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
corneæ that have suffered from keratitis. The alteration is usually in the
form of ectasiæ. 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
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