Retinal Vein Occlusion (CRVO & BRVO)

Overview

Retinal vein occlusion (RVO) is a common retinal vascular disorder in which thrombosis obstructs venous outflow from the retina, causing venous congestion, hemorrhage, and macular edema. It is classified by location as branch RVO (BRVO, occlusion of a branch retinal vein) or central RVO (CRVO, occlusion of the central retinal vein at or near the optic nerve), and by perfusion status as non-ischemic or ischemic, which has major prognostic implications. BRVO is approximately four times more prevalent than CRVO and is a significant contributor to vision loss worldwide, particularly in middle-aged and elderly populations.¹

Epidemiology & Risk Factors

RVO risk factors substantially overlap with cardiovascular risk factors generally: systemic hypertension, hyperlipidemia, diabetes mellitus, and older age are all associated with increased risk. Glaucoma/elevated intraocular pressure is a specific additional risk factor for CRVO, given the shared anatomic course of the central retinal vein and artery within the rigid optic nerve/lamina cribrosa. In BRVO specifically, occlusion typically occurs at an arteriovenous crossing point, where a rigid, atherosclerotic retinal arteriole compresses the adjacent vein that shares a common vascular sheath at that site.

Pathophysiology

BRVO pathophysiology is complex, involving venous compression at arteriovenous crossings, local inflammation, and increased vascular endothelial growth factor (VEGF) levels — all of which promote thrombus formation, venous stasis, and downstream vascular permeability changes that manifest clinically as macular edema.¹ In CRVO, the entire venous drainage of the retina is compromised, leading to more extensive hemorrhage and, in ischemic cases, more widespread retinal capillary non-perfusion. Ischemic forms of RVO (particularly ischemic CRVO) carry substantial risk of subsequent ocular neovascularization (iris, angle, retina) driven by VEGF upregulation from the ischemic retina — the same pathway responsible for neovascular glaucoma.

Clinical Presentation

Patients typically present with acute or subacute painless unilateral blurred vision or a visual field defect corresponding to the affected retinal sector (BRVO) or more diffuse vision loss (CRVO). Severity ranges widely, from mild blur in non-ischemic BRVO to marked vision loss in ischemic CRVO.

Exam Findings

• Dilated, tortuous retinal veins with flame-shaped and dot-blot hemorrhages distributed in the sectoral (BRVO) or diffuse, all-quadrant (CRVO) pattern of the affected venous drainage territory
• Macular edema, best characterized on optical coherence tomography (OCT), the principal driver of vision loss in most RVO patients
• Cotton-wool spots, more prominent in ischemic forms
• Optic disc edema/hyperemia, more prominent in CRVO
• Iris or angle neovascularization (rubeosis) in ischemic CRVO, typically appearing weeks to a few months after the occlusion ("90-day glaucoma")

Differential Diagnosis

• Diabetic retinopathy (can mimic hemorrhage pattern but typically bilateral, with a longer disease course and characteristic diabetic features)
• Ocular ischemic syndrome (from carotid disease, can produce retinal hemorrhages but with a different distribution and associated anterior segment findings)
• Hypertensive retinopathy (typically bilateral, less focal hemorrhage than RVO)
• Hyperviscosity syndromes/blood dyscrasias in atypical or bilateral presentations, particularly in younger patients

Management

Diagnosis is confirmed by fundus exam and OCT (to characterize and quantify macular edema), with fluorescein angiography used to assess perfusion status (distinguishing ischemic from non-ischemic disease) and guide treatment planning.¹ Anti-VEGF therapy (e.g., ranibizumab, aflibercept, bevacizumab) is the primary treatment for RVO-associated macular edema, given as a series of intravitreal injections. Laser photocoagulation (grid laser for macular edema in BRVO, panretinal photocoagulation for ischemic disease with or established neovascularization) and intravitreal corticosteroids (e.g., dexamethasone implant) are complementary treatment options.¹

A meta-analysis found that combination anti-VEGF plus corticosteroid therapy produced somewhat greater visual acuity improvement than anti-VEGF monotherapy at 6 months for both CRVO and BRVO, with the benefit more pronounced in BRVO, though differences in central macular thickness reduction between approaches were inconclusive.² Emerging treatments under investigation include gene therapy, peptide-based agents, and small-molecule inhibitors, though recurrence of macular edema and treatment resistance remain significant ongoing challenges.¹

A practical, perioperative consideration: in RVO patients requiring cataract surgery, anti-VEGF pretreatment within about 35 days before surgery was associated with a significantly lower incidence of postoperative macular edema compared with pretreatment given earlier, an effect particularly pronounced in eyes with ischemic RVO on angiography.³

Complications

• Persistent or recurrent macular edema despite treatment
• Neovascular glaucoma, particularly following ischemic CRVO ("90-day glaucoma")
• Vitreous hemorrhage from retinal or disc neovascularization
• Chronic vision loss from macular ischemia or longstanding untreated edema
• Postoperative macular edema after cataract surgery in RVO eyes, particularly without adequately timed anti-VEGF pretreatment³

Clinical Pearls

• BRVO is roughly four times more common than CRVO¹
• Ischemic CRVO carries substantial risk of neovascular glaucoma, classically emerging around 90 days after the occlusion — close follow-up during this window is essential
• Anti-VEGF therapy is first-line for RVO-associated macular edema; combination anti-VEGF plus corticosteroid may offer modestly better visual outcomes at 6 months, especially in BRVO²
• Anti-VEGF pretreatment within about 35 days before cataract surgery in RVO patients is associated with lower postoperative macular edema risk, particularly in ischemic RVO³
• Fluorescein angiography's role in distinguishing ischemic from non-ischemic RVO is central to prognosis and monitoring intensity, not just diagnosis

Common Pitfalls

• Assuming all RVO is the same regardless of ischemic status — ischemic disease requires closer neovascularization surveillance
• Overlooking the "90-day glaucoma" window after ischemic CRVO, missing early rubeosis
• Planning cataract surgery in an RVO patient without considering anti-VEGF pretreatment timing
• Treating macular edema with anti-VEGF monotherapy indefinitely without considering adjunctive corticosteroid therapy in refractory cases
• Missing an underlying systemic risk factor (uncontrolled hypertension, glaucoma) that, if addressed, reduces recurrence or fellow-eye risk