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GLAUCOMA

A SYMPOSIUM PRESENTED AT A MEETING OF THE
CHICAGO OPHTHALMOLOGICAL SOCIETY,
NOVEMBER 17, 1913.

EDITED BY

WILLIS O. NANCE, M.D.,

PRESIDENT CHICAGO OPHTHALMOLOGICAL SOCIETY (1913); OPHTHALMIC
SURGEON, ILLINOIS CHARITABLE EYE AND EAR INFIRMARY; FORMER
OCULIST AND AURIST, COOK COUNTY HOSPITAL; EDITOR
JOURNAL OF OPHTHALMOLOGY AND OTO-LARYNGOLOGY,

AND

WESLEY HAMILTON PECK, M.D.,

PRESIDENT CHICAGO OPHTHALMOLOGICAL SOCIETY (1914); FORMER
PROFESSOR OPHTHALMOLOGY, CHICAGO EYE, EAR, NOSE AND
THROAT COLLEGE; ASSISTANT SURGEON, ILLINOIS
CHARITABLE EYE AND EAR INFIRMARY;
OPHTHALMIC SURGEON, OAK
PARK HOSPITAL.

1914
CHICAGO MEDICAL BOOK COMPANY
CHICAGO


COPYRIGHT 1914
BY
CHICAGO MEDICAL BOOK COMPANY




CONTRIBUTORS

EDWARD JACKSON, A.M., M.D.
Prof. Ophth. Univ. Colo.; Emer. Prof. Ophth. Phila. Polyclinic; Ex-Ch.
Sec. Ophth. A.M.A.; Ex-Pres. Am. Acad. Med. and Am. Acad. Ophth. and
Oto-Laryng.; Mem. Am. Ophth. Soc. and Honorary Mem. Chicago Ophth.
Society.

JOHN ELMER WEEKS, M.D., D.Sc.
Prof. Ophth. Univ. and Bellevue Hosp. Med. Coll., N.Y.; Ophth. Surg.
N.Y. Eye and Ear Inf.; Mem. Am. Ophth. Soc.; Hon. Mem. Chicago Ophth.
Soc. and Royal Hungarian Med. Soc. Budapest.

GEORGE EDMUND DE SCHWEINITZ, A.M., LL.D., M.D.
Prof. Ophth. Univ. Penn.; Ophth. Surg. Univ. Hosp., Phila. Hosp.,
Orthop. Hosp. and Inf. for Nerv. Dis.; Consult. Ophth. Surg, Phila.
Polyclinic; Honorary Member Chicago Ophth. Soc.

ROBERT HENRY ELLIOT, M.D., B.S. LOND., Sc.D. EDIN., F.R.C.S. ENG., ETC.,
LIEUT.-COLONEL, I.M.S.
Supt. Gov. Ophth. Hosp., Madras. India; Prof. Ophth. Med. Coll., Madras;
Fellow Univ. of Madras; Honorary Member Chicago Ophthalmological
Society, U.S.A.

CASEY A. WOOD, M.D., C.M., D.C.L.
Prof. Ophth. Univ. Ill.; Late Prof. Ophth. N. W. Univ.; Ex-Pres. Am.
Acad. of Med.; Am. Acad. Ophth. and of the Chicago Ophth. Soc.;
Ophthalmic Surg. St. Luke's Hosp.; Consulting Ophth. Surg. St. Luke's
and Cook County Hosp.; Ex-Ch. Ophth. Sec. A.M.A.; Editor System Ophth.
Therapeutics. Sys. Ophth. Operations and American Encylopedia
Ophthalmology.

FRANCIS LANE, A.B., M.D.
Pathologist and Asst. Ophthalmic Surgeon Ill. Char. Eye and Ear Inf.;
Instructor in Ophth. Rush Med. Coll.; Asst, Ophth. Surg. Presbyterian
Hospital.

E. V. L. BROWN, M.D.
Asst. Prof. Pathology of the Eye, Univ. Chicago; Asst. Prof. Ophth. Rush
Med. College; Ophth. Surg. Ill. Eye and Ear Inf. and Cook County Hosp.;
Mem. Am. Ophth. Soc.

NELSON M. BLACK, PH.G., M.D.
Author of The Development of the Fusion Center in the Treatment of
Strabismus; Examination of the Eyes of Transportation Employes;
Artificial illumination a Factor in Ocular Discomfort, etc.

FRANK C. TODD, M.D.
Prof. Ophth. and Oto-Laryng., Univ. Minn.; Chairman Sec. Ophth. A.M.A.
and second Vice-Pres. A.M.A.; Ophth. Surg. Univ. and Hill Crest
Hospital.

ALBERT EUGENE BULSON, JR., B.S., M.D.
Prof. Ophth. Ind. School Med.; Ex-Ch. Sec. Ophth. A.M.A.; Ophth. Surg.
St. Joseph's Hospital; Editor Jour. Ind, Slate Med. Assn.




DEDICATED TO
DR. EDWARD JACKSON
DR. JOHN E. WEEKS
DR. GEORGE EDMUND DE SCHWEINITZ
LIEUTENANT COLONEL ROBERT HENRY ELLIOT
HONORARY MEMBERS
BY THE CHICAGO OPHTHALMOLOGICAL SOCIETY
IN RECOGNITION OF THEIR SPLENDID ACHIEVEMENTS
IN THE DOMAIN OF OPHTHALMOLOGY




ABSTRACTS.


I. Etiology and Classification of Glaucoma.

Abstract:--

Etiologic factors include: obstruction of lymph spaces, especially the
angle of the anterior chamber; blood pressure, arterial, capillary and
venous; affinity of tissues for fluids; alterations of the intra-ocular
fluids; inflammations in the eye ball; and failure of a nerve apparatus
to control fluid in the globe. Classification: various types of glaucoma
constituting clinical entities must be recognised, as: simple glaucoma,
recurring exacerbations, congestive, mechanical, and increased tension
arising during uveal inflammations.

DR. EDWARD JACKSON, Denver.

Discussion by DR. FRANCIS LANE, Chicago.


II. Pathology of Glaucoma.

Abstract:--

(a) Changes taking place in corneal tissue.

(b) Iris angle with particular reference to the ligamentum pectinatum.

(c) Variations in the condition of the ciliary body.

(d) Consideration of the anatomical changes that take place in glaucoma
secondary to retinal and chorioidal hemorrhage.

DR. JOHN E. WEEKS, New York City.

Discussion by DR. E. V. L. BROWN, Chicago.


III. Concerning Non-surgical Measures for the Reduction of Increased
Intra-ocular Tension.

Abstract:--

(a) The use of myotics; their preparation, method of administration, and
explanation of their action.

(b) Reduction of increased intra-ocular tension by means of various
mechanical measures, notably massage, vibration massage, suction
massage, electricity and diathermy.

(c) Indirect reduction of increased intra-ocular tension, brought about
by lowering the general vascular pressure.

(d) The relation of osmosis, lymphagogue activity, the absorption of
edema, the stimulation of capillary contractility, and the lowering of
the affinity of ocular colloids for water in their relation to the
reduction of increased intra-ocular tension.

DR. GEORGE EDMUND DE SCHWEINITZ, Philadelphia.

Discussion by DR. NELSON M. BLACK, Milwaukee.


IV. Trephining for Glaucoma.

Abstract:--

(a) The aim of the operation is the formation of a foreign-body-free
fistula.

(b) It is most important to leave uveal tissue untouched.

(c) Method of doing this explained.

(d) The area available for trephining.

(e) Method of increasing that area.

(f) Cornea splitting.

(g) Placing of trephine.

(h) Technique of using trephine.

(i) The operation is not difficult.

(j) The operation valuable as a prophylactic measure.

DR. ROBERT H. ELLIOT, F.R.C.S., Lieut.-Col. I.M.S., Madras, India.

Discussion by DR. FRANK C. TODD, Minneapolis.


V. Operations Other than Scleral Trephining for the Relief of Glaucoma.

Abstract:--

Most of the ordinary surgical procedures employed for lowering
intra-ocular tension furnish a permanent cure of certain fairly well
defined varieties of glaucoma. They also relieve the symptoms and retard
the progress of other varieties of the disease, even if they do not
perform a cure. In a third class of cases, they either have no effect
whatever in arresting the disease or they hasten its march towards
blindness.

What operative procedure gives, on the whole, the best results? In other
words, what operation is the easiest of performance, is the least likely
to be attended by serious complications and is available for the largest
number of cases? Reasons for believing that of the better known
procedures simple iridectomy is the least effective, while those
interventions producing a large, thin, scleral filtration-cicatrix are
the most valuable.

DR. CASEY A. WOOD, Chicago.

Discussion by DR. A. E. BULSON, JR., Fort Wayne




Etiology and Classification of Glaucoma

BY

EDWARD JACKSON, M.D.,

Denver.


It is convenient to start with the conception that glaucoma is increased
tension of the eyeball, plus the causes and effects of such increase;
although a broad survey of the facts may reveal a clinical entity to be
called glaucoma, without increased tension constantly or necessarily
present, and cases of increased intra-ocular tension not to be classed
as glaucoma.

The physiologic tension of the eyeball is essential to ocular
refraction, and closely related to ocular nutrition. Fully to understand
the mechanism for its regulation would carry us far toward an
understanding of the causes of glaucoma. Normal tension is maintained
with a continuous flow of fluid into the eye and a corresponding
outflow. Complete interruption of the nutritional stream would be speedy
death; partial interruption may be held responsible for most of the
visual impairment and pain of glaucoma.

The balance of intra-ocular pressure is not maintained by the slight
distensibility of the sclero-corneal coat. Increased pressure does not
open new channels for the escape of intra-ocular fluid; if, indeed, it
does not tend to close the normal channels.

The affinity of the tissues for water, or, as Fischer explains it, the
affinity of the tissue colloids for water, seems too little related to
the requirements of ocular function to furnish the needed regulation of
tension. The lymph spaces and blood-channels of the eye are large, as
compared with the mass of its tissue colloids. In these spaces and
channels must be sought a means for rapid response to the need for
regulation of intra-ocular tension. Fischer has shown, that when the
enucleated eyeball is placed in a weak solution of hydrochloric acid,
the swelling of the tissue colloids is sufficient in a few hours, to
burst the sclero-corneal coat. But this is an eye in which all
nutritional changes have ceased. He brings together many facts to
support the view that in the living tissues impaired circulation, and
especially diminished oxidation, are the chief causes of increased
affinity of the colloids for water. Such affinity increased by the
impairment of the intra-ocular circulation, may well constitute a factor
making for malignancy in glaucoma. But it can hardly explain the
original departure from a normal pressure balance.

We must assume that intra-ocular pressure is kept down to the normal
limit, by the prompt response of a regulative mechanism, which
diminishes the flow of fluid into the eye, or permits its more rapid
escape, whenever fluid tends to accumulate in the eye and increase its
tension.

Little has been done to show that increase of fluid entering into the
eye is the cause of glaucoma. A normal, or even a low arterial blood
pressure is sufficiently above the normal intra-ocular pressure to
furnish a source of increased fluid in the eye. Increased arterial
pressure has been found in a large proportion of cases of glaucoma; and
may be necessary to the production of the highest intra-ocular tension.
A sudden relaxation of the arterial walls, that would permit the
arterial blood pressure to make itself felt in the eye, might cause an
important rise of intra-ocular tension and may be a factor in the
etiology of acute attacks. It affords a possible mechanism through which
may be produced the recognized glaucomatous effects of certain nerve
disturbances. But such attacks are not commonly associated with
noticeable flushing of the head and face generally; and paralysis of the
cervical sympathetic is known to lower the intra-ocular tension.

Capillary blood pressure must lie between the arterial blood pressure
and the venous blood pressure. It must be closely associated with the
nutritional processes like secretion or inflammation; beyond this we
know little about it. The association of increased blood pressure with
glaucoma seems to be generally an indirect one through vascular lesions
and disturbances of nutrition.


_Obstructed Outflow_

A reservoir with a free outlet can only fill during a flood; and then
quickly empties itself again. The outflow channels in the normal eye
provide for carrying away of the waste products of such an active
nutrition, that it is hard to think they will become inadequate in
glaucoma until there has been a marked decrease from their normal
capacity. Priestley Smith has pointed out that the glaucomatous eye
softens more slowly than the normal eye after enucleation, in spite of
the fact that a greater force is operating to drive fluid out of the
eye. In his recent tonometric studies Schoenberg noted that under
manipulation the glaucomatous eye softened more slowly than the normal
eye; and suggests this diminished drainage as an important evidence of
glaucoma.

Obstructed outflow might begin in an abnormal tendency of the tissues to
retain fluid, a tendency that Fischer might locate in the colloids. The
increase of intra-ocular pressure noted in cases of uveal inflammation,
to be presently referred to, may be due to some such tendency. But it is
rational to ascribe to obstruction of the filtration angle of the
anterior chamber, the important part it has been supposed to play in the
pathology of glaucoma. However this obstruction may be brought about,
whether by thickening of the iris root during dilatation of the pupil,
pushing forward of the iris root by the larger ciliary processes of age,
or the enlarged crystalline lens pressing on the ciliary processes; or
by inflammatory adhesion of the iris to the filtration area; ballooning
of the iris, or its displacement by traumatic cataract; or adhesion to
the cornea after perforating ulcer in the secondary glaucomas; or
whether the obstruction is due to the accumulation of experimental
precipitates, as shown by Schreiber and Wengler, or possibly of pigment
granules into Fontana's space; or a process of sclerosis closing the
spaces by contraction of new-formed connective tissue, or the covering
over with proliferating implanted epithelium following injury opening
the anterior chamber; glaucoma follows impairment of this drainage
space, and lessened outflow through it. This blocking of the angle of
the anterior chamber must be regarded as an established fact in the
etiology of glaucoma. But because it is so definitely established, and
because so much work has been done with reference to it, we may attach
to it an undue importance.

The escape of the outflow of fluid from the eye is ultimately through
the veins. The general venous blood pressure is so low (often negative
in the great veins of the neck during inspiration) that no obstacle can
come from it to the ocular outflow. The venous blood pressure permits
the eyeball to become perfectly soft. We have all seen tension of 5 mm.,
or even less; and general venous pressure does not rise to the normal
intra-ocular tension. Increased intra-ocular pressure requires that
there must be some obstacle that keeps the intra-ocular fluid from
reaching the general venous system. This may be in the lymph drainage
system of the eye; but it may also be in the ocular veins themselves.

