Retinal vein occlusions cause vision loss through macular edema and ischemia. Anti-VEGF injections significantly improve visual outcomes compared to observation or laser in clinical trials. OCT guides treatment decisions; OCTA provides additional ischemia assessment. Persistent edema, ischemic complications, and treatment burden remain challenges.
Pathophysiology and types
Retinal vein occlusions occur when retinal veins become blocked, typically at arteriovenous crossings (branch RVO) or at the lamina cribrosa (central RVO). Thrombosis leads to hemorrhages, edema, and potentially ischemia. Risk factors include hypertension, cardiovascular disease, and glaucoma. BRVO affects sectoral retina; CRVO affects the entire retina.
Clinical presentation
Patients present with sudden, painless vision loss or visual field defects. Fundus exam shows hemorrhages, dilated tortuous veins, cotton-wool spots, and edema in the affected area. OCT confirms macular edema and quantifies severity. Visual acuity at presentation and degree of ischemia influence prognosis.
The role of anti-VEGF therapy
Randomized controlled trials (CRUISE for CRVO, BRAVO for BRVO, and others) demonstrated that anti-VEGF injections significantly improve visual acuity and reduce macular edema compared to observation or laser. Ranibizumab, aflibercept, and brolucizumab are FDA-approved. Anti-VEGF became first-line therapy for macular edema from RVO.
Treatment patterns and burden
Many patients require multiple injections over months to years to control edema. Treatment intervals can sometimes be extended using treat-and-extend or pro re nata protocols. Some patients respond dramatically; others have persistent edema despite frequent injections. Predictors of treatment response are imperfect.
Corticosteroid alternatives
Intravitreal corticosteroid implants (dexamethasone, fluocinolone) provide longer-duration edema control but carry risks of cataract and glaucoma. They are often used in pseudophakic patients, those with incomplete anti-VEGF response, or when frequent monitoring is infeasible. Comparative effectiveness versus anti-VEGF is context-dependent.
Ischemia and complications
Ischemic CRVO can develop neovascular glaucoma, a sight-threatening complication requiring prompt panretinal photocoagulation or anti-VEGF treatment. OCTA may enable earlier ischemia detection than fluorescein angiography. Wide-field imaging documents peripheral ischemia. Close monitoring is essential in ischemic cases.
Imaging for treatment decisions
OCT-measured central retinal thickness guides treatment initiation and monitors response. Qualitative fluid assessment (intraretinal vs subretinal) may influence treatment choice. OCTA assesses macular perfusion and can detect areas of capillary dropout. Autofluorescence may reveal chronic RPE changes in long-standing cases.
Long-term outcomes
Many patients achieve significant vision improvement, but recovery to baseline acuity is variable. Chronic edema, permanent macular damage, and persistent ischemia limit outcomes in some cases. Natural history is variable—some RVOs resolve spontaneously (more common in BRVO); others progress. Early treatment and close monitoring optimize outcomes but cannot guarantee full recovery.
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