd.

Footnote 677:

  London Medical Gazette, 1839–40, p. 266.

Footnote 678:

  Hoffman, Medicina Rationalis Systematica, i. 198.

Footnote 679:

  Magazin für die gerichtlichen Arzneikunde, ii. 473.

Footnote 680:

  Ueber die Arsenic-Vergiftung, 63.

Footnote 681:

  Gmelin’s Geschichte der Mineralischen Gifte. Gmelin attempts to show
  from symptoms, that the Popes Pius Third and Clement Fourteenth died
  of arsenic secretly and gradually given, p. 107.

Footnote 682:

  Curat. Medic. C. ii. Obs. 33.

Footnote 683:

  De Cicuta, p. 289.

Footnote 684:

  Quoted by Hahnemann, über die Arsenic-Vergiftung, p. 41.

Footnote 685:

  Cours de Médecine Légale, p. 121.

Footnote 686:

  London Medical Gazette, 1842–43, i. 351; from Gazette Médicale, 1842,
  Nov. 5.

Footnote 687:

  Elémens de Médecine Opératoire.

Footnote 688:

  Annales d’Hyg. Publ. et de Méd. Lég. xi. 461.

Footnote 689:

  Journ. de Chimie Médicale, 1836, 482.

Footnote 690:

  On Phagedæna Gangrænosa, or Med. Phys. Journal, xl. 238.

Footnote 691:

  De Arsenici usu in Medicina, p. 158.

Footnote 692:

  Aufsätze und Beobachtungen, i. 43.

Footnote 693:

  Paris and Fonblanque, ii. 222.

Footnote 694:

  Médecine, Légale, iv. 226.

Footnote 695:

  Ansiaulx, Clinique Chirurgicale, and Henke’s Zeitschrift für die
  Staatsarzneikunde, ii. 188.

Footnote 696:

  Acta Hafniensia, iii. 178.

Footnote 697:

  Hippocrates Chymicus, c. 24. p. 213.

Footnote 698:

  Casus Medicinales, lib. vii. cas. 11.

Footnote 699:

  Die Wirkung der Arzneimittel und Gifte, i. 299.

Footnote 700:

  Journal der Praktischen Heilkunde, lxxii. v. 134.

Footnote 701:

  London Medical Gazette, 1837–38, i. 585.

Footnote 702:

  Buchner’s Repertorium für die Pharmacie, lxix. 271.

Footnote 703:

  Dublin Journal of the Medical Sciences, xx. 422.

Footnote 704:

  Eph. Curios. Naturæ, Dec. iii. An. 9 and 10, Obs. 220.

Footnote 705:

  Sur les Contrepoisons de l’Arsénic, p. 112.

Footnote 706:

  Mem. of London Medical Society, ii. 397.

Footnote 707:

  Recueil Périod. de la Soc. de Med. vi. 22.

Footnote 708:

  Acta Germanica, ii. 33.

Footnote 709:

  Knape und Hecker’s Kritische Annalen der Staatsarzneikunde, i.
  143–159.

Footnote 710:

  Die Wirkung der Arzneimittel und Gifte, i. 241.

Footnote 711:

  Einige auserlesene Medizinisch-gerichtliche abhandlungen von Schmitt,
  Bachmann, &c. p. 40.

Footnote 712:

  State Trials, xviii.

Footnote 713:

  Ephem. Academ. Cæsareo-Leopoldinæ, 1715. Obs. cxxvi.

Footnote 714:

  Horn’s Archiv für Medizinische Erfahrung, 1834, 755.

Footnote 715:

  Guy’s Hospital Reports, 1841, vi. 278.

Footnote 716:

  Aufsätze und Beobachtungen, i. 53, and v. 107.

Footnote 717:

  Diss. Inaug. Tubingæ, 1808, de Effectibus Arsenici in varios
  organismos, p. 39.

Footnote 718:

  Diss. Inaug. Edin. 1813, de Venen. Mineralibus, pp. 5, 6, 12.

Footnote 719:

  Edin. Med. and Surg. Journal, xviii. 171.

Footnote 720:

  London Medical Gazette, xiv. 62.

Footnote 721:

  Praktisches Handbuch, iii. 232 and 304.

Footnote 722:

  Dissert. Exp. 36.

Footnote 723:

  Edin. Med. and Surg. Journal, xxvii. 453.

Footnote 724:

  Nordisches Archiv, i. 334.

Footnote 725:

  Jaeger, p. 40.

Footnote 726:

  Edin. Med. and Surg. Journal, xxvii. 453.

Footnote 727:

  Schlegel, Collect. Opusc. &c. 423.

Footnote 728:

  Aufsätze und Beobachtungen, i. 58.

Footnote 729:

  Edinburgh Med. and Surg. Journal, xxxiii. 66.

Footnote 730:

  Metzger’s System der gerichtlichen Arzneikunde, von Remer, 1820, p.
  257.

Footnote 731:

  Edin. Med. and Surg. Journal, xxix. 25.

Footnote 732:

  Edin. Med. and Surg. Journal, xxvii. 453.

Footnote 733:

  Guy’s Hospital Reports, 1837, ii. 29, and 1841, vi. 266.

Footnote 734:

  Gmelin’s Geschichte der Mineralischen Gifte, 124, Foderé,
  Médecine-Légale, iv. 127. Sallin, Journal Gén. de Médecine, iv.

Footnote 735:

  Edin. Med. and Surg. Journal, xxix. 25.

Footnote 736:

  Journal Complémentaire, i. 106.

Footnote 737:

  Trial of Medad Mackay at Allegany, 1821. The prisoner was found not
  guilty. But the presence of arsenic in the stomach was proved by
  several tests.

Footnote 738:

  Philosophical Transactions, cii. 216.

Footnote 739:

  Archives Gén. de Médecine, 1. 107.

Footnote 740:

  Harles de Arsenico, 153, and Renault sur les Contrepoisons de
  l’Arsénic.

Footnote 741:

  Morbid Anatomy, p. 128.

Footnote 742:

  Metzger in Schlegel’s Opuscula, iv. 23. Pyl’s Aufs. und Beob. i. 60.
  Platner, Quæstiones Medicinæ Forenses, 206.

Footnote 743:

  Medicina Forensis, Cent. v. Cas. 45, quoted by Wibmer.

Footnote 744:

  Beiträge zur gerichtlichen Arzneikunde, iv. 221.

Footnote 745:

  Bernt, Beiträge zur gerichtlichen Arzneikunde, iv. 221.

Footnote 746:

  Metzger’s Materialien für die Staatsarzneikunde, ii. 95.

Footnote 747:

  ii. 284.

Footnote 748:

  Edin. Med. and Surg. Journal, xxvii. 457.

Footnote 749:

  Ibid, xxxiii. 66.

Footnote 750:

  Sproegel’s Dissert. Exp. xxxi.

Footnote 751:

  Pfaff and Scheele’s Nordisches Archiv. i. 345.

Footnote 752:

  Archives Gén. de Med. vii. 1.

Footnote 753:

  Ibidem, vii. 285.

Footnote 754:

  Repertorium für die Pharmacie, xxiv. 144.

Footnote 755:

  Archives Gén. de Méd. ii. 58.

Footnote 756:

  Edin. Med. and Surg. Journal, xviii. 171.

Footnote 757:

  Elements of Juridical Medicine, 76.

Footnote 758:

  Morbid Anatomy, p. 128.

Footnote 759:

  Case of Mr. Blandy, State Trials, xviii.

Footnote 760:

  Bachmann’s Essay (see p. 259).

Footnote 761:

  Houlton in London Med. Gazette, xiv. 712.

Footnote 762:

  Diss. Inaug. Edin. 1813, pp. 11 and 12.

Footnote 763:

  Diss. in Haller’s Disp. de Morbis, vi. Exp. xxxvi.

Footnote 764:

  London Med. Gazette, x. 115.

Footnote 765:

  Gazette Médicale de Paris, 1839, No. 20.

Footnote 766:

  Neues Magazin, I. iii. 508.

Footnote 767:

  Zeitschrift für die Staatsarzneikunde, i. 32.

Footnote 768:

  Annales d’Hyg. Publique, xi. 461.

Footnote 769:

  London Med. Gazette, xiv. 62.

Footnote 770:

  Archives Gén. i. 147.

Footnote 771:

  Nouvelle Bibliothèque Médicale, 1829, i. 395.

Footnote 772:

  Jaeger, de Effectibus Arsenici, p. 40.

Footnote 773:

  Bachmann’s Essay, p. 41, or above, p. 259.

Footnote 774:

  Aufsätze und Beobachtungen, i. 50.

Footnote 775:

  Wibmer. Die Wirkung der Arzneimittel und Gifte, i. 281, 283.

Footnote 776:

  Phil. Trans. cii. 214.

Footnote 777:

  De Arsenici usu in Medicina, 1811, p. 154.

Footnote 778:

  Journal de Chimie Médicale, 1839, p. 127.

Footnote 779:

  Practisches Handbuch, iii. 229.

Footnote 780:

  De Venenis Mineralibus. Diss. Inaug. Edinburgi, 1813.

Footnote 781:

  Historia Circutæ, 288.

Footnote 782:

  Augustin’s Repertorium. Neue Entdeckungen betreffend die Kennzeichen
  der Arsenic-vergiftung, I. i. 30.

Footnote 783:

  Geschichte der Mineralischen Gifte.

Footnote 784:

  Essay on Mineral Poisons, 36.

Footnote 785:

  Quæst. Medicinæ Forenses, 206.

Footnote 786:

  Jaeger, de Effectibus Arsenici, p. 47.

Footnote 787:

  Magazin für die gesammte Heilkunde, xx. 485.

Footnote 788:

  Bulletins de l’Acad. Roy. de Méd. v. 137.

Footnote 789:

  Geiger’s Magazin für Pharmacie, xxxii. 301, from Seeman’s Dissert.
  Inaug. Berolini, 1824.

Footnote 790:

  For an excellent analysis of the case of Ursinus and the experiments
  of Klanck, see Augustin—Neue Entdeckungen betreffend die Kennzeichen
  der Arsenic-vergiftung und Berichtigung älterer Angaben über diesen
  Gegenstand,—in Augustin’s Repertorium, I. i. 36.

Footnote 791:

  Bachmann, Einige auserlesene gerichtlich-medizinische abhandlungen,
  von Schmidt, Bachmann, und Küttlinger. Nürnberg, 1813.

Footnote 792:

  Hufeland’s Journal, xix. iv. 11, and xxii. i. 166.

Footnote 793:

  Archives Gén. de Med. xxi. 615, or Revue Médicale, 1830, i. 165.

Footnote 794:

  Annales d’Hygiène Publique, 1837, xviii. 466; and Journal de
  Pharmacie, 1837, 386.

Footnote 795:

  Edin. Med. and Surg. Journal, xxvii. 457.

Footnote 796:

  De veneficio caute dijudicando, in Schlegel’s Opuscula, iv. 23.

Footnote 797:

  Edin. Med. Chir. Trans. ii. 284.

Footnote 798:

  Dr. Symonds’s Account of the Examination, &c., Trans. of Provincial
  Med. and Surg. Association, iii. 432.

Footnote 799:

  Lancet, 1843–44, ii. 801.

Footnote 800:

  Dissertatio de vera Chemiæ Organicæ notione, additis experimentis de
  vi Arsenici in corpore organico mortuo. 1822. Quoted fully by Wibmer,
  die Wirkung der Arzneimittel und Gifte, i. 312.

Footnote 801:

  Elémens de Chymie, ii. 343.

Footnote 802:

  See this work, First Ed. 1829, p. 258.

Footnote 803:

  Kopp’s Jahrbuch, ii. 226.

Footnote 804:

  Bernt’s Beiträge zur gerichtlichen Arzneikunde, iv. 219.

Footnote 805:

  Ueber eine Vergiftung durch weissen Arsenic—Rust’s Magazin für die
  gesammte Heilkunde, v. 61.

Footnote 806:

  Edin. Med. and Surg. Journal, xviii. 172.

Footnote 807:

  De usu Arsenici, 164.

Footnote 808:

  Journal de Pharmacie, 1837, p. 386.

Footnote 809:

  Revue Médicale, 1828, ii. 470.

Footnote 810:

  Knape und Hecker’s Kritische Jahrbücher, ii. 76.

Footnote 811:

  Henke’s Zeitschrift für die Staatsarzneikunde, xxxix. 176.

Footnote 812:

  Toxicologie Générale, ii.

Footnote 813:

  Sur les Contrepoisons de l’Arsenic, pp. 33, 35.

Footnote 814:

  London Med. and Phys. Journal, xlvi. 466, 545. Mr. Edwards, Ibidem,
  xlix. 117. Mr. Buchanan, London Med. Repository, xix. 288.

Footnote 815:

  Journal Gén. de Médecine, 1813 and 1815, p. 363.

Footnote 816:

  Toxicologie Gén. i. 429.

Footnote 817:

  Das Eisenoxydhydrat, ein Gegengift der Arsenigen saüre, Göttingen,
  1834.

Footnote 818:

  Annales d’Hygiène Publique, xiv. 134.

Footnote 819:

  Probationary Essay, Edin. Roy. Coll. of Surgeons, 1839.

Footnote 820:

  London Medical Gazette, xv. 220.

Footnote 821:

  Lancet, 1834–35 p. 232.

Footnote 822:

  Edinburgh Medical and Surgical Journal, liv. 106.

Footnote 823:

  Buchner’s Repertorium für die Pharmacie, lxvi. 126.

Footnote 824:

  Journal de Chimie Médicale, 1841, p. 240.

Footnote 825:

  Mr. Kerr in Edin. Med. and Surg. Journal, xxxvi. 97.

Footnote 826:

  London Med. Repository, ix. 456.

Footnote 827:

  Med. and Phys. Journal, xxix.

Footnote 828:

  Journal de Chimie Médicale, 1839, p. 189.

Footnote 829:

  Bulletins de l’Acad. Roy. de Méd. iii. 1124.

Footnote 830:

  Ibidem, 1840, vi. 135.

Footnote 831:

  Bulletins de l’Académie Roy. de Médecine, 1840, vi. 136.

Footnote 832:

  Journal de Chimie Médicale, 1840, p. 711.

Footnote 833:

  Ibidem, 1843, p. 265.

Footnote 834:

  Ibidem, 1841, p. 258.

Footnote 835:

  Kopp’s Jahrbuch der Staatsarzneikunde, iv. 354.

Footnote 836:

  Devergie. Annales d’Hyg. Publ. xi. 418.

Footnote 837:

  Toxicologie Gén. i. 241.

Footnote 838:

  Medical Jurisprudence, ii. 208.

Footnote 839:

  Annales d’Hyg. Publ. et de Méd. Lég. xi. 411.

Footnote 840:

  Philosophical Transaction, 1831, cxxi. 155, 160.

Footnote 841:

  Annales de Chimie, xliv. 176, and Orfila, Toxicol. Gén. i. 243.

Footnote 842:

  Taddei, Recherches sur un nouvel Antidote contre le sublimé corrosif.

Footnote 843:

  Berthollet, sur la Causticité des sels Métalliques. Mém. de l’Acad.
  1780.

Footnote 844:

  Toxic. Gén. i. 245.

Footnote 845:

  Recherches, &c. p. 60.

Footnote 846:

  Journal de Chimie Médicale, 1837, p. 161.

Footnote 847:

  Poggendorff’s Annalen der Physik und Chemie, xxviii, 135.

Footnote 848:

  Annalen der Pharmacie, xxiv. 36.

Footnote 849:

  Annales de Chimie, xliv. 176.

Footnote 850:

  Toxicologie Générale, i. 301.

Footnote 851:

  Annales d’Hygiène Publique, xxviii. 424.

Footnote 852:

  Dr. Bigsby in London Medical Gazette, vii. 329.

Footnote 853:

  Philosophical Transactions, cii. 222.

Footnote 854:

  Tentamen Inaugurale de Venenis Mineralibus, Edinb. 1813, p. 36.

Footnote 855:

  Orfila, Toxicologie Gén. i. 257.

Footnote 856:

  Journal de Physiologie, i. 165 and 242.

Footnote 857:

  Toxicologie, i. 261.

Footnote 858:

  Journal de Physiologie, i. 165.

Footnote 859:

  Autenrieth und Zeller über das Daseyn von Quecksilber in der Blutmasse
  der Thiere. Reil’s Archiv für die Physiologie, viii. 216.

Footnote 860:

  Horn’s Archiv für Medizinische Erfahrung, 1823, ii. 417.

Footnote 861:

  Diss. Inaug. Tubingæ, 1808, sistens experimenta quædam circa effectus
  hydrargyr in animalia viva, pp. 25, 31, also Reil’s Archiv, _ut
  supra_.

Footnote 862:

  Tract. de Morb. Gall. in Opera Omnia, pp. 728, 729.

Footnote 863:

  Archiv für Medizinische Erfahrung, 1810, ii. 252.

Footnote 864:

  Corvisart’s Journ. de Méd. xxvii. 244.

Footnote 865:

  Dec. I. Ann. i. Obs. 8.

Footnote 866:

  Journ. der Prakt. Heilkunde, li. 5, p. 117.

Footnote 867:

  Mem. of Lond. Med. Soc. v. 112.

Footnote 868:

  Seltene Beobachtungen zur Anat. Physiol. und Pathol. Berlin, 1824, ii.
  36. Quoted by Marx, die Lehre von den Giften, I. ii. 163.

Footnote 869:

  Die Wirkung der Arzneimittel und Gifte, iii. 86.

Footnote 870:

  Zeller, in Reil’s Archiv. viii. 233.

Footnote 871:

  Nouvelle Bibliothèque Médicale, 1828, iv. 17 and 18.

Footnote 872:

  See the last Edition of this work, p. 366.

Footnote 873:

  See my Dispensatory, 1842, p. 507.

Footnote 874:

  Reil’s Archiv., viii. 228.

Footnote 875:

  Journal der Praktischen Heilkunde, lx. 115.

Footnote 876:

  Toxicologie 3te Auflage, 539.

Footnote 877:

  Ibidem, 433.

Footnote 878:

  Journal de Chimie Médicale, 1842, p. 428.

Footnote 879:

  Buchner’s Repertorium für die Pharmacie, lxxvi. 249.

Footnote 880:

  Journal de Chimie Médicale, 1843, p. 137.

Footnote 881:

  Hodgson’s Trial, Edin. Med. and Surg. Journal, xxii. 439, also a case
  by Mr. Blacklock, Ibid. xxxvi. 92.

Footnote 882:

  Case by Ollivier in Archives Gén. de Méd. ix. 100; also one by Mr.
  Valentine, Edin. Med. and Surg. Journal, xiv. 471.

Footnote 883:

  Case by Fontenelle, Arch. Gén. de Méd. v. 345; also Hodgson’s Trial.

Footnote 884:

  Hodgson’s Trial; also Orfila, Tox. Gén. i. 263: and Mr. Valentine’s
  5th case, the only survivor.

Footnote 885:

  Hodgson’s Trial; also Mr. Buchanan’s case in Lond. Med. Repos. xix.
  374.

Footnote 886:

  Mr. Valentine’s Cases, Edin. Med. and Surg. Journal, xiv. 470.

Footnote 887:

  Mr. Anderson’s case in Edin. Med. and Surg. Journal, xiv. 474.

Footnote 888:

  Essay on Mineral Poisons, p. 52.

Footnote 889:

  Dumonceau in Journ. de Med. lxix. 36; Orfila, Tox. Gén. i. 264; and
  Blacklock’s case.

Footnote 890:

  Edin. Med. and Surg. Journal, xiv. 468.

Footnote 891:

  Ibid. xliv. 26.

Footnote 892:

  xli. 204.

Footnote 893:

  London Medical Gazette, viii. 616.

Footnote 894:

  Edin. Med. and Surg. Journal, xxxvi. 92.

Footnote 895:

  Archives Gén. de Méd. ix. 99.

Footnote 896:

  Orfila, Tox. Gén. i. 265.

Footnote 897:

  Mr. Valentine’s cases.

Footnote 898:

  Ollivier’s case, and Fontenelle’s.

Footnote 899:

  Case by Devergie in Arch. Gén. de Méd. ix. 463.

Footnote 900:

  Houlston, in London Med. Journal, vi. 271.

Footnote 901:

  Arch. Gén. de Méd. ix. 463.

Footnote 902:

  Toxicol. Gén. i. 263.

Footnote 903:

  Journal de Chimie Médicale, 1842, p. 294.

Footnote 904:

  Edin. Med. and Surg. Journal, xiv. 468.

Footnote 905:

  Mr. Valentine’s 4th case.

Footnote 906:

  London Medical Gazette, viii. 616.

Footnote 907:

  London Medical Gazette, vii. 329.

Footnote 908:

  Ibidem, 1842–43, i. 556.

Footnote 909:

  Mr. Valentine’s case 1st.

Footnote 910:

  Case in Med. and Phys. Journal, xli.

Footnote 911:

  Case by Dr. Anderson in Edin. Med. and Surg. Journal, vii. 437.

Footnote 912:

  Beddoes’ Contributions to Physical and Medical Knowledge, 1799, p.
  231.

Footnote 913:

  London Medical Gazette, 1842–43, i. 941.

Footnote 914:

  Edinburgh Med. and Surg. Journal, li. 114.

