{'fraction_non_alphanumeric': 0.02047952047952048, 'fraction_numerical': 0.006993006993006993, 'mean_word_length': 5.6544850498338874, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Medical and Surgical Management of Central Retinal Vein Occlusion

Central retinal vein occlusion (CRVO) remains one of the leading causes of blindness among the retinal vascular disorders. In fact, retinal vein occlusions are second only to diabetic retinopathy in causing visual loss. The fundus of a patient with a CRVO has been likened to a “bloodand-thunder” appearance, referring to the extensive, four-quadrant intraretinal hemorrhages, venous tortuosity, and capillary nonperfusion. In some cases, retinal ischemia subsequently induces anterior segment neovascularization, which then leads to neovascular glaucoma. This complication usually occurs 90 days after the initial examination and has been reported in 8% of CRVO overall. The Central Retinal Vein Occlusion Study (CVOS) classified CRVOs as perfused (nonischemic) if fewer than 10 disc areas of retinal capillary nonperfusion are noted on fluoroscein angiography; nonperfused (ischemic) if more than 10 disc areas of capillary nonperfusion are identified; and indeterminate if intraretinal hemorrhages prevent interpretation of the angiogram. Despite recent advances, the visual prognoses for patients with the ischemic form of the disease are extremely poor, with fewer than 10% maintaining a visual acuity better than 20/400. Unfortunately, there is no effective treatment of CRVO. Histopathological studies suggest that most or all cases of CRVO result from intraluminal thrombus formation at or just posterior to the lamina cribrosa. Many congenital and acquired blood protein defects are now known that predispose individuals to a hypercoagulable state and an increased risk of thrombus formation. These prothrombotic states are secondary to deficiencies in the physiological anticoagulants, such as antithrombin III and protein C and S and the presence of antiphospholipid antibodies. Thus, such preventative measures as adequate anticoagulation for these individuals may be used to prevent thrombus formation in the retinal vein.