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Angle-Closure Glaucoma Secondary to Occlusion of the Central Retinal Vein

Malik Y. Kahook, MD and David L. Epstein, MD, MMM

Occlusion of the central retinal vein is not ordinarily thought to affect the depth of the anterior chamber, but occasionally, within a few days after vein occlusion, the lens and iris move forward, producing conspicuous shallowing of the anterior chamber in the affected eye. This is especially appreciated when one compares the axial depth of the anterior chamber in the affected eye with that in the contralateral normal eye.^1–4 In some cases, there has been enough shallowing to cause the angle to close. In such cases, angle-closure glaucoma has usually been diagnosed within 2 or 3 weeks after vein occlusion. The shallowing is reversible, and the anterior chamber does return to its original depth within a few weeks. The problem of angle-closure glaucoma then disappears if no synechiae have formed, but subsequent neovascular glaucoma may develop.

In the past, before this entity was clearly distinguished from other forms of angle-closure glaucoma, most cases were treated with pilocarpine and aqueous humor suppressants, which sufficed to keep the angle open until the spontaneous deepening and resolution of the glaucoma took place. We encountered one case in which treatment with pilocarpine, a carbonic anhydrase inhibitor, and oral osmotics did not relieve unilateral angle-closure glaucoma secondary to occlusion of the central retinal vein. However, when the pilocarpine was discontinued and a cycloplegic (cyclopentolate) was administered, the anterior chamber deepened, and the angle opened. Bloome reported 2 cases in which there was a good response to a cycloplegic and acetazolamide.³ Treatment with cycloplegic agents seems logical in this condition, and although we still have much to learn, cycloplegics should be used as initial treatment instead of miotics.

We assume that an abnormal accumulation of blood or fluid in the posterior segment is responsible for pushing the vitreous and lens forward. This fluid is gradually reabsorbed, allowing the vitreous and lens to recede to their normal position. Angle closure appears to be caused by abnormal resistance to flow of aqueous humor through the pupil from the posterior chamber to anterior chamber due to the forward position of the lens, analogous to the mechanism in primary angle-closure glaucoma in which the lens is also forward, but on a permanent rather than a transient basis; that is, the mechanism for the closure of the angle in this entity seems to involve a secondary pupillary block mechanism. In some cases of this type, peripheral iridectomy has been done and has relieved the angle-closure glaucoma without altering the position of the crystalline lens.

Before the availability of laser iridectomy, we believed that, in this particular kind of angle-closure glaucoma, it was best to treat the condition medically rather than by iridectomy. We learned that in most cases, the underlying condition cleared in a few weeks, even if the angle was only minimally open in this interval. With the relative ease of laser iridectomy, we now recommend that it be performed if the eye is not totally blind to prevent chronic synechial glaucoma, unless medical (cycloplegic) therapy opened the angle so well that synechiae formation would be unlikely. Gonioscopy of the fellow eye is important because it may be occludable.

The occurrence of shallowing of the anterior chamber and angle-closure glaucoma secondary to occlusion of the central retinal vein is not directly related to the risk of developing neovascular glaucoma later.⁵ The proportion of eyes that have developed neovascular glaucoma has not been more or less than is expected after ordinary occlusion of the central retinal vein without axial shallowing.

This condition must always be considered in the differential diagnosis of unilateral angle closure. Other causes of transient unilateral shallowing of the anterior chamber with or without angle-closure glaucoma include panretinal photocoagulation,6,7 choroidal hemorrhage,⁸ massive retinal detachment secondary to macular degeneration,⁹ uveal effusion,¹⁰ and massive vitreous hemorrhage.¹¹

The capacity of the vitreous to normally give up fluid and reduce its volume to compensate for the expanded posterior segment volume from the central retinal vein occlusion is believed to explain why this syndrome of angle-closure glaucoma is uncommon. Presumably, the condition occurs in patients with more turgid vitreous. A systematic analysis of the difference between affected and unaffected patients with central retinal vein occlusion would be of interest. However, we suspect that slight axial shallowing (without angle closure) occurring acutely after central retinal vein occlusion may be more common than realized.

REFERENCES

1.      Hyams SW, Neumann E. Transient angle-closure glaucoma after retinal vein occlusion. Br J Ophthalmol. 1972;56:535-355.

2.      Grant WM. Shallowing of the anterior chamber following occlusion of the central retinal vein. Am J Ophthalmol. 1973;75:384-389.

3.      Bloome MA. Transient angle-closure glaucoma in central retinal vein occlusion. Ann Ophthalmol. 1977;9:44-48.

4.      Mendelsohn AD, Jampol LM, Shoch D. Secondary angle-closure glaucoma after central retinal vein occlusion. Am J Ophthalmol. 1985;100:581-585.

5.      Hayreh SS, Rojas P, Montague P, et al. Ocular neovascularization with retinal vascularization occlusion-III. Incidence of ocular neovascularization with retinal vein occlusion. Ophthalmology. 1983;90:488-506.

6.      Boulton PE. A study of the mechanisms of transient myopia following extensive xenon arc photocoagulation. Trans Ophthalmol Soc UK. 1973;93:287-300.

7.      Mensher JH. Anterior chamber depth alteration after retinal photocoagulation. Arch Ophthalmol. 1977;95:113-116.

8.      Christensen L. Narrow angle glaucoma. Trans Am Acad Ophthalmol Otolaryngol. 1963;67:71-74.

9.      Wood WJ, Smith TR. Senile disciform macular degeneration complicated by massive hemorrhagic retinal detachment and angle closure glaucoma. Retina. 1983;3:296-303.

10.    McDonald PR, de la Paz V Jr, Sarin LK. Nonrhegmatogenous retinal separation: With choroidal detachment (uveal effusion). Am J Ophthalmol. 1965;59:820-827.

11.    Doden W. Sekundarglaukom bei Periphlebitis retinae. Ophthalmologica. 1961;142:506-511.