Retinal Vein Occlusion

Retinal vein occlusion (RVO) is a retinal vascular disorder in which the central vein that drains blood from the capilaries of the retina gets occluded or blocked. Since the central retinal artery and vein are the sole source of blood supply and drainage for the retina, such occlusion can lead to severe damage to the retina and blindness, due to ischemia and edema. Retinal vein occlusion is essentially an obstruction of a portion of the venous circulation that drains the retina. With blockage, a pressure build up takes place in the capillaries, leading to hemorrhages and leakage of fluid and blood. Then, this can lead to macular edema with leakage near the macula. Macular ischemia occurs when these capillaries, which supply oxygen to the retina, manifest leakage and nonperfusion. Neovascularization is the most devastating pathologic complication with the development of abnormal blood vessel growth.

Complete loss of vision in retinal vein occlusion (RVO) are due to macular edema, macular ischemia, and neovascular glaucoma. The precise pathologic event in RVO is intraluminal thrombus formation, which can be associated with the abnormalities of blood flow, its constituents, and vessels consistent with the Virchow triad. Central retinal vein occlusion has been likened to a neurovascular compartment syndrome at the site of the lamina cribrosa or closure of the final retinal vein located at the optic nerve.

There are two types of retinal vein occlusion: 1) central retinal vein occlusion, when the central retinal vein at the optic nerve gets clogged up; 2) branch retinal vein occlusion, which is an obstruction at a branch of the retinal vein. The two forms have both differences and similarities in pathogenesis and clinical presentation.

Retinal vein occlusion is usually divided into nonischemic and ischemic types. Such a distinction is relevant to the clinician, since two thirds of patients with the ischemic type develop the dreaded complications of macular edema, macular ischemia, and neovascularization that lead to blindness. Most investigators accept that these two entities represent varying degrees of the same underlying disease process. Yet, other clinicians and researchers argue that ischemic and nonischemic types are distinct clinical entities. In both types, blockage of the retinal vein occurs, but the nonischemic type is able to maintain better relative blood flow to the retina through collaterals, preventing the dreaded complications known of the ischemic type. The ischemic type of CRVO predisposes to anterior neovascularization called rubeosis irides. With this, high-pressure neovascular glaucoma develops. Neovascularization in the back of the eye can lead to vitreous hemorrhage and retinal detachments.

Visual recovery in retinal vein occlusion has been found to be highly variable, and the presenting visual acuity to be the best predictor of final visual acuity. The natural history of the nonischemic type carries a good prognosis for a return of satisfactory visual acuity. Sixty-five percent of eyes with an initial acuity of 20/40, had the same 20/40 acuity or better on final evaluation. In about 50% of patients, vision may be 20/200 or worse, of which, 79% showed deterioration in visual acuity on follow-up. In a third of patients with branch retinal vein occlusion, visual acuity ends up better than 20/40. However, almost two thirds of patients have evidence of some visual loss secondary to macular edema, macular ischemia, macular hemorrhage, and vitreous hemorrhage. Nonischemic CRVO may resolve completely without any complications in about 10% of cases. One third of patients may progress to the ischemic type, commonly in the first 6-12 months after presentation. In more than 90% of patients with ischemic CRVO, final visual acuity may be 20/200 or worse.