Footnote 915:

  Ibidem, xiv. 474.

Footnote 916:

  Manual of Medical Jurisprudence, 162.

Footnote 917:

  Lond. Med. and Phys. Journal, xli.

Footnote 918:

  Toxic. Générale, i. 282, from Degneri Historia Med. de Dysent. Bilios.
  Contag. 250.

Footnote 919:

  Lond. Med. and Phys. Journal, xli. 204.

Footnote 920:

  Reports of Medical Cases, ii. 337.

Footnote 921:

  Lancet, 1838–39, i. 215.

Footnote 922:

  M. Colson in Arch. Gén. de Méd. xii. 84.

Footnote 923:

  Dr. Ramsbotham in Lond. Med. Gazette, i. 775.

Footnote 924:

  Dr. Crampton, Trans. Dublin College of Physicians, iv. 91.

Footnote 925:

  See page 335.

Footnote 926:

  Rust’s Magazin, xxv. 578.

Footnote 927:

  Journal der Praktischen Heilkunde, ix, ii. 201.

Footnote 928:

  Lond. Med. and Phys. Journal, xxvi. 452.

Footnote 929:

  Ibid. xxvii. 275.

Footnote 930:

  Trans. Lond. Coll. Phys. i. 34.

Footnote 931:

  Revue Medicale, 1828, iv. 76.

Footnote 932:

  Ibidem, 1829, i. 467, from Osservatore Medico di Napoli, Febb. 1829.

Footnote 933:

  Dr. Tott, in Rust’s Magazin für die gesammte Heilkunde, xxxv. 50.

Footnote 934:

  Journ. de Chem. Med. ix. 197.

Footnote 935:

  London Medical Gazette, 1837–38, ii. 578.

Footnote 936:

  De Ptyalismo Febrili. Diss. Inaug. Lipsiæ, in Halleri Disput. de Morb.
  Histor. i. 469.

Footnote 937:

  See Evidence of Mr. Bromfield on the Trial of Miss Butterfield for the
  murder of Mr. Scawen, p. 40.

Footnote 938:

  London Medical Gazette, 1839–40, ii. 875.

Footnote 939:

  Lancet, 1843–44, i. 60.

Footnote 940:

  London Medical Gazette, 1841–42, i. 338.

Footnote 941:

  Swédiaur on Venereal Diseases, ii. 251.

Footnote 942:

  Colson in Arch. Gén. de Méd. xii. 99.

Footnote 943:

  Flora Suecica.

Footnote 944:

  On the Venereal Disease, ii. 143.

Footnote 945:

  Colson in Arch. Gén. de Méd. xii. 99.

Footnote 946:

  The exact time is not mentioned.

Footnote 947:

  Trial by Gurney and Blanchard, pp. 39, 47.

Footnote 948:

  Principles of Forensic Medicine, 2d Ed. 118.

Footnote 949:

  Trans. of the Prov. Med. and Surg. Association, ii. 262.

Footnote 950:

  Mead’s Medical Works, p. 202.

Footnote 951:

  Male’s Juridical Medicine, 89.

Footnote 952:

  Archives Gén. de Méd. xl. 254.

Footnote 953:

  Ibid. xii. 100.

Footnote 954:

  Trans. Dublin Coll. Physicians, iii. 236.

Footnote 955:

  Appendix to his Traité de la Colique Metallique, p. 275.

Footnote 956:

  Edin. Med. and Surg. Journal, viii. 376, and ix. 180.

Footnote 957:

  Reports of Medical Cases, ii. 495.

Footnote 958:

  Fernelius, de Lues Ven. Curat. c. vii.

Footnote 959:

  London Med. and Phys. Journal, lxvii. 394.

Footnote 960:

  Arch. Gén. de Méd. xiv. 109.

Footnote 961:

  Mém. de l’Acad. des Sciences, 1719, p. 474.

Footnote 962:

  Edin. Med. and Surg. Journal, viii. 195.

Footnote 963:

  London Medical Repository, xvi. 458.

Footnote 964:

  Mémoires de l’Acad. de Chirurgie, iv. 154.

Footnote 965:

  Wibmer. Die Wirkung der Arzneimittel und Gifte, iii. 46.

Footnote 966:

  Diss. Inaug. de Effectibus Liquidorum in vias aëriferas applicatorum,
  p. 35.

Footnote 967:

  Hufeland’s Journal, xlii.

Footnote 968:

  Mr. Hill in Edin. Med. Ess. iv. 38.

Footnote 969:

  Corvisart’s Journal, xxv. 209.

Footnote 970:

  London Journal of Science, x 354.

Footnote 971:

  Edin. Med. and Surg. Journal, vi. 513, and London Medical and Physical
  Journal, xxvi. 29.

Footnote 972:

  Horn’s Archiv für Medizinische Erfahrung, 1831, 519.

Footnote 973:

  Edin. Med. and Surg. Journal, vii. 437.

Footnote 974:

  Ibidem, xliv. 26.

Footnote 975:

  Medizinisch-Chirurgische Zeitung, 1833, v. 330.

Footnote 976:

  Repertorium für die öffentl. und gerichtl. Arzneiwissenschaft, i. 223.

Footnote 977:

  Annalen der Gesetz-gebung, iii. 55.

Footnote 978:

  Journ. de Physiologie, i.

Footnote 979:

  Annals of Philos. xiv. 241, 321.

Footnote 980:

  See my Dispensatory, 1842, p. 500.

Footnote 981:

  Acta Naturæ Curiosorum, Dec. ii. Ann. vi. Obs. 231.

Footnote 982:

  Journal de Médecine, l. 3.

Footnote 983:

  Dr. Sigmond in Lancet, 1837–38, i. 228, from Turner’s Treatise on
  Diseases of the Skin.

Footnote 984:

  Ibidem, p. 227.

Footnote 985:

  I. 240.

Footnote 986:

  Opera Omnia, p. 729.

Footnote 987:

  Arch. Gén. de Médecine, xix. 330.

Footnote 988:

  Sur l’usage et les Abus des Caustiques. Paris, 1817. Quoted by Wibmer
  Smith found two drachms kill a dog when swallowed, and half a drachm
  proved fatal in two dogs when applied to a wound.

Footnote 989:

  Lancet, 1836–37, i. 401.

Footnote 990:

  London Medical Gazette, xiii. 117.

Footnote 991:

  Cours de Médecine-Légale.

Footnote 992:

  Handbuch der Toxicologie, 1838, p. 250.

Footnote 993:

  Wibmer. Die Wirkung der Arzneimittel und Gifte, iii. 66.

Footnote 994:

  Ibidem, iii. 647.

Footnote 995:

  Arch. Gén. ix. 102.

Footnote 996:

  Thibert, Anatomie Pathologique, extracted in the American Journal. of
  Med. Science, April, 1842, p. 490.

Footnote 997:

  De Medicamentis insecuris et infidis, in Oper. Omn. vi. 314.

Footnote 998:

  Miscellanea Curiosa, 1692. Dec. ii. Ann. x. p. 34.

Footnote 999:

  Die Wirkung der Arzneimittel und Gifte, iii. 72.

Footnote 1000:

  Johnson on Tropical Climates, pp. 45, 151, 267.—Annesley on the
  Diseases of India.—Musgrave on Mercury, in Edin. Med. and Surg. Journ.
  xxviii. 42.

Footnote 1001:

  Dr. Fletcher. American Journal of Med. and Phys. Sciences, vii. 561.

Footnote 1002:

  Miscellanea Curiosa, l. c.

Footnote 1003:

  Die Wirkung der Arzneimittel und Gifte, iii. 72.

Footnote 1004:

  London Medical Gazette, 1837–38, ii. 610.

Footnote 1005:

  M. Mialhe in Annales de Chimie et de Physique, Juin, 1842.

Footnote 1006:

  Manual of Medical Jurisprudence, p. 178.

Footnote 1007:

  For the documents in this trial I am indebted to my late colleague Dr.
  Duncan, Junior, who was concerned in it.

Footnote 1008:

  Toxicol. Gén. i. 310.

Footnote 1009:

  Recherches sur un Nouvel Antidote contre le sublimé corrosif, p. 34.

Footnote 1010:

  Toxicol. Gén. p. 311.

Footnote 1011:

  Taddei, Recherches, &c. p. 92.

Footnote 1012:

  Edin. Med. and Surg. Journal, xxii. 438.

Footnote 1013:

  As in Devergie’s Case (Arch. Gén. ix 468), in which they were as big
  as peas.

Footnote 1014:

  Ibidem.

Footnote 1015:

  Devergie in Arch. Gén. ix 468.

Footnote 1016:

  Sir B. Brodie in Philos. Trans. 1812.

Footnote 1017:

  Edin. Med. and Surg. Journ., xiv. 472, 473.

Footnote 1018:

  London Medical Gazette, viii. 618.

Footnote 1019:

  Recherches sur un Nouvel Antidote, &c. p. 61.

Footnote 1020:

  Archives Gén. de Méd. ix. 470.

Footnote 1021:

  Journal de Chim. Médicale, viii. 268.

Footnote 1022:

  Orfila, Traité de Médecine Légale, iii. 134.

Footnote 1023:

  Edin. Med. and Surg. Journal, li. 115.

Footnote 1024:

  The reader may apply this statement to the trial of Mr. Angus, p. 118.

Footnote 1025:

  Edin. Med. and Surg. Journal, vii. 151.

Footnote 1026:

  Augustin’s Repertorium, B. i. H. ii. 11.

Footnote 1027:

  xli. 207.

Footnote 1028:

  Journal de Médecine, l. iii. 15, or Recueil Périodique de la Soc. de
  Méd. vii. 343.

Footnote 1029:

  Revue Medicale, 1830, ii.

Footnote 1030:

  Toxicologie Gén. i. 313.

Footnote 1031:

  Corvisart’s Journal de Médecine, xxxviii. 77.

Footnote 1032:

  Dissert. Inaug. p. 36.

Footnote 1033:

  See my Dispensatory, p. 518. Dr. Wright’s Thesis on certain points
  connected with the action of mercury and its salts has not yet been
  published.

Footnote 1034:

  London Med. Repository, xix. 408.

Footnote 1035:

  Trans. of Dublin Coll. of Phys. iii. 310.

Footnote 1036:

  Journal de Chim. Méd. Mars, 1825.

Footnote 1037:

  Recherches sur un Nouvel Antidote, &c. p. 26.

Footnote 1038:

  Giornale di Fisica, 1826, vi. 170, and Buchner’s Repertorium für die
  Pharmacie ii. 229.

Footnote 1039:

  London Medico-Chirurgical Review, v. 612.

Footnote 1040:

  Buchner’s Repertorium für die Pharmacie, iv. 51.

Footnote 1041:

  Annales d’Hygiène Publique, xxviii. 427.

Footnote 1042:

  Journal de Chimie Médicale, 1843, p. 10.

Footnote 1043:

  Dr. Hort. American Journal of Med. Science, vi. 540.

Footnote 1044:

  Edin. Med. and Surg. Journal, xxix. 218.

Footnote 1045:

  Lond. Med. Repos. N. S. vi. 368.

Footnote 1046:

  Lond. Med. Gazette, 1836–37, ii. 144.

Footnote 1047:

  Burnett on Criminal Law, 547.

Footnote 1048:

  Journal de Chimie Médicale, 1842, p. 771.

Footnote 1049:

  Dégrange, London Medical Gazette, 1842–43, i. 495.

Footnote 1050:

  Falconer on the Poison of Copper, p. 23.

Footnote 1051:

  Expériences sur l’Empoisonnement par l’oxyde de Cuivre. Diss. Inaug.
  Paris, 1802. Quoted in Orfila’s Toxicol. i. 502.

Footnote 1052:

  Sur l’usage prétendu dangereux de la vaisselle de cuivre dans nos
  cuisines. Histoire de l’Acad. Roy. des Sciences de Berlin, 1756, p.
  12.

Footnote 1053:

  Toxicol. Gén. 1843, i. 612.

Footnote 1054:

  Beck’s Medical Jurisprudence, 460.

Footnote 1055:

  Falconer, &c. pp. 48, 98, 110.

Footnote 1056:

  Sur l’usage, &c. p. 12.

Footnote 1057:

  Falconer, &c. p. 63.

Footnote 1058:

  Histoire de l’Acad. de Berlin, 1756, p. 16.

Footnote 1059:

  Falconer, &c. p. 79.

Footnote 1060:

  Annales de Chimie, lvii. 79, 81.

Footnote 1061:

  Practisches Handb. für Physiker, iii. 312, Case 49.

Footnote 1062:

  Fabricii Hildani Opera omnia. Genevæ, 1682. De Dysenteria, p. 669.

Footnote 1063:

  Orfila, Toxicol. Générale, i. 507.

Footnote 1064:

  Trans. London College of Physicians, iii. 80.

Footnote 1065:

  On the Poison of Copper, 86.

Footnote 1066:

  On the Poison of Copper, 88; also Paris and Fonblanque’s Medical
  Jurisprudence, ii. 289.

Footnote 1067:

  Annales de Chimie, lvii. 80.

Footnote 1068:

  On the Poison of Copper, p. 18.

Footnote 1069:

  Annales, &c. p. 80.

Footnote 1070:

  Medical Observations and Inquiries, ii. 11.

Footnote 1071:

  On the Poison of Copper, 106.

Footnote 1072:

  Proust, Annales de Chimie, lvii. 83.

Footnote 1073:

  Geschichte der Mineralischen Gifte, p. 77.

Footnote 1074:

  Lond. Med. Journal, ii. 411, from Journ. de Méd.

Footnote 1075:

  Archives Gén. de Méd. xix. 471.

Footnote 1076:

  Annales d’Hygiène Publ. et de Méd. Légale, iii. 342.

Footnote 1077:

  Archives Gén. de Méd. xxi. 145.

Footnote 1078:

  Buchner’s Repertorium für die Pharmacie, xxxiii. 236.

Footnote 1079:

  Pignant in Journ. de Chim. Méd. viii. 339.

Footnote 1080:

  Toxicologie Gén. 1826, i. 510.

Footnote 1081:

  Schweigger’s Journal der Chemie, xvi. 340, 436.

Footnote 1082:

  Journal de Pharmacie, xvi. 505.

Footnote 1083:

  Bulletins de la Société Roy. de Méd. 1838–39, p. 113.

Footnote 1084:

  Journal de Chimie Médicale, 1840, p. 475.

Footnote 1085:

  Ibid. viii. 442, 573.

Footnote 1086:

  L’Experience, Avril 27, 1843.

Footnote 1087:

  Journal de Chimie Méd. ix. 147.

Footnote 1088:

  Ibidem, 1840, p. 28.

Footnote 1089:

  Toxicologie Gén. 1843, i. 637.

Footnote 1090:

  Orfila. Toxic. Gén. i. 511.

Footnote 1091:

  ibid. Toxic. i. 513.

Footnote 1092:

  Buchner’s Repertorium für die Pharmacie, lxxvi. 352.

Footnote 1093:

  Toxicol. Générale, i. 515.

Footnote 1094:

  Edinburgh Med. and Surg. Journal. lvi. 110.

Footnote 1095:

  Utrum per viventium adhuc anim. membr. et arter. pariet. mat.
  ponderab. permeare queant, 13.

Footnote 1096:

  Ueber die Wirkung des Kupfers auf den thierischen Organismus, in
  Buchner’s Repertorium für die Pharmacie, xxxii. 337, 1829.

Footnote 1097:

  Ibidem, lxxii. 56.

Footnote 1098:

  Journal de Chimie Médicale, 1840, p. 475.

Footnote 1099:

  Observations sur les effets des vapeurs méphitiques, 437.

Footnote 1100:

  Orfila, Toxicol. Gén. i. 500.

Footnote 1101:

  Annales d’Hygiène Publique, 1840, xxiv. 100.

Footnote 1102:

  Arch. Gén. de Médecine, xix. 329.

Footnote 1103:

  _Ut supra_, 103, 106.

Footnote 1104:

  Corvisart’s Journal de Médecine, xviii. 54.

Footnote 1105:

  _Ut supra_, 108, 110, 113.

Footnote 1106:

  _Ut supra_, xviii. 56.

Footnote 1107:

  Journal de Chimie Médicale, 1841, p. 309.

Footnote 1108:

  Toxicol. Gén. i. 519.

Footnote 1109:

  Aufsätze und Beobacht. aus der gericht. Arneiwiss. viii. 85.

Footnote 1110:

  Practisches Handbuch für Physiker, iii. 308.

Footnote 1111:

  Journ. de Chimie Médicale, v. 413.

Footnote 1112:

  Die Wirkung der Arzneimittel und Gifte, ii. 253.

Footnote 1113:

  Trans. London Coll. Phys. iii. 88.

Footnote 1114:

  Quoted by Dr. Thomson in Lancet, 1836–37, ii. 640.

Footnote 1115:

  Traité des Maladies des Artizans, p. 78.

Footnote 1116:

  Traité de la Colique Métallique, p. 103.

Footnote 1117:

  London Medical Gazette, 1838–39, i. 195, 697.

Footnote 1118:

  Gangrene could not have taken place in thirteen hours. The appearance
  must have been black extravasation, which has often been mistaken for
  gangrene. See page 267.

Footnote 1119:

  Portal sur les effets des vapeurs méphitiques, 436, 439.

Footnote 1120:

  Orfila, Tox. Gén. i. 530.

Footnote 1121:

  Dict. des Sciences Médicales, vii. 564.

Footnote 1122:

  Orfila, Tox. Gén. i. 534.

Footnote 1123:

  Orfila, Tox. Gén. i. 535.

Footnote 1124:

  Ibidem, i. 539.

Footnote 1125:

  Ibidem, i. 540.

Footnote 1126:

  Ibidem, i. 541.

Footnote 1127:

  Journal de Pharmacie, xviii. 570.

Footnote 1128:

  London Medico-Chirurgical Review, v. 611.

Footnote 1129:

  Taylor’s Medical Jurisprudence, 1844, p. 206.

Footnote 1130:

  Orfila, Toxicol. Générale, i. 466.

Footnote 1131:

  Edinburgh Med. and Surg. Journal, xxviii. 71.

Footnote 1132:

  Ibid, xxviii. 71.

Footnote 1133:

  Journal de Chimie Médicale, 1840.

Footnote 1134:

  Memoire sur l’Emétique, or Orfila, Toxicol. Gén. i. 469.

Footnote 1135:

  De Effectibus liquidorum, &c. p. 32.

Footnote 1136:

  Diss. Inaug. de Venenis Mineral. Edin. 1813. P. 23.

Footnote 1137:

  Diction. de Méd. et de Chir. Pratiques, Art. Antimoine, iii. 69.

Footnote 1138:

  Journal de Chim. Médicale, 1840, p. 291, and Orfila, Toxicologie
  Générale, 1843, i. 475.

Footnote 1139:

  Annales d’Hygiène Publique, xxix. 427.

Footnote 1140:

  Buchner’s Repertorium für die Pharmacie, lxxviii. 107, from Comptes
  Rendus de l’Institut.

Footnote 1141:

  Orfila, Toxicol, i. 74.

Footnote 1142:

  Ibid. i. 478.

Footnote 1143:

  Bulletins des Sciences Médicales, xvii. 243.

Footnote 1144:

  Taylor’s Medical Jurisprudence, 205, from Casper’s Wochenschrift.

Footnote 1145:

  Edin. Med. and Surg. Journal, xxii. 227.

Footnote 1146:

  Laennec, Auscultation Médiate, i. 493.

Footnote 1147:

  On the Nature and Treatment of Cholera, p. 24.

Footnote 1148:

  Mr. Greenwood, Lancet, 1835–36, ii. 142.

Footnote 1149:

  Renauld in Journ. Univ. des Sciences Médicales, xvii. 120.

Footnote 1150:

  Mem. of Lond. Med. Soc. ii. 386.

Footnote 1151:

  Ibidem, v. 81.

Footnote 1152:

  Corvisart’s Journ. de Med. xxvi. 221.

Footnote 1153:

  Mem. of Lond. Med. Soc. iv. 79.

Footnote 1154:

  Journal de Chimie Médicale, iv.

Footnote 1155:

  Lond. Med. Repos, xvi. 357.

Footnote 1156:

  London Medical Gazette, xii. 496.

Footnote 1157:

  Lohmerer in Journal de Chimie Médicale, 1840, p. 629.

Footnote 1158:

  Orfila, Toxicol. Générale, i. 480.

Footnote 1159:

  De Medicamentis Venenorum vim habentibus. Opera Omnia, T. 1. p. ii.
  213.

Footnote 1160:

  Diss. Inaug. de Effectibus liquidorum, &c. p. 32.

Footnote 1161:

  Archives Générales de Médecine, xlvii. 364.

Footnote 1162:

  Orfila, Toxicol. Générale, i. 475.

Footnote 1163:

  Bulletins des Sciences Médicales, vi. 259.

Footnote 1164:

  Bulletins de l’Acad. Roy. de Médecine, 1840, vi. 140.

Footnote 1165:

  Manual of Medical Jurisprudence, 1844, p. 209.

Footnote 1166:

  Toxicologie Générale, i. 555.

Footnote 1167:

  Orfila, Journal de Chimie Médicale, 1842, p. 346.