Experimentally the eyeball can be made to burst by tying all the venous
outlets from it. I have seen very high intra-ocular tension develop in a
few hours after general thrombosis of the orbital veins. The absence of
the canal of Schlemm is noted in congenital buphthalmos. The enlargement
of the anterior perforating veins is an old symptom of chronic glaucoma.
Obstruction to outflow of blood through the vorticose veins, by the
increased intra-ocular pressure, has long been a recognized explanation
of the malignant tendency of glaucoma--a part of the vicious circle
established in this disease. There is reason that we should give careful
attention to the views of Heerfordt and Zirm, that obstruction to the
venous outflow may be the effective cause of the disease. Zirm believes
the venous plexus of the choroid is an essential part of the mechanism
for the regulation of intra-ocular tension, the necessary vaso-motor
control depending on nerve centers situated in the iris.


_Nerve Control_

The accurate control of normal intra-ocular pressure, by mutual
adjustment of inflow and outflow of fluid, is scarcely conceivable
without some highly specialized, extremely sensitive nerve mechanism to
preside over it. This is suggested by analogy with the regulation of
secretion in the lacrimal, salivary, or peptic glands, or the
maintenance of blood pressure in the heart and arteries. Clinical
observations point the same way. Many patients connect their attacks
(especially their earlier ones of ocular discomfort, impaired vision,
haloes around the light, and dilated pupil) with social excitement,
anxiety, worry, anger or fatigue. A patient of mine gave up her card
parties, because an exciting game generally ended in blurred vision, a
rainbow around the light, and a dilated pupil, and sometimes an aching
eye. Another woman watching beside her dying husband and exposed to
extreme cold, had her first attack of glaucoma, so severe as to destroy
the sight of one eye. The other eye, also affected at the time,
recovered good vision, and has remained several years without a second
attack and without treatment.

Laqueur's first attack occurred at the end of a long exhausting morning
in the operating room, with luncheon delayed two hours. The connection
of his later attacks with anger, worry, embarrassment, even the
excitement of watching a play at the theatre, was noted again and
again. In Javal's case, the attack fatal to one eye came at the
culmination of an exciting electoral campaign. The other eye was
stricken at the termination of the Dreyfus case, in which Javal was
intensely interested. There seems to be a special liability to glaucoma
among those residing at high altitudes, best explained by nerve
influence. The frequency of glaucoma among Jews may be due to a small
cornea, as suggested by Priestley Smith; but it is quite as reasonable
to connect it with a racial excitability or nervous instability. More
definite knowledge of the nervous mechanism concerned in the regulation
of intra-ocular pressure and the production of glaucoma is much needed.


_Alterations of Fluids and Tissues_

The influence of increased affinity of the tissues for fluid has already
been referred to. That a similar obstacle to the escape of fluid from
the eyeball might be due to a change of character in the fluid, is a
conception that has been entertained as a working hypothesis, and much
experimental and analytical work has been done to test its correctness.
This work has been so slightly related to practical ophthalmology, and
so contradictory in its results that alterations in the fluids can only
be regarded as a possible etiologic factor. Glaucoma secondary to
intra-ocular hemorrhage, operations on the lens or its capsule, or
severe nutritional disturbance may be capable of such explanation.


_Different Kinds of Glaucoma_

A better grasp of the etiology of glaucoma may be attained by
considering separately various types of cases; although perfectly
typical cases may be rare; and cases of mixed type and etiology much
more frequent.

Simple glaucoma has been recognized as closely related to atrophy of the
optic nerve with deep excavation. No line of demarcation can be drawn
between them, except by reserving the term of glaucoma for cases that
depart from the pure type, terminating in glaucoma of some other kind,
which is no more significant than the passage of a conjunctivitis into a
keratitis, or an iritis into a glaucoma. Cases of simple glaucoma do run
their course of many years to complete blindness, or to death, without
exacerbations, inflammation, or characteristic pain. In such cases the
intra-ocular tension does not rise suddenly; and it may be little or not
at all elevated above the usual normal limit.

For nine years I have watched the progress of such a glaucoma in a man
now aged 87, with slow development of glaucomatous cupping of the optic
disc, now more than 3 D. deep. The tension has never been noted at more
than Plus T (?), and when taken with the tonometer varied from 9 to 32
mm. for the worse eye, and 13 to 24 mm. for the other. Similar cases in
which the tension lay within the commonly accepted normal limits have
been reported recently by Bietti and Stock.

In the eye there is probably a normal equilibrium between blood
pressure, tissue activity, and intra-ocular tension. This may be
destroyed either by increasing the intra-ocular tension, or lowering the
tissue activity, or the blood pressure. Lowered blood pressure has been
suggested by Paton as an explanation of symptoms usually ascribed to
vascular obstruction. Rising blood pressure may be required in old age
to compensate for diminished tissue activity; and it is conceivable,
under normal intra-ocular tension, that diminished nutritional activity
may result in the same symptoms as are produced in other eyes by
increased tension. Glaucoma is probably not so much an increase of
tension as a loss of balance between intra-ocular tension and
nutritional activity.

In contrast with the above are the cases marked by sudden elevations of
ocular tension recurring repeatedly over long periods without permanent
visual impairment. Laqueur's case continued of this character for six
years, under the use of miotics, and then was cured by iridectomy, the
cure remaining permanent with normal vision until his death after 30
years. Millikin has reported the case of a patient who in five years had
"many hundreds" of attacks, in which vision was impaired, haloes
appeared about the light, the pupil dilated, the cornea became steamy,
and tension rose to plus T. 1 or plus T. 2. After iridectomy the attacks
ceased, leaving no pathological cupping of the disc, full vision, and a
good field. I have seen cases of this type in women under middle age,
and of marked nervous instability.

A third type which will come to be more generally recognized, as the
tonometer comes to be more widely used, includes cases in which there is
little beside the increase of intra-ocular tension to justify their
mention in a discussion on glaucoma. A patient, then aged 21, suffered
three years ago from a scotoma almost central; and was first seen six
months after that with a macular choroidal atrophy and abnormal
pigmentation. She suffered, we afterwards concluded, from choroidal
tuberculosis. A recurrence involving adjoining choroid occurred fourteen
months ago. There was at the start pain, slight dilatation of the pupil,
and slight general hyperemia of the globe. The tension of the eyeball
rose to 60 mm., that of the fellow eye being 20 mm. Under miotics the
tension fell at first but slightly. It was 55 mm. at the end of a week;
but after two weeks came down to normal, 20 mm. A month later the
tension rose to 28 mm., but for a year has continued normal; the eye did
well under tuberculin treatment, and without any local treatment. In
September of this year I had two cases of iritis in which the
intra-ocular tension rose to 45 and 52 mm., respectively, and gradually
returned to normal, with the cure of the iritis under atropine. In one
of these cases, a lady of 70, I used atropine also in the other eye,
but the tension of that eye remained normal, 22 to 24 mm., throughout.
After needling the lens in young people I have seen a rise of
intra-ocular tension to 50 and 60 mm., maintained for many days, with
considerable general deep hyperemia, and soreness of the globe, followed
by gradual return to normal tension, and no permanent impairment of
vision or the visual field.

One other type may be mentioned. That of an elderly patient with marked
vascular disease, often renal involvement, and distinctly impaired
nutrition. There may be renal retinitis or retinal hemorrhages. The case
may easily become one of hemorrhagic glaucoma. It may run a very chronic
course. But it may become suddenly worse, or go on to complete blindness
with pain, demanding enucleation, after some temporary perturbation, as
the performance of a glaucoma operation. It is pre-eminently the kind of
a case you would prefer would go to some one else.

Each of these types illustrate a distinct cause or group of causes. The
first type brings us near to what may be the essential nature of
glaucoma, impairment of ocular nutrition by the intra-ocular tension,
which is generally elevated, but may not be above the usual normal. A
special weakness in the nutrition of nerve tissue may be assumed. It
would help to explain the cavernous atrophy of the optic nerve
associated with simple glaucoma. The second type shows impairment of the
regulative mechanism permitting rapid rise of the intra-ocular pressure.
In persons of good nerve nutrition and strong recuperative power, it may
exist for years without doing permanent damage. But joined to causes of
the first type, lowered nutritive activity, it causes rapid and
permanent loss of sight. The third group are cases associated with
glaucoma only as causes. In eyes with low nutritive power, or subject to
exacerbations of increased intra-ocular pressure, uveal inflammations
may prove disastrous. The fourth type shows the results of the
combination of the causes of the other types; with the elements of acute
or slow malignancy added--the impaired circulation and lowered oxidation
producing some degree of edema of the tissues that insures a fatal
result.

This is no complete presentation of my subject, but a selection of facts
bearing on the etiology, to serve as a foundation for the discussion of
those practical aspects of glaucoma which are to claim your attention
through the papers and remarks of subsequent speakers.




Dr. Edward Jackson's Paper on Etiology and Classification of Glaucoma

Discussion,

FRANCIS LANE, M.D.

Chicago.


Not one of the theories thus far propounded to explain the essential
cause of increased intra-ocular tension is satisfactory. Our present day
knowledge apparently ceases with a more or less incomplete understanding
of the mere circumstance under which increase of tension in general
depends.

The question of the source of the normal intra-ocular pressure must
first be solved before any discussion of a pathological increase can be
engaged in. This question primarily hinges on whether the corneo-sclera
is to be regarded as an unelastic capsule with a fixed volume, or as a
yielding envelope with an ever changing capacity.

This brings us at once to the consideration of that theory which
probably has held our attention for the longest period of time, _i. e._,
the volumetric theory. According to it, the normal intra-ocular tension
depends on the volume of fluids within the eyeball. Any variation in the
quantity of the contents gives rise to a change in the pressure,
therefore, the globe has been regarded as "an elastic capsule, whose
capacity, form, and internal pressure depend on the balance struck
between a constant inflow, or formation of aqueous, and a proportionate
outflow or resorption." (Henderson.)

Hill has satisfactorily demonstrated that, under physiological
conditions, the hydrostatic pressure within the eye and the skull is
identical; it rises and falls simultaneously; it is the same as the
cerebral venous pressure; it is constantly varying, depending directly
on the general circulation. Upon these findings Henderson based his
opinion that the physiological properties of the tunica fibrosa and the
skull are identical, realizing at the same time, that the rigidity of
the corneo-sclera, because of its fibrous nature, is not as firm as the
cranium. In accepting this belief the inference was that the cubic
capacity of both coverings is fixed. Applying these conclusions to the
eye, it can be said that the pressure of the fixed intra-ocular volume
varies with the venous tension within the bulb, which in turn is
influenced by the general circulation. Such a conception, while not
strictly in accord with recognized physiological teachings, proves that
the normal intra-ocular pressure is not a question of volume content,
but that it is purely a question of pressure of a fixed volume within an
unyielding capsule. Dr. Jackson virtually puts aside the volumetric
theory with his statement, that "the balance of intra-ocular pressure is
not maintained by the slight distensibility of the sclero-corneal coat."
Further discussion on the inadequacy of the volumetric theory need not
detain us.

It is well to recall a few anatomical features because of their bearing
on the theories herein considered.

1. The angle of the anterior chamber is a true angle and not an annular
sinus.

2. The meshwork of the iris angle (ligamentum pectinatum), a cellular
structure at birth, undergoes a progressive and physiological fibrosis
with early subsequent sclerosis, until finally it becomes a fibrous
structure. The individual strands of this meshwork are more than two
times as large at advanced age as at birth, consequently the alveoli of
the meshwork becomes markedly reduced in size.

3. The spongy nature of this meshwork affords free access of aqueous to
the venous sinus of Schlemm, thence by tributaries into the
supra-choroidal space and anterior uveal venous system.

4. Fuchs's iris cripts afford direct access of aqueous to the veins of
the iris.

Furthermore, two simple principles are taught by physics: Fluids are
incompressible and they seek the lowest hydrostatic level. The
application of these perfectly obvious principles to the eyeball makes
the intra-ocular pressure the same as that within the elastic venous
walls, which is the lowest circulating pressure within the bulb.

To summarize: The aqueous has direct access to the anterior uveal venous
system; the physiological thickening of the strands of the meshwork of
the iris angle supplies a mechanical obstruction between the anterior
chamber and the venous sinus of Schlemm; intra-ocular pressure stands at
the same level as the intra-venous, consequently, the hydrostatic
pressure is the same on both sides of the iris angle meshwork, because
the canal of Schlemm is a secondary venous system; lastly, the outflow
of aqueous into the venous sinus is by diffusion, not by filtration,
because the pressure is the same on both sides of the meshwork.

These facts and deductions have given rise to the present day
circulatory theory of intra-ocular pressure, so we now can approach the
predisposing and exciting factors which determine glaucoma.

The central fact to be borne in mind is, if the physiological pressure
is vascular in origin and nature, the pathological pressure must
likewise be derived from the same source.

Sclerosis of the meshwork of the iris angle is the predisposing factor
because it hinders free access of aqueous into the venous sinus of
Schlemm. Sclerosis alone, however, will not cause glaucoma so long as
access to the iris veins can keep the intra-ocular pressure at the
intra-venous level, and, too, as long as the exciting cause is absent.

The exciting cause is vascular, maintained and influenced by the general
circulatory pressure. A rise of the general vascular tension alone will
not cause glaucoma, because any alteration in intra-ocular pressure
resulting would be purely a temporary change, easily taken care of by
the extensive access of aqueous to the intra-ocular venous system. When
these two factors coexist in their varying combinations, pathological
increase of pressure results--in short, glaucoma.

Syphilis, rheumatism, gout, auto-intoxication and many other
constitutional disorders are well recognized agencies which induce
sclerosis in body tissues, so there can be little doubt that these
conditions produce pathological sclerosis of the meshwork of the iris
angle. Psychic disturbances, congested portal or renal system, hard
mental or muscular work, etc., etc., induce increased pressure of the
general circulation, and so simultaneously the intra-ocular pressure.

According to the edema theory advanced by Fischer, glaucoma is
"essentially an edema of the eyeball, and for its production we must
hold responsible the same circumstances which are responsible for a
state of edema in any other part of the body." The magnificent
experimental work of this investigator has shown that edema is nothing
more or less than an increased capacity of the protein colloid tissues
for water; that the most important factor leading to this increased
hydration capacity is an abnormal production or accumulation of acid
content, effected by those agencies which are instrumental in causing
sclerosis and an increase of blood pressure.

It seems that both of these theories afford an explanation for many of
the secondary pathological manifestations which characterize the
intra-ocular tissues during a glaucomatous onset.

