Signs and Symptoms
Patients with neovascular glaucoma (NVG) may be asymptomatic, but more typically present with a chronically red, painful eye which often has significant vision loss. Further, there will be significant concurrent vascular disease such as diabetes, hypertension, carotid artery disease, or giant cell arteritis (GCA). There frequently is an antecedent history of a retinal vessel occlusion or chronic uveitis.
There will be visible neovascularization of the iris (NVI) and angle (NVA). Only rarely will NVA develop without NVI. The patient typically has significant corneal edema and elevated intraocular pressure, often exceeding 50-mm-Hg. There may be a shallow anterior chamber. Gonioscopically, there will be total or near-total angle closure. Funduscopically, there typically will be evidence of retinal vessel occlusion (either artery or vein), ocular ischemic syndrome or diabetic retinopathy.
Ischemia to ocular tissues is theorized to be the genesis of NVG. The most common causes of NVG include ischemic central retinal vein occlusion (CRVO), diabetic retinopathy, and carotid artery disease and ocular ischemic syndrome (OIS). Less common causes of NVG include hemi- and branch retinal vein occlusion, retinal artery occlusion, and GCA. In terms of retinal vein occlusions, NVG typically develops within three months of the occlusion. In terms of retinal artery occlusions, NVG typically develops within four weeks of the occlusion.
In ischemic retinal disease, hypoxia induces vascular endothelial growth factor (VEGF), a vasoproliferative substance, with acts upon healthy endothelial cells of viable capillaries to stimulate the formation of a fragile new plexus of vessels (neovascularization). In cases of extreme retinal hypoxia, there are essentially very few viable retinal capillaries available. In that instance, VEGF is theorized to diffuse forward to the nearest area of viable capillaries, namely the posterior iris. Neovascularization buds off of the capillaries of the posterior iris, grows along the posterior iris, through the pupil, along the anterior surface of the iris, and then into the angle. Once in the angle, the neovascularization, along with its attendant fibrovascular support membrane, acts to both physically block the angle as well as bridge the angle and physically pull the iris and cornea into apposition, thus blocking the trabecular meshwork. Peripheral anterior synechiae with permanent angle closure happens quickly. The result is a secondary angle closure without pupil block. Due to the extremely elevated intraocular pressure, there will be a modest amount of inflammation.
If there is any degree of inflammation and ocular pain, prescribe a topical cycloplegic such as atropine 1% b.i.d. as well as a topical steroid such as Pred Forte, Vexol, or Flarex q.i.d. Aqueous suppressants may be used in order to temporarily reduce IOP. However, chronic medical therapy is not indicated for neovascular glaucoma. Aqueous suppressants will temporize IOP and lead to a false sense of security as the neovascular process will continue with further angle closure.
Ultimate management of NVG involves eradication of the vessels. This is best accomplished with pan-retinal photocoagulation to destroy ischemic retina, minimize oxygen demand of the eye, and reduce the amount of VEGF being released. PRP tends to be effective in causing regression and involution of anterior segment neovascularization. If a significant amount of the angle is in permanent synechial closure, filtering surgery must then be employed.
Other reports in this section
Eyelids & Eyelashes | Conjunctiva & Sclera | Cornea
Uvea | Vitreous & Retina | Optic Nerve & Brain | Oculosystemic Disease
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