Footnote 1168:

  Horn’s Archiv für Medizinische Erfahrung, 1823, ii. 415.

Footnote 1169:

  Toxicol. Gén. 1843, ii. 10.

Footnote 1170:

  Recherches Chimiques sur l’Etain, Paris, 1781.

Footnote 1171:

  See Wibmer, die Wirkung der Arzneimittel und Gifte, v. 168.

Footnote 1172:

  Toxicologie Gén. 1843, ii. 5.

Footnote 1173:

  Medical Times, Oct. 9, 1841.

Footnote 1174:

  Edinburgh Med. and Surg. Journal, lvi. 119.

Footnote 1175:

  Toxicol. Gén. i. 581.

Footnote 1176:

  De Effect. Liquid. ad vias aëriferas applic. Tübingæ, 1816, p. 33.

Footnote 1177:

  London Medico-Chirurgical Transactions, vii. 2. Journal der
  Practischen Heilkunde, Juli, 1824.

Footnote 1178:

  Wibmer. Die Wirkung, &c. i. 212, from Rust und Casper’s Kritische
  Repertorium, xix. 454.

Footnote 1179:

  Journal de Chimie Médicale, 1842, p. 351.

Footnote 1180:

  Ibid. 1843, p. 348.

Footnote 1181:

  Annales d’Hygiène Publique, xxix. 430.

Footnote 1182:

  Journal de Chimie Médicale, 1839, p. 434.

Footnote 1183:

  Orfila, Toxicol. Générale, i. 593.

Footnote 1184:

  Magendie, Formulaire pour les nouveaux Médicamens.

Footnote 1185:

  Toxicol. 241.

Footnote 1186:

  Medicina Rationalis Syst. ii. c. 8. Sect. 12.

Footnote 1187:

  Toxicol. Gén. i. 501.

Footnote 1188:

  Journal de Chimie Médicale, 1842, p. 344.

Footnote 1189:

  Bulletins des Sciences Méd. xx. 188. From the Heidelberg Klinische
  Annalen, also Wibmer, Die Wirkung der Arzneimittel und Gifte, i. 416.

Footnote 1190:

  Versuche über die Wirkungen des Baryts, Strontians, Chrom, &c. auf den
  thierischen Organismus. 1824.

Footnote 1191:

  Buchner’s Repertorium für die Pharmacie, lxix. 387.

Footnote 1192:

  London Medical Gazette, 1843–44, ii.

Footnote 1193:

  Ed. Med. and Surg. Journ. xxvi. 133.

Footnote 1194:

  Journal de Chimie Médicale, 1842, p, 353.

Footnote 1195:

  Toxicologie Gén. i. 569.

Footnote 1196:

  Edinburgh Med. and Surg. Journal, lvi. 110.

Footnote 1197:

  Journal de Chimie Médicale, 1842, p. 353.

Footnote 1198:

  Médecine Légale, iv. 165.

Footnote 1199:

  Guy’s Hospital Reports, vi. 17.

Footnote 1200:

  Orfila, Tox. i. 573.

Footnote 1201:

  Journal Gén. de Médecine, lvi. 22.

Footnote 1202:

  Materialien für die Staatsarzneikunde, i. 122.

Footnote 1203:

  Horn’s Archiv, 1824, ii. 259.

Footnote 1204:

  Buchner’s Repertorium für die Pharmacie, xxvii. 317, and xxxiii. 104.

Footnote 1205:

  Henke’s Zeitschrift für die Staatsarzneikunde, xxiii. 164.

Footnote 1206:

  Magazin für die gesammte Heilkunde, xxi. 563.

Footnote 1207:

  Annales de Chimie, lxxxvi. 59.

Footnote 1208:

  Orfila’s Toxicologie, i. 567, from the Procès-verbal of the public
  meeting of the Society of Liége in 1813.

Footnote 1209:

  See Dr. Babington’s Paper in Guy’s Hospital Reports, vi. 16.

Footnote 1210:

  Journal de Chimie Médicale, 1839, p. 389, from Casper’s Wochenschrift.

Footnote 1211:

  Aufsätze und Beob. ii. 12.

Footnote 1212:

  Versuche über die Wirkung des Baryts, &c.

Footnote 1213:

  Toxicologie Gén. 1843, ii. 44.

Footnote 1214:

  Magazin für die gesammte Heilkunde, xxi. 247.

Footnote 1215:

  I shall take an early opportunity, with the permission of Messrs
  Dewar, of publishing some of the details of these two cases, which are
  most interesting in various respects.

Footnote 1216:

  Versuche über die Wirkung des Baryts, &c. Heidelberg, 1824.

Footnote 1217:

  Horn’s Archiv für Medizinische Erfahrung, 1830, ii.

Footnote 1218:

  British Annals of Medicine, i. 41.

Footnote 1219:

  Ibidem, 132.

Footnote 1220:

  Schubarth, Journal der Praktischen Heilkunde, lii. 101.

Footnote 1221:

  See a paper by myself in Edinburgh Royal Society Trans., 1842, xv.
  276, 274.

Footnote 1222:

  Buchner’s Repertorium für die Pharmacie, xxxviii. 125.

Footnote 1223:

  Mem. de l’Acad. des Sc. 1787, 281, sur les vins lithargyriés.

Footnote 1224:

  Vitruv. de Architectura, L. viii. c. 7, Quot modis ducantur aquæ.
  Editio Dun. Barbari, 1567, pp. 262, 265.

Footnote 1225:

  De Medic. secundum locos, lvii.

Footnote 1226:

  Researches into the Properties of Spring Waters, 1803, p. 193.

Footnote 1227:

  Annales de Chim. lxxi. 197, l’an 1809.

Footnote 1228:

  Experiments in Scudamore’s analysis of Tunbridge Water, 1816.

Footnote 1229:

  A Treatise on Poisons, &c. First Edition, 1829.

Footnote 1230:

  Philosophical Magazine. Third Series, v. 81, 1834.

Footnote 1231:

  Guy’s Hospital Reports, 1838, iii. 60.

Footnote 1232:

  Transactions of the Royal Society of Edinburgh, 1842, xv. 265.

Footnote 1233:

  Toxicologie Gén. 1843, i. 657.

Footnote 1234:

  Transactions of the Royal Society of Edinburgh, xv. 265.

Footnote 1235:

  The statement here given of these phenomena is somewhat different from
  what is contained in the last edition of this work. The present
  account is derived from ulterior experiments, partly published in my
  paper in the Edinburgh Transactions. The discrepancies formerly
  prevailing between my own researches and those of Captain Yorke are
  now completely reconciled.

Footnote 1236:

  Journal de Chim. Méd. ix 714.

Footnote 1237:

  Annales d’Hyg. Publ. et de Méd. Lég. iv. 55. 1830.

Footnote 1238:

  Journal de Chim. Médicale, ix. 716. This adulteration has likewise
  since then attracted attention in London. See British Annals of
  Medicine, 1837, i. 15.

Footnote 1239:

  Annales de Chimie, lxxi. 197.

Footnote 1240:

  In distilled water containing a 12,000th of anhydrous _arseniate of
  soda_ three lead rods weighing 71·235 grains became in thirty-three
  days 71·240; in a solution of a 15,000th the lead, though slightly
  whitened, retained its weight exactly, weighing at the end, as at the
  beginning, of the experiment 62·622 grains. In distilled water
  containing a 35,000th of anhydrous _phosphate of soda_, three lead
  rods, which weighed together 73·949 grains, became in thirty-two days
  73·946; and in a comparative experiment with a solution containing a
  27,000th they gained 0·015.

Footnote 1241:

  Sometimes, however, a minute trace of white powder is attached to the
  bottom of the glass wherever the lead touches it. This is carbonate of
  lead at first, and afterwards a mixture like that described in the
  text.

Footnote 1242:

  Mr. Morson in Pharmaceutic Journal, ii. 355.

Footnote 1243:

  On Spring Waters, p. 23.

Footnote 1244:

  Tronchin de Col. Pict. 66.—1757.

Footnote 1245:

  De la Colique Métallique, 99, from Wanstroostwyk de l’Electricité
  Médicale, p. 224.

Footnote 1246:

  Appendix to Dr. Scudamore’s Analysis of the Mineral Water of
  Tunbridge, p. 51.

Footnote 1247:

  Some effect may perhaps be also owing to a difference between the
  proportion of saline matter contained in the water of the Crawley
  spring, which has been introduced into the city since Dr. Thomson
  resided here, and the proportion in the water with which the city was
  at that time supplied, I am not aware, however, of the difference
  between them, or that any material difference does exist.

Footnote 1248:

  Trans. of London College of Physicians, ii. 400.

Footnote 1249:

  Hints on a mode of procuring Soft Water at Tunbridge—Journal of
  Science, xiv. 352.

Footnote 1250:

  Scudamore’s Pamphlet—Appendix—_passim_.

Footnote 1251:

  Ibidem, p. 47.

Footnote 1252:

  Edinburgh Royal Society Transactions, xv. 265.

Footnote 1253:

  On Spring Waters, p. 14.

Footnote 1254:

  Ibidem, 116.

Footnote 1255:

  De la Colique Métallique, p. 98.

Footnote 1256:

  Dr. Duncan’s Medical Commentaries, xix. 313.

Footnote 1257:

  Comment. ad Boerhaave. § 1060, T. iii. 347. Edit. Lugd. Batav. 1753.

Footnote 1258:

  Scudamore on the Analysis of Tunbridge Water, Appendix, 51, 53.

Footnote 1259:

  Rozier. Observations sur la Physique, xiii. 145.

Footnote 1260:

  Annales d’Hygiène Publique, 1842, xxvii. 111.

Footnote 1261:

  Ann. de Chim. lvii. 82.

Footnote 1262:

  Zoonomia, ii. 130.

Footnote 1263:

  Trans. of London College of Physicians, iii. 227.

Footnote 1264:

  On the Diseases of the Army in Jamaica, p. 269.

Footnote 1265:

  Philosophical Magazine, liv. 229.

Footnote 1266:

  Trans. of London College of Physicians, i. 216.

Footnote 1267:

  On the Cause of the Endemical Colic of Devonshire. Transactions of the
  London Coll. of Phys., i. ii. and iii.

Footnote 1268:

  Annales d’Hygiène Publique, 1842, xxvii. 104.

Footnote 1269:

  Elements of Medical Jurisprudence, ii. 319.

Footnote 1270:

  Zeitschrift für die Staatsarzneikunde, 1827, xiii. 151.

Footnote 1271:

  Mérat de la Colique Métallique.

Footnote 1272:

  Diss. Inaug. sur la Collique de Madrid. Analyzed in Corvisart’s
  Journal de Médecine, xxxiv. 208.

Footnote 1273:

  Hohnbaum, &c. p. 157.

Footnote 1274:

  Geschichte der Mineralischen Gifte, 194.

Footnote 1275:

  Note in an Essay by his Son,—Ueber Vergiftung durch Käse. Horn’s
  Archiv. 1828, i. 83.

Footnote 1276:

  Gmelin’s Geschichte der Mineralischen Gifte, 216.

Footnote 1277:

  Cockelius, Acta, &c. Dec. i. An. iv. Obs. 30. Brunnerus, Ibidem, Obs.
  92. Vicarius, Ibidem, Obs. 100. Riselius, Ibidem, Dec. i. An. v. Obs.
  251.

Footnote 1278:

  Paris and Fonblanque’s Med. Jurisprudence, ii. 347.

Footnote 1279:

  De la Colique Métallique, 212.

Footnote 1280:

  Toxicologie Gén. i. 616.

Footnote 1281:

  Dr. Macculloch on the Art of Wine-making, in Edin. Horticultural Mem.
  i. 134.

Footnote 1282:

  Sur les Vins lithargyriés Mém. de l’Académie, 1787, p. 280.

Footnote 1283:

  Journal Gén. de Médecine, xliv. 321.

Footnote 1284:

  Edin. Medical and Surgical Journal, viii. 213.

Footnote 1285:

  Dehaen, Ratio Medendi, P. x. c. viii. § 1.

Footnote 1286:

  Repertory of Arts, First Series, viii. 262.

Footnote 1287:

  Trans. of Lond. Med. Society, i., or Edin. Med. and Surg. Journal,
  viii. 211.

Footnote 1288:

  The precipitate formed by the acetate of lead with albumen is
  dissolved by nitric acid. From that formed with milk the acid removes
  the oxide of lead entirely, leaving the casein.

Footnote 1289:

  Journal de Chimie Médicale, 1842, 339.

Footnote 1290:

  Toxicologie Générale, i. 630.

Footnote 1291:

  Edin. Med. and Surg. Journal, lvii. 117.

Footnote 1292:

  Journal de Physiologie, i. 284.

Footnote 1293:

  Diss. Inaug. p. 27.

Footnote 1294:

  De Effectibus liquidorum in vias aëriferas, &c. p. 43.

Footnote 1295:

  De effectu plumbi in organismo animali sano, &c. auctore Carol.
  Wibmer. Monachii, 1829, p. 29.

Footnote 1296:

  Treatise on Poisons, Edition 1836, p. 509.

Footnote 1297:

  Bulletin de l’Académie Roy. de Méd. 1840, vi. 283, and Toxicologie
  Gén. 1843, i. 668, 684.

Footnote 1298:

  Journal de Chim. Med. 1842, 344.

Footnote 1299:

  Guy’s Hospital Reports, 1841, vi. 175.

Footnote 1300:

  Archives Gén. de Médecine, liv. 106.

Footnote 1301:

  London Med. Chir. Trans., 1842, xxv. 115.

Footnote 1302:

  Annales d’Hygiène Publique, xx. 463, xxiv. 180.

Footnote 1303:

  Ibidem, xxi. 164.

Footnote 1304:

  L’Experience, Avril 27, 1843.

Footnote 1305:

  Toxicologie Gén. 1843, i. 670.

Footnote 1306:

  Arch. Gén. de Médecine, xix. 328.

Footnote 1307:

  Corvisart’s Journal de Médecine.

Footnote 1308:

  Krüger in Rust’s Magazin für die gesammte Heilkunde, xi. 535.

Footnote 1309:

  Lancet, 1838, i. 786.

Footnote 1310:

  Toxicologie Gén. i. 690.

Footnote 1311:

  Manual of Medical Jurisprudence, 189.

Footnote 1312:

  Experimental Inquiry on Iodine, p. 140.

Footnote 1313:

  London Medical Gazette, v. 538.

Footnote 1314:

  Lond. Med. Repos. N. S. vi. 368.

Footnote 1315:

  Comment. 1060, T. iii. p 347. Editio Dan Barbari.

Footnote 1316:

  Trans. Coll. Phys. London, iii. 426.

Footnote 1317:

  Journal Universel, xx. 351.

Footnote 1318:

  Bulletin de la Soc. Roy. de Méd. 1840, vi. 283.

Footnote 1319:

  Manual of Medical Jurisprudence, p. 186.

Footnote 1320:

  London Medical Repository, 1824, N. S. iii. 37.

Footnote 1321:

  Edinburgh, Phys. and Lit. Essays, i.

Footnote 1322:

  Traité des Maladies de Plomb. 1843.

Footnote 1323:

  London Medical Gazette, 1839–40, 1, 687.

Footnote 1324:

  Mérat de la Colique Métallique, 51.

Footnote 1325:

  Ibid., p. 55.

Footnote 1326:

  Tronchin de Colica Pictonum. Genevæ, 1757.

Footnote 1327:

  Archives Gén. de Médecine, liv. 111.

Footnote 1328:

  Louis, Recherches Pathologiques

Footnote 1329:

  London Medical Gazette, 1837–38, ii. 158.

Footnote 1330:

  British Annals of Medicine, i. 145.

Footnote 1331:

  London Med.-Chir. Transactions, xxii. 82.

Footnote 1332:

  Lancet, 1838–39, i. 65.

Footnote 1333:

  Reports of Medical Cases, p. 394.

Footnote 1334:

  Lambe on Spring Waters, p. 71.

Footnote 1335:

  Hufeland’s Journal der Praktischen Heilkunde, Mars, 1839.

Footnote 1336:

  Archives Gén. de Médecine, liv. 106.

Footnote 1337:

  Transactions of London Coll. of Phys. i. 236, 301, 304.

Footnote 1338:

  Annali Universali di Medicina, 1837, iv. 426.

Footnote 1339:

  Lancet, Dec. 31, 1842.

Footnote 1340:

  Trans. of Lond. Coll. Phys. i. 311.

Footnote 1341:

  Ibid. iii. 435.

Footnote 1342:

  Archives Gén. de Médecine, 1838, i. 353.

Footnote 1343:

  Ibid., liv. 106.

Footnote 1344:

  London Medical Gazette, April, 1843.

Footnote 1345:

  On the Poison of Lead, p. 22.

Footnote 1346:

  De la Colique Métallique.

Footnote 1347:

  De Colica Pictonum, p. 56.

Footnote 1348:

  Ibid. p. 65.

Footnote 1349:

  De la Colique Métallique, p. 23.

Footnote 1350:

  Journal de Chim. Médicale, 1840, 328.

Footnote 1351:

  Ibid. _passim_.

Footnote 1352:

  Calcineur,—a calciner of gypsum, I believe.

Footnote 1353:

  Annales d’Hygiène Publique, xix. 23, xxv. 543, xxviii. 226.

Footnote 1354:

  Journal Universel, xx. 353.

Footnote 1355:

  Annales d’Hygiène Publique, xxi. 149.

Footnote 1356:

  Corvisart’s Journ. de Médecine.

Footnote 1357:

  British Annals of Medicine, i. 205.

Footnote 1358:

  De la Colique Métallique, p 213.

Footnote 1359:

  Trans. of Lond. Med. Society, 1810, or Edin. Med. and Surg. Jour.
  viii. 211.

Footnote 1360:

  Tronchin de Colica Pict. p. 117.

Footnote 1361:

  De effectibus liquidorum ad vias aërif. applic. p. 43.

Footnote 1362:

  British Annals of Medicine, i. 205.

Footnote 1363:

  Trans. of Lond. Coll. of Physicians, i. 469.

Footnote 1364:

  Trans. of Lond. Coll. Phys. i. 317.

Footnote 1365:

  Annales d’Hygiène Publique, xxviii. 234.

Footnote 1366:

  London Med. Chir. Transactions, 1839, xxii. 87.

Footnote 1367:

  Traité des Maladies de Plomb, 1839, and Annales d’Hygiène Publique,
  1842, xxviii. 232.

Footnote 1368:

  Trans. of London Coll. of Phys., ii. 83.

Footnote 1369:

  Transactions Médicales, 1832, or, Annales d’Hygiène, 1841, xxv. 463,
  and xxvi. 543.

Footnote 1370:

  Annales d’Hygiène, xxv. 466.

Footnote 1371:

  Clark, in Edin. Med. Comment, xi. 102. Berger, in Horn’s Archiv für
  Mediz. Erfahrung, xi. 344. London Med. and Phys. Journ. xxvi. 46.

Footnote 1372:

  Ratio Medendi, P. I. c. ix. de Variis.

Footnote 1373:

  Trans. of London Coll. of Phys. ii. 457.

Footnote 1374:

  Ed. Phys. and Lit. Ess. i. 521.

Footnote 1375:

  Annales d’Hygiène Publique, xxv. 466.

Footnote 1376:

  Archives Gén de Médecine, xli. 136.

Footnote 1377:

  Annales d’Hygiène Publique, xv. 22.

Footnote 1378:

  Annales d’Hygiène Publique, xv. 36.

Footnote 1379:

  Annales d’Hygiène Publique, xix. 14.

Footnote 1380:

  Annales d’Hygiène Publique. 1842, xxviii. 217.

Footnote 1381:

  Philosophical Transactions, 1812, p. 218.

Footnote 1382:

  Toxicologie Gén. i. 208.

Footnote 1383:

  Versuche über die Wirkungen, &c.

Footnote 1384:

  Diss. Inaug. de effectibus liquidorum ad vias aërif. applic. p. 30.

Footnote 1385:

  Nicholson’s Journal, First Series, i. 529.

Footnote 1386:

  Ed. Med. and Surg. Journ., lvi. 114.

Footnote 1387:

  Orfila, Toxicol. Gén. i. 213.

Footnote 1388:

  Observations sur la Strontiane. Ann. de Chimie, xxi. 119.

Footnote 1389:

  Diss. Inaug. de venenis Mineralibus, p. 31.

Footnote 1390:

  Annales d’Hygiène Publique, 1842, xxix. 425.

Footnote 1391:

  Ibidem, xxviii. 216.

Footnote 1392:

  Journal of Science, iv. 382.

Footnote 1393:

  Henke’s Zeitschrift für die Staatsarzneikunde, 1835, xxx. 1.

Footnote 1394:

  Medical Commentaries, xix. 267.

Footnote 1395:

  London Medical Gazette, 1833–34, ii. 487.

Footnote 1396:

  Parkes’s Chemical Essays, ii. 219.

Footnote 1397:

  Essay on Poisons, p. 143.

Footnote 1398:

  Toxicologie Gén. i. 216.

Footnote 1399:

  Observations sur la Strontiane, Annales de Chimie, xxi. 119.

Footnote 1400:

  Versuche über die Wirkungen, &c.

Footnote 1401:

  Edin. Med. and Surg. Jour. lvi. 113.

