Overview of Neovascular Glaucoma (NVG)

Neovascular glaucoma (NVG) is a devastating secondary glaucoma, often seen as an end-stage

complication of retinal ischemia.  First documented in 1871, historically, it has been referred to as hemorrhagic glaucoma, thrombotic glaucoma, congestive glaucoma, rubeotic glaucoma, and diabetic hemorrhagic glaucoma.  Numerous secondary ocular and systemic diseases that share one common element, retinal ischemia/hypoxia and subsequent release of a vascular endothelial growth factor (VEGF), cause NVG. VEGF causes new blood vessel growth from preexisting vascular structures. Depending on the progression of NVG, it can cause glaucoma either through secondary open-angle or secondary closed-angle mechanisms. This is accomplished through the growth of a fibrovascular membrane over the trabecular meshwork (TM) in the anterior chamber angle, resulting in obstruction of the meshwork and/or associated peripheral anterior synechiae.  The IOP may become significantly elevated and difficult to control, resulting in advanced glaucomatous optic neuropathy and irreversible visual loss.

The most common conditions associated with NVG are proliferative diabetic retinopathy (PDR), central retinal vein occlusion (CRVO), and ocular ischemic syndrome.  The list of associated ocular diseases is extensive and the majority (up to 97%) are associated with an underlying process of retinal ischemia and hypoxia.

Early treatment is paramount in preventing permanent visual loss.  Initial treatment involves both medical and surgical treatment.  Medical therapy involves lowering the IOP, starting topical steroids and cycloplegics.  IOP lowering is best done with aqueous suppressants. Prostaglandins may not be as effective as their mechanism of action (the increase of uvealscleral outflow) may be interrupted by the neovascular obstruction of the TM.  Surgical therapy begins with identifying the etiology of the underlying retinal ischemia.  If the patient has ocular ischemic syndrome then appropriate medical consultation for vascular imaging and subsequent carotid surgery is warranted. In the setting of PDR or CRVO, reducing the amount of viable retina via retinal ablation is known to inhibit and even to reverse new vessel proliferation in the anterior segment.  Retinal ablation is achieved via panretinal photocoagulation (PRP) or cryophototherapy because of media opacities (ie, corneal edema, cataract, vitreous hemorrhage) or other patient factors.  As an adjunct to retinal ablation, injectable intraocular medications such as bevacizumab (Avastin) and ranibizumab (Lucentis) are increasingly being used to block the angiogenic factors that promote the formation of new vessels, thereby reversing the neovascularization process.  If the aforementioned treatments are not successful in controlling IOP and the patient has useful vision in the affected eye then the next step is incisional surgery.  Surgical modalities include trabeculectomy with an antifibrotic agent(mitomycin-C or 5-fluorouracil) and glaucoma drainage implant surgery (GDI). Trabeculectomy in NVG has a significant failure rate so GDIs such as Baerveldt, Ahmed, and Molteno implants are commonly the 1st glaucoma surgery performed.

Generally, NVG carries a very guarded prognosis. Prognosis is highly dependent on diagnosis and treatment of NVG early in its course.  The later it is diagnosed the worse the visual prognosis.  If NVG is caught early then our patients can be spared its devastating effects.