Produced by Ron Swanson





[Frontispiece: Plate I. Occlusion of the Bile, and Pancreatic Ducts.]




JAUNDICE: ITS PATHOLOGY AND TREATMENT.

WITH THE APPLICATION OF PHYSIOLOGICAL CHEMISTRY TO THE DETECTION AND
TREATMENT OF DISEASES OF THE LIVER AND PANCREAS.




BY GEORGE HARLEY, M.D.,

Professor of Medical Jurisprudence in University College, London;
Assistant Physician to University College Hospital; Formerly President
of the Parisian Medical Society; Cor. Memb. of the Academy of Sciences
of Bavaria, and of the Royal Academy of Medicine of Madrid.




So rapid is the advance of science, that the theory regarded as true
to-day, may be recognised as false to-morrow. The facts, however, on
which the theory is based, if rightly observed, remain unaltered, and
unalterable.




LONDON:
WALTON AND MABERLY,
UPPER GOWER STREET, AND IVY LANE, PATERNOSTER ROW.
MDCCCLXIII.




LONDON:
WILLIAM STEVENS, PRINTER, 37, BELL YARD,
TEMPLE BAR.




TO

WILLIAM SHARPEY, M.D., LL.D., F.R.S.,
Professor of Anatomy and Physiology in University College, London,

AS A SMALL TOKEN OF A COLLEAGUE'S ESTEEM FOR A PROFOUND THINKER, A
SOUND REASONER, AND A TRUE FRIEND.




PREFACE.


"Time being money," quite as much to the professional as it is to the
mercantile man, the author has endeavoured in the accompanying
monograph not only to condense his material, but to exclude the
consideration of any question not directly bearing upon the pathology
or treatment of jaundice; indeed, as stated in the Introduction, one of
the chief objects of the author having been to point out how valuable
an adjunct modern physiological, and chemical knowledge is in the
diagnosis, and treatment of hepatic and pancreatic disease, he has
neither dwelt on the literature nor discussed the old theories of the
mechanism of jaundice, but limited himself almost entirely to a brief
exposition of his own views. For the sake of brevity, he has at page
132 put into a tabular form the pathology of jaundice, according to the
opinions expressed in the body of the volume.

As the object of all theory, and the aim of all science, is to insure
wise practice, the author desires to call special attention to that
portion of the work devoted to the chemistry of the excretions,
feeling, as he does, that we are entering upon the threshold of an
important department of medical inquiry, which, sooner or later, will
be followed by valuable practical results. He would also direct the
special attention of his readers to the chapter devoted to treatment,
being sanguine enough to imagine that the adoption of the principles he
has enunciated regarding the mode of action, and administration of the
remedies usually employed in hepatic affections, may conduce to a more
rational and successful method of treatment than has hitherto been
employed. He even goes far enough to hope that the result of the
treatment, as shown in the cases cited, will not only justify the
adoption of the principles on which it is founded, but also prove a
strong incentive to others to follow the line of diagnosis he has
striven to inculcate.

In some portions of the volume the statements of the author may,
perhaps, appear to be rather dogmatic; if so, he would remind his
readers that this has arisen from the circumstance of so many old
dogmas, and deeply-rooted prejudices having to be combated, for he is
quite alive to the fact, that what we regard as scientific truth is in
no case incontrovertible certitude, and that the deductions of to-day,
in an advancing science like that of medicine, may require material
alteration when viewed in the light of the morrow. But he is equally
convinced of the fact, that if men fold their arms, and refrain from
acting until every link in the chain of knowledge is forged, all
progress will be arrested, and the day of certainty still further
postponed.

Too long have we reversed the natural order of things, and commenced
the study of medicine where we ought rather to have left it off. Too
long have we striven, by studying pathology ere we were sufficiently
acquainted with physiology, to place the pyramid on its apex instead of
on its base; and thus it is we remained so long ignorant of the
fundamental doctrine, that the same laws which regulate health,
regulate disease. Nature does nothing on a small scale, and the more we
study her the more we admire the uniformity, and extensive
applicability of her laws. If we pry into the ultimate structure of our
bones, we find they receive their nutriment by a system of irrigation,
carried on through lakes, and rivers (lacunæ, and canaliculi); and if
we examine the periosteum surrounding them, the ligaments attaching
them, or the muscles covering them, we still find, that,
notwithstanding the diversity in structure, and use, the one system of
irrigation pervades them all. We may even go a step further, and say
that the same law which governs the animal governs also the vegetable
kingdom. Indeed, the further science advances, the more apparent does
it become, that not only the animal, and vegetable, but even the
organic, and inorganic, form but one world, regulated by the same laws.

A knowledge of organization, important though it be, is yet less
indispensable to the physician than a knowledge of healthy function,
for it is the latter which elucidates the dark problems of life, it is
the latter which proves the golden key to the comprehension of disease.

Although not even the most ardent admirers of medicine can say, that it
as yet merits the name of an exact science, this ought neither to
destroy our hopes nor trammel our labours. With the stethescope,
microscope, and other physical means of diagnosis a new era dawned upon
our art; and now the members of the new school which is rising up, and
carrying chemistry into the domains of medicine, are the pioneers of
the revolution which is soon to follow. If we look back to what the
exact sciences of to-day were in former times, we shall find they were
much less perfect then, than medicine is now. Astronomy and chemistry
were but astrology and alchemy. If, then, we draw a picture of the
future from the progress of the past, we need have no hesitation in
saying that chemistry rightly applied, and physiology justly
interpreted will, ere many generations pass away, reveal the deepest
secrets of diseased action, and although unable to banish death, will
yet enable the practitioner to follow with unerring certainty the
various morbid changes occurring in the frame.

77, HARLEY STREET, CAVENDISH SQUARE,
  _March, 1863_.




CONTENTS.

                                                                   PAGE
INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . .    1

Pathological conditions with which jaundice is associated--Those
    of the liver itself--Those of the bile-ducts--General
    affections of other organs of the body exerting an influence
    on the biliary secretion--Zymotic diseases--The effects of
    certain poisons  . . . . . . . . . . . . . . . . . . . . . . .    3

Frerichs's theory of jaundice--Theory of jaundice hitherto most
    favoured in England--Dr. Budd as its exponent  . . . . . . . .    6

Nature of bile--Biliverdine--Bile acids; glycocholic, and
    taurocholic acids--Cholesterine--Bile resin--Sugar--Inorganic
    constituents--Specific gravity, reaction, and colour of normal
    bile . . . . . . . . . . . . . . . . . . . . . . . . . . . . .    7

Manner in which bile is secreted--Liver both a formative and
    excretive organ--Animals without gall-bladders--Effects of
    food on the colour and quantity of the bile  . . . . . . . . .   11

Is bile essential to life?--Effect on the system of absence of
    bile in the digestive process--Death from starvation as a
    result--Benefit derived from an additional quantity of
    food--Uses of bile in the animal economy--Necessary to the
    absorption and assimilation of food--Bile as a digestive
    agent--Its action on the chyme--Experiments on its influence
    over the absorption of fatty matter--Its relation to the
    pancreatic juice--Bile taken internally by Caffres . . . . . .   13

General view of the mechanism of jaundice--Two great
    divisions--Jaundice from suppression, and jaundice from
    re-absorption--1st subdivision: jaundice arising from
    enervation, disordered hepatic circulation, and absence of
    secreting substance--2nd subdivision: jaundice arising from
    congenital deficiency of the bile-ducts, and from accidental
    obstruction of the bile-ducts  . . . . . . . . . . . . . . . .   19

General view of the pathology of jaundice from suppression,
    showing how the coloration of the skin, and urine is produced
    in such cases  . . . . . . . . . . . . . . . . . . . . . . . .   20

Mechanism of jaundice as a result of enervation--Influence of
    nervous system on secretion--Effect of mental emotion on
    biliary secretion, as observed in dog with biliary
    fistula--Action of fright in paralyzing nerve force  . . . . .   22

Mechanism of jaundice from hepatic congestion--Active
    congestion--General view of the effects of congestion on
    glandular secretion--Reason why the biliary secretion is not
    usually completely arrested--The absence of pipe-clay stools
    explained--Example of jaundice from hepatic
    congestion--Jaundice from zymotic disease, and other cases of
    blood-poisoning, have a similar mechanism--Example of jaundice
    following upon ague--Effect on the urine--Analysis of the
    urine a clue to the nature of the case . . . . . . . . . . . .   24

Passive congestion of the liver as a cause of jaundice--Cases
    associated with heart disease, pneumonia, &c.--Explanation of
    the reason why jaundice is so frequently absent in such cases    29

Mechanism of jaundice arising from suppression consequent upon
    absence of the secreting substance--Cancer, tubercle,
    &c.--Effects of the position of the morbid deposit in
    modifying the result . . . . . . . . . . . . . . . . . . . . .   31

Jaundice arising from acute, or yellow atrophy of the liver--State
    of the urine in such cases--Presence of
    bile-acids--Pettenkofer's test--Tyrosine and leucine in the
    urine--An example of the affection occurring in a young
    woman--Exciting cause--State of the liver tissue--Poisonous
    effects of glycocholate of soda injected into the circulation    34

Mechanism of jaundice arising from the re-absorption of the
    secreted but retained bile--Jaundice arising from a
    congenital deficiency of the ducts--History of a case  . . . .   39

Pathology of jaundice resulting from the accidental obstruction of
    the bile-ducts--Mode of formation of gall-stones--Jaundice
    only present when the stone is lodged in common duct--How
    gall-stones may imperil life without inducing jaundice--Modes
    of escape from the gall-bladder--Presence of foreign bodies,
    such as cherry-stones in gall-duct--Jaundice arising from
    hydatids impacted in the common duct . . . . . . . . . . . . .   42

Mechanism of permanent jaundice from obstruction--Resulting from
    organic disease--Cancer of head of pancreas--Effect of the
    dilatation of the bile-ducts in the liver--Effect on the
    nutrition of the parenchyma of liver--Different stages in
    size through which the liver passes--Difficulties of
    diagnosis--Cause often obscure--Key to its detection . . . . .   46

Analysis of the intestinal secretion an aid to the diagnosis of
    obscure cases of abdominal disease--Colour, nature, and
    chemical composition of the stools--Changes produced in them
    by different foods, and remedies . . . . . . . . . . . . . . .   51

Examination of the renal secretion--Diagnostic value of the colour
    of the urine--Colour produced by urohæmatin to be
    distinguished from that produced by biliverdine--Simple method
    of separating the pigment from the urine--Advantage of at the
    same time ascertaining the quantity of uric acid
    present--Effect of the bile pigment becoming deposited in the
    kidneys--Production of secondary disease . . . . . . . . . . .   55

Diagnostic value of the presence of the bile-acids in the
    urine--Views of Frerichs, Städler, and Kühne--Hoppe's method
    of detecting the bile-acids--Frerichs's theory of the
    transformation of bile-acids into biliverdine shown to be
    untenable  . . . . . . . . . . . . . . . . . . . . . . . . . .   58

Diagnostic value of the presence of tyrosine, and leucine in the
    urine--Microscopic appearances of these substances--Mode of
    separating them from urine--Chemical tests . . . . . . . . . .   63

Melanine in the urine in cases of cancer of the liver--The
    characters by which it is to be distinguished from bile
    pigment--Case related showing the value of the test  . . . . .   68

Diagnostic value of ascertaining the quantity of urea, and uric
    acid, as well as the presence of sugar in the urine in obscure
    cases of jaundice--History of a case illustrating the value of
    such knowledge--Significance of the presence of fatty acids in
    the fæces in the diagnosis of pancreatic disease--Pancreatine
    administered--Effect of bile-poisoning on the memory--Analysis
    of the patient's urine--Diagnostic value of the quantity of
    its constituents pointed out--Appearance of sugar as the
    forerunner of a fatal termination alluded to--Disappearance of
    bile-acids, and appearance of tyrosine and leucine in the
    latter stages of the disease--Post-mortem appearances
    described--Occlusion of bile, and pancreatic ducts--Analysis
    of healthy and diseased bile--Change in the proportion of the
    organic greater than in that of the inorganic
    constituents--Microscopic appearances of liver--Presence of
    crystals of cystine, as well as of tyrosine in the hepatic
    parenchyma . . . . . . . . . . . . . . . . . . . . . . . . . .   70

Jaundice from obstruction in its latter stage complicated with
    jaundice from suppression  . . . . . . . . . . . . . . . . . .   89

Epidemic jaundice--Among soldiers--Among pregnant women--Among the
    entire civil population--Its mechanism--Its cause--Case of
    jaundice supervening upon scarlatina . . . . . . . . . . . . .   90

Artificial jaundice--Mode of production--Experiments
    related--Tyrosine, and leucine supposed to be the result
    either of the arrested, or of the retrograde metamorphosis of
    glycocholic, and taurocholic acids--Biliary acids detected in
    the blood--Poisonous nature of the constituents of the
    bile--Condition of the blood in bile-poisoning . . . . . . . .   95

Treatment of jaundice--Totally different in jaundice from
    suppression and in jaundice from obstruction--Benefit of
    mercury in cases of jaundice--General theory regarding the
    action of mercurials--Benefit of acids, and of alkalies--Their
    mode of action explained--Theory of their action in cases of
    gall-stones--Lithia water--Treatment of jaundice by benzoic
    acid--Cases illustrating its mode of action--Podophyllin a
    bane, and an antidote in cases of jaundice--Its pernicious
    effects in cases of obstruction pointed out--Author's theory
    of its action in such cases--Method of detecting gall-stones
    in the stools--Sulphuric ether, and chloroform in cases of
    gall-stones--Taraxacum . . . . . . . . . . . . . . . . . . . .  101

Difficulties in the treatment of jaundice from obstruction pointed
    out--Derangements arising from absence of bile in the
    digestive process--Good effects of an additional quantity of
    food--Establishment of an artificial biliary fistula shown to
    be less hazardous than usually imagined--Mode of operation
    explained--Treatment of permanent jaundice by prepared
    bile--New mode of preparing bile pointed out--Theory of its
    action--Time of administration shown to be of much
    importance--Bile put into capsules--Benefits derived from bile
    given in this form . . . . . . . . . . . . . . . . . . . . . .  122

Tabular view of the pathology of jaundice according to the
    author's views . . . . . . . . . . . . . . . . . . . . . . . .  132

INDEX  . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  133




DESCRIPTION OF PLATES AND WOODCUTS.


PLATE I.

Represents the condition of the parts in a fatal case of permanent
jaundice, in which both the bile, and pancreatic ducts were completely
occluded.

_(a)_ Atrophied liver.

_(b)_ Transverse section of the left lobe, showing the mouths of the
enormously distended gall-ducts.

_(c)_ Enlarged gall-bladder.

_(d)_ Dilated cystic duct.

_(e)_ Distended hepatic, and common duct.

_(f)_ Ulceration in duodenum, in the situation of the opening of the
gall-duct into the intestines.

_(g)_ Pancreas with enlarged head _(h)_, and enormously distended duct.


PLATE II.

External surface of the left kidney, denuded of its capsule, in a case
of permanent jaundice.

_(a)_ Small specks of bile pigment deposited in the renal tissue, and
blocking up the urine tubes.

_(b)_ Small abscesses scattered throughout the tissue of the kidney.


WOODCUTS.


Fig. 1. Crystals of glycocholate of soda, mag. 90 diam.--Page 8.

 "   2. Taurocholate of soda, as found in the form of globules of
          various sizes.--Page 9.

 "   3. Crystals of cholesterine.--Page 9.

 "   4. Crystals of pure tyrosine.--Page 63.

 "   5. Spiculated balls of tyrosine, from the urine of a case of acute
          atrophy of the liver.--Page 64.

 "   6. Globules of leucine.--Page 66.

 "   7. Cholesterine crystals.--Page 82.

 "   8. _(a)_ Crystals of cystine.
        _(b)_ Hepatic cells, showing entire absence of fat globules.
        _(c)_ Caudate or spindle-shaped cells, from epithelial lining
                of hepatic ducts.--Page 86.


{1}

JAUNDICE: ITS PATHOLOGY AND TREATMENT.




INTRODUCTION.


Having entitled this monograph "Jaundice, its Pathology and Treatment,"
it may, perhaps, be necessary for me to state at the beginning that by
so doing it is not to be supposed that I regard jaundice as a disease
_per se_. On the contrary, I look upon it in the same light as I do
albuminuria, which is not of itself a disease, but only the most
prominent symptom of several widely-differing pathological conditions.
So also the peculiar state of body characterised by yellow skin,
saffron-coloured urine, and pipe-clay stools, is itself but a symptom
of morbid action. It may be asked, "Then why do you treat of jaundice
as if it were a disease?" To this I reply, "Because, although {2} the
condition called jaundice be merely a manifestation of morbid action,
and one, too, requiring neither skill nor experience to detect, the
proper comprehension of its true mechanism is of much practical
importance to the physician, for without this knowledge it is
impossible for him to treat it with any chance of success. Nay, even
the remedies for jaundice become dangerous weapons, if unskilfully
applied." In fact, it is almost unnecessary to apologise for treating
of jaundice as a disease _per se_; for, notwithstanding all that has
been written upon the subject, it is universally admitted that the
simplicity of its diagnosis is only equalled by the obscurity of its
pathology, and the uncertainty of its treatment; and no one at all
conversant with the literature of jaundice can be in the least degree
surprised at this statement. On the contrary, on glancing at the
immense variety of morbid states, and known pathological conditions
with which it is associated, he cannot fail to admit its truth.

Some of the pathological conditions are closely allied; others are
widely separated--so widely, indeed, that at first sight it is
impossible to discover from whence emanates the common symptom. We find
jaundice connected with diseases of the liver, of the neighbouring
organs, and of the general system. In some diseased conditions, {3}
jaundice presents itself when least expected. At other times it is
absent when, apparently, it ought to be present. On the other hand,
again, there are cases in which jaundice is evidently merely a symptom,
and others in which it seems to be in itself the disease. We have
temporary jaundice from transient derangements, and we have permanent
jaundice from stationary causes. There are cases in which the cause of
jaundice is visible after death to the naked eye. There are others
where the minutest research is baffled in ascertaining the cause. That
this is no exaggerated view of the case the following table will
show:--

               JAUNDICE IS MET WITH,
    Firstly, IN DISEASES AFFECTING THE LIVER--
  _(a)_ Cancer.
  _(b)_ Tubercle.
  _(c)_ Cirrhosis.
  _(d)_ Inflammation.
  _(e)_ Atrophy.
  _(f)_ Amyloid, and
  _(g)_ Fatty degeneration.

    Secondly, IN DISEASES OF THE BILE-DUCTS--
  _(a)_ Congenital deficiency.
  _(b)_ Accidental obstruction. The latter arising from gall-stones,
          hydatids, foreign bodies {4} (such as cherry-stones and
          entozoa) entering from the intestines.
  _(c)_ Ulcer of the duodenum.
  _(d)_ Tumours of the pancreas.

    Thirdly, IN AFFECTIONS OF OTHER ORGANS OF THE BODY EXERTING AN
    INFLUENCE ON THE BILIARY SECRETION--
  _(a)_ Diseases of the nervous system.
  _(b)_ Diseases of the lungs.
  _(c)_ Diseases of the heart.
  _(d)_ Imperfect establishment of the extra-uterine circulation
          (infantile jaundice).
  _(e)_ Dyspepsia.
  _(f)_ Torpidity of the bowels, and consequent accumulation of fæces
          in transverse colon.
  _(g)_ Pregnancy.

    Fourthly, IN A VARIETY OF ZYMOTIC DISEASES--
  _(a)_ Typhus.
  _(b)_ Yellow fever.
  _(c)_ Ague.
  _(d)_ Pyæmia.
  _(e)_ Epidemic jaundice.

    Fifthly, AS A RESULT OF THE INJURIOUS EFFECTS OF CERTAIN POISONS--
  _(a)_ Snake bites. {5}
  _(b)_ Alcohol.
  _(c)_ Chloroform, etc.

Can it be wondered, then, that a state so easily diagnosed is
nevertheless so difficult to comprehend?

Notwithstanding the apparent incongruity of the diseases with which the
one common symptom of jaundice is associated, I trust to be able to
reconcile these discrepancies, and prove that the seeming discord is
but "harmony not understood."

All physicians, I think, admit that the peculiar state of the system to
which the name of jaundice has been applied, is essentially due to some
derangement of the biliary function, the exact nature of the
derangement being alone the point of contention. I need not, therefore,
waste the time of my readers, either by giving an account of the
literature or a detail of the symptoms of jaundice. Even in discussing
its pathology, I shall strictly limit myself to the consideration of
the opinions at present held by the more advanced of our pathologists;
the object of this monograph being, not to pourtray the views of
others, but to give a brief _exposé_ of my own, and to point out how
modern physiology, and chemistry have not only thrown a new light on
its pathology, but have also given us a clue to its successful
treatment.