Footnote 1402:

  Toxicol. Gén. i. _passim_.

Footnote 1403:

  Supplement to Dr. Duncan’s Dispensatory, p. 53.

Footnote 1404:

  Buchner’s Repertorium für die Pharmacie, vi. 175.

Footnote 1405:

  Ibidem, xxxvii. 203.

Footnote 1406:

  Toxicologie Gén. i. 710.

Footnote 1407:

  Edin Med. and Surg. Journal, li. 341.

Footnote 1408:

  Phil. Trans. 1760, li. 662.

Footnote 1409:

  Journal of Science, iii. 51.

Footnote 1410:

  Aufsätze und Beobachtungen, i. 79.

Footnote 1411:

  Edin. Med. and Surg Journal, xlix. 488.

Footnote 1412:

  Toxicol. Gén. i. 712.

Footnote 1413:

  Toxicol. Gén. i. 713.

Footnote 1414:

  Archives Gén. de Méd. viii. 615.

Footnote 1415:

  Journal de Chim. Méd. viii. 671.

Footnote 1416:

  Orfila, Toxicol. Gén. 714.

Footnote 1417:

  Botanical Arrangement, ii. 501. Stokes’s Edition.

Footnote 1418:

  See on this subject Deyeux in Ann. de Chim. lxxiii. 106.
  Boutron-Charlard et Henri, in Journal de Pharmacie, x. 466. Bussy et
  Lecanu, ibid. xii. 481.

Footnote 1419:

  Tractatus de Venenis in Opp. I. i. 308, quoted by Marx, die Lehre von
  den Giften, i. 128.

Footnote 1420:

  Manual of Medical Jurisprudence, 224.

Footnote 1421:

  Toxicol. Gén. i. 706.

Footnote 1422:

  Ibidem, i. 715.

Footnote 1423:

  Mr. Bennet in London Medical Gazette, ix. 7.

Footnote 1424:

  Med. Facts and Observations, vii. 293.

Footnote 1425:

  Journal de Pharmacie, xxii. 118.

Footnote 1426:

  Journ. de Chim. Méd. i. 343.

Footnote 1427:

  Ibidem, i. 483.

Footnote 1428:

  Flora Médicale des Antilles, iii. 14.

Footnote 1429:

  Flore Médicale des Antilles, iii. 27.

Footnote 1430:

  Landsberg. Therapeutische und Toxikologische Würdigung der Grana
  Tiglii. Horn’s Archiv für Medizinische Erfahrung, 1831, 565.

Footnote 1431:

  Journal de Chim. Médicale, 1839, 509.

Footnote 1432:

  Journal de Pharmacie, iv. 289.

Footnote 1433:

  Toxicol. Gén. i. 679.

Footnote 1434:

  Nouv. Bibliothèque Medicale, Mai, 1827, p. 221.

Footnote 1435:

  Neues Magazin. i. 3, p. 557.

Footnote 1436:

  Toxicol. Gén. i. 680.

Footnote 1437:

  Journal de Pharmacie, x. 416.

Footnote 1438:

  Toxicol. Gén. i. 691.

Footnote 1439:

  Observat. Medicinales, iv. c. 27, p. 218.

Footnote 1440:

  Toxicol. Gén. i. 695.

Footnote 1441:

  London Courier, Sept. 9, 1823.

Footnote 1442:

  Toxicol. Gén. i. 695.

Footnote 1443:

  Annales d’Hygiène Publique et de Méd. Lég. viii. 333.

Footnote 1444:

  Edin. Med. and Surg. Journal, xxxv. 339.

Footnote 1445:

  Journal of the Royal Institution, i. 532.

Footnote 1446:

  Toxicol. Gén. i. 754.

Footnote 1447:

  Toxicologie Gén. i. 754.

Footnote 1448:

  Journal de Chimie Médicale, 1836, 273.

Footnote 1449:

  Histoire des Plantes Vénéneuses de la France, p. 178.

Footnote 1450:

  Ibidem, 180.

Footnote 1451:

  Buchner’s Repertorium für die Pharmacie, lxviii. 346.

Footnote 1452:

  Die Wirkung der Arzneimittel und Gifte, i. 17.

Footnote 1453:

  Historia Stirpium Helvet.

Footnote 1454:

  Rust’s Magazin für die Gesammte Heilkunde, xx. 451.

Footnote 1455:

  Ann. de Chim. et de Phys xii. 358.

Footnote 1456:

  Schweigger’s Journal der Chimie, xxv. 369.

Footnote 1457:

  Toxicol. Gén. i. 739.

Footnote 1458:

  Ibidem, 741.

Footnote 1459:

  Journal de Chim. Méd. v. 567.

Footnote 1460:

  Toxicol. Gén. i. 703.

Footnote 1461:

  Lancet, 1837–38, i. 44.

Footnote 1462:

  Hist. des Plantes Venen. de la Suisse, p. 140.

Footnote 1463:

  Flora Suecica, No. 338.

Footnote 1464:

  Withering’s Arrangement, i. 403, Stokes’s Edition.

Footnote 1465:

  Descourtils. Flora Médicale des Antilles, iii. 57.

Footnote 1466:

  Buchner’s Repertorium, lxviii. 80.

Footnote 1467:

  Toxicologie Gén. ii.

Footnote 1468:

  Horn’s Archiv für Mediz. Erfahrung, 1824, i. 65.

Footnote 1469:

  Die Wirkung der Arzneim. und Gifte, ii. 388.

Footnote 1470:

  Acta Curios. Nat. Dec. I. Ann. viii. p. 139.

Footnote 1471:

  Trial of Webb. Lond. Med. Gaz. xiv. 612. Inquest on Rebecca Cross.
  Ibidem, 759. Case by Drs. Labatt and Stokes. Dublin Journ. of Med. and
  Chem. Science, iv. 237.

Footnote 1472:

  Analysis by Mr. West in the first of these cases.

Footnote 1473:

  Annali Universali di Medicina, 1839, iii. 41.

Footnote 1474:

  Toxicol. Gén. i. 744.

Footnote 1475:

  Repertorium für die Pharmacie, xxxvii.

Footnote 1476:

  Dissertation Inaugurale, quoted in Orfila, Toxicol. Gén. i. 683.

Footnote 1477:

  Tox. Gén. i. 758. The drug must have been much adulterated, as it very
  generally is; for half a scruple is an active purgative to man.

Footnote 1478:

  Orfila, Toxicol. Gén. i. 724.

Footnote 1479:

  Méd. Légale, iv. 430.

Footnote 1480:

  Ibid. iv. 431.

Footnote 1481:

  Die Wirkung der Arzneimittel und Gifte, iii. 191.

Footnote 1482:

  Annales de Chimie, lxxvi.

Footnote 1483:

  Annales d’Hygiène Publique, xxviii. 347.

Footnote 1484:

  Revue Medicale, 1828, ii. 475.

Footnote 1485:

  Toxicol. Gén. ii. 4.

Footnote 1486:

  Edin. Med. and Surg. Journal, li. 344.

Footnote 1487:

  Orfila, Toxicol. Gén. ii. 28.

Footnote 1488:

  Annales de la Med. Physiologique, Octobre, 1829—extracted in Edin.
  Med. and Surg. Journal, xxxiv. 214.

Footnote 1489:

  London Medical Gazette, 1841–42, i. 63.

Footnote 1490:

  Hufeland’s Journal der Praktischen Heilkunde, lii. 2, 112.

Footnote 1491:

  See an interesting case in Memorie della Soc. Med. di Genova, ii. 1,
  p. 29.

Footnote 1492:

  Graaf’s Cases, and Rouquayrol’s.

Footnote 1493:

  Lib. xxi. des Venins.

Footnote 1494:

  See the case in Memorie della Soc. Med. di Genova, ii. 1, p. 29.

Footnote 1495:

  Toxicol. Gén. ii. 23.

Footnote 1496:

  Hufeland’s Journal, lii. 2, 114.

Footnote 1497:

  Mem. dell’ Acad. de Torino, 1802–3.

Footnote 1498:

  Toxicol. Gén. ii. 30.

Footnote 1499:

  Medizinische-Chirurgische Zeitung, 1834, iv. 298, from American
  Journal of Medical Science.

Footnote 1500:

  Taylor’s Manual of Medical Jurisprudence, 228.

Footnote 1501:

  Medical Jurisprudence, 574, from New York Med. and Phys. Journal.

Footnote 1502:

  Mem. della Soc. Med. di Genova, ii. 1, 29.

Footnote 1503:

  Report of the Coroner’s Inquest in Standard Newspaper, Jan. 1841.

Footnote 1504:

  Archiv. für Medizinische Erfahrung, 1834, i. 61–64.

Footnote 1505:

  Annales d’Hygiène Publique, xxviii. 383.

Footnote 1506:

  Revue Médicale, 1828, ii. 475.

Footnote 1507:

  Magazin für die gesammte Heilkunde, xviii. 109.

Footnote 1508:

  Journal Complémentaire, xviii. 184.

Footnote 1509:

  Cuvier, Règne Animal, v. 63.

Footnote 1510:

  Edin. Med. and Surg. Journal, iv. 393.

Footnote 1511:

  Memoirs of the London Medical Society, v. 94.

Footnote 1512:

  Edin. Philos. Journal., i. 194.

Footnote 1513:

  Lond. Med. Repository, iii. 445.

Footnote 1514:

  Edin. Med. and Surg. Journal, xxix. 86.

Footnote 1515:

  Toxicol. Gén. ii. 37.

Footnote 1516:

  Médecine Légale, iv. 85.

Footnote 1517:

  1er Mars, 1812; 1er Octobre, 1812; 21 Mars, 1813; Avril, 1813.

Footnote 1518:

  De Mytilorum quorundam veneno,—Acta Physico-Medica
  Acad.—Cæsareo-Leopoldino-Carol. &c. 1744. Appendix, p. 124.

Footnote 1519:

  De Mytilorum, &c. p. 115.

Footnote 1520:

  Edin Med. and Surg. Journal, xxix. 88.

Footnote 1521:

  Voyage of Discovery, ii. 285.

Footnote 1522:

  Orfila, Toxic. Gén. ii. 44.

Footnote 1523:

  Annales d’Hygiène Publique, xvii. 360.

Footnote 1524:

  De Mytilorum, &c. p. 117, 121, 124.

Footnote 1525:

  Toxicol. Gén. ii. 45.

Footnote 1526:

  De Mytilorum, &c. p 134.

Footnote 1527:

  Journal de Pharmacie, v. 25, from Essai Medical sur les huitres.

Footnote 1528:

  London Med. Repository, xiii. 58.

Footnote 1529:

  Trans. London Coll. of Phys. v. 109.

Footnote 1530:

  Journal de Pharmacie, v. 509.

Footnote 1531:

  For a severe case, not fatal, occurring in Kent, see London Medical
  Gazette, xii. 464.

Footnote 1532:

  Magazin für die gesammte Heilkunde, xx. 155.

Footnote 1533:

  Bulletins des Sciences Medicales, x. 92.

Footnote 1534:

  Ibidem, xx. 195.

Footnote 1535:

  Journal der Praktischen Heilkunde, 1829, ii. iv. 120.

Footnote 1536:

  Rust’s Magazin für die gesammte Heilkunde, xxxii. 361.

Footnote 1537:

  Robineau-Devoidy in Archives Gén. de Méd. xxi. 626.

Footnote 1538:

  Giornale di Fisica. ix. 458, and Meckel’s Archiv für Anat. und
  Physiol. iii. 639.

Footnote 1539:

  Edin. Med. and Surg. Journal, xviii.; Phil. Trans. 1810.

Footnote 1540:

  Wibmer, Die Wirkung der Arzneimittel und Gifte, i. 200.

Footnote 1541:

  Journal de Médecine, 1765.

Footnote 1542:

  Gazette de Santé, 1776.

Footnote 1543:

  Archives Gén. de Médecine, xi. 30.

Footnote 1544:

  Trans. of Med. and Phys. Soc. of Calcutta, iv. 442.

Footnote 1545:

  Histoire d’une Maladie très-singulière, &c. in Hist. de l’Académie des
  Sciences, 1766, i. 97.

Footnote 1546:

  London Med. and Phys. Journal, lvii. 342.

Footnote 1547:

  Dr. Duncan’s Cases of Diffuse Inflammation of the cellular texture—in
  Edin. Med. Chirurg. Trans. i. 455, 470, 1824. Also,

Footnote 1548:

  Mr. Travers on Constitutional Irritation, 1826.

Footnote 1549:

  Rust’s Magazin, xxiv. 490. Also Annali Univ. di Med. 1811, iii. 449.

Footnote 1550:

  Ibidem, xxv. 108.

Footnote 1551:

  Kopp’s Jahrbuch, v. 67, and vi. 95.

Footnote 1552:

  Rust’s Magazin, xxv. 105.

Footnote 1553:

  Revue Médicale, 1827, ii. 488.

Footnote 1554:

  Journal der Praktischen Heilkunde, liv. iii. 62.

Footnote 1555:

  Magazin der Ausländischen Literatur, iii. 460, v. 168.

Footnote 1556:

  I have taken the liberty of applying this term to an establishment
  unique perhaps in the history of the world. The Voirie et Chantier
  d’Ecarrissage of Montfaucon, which has existed close to the walls of
  Paris for several centuries, is an enclosure of many acres, where the
  contents of the necessaries of the city are collected in enormous
  pits, and where horses, dogs, and cats are flayed to the amount of
  forty or fifty thousand annually. The fat is melted for blowpipe
  lamps; the bones are in a great measure burnt on the premises for
  fuel; the intestines are made into coarse gut for machinery; the
  flesh, blood, and garbage are heaped to putrefy for manure; and in
  summer a bed of compost is spread to breed maggots for feeding
  poultry. There is no drain. Description cannot convey an idea of the
  stench. The committee of the Board of Health, appointed to make
  inquiries into the best mode of abating the nuisance, in vain
  attempted to penetrate into the place. Yet the workmen and their
  families are stout, healthy, and long lived.

Footnote 1557:

  Des Chantiers d’Ecarrissage. Annales d’Hyg. Publ. et de Méd. Lég.
  viii. 139. Sur l’enfouissement des Animaux morts de maladies
  contagieuses. Ibid. ix. 109.

Footnote 1558:

  Journal de Physiologie, ii. 1, and iii. 81.

Footnote 1559:

  Journal des Progrès des Sciences Médicales, 1827, vi. 181.

Footnote 1560:

  Journal de Physiologie, iii. 85.

Footnote 1561:

  De divers accidens graves occasionnés par les miasmes d’animaux en
  putréfaction. Mém. de la Soc. de Med. i. 97.—London Med. Chirurg.
  Review, vi. 202.

Footnote 1562:

  Annales d’Hyg. Publique et de Med. Légale, vii. 216.

Footnote 1563:

  Ibidem, viii. and ix. _ut supra_.

Footnote 1564:

  Dr. Duncan, Edin. Med. Chirurg. Trans. i. 502 and 520.

Footnote 1565:

  Neue Beobachtungen über die Vergiftungen durch dens genuss
  geraücherten Würste. Tübingen, 1820.—Das Fettgift, oder die Fettsaüre,
  und ihre Wirkungen auf den thierischen Organismus. Tübingen, 1822.

Footnote 1566:

  De Veneni Botulini viribus et natura. Diss. Inaug. Berolini, 1828.

Footnote 1567:

  De Veneno in Botulis. Commentatio in certamine lit. a gratioso Med.
  Ord. Berol. Præmio ornata, 1828. Analyzed by Dr. Arrowsmith in Edin.
  Med. and Surg. Journal, xxxiii. 28.

Footnote 1568:

  Horn’s Archiv, 1828, i. 558.

Footnote 1569:

  Röser, in London Med. Gazette, 1842–43, i. 271.

Footnote 1570:

  Weiss, die neuste Vergift. durch Verdorbene Würste, &c. mit Vorrede
  und Anhang begleitet, von Dr. J. Kerner. Carlsruhe, 1821.

Footnote 1571:

  Horn’s Archiv, 1828, i. 596.

Footnote 1572:

  Toxicologie, Zweite Auff. 1829, p. 136.

Footnote 1573:

  Das Wurst-fett-gift. oder neue Untersuchung, &c. Archiv für
  Medizinische Erfahrung, 1829, i. 30 and 75.

Footnote 1574:

  Hufeland’s Journal, lvii. 2, 106.

Footnote 1575:

  Magazin für die gesammte Heilkunde, xxi. 247.

Footnote 1576:

  Die Chemische Ausmittelung des Käsegifts. Horn’s Archiv, 1827, i. 203.

Footnote 1577:

  Ueber die Vergiftung durch Käse. Horn’s Archiv, 1828, i. 65.

Footnote 1578:

  Ann. de Chimie et de Physique, xxxvi. 159.

Footnote 1579:

  Archives Gén. xv. 460.

Footnote 1580:

  Rust’s Magazin, xxvii. 193.

Footnote 1581:

  Horn’s Archiv. 1828, i. 76.

Footnote 1582:

  Rust’s Magazin, xvi. 111.

Footnote 1583:

  London Medical and Physical Journal, xlvi. 68.

Footnote 1584:

  Orfila, Médecine-Légale, ii. 322.

Footnote 1585:

  Archives Gén. de Méd.

Footnote 1586:

  Journ. de Chim. Méd. viii. 726.

Footnote 1587:

  Annales d’Hygiène Publique, xxi. 234.

Footnote 1588:

  Annales d’Hygiène Publique, xx. 413.

Footnote 1589:

  Journal de Chimie Med. 1842, 872.

Footnote 1590:

  Journal of the Institution, ii. 414, from Hufeland Journal.

Footnote 1591:

  Bulletins des Sciences Méd. xx. 197.

Footnote 1592:

  London Med. Gazette, xiv. 656.

Footnote 1593:

  London Med. Repository, Third Series, iii. 372.

Footnote 1594:

  Edin. Med. and Surg. Journal, xlvi. 293.

Footnote 1595:

  London Medical and Physical Journal, xxxv. 100.

Footnote 1596:

  Observations on Surgery. 276.

Footnote 1597:

  London Medico-Chirurgical Transactions, xii. 52.

Footnote 1598:

  Annales d’Hygiène Publique, xxi. 188.

Footnote 1599:

  Sur les Blessures par armes de guerre, i. 82. Also, Lond. Med. Gaz.
  1838–39, ii 799.

Footnote 1600:

  London Med. Gazette, 1836–37, ii. 275.

Footnote 1601:

  Ueber den Selbstmord, p. 168, from Schmucker’s Vermischte Chirurgische
  Schriften.

Footnote 1602:

  Diss. Inaug., Paris, 1810. Analyzed in Sedillot’s Journal de Méd.
  xxxix. 331.

Footnote 1603:

  Saggi scient. e litter. dell’ Acad. di Padova, T. iii. P. ii. p. 1,
  quoted in Marx, die Lehre von den Giften, I. ii. 196.

Footnote 1604:

  Meyan, Causes Célèbres. Edit. 2, 1808. T. ii. 324, quoted by Marx, die
  Lehre von den Giften, I. ii. 298.

Footnote 1605:

  Ann. d’Hyg. Pub. et de Méd. Lég. iii. 365.

Footnote 1606:

  Midland Medical and Surgical Reporter, i. 47, 1828.

Footnote 1607:

  Instruction sur le Traitement des Asphyxiés, &c. p. 118.

Footnote 1608:

  Med. and Surg. Journal, xxii. 233.

Footnote 1609:

  Arch. Gén. de Méd. xiii. 372.

Footnote 1610:

  London Medico-Chirurgical Transactions, xii. 1.

Footnote 1611:

  Philosophical Transactions, xlix. 477, 483.

Footnote 1612:

  Magazin für die gesammte Heilkunde, xxi. 549.

Footnote 1613:

  Annales de Hygiène Publique, 1842, xxvii. 397.

Footnote 1614:

  London Med. Gazette, 1837–38, i. 177.

Footnote 1615:

  London Courier, Oct. 1, 1828.

Footnote 1616:

  London Med. Gazette, 1839–40, i. 559.

Footnote 1617:

  Journal de Chim. Méd. vi. 265.

Footnote 1618:

  Ibidem, vi. 458.

Footnote 1619:

  Archives Gén. de Méd. xxi. 616, or Journ. de Chim. Méd. v. 621, and
  vi. 63.

Footnote 1620:

  Journal de Pharmacie, xvi. 322, or Journ. de Chim. Méd. vi. 263.

Footnote 1621:

  Annales d’Hyg. Publique et de Méd. Légale, viii. 25.

Footnote 1622:

  Journal de Chim. Med. iv. 275.

Footnote 1623:

  Annales d’Hyg. Publique et de Med. Légale, i. 235.

Footnote 1624:

  Dictionnaire de Méd. et Chirurg. Pratiques, v. 124.

Footnote 1625:

  Recherches sur l’Apoplexie, p. 70.

Footnote 1626:

  Beiträge zur Gerichtlichen Arzneikunde, iii. 40.

Footnote 1627:

  London Medical and Physical Journal, xlvii. 181.

Footnote 1628:

  Recherches sur l’Apoplexie, 212.

Footnote 1629:

  Ibidem, p. 214.