Fischer criticizes the Henderson theory on the ground that increased
blood pressure alone does not lead to edema--edema is thwarted by high
blood pressure. On the other hand, if Fischer believes that sclerosis of
the meshwork of the iris angle is a result and not a cause of glaucoma,
then it would seem that Henderson has the better of the argument. The
physiological changes in this structure, which take place with advancing
age, can rightfully be looked upon as a predisposing factor in glaucoma.

Dr. Jackson has presented all other phases of this part of the
symposium in such a comprehensive manner that nothing further remains to
be said.




Pathology of Glaucoma

BY

JOHN E. WEEKS, M.D.,

New York City.


In reviewing the pathology of glaucoma it seems proper to consider the
various structures and tissues of the eye in logical order.

_Lids and Conjunctiva._ "The only change observed in these tissues is a
reflex edema, excited apparently by pressure on the ciliary nerves and,
probably, irritation of the vaso-motor fibers of the sympathetic."

_Lachrymal Gland._ Hyper secretion due to reflex irritation.

_Cornea._ As has been shown by Priestley Smith, the cornea in
glaucomatous eyes is, as a rule, smaller than in non-glaucomatous eyes,
the mean of a series of measurements being 11.1 mm. horizontally and
10.3 mm. vertically in glaucomatous and 11.6 mm. horizontally and 11
mm. vertically in non-glaucomatous eyes. In cases of considerable
increase of tension, particularly if the onset is sudden, the
circulation of lymph in the cornea is interfered with, the anterior
layers of the cornea become edematous, the spaces between the lamellae
filled with albuminous fluid. Some of this fluid finds its way through
Bowman's membrane, apparently by way of the minute channels which permit
the passage of small nerve twigs, and enters the epithelial cell layer.
The fluid finds its way between the epithelial cells in the deeper
layers, apparently being taken into some of the superficial cells by
imbibition. Some of the swollen surface cells open spontaneously and
discharge their contents, others drop off. The process causes a
roughening of the surface of the cornea and produces a faint haziness.
There is another form of haziness that develops on sudden rise in
tension and completely disappears on subsidence of the tension. This is
due, as has been shown by V. Fleischl (Sitzungsberichle d. Weiner Akad.
d. Wissensch, 1880) and others, to increased tension on the fibrillae of
the cornea, a double refraction being induced. In cases of long
continued increase of tension minute permanent vesicles form in the
epithelial layers, particularly in the superficial portion. Anaesthesia
of the cornea develops, due to pressure on the nerve fibers that are
distributed to the epithelium, the compression probably occurring along
the course of the long ciliary nerves, from which the corneal nerves are
derived, as they pass between the choroid and the unyielding sclera
(Collins & Mayou).

In advanced cases of glaucoma after the congestive period has subsided
the cornea becomes somewhat condensed, the lymph spaces contracted; a
condition of sclerosis obtains. Alteration in the shape of the cornea
occurs only rarely in adult life. When it does occur it takes place in
corneæ that have suffered from keratitis. The alteration is usually in
the form of ectasiæ. In infancy and early youth (buphthalmia) the cornea
may become uniformly enlarged and globular. Often, however, the
enlargement of the cornea is irregular. Increase in tension may produce
fissures in Descemet's membrane. These occur more frequently in the
cornea that have suffered a change in shape, as in buphthalmos. Gaps
occur in the elastic membrane which become covered by endothelium. Some
cloudiness may be seen in the corneal lamellae adjacent to these
fissures, in some cases due evidently to the filtration of aqueous humor
through defective endothelium. Prolonged high intra-ocular tension may
be accompanied, particularly in cases of secondary glaucoma, by
vesicular and bullous keratitis.

In acute glaucoma the sclera appears to be edematous and slightly
thickened. As the disease progresses the sclera becomes denser than
normal. The oblique openings--passages for the venae vorticosae--are
said to be narrowed. The openings for the passage of the anterior
ciliary vessels are enlarged in many, particularly in advanced cases.
Minute herniae at these openings are sometimes present. Dilatation and
tortuosity of the anterior ciliary veins are due apparently to excessive
flow of blood through them on account of the abnormally small amount
carried off by the venae vorticosae. In the stage of degeneration,
ectasae of the sclera occur most frequently near the equator of the
globe. Spontaneous rupture may take place.

_Anterior Chamber._ The anterior chamber is shallow, as a rule. This is
almost without exception in primary glaucoma in adults. In secondary
glaucoma in which occlusion of Fontana's spaces occurs as a result of
the deposition of fibrin or other inflammatory products the anterior
chamber may be of normal depth, or deeper than normal. Very deep
anterior chamber may occur in glaucoma, due to retraction of lens and
iris following fibrinous or plastic exudation into the vitreous, or
when it occurs in congenital glaucoma, due to enlargement of the globe.

_Aqueous Humor._ The aqueous humor, as has been pointed out by
Uribe-Troncoso (Pathoginie du Glaucome 1903) contains a greatly
increased quantity of albuminoids and inorganic salts in glaucoma. In
acute glaucoma the increase of albuminoids (blood proteids) is greater
than in chronic glaucoma. The aqueous humor becomes slightly turbid in
acute attacks, coagulating more readily than the normal. The plastic
principle contained in the aqueous is rarely sufficient to cause
adhesion between the margin of the iris and the lens capsule, but the
colloid nature of the aqueous, according to Troncoso, lessens its
diffusibility and prevents its free passage into the lymph channels. The
increase in albuminoids is a consequence of congestion and venous stasis
and does not precede the attack.

_Filtration Angle._ The changes that occur in the filtration angle
before it is encroached upon by iris tissue are sclerosis of the
ligamentum pectinatum in adults to which Henderson (Trans. Ophth. Soc.
U.K. Vol. xxviii) has called our attention; the accompanying sclerosis
of the other tissues to the inner side of Schlemm's canal; and, in some
cases, the deposition of pigmented cells derived from the iris and
ciliary processes (Levinsohn) which serve to obstruct the lymph spaces.
In many of the cases of acute glaucoma and almost all of the cases of
chronic glaucoma of long standing the filtration angle becomes blocked
by the advance of the root of the iris.

_Iris._ In acute glaucoma the iris is congested and thickened. It is
pushed forward and may lie against the cornea at its periphery. When the
attack subsides, the iris falls away from the cornea. Aside from the
congestion, the primary changes that take place in the iris are
indicative of paresis of the fibers of the motor oculi that supply the
sphincter pupillae, and stimulation of the fibers from the sympathetic
producing vasomotor spasm. The long diameter of the pupil apparently
lies in the direction of the terminal vessels of the two principal
branches of each long ciliary artery which form the circulus iridis
major, where the vasomotor spasm would have the greatest effect in
lessening the blood supply. The haziness of the cornea and slight
turbidity of the aqueous contribute greatly to the apparent change in
the color of the iris. In cases of simple chronic glaucoma there is but
little evidence of edema of the iris. If the iris lies in contact with
the sclera and cornea for some time, it becomes adherent (peripheral
anterior synechia). As the disease progresses, the stroma of the iris
atrophies and contracts. There is very little evidence of small-cell
infiltration or the formation of cicatrical tissue. Numerous slits may
develop in the iris through which the fundus of the eye may be seen
(polycoria). The pigment layer does not atrophy in proportion to the
stroma of the iris; by the contraction of the stroma of the pigment
layer is doubled upon itself at the pupillary margin, forming a black
ring of greater or less width (ectropian uveae). The iris becomes
attached to the pectinate ligament and to the endothelium of Descemet's
membrane. In a very few cases the closure of the angle is not complete
at the apex, a small space remaining comparatively free for a long time.
The adhesion of the iris to the pectinaform ligament and cornea is not
uniform at all parts of the periphery; it varies in width. Portions of
the iris angle may remain open while other parts are closed. Where the
iris tissue lies in contact with the cornea, the stroma of the iris
almost totally disappears. In some cases the iris becomes totally
adherent to the cornea.

_Ciliary Body and Chorioid._ In acute glaucoma there is congestion of
the entire uveal tract, the congestion partaking more of a venous stasis
than of an active or arterial congestion. The vessels of the ciliary
process, which are larger and more tortuous in adults of advanced years
than in the young, become enormously distended, causing almost complete
obliteration of the perilental space. They press against the root of the
iris and the equator of the lens, forcing them forward. There is edema
of the ureal tract, apparently from transudation of serum. Many small,
and sometimes rather large hemorrhages may occur. There is but little
small cell infiltration, indicating almost total absence of what is
ordinarily recognized as true inflammation. It is probable that the
secretion from the glandular zone of the ciliary body is increased.

On subsidence of the congestion, as after miotics or iridectomy, the
tissues may return to very nearly a normal condition. The iris recedes
from contact with the ligamentum pectinatum and cornea and the
filtration angle is again open. In some cases the iris becomes adherent
to the head of the ciliary processes and, when atrophy of the ciliary
body occurs, is drawn backward at the base of the iris by the receding
tissues. If the hypertension persists or is repeated at varying periods,
a slow atrophy of the uveal tract sets in. Eventually the ciliary body
becomes very much reduced in thickness, is flattened out, the ciliary
processes reduced in size and the blood vessels disappear or are reduced
much in caliber. Those that persist possess walls that are much
thickened. This is particularly true of hemorrhagic glaucoma.

In advanced absolute glaucoma the chorioid may become reduced to a very
thin membrane consisting of connective tissue and pigmented cells,
scarcely distinguishable even by moderate powers of the microscope.
Atrophy is marked in the vicinity of the venae vorticosae. Czermak and
Birnbacher describe proliferation of the endothelium of the large veins
with contraction and obliteration of their lumen.

_Optic Nerve and Retina._ In the acute form the retina and optic nerve
present the same condition that is present in the vascular tunic;
namely, that of venous stasis with the consequent edema. Frequently
minute hemorrhages occur in the retina, particularly in violent acute
attacks. Cupping of the discs slowly develops, causing more or less
stretching of the nerve fibers over the edge of the cup. The gradual
diminution of the field of vision is due in greater part to death of
peripheral nervous elements of the retina, those parts of the field
farthest removed from the large arterial trunks suffering first. The
arrangement of the arteries at the disc, passing out as they do from the
nasal side, of necessity make the vessels that pass to the temporal part
of the retina longest and of less caliber. These vessels and their
terminals are first to suffer marked diminution in size; death of the
perceptive elements supplied with nutrition by these vessels follows.
For this reason the nasal part of the field of vision is more often the
first to disappear. In congestive (inflammatory) glaucoma, the typical
field of vision shows most marked contraction on the nasal side. The
disturbance of the nutrition of the retina accounts in greater part for
the various forms of visual field met with.

Death of all of the perceptive elements of the retina eventually occurs.
The loss of nutrition is apparently not the whole cause of blindness.
Atrophy of the nerve fibers follows death of retinal neurons, but
atrophy of some of the nerve fibers may be, and probably is, due to the
pressure and traction exerted upon them at the margin of the disc. It is
probable that too much importance has been given to this mode of
interference with the nerve fibers. However, the change in the position
of the lamina cribrosa must exert a deleterious effect, particularly on
those fibers which pass through the peripheral meshes, the shape of
which must necessarily be much distorted. In glaucoma simplex, which is
largely devoid of marked congestive periods (acute attacks), a
surprisingly high degree of acuity of vision may exist with a deep
excavation and pale nerve. Careful studies of the retinal vessels in
glaucoma (Verhoeff Arch. of Ophth. XLII. p. 145; Opin. Soc. Française
d'Ophth. 1908) disclose the fact that an increase in the elastic tissue
and connective tissue elements occurs in _some cases_, also
proliferation of the endothelial cells, which serve to irregularly
narrow and, in some instances, obliterate the lumen of the vessel.
Arteries and veins are both affected. Hyaline degeneration of the media
also occurs. The process is not uniform.

_Glaucomatous Cup._ The excavation of the disc progresses slowly and is
due in part to stretching the fibers of the lamina cribrosa pressing
this structure outward, and partly to atrophy and disappearance of the
nerve tissue and much of the vascular tissues in the nerve head. The
displacement backward of the lamina cribrosa may cause that structure
to lie behind the outer surface of the sclera. Atrophy and cystic
degeneration of the nerve trunk follows destruction of retinal neurons
and cupping of the disc. Neuroglia remains in part. Connective tissue
elements increase in the optic nerve as the nerve fibers disappear.

_Glaucomatous Ring._ The development of the pale circle which surrounds
the disc, particularly in glaucomatous eyes, is due to a very slight
recession of the pigment layer of the retina and of the margin of the
chorioid at this point with some atrophy, apparently consequent on the
beginning retraction of the lamina cribrosa and slightly increased
pressure of the nerve fiber layer on the underlying tissues at the
margin of the disc. This permits the sclera to show through a very
little at this part. In some eyes in which there is a beginning
sclero-chorioiditis posterior, the condition is very similar to that
presented by the glaucomatous ring.

_Field of Vision._ The two pathological processes that operate to
destroy the function of the retina suffice to produce scotomata in the
field of vision of varying shapes. The typical glaucomatous field in the
acute cases shows a defect most pronounced to the nasal side. As has
been shown by Bjeraum, the blind spot corresponding with the optic disc
is enlarged in glaucoma, a relative scotoma often connecting it with the
blind nasal portion of the field either above or below the horizontal
meridian (Straub). The field in a simple glaucoma is apt to approach
concentric limitation; namely, more like the field in simple atrophy.
This is consistent with the fact that simple glaucoma in many cases
possesses the characteristics of glaucoma plus atrophy of the optic
nerve.

_Vitreous._ During the acute attack, the vitreous may become slightly
turbid by transudation of serum from the vessel of the ciliary body and
the chorioid and may become filled with fibrin. In some chronic cases
in which absolute glaucoma is reached the development of small blood
vessels in convoluted loops springing from the vessels of the discs has
been observed. Any process that increases the volume of the contents of
the vitreous chamber, as hemorrhage, neoplasm, profuse serous or plastic
exudation, may by pushing iris and lens forward produce an attack of
acute glaucoma.

_Buphthalmos._ Reis (Graefe's Arch. f. Ophth. V. LX. 1905) states that
there is always obliteration of the anterior scleral venous channels
(Schlemm's canal) in buphthalmos. Seefelder (Graefe's Arch. V. LXIII.
1906) mentions the abnormal position and abnormal narrowing of Schlemm's
canal and the imperfect and insufficient differentiation of the
cornea-scleral junction. In all of the cases in which the eye has been
examined microscopically obliteration of Schlemm's canal has been
reported. This is thought to be a defect in development. Magitot (Ann.
d'Oculis CXLVII) suggests that injury to mesoderm which pushes itself
between the ectoderm and anterior surface of the lens would account for
the failure in development of Schlemm's canal. The changes that occur in
the tissues of the eye appear to be largely due to the stretching
consequent on the more or less uniform distentions of the globe as a
result of hypertension.

