Retinal Vein Occlusion (CRVO & BRVO)

The central retinal vein drains the entire retina and passes through the rigid lamina cribrosa alongside the central retinal artery, sharing a common adventitial sheath — the same tight anatomic relationship that makes the vein vulnerable to compression at that fixed point. Retinal branch veins similarly cross branch retinal arterioles at fixed points, sharing a common vascular sheath there too.

Retinal vein occlusion (RVO) is classified by location as branch RVO (BRVO) or central RVO (CRVO), and by perfusion status as non-ischemic or ischemic — a distinction that drives prognosis and management far more than the branch/central distinction alone. BRVO is roughly four times more common than CRVO.¹

In BRVO, a rigid, atherosclerotic retinal arteriole compresses the adjacent vein at a shared arteriovenous crossing point, and pathophysiology further involves local inflammation and increased vascular endothelial growth factor (VEGF), promoting thrombus formation, venous stasis, and vascular permeability changes that manifest as macular edema.¹ CRVO similarly involves thrombosis, but affects the entire venous outflow of the retina, producing more extensive hemorrhage and, when ischemic, widespread capillary non-perfusion. Ischemic RVO upregulates VEGF from the hypoxic retina, driving neovascularization of the iris, angle, and retina — the mechanism behind neovascular glaucoma.

Patients present with acute or subacute painless unilateral blurred vision or a sectoral field defect (BRVO) or more diffuse vision loss (CRVO). Exam shows dilated, tortuous veins with flame-shaped and dot-blot hemorrhages in the affected venous territory, macular edema on OCT, cotton-wool spots (more in ischemic disease), disc edema (more in CRVO), and — in ischemic CRVO — iris/angle neovascularization typically emerging around 90 days after the occlusion.

Key differentials include diabetic retinopathy (usually bilateral, longer course), ocular ischemic syndrome from carotid disease (different hemorrhage distribution, anterior segment findings), hypertensive retinopathy (bilateral, less focal hemorrhage), and hyperviscosity/blood dyscrasias in atypical or bilateral presentations, especially in younger patients.

OCT characterizes and quantifies macular edema and guides re-treatment decisions. Fluorescein angiography assesses perfusion status — distinguishing ischemic from non-ischemic disease — which is central to prognosis and the intensity of neovascularization surveillance required, not just to diagnosis.¹

Anti-VEGF therapy (ranibizumab, aflibercept, bevacizumab) is first-line treatment for RVO-associated macular edema. Laser photocoagulation (grid laser for macular edema in BRVO, panretinal photocoagulation for ischemic disease with neovascularization) and intravitreal corticosteroids (e.g., dexamethasone implant) are complementary options.¹ A meta-analysis found combination anti-VEGF plus corticosteroid produced somewhat greater visual acuity improvement than anti-VEGF monotherapy at 6 months, with benefit more pronounced in BRVO.²

A key perioperative point: in RVO patients needing cataract surgery, anti-VEGF pretreatment within about 35 days before surgery was associated with significantly lower postoperative macular edema risk than earlier pretreatment, especially in ischemic RVO.³

• BRVO is about four times more common than CRVO¹
• Ischemic CRVO carries substantial neovascular glaucoma risk, classically around 90 days after occlusion — surveil closely during this window
• Anti-VEGF is first-line for macular edema; adding corticosteroid may modestly improve visual outcomes at 6 months, especially in BRVO²
• Timing anti-VEGF pretreatment appropriately before cataract surgery in RVO patients lowers postoperative macular edema risk³
• Common pitfall: treating all RVO identically regardless of ischemic status, missing the need for closer neovascularization surveillance in ischemic disease
• Common pitfall: missing the 90-day glaucoma window after ischemic CRVO