Chapter 1

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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

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.

(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.

(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.

(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

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.