_Cornea._ This portion of the fibrous membrane is enlarged, globous or
flattened, irregularly thinned, particularly at the periphery, where it
may be as thin as tissue paper, nebulous because of the stretching of
its fibers principally, but in some degree (differing in different
cases) to edema of the epithelial layer. Fissures occur in Descemet's
membrane.

_Anterior Chamber._ This is very deep in the greater number of cases.
However, this rule has many exceptions.

The vascular tunic may be congested in young infants, but atrophy soon
develops and may reach an extreme degree. The sclera ordinarily becomes
quite thin throughout, but may retain almost a normal thickness at the
equator of the globe and posteriorly. Posterior sclera ectasae may
develop. The iris, as a rule, hangs free from the cornea, often
tremulous because of retraction of the lens beyond the iris plane. In
some cases the iris is partly or totally adherent to the posterior
surface of the cornea.

The vascular membrane (iris, ciliary body and chorioid) and the retina
become atrophic, the atrophy varying in degree in various parts.
Detachment of the retina may occur, often preceded by or accompanied by
subretinal hemorrhage. The optic disc becomes deeply cupped and the
tissues of the optic disc and optic nerve extremely atrophied. The
crystalline lens may become cataractous and shrunken. Spontaneous
rupture of the suspensory ligament with consequent subluxation of the
lens may follow.

_Secondary Glaucoma._ The pathological conditions that precede
secondary glaucoma are many and differ widely. They may be briefly
classified as:

1. Those that cause a partial or complete closure of the lymph spaces
and Schlemm's canal by cicatrical contraction, as in sclero-keratitis.

2. Those that cause obstruction to the lymph spaces at the filtration
angle by the deposition of fibrin or cellular elements, as in iritis,
hemorrhage into the anterior chamber, etc.

3. Those that cause obstruction of the filtration angle by advancement
of the iris and lens, as occurs when the volume of the contents of the
vitreous chamber is increased, as from retinal or chorioidal hemorrhage
or neoplasm.

The various changes are so numerous that they need not be described
further here. The ultimate changes due to high tension resemble those
already described.




Dr. John E. Weeks' Paper on Pathology of Glaucoma

Discussion,

E. V. L. BROWN, M.D.,

Chicago.


I would like to emphasize one of the newer features of the pathologic
anatomy of glaucoma, one which has received too little attention in this
country: the _lacunar_ or _cavernous atrophy_ of the _optic nerve_.

The name accurately describes the condition. Tiny clear spaces form in
the lamina cribrosa and in front and behind it in the nerve tissue.
Their exact nature is unknown. Usually they are entirely empty, often
they are traversed by fine glial fibers. They seem to be in no relation
to the blood vessels. Adjoining lacunae are supposed to fuse to form
larger cavernae and these finally merge and constitute the final
glaucoma cup. The lamina may then bridge across the space like a cord,
or lie back against the end of the nerve trunk.

Schnabel considered all glaucoma cups to be formed in this way,
independent of tension. His views were strongly supported by Elschnig,
but as vigorously opposed by others. Axenfeld cites the fact that the
glaucoma cup may disappear after operation. (I myself have seen a cup of
7 D. reduced to 1 D. in the course of a year after the tension had been
lowered from 62 to 12.) Stock found the same lacunae in eight cases of
myopia. The last extended study of the subject was made by E. v. Hippel,
who found lacunae in 20 of 33 cases (60 per cent); enough certainly to
make one look for them carefully in every case. He publishes a large
number of excellent photo-micrographs, but none more typical than one I
have in my possession.

I have been especially interested in this subject because I have met
with a complete and total glaucoma cup, with the typical (ampulliform)
undermining of the scleral ring, in a pair of eyes without increased
tension. The (Schiotz) tonometer was used daily for 70 consecutive days
and never registered more than 12-14 mm. Hg. The man had been blinded by
wood alcohol. At the time I could find no other report in the
literature, but overlooked a publication by Lewin and Guillery.
Friedenberg has since reported cases of the same nature.

If other conditions than increased tension can produce a typical
(ampulliform) glaucomatous excavation of the disc, why may not the
cavernous atrophy and cup in glaucoma be due in part at least to similar
processes, possibly in the nature of a toxic oedema of the nerve, either
in association with tension or independent of it, as contended for by
Schnabel?




Concerning Non-Surgical Measures for the Reduction of Increased
Intra-ocular Tension

BY

GEORGE EDMUND DE SCHWEINITZ, M.D.,

Philadelphia.


Only a few years ago the literature of glaucoma was big with discussions
of the comparative value of the surgical and non-surgical treatment of
glaucoma, and especially of the chronic types of this disease. Now,
thanks to the achievements of Lagrange, Fergus, Herbert and Elliot, the
value of a filtering cicatrix, although known for a long time, has
attained increased importance, due to the improvement and elaboration of
operative technic, and the medical journals of the day are weighted with
opinions and experiences from all over the world as to these surgical
measures. But true as this is, we are not yet in a position to discard
non-surgical procedures (1) because operation is not always possible,
(2) because operation is not always permitted, and (3) because in
certain circumstances operation is not advisable. Hence a glance at the
non-surgical methods of reducing increased intra-ocular tension is not
out of place, and for convenience they may be catalogued as follows:

1. Myosis produced by means of solutions of various drugs, a myosis
followed by reduction of intra-ocular tension.

2. Reduction of tension by means of various mechanical measures, notably
massage, vibration massage and suction massage, and by means of
electricity and diathermy.

3. Indirect reduction of intra-ocular tension, accomplished by lowering
general vascular pressure.

4. Reduction of ocular tension by stimulation of osmosis, of lymphagog
activity, of absorption of edema, and of capillary contractility, and by
decreasing affinity of ocular colloids for water.

1. _The Myotics._ Of these, eserin (physostigmin) and pilocarpin, with
their respective salts, the sulphate and the salicylate in the first
instance, and the hydrochlorid and the nitrate in the second, are well
established in favor and efficiency. Personally, it has always seemed to
me that the salicylate of eserin is preferable to the sulphate, but I
have not persuaded myself that the nitrate of pilocarpin possesses
material advantages over the hydrochlorid, although some authors prefer
it. With arecalin, the alkaloid of the Betel nut, I have no experience,
nor have I used its mixture with eserin, recommended by Merck as more
potent than either of the drugs in separate solution.

The substance isophysostigmin, found with eserin in Calabar bean,
according to Ogiu, exceeds in its myotic activity the sulphate of
eserin, _i. e._, 1/80 of a grain of the drug is equal to 1/60 of a grain
of the sulphate of eserin, but it is certainly not less irritating than
physostigmin, and according to Stephenson's researches, is more so, and
in this sense has no superiority over the usual alkaloid. In general
terms, it may be said that the time has not arrived to make a preachment
"on the passing of eserin and pilocarpin."

_Physiologic Action._ Concerning the ocular, physiologic action of the
two chief alkaloids respectively of Calabar Bean and of Jaborandi, there
still exists difference of opinion. It has always been easy to attribute
the myotic action of these drugs, or at least, of eserin, to their
stimulant action on the peripheral ends of the oculo-motor, thus causing
sphincter contraction, and to a depressing action on the sympathetic
fibers, thus causing removal of the action of the dilatator of the iris.
But complete experimental proof of such action is wanting, and it is
probable that myosis follows a direct stimulation of the sphincter
muscle fibers, aided, perhaps, by contraction of the iris vessels,
although the last named effect is denied by so competent an authority as
Hobart Hare.

Exactly how the myotics reduce intra-ocular tension is not definitely
proven. Usually it is taught that because of the myosis the base of the
iris wedged in the angle of the anterior chamber is loosened and
withdrawn, precisely as a fold in a coat is straightened by a tug on the
fabric beneath it. Experiments, however, for example, by E. E.
Henderson, have shown that the rate of filtration in an eye with
artificially raised pressure is considerably larger when it is under the
influence of eserin than it is when under the influence of atropin; that
is by the contraction of the pupil the iris-surface filtration is
increased and consequently the pressure is reduced. We all know that
Thomas Henderson maintains that the results of iridectomy are beneficial
because the raw edges of the coloboma, which do not cicatrize, permit
access of the aqueous to the iris veins, and that myotics, inasmuch as
they contract the pupil, open the iris crypts and therefore act, less
efficiently, perhaps, but act none the less like an iridectomy. The
normal intra-ocular pressure is uninfluenced by myotics because this
pressure represents the lowest circulatory pressure in the eye, and
further contact between aqueous and veins cannot reduce it below this
level, another point which is made by Thomas Henderson in support of his
contention.

The clinical fact remains that either by mechanical means, as it were,
in the liberation of a plugged filtering angle, or by the increasing of
iris-surface filtration, the myotics markedly reduce the abnormal
intra-ocular pressure.

_Methods of Administration and Indications._ With the methods of
administration of the myotics we are all so familiar that time need not
be wasted in their reiteration, except to refer to a few practical
points. In acute glaucoma, and every one knows that in this disease
their action is often prompt and sometimes curative, eserin in a
strength of one to four grains to the ounce may be instilled with
sufficient frequency to establish myosis, and its action in this respect
is enhanced if the congestion of the eye is lowered by measures to which
I shall refer later. There is a good deal of clinical evidence to
indicate that in this type of glaucoma, as well as in the so-called
sub-acute varieties, myotic activity is increased by a mixture of
pilocarpin and eserin in the same solution, exactly as a mixture of
arecalin and eserin is more potent than either of the drugs in separate
solution.

Prior to the happy advent of technically correctly placed filtering
cicatrices, a large number of surgeons depended almost exclusively on
the use of myotics in so-called simple, chronic or non-inflammatory
glaucoma. This is not the place to introduce a discussion of the
comparative value of iridectomy and myotic treatment in simple glaucoma
as based upon statistical records. We must wait now for a sufficient
period of time and then compare the value of myotic treatment with that
of operations by means of which satisfactory filtration is produced. We
are somewhat in the position that general surgeons occupied when aseptic
methods first became prevalent. We do not usually compare the statistics
of early aseptic days with those of the pre-antiseptic period, and I do
not think we ought to compare the statistics of myotic treatment with
ordinary iridectomy any longer, but that we should wait until we can
make a comparison between the results of prolonged myosis and those of
an improved modern technic which establishes a permanent filtration. In
the meantime the patients who will not or cannot submit to operation
must be reckoned with. Doubtless many patients with chronic glaucoma can
be satisfactorily managed with myotic treatment, although personally I
have always advocated operation when this could be performed, but it
cannot always be performed. This rule should guide us, namely, to begin
with a comparatively weak solution of the selected drug, for example, as
Posey has advocated a tenth of a grain of salicylate of eserin to the
ounce, and the strength gradually increased so that at the end of some
months the patient is using a solution 1 grain to the ounce; or if the
pilocarpin is preferred, solutions in double these strengths. It is my
own belief, and that of many who have studied this subject, that if,
without eserin irritation, a myosis can be maintained, and if the
treatment can be begun early enough, the chances of preserving vision
and the field of vision are good. I believe that the two most important
instillations during the twenty-four hours of the number necessary to
maintain this myosis are on retiring and if possible in the very early
morning, some time between two and four o'clock. Most patients can be
taught to wake themselves at the proper period of time, and are little
inconvenienced by this disturbance of their sleep. I believe that eserin
irritation is most successfully avoided, not by preparations of the
myotics in combination with the antiseptics, for example, tricresol,
which has been so much advocated, but by ordering very small quantities
of the solution, insisting that it shall be frequently renewed and
sterilized at each preparation, and that a half an hour after its
instillation, during the day time at least, the eye shall be thoroughly
flushed with some mild antiseptic solution, for example, boric acid and
sodium chlorid. Whether the action of the eserin on the choroidal
circulation, which is maintained by Wahlfours, aids in this favorable
action of the myotics remains to be proved. It has been maintained by
this author and by others who have followed him.

The great trouble with myotic treatment is not its lack of efficiency,
but the difficulty of carrying it out successfully on ambulant
patients, even in the better walks of life. It is hard successfully to
maintain in a patient with chronic glaucoma what I may call an eserin
life, just as it is hard to maintain in a person with an enlarged
prostate a catheter life and escape infection, resulting, if it occurs,
in the one instance in a difficult and stubborn conjunctivitis, and in
the other in a cystitis. Still, we are obliged to use myotics, and the
way to employ them to the patients' best advantage, I have ventured to
repeat in spite of the universal familiarity with the methods. Perhaps
we may reach that happy day when, especially with improved tonometric
methods, increased skill in measuring the rate of filtration and better
instruments for determining the light sense, we can anticipate the
advent of glaucoma and get ahead of the ocular and visual deterioration
which increased tension produces, by performing preventive operations
which shall aid nature's filtration channels in the establishment of an
artificial one. But increased tension is not the whole story of
glaucoma, and a filtering cicatrix is not the last word in surgical
therapeutics, and there is much to learn.

2. _Reduction of tension by means of various mechanical measures,
notably massage, and by means of electricity and diathermy._ Massage is
of ancient lineage. In general terms, in so far as ocular massage is
concerned, it may be applied to the eye with the finger tips (ordinary
massage), by means of various instruments (vibration massage), and with
the help of certain suction cups (suction massage, which is indeed a
form of vibratory massage). Many authors are satisfied with their
results without the employment of any instrument, and prefer simple
massage with the tip of the finger to any form of the instrumental
variety, to quote the words of Casey Wood. At one time in my career I
experimented very extensively with massage, not alone for the purpose
of reducing intra-ocular tension, but in various diseases of the lid and
cornea, and taught a trained nurse, who herself had a nebulous cornea,
to make what I may call a specialty of this particular therapeutic
procedure. She became exceedingly skillful and was quite faithful. We
believed that the best results were obtained in a seance of two or three
minutes, the finger tip being used over the lid, and the surface of the
cornea lubricated with a drop of pure olive oil, although in glaucoma
the addition of the oil is not necessary. Four movements were utilized,
the first a stroking movement in lines radiating from the central
pressure, very much as the spokes of a wheel radiate from the hub,
second a circular movement, third a pressure movement, a little dipping
motion, so that the cornea was slightly depressed, and finally, a gentle
tapping movement, precisely the same, except that it was a diminutive
one, as the tapping movement that the Swedish masseur makes. Usually
each movement occupied from a half to one minute, according to the
results desired. I agree with Casey Wood that such a technic furnishes
just as good results as any one with the aid of an instrument.

