Abstract
Neovascular glaucoma (NVG) is an aggressive type of glaucoma, which often results in poor visual outcomes. Most NVG patients have severe underlying systemic and ocular pathology which causes NVG as a late presentation of their primary systemic and/or ocular disease. This makes NVG very difficult to treat. The key to adequate treatment of this devastating ocular disease is an understanding of its pathogenesis, which has recently been better elucidated. Weiss and colleagues first proposed the term “neovascular glaucoma” in 1963, when they described a severe glaucoma associated with the presence of new iris and angle vessels. (1) These patients present with elevated intraocular pressure (IOP) and neovascularization of the iris and angle, often with hyphema and other ocular findings, such as ectropion uveae (Figure 1). The myriad medical conditions resulting in NVG all lead to a final common pathway of profound retinal ischemia. This ischemia induces retinal production of vasoproliferative factors, including vascular endothelial growth factor (VEGF), which diffuse anteriorly and lead to anterior segment neovascularization of the iris (NVI) and neovascularization of the angle (NVA). Patients with NVI and NVA may have normal IOP in the early stages. If left untreated, the fibrovascular scaffolding of these vessels cross the angle and IOP becomes markedly elevated, though the angle may still be gonioscopically open. Ultimately, in the absence of definitive treatment, these fibrovascular membranes contract and produce synechial angle closure and ectropion uveae with intractable elevation of IOP and damage to the optic nerve with subsequent vision loss. Open in a separate window Figure 1 NVG with florid NVI and ectropion uveae
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