
doi: 10.1159/000337157
pmid: 22517123
Retinal vein occlusion (RVO) encompasses two conditions: central RVO, in which the major outflow vessel of the retina is obstructed, and branch RVO, in which a proximal branch of the central retinal vein is obstructed. In both conditions, there is increased intraluminal and interstitial pressure throughout the retina drained by the obstructed vessels, resulting in reduced arterial perfusion, which is exacerbated by preexistent arterial insufficiency, and in variable amounts of retinal ischemia. Retinal ischemia causes increased production of vascular endothelial growth factor (VEGF), which causes vascular leakage and macular edema. High levels of VEGF also promote retinal hemorrhages and exacerbate capillary nonperfusion. Intraocular injections of a VEGF-binding protein reduce vascular leakage, resulting in improvement in macular edema, accelerate resorption of retinal hemorrhages, and prevent worsening of capillary nonperfusion. The ideal regimen has not been defined, but it appears that monthly injections early in the course control edema and may help to limit disease severity in a large percentage of patients. Over time, treatment should be individualized based upon timing and severity of recurrent edema and/or progression of nonperfusion. The role of adjunctive treatments is yet to be defined, but it is clear that VEGF antagonists provide excellent first-line treatment that has dramatically improved visual outcomes in patients with RVO.
Bevacizumab, Vascular Endothelial Growth Factor A, Receptors, Vascular Endothelial Growth Factor, Ranibizumab, Recombinant Fusion Proteins, Retinal Vein Occlusion, Humans, Angiogenesis Inhibitors, Aptamers, Nucleotide, Antibodies, Monoclonal, Humanized
Bevacizumab, Vascular Endothelial Growth Factor A, Receptors, Vascular Endothelial Growth Factor, Ranibizumab, Recombinant Fusion Proteins, Retinal Vein Occlusion, Humans, Angiogenesis Inhibitors, Aptamers, Nucleotide, Antibodies, Monoclonal, Humanized
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