Referring particularly to the reduction of intra-ocular tension, many
surgeons have been impressed with the value of various instruments.
Thus, Ohm, who has worked particularly in the reduction of the increased
tension of secondary glaucoma, for example, after discussion of lamellar
cataract, advocates the Piesbergen instrument, which makes 3,000
vibrations a minute, and is applied over the closed lids. I think the
instrument best known is the one introduced by Malakow. For this purpose
the point of an Edison electric pen is armed with a small ivory ball,
and the vibration rate varies from 200 to several thousand a minute, the
rapidly revolving ball being passed over the closed lids, in some
instances directly upon the cornea itself. I am frankly afraid of these
vibrating machines, and again make a plea for the finger tip, just as I
am afraid of a Von Hippel trephine, and prefer one which is rotated with
the fingers.

A special investigation of pressure massage according to the method of
Domec has been made by Paul Knapp of Basel. This, as you know, consists
in applying the thumb to the cornea through the closed lids, and making
repeated pressures upon it at the rate or 60 to 100 a minute. He checked
his results with the tonometer after 200, 500 and 1,000 pressures, and
found that even in normal eyeballs such massage was followed by a fall
of intra-ocular tension, the average being nearly 9 mm. after a thousand
pressures. Within three-quarters of an hour the tension returns to the
normal. In acute glaucoma such massage is not available, but it is of
assistance in encouraging a reduction of the intra-ocular tension and
keeping it at a normal grade after operative work, particularly after a
filtering cicatrix has been made, as was well shown by Weeks in his
study of glaucomatous eyes operated upon by the Lagrange method. It is
interesting to remember that Paul Knapp, in the course of this
investigation, observed reduction of the tension after the use of
holocain.

Another method of reducing the intra-ocular tension is by the suction
method, which consists in the use of certain cups from which the air is
exhausted by means of a suction apparatus. Domec uses an elliptical eye
cup, the concave margins of which fit closely about the globe. The air
is exhausted with each respiration of the patient and from 50 to 200
tractions are made at each sitting. Domec is of the opinion that this
method succeeds in two ways, namely, in producing analgesia by traction
on the ciliary nerves, and in reducing intra-ocular tension.

Unfortunately, it is difficult for regular physicians to make reference
to massage of the eyeball lest their words should be misquoted by
irregular practitioners who employ this method, selling various
instruments to trusting patients, and attributing to this simple and
often beneficial procedure all sorts of marvelous influences. Doubtless
all of us have seen eyes utterly ruined because the patient has trusted
to the advertisements of these people, and has continued to use some
foolish little suction pump, when what his eye needed was operative
procedure or skilled therapeutics.

If I should sum up my opinion of massage in the reduction of
intra-ocular tension, I would say that it is useful in enhancing the
action of myotics, and particularly useful, as Domec, Knapp, Ohm, Weeks
and many others have shown, after the filtering angle has been opened by
a proper operative procedure. It seems to me that it is distinctly our
duty to inform patients that it is no panacea, and that they must never
trust themselves in the hands of irregular practitioners who pretend to
cure all ocular ills with massage.

_Electricity._ The credit of first using high frequency currents in the
treatment of glaucoma belongs to Truc, Imbert and Marques, and Roure's
experiments indicate that this current suitably applied appears to have
an influence not only in reducing the arterial tension, but also the
ocular tension. Thus, in an interesting series of experiments he has
been able to reduce an arterial pressure of 200 mm. to 140 mm., and an
ocular tension of plus 2 to the normal after eighteen applications of
the high frequency current. The current is applied for ten to fifteen
minutes at a time twice a week. Some surgeons, for example, Würdemann,
have suggested the use of electricity combined with massage, and have
apparently achieved satisfactory results.

The constant current has also been much employed for the purpose of
reducing intra-ocular tension. Coleman quotes Le Prince's observations,
who applies the negative pole to the eye and the positive pole to the
neck, gradually passing a current of 30 to 40 ma. during a quarter of an
hour, and who reports notable diminution of tension. Coleman points out
that in his own experience he has not found any patient who would
willingly tolerate more than 19 ma. of current with an ordinary sized
electrode, although he grants that it is possible that Le Prince used a
very large electrode. Unfortunately he does not mention its size.
Ziegler of my own city, who has studied most scientifically and
intelligently the use of electricity in diseases of the eye, announces
this rule: The positive pole should be used in all inflammatory
processes of the eye, glaucoma excepted, and with this rule Coleman
agrees. Now, although the negative pole is a stimulant and therefore not
generally indicated in inflammation, as Coleman points out, the object
in view is to diminish the density of the ocular capsule and its
tension, hence the negative rather than the positive pole should be
used, inasmuch as the former, according to him, while it is a sedative,
hardens tissue and would tend to increase intra-ocular tension by
diminishing excretion. Moreover, in chronic glaucoma the ordinary
inflammatory processes are not present, indeed, primary acute glaucoma
itself is not an inflammation.

I have no personal experience in the use of the constant current with
negative pole application to the eye in the reduction of increased
intra-ocular tension, but quote for our general benefit the opinions of
those who have employed it. I have always been very frankly pessimistic
in regard to the therapeutic value of electricity in ocular disorders.
Perhaps I am wrong; I am willing to be enlightened. There seems little
doubt that Truc and Imbert's observations that high frequency currents
can temporarily reduce intra-ocular tension is correct, that they are
able to relieve the pain of primary and of secondary glaucoma would
seem to be proved by many observations, some of which I have myself
made, and other very accurate and excellent ones have been made by
Risley in Philadelphia.

A word might be said in regard to _diathermy_. According to Zahn, the
method of applying diathermy to the human eye is to take a layer of
cotton wool 1 cm. thick soaked in a 2 per cent solution of sodium
chlorid, which is applied close to the outside of the lids. On this is
put an electrode 15 cm. in size with a large indifferent electrode
applied to the back of the neck. It is not germane to the subject to
name the various ocular diseases which were treated in this manner, but
Clausnizer has made an investigation of the influence of diathermy on
intra-ocular tension. In a number of diseases, for example,
iridocyclitis, the method produced distinct rise of pressure. In one, a
patient with secondary glaucoma, prior to the diathermic application
the tension was 37½ mm., after the passage of the current it had
fallen to 28 mm., but the next morning the tension rose to 45 mm. In a
patient with chronic glaucoma no definite alteration of tension could be
found. This observation is mentioned, not because it puts us in
possession of a valuable therapeutic measure, but largely because it is
a good example of how in this disease it is wise to investigate any
method which furnishes a hope of relief.

In a few instances endeavor has been made to reduce the intra-ocular
tension, or at least to relieve glaucomatous symptoms, by galvanism of
the cervical sympathetic, for example, by placing one electrode along
the whole length of this nerve in the neck and one on the back of the
neck on the opposite side, 15 to 20 ma. of current being used. Good
results have been reported by an observer named Allard. I confess that I
am entirely faithless in regard to any results that may be reached in
this manner. It is possible that as the positive pole is a sedative, if
there were any influence, the influence of sedation would be present,
but certainly it has over and over again been experimentally proved that
irritation of the cervical sympathetic quite rapidly produces elevation
of intra-ocular tension of 2 to 4 mm. In some experimental work the
primary elevation of intra-ocular tension was followed by a secondary
drop.

3. _Indirect reduction of increased intra-ocular tension brought about
by lowering general vascular pressure._ Much has been written in regard
to the association between increased vascular pressure and increased
intra-ocular pressure. It is not my province to analyze observations
often contradictory and not infrequently inaccurate. This much seems to
be established: First, that at corresponding ages there is usually a
higher average blood pressure in glaucomatous subjects than there is in
non-glaucomatous subjects; second, that arteriosclerosis and therefore
usually increased blood pressure, with all its concomitant conditions,
is correctly classified as an exciting cause of glaucoma; and third,
that the regulation of this increased blood pressure is part of the
advantageous management of increased intra-ocular pressure, although it
may be too much to say, as Gilbert has, that blood pressure and
intra-ocular pressure rise and fall together. It may be true, as Thomas
Henderson says, that the intra-ocular pressure is influenced by changes
in the general arterial or general venous pressures, whereby a rise in
general arterial pressure induces a proportionate rise in the
intra-ocular pressure, but it would seem that future investigations must
confirm this statement before it can be entirely accepted, as well as
his further statement that the effect of an increased general venous
pressure is a direct one, producing millimeter for millimeter a
corresponding increase in the intra-ocular pressure.

Now, it goes without saying, if these data are correct, or even only
partly correct, that part of the treatment of the increased intra-ocular
pressure state must be constitutional in that the vascular pressures
should be lowered in order that the beneficial effect of their
relationship to the intra-ocular pressure shall be established. It is
further a great mistake to drive down a high arterial pressure simply
because that exists. In other words, it is often necessary from the
general standpoint that a certain amount of plus pressure shall remain
if the patient's general well-being is to be maintained. There must
always be a differential diagnosis between plus pressure and what may be
called over plus pressure. That is to say, a man may be perfectly
comfortable and properly need, for example, a pressure of 160 or 165
mm., which is above the physiologic limit, but which is a plus pressure,
while some disturbance in his general life may add to that 10, 15 or 20
mm. more of pressure, which is then the over plus amount. This over
plus amount may be in association with a rise of intra-ocular pressure,
and must be eliminated if the latter is to be controlled by a
non-operative procedure, or, indeed, by an operative one.

It is no easy matter to determine the presence of increased venous
pressure, although there are tolerably accurate instrumental technics,
and yet, as Henderson points out, it is just this increased general
venous pressure which is often detrimental. Therefore the perfunctory
use of such drugs as nitrite of amyl and the other nitrites may not be
in the least indicated when, for example, the venous pressure depends
upon inability of the right heart to perform its functions, and the drug
needed may, for example, be digitalis. Far better than pressure-reducing
drugs like nitrite of amyl, urgently indicated in some instances and for
some purposes, is the regulation of life and the restoration to their
normality of the metabolic processes, the elimination of the worry
which is usually the exciting agent that brings about the over plus
pressure, which may have as one of its expressions an acute rise of
intra-ocular tension. I believe that in the management of a case of
glaucoma, whether it be chronic or chronic with sub-acute exacerbations,
the greatest care with the aid of an expert clinician must be exercised
to find out exactly what mean pressure of the arterial and venous system
best conforms with the patient's general welfare, and I am bitterly
opposed, and I think with right, to the sudden reduction of tensions,
except in emergencies, without a perfect understanding of the facts I
have ventured to indicate. This does not for a moment mean that prior,
for example, to operative work it is not necessary to get rid by means
of drugs of an over plus tension, for surely the elimination of such an
over plus tension may be the means of preventing, for example, an
intra-ocular hemorrhage, and in this emergency we must not lose sight
of Gilbert's recent investigation, who has found that blood withdrawn to
the extent of 8 grams to each kilogram of the body weight always
produces lowering of the intra-ocular tension, appearing in six to eight
hours and lasting to the next day in simple glaucoma, and in
inflammatory glaucoma commencing the day after the venesection and
lasting two to three days. It is not necessary for me to point out the
value of free purgation and diaphoresis in this respect.

In most instances the successful maintenance of a glaucomatous life,
exclusive of operative interference, in addition to sustained myosis,
demands the investigation of the patient's metabolism, which must be
kept at the normal standard, the removal of the evil effects of
auto-infection, as we are wont to call it, and especially the
elimination of the cause which is responsible for the over plus tension
of the arteries and of the veins. This is best secured by just such
regulation of life as has been referred to, aided when necessary by the
ordinary drugs which the patient's condition indicate, and the success
of all treatments, be they operative or non-operative, is enhanced if
such a happy state of affairs can be brought about.

I am firmly convinced that every glaucomatous patient, and I now refer
to those who are the subjects of chronic progressive glaucoma, should be
carefully studied from the general standpoint by the oculist with the
aid of an expert internist, just as I am convinced that the modern
expert internist should not study his cases of cardio-vascular disease
without the help of the oculist. Perhaps I am going a little far afield,
but in justification of my statement I want to quote the opinion of Dr.
Hobart Hare, one of America's most expert clinicians, on blood pressure,
because it seems to me much harm has been done by the more or less
brutal knocking down of blood pressure simply because blood pressure
above the normal existed. "Concerning the matter of high blood
pressure," writes Hare, "independent of cerebral lesions, the longer I
study the matter the more convinced I am that this blood pressure is
devised by nature to compensate for fibroid changes in peripheral
vessels, in order that tissues which would otherwise be cut off from
adequate blood supply may receive plenty of blood, and I consider it one
of the most vital points to ascertain whether a pressure is what may be
called the patient's pathological norm, that is, the pressure which is
required in the face of vascular changes, or whether this pressure is in
excess of his pathological norm. If it is in excess, measures directed
to bring it to the pathological norm should be instituted, but if the
pressure found proves to be the pathological norm it is a bitter mistake
to lower it, be the pressure what it may. If it is lowered below the
pathological norm, all manner of disturbed cardiac action, etc., may
result. There is no more reason for reducing a blood pressure below his
pathological norm than there is for reducing it below his physiological
norm. The adjustment of a man's blood pressure to his pathological norm
often has to be as correctly done as the adjustment of a watch which is
losing or gaining time."

I shall not quote Hare's elaborate methods for determining these various
points because they do not belong to a paper of this character, but I
quote his admirable advice because it emphasizes what I believe to be an
essential in the treatment of chronic glaucoma, exclusive of operative
work, that is, the intelligent co-operation of the oculist and the
internist.

Some such thought was in the mind of Ibershoff, who quotes Sterling and
Henderson's views that the rate of secretion depends upon and varies
with the difference in the blood pressure and the tension of the
eyeball, and that the specific gravity of the secretion increases
directly with the blood pressure and inversely with the ocular tension.
Should the blood pressure be very high, paracentesis, for example, would
apparently not be the proper procedure, and the resulting difference
produced between the blood pressure and the eye tension would cause a
rapid reformation of fluid with higher specific gravity and higher
osmotic coefficient. The proper procedure in these circumstances is
first properly to reduce the blood pressure, or what I have, quoting
Hare, ventured to call the over plus pressure.

