Remember: Perform gonioscopy under low light conditions!

7.2.1Causes of Secondary Angle Closure

7.2.1.1With Pupillary Block

In eyes with thick swollen lens (phacomorphic in advanced cataract), anterior lens dislocation due to weak zonules (pseudoexfoliation, trauma, Marfan syndrome, Weil-Marchesani syndrome).

In eyes with seclusion or occlusion of the pupillae with iris bombata (bombŽ) after inßammations due to circular posterior synechiae (Figs. 7.18 and 7.19).

In eyes with aphakia with:

¥ Prolapse of the vitreous into the pupil

Fig. 7.20 Silicone oil blocking the pupil, but no angleclosure, due to an open inferior iridectomy

¥Prolapse of silicone oil into the pupil without an Ando iridectomy at 6 oÕclock (Fig. 7.20)

¥Aphakia and anterior chamber lens without a patent peripheral iridectomy (Fig. 7.21)

¥Pseudophakia (refractive lenses) in phakic eyes without iridectomy

7.2.1.2Without Pupillary Block, but with an Anterior Pulling

Mechanism

In eyes with neovascular membranes. These consist not only of new vascular structures, but they also have proliferative Þbrotic tissue. The vessels are

Fig. 7.21 Aphakia with anterior chamber lens (Þrst postoperative day) with iridectomy not patent. The peripheral iris is bowed forward and pushed into the chamber angle

Fig. 7.22 Newly formed vessels on the anterior surface of the iris in a randomized pattern in an eye with a central venous thrombosis 6 months before

thinner than normal and they do not run in a radial or circumferential pattern (Fig. 7.22). Reasons can be proliferative diabetic retinopathy, central retinal venous occlusion, occlusion of the carotid, and rarely central retinal artery occlusion. The hypoxia induces an increase in the levels of growth factors. The Þbrovascular tissue starts to proliferate at the pupillary margin of the iris, and grows towards the chamber angle (Fig. 7.23).

In eyes with iridocorneal endothelial syndrome (ICE), with progressive formation of endothelium and its basement membrane (DescemetÕs

Fig. 7.23 Chamber angle of an eye with neovascularizations of the iris. There are no structures of the chamber angle visible; the angle is completely closed

Fig. 7.24 Progressive essential iris atrophy due to proliferating endothelial cells showing ectopia of the pupil and a large hole in the iris at 12 oÕclock

membrane). These structures have an abnormal tendency for proliferation, which pulls the iris into the chamber angle. The consequences are synechiae and distortion of the pupil (corectopia) and the formation of new pupils (polycoria) in the opposite direction to the pulling, with atrophy of iris tissue. The pulling mechanisms lead to an ectropium of the pigmented layer of the iris.

¥Progressive (essential) iris atrophy: iris atrophy with marked corectopia, hole formations in the iris (pseudopolycoria), always unilateral (Figs. 7.24 and 7.25)

¥Chandler syndrome: much less iris atrophy; ectropium uveae, corneal edema

Fig. 7.25 The same eye as shown in Fig. 7.24 14 years later showing enlargement of the big hole and loss of pigmentary layer of the iris with a new large hole at 12 oÕclock. The eye went blind after several operations

Fig. 7.26 Epithelial implant cysts from 12 to 5 oÕclock in the chamber angle and the anterior chamber after extracapsular cataract extraction. The cysts are transparent and have grown slowly

¥Iris-nevus syndrome (Cogan-Reese): peduncular nodules on the iris surface combined with iris atrophy

In eyes with epithelial ingrowth after penetrat-

ing globe injuries or surgery. The epithelium proliferates within a slowly increasing cyst (Fig. 7.26).

Following argon-laser trabeculoplasty, with the laser spots placed too close to the anterior ciliary band. The inßammation and the scars will lead to peripheral anterior synechiae.

In aniridia. The small amount of peripheral iris tissue tends to cover the trabecular meshwork.

Fig. 7.27 Peripheral anterior synechiae due to a tumor of the ciliary body (between the arrows) pushing the iris forward

Fig. 7.28 Tumor of the ciliary body pushing the peripheral iris into the chamber angle. Note the heavily pigmented trabecular meshwork

In eyes with endothelial posterior polymorphous dystrophy of the cornea (Schlichting).

7.2.1.3Without Pupillary Block, but with an Anterior

Pushing Mechanism

In eyes with aqueous misdirection, ÒmalignantÓ reaction. The misdirection of the aqueous humor into the posterior compartments (behind the lens, into the vitreous body) of the eye pushes the lens- iris-diaphragm anteriorly. Uveal effusion is an additional component.

In eyes with iris or ciliary body cysts or tumors (Figs. 7.27, 7.28, and 7.29). Their real extent and size are preferentially visualized by