Part 4

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.