{6} Frerichs, the most recent writer on this subject, in his elaborate
treatise on diseases of the liver, says that jaundice may result from
one of the three following conditions:--

Firstly,--Obstruction to the escape of bile.

Secondly,--Diminished circulation of blood in the liver, and consequent
abnormal diffusion; both of these conditions giving rise to an
increased imbibition of bile into the blood, and in both cases the
liver being more or less directly implicated.

Thirdly,--Obstructed metamorphosis, or a diminished consumption of bile
in the blood.[1]

[Footnote 1: Frerichs' "Clinical Treatises on Diseases of the Liver."
New Sydenham Society's Translation, vol. i. p. 93.]

From this it is seen, that the pathology of jaundice, according to
Frerichs, is very different from what we were formerly taught. For
while he has entirely laid aside the theory of jaundice as a result of
suppressed secretion, he has introduced two perfectly new
elements--namely, abnormal diffusion, and diminished consumption. The
latter theory, being, of course, founded on the supposition that bile,
after playing its part in the digestive process, is re-absorbed into
the circulation, again to perform another function in the animal
economy, before its final excretion from the organism as effete matter.
The theory of jaundice, hitherto most favoured in England, and which
found {7} such an able exponent in Dr. Budd, is, that the disease may
arise in two ways--firstly, by a mechanical obstruction to the passage
of bile into the intestines, and the consequent re-absorption of the
detained fluid into the blood; and secondly, by a suppression of the
biliary secretion arising from some morbid condition of the liver
itself, whereby the biliary ingredients accumulate in the circulation.
Now, although I am not prepared to admit the justice of the views held
regarding the origin and function of bile, on which these opinions are
based, I nevertheless believe that in the following pages I shall be
able, by the aid of modern medical science, to prove the correctness of
the conclusions themselves. In order to do this, however, it will be
necessary for me to begin by making a few remarks on the nature of
bile, and the physiology of its secretion.


ON THE NATURE OF BILE.

In a few words, bile may be said to be composed of the following
substances:--

Firstly,--Biliverdine, a green nitrogenized, non-crystallizable
colouring matter, analogous to the green colouring matter of plants,
and like it, leaving on incineration a distinctly ferruginous ash. This
colouring matter appears, like {8} urohæmatine, and all other animal
pigments, to be a direct derivative of the colouring matter of the
blood.[2]

[Footnote 2: _Vide_ papers by the author on the colouring matter of the
urine, Pharm. Journ., November, 1852. "Urohæmatine, and its combination
with animal resin." Verh. d. Phys.-Med. Gesellschaft zu Wurzburg, Bd.
V. 1854.]

[Illustration: FIG. 1. Crystals of Glycocholate of soda, a beautiful
polariscopic object. _(a)_ Fine needle-shaped crystals, separated from
a rosette-shaped group. _(b)_ Small rosette of crystals. _(c)_
Fan-shaped groups of crystals, which are merely portions of large
rosettes that have become broken up. _(d)_ A fragment of a bundle of
needle-shaped crystals. Mag. 90 diam.]

Secondly,--Two peculiar substances, named respectively, glycocholic,
and taurocholic acid--the former yielding, when in combination with
soda, a crystallizable, the latter a non-crystallizable salt.
Taurocholic differs still further from glycocholic acid, in containing
a large percentage of sulphur, {9} and being, under the influence of
hydrochloric acid, convertible into taurine, a beautiful white
crystalline substance.

[Illustration: FIG. 2. Taurocholate of soda is found in the form of
fatty-looking globules of various sizes. They differ from fat and oil
globules, however, in being soluble in water, and insoluble in alcohol
and ether.]

Thirdly,--Cholesterine, a crystalline, fatty matter, not, however,
peculiar to bile, but found in various tissues, and secretions of the
body.

[Illustration: FIG. 3. Cholesterine crystals appear in the form of fine
transparent four-sided plates of various sizes and shapes. The crystals
are freely soluble in hot alcohol, from which they are re-deposited on
cooling.]

{10} Fourthly,--A brown resinous substance resembling, in appearance
and consistence, shoemaker's wax.

Fifthly,--Among the constituents of the bile, I may mention sugar, for
both in the normal bile of man, and of the lower animals, the ox, and
the dog, I have detected that substance. On one occasion, I even found
torulæ in the bile twenty-four hours after its removal from the
gall-bladder of a healthy dog.

Sixthly, and lastly,--a quantity of inorganic matter, consisting
chiefly of soda, potash, and iron.

The specific gravity of bile fluctuates, of course, with the percentage
of solid matter it contains. From my own observations, I consider that
healthy human bile has an average specific gravity of 1020, and
contains about six per cent. of solid matter, five per cent. of which
is organic, and one per cent. inorganic substance. When fresh, bile is
almost neutral; but it rapidly undergoes decomposition, and becomes
alkaline.

In colour, human bile is usually of a brownish yellow hue; the colour,
however, varies with its degree of concentration, the kind of food
taken, and the state of the system. As regards the effect of food, if
we may be allowed to form an opinion from experiments on dogs, it may
be said that, as a {11} rule, animal food tends to give bile a yellow,
vegetable food a green, tint.

Next, as regards the manner in which bile is secreted. For a long time
it was thought, and, indeed, some people still think, that bile exists
pre-formed in the blood, and that the liver only excretes it, as the
kidneys excrete the urinary ingredients. Another class, running to the
opposite extreme, believe that the liver is not merely the excretive,
but also the formative organ of the bile. It appears to me, however,
that neither of these extreme views is correct, and that the truth lies
between the two.

It is, in fact, not at all difficult to prove that the liver
manufactures certain biliary constituents, while it merely excretes
others. Thus, for example, the two substances glycocholic and
taurocholic acids are never to be found either in the blood, tissues,
or fluids of the healthy organism, with the single exception of those
of the liver and gall-bladder; and after extirpation of the liver
neither acid is to be found in the body at all. On the other hand, such
substances as cholesterine and biliverdine, are not peculiar to the
liver or its secretion, but are the products of several organs, and are
always to be detected in the blood, independently of the presence or
absence of the liver. These facts, therefore, clearly show that the
liver {12} is both a formative and excretive organ to some, and an
excretive only to others, of the biliary constituents.

Lastly, the general opinion is that the secretion intermits, and, like
the gastric, and pancreatic juices, bile is only formed during
digestion. Were it so, however, where would be the necessity for a
gall-bladder? Is it not to store up the secretion formed in the
intervals of digestion, and to retain it until it is required? No doubt
there are several animals, such as the horse, and the deer, that
possess no gall-bladders; but there is undoubtedly in them some special
arrangement of the digestive apparatus, rendering the presence of a
gall-bladder unnecessary. In fact, it is easily shown that the biliary
secretion in ordinary cases is continuous; for if in an animal
possessing a gall-bladder a biliary fistula be established, and the
secretion of bile carefully watched, it will be found that at no period
of the day does it entirely intermit, although it is more active at one
time than at another, the minimum of its activity being during
sleep--the maximum during active digestion. The absolute quantity of
bile secreted in the twenty-four hours is tolerably uniform, although
the daily amount is slightly influenced by the kind of food.[3]

[Footnote 3: Arnold found that dogs secreted more bile on a bread, than
on an animal diet. "Zur Physiologie der Galle," Mannheim, 1854.]


{13} IS BILE ESSENTIAL TO LIFE?

Several physiologists have given it as their opinion that bile is not
essential to life, for animals have lived for many months after the
artificial establishment of a biliary fistula, through which the bile
was allowed to flow away, and be lost to the animal. Now, although this
is perfectly true, yet it is at the same time evident that the uses of
the bile cannot altogether be dispensed with, for all the animals with
a biliary fistula lose flesh, become emaciated, and weak; the hair has
a tendency to fall off, the bowels to become irregular; and a great and
an almost constant discharge of foul-smelling gases takes place from
the intestinal canal. At length, after a shorter or longer period, the
animal sinks, and dies. The fatal termination can, however, be retarded
by allowing him an additional quantity of nourishing food, for death
from want of bile, as is too often seen in the human subject, is
nothing else than death from slow starvation. The fact just related
regarding the beneficial effects of an additional quantity of food in
prolonging life, should never be lost sight of in the treatment of
cases of obstruction of the gall-ducts, for, by attending to this
circumstance, it is often in the power of the medical man to keep his
patient alive for a considerable length of time.

{14} It may perhaps not be out of place if I here briefly enumerate the
chief uses of bile in the animal economy. In order to live, not only
must the individual particles of our frames die, but they must be
continually replaced by new materials of a similar kind; and for the
accomplishment of this important end, nature has endowed animals with a
digestive apparatus in which their food undergoes the various physical,
and chemical changes necessary to its absorption, and assimilation. In
the animal laboratory or digestive apparatus there are five important
agents constantly at work--saliva, gastric juice, bile, pancreatic
fluid, and intestinal secretion, and each of these agents has a special
and definite office to perform in the elaboration of the food.[4] At
present, however, I must limit myself entirely to the consideration of
bile.

[Footnote 4: For an explanation of these offices, see the author's
article on "The Chemistry of Digestion," in the "British and Foreign
Quarterly Review," January, 1860.]

Bile is the first digestive agent with which the food comes in contact
on leaving the stomach and entering the intestines, and immediately on
the acid chyme mixing with the alkaline bile, a white flocculent
emulsion is formed, which emulsion has been described by many writers
as a precipitation of the albuminose (digested albumen). Later {15}
researches by myself and others have, however, shown that it is not the
bile which precipitates the albuminose, but the acid of the chyme,
which in reality sets free certain ingredients of the alkaline bile. In
the majority of cases there is not even a true precipitation, for on
throwing the milky-looking mixture upon a filter, I found that almost
nothing remained behind, and the filtrate was nearly as white as the
original liquid. Further, if the albuminose be separated from the
chyme, and the chyme then brought into contact with the bile, the same
flocculent-looking milkiness still appears. Nay, more, on adding equal
parts of sheep's bile (fresh) to gastric juice drawn from a dog's
stomach in full digestion, the apparent flocculent precipitate still
appeared, although the acidity of the gastric juice remained
unneutralized; and on throwing the whole into a filter, I found that
the liquid that drained through was as milky and flocculent-looking as
the original. The office of bile in the digestive process is neither to
act on the albuminous[5] nor amylaceous portions {16} of our food; its
chief action being to assist in the absorption of fats. When bile is
mixed with neutral fat, little change is observed, but when brought in
contact with the fatty acids, an immediate emulsion takes place. Lenz
and Marcet[6] pointed out how the neutral fats of our food are
transformed into fatty acids during their sojourn in the stomach; and
Bidder and Schmidt[7] illustrated by experiments on dogs the important
part played by the bile in their absorption. A dog, which in its normal
condition absorbed on an average 7 grains of fat for every 2 pounds of
its weight, absorbed only 3, or even as little as 1 grain, after the
bile was prevented entering the intestines, in consequence of a
ligature being applied to the gall-duct.

[Footnote 5: In speaking of the properties of the bile, I may mention
that, although bile has no digestive power (properly speaking) over
albuminous substances, yet, when injected into the subcutaneous
cellular tissue of a healthy animal, it eats its way out through the
skin, just as gastric juice or lactic acid does under similar
circumstances. Even the muscles with which it comes in contact appear
to be eaten away.]

[Footnote 6: _Vide_ a Discourse on the Chemistry of Digestion, by Dr.
Marcet. Journ. of the Chem. Soc., Oct. 1862.]

[Footnote 7: "Die Verdauungssaefte und der Stoffwechsel." Leipzig,
1852.]

Further, these last-named observers found that, while the chyle in the
thoracic duct of a healthy dog contains 32 parts of fat per thousand,
that in the thoracic duct of a dog with a ligatured gall-duct, contains
only 2 parts per thousand. These facts clearly prove that bile plays an
important part in the absorption of the fatty portion of our food. Next
comes the question, "In what manner does bile aid in the absorption of
fatty matter?" {17} As is well known, fats or oils have no tendency to
mix with water, and hence diosmose between an aqueous and an oily fluid
is next to impossible. Matteucci has, however, shown that if an animal
membrane be moistened on both sides with a weak solution of potash, it
allows oil to pass through it. It has also been observed, that when the
intestine is moistened with bile, it allows oil to pass through, which
would not otherwise be the case. To illustrate this property of bile, I
performed the following experiments:--

Firstly,--A clean piece of duodenum was filled with oil, ligatured at
both ends, and suspended in water, holding in solution a small quantity
of albumen. (The albumen was added to the water merely to imitate
slightly the albuminous blood.) On examination, twenty-four hours
later, no oil was found to have escaped through the intestinal walls.

Secondly,--A second portion of intestine had its internal surface
moistened with sheep's bile before the introduction of the oil. It was
then treated in the same manner as the preceding, and on being examined
after the lapse of twenty-four hours, a small quantity of the oil was
found to have penetrated through the intestine.

Thirdly,--Into a third portion of intestine was poured equal parts of
sheep's bile, and chyme obtained from a dog in full digestion, through
a {18} fistulous opening into its stomach. After being treated for the
same length of time, and in precisely the same manner as the others,
evident signs of the oily matters of the chyme having passed through
the walls of the intestine were obtained, for they were seen as a scum
floating on the surface of the albuminous water. Moreover, the fatty
matters were not in the form of pure oil, but of a soapy substance.

The bile is thus seen to possess one of the more remarkable properties
of the pancreatic juice. There is this important difference between the
action of these two secretions on fats, however, that while bile merely
emulsions and saponifies that portion of our food which enters the
duodenum in the form of fatty acids, pancreatic juice, on the other
hand, possesses the power, not only of emulsioning and saponifying the
fatty acids, but also the neutral fats; indeed, its power seems chiefly
to be exerted upon the latter. Hence it appears that both secretions
are in a measure necessary to the complete digestion and absorption of
the oleaginous constituents of our food.

On one occasion, while experimenting with bile at University College, I
was surprised to hear Minton, the servant who was assisting me, say,
that while he was travelling with Sir Andrew Smith in South Africa, he
had oftentimes seen the {19} Caffres drink bile direct from the
gall-bladders of the animals killed by the European party, and that,
while passing the gall-bladder round to each other, they would rub
their stomachs and say,--"Mooé-ka-kolla," signifying thereby, that it
was very good. It certainly seems very extraordinary that any human
being should not only drink, but drink with pleasure, a liquid so
bitter and nauseating as bile. Perhaps the poor Caffres, however, drank
the sickening tasted bile for the same reasons as the cattle in
Caffreland, at certain periods of the year, go thousands of miles to
drink at the salt-springs. There being scarcely any chloride of sodium
in the earth, there is insufficient for the animal requirements in the
herbage on which they feed, and they are forced to supply the
deficiency by artificial means. Bile contains a large percentage of
soda, and perhaps the Caffres drink it in order to obtain that
substance, just as the animals drink the brackish water of the salt
licks, feeling that it agrees with them, without knowing why.


THE MECHANISM OF JAUNDICE.

As said in the beginning of this paper, I believe, the pathology of
jaundice may be embodied under the two heads, jaundice from suppression
{20} of the biliary functions, and jaundice from re-absorption of the
secreted but retained bile. These are at best, however, but vague
terms, and in order to make the pathology of jaundice somewhat more
definite it will be necessary for me to subdivide these two great
classes in the following manner:--

  (CLASS A.)--JAUNDICE FROM SUPPRESSION.
              Arising from:--
    (1) Enervation.
    (2) Disordered hepatic circulation.
    (3) Absence of secreting substance.

  (CLASS B.)--JAUNDICE FROM RE-ABSORPTION.
              Arising from:--
    (1) Congenital deficiency of bile-ducts.
    (2) Accidental obstruction of bile-ducts.

I shall now try to point out the pathology of these different states,
and see how far they are able to explain the occurrence of jaundice
under the various conditions already alluded to.


JAUNDICE FROM SUPPRESSION.

Although there can be no misunderstanding the meaning of the term
"jaundice from suppression," there may, nevertheless, be some
difficulty in comprehending how the skin becomes yellow, and the urine
high coloured, when the secretion {21} of bile is arrested. In order to
explain how this occurs, it will be necessary to recall to mind what
was said regarding the nature of the biliary secretion. It will be
remembered that I began by saying, that while some of the constituents
of the bile are generated in the liver itself, there are others that
exist, pre-formed in the blood.

If this view of the physiology of the biliary secretion be correct, it
is perfectly evident that when the secretion of bile is arrested, those
substances which the liver generates will be entirely wanting, while
those which it merely excretes from the blood will accumulate there as
soon as their excretion is prevented; just as urea accumulates in the
circulation when its elimination by the kidneys is stopped. Hence it is
that, as soon as the biliary secretion is in abeyance, biliverdine
accumulates in the blood (until the serum is as it were completely
saturated with the pigment), from which it exudes and stains the
tissues, and produces the colour we term jaundice. At the same time, or
even before the skin becomes yellow, the urine assumes a saffron tint
in consequence of the elimination of the colouring matter by the
kidneys.[8] From this it will be seen that I regard {22} the yellow
skin and high-coloured urine of jaundice as simply due to the deranged
secretion of biliverdine, quite independent of the presence or absence
of the other constituents of the bile, the effects produced by which
will be referred to elsewhere. Meanwhile we shall separately consider
the further pathology of the three subdivisions of jaundice arising
from suppression.

[Footnote 8: The true order of the occurrence of these changes is:--On
the second day the urine becomes high-coloured; in a day or two later
the skin assumes a yellow tint; and, in very severe cases, within the
first week or two, the sweat, the milk, the tears, the sputa, and the
serum in the thoracic and abdominal cavities, become of a more or less
decided yellow hue.]


JAUNDICE AS A RESULT OF ENERVATION.

It is now a well-established fact that all secretions are under the
direct influence of the nervous system. Stimulate a nerve supplying a
gland, and secretion is accelerated; stop the nervous action, and
secretion is as instantaneously arrested. Again, just in the same way
as volition can produce or suspend muscular movement, mental influence
can hasten or retard glandular secretion. As an illustration of this
fact, I need only call to mind the influence the mere sight of food has
in exciting the salivary secretion, and the effect of bad news in
arresting it. Exactly the same influence as is here alluded to, is
exerted by the mind over the biliary function. If, for example, {23} as
Bernard first observed, a dog with a biliary fistula be caressed, the
secretion of bile is actively continued; if, on the other hand, the
animal be suddenly ill-used, the secretion of bile is instantly
arrested. If he be again caressed, the secretion is re-established, and
the bile flows drop by drop from the end of the cannula. Here the
influence is entirely produced through the intervention of the nervous
system; and if such effects as are above described occur in the dog, we
can surely have little difficulty in understanding how the biliary
secretion can be influenced in the highly-developed organization of the
human being. Indeed, every one must have felt how quickly sad tidings
received during a meal not only destroy the appetite and retard
digestion, but occasionally alter the complexion. This effect, that all
of us must have experienced in a slight degree in our own persons,
several may have observed to a greater extent in the persons of others,
even to the production of well-marked jaundice. At this very time I
have under my care a young married lady, who during the last two years
has twice suffered from an attack of jaundice induced by witnessing her
child in convulsions, and this I regard as an example of jaundice from
enervation.

One of the reasons, no doubt, why jaundice does not more frequently
follow upon mental emotion is {24} simply on account of a certain
amount of pigment being required in order to produce a visible tinging
of the body, and it seldom happens that the emotional effect on the
biliary secretion is sufficiently permanent to permit of the requisite
amount of pigment accumulating in the blood. The reason, too, why
mental emotion is more apt to cause jaundice immediately after a meal
is, as will afterwards be better understood, on account of the
congested state of the liver at that time favouring the stoppage of the
secretion. A blow on the head, which is now and then observed to be
suddenly followed by jaundice, acts, I believe, in the same way as
fright, namely, by paralyzing the nerve force required for the
continuance of the biliary secretion.

I now pass on to the consideration of the pathology of the second kind
of jaundice from suppression, namely, jaundice resulting from hepatic
congestion.


JAUNDICE ARISING FROM HEPATIC CONGESTION.

This is one of the most common causes of the disease; but as there are
two kinds of hepatic congestion--active and passive--it will be
necessary for me to make a further subdivision, and consider each of
these separately.


{25} _Jaundice the Result of Active Congestion._

The mechanism of jaundice resulting from active congestion of the liver
is readily explained on physiological grounds.

