Part 1 (1/2)
Glaucoma.
by Various.
Etiology and Cla.s.sification 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 ent.i.ty to be called glaucoma, without increased tension constantly or necessarily present, and cases of increased intra-ocular tension not to be cla.s.sed 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 s.p.a.ces and blood-channels of the eye are large, as compared with the ma.s.s of its tissue colloids. In these s.p.a.ces 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 const.i.tute a factor making for malignancy in glaucoma. But it can hardly explain the original departure from a normal pressure balance.
We must a.s.sume 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 acc.u.mulate 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 a.s.sociated with noticeable flus.h.i.+ng 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 a.s.sociated with the nutritional processes like secretion or inflammation; beyond this we know little about it. The a.s.sociation 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, pus.h.i.+ng 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 acc.u.mulation of experimental precipitates, as shown by Schreiber and Wengler, or possibly of pigment granules into Fontana's s.p.a.ce; or a process of sclerosis closing the s.p.a.ces 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 s.p.a.ce, 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 ca.n.a.l 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 a.n.a.logy 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, embarra.s.sment, 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 alt.i.tudes, 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 a.n.a.lytical work has been done to test its correctness.