Intravitreal Ranibizumab for Treatment of Macular Edema Secondary to Retinal Vein Occlusion

R etinal vein occlusion (RVO) is a common retinal vascular disease that can lead to significant visual loss and blindness. The 15year cumulative incidences of branch retinal vein occlusion (BRVO) and central retinal vein occlusion (CRVO) are 1.8% and 0.5%, respectively, thus representing a serious public health problem. The main risk factors for RVO include age, hypertension, arteriosclerosis, diabetes, and hypercholesterolemia. Visual loss associated with RVO can be a result of macular edema, macular ischemia, and other complications associated with anterior and posterior segment neovascularization. The main strategy to reduce visual loss in these patients has been the treatment of macular edema.1 The pathophysiology of some RVOs appears to begin with the compression of the vein by the adjacent retinal artery. Systemic disease processes, such as hypertension and atherosclerosis, create hypertrophy of the arterial muscular wall, producing additional compression. This compression further narrows the retinal veins, leading to blood-flow turbulence and thrombus formation. With the thrombus formation, there is an increase in retinal venous pressure and stagnation of blood flow through the proximal capillary bed. The tissue in the distribution of these capillaries becomes ischemic, with resulting upregulation of vascular endothelial growth factor (VEGF). The release of VEGF in turn leads to increased capillary permeability, with vascular leakage and retinal edema, and in some cases eventual retinal and anterior segment neovascularization.2-4 Current treatment options for the complications associated with RVO are numerous, although the efficacy and longterm safety of most have not been demonstrated in randomized clinical trials. Macular edema has traditionally been managed with laser photocoagulation. However, laser photocoagulation results in little or no improvement in visual acuity in patients with CRVO and modest improvement relative to observation in BRVO.5,6 Other modalities currently under investigation for treatment include vitrectomy with or without sheathotomy, optic nerve decompression, creation of laser or surgical anastomoses, antiaggregative and thrombolytic therapies, isovolemic hemodilution, intravitreal and periocular steroid injection, and, recently, treatment with anti-vascular endothelial growth factor (VEGF) agents.7 There is a rationale for the use of VEGF inhibitors in RVO to reduce macular edema, an important cause of visual loss in patients with vein occlusions. Ranibizumab (Lucentis, Genentech), a humanized antibody fragment that inhibits Intravitreal Ranibizumab for Treatment of Macular Edema Secondary to Retinal Vein Occlusion