Glaucoma | Page 2

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