4. _The relation of osmosis, lymphagogue activity, absorption of edema,
capillary contractility and decreased affinity of ocular colloids for
water to the reduction of increased intra-ocular tension._ We are all
familiar with the attention which was directed some years ago to the
statements coming from French clinics that the treatment of glaucoma
should include the administration of osmotic substances as adjuvants in
the reduction of increased intra-ocular tension. Particularly was this
treatment advocated by Cantonnet in the administration of daily doses of
3 grams of chlorid of sodium, preceded, of course, by a careful urinary
examination and the estimation of the amount of urine and its contained
chlorids. Carefully this dose was increased in proper circumstances to
15 grams per diem, and in Cantonnet's original paper good results were
achieved in 12 of the 17 patients so treated. I have myself experimented
somewhat, not with the administration of sodium chlorid by the mouth,
but with the introduction by the bowel of fairly large quantities of
physiologic salt solution in patients with glaucoma whose quantity of
urinary secretion was markedly below the normal, and in one or two
startling instances, which have been reported, achieved success in the
rapid reduction of the intra-ocular tension when by this technic the
urine secretion rose to the normal amount. To be sure, myotics were
also used, but these myotics were insufficient, totally so in the two
instances noted prior to the enteroclysis.

Very interesting are the observations on the subconjunctival injections
of various substances, notably the citrate of sodium, because of its
power of decreasing the affinity of ocular colloids for water. This
method of treating increased intra-ocular tension, introduced, as you
know, by Thomas and Fischer, has met with confirmation from a number of
sources in spite of the fact that Happe's experimental study failed to
confirm Fischer's observations; indeed, he even reports in several
instances a rise of tension.

As you will remember, the strength of ordinary crystallized sodium
citrate in water should be from 4.05 to 5.41 per cent. Of this five to
fifteen minims are injected, the eye having been previously cocainized
and adrenalinized. With frequent injections the weaker of the two
solutions is mixed with 2 to 4 parts of physiologic salt solution. These
authors in no sense claim to cure glaucoma, but to ameloriate it and
reduce the tension. Weekers has used the salts of calcium, 3 grams a
day, with success in so far as lowering of tension is concerned,
although it must be stated, as a reviewer of his work has said, that his
recommendation of this drug in these respects is poorly supported. On
the other hand, Tristiano seems to have proved that calcium chlorid is
capable of lowering ocular tension and clinically may be used as an
adjuvant in the treatment of glaucoma for this purpose, largely because
he believes that he has proven that it facilitates the absorption of
edema. Darier has reported that a single subconjunctival injection of a
milligram of iodate of sodium has cleared the cornea and lessened the
intra-ocular pain in glaucoma.

What shall be said in regard to certain medicinal agents which stimulate
the lymphagogue activity of the eyeball in their relation to the
reduction of intra-ocular tension, notably of dionin? Toczyski's
experiments with this drug on the normal eye indicate that it produces
first a rise of tension, which shortly falls to the normal and sometimes
below it, the tension being high as long as the primary narrowing of the
pupil is maintained, but more than one author, particularly A. Senn,
holds an opposite view and reports acute glaucoma following its
instillation into a chronic glaucomatous eye. He believes that dionin
not only does not reduce the tension but hinders the filtration through
the anterior lymph channels by the pressure of the edema which is
produced on the veins and by the increased secretion of the ciliary
processes. In spite of this statement, most of us must agree with Karl
Grossman's observations that certainly in acute and particularly in
chronic secondary glaucoma, this is a most valuable agent, especially if
it is combined with holocain, which Paul Knapp in his well-known
research has proved can reduce the tension even of the normal eye. I
cannot think that anybody who has systematically used dionin with
holocain, the former in gradually increasing strength, beginning with 2
per cent and going up to 8 per cent, in various types of acute glaucoma,
particularly of the secondary variety, can fail to have noted a
favorable influence.

Many authors, for example, Darier, Grandclement and others, are strong
in their recommendation of adrenalin, particularly if this drug is added
to the various myotic mixtures, and yet adrenalin is certainly not
without danger in the treatment of glaucoma. McCallan has seen a number
of instances of striking increase of intra-ocular tension following this
instillation in the conjunctival sac. Harmon has had a similar
experience, as also has Senn. It is possible that in these circumstances
the solution was too strong. Should the rise of tension occur, and I
have seen it myself, it is doubtless due to the fact that this drug
dilates the pupil, which would be especially dangerous if the dilatation
should occur before contraction of the ciliary vessels; also the
narrowing of the ciliary veins by the adrenalin might by virtue of this
narrowing obstruct the gate of outflow. I have never been able to
persuade myself that, except as an adjuvant to operative work, there was
any real therapeutic value in the instillation of adrenalin.

A word in regard to the effect of general narcosis on intra-ocular
tension. Thus, Neuschuler has observed that narcosis causes an elevation
of the intra-ocular tension of from 2 to 6 degrees as measured with
Fick's tonometer. These observations were made while he was
experimenting on irritation of the sympathetic as a method of producing
increased intra-ocular tension. This is not in accord with Axenfeld's
recent observations. It is well known, this observer points out, that
after the period of excitation and muscular rigidity disappears, there
is a lowering of blood pressure in chloroform narcosis and coincidently
a sinking of the intra-ocular pressure. Not only this, the intra-ocular
tension of normal eyes during this narcosis drops several millimeters.
Only such eyes as have high hypertony, for example, in absolute
glaucoma, are unaffected during chloroform narcosis. In the light of
this observation it will be interesting to measure the tension both of
normal and glaucomatous eyes during narcosis in a large series of cases,
and if it is confirmed there will be an additional reason why in many
circumstances general narcosis is advantageous in glaucomatous patients.
Formerly I thought it was essential, if iridectomy was to be performed,
lest some sudden movement on the part of the patient might bring the
point of the knife in contact with the lens. I have rarely employed it
in corneo-scleral trephining, and yet if there is this temporary
reduction of intra-ocular pressure, it is not without a certain
therapeutic value, and the matter is mentioned as a suggestion that
additional observations along this line shall be made.




Dr. George Edmund de Schweinitz' Paper on Concerning Non-Surgical
Measures for the Reduction of Increased Intra-ocular Tension

Discussion,

NELSON MILES BLACK, M.D.,

Milwaukee.


It seems almost useless to attempt any discussion of Dr. de Schweinitz'
most terse and comprehensive paper. However, Dr. de Schweinitz mentioned
the close relationship which should exist in the non-surgical treatment
of increased intra-ocular tension between the internist and the
ophthalmologist, but neglected to mention a corresponding relation which
should exist between the rhinologist and the ophthalmologist, and
possibly between the dental surgeon and the ophthalmologist.

I would like to refer to the _now_ recognized close relationship which
exists between disease of the nasal accessory sinuses and diseases of
the eye. The definition of glaucoma found in Dr. Wood's system of
therapeutics gives rise to an hypothesis as to why disease of the nasal
accessory sinuses may be a factor in producing increased intra-ocular
tension and why treatment directed toward obtaining free drainage from
the sinuses gives good results in so many cases, especially if the
relationship is recognized sufficiently early. "Glaucoma proper is
essentially a damming or blocking of the drainage from the interior of
the eye. The chief lymph stream flows from the posterior chamber past
the margin of the lens, through the zonula of Zinn, beneath the iris,
through the pupil into the anterior chamber, thence through the tissue
at the junction of the iris and sclera into the circular canal of
Schlemm and from this space into _the external lymph channels_.
_Obstruction to the steady escape of the intra-ocular fluids at any
point in this drainage system or any undue increase of the fluids
themselves may produce glaucoma._ Probably the most important
obstruction to the exosmosis is at the angle close to Schlemm's canal."

The following hypothesis is based upon Fischer's edema theory of
glaucoma and the relation of the circulation of the eye and orbit and
that of the nose and the accessory sinuses, the minute anatomy of which
is not as yet thoroughly understood. However, sufficient work has been
done to make it appear that the lymph channels which drain the eyes and
orbits empty into the same main channel as do those which drain the
sinuses. Admitted for sake of argument that such is the case, then
disease either acute or chronic of one or more of the sinuses with the
accompanying inflammatory reaction, congestion and stasis, will cause an
increased amount of fluid to be taken care of by the lymph channels
draining these sinuses. This will in turn cause flooding of the common
lymph channel, producing a stagnation in the flow of fluid from the
orbits and eyes at the junction with the main channel, with backing up
of the fluid within these channels and retention of the waste products
within the orbits and eyes; thus will be brought about conditions most
favorable (to quote from Fischer's theory of glaucoma) "to an abnormal
production or accumulation of acid in the eye. In consequence of this
abnormal acid content the hydration capacity of the ocular colloids is
raised and glaucoma results, not because water is pushed into the ocular
colloids, but because these suffer changes which make them suck in water
from any available source."

This hypothesis also might suggest why the subconjunctival injection of
sodium citrate in addition to alkalinizing the ocular contents, may be
effective in reducing tension, _i. e._, the amount of fluid injected
beneath conjunctiva may overcome the stagnation in the lymph passages,
flush out these channels and improve ocular elimination.

Fischer in a personal letter says:

"You have two possibilities for the production of glaucoma with sinus
disease: A toxic factor due to poisons being carried into the eye; and
second, interference with a proper blood supply to the eye through
compression of the efferent or afferent blood vessels supplying the eye
from edema of the tissues about the eye consequent upon the sinus
infection. Either is associated with the production of substances which
increase the hydration capacity of the ocular colloids."

If such is the case why could not the existence of pyorrhea and blind
abscesses about the roots of the teeth be the source of the toxic
factors mentioned by Fischer? Hence the suggested association of the
dental surgeon with the ophthalmologist in these cases of apparently
idiopathic increased intra-ocular tension.

It would be well to state here a cursory examination of the mouth will
not discover root abscesses any more than such examination will
discover non-suppurative sinus disease. A careful examination of each
tooth together with radiograms of the entire maxilla are absolutely
essential to determine their presence or absence.




Trephining for Glaucoma

BY

ROBERT HENRY ELLIOT, M.D.,

London, England.


Mr. President and Members of The Chicago Ophthalmological Society:

As the hour is late I propose to take up only the principal points in
connection with my subject and to deal with each one shortly.

First: The operation of trephining is suitable, not merely for chronic
cases, but for sub-acute and acute cases of glaucoma as well. I would
urge on your attention that, of all the operations dealing with
glaucoma, this one involves the minimum of surgical violence, and
should, therefore, in acute cases be the operation of choice. It is,
moreover, much safer than any other operation I know of, and is no less
certain in its results. I do not advise trephining in the secondary
glaucoma following intumescent cataract, for in such cases the
semi-fluid lens bulges into and blocks the trephine hole. Nor for
obvious reasons do I recommend it in cases where there is reason to
believe that a communication exists between the aqueous and vitreous
chambers.

Second: The object of trephining is to tap and permanently drain the
aqueous fluid from the anterior chamber of the eye into the
sub-conjunctival space; in doing so it is essential to avoid as far as
possible all interference with the uveal tissue. The purpose of an
iridectomy is to avoid the danger of the iris in the neighborhood of the
wound being drawn and impacted in the trephined hole. We have found in a
large number of cases in which an iridectomy has been omitted, that the
results have been in no way inferior to those in which a piece of iris
has been removed, provided always that no subsequent iris prolapse
takes place. In pursuance of our purpose to avoid uveal tissue, we split
the cornea, and place the trephine as far forward as such splitting will
allow, and we bear on the trephine in such a way that it cuts through on
the corneal edge of the wound first. This insures establishing our
fistula in the most anterior position possible, and, therefore, as far
away as possible from the ciliary body and the angle of the chamber.

Third: The difficulties of the operation. Far too much stress has been
laid on these. Trephining is an operation which can be performed by any
surgeon who is used to ophthalmic manipulations, and who has good sight.
It is essential that he should work in a good light. The necessary
technique can be acquired from a written description. It is not for a
moment necessary that the surgeon who wishes to learn trephining should
see the originator of the operation at work. If, however, he feels
diffident at undertaking the procedure until he has seen it done by
another, there are many centers in this country where the operation is
now being successfully performed. I would mention amongst those which I
have visited New York, Minneapolis, St. Louis, Nashville, Louisville,
Detroit and Chicago. I have seen results of trephining by American
surgeons which could not be bettered anywhere.

Fourth: I am sure that everybody will recognize the difficulties of
operating during such a tour as I am now making. I have so far in the
last month performed over seventy trephinings in ten cities, and in
twice as many clinics. To adapt one's self to different clinical
methods, different assistants and different nurses is so difficult that,
as you are aware, many distinguished surgeons refuse to work out of
their own clinics. One cannot expect the results of such a tour to be on
a par with those one obtains in one's own quiet daily surroundings. I
am, however, confident that you will make a generous allowance for
these difficulties, and I gladly welcome the suggestion that all the
cases which I have operated on in America be collected together and
reviewed as a whole.

Fifth: In conclusion I would like to express the pleasure with which I
listened to Dr. de Schweinitz' paper. I believed from the title that
there might be a wide divergence of opinion between us. I find to my
great relief that we are in absolute accord. I know, however, that there
are in America and elsewhere able men who consider that the medical
treatment of glaucoma should be pushed as long as possible. I cannot but
feel that this is a survival of the dread that most surgeons have felt
in recommending one of the older operations for glaucoma. We have now in
our hands a method so safe, so easy and so certain that I feel sure that
this dread will ere long pass away, and that the diagnosis of glaucoma
will then be followed by a very early operation. In India I have gone
farther than this, and where one eye has shown high tension, I have
frequently trephined both. The prophylactic use of the operation is more
than justified in that land of long distances and scattered medical aid,
and where the patient is not likely to return a second time for surgical
help. This prophylactic trephining is a proposition that I put before
you today for your consideration, reminding you at the same time that
glaucoma is practically invariably a bi-lateral condition. I have seen
even in America not a few people blind in both eyes who might have
retained the sight of the second eye had the surgeon advised a double
sclerectomy when he first saw the case, despite the fact that the second
eye was then to all appearances non-glaucomatous.




Dr. Robert Henry Elliot's Paper on Trephining for Glaucoma

Discussion,

FRANK C. TODD, M.D.,

Minneapolis.


It is very difficult for one of limited experience to discuss a subject
presented so ably by Lieutenant Colonel Elliot to whom we are indebted
for the sclero-corneal trephine operation. He has already over a period
of a little over four years performed over 900 trephinings, and has made
a most careful subsequent study of the results of those operations on as
many cases as he had the opportunity to observe.

