172 ANGLE-CLOSURE GLAUCOMA

NEOVASCULAR GLAUCOMA

38.What typically causes neovascular glaucoma (NVG)?

Posterior segment (retinal) ischemia results in the production of angiogenic factors that stimulate the formation of a neovascular membrane on the iris (NVI). Vascular endothelial growth factor (VEGF) has been shown to be the primary angiogenic factor. As the membrane first grows into the angle and across the scleral spur to the TM, the angle appears anatomically open. Later, the membrane contracts, pulling the peripheral iris up to the TM and peripheral cornea, creating PAS. This latter process can occur over significant areas of the

angle very quickly (often in a few days) producing an acute angle-closure glaucoma. Common causes of NVG are CRVO (1/3), proliferative diabetic retinopathy (1/3), and carotid occlusive disease (approximately 10%).

39.How is neovascular glaucoma treated?

1.The underlying etiology of the neovascularization must be diagnosed and treated, usually with panretinal photocoagulation (PRP) or, if the lack of clear visualization of the retina precludes PRP, peripheral retinal cryotherapy for posterior segment ischemic processes. New anti-VEGF compounds injected into vitreous or AC can produce dramatic regression of NVI within 1–2 weeks.

2.Medical treatment. The percent of angle that is closed with PAS as well as the outflow resistance of the TM still open will determine the potential for successfully treating the glaucoma medically. Even if the angle is completely closed, maximal tolerated aqueous suppressant and, if necessary, hyperosmotic therapy should be used in an attempt to temporize until surgery is performed. Miotics should not be used, because they decrease uveoscleral outflow and increase inflammation.

3.Surgical treatment. One of the most important principles to remember when operating on these eyes, especially eyes with florid NVI, is to try to avoid rapid decompression of the eye; the fragile new vessels may rupture, creating a spontaneous hyphema that can significantly complicate subsequent management.

&The guarded filtering procedure (trabeculectomy) has been used to control IOP in these eyes with poor results. The success rate is somewhat better if an adjunctive antimetabolite such as mitomycin C is used. The risk of filtration failure due to fibrosis is higher, presumably owing to the presence of angiogenic factors in the aqueous.

&Aqueous tube shunts have become the procedure of choice for many glaucoma surgeons, but still have success rates of only approximately 70%, owing to the often poor prognosis of the underlying pathologic process.

4.Laser/cryo cyclodestruction. This may be a viable option in eyes with minimal visual potential, as an attempt to control IOP for long-term comfort, and to prevent the need for enucleation for pain due to high IOP. Laser is highly preferred to cryo due to higher long-term success, much lower risk of phthisis bulbi, and much less postoperative pain and inflammation.

MISCELLANEOUS

40.What are the different mechanisms of producing angle closure secondary to inflammation?

&PAS formation from any etiology

&Complete pupillary block (secluded pupil) from posterior synechiae resulting in iris bombe´

&Uveal effusion causing anterior rotation of the ciliary body (uncommon)

&Exudative retinal detachment pushing lens-iris diaphragm forward (rare)