What is retinal vein occlusion?

Retinal vein occlusion (RVO) is a blockage of one of the veins that drain blood from the retina (the light-sensing layer at the back of the eye). When a retinal vein is blocked, pressure builds up in the part of the retina drained by that vein, causing fluid leakage and bleeding. The result is sudden or gradual vision loss in the affected eye.

The two main types.

Central retinal vein occlusion (CRVO): the main retinal vein is blocked, affecting the entire retina.

Branch retinal vein occlusion (BRVO): a branch of the retinal vein is blocked, affecting a portion of the retina. BRVO is more common than CRVO and tends to have a better visual outlook on average.

Why it is a vascular event. Retinal vein occlusion is part of the broader picture of vascular disease. Risk factors overlap substantially with cardiovascular disease risk: hypertension (the strongest risk factor), diabetes, hyperlipidemia, smoking, atrial fibrillation, glaucoma (an eye-specific risk factor), and increasing age. Patients with RVO benefit from comprehensive cardiovascular risk management, not just eye-specific treatment.

How it presents. Sudden or gradual vision loss in the affected eye is the classic presentation. The vision loss can range from mild blurring to severe vision impairment depending on the location and extent of the occlusion. Some patients with milder BRVO have minimal symptoms.

The diagnostic workup.

Eye-specific: detailed retinal examination, optical coherence tomography (OCT) to assess macular edema, wide-field imaging to assess retinal ischemia and look for neovascularisation. Fluorescein angiography in selected cases to characterise the vascular anatomy.

Systemic: structured cardiovascular risk assessment including blood pressure, lipids, blood glucose, evaluation for atrial fibrillation in appropriate patients, and referral to primary care or cardiology as indicated.

The therapy options.

For macular edema (the most common cause of vision loss in RVO): anti-VEGF intravitreal injections are the modern first-line. Options include ranibizumab, aflibercept (including a high-dose formulation that extends dosing intervals), faricimab (which adds Ang-2 inhibition to VEGF-A blockade and can extend dosing intervals further), and brolucizumab. Treatment typically involves loading doses followed by maintenance based on response. Many patients require ongoing treatment over years.

Intravitreal corticosteroid implants: dexamethasone or fluocinolone implants are alternatives or additions for selected patients, particularly those with limited anti-VEGF response or for whom frequent injections are impractical.

Laser photocoagulation: focal laser for selected BRVO with persistent macular edema, sectoral laser when retinal neovascularisation develops.

For retinal neovascularisation (abnormal new vessel growth that can cause severe complications including vitreous bleeding and neovascular glaucoma): sectoral or full panretinal laser photocoagulation, anti-VEGF therapy.

Systemic management. Cardiovascular risk reduction (blood pressure control, lipid management, smoking cessation, glucose control, anticoagulation when atrial fibrillation is identified) is part of comprehensive RVO care and can reduce risk in the unaffected eye.

Emerging direction. Sustained-release delivery formulations would reduce the injection burden of long-term therapy. Mechanism-targeted programs (Tie2, complement, neuroprotection) are in late-stage trials.

What to expect. With prompt anti-VEGF treatment for macular edema, many patients achieve meaningful vision improvement and stabilisation. Long-term treatment is the rule rather than the exception in most cases. Comprehensive cardiovascular risk management is essential and reduces risk for future vascular events including in the other eye.