Anyone who has read Colonel Elliot's book on the sclera-corneal
trephining operation will be struck with the fact that he has not only
had a tremendous experience in ophthalmic surgery, but that he has made
the best of that unusual opportunity, and that to a foundation of a
careful training he has added the experience of twenty-two years of hard
painstaking work.

I have recently had the privilege of entertaining Colonel Elliot in my
own city, where I had the opportunity of assisting him and hence closely
observing his technique in eighteen trephinings. It has since been my
duty, and responsibility I may add, to care for those eighteen eyes. For
two years I have been doing the Herbert tongue flap, or a similar
operation. The results have been highly satisfactory thus far and
similar to those following the trephining operation, which operation I
have performed in a number of cases during the past ten months. My
conclusions as to these two operations are favorable to the trephining
operation because the Herbert tongue flap operation is much more
difficult, and hence less certain than the Elliot trephining operation.

The time for discussion does not permit a detailed statement of the
results nor experiences in the handling of these trephining cases. Of
the entire number five totally blind eyes were trephined. Tension was
reduced in all but one. In that one hemorrhage occurred at the time of
the operation. One of these blind eyes had not been totally blind longer
than a few weeks. Hand movement vision developed in this eye. Another
eye totally blind one year has thus far developed perception of light.
Of the cases with varying degrees of vision from hand movements to
six-ninths all but one have either remained the same or shown some
improvement. The one exception was an eye having six-ninths vision. A
small button hole iridectomy was made; prolapse of the iris into the
wound occurred four days later requiring incision. Upon incision of the
prolapse intra-ocular hemorrhage occurred, causing nearly total
blindness for two weeks. Vision is clearing fast and it remains yet to
be seen what the final results may be. One buphthalmic eye trephined by
myself gave good results.

I have as yet seen no cases of remote infection, but the report of
Axenfeld and some others would indicate that this occurred following the
Lagrange as well as the trephining operation, the then bulging
conjunctiva having become eroded and infection having taken place
through the eroded conjunctiva as shown when stained with flourescin.

The opinion, not yet conclusive, that I have thus far formed as a
consequence of my experience and the information obtained from others of
greater experience is as follows:

First: That in those cases of chronic glaucoma in which iridectomy has
been of benefit in preventing or retarding the oncoming of blindness,
the result has apparently been secured by reason of the fact that
filtration has been produced, and not merely because a piece of iris has
been removed.

Second: That in chronic glaucoma (in acute glaucoma iridectomy has
proven a satisfactory operation) when the progress of the disease
cannot be arrested by non-surgical treatment (an even in some of these,
where, for instance the patient cannot be kept under observation or will
not carry out the treatment) some form of operation intended to produce
filtration should be performed.

Third: The Elliot sclero-corneal trephining operation carefully
performed in accordance with the author's technique in the light of our
present knowledge seems to be the best and safest operation to produce
that result.

Fourth: That to glaucoma may be added buphthalmos and staphyloma, as
diseases often capable of relief by trephining and indeed toward the
relief of which trephining is the best form of operation yet presented.

Fifth: That the results secured when the operation is well done and the
after care is properly followed out are satisfactory, in that the
operation in a large proportion of cases apparently permanently lowers
the tension to normal or below normal, relieves pain, prevents the
oncoming blindness (otherwise inevitable) and in many cases causes an
improvement in the acuity of vision, in the visual field. And in
occasional cases of blindness of not too long duration, it restores some
vision, occasionally to a marked degree.

Sixth: That it is not a simple nor easy operation and should, therefore,
be performed only by an operator well trained in ophthalmic surgery. The
careful and skillful technique of the originator of the operation
perhaps accounts for his greater success in its results and those who
perform the operation should follow his technique and be capable of
handling complications that may later arise.

In conclusion, Mr. President, I wish to say that we ophthalmologists the
world over are indebted to Lieutenant Colonel Elliot not alone for his
contributions to our knowledge, but for his persistence against
precedent and criticism in establishing the facts upon which rest the
foundation for the success of his operation, and for so emphasizing the
great importance of this epoch-making achievement.

It is because we respect his wisdom gained by incessant study and
experience in a country where climatic conditions are such that a man of
ordinary energy would have failed to do even average work that we so
readily welcome the teaching of this enthusiastic evangelist.

His pilgrimage to our country will be the means of starting many in this
new field, and we shall soon be able to draw more definite and final
conclusions from our own experiences.




Operations Other than Scleral Trephining for the Relief of Glaucoma

BY

CASEY A. WOOD, M.D.,

Chicago.


In this paper I shall say a few words about the large number of
operative procedures that, apart from trephining, or, preferably,
_trepanation_, have been urged in the treatment of the various forms of
glaucoma. Their name is legion and among them we find peripheral
iridectomy; anterior sclerotomy; irido-sclerotomy; scleriritomy; de
Wecker's dialysis of the iris; Hancock's division of the ciliary muscle;
the incision of the iridian angle of de Vincentiis; sclero-cyclo-iridic
puncture; the Sterns-Semmereole _sclerotomia antero-posterior_; the
_transfixio iridis_ of Fuchs; Antonelli's peripheral iritomy; Holth's
formation of a cystoid cicatrix; Hern's operation; Terson's
sclero-iridectomy; Abadie's ciliarotomy; Ballantyne's incarceration of
iris method; Masselon's small equatorial sclerotomy; Simi's equatorial
sclerotomy; Galezowski's sclero-choriotomy; excision of the cervical
ganglion; removal of the ciliary ganglion; Querenghi's operation of
sclero-choriotomy; Bettremieux's simple anterior sclerectomy; Heine's
cyclodialysis; Herbert's wedge-isolation operation; Verhoeff's operation
with a special sclerotome; Holth's sclerectomy with a punch-forceps;
Walker's hyposcleral cyclotomy; posterior sclerotomy; T-shaped
sclerotomy; and last but not least the Lagrange form of sclerectomy with
its various modifications by Brooksbank James, myself and others.

In addition to the foregoing list--which is by no means complete--there
are several combinations of operations, as, for example, the Fergus
trephining operation, which is really a combination of a sclero-corneal
trepanation and a cyclodialysis.

So far as it is practicable there is a certain amount of wisdom in
comparing the results of an operative procedure with others with which
it is brought in competition, and I believe we are even now in a
position to form at least some idea of the comparative value of the
three methods that comprise the great majority of interventions made use
of by ophthalmic surgeons at the present time. I refer to _iridectomy_,
the _Lagrange operation_, and the _Elliot operation_. So far as regards
the last named procedure, I congratulate this Society that it has had an
opportunity of seeing a demonstration and hearing a discussion by the
famous ophthalmic surgeon who perfected it.

As regards the others let me recommend to you the complete description
of them given by Posey in _A System of Ophthalmic Operations_.

Let us consider the first of the three procedures just
mentioned--_iridectomy_--introduced by von Graefe. The mechanism of its
mode of cure is best studied in cases of acute primary glaucoma, when
there is apposition of the periphery of the iris to the cornea. In these
acute cases there is probably only a mere _apposition_, and the blocking
up of the sclero-iridian angle is largely mechanical. Here the root of
the iris is readily removed in its entirety and a really peripheral
iridectomy is easily done. When, however, a true _adhesion_ between
corneal and iridic tissue takes place the filtration angle is not so
easily opened. True peripheral adhesions are not readily broken up or
separated, and the iridectomy is, for that reason at least, not
effective. Moreover, this form of anterior synechia (resulting from a
true union of iris and cornea) is so intimate that the iris root is, by
the iridectomy, torn away only at the sclero-iridian angle at the
anterior border of the adhesion--and does not open up a channel into
Schlemm's canal. It is not, therefore, difficult to understand why
iridectomy alone in any of the forms of chronic glaucoma fails to open
up the true filtration spaces and does not provide a drain that permits
of an escape of fluid from the posterior chamber through the loose
tissue that surrounds it into the canal of Schlemm. Treacher Collins
found, after a careful examination of eyes upon which iridectomy had
been performed for glaucoma, that it is extremely rare for the initial
section to pass through the pectinate ligament, while Schlemm's canal
invariably escapes. Moreover, since the sclero-corneal incision is
uniformly oblique, the position and extent of the external wound does
not always furnish evidence of the character of the internal wound. In
all likelihood many cases of relief or cure following iridectomy are
those due to the formation of cystoid scars or minute fistulae, rather
than as a result of the removal of a portion of the iris periphery.

The best brief tabulation of the results obtained by iridectomy, in
glaucoma, is to be found in Weeks' textbook on _Diseases of the Eye_,
page 417: "Sulzer reports as follows: Acute glaucoma, 149 cases;
improved, 72.5 per cent; serviceable vision preserved, 11.3 per cent;
vision impaired at once, 4.08 per cent; very little vision, 12.12 per
cent.

"Zentmeyer and Posey: In simple glaucoma central vision increased in 60
per cent; remained the same in 20 per cent; diminished in 20 per cent.

"Wygodski: Inflammatory glaucoma, 37 cases; improvement, 76 per cent;
unimproved, 5 per cent; deterioration, 19 per cent. Sub-acute (chronic
inflammatory), 147 cases; improvement 10 per cent; unimproved (condition
the same as before iridectomy), 40 per cent; deterioration, 30 per cent;
blindness, 20 per cent. Cases operated on at an early stage gave 85 per
cent of good results. Simple glaucoma, 104 cases; improvement, O.96 per
cent; condition as before, 10.5 per cent; deterioration, 52 per cent;
amaurosis, 36.5 per cent.

"Hahnloser and Sidler: One hundred seventy-two eyes observed not less
than ten years after operation; acute inflammatory, 31 eyes; good
results, 64 per cent; relatively good, 13 per cent; blind 23 per cent;
chronic inflammatory, 37 eyes; good result, 29.9 per cent; relatively
good, 27 per cent; blind, 43 per cent; simple glaucoma, 76 eyes; good
results, 42 per cent; relatively good, 28.9 per cent; blind, 28.9 per
cent."

As far as the _Lagrange procedure_ is concerned, you will remember that
after eserinization an oblique incision is made through the sclera by
means of a narrow Graefe knife and a large conjunctival flap secured.
This is obtained by making a peripheral section of the sclero-corneal
margin with the knife and, as soon as the edge of the knife reaches the
upper limit of the anterior chamber, it is turned backward and brought
out through the sclera obliquely. The conjunctival flap thus formed is
turned back over the cornea, and the fragment of sclera that is left
attached to the cornea is removed by means of a fine pair of delicate
curved scissors. Following this an iridectomy is performed. The
conjunctival flap is now replaced and a bandage applied.

This operation opens a large filtration passage for the intra-ocular
fluids and the prompt healing of the wound with its mucous covering
prevents prolapse of the iris.

Under no circumstances must iris be left between the lips of the wound.

Although Lagrange advocated iridectomy in all cases in his first
communication, he no longer judges the procedure to be necessary in all
instances, reserving it for cases in which for any reason, such as
hypertension, prolapse is to be feared.

While Lagrange holds that it is necessary to open the anterior chamber,
Bettremieux thinks that a removal of but a portion of the thickness of
the sclera suffices. His procedure is as follows: After raising a flap
of conjunctiva from the neighborhood of the limbus a medium sized
needle, curved and flattened towards its point and firmly grasped in a
needle holder, is thrust superficially into the sclera tangentially to
the upper edge of the cornea, so as to become fixed in the capsule of
the eyeball. A small shaving of the sclera, about ½ mm. thick, 1½ to 2
mm. broad and from 2 to 3 mm. long, is then excised by means of a narrow
Graefe knife. The scleral slip is then freed from the conjunctiva at
each end and the mucous membrane brought together over the wound by fine
catgut sutures.

As you are well aware, numerous operators regard the Lagrange operation
as superior to the iridectomy of von Graefe because they believe there
is filtration through the newly formed tissue between the lips of the
operative wound. Among those of many observers the conclusions of
Ballantyne may be quoted: "The results of sclerectomy vary according to
the degree of hypertension of the eye operated on. Three varieties of
cicatrix are distinguishable according to the amount of sclera excised:
(1) that in which there is mere thinning of the sclera owing to the
excised portion not reaching the posterior surface of the cornea
(conjunctiva smoothly covers the cicatrix); (2) that represented by a
subconjunctival fistulette, due to excision of the whole thickness of
the sclera, in an eye with moderate tension (the conjunctiva lies
smoothly over the cicatrix); (3) the fistulous cicatrix with an
ampulliform elevation of the overlying conjunctiva, resulting from
excision of the whole thickness of the sclera in an eye the seat of high
tension. In cases of high tension, even a simple sclerectomy will allow
ample filtration, owing to the gaping of the wound, while in cases
without elevation of the tension, sclerectomy will be quite ineffectual.
Lagrange therefore proposes the following rules of procedure: (a) If
tensions is normal to +1, do sclerectomy without iridectomy, the amount
of sclera excised being inversely proportionate to the degree of
hypertension. (b) If tension is +1 to +3, do sclerotomy-iridectomy, the
iridectomy being added to avoid entanglement of the iris. Lagrange does
not recommend his operation for acute glaucoma. It is especially adapted
for cases of chronic simple glaucoma."

During the past ten years or more I have been doing a modification of
the Lagrange operation, the details of which (The Operative Treatment of
Glaucoma with Special Reference to the Lagrange Method, _The Canadian
Medical Association Journal_, November, 1911) I have elsewhere
published.

As stated in this paper I have modified the procedure to the extent of
removing _all_ the conjunctiva attached to the borders of the operative
wound. I admit that this intervention exposes the root of the iris and
the ciliary body, but I have never yet had the slightest infection of
the wound. I attribute this freedom from sepsis to careful cleansing of
the conjunctival sac and to other pre-operative precautions, but
especially to the use, before and after the operation, of White's
ointment--a preparation of 1-3000 mercuric chloride in sterile vaseline.
One cannot use sublimate in such a strong _watery_ solution, but the
vaseline seems to modify it and to allow of such slow absorption that it
is not only a non-irritant but a most excellent antiseptic application
in operations on the eye.

In any event the result of the Lagrange operation proper, as well as my
modification of it, is to produce a drainage-oedema about the incisional
wound which persists almost indefinitely. In many cases this swelling
amounts to a bleb which may be increased by massage of or pressure upon
the eyeball. The efficacy of the operation in lowering intra-ocular
tension is to some extent measured by the degree and the constancy of
this epibulbar oedema; indeed, I suspect that the most successful
examples are those in which sclera fistulae, minute or otherwise, form
as a sequel of the operation.

