by If rubeosis and neovascular glaucoma occur, preservation of the globe may be considered an adequate result. CURRENT TREATMENTS OF BRANCH RETINAL VEIN OCCLUSION Antiplatelet AgentsKlein and associates4 reported in the Beaver Dam Eye Study that aspirin intake was not associated with the incidence or prevalence of retinal vein occlusion. eyes (59%) improved visually, with 20 eyes (51%) improving 2 or more lines. These results are similar to those for eyes that received argon grid laser and chorioretinal anastomosis, but are worse than in eyes that received arteriovenous adventitial sheathotomy, macular decompression surgery, and intravitreous triamcinolone acetonide. Conclusions Visual benefit from intravitreous bevacizumab compares well against laser treatments for BRVO and HRVO but not as well opposed to surgical techniques and intravitreous triamcinolone acetonide. Intravitreous bevacizumab injection has a risk, cost, and convenience profile that is favorable. INTRODUCTION OVERVIEW The circulation to PHA-767491 the inner retina derives from the central retinal artery and central retinal vein. The central retinal vein forms at the nerve head by the confluence of tributaries of retinal veins and accompanies the central retinal artery, which emerges out of the nerve. Usually there are 2 main contributors, a superior and an inferior branch. Sometimes the 2 2 retinal veins remain separate until uniting within the substance of the nerve.1 The central vein then goes on through the central nerve to leave the optic nerve posterior to the globe in the orbit. Within the nerve head, as they cross the sclera foramen, the artery and vein traverse the lamina cribrosa, a rather rigid mesh of fibrous tissue. Within the retina, the retinal arteries and veins follow roughly the same paths and cross extensively. At crossings, the PHA-767491 2 2 vessels share a common wall and adventitial sheath.2 There are 2 general categories of retinal vein occlusion: central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO). These categories have both common and unique features and vary substantially as to etiology and prognosis. The common characteristics are due to occlusion of the vein and include venous congestion, ischemia, retinal hemorrhages, and retinal edema. Although retinal vein occlusions are infrequent in the population, they are a major cause of visual disability.3,4 The Blue Mountains Eye Study was a population-based study in suburban Australia with data collection at 5 and 10 years. The 10-year incidence of BRVO was 1.2% and of CRVO was 0.4%.5 Many treatments addressing congestion, ischemia, and edema have been considered, as well as efforts to treat the occlusion directly and to PHA-767491 treat the underlying systemic associations thought to predispose to progression. Generally, these treatments have been disappointing as to long-term visual outcomes. With the exception of focal argon laser photocoagulation, few treatment methods have been subjected to prospective randomized clinical trials. This thesis reviews the etiology, prognosis, and current treatment possibilities of BRVO and hemisphere retinal vein occlusion (HRVO) and Rabbit Polyclonal to Smad1 compares results in the literature with a series of BRVOs treated with bevacizumab, collected retrospectively from a large retinal practice. In both CRVO and BRVO, the occlusion occurs in PHA-767491 a location where the vein and accompanying artery run along in proximity and share an adventitial sheath. The artery wall is thicker and less flexible and impinges on the vein.6 Turbulence occurs, and the combination PHA-767491 of a narrowing of the lumen and turbulence allows endothelial cell damage and a thrombus to form. The sequelae of a venous occlusion depend on the extent of tissue involvement, ischemia, and edema created by the insufficient flow. Accordingly, CRVO affects a larger area, since the occluded vessel controls flow from the whole retina. Because the fovea is at a watershed and is usually influenced by at least 2 vessels, obstruction of a branch vessel would be likely to have less macular injury. For the central vein this narrowing occurs as the artery and vein traverse the lamina cribrosa in the optic nerve head.7 There is sharing of a common wall, and the lumen is impinged on and narrowed by the stiffness of the lamina. The stagnation of free flow associated with narrowing of the vessel lumen at the lamina causes turbulence, then thrombus formation, and ultimately occlusion of the.