The congested condition of any gland is unfavourable to secretion. We
all know, for example, that congestion of the kidney is accompanied by
a suppression of the urinary secretion, and that the secretion is
re-established as the congested condition of the organ diminishes. The
suppression of the renal secretion is no doubt due to the engorged
capillaries pressing upon the secreting structure, and ultimate
ramifications of the urine tubes, and thereby annulling their
functions. A similar explanation is equally applicable to the biliary
secretion; and just as it happens in the case of the kidney, that it is
exceedingly rare for a total suppression of its functions to take
place, so with the liver it seldom happens that the congestion is
sufficiently severe to induce complete arrest of the biliary secretion.
We find, therefore, that although there may be yellowness of the skin
and high-coloured urine in such cases, pipe-clay stools are frequently
absent, sufficient bile to tinge the fæces still finding its way into
the intestines.

Undoubtedly it must have occurred to many of my readers, that jaundice
is frequently absent in {26} cases of acute inflammation of the liver,
even running on to suppuration, and that the foregoing theory of the
pathology of such cases is therefore insufficient. At one time I was
puzzled to explain this apparent anomaly, but on subsequent
investigation the true cause became apparent, and instead of the above
fact detracting from, it tended rather to strengthen the theory. If,
for example, we closely examine cases of acute hepatitis without
jaundice, we find they are those in which only a portion of the liver
is affected. It matters not whether it be one lobe or two, the surface
or the centre of the organ, the disease is invariably circumscribed;
and there is enough hepatic tissue left in a sufficiently normal
condition to prevent the constituents of the bile accumulating in the
blood, and producing jaundice. This may even occur, as I have myself
observed, when the disease has run on to suppuration.

The most typical example of jaundice as the result of active
congestion, is to be found in those cases where it supervenes on an
attack of hepatitis, such as is met with in hot climates, where
indolent habits and high living favour portal congestion. It is
occasionally met with in England, however, and is frequently associated
with gastric derangement.

I had occasion to witness a good example of {27} this form of disease
in the person of a French gentleman, who was brought to me seven days
after his arrival in England, on account of his skin having assumed a
most intense yellow hue. It appeared that he had come to England on a
visit to some of his friends, and rather enjoying the novelty of an
English table, indulged too freely in a quantity and quality of food to
which he had hitherto been a stranger. The consequence was, that within
three days after his arrival he began to suffer from hepatic
tenderness, and dyspeptic symptoms; the skin at the same time assumed a
dusky hue, which soon merged into a decided yellowness. These symptoms
were accompanied by pipe-clay stools and saffron-coloured urine; on the
latter being tested it gave a distinct bile pigment, but no bile acid
reaction--a point which I shall afterwards have occasion to show, is of
a certain diagnostic value in obscure cases of jaundice. This
gentleman, under the influence of benzoic acid, perfectly recovered his
normal complexion in the short space of a week.

There is another form of jaundice from active congestion, viz., that
due to the presence of zymotic disease, such as ague, typhus, and other
fevers. As an illustration of this kind of affection, I shall cite one
arising from the first of these causes, namely, ague. And the best
example I {28} can give is one that has recently fallen under my
notice, and which occurred in the person of a member of our own
profession. The gentleman was for several years surgeon to one of our
large colonial hospitals, but in consequence of repeated attacks of
intermittent fever, was forced to resign the appointment, as well as a
lucrative practice, and return to England. He has now been at home for
two years, and although his general health has much improved, still
suffers from occasional attacks of his old enemy. On consulting me
regarding his case several months ago, he mentioned, that while
suffering from the above-named attacks, he occasionally suddenly passed
five or six ounces of urine as dark as chocolate, and this would recur
perhaps once in twenty-four hours, during two or three days, and then
as suddenly disappear. This urinary symptom being an unusual one, I
requested him to send me on the next occasion a specimen of the fluid.
In the beginning of last November[9] I received three samples of urine,
one passed at eight A.M., which was clear, pale, of a specific gravity
of 1025, of an acid reaction, deposited no lithates, and contained no
albumen, being in fact normal in every respect; another quantity passed
at two P.M., of {29} a chocolate brown colour, opaque, turbid, having a
specific gravity of 1032, of an acid reaction, depositing lithates,
containing albumen,[10] some sugar, and a large excess of urea (3·6 per
cent.) and urohæmatine; a third sample passed at night, of a specific
gravity of 1021, also with an acid reaction, depositing lithates in
small quantity, but containing no albumen. The percentage of urea in
this urine was exactly one-half (namely, 1·8) of what it was in the
preceding specimen passed at two P.M.

[Footnote 9: This was written last year, and therefore refers to
November, 1861.]

[Footnote 10: When examined with the microscope, this specimen of urine
was found to contain a large quantity of nucleated epithelium, and
granular cells; free granules of a hæmatine colour, granular
tube-casts, and a quantity of mucus; while the morning and evening
urines were perfectly free of any such substances.]

The varying conditions of these three urines clearly pointed to intense
congestion of the chylopoietic viscera, of a transient and periodic
character. Suiting the practice to the theory, mercurials were taken by
this gentleman in order to remove the congestion of the chylopoietic
viscera, and with the most favourable results, for, as I afterwards
learned, the jaundice and other disagreeable symptoms soon disappeared.


_Jaundice the Result of Passive Congestion of the Liver._

In this case the congestion, instead of arising from an increased flow
of blood to the liver, as {30} in the preceding, is the result of some
cause impeding the outward flow of blood from the liver. Thus for
example, passive hepatic congestion may arise from valvular disease of
the heart, or from any pulmonary affection obstructing the circulation
of blood through the lungs (pneumonia, &c.). Jaundice from the passive
form of hepatic congestion, is not so common as jaundice from the
active form, in consequence of the former being, as a rule, much
slighter than the latter. Its pathology is, however, I believe, exactly
the same, viz. the result of the engorged hepatic capillaries
compressing the secreting cells and tubes, and thereby annulling their
functions. Such being the case, it is unnecessary for me to do more
than merely allude to this cause of jaundice.

It may, perhaps, be asked--"If the foregoing statements regarding the
pathology of jaundice from congestion be correct, how does it happen
that it is not present in every severe case of gastric derangement,
fever, heart-disease, &c.?" This question is easily answered, for as
Dr. Budd has clearly put it, while speaking of the action of medicines
upon the liver--"In most persons, perhaps, a portion of the liver may
waste or become less active without sensible derangement of health,
they have more liver, as they have more lung, than is absolutely
necessary. In others, on the {31} contrary, the liver, from natural
conformation, seems just capable of effecting its purpose under
favourable circumstances." Persons inheriting this feebleness of liver,
"or in whom, in consequence of disease, a portion of the liver has
atrophied, or the secreting element of the liver has been damaged, may
suffer little inconvenience as long as they are placed in favourable
circumstances, and observe those rules which such a condition
requires;" but as soon as the balance of their hepatic circulation is
disturbed by causes like those above mentioned, jaundice makes its
appearance; such patients being, as Dr. Budd says, "born with a
tendency to bilious derangements."[11]

[Footnote 11: Diseases of the Liver, p. 55.]


JAUNDICE AS A RESULT OF SUPPRESSION CONSEQUENT UPON ABSENCE OF THE
SECRETING SUBSTANCE.

The pathology of this state is self-evident, for wherever secreting
substance is wanting, secretion cannot take place. If then, the tissue
which secretes bile be destroyed or transformed by disease, the biliary
function must be suspended, and the ingredients which it is the office
of such structure to separate from the blood, will accumulate in the
circulation, and give rise to the {32} usual chain of results following
suppression of the biliary secretion.

In cancer, tubercle, fatty and amyloid degeneration of the liver,
jaundice arises from the above-named cause. In these diseases it is
not, however, a constant symptom, and this is simply on account of
there being usually sufficient healthy tissue left to enable the
biliary secretion to be carried on. If the cancer, or other morbid
product, occupied the whole place of the secreting tissue, the biliary
function could no more be carried on by such product, than by the same
product occupying another organ of the body. In cases of jaundice
arising from absence of the secreting substance, the amount of the
jaundice depends on another cause besides the mere extent of the morbid
deposit. This is its situation. A large amount of diseased tissue may
exist in certain portions of the liver, and yet fail to produce
jaundice, while a much smaller amount of the same diseased tissue,
placed in another situation, may induce it. Should the morbid deposit,
for example, be so placed as readily to interrupt the flow of the
secreted bile, jaundice may rapidly occur, and be due as much to the
re-absorption of the secreted bile, as to the suppression of the
biliary secretion. This is, indeed, the true explanation of the fact,
that diseases affecting the {33} concave, are much more frequently
accompanied with jaundice, than those attacking the convex surface of
the liver. I might have chosen what at first sight appears a more
typical example of absence of secreting structure, namely, a case of
acute atrophy of the liver; for in such cases the hepatic tissues
sometimes dwindle down in the course of a few days to less than a
quarter of their original bulk, and give rise to intense jaundice. But
in such cases there does not appear to be a total arrest of the
secretion, until the very last stage of the disease, if it even occurs
then; and besides, if I dare form an opinion from one case, I should
say that, in consequence of the rapid disorganization of the parenchyma
of the liver, the circulation in the organ becomes much disturbed, and
gives rise to what Frerichs terms disordered diffusion. So that in
cases of acute atrophy of the liver, the jaundice, although chiefly due
to suppression, is complicated with re-absorption of the bile, as was
proved in a case I examined, by finding in the urine, not only those
products which are merely excreted from the blood, but also some of
those which are generated in the liver itself. It will be necessary for
me, therefore, to go more fully into this form of jaundice than I have
done in any of the preceding forms of the disease.


{34} JAUNDICE ARISING FROM ACUTE ATROPHY OF THE LIVER.

Acute, or yellow atrophy of the liver, is one of the most formidable of
human diseases. It is sudden in its onset, rapid in its course, fatal
in its termination. It is more common in women than in men; seldom
attacks those above thirty years of age, and occurs most frequently in
the earlier months of pregnancy. The immediate exciting cause of this
strange disease appears to be, in the majority of cases, mental
depression. The symptoms usually observed are jaundice, rapidly
followed by sickness, and vomiting; by febrile excitement, and cerebral
disturbance.

As the disease advances, the hepatic dulness diminishes; the urine
becomes scanty, and high-coloured; the bowels confined. Extravasations
of blood take place under the skin; and hæmorrhages from the nose,
vagina, or bowels are frequently observed. Lastly, delirium, or coma,
generally closes the scene, within a week after the commencement of the
violent symptoms, and within a month after the appearance of simple
jaundice. Frerichs, who has so well described these cases, even says,
"that in the severest forms, the disease may run its course, and end
fatally within twenty-four hours."[12]

[Footnote 12: "Clinical Treatises on Diseases of the Liver," vol. i. p.
197.]

{35} All cases of acute atrophy of the liver are, fortunately, not
necessarily fatal. In some the violent symptoms gradually disappear,
and recovery takes place after free evacuation of the bowels.

In every case of suspected acute atrophy of the liver, the urine ought
to be carefully examined for tyrosine, and leucine, two abnormal
products, which, according to Frerichs, are never absent. Some remarks
on the diagnostic value of these substances will be found at page 62.

Through the kindness of Dr. Wilks, I had the opportunity of examining
the liver, and analysing the urine, in a typical case of acute atrophy,
which he reported in the Pathological Society's "Transactions," vol.
xiii. p. 107. The brief history of the case is as follows:--E. K., aged
seventeen, a married woman, in the third month of pregnancy, was seized
with a bilious attack, and jaundice, after having a violent quarrel
with her husband, who accused her with infidelity. The patient was
first under the care of Mr. Bisshopp, of South Lambeth, who found her
suffering from jaundice, accompanied by some febrile symptoms, and
vomiting. In two days she became delirious, had violent screaming, and
convulsive fits, which were rapidly followed by unconsciousness. Next
day the patient was seen by Dr. Wilks; she was then quite insensible,
with slight stertorous breathing, {36} and foam on the lips. The pupils
were moderately dilated, and sensible to light. The pulse 120. The
hepatic dulness reduced to a narrow band over the lower ribs. No urine
had passed for twenty-four hours; a catheter was therefore introduced,
and twelve ounces of clear bilious-looking fluid were drawn off. This
urine I had the opportunity of analysing a few days afterwards. It was
then of a yellow-ochre colour, and contained a considerable deposit.

        The analysis gave:
  Specific gravity . . . . . . . . . . . . .    1028
  Reaction . . . . . . . . . . . . . . . . .    acid (?)
              IN 1000 PARTS.
    Water  . . . . . . . . . . . . 948·860
    Solids (organic, inorganic)  .  51·138
                                   =======
  Urea . . . . . . . . . . . . . . . . . . .  30·000
  Uric acid  . . . . . . . . . . . . . . . .   0·375
  Resin and mucus  . . . . . . . . . |
  Bile, colouring matter, and acids  |
  Urohæmatine  . . . . . . . . . . . | . . .  14·575
  Leucine, and tyrosine  . . . . . . |
  Inorganic salts  . . . . . . . . . . . . .   6·188
                                              ======

The biliary acids (contrary to what Frerichs found in some of his
cases) were present in this urine in fair quantity. With Pettenkofer's
test (sulphuric acid and sugar) a decided purple colour was obtained.

{37} When a portion of the urine was concentrated, and allowed to
crystallize slowly, beautiful crystals of both tyrosine, and leucine
were detected in it by means of the microscope. The purified urine also
showed the presence of sugar in small quantity. When the organic solids
were burned, they had a strong odour, and gave off a smoky _flame_,
thereby showing that the urine contained a considerable quantity of
fatty resin.

As calculating the constituents of the urine by _percentage_ is a very
unsatisfactory method for scientific purposes, it may be useful for me
to give the analysis of the same urine as calculated for twenty-four
hours, viz., twelve ounces, the amount drawn from the bladder shortly
before death. In that case the analysis gives:

             24 HOURS' URINE.
  Quantity . . . . . . . . . . . . .  372·00 c.c.
  Specific gravity . . . . . . . . .    1028
  Reaction . . . . . . . . . . . . .    acid (?)
  Solids (total) . . . . . . . . . .  19·038 grammes.
  Urea . . . . . . . . . . . . . . .  11·160    "
  Uric acid  . . . . . . . . . . . .   0·139    "
  Resin, and mucus . . . . . . |
  Bile pigment, and acids  . . |
  Urohæmatine  . . . . . . . . | . .   5·441    "
  Tyrosine, and leucine  . . . |
  Inorganic salts  . . . . . . . . .   2·298    "
                                      ======

During the night before her death, the patient {38} aborted, and lost a
considerable quantity of blood by the vagina. The whole duration of the
disease was merely six days, and the more urgent symptoms only
manifested themselves two days before the fatal termination.

After death the liver was found to be very small in size, not
exceeding, as was supposed, 1½ pound in weight. It was deeply stained
yellow, and its cells were found to be small, and broken up; not an
entire cell could be detected by either Dr. Wilks or myself--nothing,
indeed, but a quantity of _débris_ of hepatic tissue, and fat. The
gall-bladder was contracted, and contained only a little mucus; the
urinary-bladder was empty.

Although jaundice the result of acute atrophy of the liver, might be
thought to be a typical example of jaundice arising from a suppression
of the biliary function--the diminution in secreting substance
naturally inducing a diminution in secreting power--I have, as was
before said, been led to view it differently; because, although less
bile than usual is secreted, there is nevertheless nothing like an
entire suppression of the biliary function, as is proved,--

Firstly,--By the absence of pipe-clay stools.

Secondly,--By the deep staining of the hepatic tissue with bile
pigment, just as occurs in jaundice the result of obstruction.

{39} Thirdly,--By the presence of the biliary acids in the urine.

Fourthly,--and lastly, the violent symptoms of bile-poisoning lead to
the same conclusion, for it is not bile pigment, but the bile acids,
that induce the fatal symptoms of bile-poisoning.[13]

[Footnote 13: Six grains of pure glycocholate of soda killed a small
dog, into whose femoral vein I injected it, in the course of two hours.
In experimenting on animals, I have made the curious observation, that
although bile has the property of retarding or arresting putrefaction,
both in the intestinal canal, and out of the body, yet, when injected
into the subcutaneous cellular tissue of a healthy animal, it causes
the surrounding tissues to decompose, and become foetid, and an
artificial disease is thereby set up, whose most peculiar feature is
the engendering of a rapid putrefaction of the body after death.]


CLASS B.

THE MECHANISM OF JAUNDICE ARISING FROM THE RE-ABSORPTION OF THE
SECRETED, BUT RETAINED BILE.

In cases of this kind, the obstruction is not usually to be found
within the liver itself, but in the ducts after their exit from the
hepatic organ. The seat of the obstruction, too, is much more
frequently found near to, or at the termination of the common duct,
than close to the liver. The obstruction may be of three kinds:--

{40} Firstly,--A congenital deficiency of the bile-ducts.

Secondly,--An accidental obstruction in the course of the ducts, as
from gall-stones, hydatids, or the entrance of foreign bodies from the
intestines.

Thirdly,--From closure of the outlet of the common duct, as, for
example, from the pressure of the pregnant uterus, or distended
transverse colon, or from organic disease of the pancreas, or
neighbouring organs.

First, as regards cases of jaundice from congenital deficiency of the
ducts. Cases of this kind are rare. The best with which I am acquainted
is the one that was brought before the Pathological Society last year,
by Dr. Wilks. "The child had never passed any meconium, the motions
always being of a white colour. When a fortnight old, jaundice came on,
and continued until death, at the age of six weeks. After death, the
liver was found of a dark green colour, and, apparently, the
gall-bladder was absent. On further examination, however, the cellular
tissue, which appeared to occupy its place, was found to be occupied by
a small canal, just large enough to contain a bristle; to this,
however, no outlet could be found, and on endeavouring to discover the
hepatic ducts, these, in like manner, could not be made {41} out. The
opening of the common duct in the duodenum was natural, but no hepatic
duct could be found joining the pancreatic. It appeared, therefore, as
if the larger ducts had become shrunken and obliterated."[14]

[Footnote 14: "Medical Times and Gazette," 29th March, 1862.]

Through the kindness of Dr. Wilks, I had the opportunity of making a
microscopical examination of the liver. The hepatic cells were very
small in size, much broken up; very few possessed nuclei, and all were
deeply tinged with brownish yellow colouring matter. Scattered
throughout the hepatic tissue, I found numbers of well-formed
cholesterine crystals, like those represented in Fig. 3.

I must here mention, that jaundice does not necessarily follow upon
absence of the gall-bladder; just as in the horse, the deer, the rat,
and other animals that possess no gall-bladders, the biliary function
is perfectly well carried on, so it may be in the human subject,
labouring under a congenital or accidental deficiency of the
gall-bladder. In such cases, the hepatic ducts are pervious, and
consequently the secreted bile finds no difficulty in reaching the
intestines. In the "Edinburgh Medical Journal" (May, 1861, p. 1045,)
Dr. Alexander Simpson reports a case of {42} this kind occurring in a
child, which died when only a few weeks old. There was no trace of the
existence of a gall-bladder; but on laying open the duodenum, the
orifice of the bile-duct was at once seen in its ordinary situation,
and a drop of pale bile was expressed from it. On tracing the duct to
the liver, it was found to pass up undivided into the horizontal
fissure, where it at once broke up and branched into the hepatic tissue
of the right, and left lobes.

I shall delay entering into an explanation of the mechanism of jaundice
from obstruction, until I come to the consideration of what may be
termed _Permanent Jaundice_, as in that case one explanation will do
for all.


JAUNDICE AS A RESULT OF THE ACCIDENTAL OBSTRUCTION OF THE BILE-DUCTS.

The second class of cases, namely, those in which the obstruction is in
the course of the ducts, are of frequent occurrence, and in them the
jaundiced state is usually merely transient, for no sooner has the
obstruction been removed, than the jaundice begins to disappear. The
most common cases of this kind are those arising from gall-stones. As
every one is familiar with their history, I may merely mention, that we
may have gall-stones, and even all the most painful {43} symptoms of
gall-stones, without the slightest trace of jaundice. This, I believe,
arises in the following manner:--

Firstly,--The majority of gall-stones are formed in the gall-bladder;
their formation being due to the accidental deposition of the less
soluble parts of the bile, either as a consequence of these ingredients
being present in excess, or in consequence of the solvent, whose duty
it is to retain them in solution, being in reduced quantity. The
deposition or formation of gall-stones follows exactly the same law as
the deposition or formation of stone in the bladder.

