Produced by Bryan Ness, Martin Pettit and the Online
Distributed Proofreading Team at http://www.pgdp.net (This
book was produced from scanned images of public domain
material from the Google Print project.)
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
corneae that have suffered from keratitis. The alteration is usually in
the form of ectasiae. 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. Francaise
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.