My object in excising the conjunctiva about the sclero-corneal flap, is
to delay union of the wound edges, to widen the bridge of loose
cicatricial tissue between them, to prevent such a complete growth of
the endothelium as would cover the wound and block the exit of fluids,
and to insure intra-ocular rest.

In cases of _chronic_ increase of intra-ocular tension associated with a
quiet uveitis or an iridokeratitis, when the patient exhibits traces of
old synechiae, or where there is danger of their re-formation, I do not
hesitate to use atropia as long as the wound of operation has not
healed.

To the present time I have done 72 operations of the sort and have seen
no reason to alter the opinion of it expressed in the article mentioned.
Whatever objection may in the future arise--and I freely confess that
it _seems_ to be fraught with the dangers that many of my colleagues
have pointed out as probable--I have so far not seen a single case of
infection of the wound of operation. While I believe the
anti-glaucomatous results to be excellent, I may also claim that the
operation is of the simplest character; and it is easy of performance
and the resulting filtration-scar is large and (perhaps) more permeable
to the changed intra-ocular fluids than the quicker healing wounds of
the usual Lagrange and Elliot procedures.

It is regarded by most operators as desirable that there should not be
long delayed healing of the operative wound, and the fact that the
conjunctiva covers the incision is often spoken of as an advantage,
partly because it shields the large open area produced by the Lagrange
incision from infection.

My experience of this modified operation continues to be that it is
necessary to clear the neighborhood of the operation wound entirely of
conjunctiva. If the down-growth of epithelium into the operative wound
is permitted the effects are by no means as pronounced, and the eventual
lowering of tension is not as permanent as they otherwise would be.

Another matter: I am satisfied that the delayed filling of the wound by
connective tissue is desirable in most cases of _chronic_ glaucoma. A
complete drainage of the intra-ocular fluids that results from long
delayed union of the wound edges, allows the interior of the eye to
regain, as far as possible, the _status quo ante_. On the other hand the
comparatively early closure of the wound (or the termination of _free_
drainage and minus tension) tends to re-establish the _status
glaucamatosus_. Whether these desirable results are to be realized or
not will, of course, depend upon a future experience larger than I have
yet had. This modification of the Lagrange operation seems to be a
radical one and I do not expect its adoption until the results of an
extended trial are carefully recorded and reported.

Quite recently several operators, who have been in a position to do so,
have contrasted the results obtained by the Elliot method and those
following the Lagrange procedure. Probably the most important of these
observations is the experience of Meller (Die Sklerektomie nach Lagrange
und die Trepanation nach Elliot) set forth in a paper read by him at the
last meeting of the _Deutsche Naturforscher und Aertze_. In this report
Meller gives an account of 389 sclerectomies following the usual
Lagrange procedure. Twelve per cent of the cases were of acute glaucoma;
61.5 per cent of chronic inflammatory glaucoma, and 9 per cent of simple
glaucoma. The rest of the operations were done in other forms of the
disease. In more than half the cases the usual iridectomy was performed;
in 30 per cent the procedure was peripheral; in 4 per cent there was no
iridectomy. The patients were studied during a period of five years. In
more than half the instances there was a pale, cystic, oedematous
cicatrix; in 11 per cent the scar was ectatic, and in the remainder the
field of operation was quite flat. The form of the scar was described in
most instances, but it was not noticed that there was a definite
relation between the cicatrical formation and the intra-ocular tension.
In 70 per cent of the cases a good result followed the operation, but in
10 per cent the result was decidedly unsatisfactory. Cloudiness of the
lens set in in 4 per cent of the cases, while posterior synechiae
developed in the great majority of them. In 2.3 per cent the eye was
attacked by iridocyclitis and in 3.4 per cent enucleation was found to
be necessary. Six eyes became atrophic but were not, for various
reasons, removed. One and three-tenths per cent of the eyes operated on
were lost from late infection. Vitreous was lost in 6.2 per cent. Two
eyes became blind from expulsive hemorrhage. The large majority of
these complications arose in the eyes operated on for chronic glaucoma.
There were fewer eyes lost following the operation for glaucoma simplex
than in the other forms of the disease. Recurrences were noticed in 11.3
per cent of all the cases; in simple glaucoma 14.3 per cent as against
the acute and chronic forms with 6 per cent. A return of the glaucoma
was noticed in 7 per cent of the pale, oedematous, post-operative scars,
in 16 per cent of the flat cicatrices, and in 24 per cent of the ectatic
variety. Considerable stress is laid upon the fact of the marked
softness of the eyes after each operation. There were histological
examinations made of the eyeballs in 11 cases, in which the position of
the incision and excision, the development of the scar tissue, and the
appearance of the complications were duly set forth. The operator then
gave a history of over 178 trepanations after the Elliot method and
compares them with the procedure of Lagrange. He concludes that the
Elliot trephining operation is less dangerous, is more likely to be
followed by the development of a cystic scar, and leads to loss of the
eye in only 2.4 per cent of the eyes operated on. In Elliot's cases the
percentage of relapse was more noticeable than in the Lagrange cases
where no iridectomy was done. This observer concludes that the method of
Elliot is to be preferred to that of Lagrange, and that in the former
case iridectomy is an important factor in obtaining a favorable result.
This being the case one cannot truthfully say that trephining alone can
take the place of the old Graefe iridectomy. On the other hand,
trephining may with advantage be employed instead of iridectomy for
cases difficult or dangerous under the latter method.

Whatever difference of opinion was noticeable at the Vienna meeting, all
of those present, especially Meller, the reader of the paper just
quoted, were decidedly of the opinion that the Elliot operation is in
every respect the one best adapted to buphthalmia, or congenital
glaucoma.

In conclusion let me say that the acceptance or rejection of Colonel
Elliot's procedure or any other operation is not to be decided by the
percentage of iritis, secondary cataract, relapses, lost eyes, etc., but
by deciding whether or not his procedure in the various forms of
glaucoma gives the best results, including the preservation of
comfortable eyes. In other words, we are seeking not the operation that
will cure _every_ case of glaucoma but the one which is capable, _in the
hands of the average ophthalmic surgeon_, of relieving or curing _most_
cases of that affection.




Dr. Casey A. Wood's Paper on Operations Other than Scleral Trephining
for the Relief of Glaucoma

Discussion,

ALBERT E. BULSON, JR., M.D.,

Fort Wayne.


Increasing belief in Colonel Elliot's view that trephining should be the
operation of choice in any form of glaucoma, makes it difficult to
consider operations other than trephining in anything but a spirit of
disfavor.

Until recently the decision as to the kind of operative procedure to be
employed for the relief of glaucoma has depended on the form and stage
of the disease, and the amount and character of the vision of the
affected eye. Many operators still hold that an iridectomy is the most
valuable of all operations for acute inflammatory glaucoma, and not a
few hold that the operation has a decided place in the treatment of
simple glaucoma. The operation is not without difficulties, and one is
inclined to agree with Elliot who says that "The man who can make a
'finished iridectomy' quietly and cleanly has graduated as an ophthalmic
operator." The difficulties of an iridectomy are especially pronounced
in those cases in which the anterior chamber is extremely shallow and
the iris is pressed against the cornea. It is in such cases that the
success of the operation is increased by the addition of posterior
sclerotomy and the intelligent use of miotics prior to the performance
of the iridectomy. Even then the permanent results of the iridectomy
will be modified in proportion to the success secured in freeing the
filtration angle and opening Schlemm's canal by thorough removal of the
root of the iris.

The failure of many apparently well executed iridectomies may be
attributed to the fact that the iris is not removed to the extreme
root, and the remaining stump is sufficient to block the drainage. This
is especially apt to be the case in chronic glaucoma where the iris is
adherent to the cornea, and in efforts to free the filtration angle by
an iridectomy the iris is torn off in front of the adhesion and the
filtration angle is not opened.

As Elliot has pointed out, iridectomy is most open to attack on the
ground of safety. We have to take into account the large scleral wound
made, and the fact that this lies close to the ciliary body. The sudden
release of all tension and the simultaneous weakening of the supports of
the lens and vitreous body create very unfavorable conditions under
which to make the crucial step of the operation.

The poor results following an iridectomy in chronic glaucoma have led to
the devising of many substitute operations, of which those tending to
the production of a filtering scar are now preferred, and, experience
shows, hold out the most hope of bringing about long continued relief.
It even is considered probable that the effects of an iridectomy which
brings about more or less permanent reduction in the intra-ocular
pressure is due to the formation of a filtering scar which augments
whatever results may have been secured in the attempt to open up the
drainage into the canal of Schlemm.

Dr. Wood has referred to several of the many substitutes for iridectomy
that have been proposed, and it is unnecessary to enumerate them again
or to attempt to point out their good or bad features. It is sufficient
to say that for the average operator and the larger per cent of cases,
the operation which is easiest to perform, is attended with the least
risk and offers the best hope of permanent results should be the one of
choice. Sympathectomy has failed to secure a place in ophthalmic
surgery, sclerotomy has not been found adequate, and cyclodialysis is
not sufficiently simple of execution or permanently beneficial in its
results to give it prominence.

Of the operations proposed for the formation of a filtering cicatrix,
those of Elliot and Lagrange are justifiably the most popular. Those of
us who have had the pleasure of seeing the trephining operation done by
Col. Elliot are impressed with the fact that the operation, even in the
hands of its originator, is not, when properly done, uniformly easy of
performance. It does, however, offer the advantage of carrying with it
the minimum amount of risk, and the apparently permanent results secured
justify the ophthalmologist in acquainting himself with the technique of
the operation, for, as pointed out by Sydney Stephenson and others, "the
technique is responsible for success or failure." Furthermore, there is
no sufficient reason why the field of usefulness of the operation should
be confined to the chronic forms of glaucoma, and Col. Elliot
unhesitatingly recommends trephining as safer and more efficient than
any other operative procedures at present employed for the relief of
acute glaucoma.

The success of the Lagrange operation, which, like the Elliot operation,
aims to produce a fistulous communication between the anterior chamber
and the sub-conjunctival area, depends upon securing the removal of a
relatively large section of all of the layers of the scleral and corneal
lip of the wound, so that a permanent opening, covered by the replaced
conjunctival flap, is made. Unlike the trephine operation which was
evolved from it, the Lagrange operation requires the same kind of an
opening of the eyeball as required for a well executed iridectomy, and a
properly placed section entirely in scleral tissue, with a good sized
conjunctival flap, are elements which enter into the ultimate success or
failure of the procedure.

Aside from the dangers incident to a wide incision in the neighborhood
of the ciliary body and the possibility of accident to the lens or
vitreous body, or of intra-ocular hemorrhage, there is for the average
operator the added difficulty and danger in removing a piece of sclera
of the exact size required. The technique of the operation is even more
difficult and exacting than in the performance of the trephine
operation, and it also compares unfavorably in safety.

The advisability of removing the conjunctival flap, as advocated by Dr.
Wood, as a modification of the Lagrange operation, may be seriously
questioned, for aside from the fact that apparently no advantages in
aiding permanent filtration are added, there is, added to the objections
to the Lagrange operation already mentioned, the very serious
disadvantage of subjecting the area at the root of the iris to infection
for a prolonged period of time. The advantages of the protection
afforded by a conjunctival flap far outweigh the disadvantages of a
remotely possible interference of drainage by the blocking of the open
wound with conjunctival tissue. The fortunate experience of Dr. Wood in
not having infection in a wound which remains open and unprotected for
variable lengths of time is not likely to be the experience of any
considerable number of operators, and probably will not always be the
experience of Dr. Wood. Furthermore, the possibilities of damage by
hemorrhage from the choroidal or retinal vessels, delayed formation of
the anterior chamber and adhesion of the capsule of the lens to the
wound, and the injurious effects of even slight trauma subsequent to the
operation, including loss of vitreous, are increased by omitting the
conjunctival flap.

The modern operation for the relief of glaucoma, by which a filtering
scar is produced which permits escape of liquid from the anterior
chamber, is the one which apparently holds out the most hope of
permanently relieving the condition. While success will depend always to
a certain extent upon the personal equation, yet it seems now that for
a large majority if not all of the cases we are justified in abandoning
all other operations than trephining, notwithstanding the verdict of
Elschnig and others that fistula forming operations eventually will be
discarded in favor of iridectomy and cyclodialysis.

Late or secondary infection, not unknown following iridectomy, may
follow the trephine operation, and already some fifteen or sixteen cases
have been reported. But while this possibility is a real danger, which
improved technique may greatly minimize (Col. Elliot has not seen a case
of secondary infection in an experience of over 1200 trephining cases of
his own and a large number of others performed by his assistants and
pupils) the ultimate verdict must rest with results as compared with
other measures. At present, as pointed out by Meller, whose statistics
Dr. Wood has cited, trephining heads the list of remedial measures for
the relief of glaucoma, and it has the advantage of being applicable to
any form of the disease, to be relatively free from danger, either
immediate or remote, and to produce the highest percentage of favorable
results. The addition of an iridectomy in every case of trephining does
not unduly complicate the operation and has much to commend it in
offering the patient every possibility of relief.




INDEX

                                                PAGE
ETIOLOGY AND CLASSIFICATION OF GLAUCOMA,
  _Edward Jackson, M.D._                           9

ETIOLOGY AND CLASSIFICATION OF GLAUCOMA,
  Discussion, _Francis Lane, M.D._                28

PATHOLOGY OF GLAUCOMA,
  _John Elmer Weeks, M.D._                        37

PATHOLOGY OF GLAUCOMA,
  Discussion, _E. V. L. Brown, M.D._              57

CONCERNING NON-SURGICAL MEASURES FOR THE
REDUCTION OF INCREASED INTRA-OCULAR TENSION,
  _George Edmund de Schweinitz, M.D._             61

CONCERNING NON-SURGICAL MEASURES FOR THE
REDUCTION OF INCREASED INTRA-OCULAR TENSION,
  Discussion, _Nelson Miles Black, M.D._         101

TREPHINING FOR GLAUCOMA,
  _Robert Henry Elliot, M.D._                    107

TREPHINING FOR GLAUCOMA,
  Discussion, _Frank C. Todd, M.D._              113

OPERATIONS OTHER THAN SCLERAL TREPHINING
FOR THE RELIEF OF GLAUCOMA,
  _Casey A. Wood, M.D._                          121

OPERATIONS OTHER THAN SCLERAL TREPHINING
FOR THE RELIEF OF GLAUCOMA,
  Discussion, _Albert E. Bulson, Jr., M.D._      141