Secondly,--In some cases the gall-stone, or stones--for there may be
many, even hundreds, remain in the gall-bladder during the whole life
of the individual, without giving rise to any disagreeable results,
either as regards pain, or jaundice. In other cases, the
gall-stones--and this usually happens when they are small--get into the
cystic duct, and become lodged there; and in such a case, although the
patient may suffer intense pain, there is still no jaundice. Moreover,
it is not until the stone or stones have passed down into the common
bile-duct, that jaundice is at all likely to be induced by them. For
while a stone remains in the cystic duct, although it may completely
block it up, and effectually prevent the bile either {44} entering into
or escaping from the gall-bladder, yet, as in this situation it cannot
offer any obstacle to the direct flow of the biliary secretion from the
hepatic tissue into the intestines, there is no retention, and
consequent absorption of bile. In fact, the presence of the stone in
this position, in as far as the biliary function is concerned, only
reduces the patient to the state of a person in whom the gall-bladder
is accidentally absent; or to that of a horse, or other animal, in
which the absence of the gall-bladder is a normal condition.

Thirdly,--There are yet other ways in which gall-stones may give rise
to great discomfort, and even imperil life, without inducing jaundice.
For example, a calculus may remain in the gall-bladder until it attains
a very large size, and then ulcerate its way into the stomach,
intestines,[15] peritoneal cavity, or even out of the body through an
opening in the abdominal parietes.[16]

[Footnote 15: _Vide_ a case of this kind published by the author in the
Pathological Society's "Transactions" for 1857, p. 235.]

[Footnote 16: _Vide_ a case published by Mr. Hinton in the "Brit. Med.
Journ." of August 4th, 1860, p. 603, and one by Mr. Sympson in the same
Journal of the 7th February, 1863, p. 139.]

In fact, jaundice only appears as a complication of gall-stones when
they chance to block up the common duct, and thereby prevent the bile
entering the intestinal canal. Hence, also, the reason {45} why
jaundice, as a result of gall-stones, is more frequently transient than
permanent. If it chances to become permanent, it sooner or later leads
to a fatal termination--usually within eighteen months after complete
obstruction. Lastly, it may be mentioned that, although gall-stones are
liable to form in almost every constitution, yet it is generally
considered that they are most frequent in persons of the tubercular,
cancerous, and gouty diathesis, either hereditary or acquired.

There are other substances besides gall-stones which, by their
accidental presence in the bile-ducts, may give rise to jaundice. Thus,
for example, foreign bodies, such as cherry-stones, have found their
way from the intestine into the bile-duct, and given rise to jaundice.
Intestinal worms have been observed to do the same thing, and recently
an interesting case of jaundice, occurring in a girl aged 16, who died
after a few weeks' illness, has been reported, which resulted from the
presence of hydatids in the ductus hepaticus, and ductus communis
choledochus.[17] Hydatids of the liver itself seldom give rise to
jaundice, their position being usually such as not to interfere with
the biliary function.

[Footnote 17: Dr. Dickinson has reported this case in the Pathological
Society's "Transactions," p. 104, vol. xiii. 1862.]

There are still other cases where we find {46} transient jaundice
arising from accidental obstruction of the bile-ducts; but in them,
instead of the closure of the ducts resulting from plugging from
within, it arises from the application of pressure from without. Thus,
for example, transient jaundice is met with as the result of closure of
the common bile-duct, by pressure exerted upon it by the pregnant
uterus, or by impacted fæces in the transverse colon. Certain permanent
abdominal tumours may also lead to the same result, but these will with
greater propriety be considered under the next head.


PERMANENT JAUNDICE FROM OBSTRUCTION.

In order to give as clear a view as possible of the pathology of
permanent jaundice from obstruction, it will be necessary for me to
give the history of a case of closure of the outlet of the common
bile-duct in consequence of organic disease--such, for example, as
cancer of the head of the pancreas. A case of this kind has the further
advantage of at the same time furnishing us with a typical example of
jaundice arising from the re-absorption of the secreted, but retained
bile.

When cancer of the head of the pancreas involves the orifice of the
common bile-duct, as the tumour grows, the duct slowly, and gradually
becomes impervious to the passage of bile into the {47} intestines,
until at length the flow is completely arrested. As this gradual
process of occlusion of the outlet goes on, the duct itself becomes
more and more distended by the retained bile, till it at length attains
an enormous size. The gall-bladder being equally prevented from
emptying itself, likewise becomes stretched and dilated, until it may
at last become not only palpable to the touch, but even apparent to the
eye through the abdominal walls. This was the case in the patient whose
liver, and occluded ducts are represented in Plate I.

The distention of the bile-ducts is not limited to those situated
external to the liver, but also affects those in the substance of the
organ; and to such an extent may this be the case, that, on making a
section of a liver that has long had its common duct obstructed, a
number of large excavations are observed all over its surface, which
excavations are nothing more than the open mouths of the transverse
sections of the dilated ducts. Such a state of matters is tolerably
well represented in the section of the liver in Plate I. Further, the
effect of this obstruction to the exit, and consequent accumulation of
the biliary secretion, is not confined to the mere distention of the
ducts, but causes various changes to occur in the parenchyma of the
liver itself. The first of these is an increase {48} in the size of the
organ, arising partly from the accumulation of the bile, and partly
from the congestion caused by the pressure exerted on the vessels by
the distended ducts. In the second place, gradually as the state of
matters here described progresses, the parenchyma of the organ becomes
itself affected, partly from the direct pressure exercised upon it, and
partly from the derangement of its nutrition, produced by the
interruption to the hepatic circulation; so that, after a time, the
enlarged liver slowly, and by degrees diminishes, until it at length
regains its natural size, thereby rendering, at this period of the
disease, the diagnosis of the case extremely difficult. This state of
matters is not, however, of long duration; for, in consequence of the
continued compression of the blood-vessels and parenchyma, the
nutrition of the liver is so disordered, as to lead to a gradual
shrinking of the entire substance, or, in other words, to a general
atrophy of the organ.

It is thus seen how in _permanent occlusion_ of the common gall-duct
the liver may be found _hypertrophied_ in the _first_, of _normal
dimensions_ in the _second_, and _atrophied_ in the _third_ and _last
stage_ of the disease.

In cases of the kind here described, it is not at all unlikely that the
enlargement of the liver in the earlier, as well as its atrophy in the
later {49} stages of obstruction, may be mistaken for the cause of the
jaundice, instead of the result of the arrest of the flow of bile, and
thereby lead to a grave error in treatment. The history of the case,
together with a knowledge of the above facts, will, however, tend to
facilitate the diagnosis. Thus, it must be ascertained:--

Firstly,--If the jaundice preceded the alteration in size of the organ.

Secondly,--If there is an absence of any history of hepatitis; and,

Thirdly,--If there is no evidence of any pulmonary or cardiac mischief
likely to lead to passive congestion of the hepatic tissue.

Even with a knowledge of all these facts, however, it often baffles the
skill, and acumen of the ablest physicians to discover the cause of
jaundice. Every now and then cases are met with, where the patient
tells us that the jaundice has gradually come on without any assignable
cause, and where, after the most careful examination of his history, as
well as of his physical condition, we fail to detect a clue to the
diagnosis. Cases of this kind are far from uncommon, and this is the
more to be regretted, seeing that unless we have a clear appreciation
of the cause, it is not only difficult, but even dangerous to treat the
symptom. The injudicious administration of {50} a remedy here, may
hasten the termination we most desire to retard. The truth of this
remark will, however, be better appreciated when I come to consider the
rationale of the treatment of jaundice. Meanwhile, it may be advisable
to point out a method capable of yielding most important information,
when all the ordinary means of diagnosis fail. I allude to the
chemistry of the excretions. Although the pathological chemistry of the
excretions is as yet in its infancy, it has already given the
scientific physician a key to the detection of several diseases, and I
trust to be able to show, that even in the obscure cases of jaundice
above alluded to, it not only gives us a clue to their cause, but
presents us with a guide to their treatment.

In jaundice arising from obstruction, the pipe-clay stools are, as in
the case of jaundice from suppression, entirely due to the absence of
bile from the intestinal canal. The yellowness of the skin is in like
manner caused by the accumulation of the bile pigment in the blood,
from whence it exudes, and stains the tissues; and, lastly, the
saffron-coloured urine results in a similar way from the elimination of
the pigment from the blood by the kidneys. Instead, however, of these
three conditions arising, as in the case of jaundice from suppression,
from the arrest of the biliary functions {51} allowing certain of the
constituents of the bile to accumulate in the circulation, they are, in
the first place, the result of the re-absorption of the secreted bile
from the distended ducts, and gall-bladder. So that while in jaundice
from suppression, only those biliary products which exist pre-formed in
the blood accumulate in the circulation, in cases of jaundice from
obstruction, the biliary products which are manufactured in the liver,
equally with those which are pre-formed in the blood, find their way
back into the circulation, to be from thence eliminated with the
excretions. If then, we could ascertain the presence or absence of
these products in the excretions, we should be enabled to distinguish
between jaundice resulting from suppression, and jaundice arising from
obstruction. Let us now see what the chemistry of the excretions
teaches us; and to begin, we shall take the intestinal excretion.


ANALYSIS OF THE INTESTINAL EXCRETION AS AN AID TO THE DIAGNOSIS OF
OBSCURE CASES OF JAUNDICE.

The intestinal excretion, in the natural state, consists, firstly,--of
those portions of our food which have resisted the action of the
digestive juices; secondly,--of the excess of the modified food
remaining unabsorbed; and, thirdly,--of the excess, {52} as well as of
the effete portions of the digestive secretions themselves.
Consequently, if from any cause the digestive secretions do not act
properly, the evacuation immediately becomes abnormal, and we can
discover by analysis which of the secretions is at fault. Thus, for
example, we know that the saliva acts upon the starchy matters of our
food, the gastric juice on the albuminous, the pancreatic on the fatty,
and that the biliary secretion so modifies the chyme as to allow of its
rapid absorption by the lacteal, and portal vessels. If then, from any
cause the elaboration, or excretion of any of these digestive juices be
interfered with, more of the particular kind or kinds of food on which
it acts, passes unchanged through the intestines. Thus, if the salivary
secretion be affected, an unusual amount of unmodified starch is found
in the stool. If the gastric juice is defective, more albumen than is
normal passes away unchanged, and so on with the others.

It is clear then, that an examination of the stools must afford us
important information regarding the presence, or absence of the normal
secretions. A simple inspection of the stool will sometimes at once
tell us whether or not bile is present. If it be present, the stool
varies from a pale yellow, to a dark olive-green hue, according to the
kind, and quantity of biliary colouring matter present, and {53} the
nature of the food. It must not be forgotten however, that unless care
be taken, the colour deducible from highly-coloured food may be
mistaken for an excess of bile. This remark is still more applicable to
medicines, for mercury, bismuth, iron, and some other mineral remedies,
give rise to dark evacuations so closely resembling bilious stools in
appearance, that the only way to distinguish them, is by chemical
analysis; when, the presence of the mineral, together with the absence
of the bile pigment, and the biliary acids (which are always to be
found in normal evacuations), will at once reveal the true nature of
the case. I have seen a mistake of this kind happen, and that too,
where a patient labouring under jaundice from obstruction, was thought
to be passing the usual amount of bile in his stools, when in reality
not a particle of bile pigment was present. The colour was in this case
entirely due to the food, and ferruginous remedies. Blood from the
stomach or bowels, is also apt to be mistaken for biliary matter, more
especially when acted on by the gastric juice, which has the property
of turning red blood brown. With these exceptions, the absence of bile
from the stool, is usually very easily ascertained. For if the patient
be taking no highly-coloured food, or any of the medicines above
indicated, the stools are of a {54} dirty pipe-clay colour. This is not
due to the presence of any new or foreign matter, but solely to the
absence of bile pigment. In these cases the evacuations, besides being
white, are usually of a most offensive odour, for, among other things,
bile checks intestinal putrefaction, and the development of offensive
gases.

In addition to the colour, and odour of the fæces, in cases of
jaundice, another important indication is to be found in the presence
of fat. The presence of fat in the stools was at one time looked upon
as evidence of pancreatic, at another time of hepatic disease; now,
however, experimental physiology has taught us, that it in some measure
depends upon both. For while, on the one hand, the pancreatic secretion
emulsions the fatty part of our diet, and thereby renders it capable of
absorption, recent researches, as has been already pointed out, have
established the fact that the biliary secretion also plays an important
part in the absorption of the oleaginous constituents of our food.
Bidder and Schmidt, as was before said, have shown that a dog, after
ligature of the gall-duct, absorbs less than half the average normal
quantity of fat; and by experiment it has been found that this arises
from the circumstance that bile emulsions only the acid fats, while
pancreatic juice transforms the neutral as well as the acid {55}
oleaginous matters. The presence of fat in the stools may be due,
therefore, partly to hepatic, partly to pancreatic derangement; and I
shall immediately point out how we can turn this fact to account in
diagnosis, and discover in cases of jaundice from obstruction, whether
the seat of the obstruction be at the outlet or in the course of the
duct.


EXAMINATION OF THE RENAL SECRETION.

The urine affords us important information in all cases of jaundice. In
fact, an examination of it alone would in many cases enable us to
discover the presence or absence of this affection.


_Diagnostic Value of the Colour of the Urine._

The urine of jaundice has invariably a peculiar tint, ranging from a
saffron-yellow to a dark olive-green, or almost black hue. It must not
be forgotten that the colour of normal urine varies with the degree of
concentration. Where little is passed, being of a high, where much is
passed, of a pale colour; the depth of colour depending on the degree
of dilution of the urohæmatine. Again, it must also be remembered that
there are many diseases, which change the colour of urine very
materially, some only deepening, others actually changing the tint.
Foods, and medicines also, {56} alter the colour of the renal
secretion. Rhubarb, and santonine give to it a saffron hue, arsenious
acid gas a black colour. Bearing in mind these facts, one would
hesitate before giving a decided opinion as to the presence or absence
of icterus from a mere inspection of the urine. For this reason, it is
generally recommended in cases of jaundice to pour a little of the
urine on a white plate, and watch the play of colours produced by
strong nitric acid. This method, however, is not always satisfactory,
for the play of colours depends on the different stages of oxidation
through which the pigment passes, and other animal pigments, besides
biliverdine, unfortunately act in a somewhat similar manner.

A very simple, and more convenient way of testing the pigment without
changing its physical characters, is to separate it in combination with
uric acid. This is readily done by simply acidulating the urine with a
few drops of hydrochloric acid, and setting it aside for twenty-four
hours to crystallize. The white uric acid in crystallizing takes up the
colouring matter, and assumes the hue of the pigment present in the
urine. I have thus obtained crystals of all the different hues from a
bright golden yellow tint through the intervening shades of red, brown,
blue, olive, to a dark, almost black colour. This experiment {57} has
another advantage, for if we take a measured quantity of urine, and
collect, dry, and weigh the uric acid obtained from it, we can readily
calculate the total quantity passed in the twenty-four hours, and
thereby assist in diagnosing the presence or absence of malignant
disease of the liver, as I shall afterwards have occasion to point out.

The urine of jaundice is generally described as being of a saffron
colour; but if I may be allowed to form an opinion from my own
observations, which are tolerably numerous, I should say that it, in
colour, much more frequently resembles old ale than anything else with
which I am acquainted. On standing, the colour changes very
considerably, in consequence of the pigment becoming slowly oxidized by
its exposure to the air. When there is a very great excess of bile
pigment present in the blood, the kidneys have some difficulty in
eliminating it. Occasionally even, it chokes up the renal capillaries,
and thereby complicates the jaundice by inducing secondary disease in
the kidney. In such cases the external surface of the kidney, after the
removal of the capsule, looks as if it had been sprinkled over with
ink. The black specks vary in size from the minutest visible point to
that of a pin-head. The accompanying chromo-lithograph (Plate II.)
represents a kidney in this condition. {58} It will also be observed
that it is studded over with a number of small abscesses; but whether
these resulted from the blocking-up of the capillaries just alluded to
or not, it is impossible to say. In the case in question no albumen was
detected in the urine during life, and it was only on careful analysis,
after the post-mortem had revealed the above state of matters, that a
small quantity was discovered; and even then, had not the experiment
been carefully performed, the presence of albumen might have been
overlooked.

[Illustration: Plate II. Kidney from a Case of Permanent Jaundice.]


_Diagnostic Value of the presence of the Bile-Acids in the Urine._

All acquainted with the recent literature of jaundice know how hard a
battle is being fought between two sets of observers in Germany,
regarding the presence of bile-acids in urine. One class, with Frerichs
and Städler at their head, believe that the biliary acids are
decomposed in the blood, and are consequently never to be detected in
the urine. The other class, headed by Kühne, state as positively that
they have detected these substances in the urine. Indeed, Kühne states
that by adopting Hoppe's method,[18] he never fails to {59} detect the
presence of the biliary acids in the urine of patients labouring under
icterus, as well as in the urine of dogs with the bile-duct ligatured.
When first studying this question, I was very much perplexed by these
contradictory statements, for neither the judgment, nor the power of
observation of either of the authorities could for a moment be called
in question; and on experimenting for myself, so unsatisfactory were
the results obtained, that I almost threw the question aside in
despair. On one occasion, however, I at length met with such
unmistakeable evidence of the presence of bile-acids in the urine, that
I could no longer doubt the fact of their existence, and was forced to
search for an explanation of the previous contradictory results.
Fortunately, it was not very long before a solution to the difficulty
was obtained, and, what was of still greater importance, led to the
observation that the contradictory results arose from a circumstance
which might be turned to account, as a means of differential diagnosis.
The discovery was, that in certain cases of jaundice not a trace of the
biliary acids is to be detected in the urine, although the {60} bile
pigment is present in abundance; while in certain other cases both
biliary acids, and bile pigment occur in notable quantity. What, then,
is the cause of this difference? Simply this. In jaundice from
suppression the liver does not secrete bile; consequently no bile-acids
being formed, none can enter the circulation, and they are therefore
not to be detected in the urine. In jaundice from obstruction, on the
other hand, bile is secreted, and absorbed into the blood; and the
bile-acids not being all transformed in the circulation, as Frerichs
supposed, are eliminated by the kidneys, and appear in the urine, where
they can be detected by Hoppe's method, or even, with proper
precautions, by simply adding sulphuric acid and sugar. Here, however,
some skill and experience are requisite, in order not to confound the
colour produced by the action of the reagents on other substances with
the fine purple produced by the biliary acids. As the majority of cases
of jaundice result from suppression of the hepatic function, and as
many of the cases of obstruction ultimately merge into the former, it
is easily understood how the existence of the biliary acids in the
urine has been so frequently denied. I have myself seen, in a case of
obstruction of the common duct, the biliary acids slowly and gradually
diminished in the urine, until they at length almost entirely {61}
disappeared as the case approached a fatal termination. Here the
disappearance of the biliary acids went on step for step with the
impairment of the secreting powers of the liver, in consequence of the
pressure exercised on its parenchyma by the retained bile.

[Footnote 18: Professor Hoppe tests for bile-acids in the following
manner:--The urine is boiled with an excess of milk of lime for about
half an hour, and filtered to free it from the precipitate thus formed.
The filtrate is evaporated to dryness, decomposed with hydrochloric
acid, washed with water, and then extracted with alcohol. The alcoholic
extract contains the bile-acids, which are recognised by Pettenkofer's
test.]

The readiest mode by which the biliary acids may be detected is the
following: To a couple of drachms of the suspected urine add a small
fragment of loaf-sugar, and afterwards pour slowly into the test-tube
about a drachm of strong sulphuric acid. This should be done so as not
to mix the two liquids. If biliary acids be present, there will be
observed at the line of contact of the acid, and urine--after standing
for a few minutes--a deep purple hue.[19] This result may be taken as a
sure indication that the jaundice is due to obstructed bile-ducts. On
the other hand, the absence of this phenomenon, and the occurrence of
merely a _brown_ instead of a _purple_ tint, although, in the earlier
stages of jaundice, equally indicative of suppression, is of course,
for the reasons already given, no indication of the cause of the
suppression. That must be gleaned from other circumstances.

[Footnote 19: The immediate formation of a reddish coloured line is due
to the acid setting free urohæmatine, the normal colouring matter of
the urine.]