Footnote 1630:

  Instances of congestive apoplexy thus arising were then quoted. I may
  here add a very apposite instance of hemorrhagic apoplexy, occurring
  in similar circumstances. Dr. Jennings, an American physician,
  mentions the case of a female fifty years of age, who, after a full
  meal, tumbled down in a fit of insensibility and immediately expired,
  and in whom after death there was found enormous distension of the
  stomach with food, an extensive effusion of blood into the central
  parts of the brain, and ossification of the cerebral arteries. (London
  Med. Gazette, xvi. 735.)

Footnote 1631:

  Annales d’Hygiène Publique, xx. 170.

Footnote 1632:

  Rochoux, Recherches sur l’Apoplexie, 66.

Footnote 1633:

  Recherches sur le Ramollissement du Cerveau, p. 150.

Footnote 1634:

  Pathological and Practical Researches on Diseases of the Brain, p.
  210.

Footnote 1635:

  Recherches Pathologiques, 460, 466, and 472.

Footnote 1636:

  Archives Gén. de Méd. xxiii. 260.

Footnote 1637:

  Journal de Médecine, xiii. 315.

Footnote 1638:

  Edin. Med. and Surg. Journal, xxxii. 262.

Footnote 1639:

  London Med. Gazette, xi. 777.

Footnote 1640:

  Recherches sur le Ramollissement du Cerveau, p. 133 and 135.

Footnote 1641:

  Pathological Researches, 214.

Footnote 1642:

  Beiträge zur gerichtl. Arzneik. ii. 61, iii. 42, iv. 42.

Footnote 1643:

  Reports of Medical Cases, ii. 240, 242, 244.

Footnote 1644:

  Pathological Researches, 216.

Footnote 1645:

  Annales d’Hygiène Publique, 1841, xxvi. 399.

Footnote 1646:

  Article Epilepsie in Dictionnaire de Médecine, viii. 209.

Footnote 1647:

  Diction. de Med. xii. 512.

Footnote 1648:

  Georget, _in loco cit._ 212.

Footnote 1649:

  The body in this case was not examined.

Footnote 1650:

  Edin. Med. and Surg. Journal, x. 40.

Footnote 1651:

  Esquirol, Dict. des Sciences Méd. xii. 528.

Footnote 1652:

  Corvisart’s Journ. de Méd. xiii. 315, and xl. 81; also Prost, la
  Médecine éclairée par l’ouverture des cadavres, ii. 382, 389, 394.

Footnote 1653:

  Nouveau Journal de Médecine, ii. 269.

Footnote 1654:

  Journal Hebdomadaire et Universel, iv. 366.

Footnote 1655:

  Portal, Observations sur la nature et le traitement de l’Epilepsie, p.
  65 and 67.

Footnote 1656:

  Memorie della Soc. Méd. di Genova, i. 89.

Footnote 1657:

  Portal, _passim_.

Footnote 1658:

  On Diseases of the Brain and Spine, Cases 18, 19, 20.

Footnote 1659:

  On Chronic Inflammation of the Brain, Ed. Med. and Surg. Journal, xiv.

Footnote 1660:

  Reports of Medical Cases, ii. 14, 15.

Footnote 1661:

  Lancet, 1838–39, ii. 236.

Footnote 1662:

  On Diseases of the Brain and Spine, Cases 16 and 17.

Footnote 1663:

  Recherches sur le Ramollissement de Cerveau, 1819, 1823.

Footnote 1664:

  Recherches Anat. Pathol. sur l’Encephale. 1820.

Footnote 1665:

  See also Dr. Abercrombie on Diseases of the Brain and Spinal Cord, p.
  71.

Footnote 1666:

  Opera varia, Venetiis, 1739.—De Mortibus Subitaneis, p. 12.

Footnote 1667:

  London Medical Repository, N. S. ii. 318.

Footnote 1668:

  Recherches Anatomico-Pathologiques, 313.

Footnote 1669:

  Laennec, Revue Médicale, 1828, iv. Dance, Répertoire Gén. d’Anatomie
  Pathologique, vi. 197.

Footnote 1670:

  On the Diseases of the Brain and Spinal Cord, Case 132.

Footnote 1671:

  Ibidem, Case 131. Ollivier, Traité de la moelle épinière, Obs. 42.

Footnote 1672:

  Abercrombie, Case 138.

Footnote 1673:

  London Medico-Chirurgical Transactions, i. 157.

Footnote 1674:

  Recherches sur l’Apoplexie, p. 159.

Footnote 1675:

  Annales d’Hygiène Publique, xx. 173.

Footnote 1676:

  Archives Gén. de Med. 1838, i. 40.

Footnote 1677:

  Archives Gén. xiv. 406.

Footnote 1678:

  London Medical Gazette, viii. 47.

Footnote 1679:

  Lancet, July 31, 1841.

Footnote 1680:

  Elements of Materia Medica, 1842, p. 1738.

Footnote 1681:

  London Medical Gazette, xviii. 930.

Footnote 1682:

  Serullas Journ. de Chim. Méd. vi.

Footnote 1683:

  Edin. Med. and Surg. Journal, xxxv. 331.

Footnote 1684:

  Buchner’s Repertorium für die Pharmacie, 2te Reihe, xxxii. 104.

Footnote 1685:

  Procès de Castaing, p. 113.

Footnote 1686:

  Ann. de Chim. et de Phys. xxv. 102.

Footnote 1687:

  Toxicol. Gén. ii. 60.

Footnote 1688:

  Orfila, Tox. Gén. 1813, ii. 254.

Footnote 1689:

  Reports of Medical Cases, ii. 203.

Footnote 1690:

  Repertorium für die Pharmacie, xxxi. 174.—Professor Orfila, in the
  last edition of his Toxicologie Gén. [1843, ii. 253], has attacked in
  no very measured terms this opinion of Professor Buchner and myself.
  But, although he professes to give a literal translation of the
  passage above, he has translated it so incorrectly as wholly to
  misrepresent our opinion. The close of the paragraph, “chemical
  analysis must often fail to detect opium where there could be no doubt
  of its _having been administered_ in large quantity,” is rendered into
  French by the Parisian Professor in these words,—“l’analyse chimique,
  propre à constater l’existence de l’opium, est souvent inutile, même
  dans le cas _ou il existe_ une grande quantité de cette
  substance,”—which is a very different proposition. Orfila clearly
  overrates the utility of the process for detecting opium, both in this
  criticism and in his whole observations on the subject, by losing
  sight of the tendency of absorption to remove the poison beyond reach.

Footnote 1691:

  Bombay Med. Phys. Transactions, i. 322.

Footnote 1692:

  Die Verdauung nach Versuchen, &c.

Footnote 1693:

  Journal of Science, N. S. vi. 56.

Footnote 1694:

  Dr. Pereira states that he is obliged to differ from me upon this
  important subject for he “has several times obtained from the stomach
  of subjects in the dissecting-room a liquor which reddened the salts
  of iron” (Elements of Materia Medica, p. 1741). This fact, however,
  does not exactly touch the question. The reddening must be occasioned,
  not in the crude fluid, but with a substance obtained by the process
  of analysis for detecting meconic acid in complex organic
  mixtures,—otherwise the proposition in the text stands good.

Footnote 1695:

  Experiments on Opium. Appendix to Treatise on Febrile Diseases, vi.
  697.

Footnote 1696:

  Edin. Lit. and Phys. Essays, iii. 309.

Footnote 1697:

  Monro, Ibidem, 331, and Philip, _ut supra_, p. 680.

Footnote 1698:

  Toxicol. Gén. ii. 77.

Footnote 1699:

  Monro, Edin. Phys. and Lit. Essays, ii. 335, 324.—Charret, Revue
  Médicale, 1827, i. 515.

Footnote 1700:

  On the Operation of Poisonous Agents on the Living Body, _passim_.

Footnote 1701:

  Revue Médicale, 1827, i. 514.

Footnote 1702:

  Archives Gén. vii. 558.

Footnote 1703:

  Arch. Gén. i. 150.

Footnote 1704:

  Ann. de Chim. et de Phys. 1824, xxv, 102.

Footnote 1705:

  Journ. de Chim. Méd. 1841, 488.

Footnote 1706:

  Narrative of a Visit to the Court of Sinde, p. 231.

Footnote 1707:

  Rust’s Magazin, iii. 24.

Footnote 1708:

  Archives Gén. vii. 550.

Footnote 1709:

  Journal Universel, xix. 340.

Footnote 1710:

  American Medical Recorder, xiii. 418, from Gemeinsame Deutsche
  Zeitschrift für Geburtshilfe, 1826, i. 1.

Footnote 1711:

  Corvisart’s Journal de Médecine, xvi. 22.

Footnote 1712:

  Lond. Med. and Phys. Journal, xlix. 119.

Footnote 1713:

  De Usu Opii, iv. 149.

Footnote 1714:

  Journal Universel, xix. 340.

Footnote 1715:

  London Med. and Phys. Journal, xxxi. 468.

Footnote 1716:

  Edin. Med. and Surg. Journal, vii. 305.

Footnote 1717:

  Reports of Medical Cases, ii. 205, 206.

Footnote 1718:

  Journal de Médecine, xvi. 21.

Footnote 1719:

  Arch. Gén. vii. 552.

Footnote 1720:

  London Med. Chir. Trans. i. 77.

Footnote 1721:

  Edin. Med. and Surg. Journ. xiv. 603.

Footnote 1722:

  Journ. Universel, xix. 340.

Footnote 1723:

  Edin. Med. and Surg. Journal, vii.

Footnote 1724:

  Journ. Universel, xix. 340.

Footnote 1725:

  Melier in Archives Gén. de Méd. xiv. 406.

Footnote 1726:

  Corvisart’s Journ. de Méd. xvi. 21.

Footnote 1727:

  Lancet, 1836–37, i. 271.

Footnote 1728:

  Aufsätze und Beobachtungen, i. 93.

Footnote 1729:

  Ollivier’s case in Arch. Gén. vii. 550.

Footnote 1730:

  Corv. Journ. de Méd. xxxiv. 274.

Footnote 1731:

  Aufsätze und Beobachtungen, i. 94, 100.

Footnote 1732:

  Archives Gén. de Méd. li. 495.

Footnote 1733:

  These effects must not be confounded with those which poppy-juice has
  been known to cause when spoiled. A whole family of Jews were attacked
  with violent vomiting and purging, in consequence of partaking of a
  decoction of poppy-heads, which had been kept four days in a hot
  stove, and had consequently undergone decomposition. The usual
  narcotism was not produced at all. (Rust’s Magazin, xxii. 484.)

Footnote 1734:

  Mém. de l’Acad. des Sciences, xxxviii. 1735.

Footnote 1735:

  Toxicol Gén. from Bibliothèque Médicale, Août, 1806.

Footnote 1736:

  Corvisart’s Journal de Médecine, iv. 3.

Footnote 1737:

  Nouveaux Elémens de Thérapeutique, ii. 60.

Footnote 1738:

  London Med. and Phys. Journal, xxviii. 81. This patient took at 4 A.M.
  two ounces of wine of opium, became drowsy at 6, was capable of being
  roused at 9, vomited by emetics a liquid coloured with laudanum, and
  was kept awake for the rest of the day. But at 7 P.M. having
  previously had a cough and brown sputa from vinegar entering his
  windpipe, he became gradually more and more insensible, till at last
  he was quite comatose; and in this state he continued till his death
  on the evening of the third day. On dissection nothing was found in
  the brain or stomach attributable to opium.

Footnote 1739:

  London Med. and Phys. Journal, xxxi. 468.

Footnote 1740:

  Aufsätze und Beobachtungen, i. 85.

Footnote 1741:

  Mémoires de l’Institut—Sc. Physiques, ii. 107.

Footnote 1742:

  Practisches Handbuch für Physiker, iii. 329.

Footnote 1743:

  Edin. Med. and Surg. Journal, liv. 151.

Footnote 1744:

  Paris and Fonblanque’s Medical Jurisprudence, ii. 388.

Footnote 1745:

  Lancet, 1837–38, i. 304.

Footnote 1746:

  Pyl’s Repert. für die gerichtl. Arzneiwissenschaft, iii. 145.

Footnote 1747:

  See, for example, Parent-Duchatelet and D’Arcet on the health and
  longevity of Tobacco-manufacturers and Woodfloaters, in Annales d’Hyg.
  Publ. et de Méd. Lég. l. 169, and iii. 245.

Footnote 1748:

  Voyages en Perse, iii. 93.

Footnote 1749:

  Narrative of a Visit to the Court of Sinde, p. 230.

Footnote 1750:

  Two Years in China, 1843, p. 243.

Footnote 1751:

  Narrative, &c. p. 231.

Footnote 1752:

  Edin. Medical and Surgical Journal, xxxvii. 123.

Footnote 1753:

  Journal de Chimie Méd. iii. 24.

Footnote 1754:

  Toxicologie Gén. ii. 81, 82.

Footnote 1755:

  Journal de Chim. Méd. vii. 250.

Footnote 1756:

  Ibidem, 1842, 583.

Footnote 1757:

  Journal de Chimie Médicale, Avril, 1827, and Edin. Med. Journ. xxix.
  450.

Footnote 1758:

  Ibidem, vii. 114.

Footnote 1759:

  Bulletins de la Société Philomatique, 1818, p. 54:—Journal de Chimie
  Médicale, Avril, 1827.

Footnote 1760:

  Annali Universali di Med. xxxi. 169, xxxiv. 100.

Footnote 1761:

  Journal de Chim. Méd. v. 410.

Footnote 1762:

  Mém. de la Soc. Roy. de Médecine, i. 142.

Footnote 1763:

  Journal de Chim. Méd. vii. 135.

Footnote 1764:

  Revue Médicale, 1829, iii. 424.

Footnote 1765:

  Procés Complet d’Edme-Samuel Castaing, p. 31.

Footnote 1766:

  Edinburgh Med. and Surg. Journal, lvi. 296.

Footnote 1767:

  Toxicol. Gén. ii. 70.

Footnote 1768:

  Traité de Médecine Légale, iii. 353.

Footnote 1769:

  Ibidem, iii. 356.

Footnote 1770:

  Toxicol. Générale, ii. 70.

Footnote 1771:

  Meckel’s Archiv für Anat. und Physiol. xiv. 19.

Footnote 1772:

  Buchner’s Repertorium für die Pharmacie, xxxvi. 204.

Footnote 1773:

  Journal de Chim. Méd. ix. 223.

Footnote 1774:

  Bachner’s Toxicologie, p. 203.

Footnote 1775:

  Henke’s Zeitschrift für die Staatsarzneikunde, xiv. 456.

Footnote 1776:

  Toxicologie Générale, ii. 86.

Footnote 1777:

  Krit, Annalen der Staatsarzn. I. iii. 501.

Footnote 1778:

  Reports of Medical Cases, ii. 203.

Footnote 1779:

  Lond. Med. and Phys. Journal, Feb. 1816.

Footnote 1780:

  Magazin für die Gesammte Heilkunde, xvii. 121.

Footnote 1781:

  Kritische Jahrbücher, ii. 100. When inflammation is found, it is not
  improbably owing to irritants given to produce vomiting, but failing
  to act. This was apparently the cause in a case described by Mr.
  Stanley, Trans. London Coll. of Phys. vi. 414.

Footnote 1782:

  Journ. de Méd. xxxiv. 267.

Footnote 1783:

  The reference to this case has been lost.

Footnote 1784:

  Augustin’s Repertorium, i. 2, 12.

Footnote 1785:

  Medical Jurisprudence, ii. 394.

Footnote 1786:

  Kritische Jahrbücher, ii. 100.

Footnote 1787:

  Praktisches Handbuch für Physiker, iii. 331.

Footnote 1788:

  Corvisart’s Journal de Médecine, xxxiv. 263.

Footnote 1789:

  Magazin für die gesammte Heilkunde, iii. 24.

Footnote 1790:

  Oral evidence at the Trial, also London Journal of Science, N. S. vi.
  56.

Footnote 1791:

  Edinburgh Med. and Surg. Journal, liv. 151.

Footnote 1792:

  Revue Médicale, 1828, ii. 473, 475.

Footnote 1793:

  Sur les Contrepoisons de l’Arsénic, 93.

Footnote 1794:

  Beck’s Medical Jurisprudence, 435.

Footnote 1795:

  Edin. Med. and Surg. Journal, xxiii. 416.

Footnote 1796:

  American Journal of the Med. Sciences, vii. 555.

Footnote 1797:

  London Med. Repository, xviii. 26.

Footnote 1798:

  London Med. and Phys. Journal, xlviii. 225.

Footnote 1799:

  Reports of Medical Cases, ii. 203.

Footnote 1800:

  Diss. Inaug. de Venenis in genere. Argentorati, 1767, quoted by Marx,
  die Lehre von den Giften, I. ii. 237.

Footnote 1801:

  London Med. Gazette, 1839–40, i. 878.

Footnote 1802:

  Edin. Med. and Surg. Journal, xix. 247.

Footnote 1803:

  Ibidem, xvii. 226.

Footnote 1804:

  London Medical Gazette, xiv. 655.

Footnote 1805:

  Lond. Med. Gaz., 1840–41, i. 390.

Footnote 1806:

  London Med. Obs. and Inq., vi. 331.

Footnote 1807:

  North American Med. and Surg. Journal, July 1826.

Footnote 1808:

  London Med. and Chir. Transactions, xx. 86.

Footnote 1809:

  Toxicol. Gén. ii. 110.

Footnote 1810:

  Le Globe, vii. 525. Août, 1829.

Footnote 1811:

  London Medical Gazette, 1840–41, i. 318.

Footnote 1812:

  Annalen der Pharmacie, 1833, vii. 270.

Footnote 1813:

  Edinburgh Medical and Surg. Journal, xxxix. 381.

Footnote 1814:

  Orfila, Médecine-Légale, iii. 374.

Footnote 1815:

  Orfila, Toxicologie Gén. ii. 137.

Footnote 1816:

  Pharmaceutic Journal, 1843–44, 578.

Footnote 1817:

  Orfila, Toxicol. Gén. ii. 137.

Footnote 1818:

  Archives Gén. de Méd. i. 297.

Footnote 1819:

  Corvisart’s Journal de Méd. xxvi. 353.

Footnote 1820:

  On the Poisonous Vegetables of Great Britain, p. 3.

Footnote 1821:

  Foderé, Médecine-Légale, iv. 25.

Footnote 1822:

  Die Wirkung der Arzneimittel und Gifte, iii. 154.

Footnote 1823:

  Acta Curiosorum Naturæ. Also Wibmer, Die Wirkung, &c. 146–154.

Footnote 1824:

  Toxicologia, p. 87.

Footnote 1825:

  Neues Magazin, ii. 3, p. 100.

Footnote 1826:

  Foderé, Médecine-Légale, iv. 23. For another instance of the effects
  of the seeds, not however fatal, see Acta Helvetica, v. 333.

Footnote 1827:

  Edin. Phys. and Lit. Essays, ii. 268.

Footnote 1828:

  Medoro in Edinburgh Med. and Surg. Journal, lv. 265.

Footnote 1829:

  Toxicol. Gén. ii. 184.

Footnote 1830:

  Dr. Schlegel, in Hufeland’s Journal, liv. ii. 29.

Footnote 1831:

  Histoire des Solanum. 1813.

Footnote 1832:

  Annales d’Hyg. Publique et de Méd. Légale, viii. 334.

Footnote 1833:

  Toxicol. Gén. ii. 190.

Footnote 1834:

  Journal de Chimie Médicale, 1840, 142.

Footnote 1835:

  Dunal, &c.

Footnote 1836:

  M. Des-Alleurs in Journ. de Chim. Méd. ii. 30.

Footnote 1837:

  Bulletins de la Soc. Méd. d’Emul.—Mars, 1821.

Footnote 1838:

  Journal de Chimie Médicale, 1837, 130.

Footnote 1839:

  Journal de Pharmacie, xx. 96.

Footnote 1840:

  Revue Médicale, xvii. 265.

Footnote 1841:

  Schubarth in Journal der Praktischen Heilkunde, li. i. 125.

Footnote 1842:

  Fechner’s Repertorium der Organischen Chemie, ii. 70, 75.

Footnote 1843:

  Codex Medicamentarius, 389.

Footnote 1844:

  Archives Gén. de Médecine, xx. 386.

Footnote 1845:

  Archives Gén de Méd. xx. 386.

Footnote 1846:

  Chevallier, Annales d’Hygiène Publique, &c. ix. 337.

Footnote 1847:

  Archives Gén. de Méd. xx. 387.

Footnote 1848:

  Journ. de Chim. Méd. ii. 561.

Footnote 1849:

  Médecine-Légale, iii. 385.

Footnote 1850:

  Journal de Pharmacie, 1837, p. 27.

Footnote 1851:

  Ann. de Chim. et de Phys., xxvii. 200.

Footnote 1852:

  Hufeland’s Journal der Praktischen Heilkunde, lii. i. 92.

Footnote 1853:

  Journal de Chim. Méd. vi. 723.

Footnote 1854:

  Ibidem, 1843, 94.

Footnote 1855:

  Ann. de Chim. et de Phys. vi. 347.

Footnote 1856:

  Lancet, 1836–37, ii. 324.

Footnote 1857:

  Edinburgh Med. and Surg. Journal, li. 339.

Footnote 1858:

  Annales de Chimie, xcii. 59.

