Understanding Central Retinal Vein Occlusion (CRVO)

What Is Central Retinal Vein Occlusion?

The central retinal vein is the primary drainage vessel of the retina. It exits the eye through the optic nerve, passing through a narrow anatomical channel at the level of the lamina cribrosa. When thrombosis or compression blocks blood flow at or behind this point, venous pressure rises throughout the entire retina.

Because the central retinal vein drains all four quadrants of the retina (unlike a branch vein occlusion, which affects only one sector), the consequences of CRVO are more widespread and typically more severe. Raised venous pressure forces fluid and blood out of the retinal capillaries, causing haemorrhages, disc oedema and — most importantly for vision — macular oedema.

Ischaemic vs Non-Ischaemic CRVO

CRVO is classified by the degree of retinal ischaemia — the extent to which the retinal capillary bed is deprived of blood flow. This distinction matters because it drives prognosis and the risk of vision-threatening complications.

Non-ischaemic CRVO may convert to ischaemic over time, making close follow-up essential even in initially “good” cases.

Causes and Risk Factors

CRVO is primarily a vascular disease driven by the same risk factors as systemic cardiovascular disease:

• • Hypertension — the single most important risk factor; arterial stiffness compresses the adjacent vein at the lamina cribrosa
• • Diabetes mellitus — alters blood viscosity and endothelial function
• • Hyperlipidaemia — contributes to atheromatous change in adjacent vessels
• • Raised intraocular pressure — can compress the central retinal vein
• • Clotting disorders (thrombophilia, hyperhomocysteinaemia) — particularly relevant in younger patients without conventional risk factors
• • Vasculitis, sarcoidosis, or oral contraceptive pill use — less common causes, important in younger patients

Symptoms and Signs

The hallmark of CRVO is sudden, painless visual loss in one eye. Severity ranges from a mild blur to profound vision loss, and many patients notice the problem first thing in the morning. The vision loss reflects the degree of macular oedema and the extent of retinal ischaemia.

On examination, the characteristic fundus appearance is dramatic: diffuse flame-shaped and dot/blot haemorrhages scattered across all four quadrants of the retina — often described as the “blood and thunder” fundus. Disc oedema, dilated tortuous retinal veins and cotton wool spots are also present. Optical coherence tomography (OCT) quantifies macular oedema accurately and guides treatment decisions.

Treatment

There is no treatment that directly unblocks the occluded vein. Management therefore focuses on treating the consequences of the occlusion — principally macular oedema — and monitoring for neovascular complications.

• Anti-VEGF intravitreal injections(ranibizumab, aflibercept, bevacizumab) — First-line treatment for macular oedema. VEGF (vascular endothelial growth factor) is elevated in occluded veins and drives both oedema and neovascularisation. Injections reduce oedema and typically improve vision. Most patients require monthly loading injections followed by an ongoing maintenance regimen.
• Ozurdex (dexamethasone implant)— A sustained-release steroid implant injected into the vitreous, providing anti-inflammatory and anti-oedema effects for approximately 3–6 months. Useful in patients who cannot attend frequent injection appointments or who have suboptimal anti-VEGF response. Risks include raised IOP and cataract progression.
• Panretinal photocoagulation (PRP)— Laser applied to the peripheral retina in the setting of ischaemic CRVO with neovascularisation. Reduces VEGF drive and helps prevent neovascular glaucoma.

Systemic Workup

All patients with CRVO should have systemic assessment to identify and treat underlying risk factors. A standard workup typically includes:

• • Blood pressure — measured at every visit; hypertension must be optimally managed
• • Fasting blood glucose and HbA1c — to detect or monitor diabetes
• • Fasting lipid profile
• • Full blood examination (FBE) — including platelet count and haematocrit
• • In younger patients or those without obvious risk factors: thrombophilia screen (including protein C, protein S, antithrombin III, factor V Leiden, antiphospholipid antibodies)

A referral to the patient’s GP or a physician for ongoing cardiovascular risk factor management is an important part of comprehensive care.

Conclusion

CRVO is a serious cause of vision loss but is also highly treatable, particularly for the macular oedema component. Early diagnosis, prompt anti-VEGF therapy and vigilant monitoring for neovascular complications — combined with proper control of systemic risk factors — give patients the best chance of preserving and recovering vision. All patients with CRVO should be under the care of both an ophthalmologist and their GP or physician.

Frequently Asked Questions