It is seen that I have taken no notice of {62} Frerichs' theory
regarding the bile-acids being changed into bile pigment. I have done
so advisedly, feeling as I do, that when that observer investigates the
subject more fully, he will himself abandon such an untenable doctrine,
founded as it is, on an erroneous view regarding the nature of bile
pigment. The colour induced by sulphuric acid on the acids of the bile,
is as different in its chemical nature from animal pigment, as any two
substances can possibly be. Indeed, they have no bond of connection
whatever, except the mere tint. All animal pigments, whether they be
green, like bile-colouring matter, or red, like hæmatine, spring from
the same source, and contain iron. Besides this, the mere fact of an
increase of animal pigment being found in the urine after the
bile-acids have been injected into the circulation, to which Frerichs
attaches such importance, in reality proves nothing more, as Kühne
pointed out, than that an increased destruction of blood corpuscles has
taken place. I have found the urine of dogs loaded with dark colouring
matter after injecting chloroform, and other stimulants into their
portal veins, in order to establish artificial diabetes; and,
assuredly, in these cases the presence or absence of bile-acids in the
blood had nothing to do with the result.


{63} _Diagnostic Value of the presence of Tyrosine, and Leucine in
Urine._

There are two other abnormal products occasionally met with in the
urine of jaundice, namely, tyrosine, and leucine. These substances,
although for many years known to chemists, attracted comparatively
little attention until Frerichs discovered their diagnostic value in
hepatic disease.

[Illustration: FIG. 4.--Crystals of pure tyrosine, obtained from the
urine of a case of chronic atrophy of the liver, following upon
obstruction of the bile-duct. _(a)_ Large crystals. _(b)_ The more
common form of the stellate groups of needle-shaped crystals. _(c)_ A
few separate fragments of needle-shaped crystals.]

In that peculiar form of complaint, described as acute or yellow
atrophy of the liver, the {64} urine is said invariably to contain
tyrosine, and leucine. The presence of these substances may therefore
assist us in diagnosing the case. When tyrosine, and leucine are
present in quantity, they are very readily detected, all that is
required being slowly to evaporate an ounce of urine, to the
consistency of syrup, put it aside during a few hours to crystallize,
and then examine it with the microscope. The tyrosine is recognised by
being in fine stellate groups of needle-like crystals, as represented
in fig. 4, or spiculated balls not unlike a rolled-up hedgehog, with
the bristles sticking out in all directions.

[Illustration: FIG. 5. Spiculated balls of tyrosine, from the urine of
a case of acute atrophy of the liver. When these were re-dissolved,
purified, and re-crystallized, they assumed the form represented in
Fig. 4 _(b)_.]

{65} Tyrosine may be obtained in a pure state by adding to four ounces
of urine a solution of acetate of lead, till a precipitate ceases to
form, filtering, and freeing the liquid from the excess of lead by a
current of sulphuretted hydrogen, again filtering, and evaporating the
clear solution. The tyrosine is now colourless, and crystallizes with
the microscopic characters above alluded to, but still better marked.
Tyrosine may be further recognised by putting a few crystals on a
platinum spatula, adding a drop or two of nitric acid, and evaporating
to dryness. If present, the yellow residue thus obtained assumes a
pumpkin hue on the addition of potash, and leaves on incineration a
dark greasy stain. Frerichs recommends another test, namely, the
following:--Put the suspected substance into a watch-glass, along with
some sulphuric acid, and after they have been in contact about half an
hour, dilute the mixture with water. Next boil, and then neutralize
with carbonate of lime. Filter, and to the clean filtrate add a few
drops of perchloride of iron, devoid of free acid. The formation of a
dark violet blue colour indicates the presence of tyrosine.

Leucine is known by its flat, circular, oily-looking discs, without any
crystalline structure. At the first glance, a globule of leucine might
be mistaken for oil, not only on account of its {66} microscopical
characters, but also on account of its being lighter than water. The
globules of leucine are distinguished from those of oil by their being
soluble in water, and boiling alcohol, and insoluble in ether. Besides
this, the discs are occasionally opaque and laminated like the granules
of potato starch. They are then not at all unlike microscopic crystals
of the carbonate of lime; but the carbonate of lime crystals sink in
water.

[Illustration: FIG. 6. Dark globules of leucine of various sizes,
resembling in appearance globules of carbonate of lime.]

Both tyrosine, and leucine are usually deeply impregnated with the
colouring matter of the urine.

Since Frerichs' views were first published I have found tyrosine, and
leucine in the urine of cases of chronic, as well as of acute atrophy
of the liver. Their presence may therefore aid in diagnosing the latter
as well as the former condition of the hepatic organ.

{67} I have little doubt that future research will discover other
conditions of the liver, besides those just mentioned, in which
tyrosine, and leucine, may appear in the urine; for, as will be
subsequently pointed out at page 96, I have been successful in
producing them artificially in the urine of animals in which there was
no evidence either of acute or chronic atrophy of the liver having
taken place. In the cases cited, indeed, it will be seen that the
jaundice was the result of suppression, consequent upon congestion of
the liver, produced by blood poisoning.

It may be added that since these observations were made I have found in
the artificially concentrated urine of a case of jaundice from
obstruction consequent upon impacted gall-stone, a few balls closely
resembling leucine in shape, and size, but differing from it in being
excessively dark in colour. No tyrosine crystals were observed, and
unfortunately there was not sufficient of the leucine-like substance
present in the urine to admit of its being chemically tested. I have
thought it my duty to record this fact for the benefit of other
observers, as there can be little doubt that we are gradually verging
towards some important discovery in a diagnostic point of view.


{68} _Melanine in the Urine._

Four years ago (1858), Dr. Eiselt of Prague called attention to the
fact that in cases of melanotic cancer of the liver, melanine appears
in the renal secretion.[20] When the urine is passed it is usually
quite clear; but after standing it becomes of a dark colour, even as
dark as porter, without, however, losing its transparency. This
deepening of the colour is no doubt due to the oxidation of the
melanotic pigment, as the employment of an oxidizing agent, such as
nitric or chromic acid, causes the same change to occur instantly.

[Footnote 20: Dr. Eiselt states that he also found melanine in the
urine in a case of melanotic cancer of the eyeball.]

In addition to the cases related by Dr. Eiselt, I am able to add one of
considerable importance, as it not only offers a striking illustration
of the correctness of his views, but has the double advantage of being
an unbiassed record of facts, in consequence of its having been
observed, and recorded long before Dr. Eiselt's views were published,
and therefore at a time when the author had no idea of its
significance. The case occurred about thirteen years ago, in the wards
of the Royal Infirmary of Edinburgh. The history of the case I extract
from my private note-book. It is briefly as {69} follows:--In the month
of May a sailor was admitted into the clinical wards of the Royal
Infirmary with symptoms of jaundice from enlarged liver. He stated that
he had been a great deal abroad, in hot climates, and admitted that he
had been a hard drinker. On admission his skin was of a dusky yellow
colour, and had been so since the month of February. The liver was
considerably enlarged, and he complained of sudden violent pains in the
neighbourhood of the umbilicus. The pain was usually most severe during
the night. The urine was of a dark colour, and on the addition of
nitric acid, became nearly quite black. It contained no albumen. The
patient died ten days after admission. On post-mortem examination, the
hepatic duct was found blocked up with malignant deposit, and the liver
of a dark green colour. There was also a considerable amount of
malignant deposit in the mesentery. This patient, as frequently happens
in such cases, became delirious before death.

In jaundice arising from melanotic cancer of the liver, the recognition
of the presence of melanine in the urine would be an important aid to
the diagnosis. Care must be taken not to confound the dark olive-green
urine occasionally met with in other forms of jaundice, with the
melanotic urine just described, or both {70} patient and doctor may
become unnecessarily alarmed.[21]

[Footnote 21: While I was Resident Physician in the Royal Infirmary of
Edinburgh, in 1850, a woman, aged 28, was admitted with a universal and
bright jaundice of three weeks' standing. Her urine was high coloured,
and of a specific gravity of 1022. It contained a small quantity of
albumen, and became perfectly black on being boiled with nitric acid.
In this case there was no reason to suspect malignant disease of the
liver; the colour of the urine was, therefore, most probably due to the
bile pigment being more than usually oxidized. After a six weeks' stay
in the hospital, I dismissed the patient as cured.]


_Urea, Uric Acid, and Sugar._

The presence, and quantity of certain other substances met with in the
urine of jaundice, although not peculiar to that condition,
nevertheless afford us important information, not only as to its cause,
but also as to its probable mode of termination.

Firstly, a correct knowledge of the quantity of urea, and of uric acid
passed in the twenty-four hours is of great value; and, secondly, the
presence, or absence of sugar is a fact which ought never to be lost
sight of. The value of this statement, as well as of several of the
preceding, will, I think, be better appreciated by giving a short
account of a case of obscure disease (where a correct diagnosis, and
prognosis could not have been arrived at without the application of the
chemical knowledge referred to), than by any mere abstract {71}
treatment of the question. I shall, therefore, at once proceed to
relate the brief history of the case.

A gentleman, aged fifty, who had been a remarkably healthy man,
observed, within eighteen months of his death, that his skin gradually
assumed a more and more jaundiced tint without any assignable cause.
The stools were clay-coloured, the urine loaded with bile pigment. Soon
afterwards, the patient began to lose flesh. The liver became enlarged,
and somewhat tender to the touch; the gall-bladder being at the same
time so distended that it could be seen, as well as felt, projecting
from under the false ribs. As the case resisted the usual remedies, the
patient was recommended to try change of air. During his absence from
town, he suddenly passed a large quantity of yellow matter by stool
(supposed to be bile), and immediately afterwards the fulness in the
abdomen disappeared. On the patient's return to town, the gall-bladder
could no longer be seen or felt, and it was naturally supposed that it
had emptied itself on the occasion referred to. As, notwithstanding
this, the jaundice continued, and the health and strength gradually
declined, Dr. Prance, under whose care the patient was, sought the
assistance of a physician of distinguished reputation in these
affections. At this period, {72} however, the entire absence of
physical signs beyond the clay-coloured stools, and those directly
referrable to the jaundice, rendered it impossible for any decided
opinion to be arrived at. The liver had now resumed its natural size,
and the only thing detectable was slight tenderness on pressure, with a
doubtful fulness in the pancreatic region. These signs, associated as
they were with gradually increasing emaciation and debility, led to the
suspicion of malignant disease, either in the course of the bile-ducts,
or at the head of the pancreas. About this time it was discovered that
the patient occasionally passed a considerable amount of a
fatty-looking matter by stool--not mixed with the motion, but separate,
though upon it. After the passage of this matter, there in general
appeared to be a slight improvement in the patient's condition. The
substance in question, on cooling, solidified into a firm pale-brown
matter, resembling Windsor soap, and not at all unlike some of the
biliary products. This led to the idea that it might be composed of the
fatty acids of the bile. On one occasion a portion of it was forwarded
to me for analysis, and on subjecting it to chemical examination it
proved to be, strangely modified fish-oil, the oleine of which had
entirely disappeared. In fact, it was nothing but the sparingly soluble
fatty acids of cod-liver oil, which had {73} been transformed in the
stomach, and from which all the liquid principles had been absorbed.
This was considered an important discovery, as it not only negatived
the idea of the bile still reaching the intestines, but also proved
that the _pancreas_, as well as the _liver_, was affected. Having thus
learned that the pancreatic juice, as well as the bile, failed to reach
the intestines, an effort was made to counteract the pernicious effect
on the system caused by the absence of the former secretion, by giving
1½ grains of pancreatine in the form of pill three times a day. During
the period that the patient was taking this medicine, the quantity of
fat passed by stool was supposed to diminish. No decided improvement in
the patient's condition took place, however, and on the 2nd of November
the gentleman was brought to me by his medical attendant. At this time
the patient was much in the state already described,[22] and after a
careful physical examination, I failed to elicit any new fact of
importance. The hepatic dulness was perfectly natural; there was no
tenderness to speak of, no history of gall-stones, and {74} no evidence
of any tumour beyond the doubtful fulness in the pancreatic region. The
digestive, and other functions of the body, except those already
mentioned, seemed unimpaired, and yet the patient's strength daily
declined. As physical as well as symptomatical diagnosis proved
inadequate to unravel the mystery of this obscure case, and as chemical
means had already, in as far as it had been tried, been of advantage,
it was resolved to subject the excretions to a rigid chemical
examination. The patient was accordingly desired to collect all the
urine he passed during twenty-four hours, and while I analysed it, Dr.
Prance examined the stools, in order to ascertain their
composition--especially as regarded the amount of fatty and albuminous
matters contained in them. The urine yielded on analysis the following
result:--

                      24 HOURS' URINE.
  Quantity (55 oz.) . . . . . . . . . . . . . . . . . .  1705 c.c.
  Reaction  . . . . . . . . . . . . . . . . . . . . . .  Acid.
  Specific gravity  . . . . . . . . . . . . . . . . . .  1018.
  Colour  . . . . . . . . . . . . . . . . . . . . . .  Greenish yellow.
  Urea  . . . . . . . . . . . . . . . . . . . . . . . .  27·28 grammes.
  Uric acid (crystals large, and of a dark-green colour)  0·511   "
  Bile acids[23]  . . . . . . . . . . . . . . . . . . .  Abundant. {75}
  Bile pigment[24]  . . . . . . . . . . . . . . . . . .  Abundant.
  Albumen . . . . . . . . . . . . . . . . . . . . . . .  None.
  Sugar . . . . . . . . . . . . . . . . . . . . . . . .  None.

[Footnote 22: I noted his state to be as follows:--Skin of a black
jaundiced tint (dark green). Eyes deeply stained. Lips anæmic.
Considerable emaciation and debility. Extreme languor. Appetite good.
Tongue, and pulse not remarkable. Slight pain on pressure over the
gall-bladder. Indistinct fulness in pancreatic region, and to the left
of middle line.]

[Footnote 23: On the addition of sulphuric acid, and white sugar to the
urine, a very marked, and beautiful purple hue was obtained.]

[Footnote 24: Nitric acid at first turned the urine green, but on the
application of heat it became red, and after prolonged boiling, of a
pale straw colour. Hydrochloric acid changed the colour of the urine
immediately to a deep olive-green tint.]

The facts here elicited were interpreted as follows:--

1st,--The quantity of urea which might be said to be normal, was
considered a favourable sign, as it indicated that the stomachal
digestion was unimpaired.

2nd,--The quantity of uric acid being below the average, was likewise
regarded as favourable, tending as it did to negative the idea of
cancerous disease of the liver; the uric acid being in such cases
usually increased.

3rdly, and lastly, the presence of the biliary acids, as well as the
bile pigment, in the urine, showed that bile was still being secreted,
but re-absorbed, and this led at once to the diagnosis that the case
was one of jaundice from obstruction.

Here, then, was an important step gained. The next point was, if
possible, to ascertain the cause of the obstruction. Taking into
account the absence of any tumour, and any history of gall-stones,
together with the fact of the sudden disappearance of the enlarged
gall-bladder, my {76} first idea was that it might be a case of
hydatids blocking up the common gall-duct, and that on one occasion,
some large cyst had ruptured, and discharged itself through the
intestines. On talking the case over with Dr. Prance, however, that
idea was abandoned, and we were forced to content ourselves with the
simple fact that the case was one of jaundice from obstruction of the
common bile-duct, complicated with occlusion of the pancreatic duct,
which fact had been previously ascertained by the discovery of the
fatty acids in the fæces. About this time the patient took three grains
of benzoic acid, in the form of pill thrice a day, and it was thought,
with the advantage of slightly diminishing the jaundiced state of the
skin. But no permanent benefit was obtained, and after a time this
remedial agent had to be discontinued, in consequence of its having
induced slight dyspepsia. In the letter I received informing me of this
fact, it was also noted that there was much less both of the oily
matter, and albumen in the stools. There was, at the same time, a
considerable deposit of urates in the urine. The specific gravity
continued to be about 1018. The quantity in twenty-four hours about
forty ounces. On the 29th of November, the patient was again brought to
me, and we made a careful examination of the size, shape, and exact
position of the {77} hepatic organ. The measurements were found to be 5
inches at the extreme right, 4 inches at a line drawn perpendicularly
to the nipple, and 2¾ inches midway between nipple and sternum. Beyond
the centre of the sternum the liver did not reach. As regards the size
of the liver then, there was still nothing very remarkable.

On this occasion it was observed, that the patient's memory was not so
good as formerly, and that there was a certain amount of mental as well
as bodily languor. His hearing was likewise sluggish, the words having
occasionally to be repeated before they made an impression on the
cerebral organ. This, no doubt, arose from the poisonous effects of the
bile circulating in his blood.

It may be here mentioned, that in cases of jaundice from suppression we
seldom or never meet with those extreme symptoms of cerebral
disturbance which are so common in cases of jaundice from obstruction.
I believe the reason of this difference in the two forms of jaundice
arises from the circumstance that the really poisonous parts of the
bile are the biliary acids, and that they, like urea, are powerful
narcotic poisons. The results of the experiments on artificial jaundice
(page 95) led me to this conclusion.

As neither the symptoms nor physical signs threw any additional light
on this interesting case, {78} it was determined once more to bring
chemistry and the microscope to bear upon it, with the view of, if
possible, extending the information these methods of investigation had
already yielded. Accordingly, a specimen of the urine was again
obtained for analysis, and it yielded the following results:--

              24 HOURS' URINE.
  Quantity, (43 oz.) . . . .  1333 c.c.
  Specific gravity . . . . .  1016.
  Reaction . . . . . . . . .  Acid.
  Urea . . . . . . . . . . .  23·994 grammes.
  Uric acid  . . . . . . . .   0·266    "
  Bile pigment . . . . . . .  Abundant.
  Bile acids . . . . . . . .  Small quantity.
  Sugar  . . . . . . . . . .  A little.
    Solids (total) . .  41·989
  Organic matter . . . . . .  31·992
  Inorganic  . . . . . . . .   9·997

A marked change is here seen to have occurred in the constitution of
the renal secretion. First--the quantity of urea has notably diminished
(from 27·28 to 23·99 grammes, or in other words, from 423·84 to 370
grains.) The amount of uric acid has also fallen (from 0·511 to 0·266
grammes, or in other words, from 8 to 4 grains); while at the same time
the biliary acids have considerably decreased. These changes are also
seen to be accompanied by another, which I at once regarded {79} as a
most unfavourable sign,--namely, the appearance of sugar in the urine.
Although the quantity of sugar was as yet small, and it was associated
with a diminution in the bile acids, it nevertheless made me look
forward with gloomy forebodings, for as far as my experience goes, when
the urine becomes saccharine in the course of a chronic, and exhausting
disease, it has generally been the forerunner of a fatal termination.
This case, I am sorry to say, proved no exception to the rule. There
was, indeed, but one consolatory fact in the analysis, and that was the
diminution of the uric acid, which, as I before remarked, tended to
negative the idea of malignant disease of the liver, and this was a
great source of satisfaction to the patient.

Eight days later, 12th November, a qualitative, and quantative analysis
of the urine was again made, with the following result:--

             24 HOURS' URINE.
  Quantity (33 oz.) . . . . . . .  1023 c.c.
  Reaction  . . . . . . . . . . .  Acid.
  Specific gravity  . . . . . . .  1017.
  Urea  . . . . . . . . . . . . .  15·345 grammes.
  Uric acid . . . . . . . . . . .  ?
  Bile acids  . . . . . . . . . .  None.
  Bile pigment  . . . . . . . . .  Abundant.
  Sugar . . . . . . . . . . . . .  Increased. {80}
  Tyrosine, and leucine[25] . . .  In small quantity.
    Solids (total)  . . . .  23·426
  Organic matter  . . . . . . . .  17·698
  Inorganic . . . . . . . . . . .   5·728

[Footnote 25: On precipitating the urine with the acetate of lead,
filtering, and freeing the clear liquid from the excess of that reagent
by means of sulphuretted hydrogen, and again filtering, the liquid, on
evaporation, was found to deposit small crystals of tyrosine, and to
have floating in it, and on its surface, round balls of leucine.]

Here, is now to be observed, the rapid downward progress of the case.
Stomachal digestion, as indicated by the amount of urea, is much
impaired. The general health, as indicated by the sugar, is sadly
affected, and, to crown all, tyrosine, and leucine, the indicators of
atrophy of the liver, have made their appearance. So unfavourable was
the result of this analysis considered, that Dr. Prance felt himself
bound to fulfil a promise he had made to the family some time
previously, of warning them of approaching danger, when we had no
longer any hope of the patient's recovery.

Some time afterwards, in the beginning of December, we again saw the
patient together, and made a physical examination of the hepatic organ,
the result of which only confirmed our suspicions. The liver was
decidedly smaller. The epigastric tenderness was increased. The {81}
jaundiced tint deeper. Petechial spots had now appeared on the trunk,
and arms. The lower extremities were oedematous, and the abdomen
two-thirds filled with fluid.