Footnote 1859:

  Diss. Inaug. de Venenatis Acidi Borussici in Animalia effectibus.
  Tubingæ, 1805.

Footnote 1860:

  Recherches et Considérations sur l’Acide Hydrocyanique. Paris, 1819.

Footnote 1861:

  Journal Complémentaire, xxviii. 33.

Footnote 1862:

  Bemerkungen über die Wirkungen der Blausaure. Hufeland’s Journal der
  Praktischen Heilkunde, lii. 88.

Footnote 1863:

  Bemerkungen, &c. 85.

Footnote 1864:

  Recherches, &c. p. 136.

Footnote 1865:

  Bemerkungen, &c. 81.

Footnote 1866:

  Ibid. 82.

Footnote 1867:

  Ann. de Chim. et de Phys. vi.

Footnote 1868:

  Recherches, &c. 146.

Footnote 1869:

  Edin. Med. and Surg. Journal, li. 339.

Footnote 1870:

  Bemerkungen, &c. 83.

Footnote 1871:

  Edin. Med. and Surg. Journal, li. 39.

Footnote 1872:

  Krimer detected the acid in the blood of the heart of an animal killed
  in 36 seconds by a few drops put on the tongue. Journ. Complémentaire,
  xxviii. 37.

Footnote 1873:

  Lassaigne, Journ. de Chim. Med. ii.

Footnote 1874:

  Versuche ueber das Nervensystem, 271, quoted by Marx, die Lehre von
  den giften, I. ii. 154.

Footnote 1875:

  Ueber das Amerikanische Pfeilgift. Meckel’s Archiv. für Anat. und
  Physiol. iv. 203.

Footnote 1876:

  Recherches, &c. 221.

Footnote 1877:

  Journal de Physiol. iii. 230.

Footnote 1878:

  Annales d’Hyg. Publique et de Méd. Légale, xi. 240.

Footnote 1879:

  Journal de Chim. Médicale, 1843, 94.

Footnote 1880:

  Horn’s Archiv. 1824, i. 75.

Footnote 1881:

  Edin. Journal of Science, ii. 215.

Footnote 1882:

  Recherches, &c. 221.

Footnote 1883:

  Horn’s Archiv für Medizinische Erfahrung, 1827, i. 73.

Footnote 1884:

  Coullon, 221.

Footnote 1885:

  Revue Médicale, xvii. 271.

Footnote 1886:

  Nicholson’s Journal, xxxi. 191.

Footnote 1887:

  Ueber die giftige Wirkungen der unächten Angustura.— Hufeland’s
  Journal, xl. iii. 68.

Footnote 1888:

  Archives Gén. de Méd. iii. 269.

Footnote 1889:

  Hufeland’s Journal, lii. i. 93.

Footnote 1890:

  Wibmer. Die Wirkung der Arzneimittel und Gifte, iii. 138, from
  Harless, Jahrbuch der Medizin, ix. 1.

Footnote 1891:

  Meckel’s Archiv für Anat. und Physiol. vii. 543, 545.

Footnote 1892:

  Wibmer. Die Wirkung der Arzneimittel, &c. iii. 136.

Footnote 1893:

  Horn’s Archiv für Medizinische Erfahrung, 1830, ii. 858.

Footnote 1894:

  Recherches, &c. 127.

Footnote 1895:

  London Med. and Phys. Journal, xlvi. 359 and 363.

Footnote 1896:

  Journal der Praktischen, Heilkunde, xl. i. 85.

Footnote 1897:

  Archiv für Mediz. Erfahrung, 1813, 510.

Footnote 1898:

  Ann. de Chimie, xcii. 63.

Footnote 1899:

  Revue Médicale, 1825, i. 265.

Footnote 1900:

  Edinburgh Med. and Surg. Journal, li. 51.

Footnote 1901:

  Such as Sobernheim in his Handbuch der Toxicologie, 1838, 455.

Footnote 1902:

  Medinisch-chirurgische Zeitung, 1829. i. 377.

Footnote 1903:

  Annales d’Hyg. Publ. et de Med. Lég. ii. 497.

Footnote 1904:

  Trial of Freeman for the murder of Judith Buswell at Leicester, April
  2, 1829.

Footnote 1905:

  Professor Amos of the London University, in criticizing in his
  Lectures what I have said of this case in the first edition of the
  present work, has accused me of misstating the evidence, and grounds
  the charge on a Report by a professional Reporter, where no notice is
  taken of the phial having been wrapped up in paper, or of the
  bed-clothes having been pulled up to the chin, or of the arms being
  crossed over the trunk [Lond. Med. Gazette, viii. 577]. I have
  nevertheless thought it right to retain my original statement of the
  evidence, as it was derived from what I still consider the best
  authority,—the medical witness, who mentions the special fact on which
  he founded the most important, indeed the only important professional
  opinion in the case, and to which therefore his attention must have
  been more pointedly turned than that of any Law-Reporter. The Report
  alluded to by Professor Amos was afterwards published in the Medical
  Gazette, viii. 759.

Footnote 1906:

  Medizinisch-chirurgische Zeitung, 1829, i. 396.

Footnote 1907:

  Buchner’s Repertorium für Pharmacie, xxi. 313.

Footnote 1908:

  Edinburgh Medical and Surg. Journal, lix. 72.

Footnote 1909:

  Orfila, Annales d’Hyg. Publ. et de Méd. Lég. i. 507.

Footnote 1910:

  Dublin Medical Journal, viii. 308.

Footnote 1911:

  Edinburgh Med. and Surg. Journal, xlviii. 44.

Footnote 1912:

  Coullon, Recherches, &c. p. 200.

Footnote 1913:

  Journ. de Chim. Médicale, vii. 426.

Footnote 1914:

  Handbuch der Toxikologie, 1838, 443.

Footnote 1915:

  Annales d’Hyg. Publique, &c. xi. 240.

Footnote 1916:

  Journal de Chimie Médicale, 1843, 95, 98.

Footnote 1917:

  See Note at p. 365.

Footnote 1918:

  Beiträge zur Geschichte der Blausaure, 1809.

Footnote 1919:

  Journal Complémentaire, xvii. 366.

Footnote 1920:

  Recherches, &c.

Footnote 1921:

  Magazin für die ges. Heilkunde, xiv. 104.

Footnote 1922:

  Magazin für die ges. Heilkunde, xxiii. 375.

Footnote 1923:

  Bemerkungen, &c. Hufeland’s Journal, lii. i. 76.

Footnote 1924:

  Annales d’Hyg. Publ. et de Méd. Lég. iv. 422.

Footnote 1925:

  Rust’s Magazin, xx. 577.

Footnote 1926:

  Manual of Medical Jurisprudence, 251.

Footnote 1927:

  Edinburgh Med. and Surg. Journal, li. 52.

Footnote 1928:

  Archiv für Anatomie und Physiologie, iii. 485, vi. 37.

Footnote 1929:

  Edinburgh Medical and Surgical Journal, li. 53.

Footnote 1930:

  Lancet, 1838–39, i. 880, and ii. 14.

Footnote 1931:

  _Ut supra_, p. 52.

Footnote 1932:

  Journal Complémentaire, xvii. 366.

Footnote 1933:

  London Med. and Phys. Journal, lvii. 151.

Footnote 1934:

  Coullon, Recherches sur l’Acide Hydrocyanique, 225, _et passim_.

Footnote 1935:

  Edin. Philosoph. Journal, vii. 124 and Edin. Journal of Science, ii.
  214.

Footnote 1936:

  Archives Gén. de Méd. xi. 30.

Footnote 1937:

  Toxicologie Gén. ii. 167.

Footnote 1938:

  Archiv für Anatomie und Physiologie, 1828, p. 208.

Footnote 1939:

  Annales d’Hyg. Publ. et de Méd. Lég. i. 511.

Footnote 1940:

  Repertorium für die Pharmacie, xii. 144.

Footnote 1941:

  Dr. Geoghegan, in Lancet, 1835–36, i. 174.

Footnote 1942:

  Repertorium für die Pharmacie, xii. 141.

Footnote 1943:

  Ibidem, xii. 144.

Footnote 1944:

  London Med. and Surg. Journal, iii. 58.

Footnote 1945:

  Annales d’Hyg. Publ. et de Méd. Lég. 525.

Footnote 1946:

  Archiv für Anatomie und Physiologie, 1828, p. 208.

Footnote 1947:

  Annales d’Hyg. Publ. et de Méd. Lég. i. 518.

Footnote 1948:

  Buchner’s Repertorium für die Pharmacie, lxxv. 403.

Footnote 1949:

  Edinburgh Med. and Surg. Journal, xlviii. 44.

Footnote 1950:

  Prize Thesis “On the Presence of Air in the Organs of Circulation.”
  Edinburgh, 1837.

Footnote 1951:

  Edinburgh Medical and Surgical Journal, li. 57.

Footnote 1952:

  Formulaire pour les Nouveaux Médicamens.

Footnote 1953:

  Lancet, 1844, October 5.

Footnote 1954:

  Journal de Pharmacie, vii. 465.

Footnote 1955:

  Buchner’s Repertorium für die Pharmacie, xvi. 100.

Footnote 1956:

  Rust’s Magazin für die gesammte Heilkunde, xxxii. 494.

Footnote 1957:

  Annales de Chim. et de Phys. xliv. 352.

Footnote 1958:

  Murray, Apparatus Medicaminum, iii. 257.

Footnote 1959:

  Buchner’s Repertorium für die Pharmacie, xii. 135.

Footnote 1960:

  Fechner’s Repertorium der Organischen Chemie, ii. 65.

Footnote 1961:

  Rust’s Magazin für die gesammte Heilkunde, xxxii. 500.

Footnote 1962:

  Wepferi, Cicutæ aquaticæ Historia et Noxæ, 244; and Coullon,
  Recherches sur l’Acide Hydrocyanique, 55.

Footnote 1963:

  Toxicol. Gén. ii. 179.

Footnote 1964:

  Philosophical Transactions, 1811, p. 184.

Footnote 1965:

  Journal de Pharmacie, ii. 204.

Footnote 1966:

  Dr. Alison’s Manuscript Lectures.

Footnote 1967:

  Die Wirkung der Arzneimittel und Gifte, i. 166.

Footnote 1968:

  Recherches, &c. 60.

Footnote 1969:

  Apparatus Medicaminum, iii. 257.

Footnote 1970:

  London Med. and Phys. Journal, lvii. 150.

Footnote 1971:

  Philosophical Transactions, 1811, p. 183.

Footnote 1972:

  Journal Complémentaire, &c. xvii. 366.

Footnote 1973:

  Journal de Chimie Médicale, 1840, 92.

Footnote 1974:

  Medical Jurisprudence, ii. 402.

Footnote 1975:

  Journal de Pharmacie, viii. 304.

Footnote 1976:

  Buchner’s Repertorium, xii. 130.

Footnote 1977:

  Rust’s Magazin für die gesammte Heilk. xxxii. 497.

Footnote 1978:

  Bericht über einige Versuche über die Wirkung des Oleum Essentiale
  Laurocerasi.—Hufeland’s Journal der Praktischen Heilkunde, liv. iii.
  27.

Footnote 1979:

  Bemerkungen, &c. Journal der Praktischen Heilkunde, li. i. 125.

Footnote 1980:

  Fechner’s Repertorium der Org. Chemie, ii. 65.

Footnote 1981:

  Médecine Légale, iv. 27.

Footnote 1982:

  Apparatus Medicaminum, iii. 216.

Footnote 1983:

  Recherches, &c. p. 95.

Footnote 1984:

  Philosophical Transactions, 1739, No. 452.

Footnote 1985:

  Wibmer, die Wirkung der Arzneimittel und Gifte, ii. 90.

Footnote 1986:

  Considerations on the criminal proceedings of this country, on the
  danger of convictions on circumstantial evidence, and on the case of
  Mr. Donnellan. By a Barrister of the Inner Temple, 1781.—Phillips’s
  Treatise on the Law of Evidence, Appendix, p. 30.—Male’s Juridical
  Medicine, p. 86.—These authorities all consider the guilt of the
  prisoner doubtful.

Footnote 1987:

  Trial, &c. taken in short hand by Gurney.

Footnote 1988:

  Buchner’s Repertorium für die Pharmacie, xxviii. 416.

Footnote 1989:

  Geiseler in Repertorium für die Pharmacie, lxix. 291.

Footnote 1990:

  Recherches, &c. p. 74.

Footnote 1991:

  Journal de Chimie Médicale, 1837, 99.

Footnote 1992:

  Repertorium für die Pharmacie, lxxv. 220.

Footnote 1993:

  Bremer, Bemerkungen und Erfahrungen über die Wirksamkeit des
  Trauben-Kirschbaums.—Archiv für Medizinische Erfahrung, 1812, i. 41.

Footnote 1994:

  Buchner’s, Repertorium, xii. 130.

Footnote 1995:

  Rust’s Magazin, xxxii. 500.

Footnote 1996:

  Bemerkungen, &c. Horn’s Archiv, 1812, i. 71.

Footnote 1997:

  Journal de Pharmacie, iii. 275.

Footnote 1998:

  Buchner’s Repertorium für die Pharmacie, xxvii. 238.

Footnote 1999:

  Buchner’s Repertorium für die Pharmacie, lxix. 293.

Footnote 2000:

  Annales de Chim. et de Phys. xxxv. 72.

Footnote 2001:

  Toxikologie, 373.

Footnote 2002:

  Ueber den Selbstmord, p. 176.

Footnote 2003:

  Quæstionum Medico-legalium, T. iii. 63. Consilium 44.

Footnote 2004:

  London Courier, Jan. 16, 1823.

Footnote 2005:

  Buchner’s Toxikologie, 331.

Footnote 2006:

  Nysten, Recherches Chimico-Physiologiques, p. 11.

Footnote 2007:

  On the Presence of Air in the Organs of Circulation. Prize Thesis at
  Edinburgh, 1837.

Footnote 2008:

  Nysten, Recherches Chimico-Physiologiques, _passim_.

Footnote 2009:

  Ibidem, p. 81.

Footnote 2010:

  Rech. Chemico-Physiologiques, p. 114.

Footnote 2011:

  Diss. Inaug. utrum, per viventium adhuc animalium membranas materiæ
  ponderabiles permeare queant. Tubingæ, p. 10.

Footnote 2012:

  Nysten, Recherches, &c. p. 137.

Footnote 2013:

  Philosophical Transactions, cxiii. 508.

Footnote 2014:

  Nysten, Recherches, &c. p. 140.

Footnote 2015:

  Corvisart’s Journal de Méd. xxiv. 249.

Footnote 2016:

  Allen and Peys, also Wetterstedt. See Dr. Apjohn’s article on
  Toxicology in Cycl. of Pract. Med. iv. 238.

Footnote 2017:

  London Quarterly Journal of Science, vi. N. S.

Footnote 2018:

  Corvisart’s Journal de Méd. xxiv. 246.

Footnote 2019:

  Researches, Chemical and Philosophical, concerning nitrous oxide gas,
  p. 475.

Footnote 2020:

  Desgranges in Corvisart’s Journal de Méd. viii. 487.

Footnote 2021:

  Bulletins de la Soc. Méd. d’Emulation, Oct. 1823.

Footnote 2022:

  Zeitschrift für die Staatsarzneikunde, xvii. 383.

Footnote 2023:

  Wibmer. Die Wirkung der Arzneimittel und Gifte, ii. 109, from Archiv
  des Apothekers-Vereins, xviii. 101.

Footnote 2024:

  Hallé, Recherches sur la nature du Méphitisme des fosses d’aisance, p.
  107.

Footnote 2025:

  Edin. Med and Surg. Journal, xxviii. 361.

Footnote 2026:

  London Medical Gazette, x. 314.

Footnote 2027:

  Ibidem, 352.

Footnote 2028:

  Dictionnaire des Sciences Médicales, ii. 391.

Footnote 2029:

  Sedillot’s Journal de Médecine, xv. 28, 34.

Footnote 2030:

  Annales d’Hygiène Publique, 1829, ii. 83, 143.

Footnote 2031:

  Edin. Med. and Surg. Journal, xxviii. 361.

Footnote 2032:

  Recherches sur la nature du Méphitisme des fosses d’aisance, 1785.

Footnote 2033:

  Recherches, &c. p. 55.

Footnote 2034:

  Recherches, &c. pp. 57, 99, 144; and Nouv. Journ. de Méd. i. 237.

Footnote 2035:

  Nouv. Journal, &c.

Footnote 2036:

  Ibidem.

Footnote 2037:

  Sedillot’s Journ. de Méd. xv. 25.

Footnote 2038:

  Recherches, &c. p. 57.

Footnote 2039:

  Hallé, Recherches, &c. p. 50.

Footnote 2040:

  Annales d’Hygiène Publique, 1840, xxiii. 131.

Footnote 2041:

  Manual of Medical Jurisprudence, 1844, p. 559.

Footnote 2042:

  Hallé, Recherches, &c. pp. 46, 58.

Footnote 2043:

  London Medical Gazette, pp. 375, 410, 448.

Footnote 2044:

  Researches on Nitrous Oxide Gas, p. 467.

Footnote 2045:

  Annales d’Hyg. Publ. et de Méd. Lég. iii. 457.

Footnote 2046:

  Mr. Pridgin’s Teale in Guy’s Hospital Reports, 1839, iv. 106.

Footnote 2047:

  Annales d’Hygiène Publique, 1842, xxvii. 232.

Footnote 2048:

  M. Collard de Martigny in Arch. Gén. de Méd. xiv. 209.

Footnote 2049:

  Journal der Praktischen Heilkunde, 1831, iv. 119.

Footnote 2050:

  Collard de Martigny, 204.

Footnote 2051:

  Dr. Bird in Guy’s Hospital Reports, 1839, iv. 81.

Footnote 2052:

  Nouv. Biblioth. Méd. 1827, iii. 91.

Footnote 2053:

  Archives Gén. de Med. v. 132.

Footnote 2054:

  Foderé, Méd. Légale, iv. 37.

Footnote 2055:

  Archives, &c. p. 211.

Footnote 2056:

  Recherches on Nitrous Oxide, p. 472.

Footnote 2057:

  Nouv. Journal de Méd. ii. 196.

Footnote 2058:

  Archives Gén. de Médecine, xiv. 205.

Footnote 2059:

  Manual of Medical Jurisprudence, 1844, 555.

Footnote 2060:

  Histoire de la Soc. Roy. de Med. i. 353.

Footnote 2061:

  Nouv. Biblioth. Méd. 1827, iii. 91.

Footnote 2062:

  Collard de Martigny, Arch. Gén. de Méd. xiv. 205.

Footnote 2063:

  Orfila, Toxicol. Gén. ii. 475. Note.

Footnote 2064:

  Lancet, 1838–39, i. 260.

Footnote 2065:

  Lond. Med. Gazette, 1838–39, i. 427.

Footnote 2066:

  Dr. G. Bird in Guy’s Hospital Reports, 1839, iv. 84.

Footnote 2067:

  London Med. Chir. Transactions, i. 83.

Footnote 2068:

  Nouv. Journ. de Méd.

Footnote 2069:

  Nouv. Biblioth. Med. 1827, iii. 91.

Footnote 2070:

  Archives Gén. de Méd. xiv. 210.

Footnote 2071:

  Fallot, in Journal Complémentaire, Mai, 1829.

Footnote 2072:

  Annales d’Hygiène Publique, 1840, xxiii. 176.

Footnote 2073:

  Ibidem, xvi. 30.

Footnote 2074:

  Manual of Medical Jurisprudence, 1844, p. 557.

Footnote 2075:

  Annales, _ut supra_, 186.

Footnote 2076:

  Toxicologie Gén. 1826, ii. 474.

Footnote 2077:

  Annales d’Hygiène Publique, xxix. 53.

Footnote 2078:

  Annales, _ut supra_, p. 191.

Footnote 2079:

  Annalen der Pharmacie, 1836, xx. 156.

Footnote 2080:

  Lancet, _ut supra_.

Footnote 2081:

  Annales, &c. _ut supra_, p. 197.

Footnote 2082:

  Annales, &c. xx. 134.

Footnote 2083:

  Lancet, _ut supra_.

Footnote 2084:

  Annales, _ut supra_, 197.

Footnote 2085:

  Ibidem, p. 199.

Footnote 2086:

  Ibidem, xx. 132.

Footnote 2087:

  Devergie, _ut supra_, 200.

Footnote 2088:

  On the Constitution of Flame—Edin. New Philos. Journal, i. 224, 226.

Footnote 2089:

  Ammann.—Medicina Critica, Cas. 59, p. 365.

Footnote 2090:

  Edin. Med. and Surg. Journal, xxviii. 359.

Footnote 2091:

  Edinburgh Med. and Surg. Journal, xiii. 353.

Footnote 2092:

  Ibidem, xxxii. 345.

Footnote 2093:

  Edin. New Phil. Journal, v. 110.

Footnote 2094:

  Holwell, Narrative of the deplorable Deaths of the English gentlemen
  and others who were suffocated in the Black Hole at Fort William.

Footnote 2095:

  Smith’s Principles of Forensic Medicine, 221.

Footnote 2096:

  Instruction sur le traitement des Asphyxiés, 25.

Footnote 2097:

  Reports of Medical Cases, ii. 226, 227.

Footnote 2098:

  Horn’s Archiv für Medizinische Erfahrung, 1823, i. 93.

Footnote 2099:

  London Medical Gazette, 1838–39, i. 923.

Footnote 2100:

  Aufsätze und Beobachtungen, i. 1. and vii. 95.

Footnote 2101:

  See various cases quoted in detail in Wibmer, die Wirkung der
  Arzneimittel, &c. ii. 49, 51, 55.

Footnote 2102:

  Practisches Handbuch für Physiker, iii. 278.

Footnote 2103:

  Beiträge zur gerichtl. medizin.—Horn’s Archiv für Medizinische
  Erfahrung, 1823, i. 296.

Footnote 2104:

  Journal Complémentaire, Mai, 1829.

Footnote 2105:

  Guy’s Hospital Reports, _ut supra_.

Footnote 2106:

  Annales d’Hygiène Publique, xx. 114.

Footnote 2107:

  Revue Médicale, 1827, iii. 528.

Footnote 2108:

  Horn’s Archiv. für Medizinische Erfahrung, 1834, 746.

Footnote 2109:

  Bird, _ut supra_, iv. 93.

Footnote 2110:

  Wibmer, die Wirkung der Arzneimittel, &c. ii. 47, _et seq._

Footnote 2111:

  Nouvelle Bibliothèque Méd. 1829, i. 374.

Footnote 2112:

  René-Bourgeois, Archives Gén. de Méd. xx. 508.

Footnote 2113:

  Nysten, Recherches Chimico-Physiologiques, pp. 88, 92, 96.

Footnote 2114:

  Annales d’Hygiène Publique, xxix. 54.

Footnote 2115:

  Mr. Witter in London Philosophical Journal, 1814, xliii. 367.

Footnote 2116:

  Guérard in Annales d’Hygiène Publique, xxix. 52.

Footnote 2117:

  Nysten, Recherches, &c.

Footnote 2118:

  Davy’s Chemical and Philosophical Researches, _passim_.

Footnote 2119:

  Thenard, Traité de Chimie, iii. 675.

Footnote 2120:

  Researches, &c., p. 462.

Footnote 2121:

  Edin. Med. and Surg. Journal, xxviii. 363.

Footnote 2122:

  Journal Universel des Sc. Méd. ii. 240.

Footnote 2123:

  Archiv für Medizinische Erfahrung, 1830, ii. 859.

Footnote 2124:

  Toxikologie, 382.

Footnote 2125:

  Edin. Med. and Surg. Journal, xxviii. 363.

Footnote 2126:

  London Quarterly Journal of Science, January, 1830.

Footnote 2127:

  Buchner’s Toxikologie, 188.

Footnote 2128:

  Wibmer, Die Wirkung der Arzneimittel, &c. i. 360, 362.

Footnote 2129:

  Annalen der Pharmacie, i. 68.

Footnote 2130:

  Ibidem, 1833, or Journal de Pharmacie, xx. 87.

Footnote 2131:

  Buchner’s Repertorium für die Pharmacie, ix. 71 and 77.

Footnote 2132:

  Orfila, Toxicol. Gén. ii. 261.

Footnote 2133:

  Annalen der Pharmacie, i. 71.

Footnote 2134:

  Sedillot’s Journ. Gén. de Méd. Dec. 1813, 364.

Footnote 2135:

  Lond. Med. Obs. and Inquiries, vi. 223.

Footnote 2136:

  Journ. Universel, xxii. 239.

Footnote 2137:

  Journal de Chimie Médicale, 1837, p. 591.

Footnote 2138:

  Ibid. 1839, 122.

Footnote 2139:

  Sedillot’s Journ. de Méd. xxiv. 228.

Footnote 2140:

  Edin. Med. and Surg. Journal, ix. 380.

Footnote 2141:

  Journ. de Chim. Méd. ii. 586.

Footnote 2142:

  Sedillot’s Journal de Médecine, xxiv. 228.

Footnote 2143:

  London Medical Gazette, 1838–39, i. 681.

Footnote 2144:

  British Herbal, 329.

Footnote 2145:

  Journ. Universel, xxii. 239.—Edin. Med. and Surg. Journal, xxix. 452.

Footnote 2146:

  Plenck’s Toxicologia, 109.

Footnote 2147:

  Roux’s Journal de Med. xxiv. 310.

Footnote 2148:

  Toxicologia, 109.

Footnote 2149:

  Moyens de remédier aux Pois Végét.

Footnote 2150:

  Journ. de Chim. Méd. iii. 586.

Footnote 2151:

  Magazin für die gesammte Heilkunde, xxi. 550.

Footnote 2152:

  Toxikologie, p. 220.

Footnote 2153:

  On Vegetable Poisons, 17.

Footnote 2154:

  Nouvelle Biblioth. Méd. 1828, iii.

Footnote 2155:

  On Vegetable Poisons, p. 18.

Footnote 2156:

  Roux’s Journal de Méd. xxiv. 321.

Footnote 2157:

  Geschichte der Pflanzengifte, p. 538.

Footnote 2158:

  Die Wirkung der Arzneimittel und Gifte, i. 347–364.

Footnote 2159:

  Mag. für die gesammte Heilk. xxv. 578.

Footnote 2160:

  Journal de Chim. Méd. iv. 390.

Footnote 2161:

  Geschichte der Pflanzengifte, p. 538.

Footnote 2162:

  Histoire de l’Acad. de Paris, 1703, p. 69.

Footnote 2163:

  On Vegetable Poisons, p. 21

Footnote 2164:

  Med. Obs. and Inq. vi. 224.

Footnote 2165:

  Roux’s Journ. de Méd. xxiv. 317.

Footnote 2166:

  Geschichte des Pflanzengifte, 527.

Footnote 2167:

  Die Wirkung der Arzneimittel, &c. i. 378.

Footnote 2168:

  Gmelin, Geschichte der Pflanzengifte, 416. As examples of such crimes
  he mentions the following. Diebe und Huren um ihr Verbrechen desto
  ungehinderter zu begehen, wenn sie die Leute damit eingeschläfert
  haben; Hurenwirthinnen, um in ihren gemietheten Mägdchen alles Gefühl
  der natürlichen Schaam zu ersticken; alte Hurer um junge Mägdchen zu
  verführen; Missethäter um ihre Wächter sinnlos zu machen;
  Ehebrecherinnen, um ihre Männer zu ruhigen Zuschauern ihrer
  Schandthaten zu machen. For most of these purposes gin and whisky are
  the instruments of villany in Britain; and of late, as already
  mentioned, opium has been resorted to.

Footnote 2169:

  Journal de Chimie Médicale, 1836, 319.

Footnote 2170:

  History of the Eastern Archipelago, i. 466.

Footnote 2171:

  Schweigger’s Journal, xxvi. 98.

Footnote 2172:

  Annalen der Pharmacie, iii. 135.

Footnote 2173:

  Journal de Pharmacie, xx. 94.

Footnote 2174:

  Orfila, Tox. ii. 271.

Footnote 2175:

  Edin. Medical Commentaries, v. 163.

Footnote 2176:

  Braun in Henke’s Zeitschrift für die Staatsarzneikunde, xxix. 177.

Footnote 2177:

  Orfila, Toxicol. Gén. ii. 247.

Footnote 2178:

  Edin. Phys. and Lit. Essays, ii. 272.

Footnote 2179:

  Corvisart’s Journ. de Méd. xxiii. 157.

Footnote 2180:

  Edin. Med. and Surg. Journal, xv. 154.

Footnote 2181:

  Gmelin, Gesch. der Pflanzengifte, 421.

Footnote 2182:

  Magazin für die gesammte Heilkunde, xvii. 564.

Footnote 2183:

  Gmelin, 420.

Footnote 2184:

  Edin. Med. and Surg. Journal, xv. 154.

Footnote 2185:

  London Medical Gazette, iv. 320.

Footnote 2186:

  Henke’s Zeitschrift für die Staatsarzneikunde, xxxiii. 129.

Footnote 2187:

  Journal de Chim. Méd. vi. 722.

Footnote 2188:

  Hist. Stirp. Helvet. Indig. i. 259.

Footnote 2189:

  Vauquelin—Annales de Chimie, lxxi. 139.

Footnote 2190:

  Bulletin des Scien. Méd. xii. 177, from Geiger’s Magazin für
  Pharmacie, Nov. und Dec. 1828.

Footnote 2191:

  Edinburgh Med. and Surg. Journal, xxxix. 382.

Footnote 2192:

  Edinburgh Med. and Surg. Journal, li. 340.

Footnote 2193:

  Ibidem.

Footnote 2194:

  Philosophical Transactions, ci. 186, 181.

Footnote 2195:

  Macartney.—Orfila, Toxicol. Gén. ii. 282.

Footnote 2196:

  Blake, in Edin. Med. and Surg. Journal, liii. 44.

Footnote 2197:

  Edin. Med. and Surg. Journal, xii. 11.

Footnote 2198:

  Pflanzengifte, 550.

Footnote 2199:

  Ephem. Cur. Nat. Dec. ii.—Ann. x. p. 222.

Footnote 2200:

  On Apoplexy and Lethargy, p. 150.

Footnote 2201:

  Ephem. Cur. Nat. Dec. ii.—Ann. iv. p. 467.

Footnote 2202:

  London Medical Gazette, 1839–40, i. 561.

Footnote 2203:

  Journal de Chimie Médicale, 1839, 329.

Footnote 2204:

  Ibidem, 165.

Footnote 2205:

  Hufeland’s Journal der Praktischen Heilkunde, lxxi. iv. 100.

Footnote 2206:

  Journal de Chimie Médicale, iii. 23.

Footnote 2207:

  Gazette Med. de Paris, 28 Novembre, 1840, or Edinburgh Med. and Surg.
  Journal, lv. 558.

Footnote 2208:

  Edin. Med. and Surg. Journal, ix. 159.

Footnote 2209:

  Acta Helvetica, 1762, v. 330.

Footnote 2210:

  Journal de Chim. Médicale, 1839, 328.

Footnote 2211:

  Ibidem, 327.

Footnote 2212:

  Julia-Fontenelle, Ibidem, 1836, 652. From Mémoires du Duc de St.
  Simon.

Footnote 2213:

  Paris and Fonblanque’s Medical Jurisprudence, ii. 415.

Footnote 2214:

  Rammazini, de Morb. Opificum, 535.—Fourcroy. Essai sur les Mal. des
  Artizans, 89.—Patissier, Traité des Mal. des Art. 202.

Footnote 2215:

  Revue Médicale, 1827, iii. 168.

Footnote 2216:

  Annales d’Hygiène Publique et de Med. Lég. i. 169. 1829.

Footnote 2217:

  Gmelin’s Pflanzengifte, S. 598.

Footnote 2218:

  Philosophical Magazine, N. S. iv. 231.

Footnote 2219:

  Geiger’s Magazin für Pharmacie, xxxv. 72, 259.

Footnote 2220:

  Edin. Medical and Surgical Journal, xxxix. 383.

Footnote 2221:

  Geiger, in Magazin für Pharmacie, xxxv. 284.

Footnote 2222:

  Edinburgh Roy. Soc. Transactions, xiii. 398, 415.

Footnote 2223:

  Toxicologie Gén. ii. 303.

Footnote 2224:

  Pflanzengifte, S. 605.

Footnote 2225:

  Transactions of the Royal Soc. of Edinburgh, xiii. 383.

Footnote 2226:

  Transactions, &c. xiii. 393, 315.

Footnote 2227:

  Corvisart’s Journal de Méd. xxix. 107.

Footnote 2228:

  Philos. Transactions, xliii. No. 473, p. 18.

Footnote 2229:

  Toxicol. Gén. ii. 311.

Footnote 2230:

  Gmelin’s Pflanzengifte, p. 604.

Footnote 2231:

  Die Wirkung der Arzneimittel und Gifte, i. 172.

Footnote 2232:

  Gmelin’s Pflanzengifte, p. 603.

Footnote 2233:

  Cicut. Aquaticæ Hist. et Noxæ, 134.

Footnote 2234:

  Annalen der Pharmacie, xxxi. 258.

Footnote 2235:

  Archiv für Medizin. Erfahr. 1824, i. 84.

Footnote 2236:

  Cic. Aquat. &c. 80, and 107.

Footnote 2237:

  Journal de Chimie Médicale, 1842, 877.

Footnote 2238:

  Article Ciguë, Diction. des Sciences Méd.

Footnote 2239:

  Journal Complémentaire, xvii. 361.

Footnote 2240:

  Journal de Chimie Médicale, 1830.

Footnote 2241:

  Instead of quoting special facts on the subject of poisoning with
  Œnanthe, I have thought it better to give in the meantime a short
  analysis of a long investigation, which I have from time to time made
  on the subject, and which was read in the Royal Society of Edinburgh
  last year. This paper will be published ere long; and the references
  and experiments will then be supplied, which, if introduced here, will
  lead to disproportionate details.

Footnote 2242:

  Lond. Philos. Magazine, N. S. ii. 392.

Footnote 2243:

  Toxicol. Gén. ii. 323.

Footnote 2244:

  London Med. and Phys. Journal, xiv. 425.

Footnote 2245:

  Geschichte der Pflanzengifte, 571.

Footnote 2246:

  Wittke in Magazin für Pharmacie, xxxii. 228.

Footnote 2247:

  Prize Thesis, on the Physiological and Medicinal Properties of the
  Aconitum napellus. Edinburgh, 1844.

Footnote 2248:

  Toxicologie Gén. 1827, ii. 211.

Footnote 2249:

  Philosophical Transactions, 1811, p. 183.

Footnote 2250:

  Toxicologie Gén. 1827, ii. 211, and 1843, ii. 361.

Footnote 2251:

  Elements of Materia Medica, 1842, ii. 1804.

Footnote 2252:

  Elements of Materia Medica, 1842, ii. 1811.

Footnote 2253:

  Elements of Materia Medica, 1842, ii. 1806.

Footnote 2254:

  Thèse Inaugurale, Paris, 1822, quoted by Orfila, Toxic. Gén., 1827,
  ii. 221.

Footnote 2255:

  Journal de Chimie Médicale, iii. 344.

Footnote 2256:

  Elements of Materia Medica, ii. p. 1807.

Footnote 2257:

  Ibidem, p. 1806.

Footnote 2258:

  Lancet, 1836–37, ii. 13.

Footnote 2259:

  Annali Universali di Medicina, 1840, iii. 635.

Footnote 2260:

  Buchner’s Repertorium für die Pharmacie, lxviii. 199.

Footnote 2261:

  Journal de Chimie Medicale, 1840, 94.

Footnote 2262:

  Edinburgh Journal of Natural Science, 1830, 235.

Footnote 2263:

  Dr. Hunter. Calcutta Med. Phys. Transactions, ii. 410.

Footnote 2264:

  Northern Journal of Medicine, 1844, i. 120.

Footnote 2265:

  Journal de Pharmacie, vii. 503.

Footnote 2266:

  Orfila, Tox. Gén. ii. 225.

Footnote 2267:

  Schabel, Diss. Inaug. be Effectibus Veratri albi et Hellebori nigri,
  p. 8, Tubing.

Footnote 2268:

  Bullet. de la Soc. Méd. d’Em. Avril, 1818.

Footnote 2269:

  De Sedibus et Causis Morborum, Epist. lix. 15.

Footnote 2270:

  Wibmer, die Wirkung der Arzneimittel und Gifte, iii. 10.

Footnote 2271:

  Buchner’s Toxicologie, 272.

Footnote 2272:

  Toxicol. Gén. ii. 202.

Footnote 2273:

  Tentamen Physico-medicum de Remediis Brunsvicensibus, 176.

Footnote 2274:

  Journal de Chimie Médicale, 1842, p. 651.

Footnote 2275:

  Vogel—Journal de Physique, lxxv. 194.

Footnote 2276:

  De Effectibus Ver. alb. et Hell. nigri. Tubingæ, 1817.

Footnote 2277:

  Mag. für die gesammte Heilkunde, xiv. 547.

Footnote 2278:

  Archiv für Mediz. Erfahrung, 1825.

Footnote 2279:

  Beiträge zur Gerichtl. Arzneik. iv. 47.

Footnote 2280:

  Die Wirkung der Arzneimittel und Gifte, v. 437.

Footnote 2281:

  Diss. Inaug. De Veratriæ Ellectibus, Lipsiæ, 1836, quoted by Wibmer,
  v. 434.

Footnote 2282:

  Libellus de Colchico, 1763, p. 17.

Footnote 2283:

  Philosophical Transactions, 1816.

Footnote 2284:

  Annalen der Pharmacie, vii. 275.

Footnote 2285:

  Edin. Med. and Surgical Journal, xiv. 262.

Footnote 2286:

  Journal de Chimie Médicale, viii. 351.

Footnote 2287:

  Repertorium für die Pharmacie, lxxi. 131.

Footnote 2288:

  Annales d’Hygiène Publique, xvi. 394.

Footnote 2289:

  Ibid. xii. 397.

Footnote 2290:

  Journal de Chimie Médicale, 1839, 589.

Footnote 2291:

  London Medical Gazette, 1838–39, ii. 763.

Footnote 2292:

  Beiträge, &c. iv. 246.

Footnote 2293:

  London Medical Gazette, x. 160.

Footnote 2294:

  Repertorium für die Pharmacie, lxix. 382.

Footnote 2295:

  Ibidem, 377.

Footnote 2296:

  Magazin für Pharmacie, xxx. 237.

Footnote 2297:

  Dr. Duncan’s Dispensatory, 953.

Footnote 2298:

  Spillan, quoted by Lewins.

Footnote 2299:

  Edinburgh Medical and Surg. Journal, lvi. 186.

Footnote 2300:

  Toxicologie Gén. 1827, ii. 257.

Footnote 2301:

  Toxikologie, 349.

Footnote 2302:

  Repertorium für die Pharmacie, lxix. 384.

Footnote 2303:

  Bibliothèque Universelle de Génève, xxvi. 102.

Footnote 2304:

  Duncan’s Supplement to the Dispensatory, p. 49.

Footnote 2305:

  Elements of Materia Medica, 1842, p. 1208.

Footnote 2306:

  Dr. Morries, Edin. Med. and Surg. Journal, xxxix. 377.

Footnote 2307:

  Toxicologie Gén. ii. 286.

Footnote 2308:

  Edinburgh Med. and Surg. Journal, li. 342.

Footnote 2309:

  Wibmer, Die Wirkung, &c. ii. 312, from Schroek, de Digit. Purpurea,
  1829.

Footnote 2310:

  London Med. Gazette, 1842–43, i. 270, from Schmidt’s Jahrbücher, Aug.
  1842.

Footnote 2311:

  Dictionary of Mat. Med. and Pharmacy, 1839, 219.

Footnote 2312:

  Blackall on Dropsy, p. 173.

Footnote 2313:

  Edin. Med. and Surg. Journ. vii. 149.

Footnote 2314:

  Bidault de Villiers, Journal de Médecine, Novembre, 1817.

Footnote 2315:

  Edin. Med. and Surg. Journ. xxvii. 223, from Morning Chronicle, Oct.
  30 and 31, 1826.

Footnote 2316:

  Journal de Méd. xl. 193.

Footnote 2317:

  Williams in Medical Gazette, i. 744.

Footnote 2318:

  Toxicologie Gén. 1843, ii. 442.

Footnote 2319:

  Annales d’Hygiène Publique, 1838, xx. 180.

Footnote 2320:

  Recherches Chim. et Physiol. sur l’Ipecacuanha. Journal de Pharmacie,
  iii. 145.

Footnote 2321:

  Rust’s Magazin für die gesammte Heilkunde, xxxii. 182.

Footnote 2322:

  Magendie. Formulaire pour la Préparation, &c. de plusieurs Nouv.
  Médicamens. 5eme ed. 67.

Footnote 2323:

  Plantes Usuelles des Braziliens, Livraison, i. 3.

Footnote 2324:

  Ann. de Chim. et de Phys. x. 142.

Footnote 2325:

  Journal de Pharmacie, viii. 401.

Footnote 2326:

  Ann. de Chim. et de Phys. x. 153.

Footnote 2327:

  Pelletier and Caventou, Ibidem, xxvi. 56.

Footnote 2328:

  Annales de Chim. et de Phys. xxvi. 44.

Footnote 2329:

  Archives Gén. de Méd. xii. 463.

Footnote 2330:

  Edinburgh Medical and Surgical Journal, li. 338.

Footnote 2331:

  Transactions of Provinc. Med. and Surg. Association, ii. 215.

Footnote 2332:

  Journal de Chimie Médicale, 1837, 481.

Footnote 2333:

  Elements of Materia Medica, ii. 1310.

Footnote 2334:

  Buchner’s Repertorium für die Pharmacie.

Footnote 2335:

  Archives Gén. de Méd. viii. 22.

Footnote 2336:

  British Annals de Medecine, i. 106.

Footnote 2337:

  Magazin für die gesammte Heilkunde, xvii. 119.

Footnote 2338:

  Cicutæ Aquat. Hist. Noxæ, p. 295.

Footnote 2339:

  Magendie, Journal de Physiol. ii. 361.

Footnote 2340:

  Cicutæ Aquat. Hist. et Noxæ, p. 198.