On the 31st December, I received a sample of urine, and a note saying
that the patient had slightly rallied. But on examining the urine, it
was found to have a neutral reaction--it had previously always been
acid--to be of a specific gravity of 1019, and on standing, to deposit
a copious sediment of lithates, coloured intensely yellow with the bile
pigment. Curiously enough, the bile-acids had reappeared; but only in
quantity sufficient to admit of their being detected. In spite of these
trifling changes for the better, the ominous one of an increased amount
of sugar was still there.

A few days later, and just before his death, the patient had the
benefit of another physician's opinion, which, although it differed
somewhat from the foregoing, was, nevertheless, equally unfavourable,
for he considered it a case of malignant disease.

The gentleman having noticed that his case excited considerable
interest, and some difference of opinion among his medical attendants,
directed that his body should be examined after death; and as this wish
was seconded by his wife, {82} a lady of superior mind and
accomplishments, a post-mortem examination was accordingly made, with
the following results:--

Firstly,--The pancreatic duct, as had been suspected, was found
completely occluded at its outlet, and so distended by the accumulated
secretion, that it readily admitted the point of the little finger.
(Vide Plate I., _g_.)

Secondly,--The orifice of the common bile-duct was in like manner
completely obliterated, and the duct itself immensely distended with
dark thick tarry bile, which on microscopic examination, was found
loaded with beautiful crystals of cholesterine. (Fig. 7.)

[Illustration: FIG. 7.]

The gall-bladder was enlarged to the size of a swan's egg, and
contained thick tarry fluid; but no gall-stones, or masses of
inspissated bile. The hepatic duct was greatly enlarged, easily
admitting {83} the point of the finger. The cystic duct was also
dilated, though in a much less degree. (Vide Plate I., _c_. _d_. _e_.)

Thirdly,--The gall-bladder, duodenum, abdominal parietes, and in fact
all the abdominal viscera, were intensely stained, almost blackened, by
the osmosed bile.

Fourthly,--The bile, on analysis, was found to contain in one thousand
parts:--

    Water . . . .  694·45
    Solids  . . .  305·55
                   ------
                  1000·00
                  =======

  Pigment . . . . |
  Bile-acids  . . | Organic matter  .  288·99
  Cholesterine  . |

  Soda  . . . . . |
  Potash  . . . . | Inorganic salts .   16·56
  Iron  . . . . . |

Whereas a specimen of normal bile taken from the gall-bladder of a
woman aged sixty-one, was of a specific gravity of 1020, and contained
in 1000 parts:--

    Water . . . .  933·27
    Solids  . . .   66·73
                   ------
                  1000·00
                  =======
{84}
  Pigment . . . . |
  Bile acids  . . | Organic matter  .  56·73
  Cholesterine  . |
  Sugar . . . . . |

  Soda  . . . . . |
  Potash  . . . . | Inorganic salts .  10·00
  Iron  . . . . . |

The difference in composition of these two biles is very striking. The
one contains more than four times as much solid matter as the other;
and if the relative amount of organic, and inorganic substances be
compared, the curious fact is observed, that the difference in the
amount of solids in the two cases, is almost entirely due to the change
in quantity of organic matter. The inorganic salts have not even so
much as doubled themselves in the abnormal bile. Whence is this? Soda
is the chief inorganic substance found in bile, and we have seen that
it occurs in the form of glycocholate, and taurocholate of soda,
substances which, as before remarked, are re-absorbed from the
distended ducts, and gall-bladder into the circulation, from whence
they are constantly being eliminated with the urine; and this, no
doubt, is one of the causes why the inorganic salts are proportionally
in such small quantity in the abnormal bile of jaundice from
obstruction.

{85} Fifthly,--In the abdomen was a considerable quantity of dark
straw-coloured serum, which on the addition of strong sulphuric acid
became of a fine emerald-green colour, in consequence of the presence
of bile. Traces of sugar were also present in the effused liquid. The
serum had only collected in the latter weeks of the patient's life, and
after the shrinking of the liver was observed to have begun.

Sixthly,--The liver was small in size, excessively dense, and very
heavy. Externally, it had a dark olive hue, and on section presented a
most curious appearance. The section was of an almost uniform
yellowish-green colour, and studded over with excavations (Plate I.,
_b_), from which thick bile streamed in all directions. The apparent
excavations were nothing more or less than immensely distended ducts.
On looking into the ducts, it was observed that they presented the
appearance of possessing valves. On microscopical examination, the
hepatic cells were found smaller than normal, as if partially
atrophied. The nuclei were unusually well marked, in consequence of the
fat granules being almost entirely absent. (Fig. 8, _b_.) In the field
of the microscope were a number of caudate or spindle-shaped cells
(Fig. 8, _c_.), from the epithelial lining of the ducts. In the hepatic
tissue were found some beautiful {86} stellate crystals, as well as a
number of separate needles of tyrosine. A few small crystals of cystine
were also found. (Fig. 8, _a_.)

[Illustration: FIG. 8.]

Seventhly,--The kidneys were enlarged, pale, and fatty-looking; and all
over the surface of the section, as well as immediately under the
capsules, which were very loosely attached, were small abscesses. The
surface was also studded with numerous minute dark bile-pigment points,
and it is possible that the abscesses were the result of the blocking
up of the capillary vessels by the pigment deposit, as previously
alluded to, page 57.

Eighthly,--The head of the pancreas was considerably enlarged, and on
cutting into it, a quantity of pus oozed out from an abscess in its
interior. The abscess was found to communicate with a large ulcerated
spot in the duodenum. (Plate I., _f_.) On microscopical examination,
the {87} tumour of the pancreas was found to consist of an hypertrophy
of the normal gland tissue, being, in fact, a chronic inflammatory
tumour of the gland substance.

In no portion of the body was a trace of cancer detected, nor any
enlargement of the mesenteric or other glands, to justify even a
suspicion of malignant disease. So the opinion arrived at regarding the
pathology of this case is, that the disease originated in an
inflammatory affection of the pancreas, during the progress of which,
the openings of the bile, and pancreatic ducts became blocked up; the
interruption to the excretion of the bile giving rise to the jaundice,
and at the same time inducing engorgement, and enlargement of the
liver. The inflammatory affection of the pancreas had probably ended in
the formation of an abscess, which, pushing the enlarged liver
forwards, admitted of the distended gall-bladder being seen, and felt
through the abdominal parietes. At length the abscess burst, and
suddenly emptied itself into the duodenum; the yellow fluid discharged
from the intestines being not bile, as the patient had supposed, but
pus. No sooner had the abscess emptied itself, than the liver returned
to its natural position, and thus accounted for the distended
gall-bladder so suddenly ceasing to be seen or felt. The ulcer in the
duodenum appears {88} to be the mouth of the abscess, which has
probably been prevented closing, partly on account of the occasional
draining away of pus, which, being in small quantity, and mixed with
the stools, escaped detection; and partly to the constant irritation of
the passage of the food, there being no bile or pancreatic fluid to
neutralize the acidity of the chyme. This might even be sufficient of
itself to delay the healing process. The ultimate gradual atrophy of
the liver would arise from the continued pressure of the distended
bile-ducts interrupting the hepatic circulation, as formerly pointed
out at page 48. Lastly, there being no bile or pancreatic juice
admitted into the intestines, the greater part of the food taken passed
out of the body unabsorbed, and the patient, though possessing an
excellent appetite, and taking plenty of food, actually died of slow
starvation.

My object in giving such prominence to this interesting case, is to
show how valuable an adjunct physiological chemistry is to the other
methods of diagnosis in obscure diseases of the abdominal organs, and
to encourage others to follow in the same path; for it must be
remembered that the foregoing was no dead-house diagnosis, but that
every fact here stated was discovered and recorded before death.

{89} Having now explained the mechanism of the two forms of
jaundice--that arising from suppression, and that induced by
obstruction--it only remains for me to remind my readers, that there is
frequently a combination of the two conditions. Jaundice from
obstruction, for example, cannot long exist without becoming
complicated with jaundice from suppression. The continued backward
pressure exerted on the hepatic parenchyma by the over-distended
bile-tubes, sooner or later impedes the circulation in the organ to an
extent sufficient to induce an impairment, if not an almost total
arrest of the biliary secretion. Hence it is, that in the last stage of
jaundice from obstruction, the biliary acids gradually diminish, and at
last finally disappear from the urine. We have it, nevertheless, in our
power to distinguish between the two forms of disease--for whereas, in
jaundice arising from simple suppression, there is only an absence of
the bile-acids; in jaundice from obstruction, complicated with
suppression, the absence of the bile-acids is usually associated with
the presence of tyrosine, and leucine. For before complete suppression
occurs as a result of obstruction, the hepatic tissue has already had
its nutrition so impaired, as to admit of the formation of these
foreign substances. Lastly, the history of the case will of itself be
an important guide.


{90} EPIDEMIC JAUNDICE.

It is seldom that jaundice attacks persons in an epidemic form; as it
does so occasionally, however, and that too in almost all countries, it
is necessary that I should say a few words on its pathology. In a
quotation, in the "Medical Times and Gazette," from the "Recueil de
Mémoires de Médecine Militaire," vol. iii. p. 374, it is stated that,
"M. Martin gave an account of an epidemic of jaundice which he had the
opportunity of observing among the artillery and engineers of the
French army stationed at Pavia during the Italian war. It commenced
during the great heats of August, and terminated by the end of October.
There occurred 71 cases in an effective of 1022 men. The causes he
considers to have been the unusual heat, which gave rise to great
congestion of the liver, the fatigue of long marches (the mounted men
suffering oftener in proportion than the unmounted), indulgence in
alcoholic drinks, and marsh miasmata. Great increase in the size of the
liver in most of the cases, and of the spleen in many, was observed,
and all complained of pain in the epigastrium and in the hypochondria.
In fact, this last was the first symptom of the approaching jaundice.
None of the cases proved fatal. Professor San-Galli {91} informed M.
Martin that a similar epidemic prevailed in the town of Pavia at the
same time."

That jaundice may also occur in an epidemic form among pregnant women,
has been shown by Dr. Saint-Vel, who relates that, "In 1858 the island
of Martinique was, without appreciable cause, visited by an epidemic of
jaundice, remarkable for its severity in pregnant women. It broke out
at St. Pierre towards the middle of April, attained its maximum height
in June and July, and terminated towards the end of the year. All races
were attacked; the patients were mostly adults; no liver-complication
could be detected; nor could any resemblance be traced between the
disease and yellow fever. It was fatal to females only, especially
during pregnancy. Of thirty pregnant women who were attacked at St.
Pierre, ten only arrived at the full period of pregnancy without
presenting any other symptoms than those of ordinary jaundice. The
other twenty all had abortion or premature labour a fortnight or three
weeks after the commencement of the attack, and died in a state of
coma, which appeared a few hours before or after the expulsion of the
foetus. The females who died were from the fourth to the eighth month
advanced in pregnancy. In some cases, slight delirium preceded the
coma, which was never interrupted, but became more and more {92}
profound up to the time of death. Its longest duration, in two cases,
was twenty-four and thirty-six hours. It was not preceded by any
notable modification of the general sensibility, nor of the respiration
or circulation. Hæmorrhage was absent, except in one case, where a
female had it before delivery. When death was delayed till three or
four days after delivery, the lochia were healthy. Almost all the
children were still-born; some lived a few hours; one alone survived.
None of the infants had the icteric colour; nor was there any sign of
jaundice in the ten children born at the full term."

The foregoing translation from the "Gazette des Hôpitaux," 20th
November 1862, appeared in the "British Medical Journal" of the 7th of
February, 1863, p. 141.

We have it further stated in the "Lancet" of the 21st February 1863,
under the head of the "Health of Rotherham," that, "scarcely had the
late fatal epidemic of fever subsided ere another, less fatal, but as
widely spread, took its place. In last November several persons were
attacked with jaundice, and now not less than 150 persons are suffering
from it. None of those who were attacked by the late fever are
suffering from the present epidemic."

When we reflect on the facts here related, we {93} can have little
difficulty in forming an opinion of the pathology of jaundice occurring
in an epidemic form. Its mechanism seems to be precisely similar to
that of the isolated cases of the disease which are every now and then
met with as the result of blood-poisoning. I have recently seen a case
of well-marked jaundice supervene on an attack of scarlet fever, and as
it affords a tolerably good illustration of the pathology of such
cases, it may, perhaps, be briefly given with advantage.

A London cabman, aged 23, was admitted under my care into University
College Hospital, on the 2nd March of the present year. He stated that
he had always enjoyed good health, but that lately he had been much out
of spirits, in consequence of the death of one of his relatives. On the
25th February, after three days' illness, a scarlatinal rash appeared
all over his chest, and extremities, and four days later (the day
before his admission), he became jaundiced. March 3rd. His skin is now
of a bright yellow colour, and when the finger is rapidly drawn across
it, a pink line immediately takes the place of the yellowness, showing
that there is still great subcutaneous vascularity. The throat is sore,
and there is considerable difficulty in swallowing. The conjunctivæ are
intensely yellow--proportionally more so than the skin, in consequence
of the scarlatinal hue being still {94} blended with the tint of the
latter. The urine is high coloured, has a slight deposit of urates;
contains a large amount of bile pigment, but no bile-acids. The stools
have not been observed to be clay-coloured. The liver is enlarged
(dulness extends 5½ inches in a perpendicular direction), and tender on
pressure. He complains of pain in the hepatic region on taking a deep
inspiration, and of a general uneasiness at other times. Has no
sickness or vomiting. The mucous membrane of the tongue is red and
raw-looking; flakes of epithelial fur are readily detached from it.

The case was at once diagnosed as one of jaundice from suppression. Its
mechanism being supposed to be identical to that of the cases discussed
at pages 25-9 under the head of jaundice arising from active congestion
of the liver induced by blood-poisoning, a dose of calomel and jalap
was accordingly administered, with the view of removing the portal
congestion, and with the most satisfactory result; for, notwithstanding
the jaundice being complicated with scarlatina, a very decided
improvement in the colour of the skin took place within twenty-four
hours, the other symptoms remaining as before. March 10th. The calomel
and jalap was repeated on the 4th, and since then the skin has
gradually become paler. It is now scarcely tinged.

{95} To return to the cases of epidemic jaundice; they, as I have just
hinted, are due to a precisely similar cause--blood-poisoning--either
the direct result of miasmata, or of contagion.

A further explanation of the reason why jaundice occurs in an epidemic
form, may be found in the circumstance that in all febrile states of
the general system some one or other of the internal organs is liable
to become congested. For example, typhus is, as a rule, complicated
with cerebral congestion, typhoid with mesenteric, ague with splenic,
scarlatina with renal, and so on. It is not, however, necessary that
the organs should be affected in the same relation to the disease as is
here given. On the contrary, in one epidemic of typhus, the brain may
be congested, in another the lungs, and in a third the liver; and so
also with other fevers. Hence we can have little difficulty in
understanding why epidemics of jaundice every now and then occur,
seeing that they are but the secondary results of other epidemic
affections, although, as occasionally happens, the jaundice is the
chief, if not the only well-marked symptom.


ARTIFICIAL JAUNDICE.

What is the source of the tyrosine, and leucine found in the urine, in
cases like those previously described? Being well aware that the
physiologist {96} has it in his power to produce almost any
pathological state or artificial disease at pleasure, I set about
imitating on an animal the effects produced in the human subject by
obstruction of the bile-ducts. Hitherto, artificial jaundice has been
usually induced either by ligaturing the gall-ducts or injecting bile
into the circulation; but as both of these methods were in the present
instance objectionable--the first on account of the constitutional
disturbance liable to be induced by the severity of the operation; the
second from the bile being all at once thrown into the circulation, and
thereby producing toxic effects, besides the danger of its too rapid
elimination by the urine--I adopted another plan, which came much
nearer to the state induced by disease in man--I took the bile of three
healthy dogs, and injected it under the skin of a fourth. In this case
the effects of the operation were almost _nil_, and the bile was at the
same time placed in a position favourable for its slow absorption, just
as in the human subject. During the first two days the animal remained
comparatively well, the urine was normal in appearance, and contained
neither bile-pigment, nor bile-acids. But on the third day the animal
became ill, and on the fourth jaundice set in. He died on the fifth.
After death the urine was found to contain not only {97} bile-pigment,
and bile-acids, but also the diseased products, leucine, and tyrosine;
and what was more interesting still, the urine was loaded with sugar,
just as occurred in the case imitated.

It will be remembered that in speaking of the bile-acids, I mentioned
that while glycocholic acid is a crystalline, taurocholic is a
non-crystalline substance. Tyrosine, and leucine stand in a similar
relation to each other; tyrosine being crystallizable, leucine
non-crystallizable. Now, taking this fact into account, together with
the fact, that when the bile-acids are allowed slowly to enter the
circulation, they reappear in the urine, accompanied with tyrosine, and
leucine; and also with the third fact of these latter substances being
found in the liver when the biliary function is interfered with, I am
inclined to look upon tyrosine, and leucine as the products either of
the arrested, or of the retrograde metamorphosis of glycocholic, and
taurocholic acids. Moreover, I have found in one case, after injecting
bile in the way before mentioned, into the cellular tissue, crystals of
tyrosine spontaneously form in the bile taken from the animal's
gall-bladder after death, and merely allowed slowly to evaporate. This
result strengthens the foregoing opinion.

Frerichs states that he has never detected the biliary acids in the
blood, even after bile had {98} been injected into the circulation. In
a remarkable case where 1 oz. of ox-bile killed a dog in less than five
minutes from the time it began to be slowly injected into the jugular
vein, I detected the bile-acids in a clear extract of the blood, with
facility. This leads me to mention that, contrary to the statement of
Frerichs, and in accordance with that of Kühne, the injection of the
pure bile-acids into the blood is very dangerous, and that even the
injection of pure bile into the cellular tissue, often proves fatal in
the course of twenty-four hours, thereby showing that the constituents
of the bile are highly poisonous.

In illustration of these facts I may cite the following experiments:--

Into the cellular tissue of the back of a full-grown, and
healthy-looking terrier dog, I injected the bile taken from the
gall-bladders of three healthy dogs, two of which had just been killed,
the other had been dead a few hours. The bile was in the first two
cases neutral, in the third faintly alkaline. All the biles seemed
perfectly normal. They contained no crystals of any kind. Eighteen
hours after the operation the animal appeared quite well, and took his
food heartily. Four hours later a remarkable change took place. The dog
looked dull and drowsy, and could not sustain himself on his legs; when
left to himself, he {99} lay on his side, and made not the slightest
movement. He was not only paralyzed, but even the nerves of sensation
had ceased to act, for when his tail, and feet were pinched, he was
quite insensible to pain. The pupils were dilated, and the body felt
cold. Death occurred twenty-three hours after the operation. Urine, and
fæces were passed in small quantity immediately before death. The urine
was strongly alkaline, and effervesced on the addition of sulphuric
acid, thereby showing that it contained alkaline carbonates. Prismatic
phosphatic crystals were present in the still fresh urine.

When tested for bile-acids, only the faintest trace was obtained, after
the urine had been cleared with the acetate of lead and sulphuretted
hydrogen.

The tissues of the abdomen and thorax were oedematous, but, within an
hour after death, had not the disagreeable odour found in animals
killed by injecting pure bile-acid. (_See_ foot-note at p. 39.)

This experiment was again repeated with alkaline bile. Two ounces of
ox-bile of a specific gravity of 1025 were injected under the skin of a
large pointer dog. In twenty-four hours the animal was dead; the
sub-cutaneous tissue all round the seat of the injection, red,
inflamed, and infiltrated with {100} blood. The urinary bladder was
empty. The gall-bladder contained 1½ ounces of dark bile of a specific
gravity of 1040. When examined with the microscope, the blood was found
to contain a large excess of white corpuscles.[26]

[Footnote 26: It has just been said that the blood contained a large
amount of white blood corpuscles. This reminds me of a fact that I have
omitted to mention--namely, that in a case of severe jaundice from
suppression, in consequence of cirrhosis of the liver, I found that the
blood possessed a very treacle-like aspect. The serum was of a dingy
yellow hue, and felt somewhat sticky to the fingers. Under the
microscope the blood corpuscles were found to be large, and flabby, had
a great tendency to adhere together by the edges, and become flattened
on the sides whenever they came in contact. Moreover, the corpuscles
looked as if they had no distinct cell-wall; some, and that too, in the
freshly drawn blood, gave off buds, others split into two, each half
when separate looking like a distinct blood corpuscle. In fact, the
blood looked more as if it had been acted upon by some powerful
chemical agent than anything else. I again examined it after the death
of the patient, and found it presented all the above characters in a
still more marked degree. To the naked eye it had a viscid, tarry
appearance.]