Footnote 2341:

  Archives Gén. de Médecine, xlvi. 365.

Footnote 2342:

  Lond. Med. Repository, xix. 448.

Footnote 2343:

  Glasgow Medical Journal. August, 1830.

Footnote 2344:

  British Annals of Medicine, i. 103.

Footnote 2345:

  Archives Gén. de Méd. viii. 17.

Footnote 2346:

  Nouv. Journ. de Méd. x. 157.

Footnote 2347:

  Tacheron, London Med. Repository, xix. 456.

Footnote 2348:

  Med. Rat. System, ii. 175.

Footnote 2349:

  Journ. der Practischen Heilkunde, iv. 492.

Footnote 2350:

  Hillefeld, Exp. quædam circa venena. Gott. 1760. Quoted by Marx, die
  Lehre von den Giften, i. ii. 26.

Footnote 2351:

  Rossi, Exp. de nonnullis plantis quæ pro venenatis habentur. Pisis,
  1762. See Marx, i. ii. 29.

Footnote 2352:

  Trans. of the Calcutta Med. and Phys. Soc. i. 138.

Footnote 2353:

  Arch Gén. de Méd. viii. 18.

Footnote 2354:

  I have not altered the statement as to this point in the former
  editions. Yet I strongly suspect that authors, who describe the spasm
  which precedes death to continue as it were into the rigidity which
  occurs after death, must have observed inaccurately. For in the
  numerous experiments I have made and witnessed in animals, flaccidity
  invariably took place at the time of death, and continued for a
  moderate interval.

Footnote 2355:

  Repertorium für die Pharmacie, lxv. 80.

Footnote 2356:

  Le Globe, vii. 525.—Août 19, 1829.

Footnote 2357:

  Henke’s Zeitschrift für die Staatsarzneikunde, ii. 169.

Footnote 2358:

  Ann. de Chim. et de Phys. xxvi. 44.

Footnote 2359:

  Orfila, Toxicol. Gén. ii. 364.

Footnote 2360:

  Journal de Chim. Méd. vi. 593.

Footnote 2361:

  Botanic Garden, ii. 256.

Footnote 2362:

  See my Dispensatory, p. 395. Orfila adheres to the old error in the
  last edition of his Toxicology, in 1843.

Footnote 2363:

  Magendie, Journ. de Physiologie, iii. 267.

Footnote 2364:

  Toxicol. Gén. ii. 377.

Footnote 2365:

  Ueber die giftige Wirkungen der unächten Angustura.—Hufeland’s
  Journal, xl. iii. 68.

Footnote 2366:

  Journal de Pharmacie, ii. 507.

Footnote 2367:

  Meckel’s Archiv für Anatomie und Physiologie, i. 1.

Footnote 2368:

  Ueber das Amerikanische Pfeilgift. Meckel’s Archiv für Anatomie und
  Physiologie, iv. 65.

Footnote 2369:

  Reported by Dr. Reid Clanny in Lancet, 1838–39, ii. 285.

Footnote 2370:

  Toxicol. Gén. ii. 400.

Footnote 2371:

  Annali Univ. di Med. xxxvi. 102.

Footnote 2372:

  Diss. Inaug. Tubingæ, 1819, p. 9.

Footnote 2373:

  Experimental Essays, 128.

Footnote 2374:

  Orfila, Toxic. Gén. ii. 406.

Footnote 2375:

  Ibid., 407.

Footnote 2376:

  London Med. Gazette, xi. 772. From American Journal of Med. Science.

Footnote 2377:

  Rust’s Magazin für die gesammte Heilkunde, xxv. 88.

Footnote 2378:

  Toxicol. Gén. ii. 400.

Footnote 2379:

  Annali, &c. xxxvi. 106.

Footnote 2380:

  Ann. de Chimie, lxxx. 109.

Footnote 2381:

  Buchner’s Repertorium für die Pharmacie, xxiv. 55.

Footnote 2382:

  Orfila, Toxicol. Gén. ii. 411.

Footnote 2383:

  Cicut. Aquat. Hist. p. 186.

Footnote 2384:

  Toxicol. Gén. ii. 412, 414.

Footnote 2385:

  Ibidem, ii. 410.

Footnote 2386:

  Annales d’Hygiène Publique, xxix. 346.

Footnote 2387:

  Beiträge zur Gerichtl. Arzneikunde, iii. 241.

Footnote 2388:

  Mulder in Pharmaceutisches Central-Blatt, 1838, p. 511.

Footnote 2389:

  Orfila Toxicol. Gén. ii. 396.

Footnote 2390:

  Philos. Trans. 1811.

Footnote 2391:

  Diss. Inaug. sistens historiam Veneni Upas antiar, &c. Tubingæ, 1815.

Footnote 2392:

  Diss. Inaug. de Veneno Upas antiar, Tubingæ, 1815, p. 27.

Footnote 2393:

  Buchner’s Repertorium, xxxi., and Hufeland’s Journal, lxviii. iv. 43.

Footnote 2394:

  Mém. de l’Acad. des Sciences, 1739, p. 47.

Footnote 2395:

  Journal de Chim. Méd. iv. 528.

Footnote 2396:

  London Medical and Physical Journal, April, 1829.

Footnote 2397:

  Mémoires de la Soc. de Phys. et d’Hist. Nat. de Génève, v. 194.

Footnote 2398:

  Lancet, 1836–37, i. 394.

Footnote 2399:

  Ibid.

Footnote 2400:

  Rust’s Magazin für die gesammte Heilkunde, xxiii. 374.

Footnote 2401:

  Essays, &c. iii. 257.

Footnote 2402:

  On the Esculent Fungi of Great Britain. Mem. Wernerian Society, iv.
  339.

Footnote 2403:

  Toxicol. Gén. 417–428.

Footnote 2404:

  London Med. and Phys. Journal, iii. 41.

Footnote 2405:

  Ibid. xxxvi. 451.

Footnote 2406:

  Edinburgh Med. and Surg. Journal, xlix. 192.

Footnote 2407:

  Journal de Chimie Médicale, 1835, 488.

Footnote 2408:

  Annali Universali di Medicina, 1842, i. 549.

Footnote 2409:

  Journal de Chimie Médicale, 1839, 325.

Footnote 2410:

  Journal de Pharmacie, 1837, 369.

Footnote 2411:

  Foderé, Médecine Légale, iv. 61, and 58.

Footnote 2412:

  Ibidem.

Footnote 2413:

  Haller, Hist. Stirp. Helv. Indig. ii. 328.

Footnote 2414:

  Bongard, London Medical Gazette, 1838, i. 414.

Footnote 2415:

  Ibidem.

Footnote 2416:

  Greville, p. 344, from Langsdorf’s Annalen der Wetterrauischen
  Gesellschaft.

Footnote 2417:

  Foderé, Médecine Légale, iv. 59.

Footnote 2418:

  Journal de Chimie Médicale, 1839, 322.

Footnote 2419:

  Edin. Med. and Surg. Journal, ix. 379.

Footnote 2420:

  Médecine Légale, iv. 55, _et passim_.

Footnote 2421:

  Toxicol. Gén. ii. 445.

Footnote 2422:

  Essai Sur les Propriétés Médicales des Plantes, 320.

Footnote 2423:

  Mem. Wernerian Soc. iv. 342.

Footnote 2424:

  Ann. de Chimie, lxxix. 265; lxxx. 272; lxxxvii. 237.

Footnote 2425:

  Archives Gén. de Méd. xi. 94.

Footnote 2426:

  Repertorium für die Pharmacie, lxvi. 117.

Footnote 2427:

  Traité des Champignons.—Also Mém. sur les Champignons coëffés. Mem. de
  la Soc. Roy. de Méd. i. 431.

Footnote 2428:

  London Med. and Phys. Journal, xxxvi. 451.

Footnote 2429:

  Edinburgh Medical and Surgical Journal, xlix. 192.

Footnote 2430:

  Annali Universali di Medicina, 1842, i. 549.

Footnote 2431:

  Corvisart’s Journ. de Méd. xxxi. 323, from Vadrot. Diss. Inaug. sur
  l’empoisonnement par les Champignons.

Footnote 2432:

  Orfila, Toxicol. Gén. ii. 433.

Footnote 2433:

  Picco—Mem. de la Soc. Roy. de Méd. 1780–81, p. 355.

Footnote 2434:

  Geschichte der Pflanzengifte, 639.

Footnote 2435:

  Aymen, in Hist. de la Soc. Roy. de Méd. i. 344.

Footnote 2436:

  Rust’s Magazin für die gesammte Heilkunde, xvi. 115.

Footnote 2437:

  Persoon, Traité sur les Champignons comestibles, 157.

Footnote 2438:

  Journal de Pharmacie, Sept. 1836.

Footnote 2439:

  Edwards in Lancet, 1836–37, ii. 512.

Footnote 2440:

  Picco—Hist. de la Soc. &c. pp. 357, 359.

Footnote 2441:

  Hist. de la Soc. &c. p. 357.

Footnote 2442:

  Ibidem.

Footnote 2443:

  Repertorium für die Pharmacie, lxvi. 117.

Footnote 2444:

  Quæstiones Medicinæ Forenses, 1824, p. 206.

Footnote 2445:

  Repertorium für die Pharmacie, xiv. 311.

Footnote 2446:

  In the Philosophical Transactions for 1762 an account is given of a
  family of eight people in Suffolk, who had the gangrenous form of the
  disease induced by spurred rye. They had lived on damaged wheat, but
  never used rye meal. See Dr. Wollaston’s paper, lii. 523, and Mr.
  Bone’s Letter, Ibid. 526.

Footnote 2447:

  The Phalaris canariensis and aquatica, Panicura miliaceum Phleum,
  pratense, Alopecurus pratensis and geniculatus, Agrostis stolonifera,
  Aira cristata, Poa fluitans, Festuca duriuscula, Arundo arenaria and
  cinnoides, Lolium perenne, Elymus arenarius and europæus, Triticum
  spelta, junceum and repens, Holcus avenaceus and lanatus, Dactylis
  glomerata, besides those mentioned in the text.—See Robert,
  Erläuterungen und Beiträge zur Geschichte des Mutterkorns.—Rust’s
  Magazin für die gesammte Heilkunde, xxv. 8.

Footnote 2448:

  Mémoire sur la Sologne, in Hist. de la Soc. Roy. de Méd. i. 61.

Footnote 2449:

  Mem. sur la mal. du Seigle appellée Ergot. Hist. de la Soc. Roy. de
  Méd. i. 427.

Footnote 2450:

  Robert’s paper, _passim_.

Footnote 2451:

  Hecker’s Jahrbücher der Staatsarzneikunde, i. 240.

Footnote 2452:

  Robert, in Rust’s Magazin, xxv. 20. Tessier seems to have been of the
  same way of thinking.

Footnote 2453:

  Tillet, Dissertation sur la cause qui corrompe les bles—Fontana,
  Lettre sur l’Ergot. Journ. de Phys. vii. 42.—Réad, Traité sur le
  Seigle Ergoté. 1771.

Footnote 2454:

  Annals of Philosophy, N. S. xi. 14.

Footnote 2455:

  Flore Française, VI.—Robert’s paper, p. 15.

Footnote 2456:

  Inquisitio in Secale cornutum, &c. Commentatio præmio regio ornata,
  Gottingæ, 1831. Analyzed in Annalen der Pharmacie, i. 129.

Footnote 2457:

  Linnæan Transactions, 1840, xviii, 449.

Footnote 2458:

  Ibidem, 453.

Footnote 2459:

  Ibidem, 475.

Footnote 2460:

  Lettre sur l’Ergot. Journal de Physique, vii. 42.

Footnote 2461:

  Lorinser, Beob. und Vers. über die Wirkung des Mutterkorns, 1824,
  noticed in Robert’s paper, p. 28.

Footnote 2462:

  Edinburgh Medical and Surgical Journal, lii. 306. Harveian Prize
  Essay.

Footnote 2463:

  Linnæan Transactions, xix. 140.

Footnote 2464:

  Tessier, 421.

Footnote 2465:

  Ibid. 428.

Footnote 2466:

  Robert, 28.

Footnote 2467:

  Bulletins de la Soc. Philomatique, 1817, 58.

Footnote 2468:

  Buchner’s Repertorium für die Pharmacie, iii. 65.

Footnote 2469:

  Rust’s Magazin, xxv. 43, also Keyl, Dissertatio de Secali Cornuto
  ejusque vi in corpus humanum salubri et noxia.

Footnote 2470:

  Rust’s Mag. für die gesammte Heilk. xxv. 47.

Footnote 2471:

  Annalen der Pharmacie, i. 159.

Footnote 2472:

  Edinburgh Medical and Surgical Journal, lii. 302, and liv. 51.

Footnote 2473:

  Repertorium für die Pharmacie, lxxv. 168.

Footnote 2474:

  Annalen der Pharmacie, i. 180.

Footnote 2475:

  Annali Universali di Medicina, 1839, iv. 12.

Footnote 2476:

  Edinburgh Medical and Surgical Journal, lii. 119, liii. 1.

Footnote 2477:

  Robert’s paper, p. 223, also Lorinser’s Versuche, &c. of which there
  is an analysis in Edinb. Med. and Surg. Journal, xxvi. 453.

Footnote 2478:

  Taube—Geschichte der Kriebelkrankheit, quoted in Robert’s paper, p.
  209.

Footnote 2479:

  Journal der Praktischen Heilkunde, lxxiii. iv. 3, and lxxiv. v. 71,
  vi. 3.

Footnote 2480:

  Descriptio morborum ex usu clavorum secalinorum cum pane, 1717. A full
  extract is given of this work in Acta Eruditorum, An. 1718. Lipsiæ, p.
  309.

Footnote 2481:

  L’Abbé Tessier, Mém. sur les effets du Seigle Ergoté. Hist. de la Soc.
  Roy. de Méd. ii. 611.

Footnote 2482:

  Robert, in Rust’s Magazin, xxv. 205.

Footnote 2483:

  Ibid. 200.

Footnote 2484:

  Ibid. 204.

Footnote 2485:

  Ibid. 231, 232.

Footnote 2486:

  Stearn’s in New York Med. Rep. 1307.—Bigelow in New England Journal of
  Med. and Surg. v.—Prescott in Lond. Med. and Phys. Journ. xxxvi.

Footnote 2487:

  Edinburgh Medical and Surgical Journal, liii. 29.

Footnote 2488:

  Revue Médicale, 1829, iii. 332.

Footnote 2489:

  Hist. de la Soc. Roy. de Méd. i. 346.

Footnote 2490:

  Sedillot’s Journ. Gén. de Méd. xiv. 200.

Footnote 2491:

  Journal de Chimie Médicale, viii. 558.

Footnote 2492:

  Journal de Chimie Médicale, vii. 122.

Footnote 2493:

  Guérard in Annales d’Hygiène Publique, xxix. 35.

Footnote 2494:

  Orfila, Toxic. Gén. ii. 466, from Seeger, Diss. Inaug. Tubingæ, 1760.

Footnote 2495:

  Sur les Effets de l’Ivraie.—Nouv. Journ. de Méd. vi. 379.

Footnote 2496:

  Orfila, Toxicol. Gén. ii. 466.

Footnote 2497:

  London Med. and Phys. Journal, xxviii. 182.

Footnote 2498:

  Buchner’s Toxikologie, 174.

Footnote 2499:

  Annalen der Pharmacie, xvi. 318.

Footnote 2500:

  Hist. de la Soc. Roy. de Méd. ii. 297.

Footnote 2501:

  Repertorium für die Pharmacie, xlviii. 160.

Footnote 2502:

  Nouvelle Bibliothèque Méd. iii. 439.

Footnote 2503:

  Journal de Pharmacie, ii. 397.

Footnote 2504:

  Journ. de Pharm., ii. 397.

Footnote 2505:

  London Medical and Physical Journal, lxii. 86.

Footnote 2506:

  Lancet, 1840–41, 552.

Footnote 2507:

  Hist. des Plantes Ven. de la Suisse, 1776, p. 49.

Footnote 2508:

  Bulletins de la Société de Pharmacie, 1809, p. 48.

Footnote 2509:

  Cases and Observations in Medical Jurisprudence.—Edinburgh Medical and
  Surgical Journal, 1843, lx. 303.

Footnote 2510:

  Journal de Pharmacie, iv. 340, 554.

Footnote 2511:

  Philosophical Transactions, ci. 118.

Footnote 2512:

  Toxicol. Gén. ii. 451.

Footnote 2513:

  Edin. Med. and Surg. Journal, xl. 277.

Footnote 2514:

  Cooke on Nervous Diseases, i. 219.

Footnote 2515:

  Lancet, 1839–40, i. 466.

Footnote 2516:

  Ibid., 1838–39, ii. 233.

Footnote 2517:

  Edinburgh Medical and Surgical Journal, liv. 147.

Footnote 2518:

  Edin. Medical and Surg. Journal, xl. 278.

Footnote 2519:

  Edinb. Med. and Surg. Journal, xii. 489, from Bedingfield’s Compendium
  of Med. Practice.

Footnote 2520:

  Toxicol. Gén. ii. 454.

Footnote 2521:

  Die Lehre von den Giften, I. ii. 306.

Footnote 2522:

  Journal de Chimie Médicale, 1839, 129.

Footnote 2523:

  Corvisart’s Journ. de Méd. xvii. 43.

Footnote 2524:

  Aufsätze, v. 94.

Footnote 2525:

  Bright’s Reports of Medical Cases, i. 1.

Footnote 2526:

  See on this subject, Grötzner, über die Truncksucht unde ihre
  Folgen.—Rust’s Mag. für die ges. Heilkunde, xx. 522.

Footnote 2527:

  Edin. Medical and Surg. Journ. xl. 292.

Footnote 2528:

  Beiträge zur Gerichtl. Arzneik. ii. 59, iii. 38.

Footnote 2529:

  On Nervous Diseases, i. 219.

Footnote 2530:

  Beiträge zur Gerichtl. Arzneik. iii. 38.

Footnote 2531:

  Edin. Med. and Surg. Journal, xl. 282, 284, 293.

Footnote 2532:

  Répertoire Gén. Anat. et de Physiol. Pathologique, i. 51.

Footnote 2533:

  Magazin für die ges. Heilkunde, xxi. 522.

Footnote 2534:

  Treatise on Nervous Diseases, i. 222.

Footnote 2535:

  Edin. Medical and Surgical Journal, xl. 293.

Footnote 2536:

  Rust’s Magazin für die gesammte Heilkunde, xxv. 126.

Footnote 2537:

  Prize Inaugural Dissertation, on the presence of alcohol in the brain
  after poisoning with it. Edinburgh, 1839, _passim_.

Footnote 2538:

  Cases and Observations in Medical Jurisprudence.—Edin. Med. and Surg.
  Journal, xxxi. 239.

Footnote 2539:

  Edin. Medical and Surgical Journal, xl. 295.

Footnote 2540:

  Smith, London Medical Gazette, ix. 502.

Footnote 2541:

  Toxicol. Gén. ii. 456.

Footnote 2542:

  Journal of Science, iv. 158.

Footnote 2543:

  Midland Med. and Surg. Reporter, i., or Edin. Med. and Surg. Journal,
  xxxv. 452.

Footnote 2544:

  Fechner’s Repertorium für Organischen Chemie, i. 1078.

Footnote 2545:

  Toxikologie, 395.w

Footnote 2546:

  Diction. des Scien. Méd. xxi. 605.

Footnote 2547:

  Journal Universel. Novembre, 1829.

Footnote 2548:

  Henke’s Zeitschrift für die Staatsarzneikunde, xxx. 425.

Footnote 2549:

  Horn’s Archiv für Med. Erfahrung, 1824, i. 89, 91.

Footnote 2550:

  Duncan’s Dispensatory, 12th edition, p. 552.

Footnote 2551:

  Lancet, 1832–33, ii. 598.

Footnote 2552:

  Lancet, 1833–34, i. 902.

Footnote 2553:

  Natural, Chemical, Medicinal, and Physiological Properties of
  Creasote. Harveian Prize Essay, 1836, p. 66 to 99.

Footnote 2554:

  Medico-Chirurgical Transactions, xix.

Footnote 2555:

  Elements of Materia Medica, 1842, i. 419.

Footnote 2556:

  lii. 291.

Footnote 2557:

  Edin. Med. and Surg. Journal, xxxiii. 61.

Footnote 2558:

  Journal Universel des Sc. Méd. xvii. 120.

Footnote 2559:

  London Med. and Phys. Journal, xlix. 119.

Footnote 2560:

  Martin-Solon. Journal Hebdomadaire, viii. 73.

Footnote 2561:

  Gueneau de Mussy. Archives Gén. de Med. Deuxiême Série, i. 594.


                                THE END.

------------------------------------------------------------------------




                          TRANSCRIBER’S NOTES


 1. P. 476, changed “exasperated by the use of oil” to “exacerbated by
      the use of oil”.
 2. P. 513, changed “I may here add a very opposite instance of
      hemorrhagic apoplexy” to “I may here add a very apposite instance
      of hemorrhagic apoplexy”.
 3. P. 712, added missing anchor for the last footnote.
 4. Silently corrected typographical errors and variations in spelling.
 5. Archaic, non-standard, and uncertain spellings retained as printed.
 6. Enclosed italics font in _underscores_.