These results rather militate against the theory of the bile being
re-absorbed, in an unchanged state, into the circulation, after the
completion of the digestive process.


{101} TREATMENT OF JAUNDICE.

After what has been said regarding the pathology of jaundice, I need
scarcely remark that the treatment must vary according to the kind of
disorder we have to deal with. A line of treatment found to be
beneficial in one case of jaundice, might prove very hurtful in
another. For, as has been shown in the foregoing pages, jaundice from
suppression, and jaundice from obstruction, are, it might be said, two
entirely different diseases, with only the symptoms of yellow skin,
high-coloured urine, and pipe-clay stools in common. The success of our
treatment will therefore depend on our powers of diagnosis.

The general principles upon which the treatment of jaundice must be
founded are as follows:--

The first and great object is, of course, as in the case of every other
disease, to remove, if possible, the exciting cause. When that is
accomplished, we can with safety turn our attention to the removal of
its effects. I need not here detail the different exciting causes which
it is our duty to remove. I have indicated them elsewhere, and the mere
mention of some of their names is sufficient to denote the line of
treatment which ought to be adopted. Thus, for example, if it be {102}
ascertained from there being symptoms of tenderness, &c., in the
hepatic region, that the jaundice arises from active congestion of the
liver, the first object would of course be to subdue the congestion of
that organ by means of leeches, hot fomentations, saline purgatives,
&c., according to the age, sex, and constitution of the patient. On the
other hand, if the jaundice be the result of passive congestion of the
liver, we know well that so long as the exciting cause exists
elsewhere, it will be worse than futile to attempt the removal of the
hepatic congestion by direct means. In such a case, therefore, if to
remedy the cause is beyond our power, our object will be to concentrate
our efforts on the mitigation of its effects. Thus I might go through
the whole list of causes of jaundice, and point out what appears to be
the most appropriate treatment of each; but I think the time of my
readers and my space, will be more profitably employed, if, instead of
doing so, I turn my remarks chiefly to the therapeutical action of
those remedies which we are constantly employing in the treatment of
jaundice. The first remedy that merits special notice is mercury.

The benefit of mercury in cases of liver disease cannot be denied; but
the injudicious employment of this drug in cases of jaundice, has
frequently been followed by the most disastrous results. {103} There
was a time when mercury was administered in all cases of jaundice,
irrespective of their cause; now, however, men are fortunately becoming
more careful in the employment of this drug. But there is still a
mistaken notion regarding the therapeutical action of mercurial
preparations. It was at one time thought that they stimulated the liver
to secrete bile, and now since physiology has shown that they possess
no such action, many have gone to the opposite extreme, and declared,
that if mercurials do not stimulate the liver to secrete bile, their
benefit in hepatic disease has been a delusion; and the dark stools
following upon their employment but the result of the sulphuret of
mercury formed in the intestines. I take a very different view of the
matter; for though believing that mercury does not directly stimulate
the liver to secrete bile, I nevertheless opine that it has an
important indirect effect in reinducing the biliary secretion, and
thereby curing certain cases of jaundice.

The action of mercurials seems to me, to be this--mercury is a powerful
antiphlogistic--it reduces the volume of the blood by its purgative
properties, and it impoverishes the blood by its direct action on the
red corpuscles. It has been poetically said by Dr. Watson, that mercury
can blanch the rosy cheek to the white of the lily; {104} and nothing
is more true, for in experiments on animals, I have found the prolonged
use of mercury reduce the red blood corpuscles to a minimum. From this
it is easy to understand how mercury acts in inflammatory affections;
and as in the majority of cases of jaundice from suppression, the
stoppage of the biliary secretion is due to active congestion of the
liver, mercury proves beneficial in such cases, not by stimulating the
biliary secretion, but simply by removing the obstacle to its
re-establishment, namely, the hepatic congestion.

As a good illustration of the correctness of this theory regarding the
action of mercurials in cases of jaundice arising from congestion, I
may be allowed to quote the following case, which appeared among the
Hospital Reports of the "Lancet" of the 7th December, 1861. The case is
headed, "Intense Congestion of the Liver, simulating an Abdominal
Tumour:"--

Alex. E----, aged forty-eight, was admitted into St. Bartholomew's
Hospital, under the care of Dr. Farre, on the 17th October, 1861. The
patient had, it appeared, been suffering from jaundice during six
weeks. He stated that the tumour in the epigastrium began about the
same time as the yellowness of the skin.

On examination, a prominent swelling was {105} noticed in the
epigastric region, possessing an indistinct feeling of fluctuation, but
it was found to be continuous with the liver. The motions were not
bilious, but were of a clay colour, and the urine looked like pure
bile. Three grains of blue pill and two of Barbadoes aloes were ordered
every night. By the 25th the hepatic tumour was less, and the icterus
was disappearing. On November 4th the urine was clearer and full of
lithates. The conjunctivæ were the only parts observed of a yellow
colour.

November 11th.--Although the pills had been continued up to this date,
the mouth was not sore. The urine and stools were natural, and the
patient was convalescent. A few days afterwards he left the hospital.

The result of the case clearly proved not only that the swelling was
from a highly congested liver, but also that the jaundice depended on
this state.

In this case it is evident that the primary beneficial action of the
mercury was to reduce the congested state of the hepatic organ, and no
one, I think, would venture to say that this was accomplished by the
power the mercury possessed of exciting the liver to secrete bile.

If, then, the above view of the therapeutical action of mercurials be
correct, it is easy to understand how, in cases of jaundice from
permanent {106} obstruction of the gall-duct, the administration of
mercury or any other lowering medicine, must prove detrimental by
hastening the fatal termination.

Although mercury has not, there are some substances which have, the
power of exciting the flow of bile, just as there are substances which
excite the flow of saliva. Among these the mineral acids, and soluble
alkalies, hold the first rank. It may seem strange that acids, and
alkalies, should be here placed in juxta-position; but the reason of
this arrangement will immediately appear.

According to a physiological law, acid substances have the power of
exciting alkaline secretions, and alkaline substances of stimulating
acid secretions.

Bile being an alkaline secretion, we can therefore have no difficulty
in understanding how the mineral acids act in cases of jaundice from
suppression, induced, for example, by enervation. They simply stimulate
the secretion of bile.

It is not so easy, however, to comprehend the action of alkalies in
similar cases. My explanation of their action is as follows:--When
taken after food, and when taken on an empty stomach, the action of an
alkali is entirely different. After food, and during digestion, the
stomach contains a {107} quantity of acid gastric juice, and an alkali
taken then, only neutralizes the acid. On the other hand, when an
alkaline substance is introduced into an empty stomach, it acts
according to the general law of exciting an acid secretion;
consequently, an immediate flow of gastric juice takes place. And I
believe it is the excess of this acid gastric juice, which, on reaching
the duodenum, stimulates the secretion, and excites the flow from the
gall-bladder of the alkaline bile, just as the mineral acids do under
similar circumstances. One remark further is, however, necessary. The
quantity of alkali employed for the purpose of stimulating the
secretion, or of exciting the flow of the already secreted bile must be
small, for if much be used, the greater part of the gastric juice will
be rendered useless, in consequence of its being neutralized as fast as
it is secreted. It may be laid down as a general rule, that when we
desire to increase the flow of bile by means of a mineral acid, the
acid must be given _after food_. When, on the other hand, an alkali is
selected for that purpose, the alkali must be administered _before
food_.

For obvious reasons, both alkalies and acids are counter-indicated in
cases of jaundice resulting from active congestion of the liver; and it
is equally evident that they can be of no direct {108} service in
jaundice arising from occlusion of the bile-duct, where our object
would be rather to diminish than to increase the secretion of bile.

Alkalies, or at least some alkalies, possess certain other properties
besides those to which allusion has just been made, which may be
usefully turned to account in the treatment of hepatic diseases. For
example, we have been long told that alkaline carbonates are valuable
remedies in cases of gall-stones, in consequence of their possessing
the power of dissolving biliary calculi. Now, although I am not
sufficiently enthusiastic to believe that alkalies can have much effect
in dissolving gall-stones when once formed, I nevertheless believe that
they are of the utmost advantage in preventing and arresting their
deposition. The alkali to which I give preference is the carbonate of
soda, and the reason why I prefer it to the carbonate of potash, is in
consequence of my believing that the advantages derived from
administering alkalies in cases of incipient gall-stones are entirely
due to our being able thereby to increase the amount of glycocholate,
and taurocholate of soda present in the bile; both of which substances,
separately or combined, retain cholesterine in a soluble form; and, as
is well known, by far the greater number of biliary calculi are
composed almost entirely of pure cholesterine.

{109} The carbonate of soda has yet another advantage. It was long ago
observed by Dr. Prout that gall-stones are very common in persons of a
gouty, and rheumatic tendency of body, a fact which I have myself been
able to confirm on several occasions, by making a quantitative analysis
of the uric acid in the twenty-four hours' urine, as recommended at
page 56. In such cases the carbonated alkali is of double service, for
while increasing the solvent in the bile, it at the same time
counteracts the uric acid diathesis. In a case of gall-stones, in a
woman aged 36, where there was an almost daily deposit of fine
crystalline uric acid in the urine, it was found necessary to continue
the administration of ten grains of soda, with five of rhubarb, three
times a-day during two months, before this tendency to lithic acid
deposit was entirely overcome.

Recently I have prescribed lithia water to persons of the uric acid
diathesis in whom I had reason to suspect the existence of a
predisposition to gall-stones; and when it was necessary to combine it
with stimulants, sherry has been the wine selected. For some further
remarks on the treatment of gall-stones, see pages 114, 119, and 123.

There is a remedy to which I wish to call special attention, namely,
benzoic acid. This substance was first recommended as a remedy in {110}
jaundice by a German physician, about six years ago. Since then, I have
tried it several times, and found it of benefit in jaundice arising
from suppression. In those cases of obstruction, on the other hand, in
which I tried it, it appeared to be anything but beneficial. I give it
in the form of pill, three times a day. Dr. Green, one of my former
pupils, who has just returned from India, tells me that he acted on my
suggestion, and tried it in a case of well-marked jaundice, following
an attack of delirium tremens; and that by the end of eight days it
would have required an experienced eye to detect the tinging of the
conjunctivæ.

The following may be cited as a tolerably good example of the value of
benzoic acid in cases of jaundice from enervation:--

William M----, aged eleven years, labouring under an acute attack of
severe jaundice, came under my care at University College Hospital on
the 2nd of February. The patient appeared to be a moderately developed,
and very intelligent boy. The jaundiced condition of the skin, his
mother said, was first noticed on the 30th of January, only two days
before he came to the hospital. It was further ascertained that,
although the boy had for some length of time been subject to monthly
attacks of severe headache, and bilious vomiting, he had never before
suffered from {111} jaundice. On the present occasion he complained of
headache, but it was unaccompanied either by sickness or vomiting. On
examination the liver was found normal in size, and not in the least
tender on pressure. The bowels were moderately open, and the stools not
clay-coloured. The urine was of a deep orange tint, and the skin of a
dark yellow hue. There was an abundance of bile pigment, but not a
trace of bile-acids in the urine.

As the jaundice appeared to be the result of enervation, brought on by
over mental exertion, the boy was ordered to be kept from school, and
not allowed to read any books (his mother said he was always reading).
At the same time three grains of benzoic acid were ordered to be taken
thrice a-day.

9th February.--The skin was now very much paler, the yellow colour
being nearly gone. The conjunctivæ were still yellow, although less so
than at last visit. The urine remained unchanged in colour. He was
ordered to continue the medicine.

16th February.--Skin perfectly normal in colour; if anything perhaps a
shade whiter than natural. Conjunctivæ no longer yellow. Dismissed
cured.

In this case no medicine whatever, except the benzoic acid, was given.

As far as my experience goes, benzoic acid {112} appears to be most
useful in jaundice arising from enervation or from active congestion,
as in the case related at page 27; but in cases of the latter kind it
seems to be of little service until the acute symptoms have
disappeared. I am still rather doubtful regarding the mode in which it
acts, although one point seems clear, namely, that it hastens the
re-absorption from the tissues, and elimination from the body, of the
bile-pigment. It thus appears to play the part of a whitewash; for, as
one of my lady patients once graphically said, the medicine had
bleached her. On one occasion I tried benzoic acid in a case of
jaundice following upon an attack of ague; but it proved of no service.
Indeed, quinine, combined with mercurials, seemed in that case to be
the only remedy.

There is another drug which proves of service in jaundice from
suppression, namely, podophyllin, or May-apple. This remedy, which was
first introduced from America, is supposed to possess both the
alterative and purgative properties of mercury. As an alterative, it is
given in doses varying from 1/8 to ¼ of a grain, three times a-day; as
a purgative, from ¼ to 1 grain, as a single dose. I have given this
remedy a tolerably fair trial, and although it seems to be very useful
as a purgative in hepatic disease, and to increase the flow of bile, I
have found it open to two objections: {113} firstly, its action is
slow, and not always certain; and, secondly, in delicate females it
gives rise to a good deal of griping. This latter objection can,
however, to a certain extent, be counteracted, by combining the remedy
with hyoscyamus. On the whole, I prefer mercurials to podophyllin, and
only administer the latter in slight cases of jaundice, or in those
where mercurials are counter-indicated.

For example, in cases of feeble liver, where there is an insufficient
secretion of bile from want of nervous power, podophyllin is decidedly
of service, for in such cases mercury is of course counter-indicated.
Moreover, podophyllin can be advantageously combined with vegetable
tonics, and, when given along with gentian or quinine, forms an
admirable hepatic stimulant in some of the cases usually denominated
"torpid liver."

I cannot refrain from making a few remarks on what I consider the
injudicious employment of podophyllin. Like every new remedy, it has to
run the risk of falling into disfavour, in consequence of its too
ardent admirers blindly prescribing it in all cases of hepatic disease;
in many of which it must of necessity prove unsuitable, if not even
detrimental. In cases of jaundice, for example, podophyllin is at one,
and the same time, the bane, and the antidote. The bane in _all_ cases
of {114} jaundice from obstruction, the antidote in a _few_ cases of
jaundice from suppression. Having already indicated the cases in which
it may be administered with advantage, I shall now call attention to
one of those where it cannot be employed without injury, and one in
which it is, nevertheless, frequently given. The case I allude to is
that of gall-stones. When once a gall-stone has formed, and is blocking
up the common bile-duct, thereby causing jaundice from obstruction, it
is easy enough to understand why a substance like podophyllin, which
increases the biliary secretion, is to be avoided. It is not, however,
so easy to understand why the remedy is equally counter-indicated,
either during the formation or sojourn of a gall-stone in the
gall-bladder. This, therefore, I must explain. In speaking of the mode
of formation of gall-stones in the gall-bladder (page 43), I have
stated that their formation is due to the deposition of the less
soluble parts of the bile, either as a consequence of these ingredients
being in excess, or in consequence of the solvent, whose duty it is to
retain them in solution, being in reduced quantity. It follows, then,
as a natural result, that the longer bile sojourns in the gall-bladder,
and the thicker it becomes, the more likely are its constituents to be
deposited, and increase the size of the already existing concretion,
{115} or give origin to a new formation. It may be further added, that
the greater the amount of bile secreted, the longer is it likely to
remain in the gall-bladder, and the more concentrated to become; for,
as is well known, there is a constant absorption of the aqueous
particles of the bile going on during the whole time it is stored up in
its reservoir. If, then, during the intervals of digestion, the liver
secretes merely sufficient bile to meet the requirements of the
succeeding meal, by the end of the digestive process the gall-bladder
will be entirely emptied of its contents, and ready to receive a fresh
supply. Whereas, if the liver secretes more bile during the intervals
of digestion than the wants of the system require; after the completion
of each succeeding meal the excess of bile will remain behind in the
gall-bladder, and, while becoming stored up with that subsequently
secreted, of necessity, favour the increase or excite the formation of
gall-stones in persons predisposed to them. There being nothing more
conducive to the deposition of biliary calculi than a well-filled
gall-bladder.

As a warning against the indiscriminate use of podophyllin, I may cite
the following case, which has come under my notice as these sheets are
passing through the press. A few weeks ago I received a telegram
requesting me to visit, as {116} early as possible, a lady dwelling in
the neighbourhood of St. John's Wood. On my arrival I found the lady
suffering from a well-marked jaundice, and considerably prostrated in
consequence of her having just arrived from Brighton, where she had
gone for the benefit of her health, but where, instead of getting
better, she got considerably worse. The history of the case was, that
the lady had been seized with pain in the back (middle of dorsal
region) about three weeks before I saw her. That there had been great
tenderness in the region of the gall-bladder--so much so, that she
could scarcely tolerate the pressure of her stays; and that she had
suffered from occasional attacks of sickness after eating.

On examining the patient I found the liver enlarged, and tender on
pressure. The gall-bladder much distended, and easily felt. The skin of
a yellow hue. The stools of a pale tint. The urine very dark-coloured,
and loaded with lithates. I had, consequently, no difficulty in
diagnosing the case as one of gall-stone impacted in the common
bile-duct; but on communicating my suspicions to the patient, I was
informed that such could not possibly be the case, for during a
considerable time past she had been carefully treated with podophyllin.
Indeed, I learned to my surprise that she had taken from a quarter to
{117} half a grain of that substance nearly every day during the six
previous months!

This incidental piece of information, instead of shaking my opinion, as
the patient had apparently expected, only tended to strengthen my
suspicions, for the reasons previously given, namely, that the
podophyllin must have tended to keep the gall-bladder constantly full
of bile. I accordingly prescribed for the case as one of impacted
gall-stone, and left instructions that the stools should be carefully
examined for its appearance.

On the following day the patient felt better; but the jaundiced tint
was deeper, the stools paler, and the urine still high-coloured. The
deposit of lithates had, however, slightly diminished. Still, feeling
certain that the case was one of impacted gall-stone, I ordered the
medicine to be repeated, and the stools to be again carefully
examined.[27] On my arrival at the patient's house the next day, the
maid met me with an expression of satisfaction which could not be
misinterpreted, and I had scarcely entered the sick chamber when, with
an {118} air of triumph, she showed me a gall-stone about the size of a
large garden-pea, or small field-bean. It had been passed that morning
about 11 o'clock, that is to say about fifteen hours after the second
dose of medicine. On analysis the stone was found to consist almost
entirely of cholesterine, and I have not the smallest doubt in my own
mind that to the constant use of the podophyllin may, in a great
measure, be attributed its formation. Unfortunately the stone had been
accidentally broken before I saw it, and I was consequently unable to
ascertain decidedly whether it was a solitary calculus, or one of many.
Had it been one of several, it would of course have possessed facets.
One facet would have indicated that the stone was one of two; two
facets that three stones existed; three facets, that the gall-bladder
had contained at least four calculi; while four or more facets would
denote that the stone was one of many; whereas, if it was a solitary
calculus, no such markings would be present.

[Footnote 27: We are sometimes told to add water to the stools, and
that if gall-stones are present they will be found floating on the
surface. I have never yet been able to detect a gall-stone in this way.
The plan I recommend is, therefore, to mix the stool freely with water,
and either decant the supernatant fluid, and then add fresh portions of
water till the whole of the soluble matter is removed, or to strain the
mixture through a hair-sieve. The gall-stone in either case remains
behind, and can be readily detected.]

I may merely add, in conclusion, that from the time the stone passed,
the stools resumed their normal colour--the first two or three were
much darker than natural, in consequence of the sudden escape of the
pent-up bile--the urine gradually became pale, and clear, and the skin
regained its wonted hue. The latter change was expedited by {119} the
administration of benzoic acid, and in a week from my first visit, a
stranger would have been quite unable to detect that the patient had
laboured under a recent attack of jaundice.

A few years ago a mixture of sulphuric ether, and turpentine was very
extensively used, especially in France, as a solvent for gall-stones.
This line of treatment was adopted on account of the well-known
solubility of cholesterine in sulphuric ether, and it was thought that
the remedy would act upon the cholesterine concretions in the
gall-bladder in the same manner as it did out of the body. After a
time, faith in the powers of the mixture became shaken, and it at
length gradually ceased to be employed.

Within the last year or two, Dr. Bouchut[28] has revived the same
theory with another form of remedy, namely, chloroform, which he
administers internally, with the view of dissolving any inspissated
bile or biliary calculi that may be lodging in the gall-bladder. Dr.
Bouchut states that he has treated one case of gall-stones in this
manner with success. Now, although I have not the slightest desire to
throw discredit on the statement of Dr. Bouchut, I must candidly admit
that I am very much inclined to doubt the accuracy of his observations.
In the first place, it is always {120} extremely difficult to ascertain
the existence of biliary concretions so long as they remain in the
gall-bladder, and it is equally difficult to know, after gall-stones
have been once passed by a patient, whether or not all have come away.
If, then, we administer chloroform to a patient, either before or after
a gall-stone has actually passed, we cannot, with anything approaching
to certainty, attribute the cessation of his symptoms to the
circumstance of the chloroform having dissolved a gall-stone. In fact,
on physiological grounds, I very much doubt the efficacy of either
sulphuric ether or chloroform as solvents of gall-stones in the living
body. Sulphuric ether, and chloroform would no doubt dissolve a
concretion of cholesterine in the gall-bladder were they admitted into
that viscus in sufficient quantity, and in a pure state. But we have no
proof that such is the case. On the contrary, we know, at least in as
far as chloroform is concerned, that exactly the opposite is the fact;
for no sooner does chloroform become absorbed, and mingled with the
constituents of the blood, than it becomes decomposed, the chlorine
combining with the blood, and the formic acid being set free.[29] And
even supposing that sulphuric ether and chloroform existed in the blood
in a free state, they could not possibly do so in a sufficiently {121}
concentrated form to be able to act as solvents of biliary calculi.

[Footnote 28: "Edin. Med. Journ." 1861, p. 398.]

[Footnote 29: Jackson, Comptes Rendus, February 25th, 1856.]

My own experiments on animals have shown me how rapidly fatal even
small quantities of chloroform are when injected into the circulation,
and a similar remark is equally applicable to sulphuric ether. A few
drops of these substances can very readily be injected into the
circulation with impunity;[30] but the quantity must not be increased
beyond a certain amount, far less than could possibly dissolve a single
grain of cholesterine, otherwise immediate death follows the operation,
by inducing a state of body closely resembling rigor mortis, from which
the animals never recover. I am, therefore, completely at a loss to
understand how these remedies can be of service in dissolving
gall-stones in the living body; and as I make it a rule as seldom as
possible to prescribe a remedy without a knowledge of its physiological
action, I have not yet ventured on an empirical trial of the effects of
sulphuric ether or chloroform administered internally in cases of
gall-stones. For some remarks on the passage of biliary calculi, see
page 123.

[Footnote 30: Vide the Author's paper on a new method of producing
diabetes artificially in animals, by the injection of
stimulants--alcohol, ether, chloroform, ammonia, &c.--into the portal
circulation. Comptes Rendus de la Societé de Biologie de Paris. 1853.]

{122} Taraxacum has been widely used in hepatic disease associated with
jaundice, and is believed to be particularly well adapted to cases
arising from congestion. As in such cases I generally trust to more
potent drugs, my experience with this remedy has been too limited to
admit of my offering an opinion of its value.

The majority of cases of jaundice from obstruction, are much less under
the power of remedial agents than those arising from suppression, for
we have here three distinct conditions to combat: Firstly,--The
derangements originating in the absence of bile from the digestive
canal. Secondly,--The morbid effects arising from its accumulation in
the ducts, and consequent interruption to the hepatic functions.
Thirdly,--The general poisonous action on the system, of the
re-absorbed bile.

As regards the first of these effects,--namely, the derangements
arising from an absence of bile from the digestive canal, it may be
said that if these were the only difficulties with which we had to
contend in cases of jaundice from obstruction, they could easily be
overcome. For, in the first place, the absence of bile is not attended
with any immediate danger, a circumstance which has led to the common
belief that the presence of bile is not absolutely essential to life.
Experiments on dogs {123} with biliary fistulæ, like those before
referred to, as well as cases in the human subject, have proved that
life may be sustained, under certain conditions, for a very long
period, without bile reaching the intestines. Indeed, the only
immediate bad effects which appear to result from its absence, are
costive bowels, great flatulence, and extremely offensive stools. The
indirect bad results,--namely, loss of flesh, &c., as has been proved
by experiments on animals, can be counteracted by giving an additional
amount of food; and even the direct results of constipation,
flatulence, and foetor, may be overcome by appropriate remedies.

The secondary morbid effects, namely, those arising from the
accumulation of bile in the ducts, are unfortunately not so easily
under control. Could we remove the cause of obstruction, these would,
of course, immediately cease. This, however, is seldom in our power,
except in the case of gall-stones, the expulsion of which we can aid in
various ways. In general, we can very successfully aid the passage of a
stone through the ducts by administering an anodyne containing a full
dose of the tincture of belladonna, which apparently assists in
dilating the duct. Placing the patient in a warm bath is also of
service; and when the paroxysms of pain are very severe, the occasional
inhalation of the vapor from a couple {124} of drachms of sulphuric
ether poured on a handkerchief, made into the form of a cup, is
generally attended with great relief. Each of these modes of treatment
may be followed either by a brisk emetic, or purgative, in the hope
that the efforts of vomiting or purging may hasten the expulsion of the
stone, either by the mouth or rectum.

It ought never to be forgotten, that the evil results of a gall-stone
do not always cease when it has reached the intestinal canal. Even
death itself has resulted from the impaction of a gall-stone in the
duodenum. When we have any suspicion that the stone is large, our
treatment must therefore be continued until its extrusion by the mouth
or rectum has been accomplished.

When the occlusion of the common bile-duct is caused by an organic
tumour, no treatment of ours can be expected to remove the obstacle,
and sooner or later the patient is carried to an untimely grave. Our
efforts of relief in such a case ought therefore to be directed to
another channel; and here, in order to give the sufferer at least some
chance of recovery, even although it be little better than a forlorn
hope, I cannot refrain from recommending, in cases of permanent
occlusion of the duct, in which there is great distension of the
gall-bladder, the establishment of an artificial biliary fistula. Were
this done, the patient would be placed, as {125} nearly as possible, in
the same condition as an animal in which the operation has been
performed for physiological purposes, and, we might almost hope, with
an equally favourable result, at least, in as far as the biliary
functions are concerned. In the first place, we would have removed all
the derangements resulting from the interruption to the flow of bile,
and consequent upon the distension of the ducts. In the second place,
we would have obviated the danger arising from the poisonous effects of
the re-absorbed bile, which the experiments previously cited (page 98)
show are of no trifling nature; and, lastly, we would only require to
combat the evils arising from the absence of the biliary secretion in
the digestive process, which, as was before said, can to a certain
extent be overcome by giving an additional quantity of food, and paying
attention to the bowels. In these remarks I have omitted taking into
consideration the effects that might arise from the tumour, or other
obstructing cause to the biliary secretion, for these would in no way
be directly influenced by the establishment of the biliary fistula.

The artificial establishment of a biliary fistula in the human subject,
is not such an Utopian idea as might at first be imagined. Distended
gall-bladders having been several times tapped with {126} success, both
in this and other countries, and the permanent establishment of a
fistula, if done in the manner I shall immediately point out, would, in
my opinion, be a much less hazardous operation than simple tapping.
Biliary fistula in dogs are generally made in a single operation, by
cutting through the abdominal parietes, seizing the gall-bladder,
stitching it to the lips of the wound, and inserting a cannula. Here
there is always some danger of the wound not healing by the first
intention, and of the passage of bile into the abdominal cavity. In the
case of the human subject, I should, therefore, recommend the inducing
of the adhesion of the gall-bladder to the abdominal parietes by means
of an escharotic, before making the opening; in which case, I can
scarcely imagine that the operation would prove one either of
difficulty or danger. But even supposing that it were not entirely free
from either, it would still surely be preferable to give the patient at
least a chance of prolonging his life, rather than to permit a fatal
affection to run its uninterrupted course, which we know can, at best,
be calculated by months only.

In those cases of jaundice from obstruction, where it might be
considered inadvisable to adopt the plan here suggested, we ought in
our treatment carefully to avoid the common error of {127}
administering mercury, or other substances supposed to have the power
of augmenting the biliary secretion. We must equally avoid the
administration of foods likely to produce a similar effect, for the
sufferings of the patient are not so much due to a deficient secretion,
as to a want of biliary excretion. Our whole energies should be
directed to sustaining the strength of the patient, and mitigating, if
possible, the physical effects of the accumulation of the bile in the
gall-bladder and biliary ducts, as well as the poisonous action of the
re-absorbed secretion. This, I believe, we can best do by administering
light and readily digested food, keeping the bowels open by gentle
purgatives, and favouring the elimination of the biliary constituents
from the blood by mild diuretics. Our object may be still further
advanced by artificially supplying the place of the absent bile in the
digestive process. _Not, however, in the way usually adopted, of giving
inspissated bile along with the food;_ a method of treatment which
originated ere modern physiology rent the veil of therapeutical
empiricism. In the first place, the bile prepared according to the
method indicated in the pharmacopoeias, has its most essential
properties destroyed during the process of preparation. And in the
second place, we have hitherto been instructed to administer it {128}
at the very time which modern research has proved to be the most
unsuitable that could possibly be devised. In administering bile
immediately after food, as is usually done, we most effectually produce
the contrary result to what is intended. When bile mingles with gastric
juice, it destroys the digestive power of the latter, so that by giving
the bile immediately or soon after a meal, we really diminish instead
of increase the digestive functions. My experiments, both chemical, and
physiological, have led me to propose not only a new method of
preparing bile for medicinal purposes, but also to suggest an entirely
new mode of administering it.

Firstly,--As regards the method of preparation. Nothing can be more
simple, and at the same time more effectual. Fresh bile, taken directly
from the gall-bladder of the newly killed pig, is filtered, through
very porous filter-paper, to free it from mucus; it is then as rapidly
as possible evaporated to dryness at a temperature not exceeding 160°
Fahr. The bile, as soon as dried, is ready for use. Simple as this
operation appears in theory, there are two practical difficulties
connected with it--1st, Bile filters very slowly, and consequently
little must be put into the filter at a time. 2nd, Bile is rather
hygroscopic, and consequently, in order to get it dried quickly, it is
necessary {129} to spread it over a large surface. If the bile has been
well prepared, that is to say, thoroughly freed by filtration from its
ferment mucus, and well dried, it will keep in stoppered bottles for
many months without losing any of its active properties.

Having stated that bile as at present employed more frequently does
harm than good, by retarding instead of hastening the digestive
process, I have now to point out the manner in which it may be given
with advantage.

If bile be administered, as I propose, at the _end_ of stomachal
digestion, it will, as in the healthy organism, act on the chyme at the
proper moment, and thereby render it fit for absorption. In order still
further to ensure the action of the bile being delayed until the food
is in a condition favourable to its action, that is to say, until it is
ready to pass from the stomach into the duodenum, I have had the bile,
as above prepared, put into capsules,[31] which are not readily acted
on by the gastric juice. While in the stomach, the capsules, however,
swell up from the size of a pea to that of a small gooseberry, and at
the same time become so soft that they will readily burst in passing
the pylorus into the duodenum, and thereby allow {130} the bile to
escape, and come in contact with the food at the precise moment its
action becomes requisite in the digestive process.[32] The capsules not
only preserve the active properties of the bile for an almost
indefinite period, but they have the advantage of most effectually
preventing the patient tasting the remedy.

[Footnote 31: The capsules were made by Savory and Moore, and I have
every reason to be satisfied with the manner in which they accomplished
the object in view.]

[Footnote 32: Prepared bile, made up into an ordinary pill, dissolves
in gastric juice in a quarter of an hour. When the pill is silvered it
is dissolved in half an hour, and when gilded, in forty minutes.
Whereas, in the same specimen of gastric juice, the capsules prepared
for me by Savory and Moore, although swollen to more than three times
their original size, were nevertheless intact at the end of an hour and
a half. They readily broke on being gently squeezed between the finger
and thumb, it is not therefore probable that they would pass the
pylorus in this condition without giving way, and allowing their
contents to escape.]

Each capsule contains five grains of the prepared bile; and five grains
is equal to one hundred grains of liquid bile fresh from the
gall-bladder. Two capsules therefore represent two hundred grains of
pure bile, a quantity (though less, perhaps, than the healthy organism
consumes during each digestion) which in most cases would be sufficient
for the wants of the system. If, however, a larger amount be considered
necessary, there is no reason why three or more capsules should not be
given. By the administration of prepared bile in the manner here
described, the physician is enabled to imitate nature, and {131} supply
an important element to the system; which, although incapable of curing
the disease, can nevertheless ward off for a time the fatal
termination.[33]

[Footnote 33: It is not alone in cases of jaundice that the prepared
bile may be of service, but also in the various forms of duodenal
dyspepsia, so common among the literary classes, consequent upon either
a deficient quantity, or an abnormal quality of bile.]


{132} TABULAR VIEW OF THE PATHOLOGY OF JAUNDICE, ACCORDING TO THE
AUTHOR'S VIEWS.

         |From        |Enervation. . . . . . |Fright.
         |Suppression.|                      |Anxiety.
         |            |                      |Over-mental exertion.
         |            |                      |Concussion of Brain.
         |            |
         |            |Congestion |Active. . |Hepatitis.
         |            |of Liver.  |          |Direct Violence.
         |            |           |          |Dyspepsia.
         |            |           |          |Ague.
         |            |           |          |Typhus.
         |            |           |          |Typhoid.
         |            |           |          |Scarlatina.
         |            |           |          |Pyæmia.
         |            |           |          |Yellow Fever.
         |            |           |          |Poison.
Jaundice.|            |           |
         |            |           |Passive.  |Heart Disease.
         |            |                      |Pneumonia.
         |            |                      |Pleurisy.
         |            |                      |Imperfect Circulation
         |            |                      |  in the Newborn.
         |            |
         |            |Absence of Secreting  |Cancer.
         |            |  Substance.          |Cirrhosis.
         |                                   |Fatty Degeneration.
         |                                   |Amyloid Degeneration.
         |                                   |Atrophy.  |Acute.
         |                                   |          |Chronic.
         |
         |From        |Congenital Deficiency |Small Ducts (?)
         |Obstruction.|  of Ducts.           |Common Duct.
                      |
                      |Accidental Obstruction|Gall-stones.
                      |  in course of Duct.  |Hydatids.
                      |                      |Foreign Bodies
                      |                      |  from Intestines.
                      |
                      |Closure of Outlet. .  |Pressure of Pregnant
                                             |  Uterus.
                                             |Impacted Fæces in
                                             |  Transverse Colon.
                                             |Organic Disease of
                                             |  Pancreas, or of
                                             |  neighbouring Organs.
                                             |Abscess in Head of
                                             |  Pancreas.
                                             |Ulcer of Duodenum.


{133}

INDEX.


A.

Abscess in kidney, 58
  in pancreas, 86

Acids, treatment by, 106
  of bile, 8, 36, 58

Acute atrophy of liver, 34

Ague, jaundice in, 28
  urine in, 28

Albumen in urine of ague, 28

Albuminose, 14

Alkalies, treatment by, 106

Artificial jaundice, 95

Atrophy of liver, 34


B.

Benzoic acid, treatment by, 109

Bidder's researches, 16

Bile, acids of, 8, 36, 58
    tests for, 58, 61
  action of, on albumen, 14
  action on fats, 16
  analysis of, 83
  colour of, 10
  diseased, 83
  drunk by Caffres, 19
  effects of food on, 11
  inorganic constituents, of, 10
  pigment in kidneys, 57, 86
  mode of secretion, 11
  nature of, 7, 83
  in digestive process, 15
  essential to life? 13
  specific gravity of, 10
  treatment of jaundice by, 127
  resin, 10

Biliary fistula, 124

Biliverdine, 7, 56

Blood in jaundice, 100

Budd's (Dr.), views, 7, 30


C.

Cancer of liver, 32
  of pancreas, 46

Carbonate of soda, treatment by, 108

Cherry-stones in bile-ducts, 45

Cholesterine, 8, 82, 108

Colour of bile, 10

Congestion, hepatic, 24, 104

Cystine, 86


D.

Diseases with which jaundice is associated, 3

Dyspepsia, 26


E.

Eiselt (Dr.), 68

Enervation, 22, 110

Epidemic jaundice, 90


F.

Farre (Dr.), case, 104

Fat in fæces, 54, 72
  absorption of, 16

Flatulence, 13

Frerichs on mechanism of jaundice, 6, 33

Fright, effect of, 23


G.

Gall-bladder, absence of in animals, 12, 41
  congenital deficiency of, 40

Gall-stones--
  mode of escape from gall-bladder, 44
  mode of formation, 43
  in common duct, 44
  in gall-bladder, 43
  in intestines, 123
  treatment of, 108, 114, 119, 123
  carbonate of soda in, 108
  chloroform in, 119
  podophyllin in, 115
  sulphuric ether in, 119

Glycocholic acid, 8, 97

Glycocholate of soda, 8
    injected into blood, 39


H.

Heart disease, jaundice in, 30

Hepatic congestion, 24, 104

Hoppe's method, 58

Hydatids in bile-ducts, 45


I.

Impacted fæces, effect of, 46

Inflammation of liver, 24, 104

Inorganic constituents of bile, 10, 83

Intestinal excretion, analysis of, 51

Introduction, 1


J.

Jaundice, artificial, 95
  from acute atrophy of the liver, 34
    absence of bile-duct, 40
    absence of gall-bladder, 41
    absence of secreting substance, 31
    ague, 27
    blood-poisoning, 27, 93
    blow on head, 24
    cancer, 32
    enervation, 22, 110
    entozoa, 45
  epidemic, 90
  from fright, 23
    gall-stones, 42, 116
    hepatic congestion, 24, 104
    mental emotion, 22, 110
    active hepatic congestion, 25, 104
    passive hepatic congestion, 29
    disease of the pancreas, 46
    pregnancy, 46
    obstruction, 39, 71
    scarlatina, 93
    suppression, 20
    typhus, 27
    tubercle, 32
    zymotic disease, 27, 90
  mechanism of, 19
  treatment of, 101


K.

Kidneys as eliminating organs, 11

Kühne's views, 58, 98


L.

Lenz's experiments, 16

Leucine, 63, 80, 95

Liver cells, 38, 85

Liver, extirpation of, 11


M.

Marcet (Dr.), 16

Martin (Dr.), 90

Matteucci (Prof.), 17

Melanine in urine, 68

Mercurials, treatment by, 102

Milk in jaundice, 22


O.

Obstruction, of bile-duct, 71
  of pancreatic duct, 71
  treatment in jaundice from, 122


P.

Pancreas, abscess in, 87

Pancreatine, 73

Pancreatic juice, 18
    absence of, 73

Pathology of jaundice, tabular view of, 132

Pathological conditions with which jaundice is associated, 3, 132

Pettenkofer's test, 36

Pipe-clay stools, 52

Pneumonia, jaundice in, 30

Podophyllin, treatment by, 112
  in cases of gall-stones, 114

Prance (Dr.), 71

Pregnancy, jaundice in, 91

Pregnant uterus, effect of, 46

Prepared bile, treatment by, 127


S.

Saint-Vel (Dr.), 91

Scarlatina associated with jaundice, 93

Schmidt's researches, 16

Specific gravity of bile, 10, 83

Sputa in jaundice, 22

Stools, fat in, 54, 72
  colour of, 52

Sugar, a normal constituent of bile, 10
  in urine, 70

Sulphuric ether, 119

Suppression, jaundice from, 20

Sweat in jaundice, 22


T.

Table of the pathology of jaundice, 132

Taurocholate of soda, 8

Taurocholic acid, 8, 97

Tears in jaundice, 22

Theories regarding mechanism of jaundice, 5

Treatment of jaundice, 101
  by acids, 106
  by alkalies, 106
  by benzoic acid, 109
  by biliary fistula, 124
  by carbonate of soda, 108
  of gall-stones, 108, 114, 119, 123
  by Lithia water, 109
  by mercurials, 102
  of jaundice from obstruction, 122
  by podophyllin, 112
  by prepared bile, 127
  by taraxacum, 122

Tubercle, 32

Tyrosine, 63, 80, 95


U.

Urea, 70

Uric acid, 56, 70

Urine, analysis of, 55
    in acute atrophy, 36
  in jaundice from ague, 28
  in obstruction of bile-duct, 74, 78, 79
  bile-acids in, 36, 58, 74, 97
  colour of, 55
  tyrosine and leucine in, 36, 80, 95
  melanine in the, 68
  uric acid, 56, 70
  sugar in, 70

Urohæmatine, 7, 55


W.

Wilks's cases, 35, 40


Y.

Yellow atrophy of liver, 34




WILLIAM STEVENS, PRINTER, 37, BELL YARD, TEMPLE BAR.