You wake up one morning and one eye is blurry. No pain, no warning. Retinal vein occlusion is the second most common retinal vascular disease after diabetic retinopathy, and treatable when caught on time.

Retinal vein occlusion (RVO) happens when one of the veins draining blood from the retina becomes blocked. Blood and fluid back up behind the blockage, leaking into the retinal tissue and causing swelling. If the swelling involves the macula, the central area responsible for sharp vision, central vision blurs rapidly. It is not painful. It is not gradual. Most patients notice it when they wake up or cover one eye by chance and discover the other is blurred. The blockage itself cannot be reversed. But the fluid it causes — which is what actually damages vision — is now very treatable.

BRVO vs CRVO: What Is the Difference?

Why Does It Happen?

The retinal veins run alongside retinal arteries, sharing a common fibrous sheath at crossings. When an artery is stiff and thickened from years of hypertension or atherosclerosis, it compresses the adjacent vein at these crossing points. The compressed vein develops turbulent flow, clotting, and eventually occlusion. This is why the risk factors for RVO are almost identical to those for heart attack and stroke: high blood pressure, diabetes, high cholesterol, smoking, and cardiovascular disease. An RVO is a vascular event. In the eye, yes, but driven by the same underlying process as a heart attack or stroke.

In younger patients, particularly those under 50 with no obvious cardiovascular risk factors, a blood clotting disorder or inflammatory condition should be considered. Conditions such as antiphospholipid syndrome, hyperhomocysteinaemia, and inflammatory diseases including uveitis can cause RVO without the typical vascular risk profile. A haematological screen is appropriate in atypical presentations.

How Vision Is Lost: Macular Edema

The occlusion itself doesn’t directly damage vision. What damages vision is the consequence: fluid leaking from the congested, damaged retinal vessels accumulates in the macula. The retinal layers swell and cystic spaces form, distorting the delicate photoreceptor arrangement that makes sharp central vision possible. This is cystoid macular edema, and it is what you are looking at in the OCT scan above.

The OCT cross-section shows the macula in profile. In a healthy eye, the central fovea has a characteristic dip and the retinal layers are thin and smooth. In RVO with macular edema, the fovea is obliterated by swelling, the layers are thickened, and large fluid-filled spaces (cysts) are visible as dark voids within the retinal tissue. The degree of edema correlates directly with how blurred vision is, and reducing the edema with treatment restores it.

Symptoms

Almost always sudden and painless. The typical presentation is blurred or distorted vision in one eye noticed on waking or discovered by chance when covering the other eye. In BRVO confined to the periphery, vision may be normal and the condition only discovered at a routine eye examination. In CRVO, vision loss is usually significant from the outset. Some patients notice a shadow or scotoma rather than generalised blurring if the edema is eccentric rather than central.

Diagnosis

The fundus appearance is usually diagnostic. Flame-shaped hemorrhages, dilated tortuous veins, cotton wool spots, and disc swelling in the distribution of the affected vein are immediately recognisable. An OCT scan quantifies the degree of macular edema and establishes a baseline to assess treatment response. Fluorescein angiography maps areas of retinal ischemia, vessel leakage, and any neovascularisation. The degree of ischemia on angiography is one of the most important prognostic indicators in CRVO.

Treatment

Anti-VEGF injections

Anti-VEGF medications are the first-line treatment for macular edema from both BRVO and CRVO. They reduce vascular leakage and fluid accumulation, allowing the macula to thin and vision to recover. Treatment typically starts with monthly injections, then transitions to a treat-and-extend or as-needed protocol based on OCT findings at each visit. Many patients need ongoing treatment for months to years. Stopping prematurely often leads to fluid returning and vision declining.

Intravitreal steroids

For patients who respond incompletely to anti-VEGF injections, intravitreal corticosteroids are an alternative. The dexamethasone implant (Ozurdex) is a slow-release rod injected into the vitreous that delivers steroid over three to four months. It can be particularly effective in CRVO and in cases where anti-VEGF response has plateaued. The main side effects are raised intraocular pressure and accelerated cataract formation, both of which require monitoring.

Laser treatment

Sector pan-retinal photocoagulation (PRP) laser is used when significant retinal ischemia has led to neovascularisation, the growth of abnormal new blood vessels on the retina or iris that can cause neovascular glaucoma. Laser reduces the ischemic drive for new vessel growth. It does not improve vision and does not treat macular edema, but it prevents the sight-threatening complication of neovascular glaucoma, which is one of the most serious consequences of untreated ischemic CRVO.

Treating the underlying cause

This is as important as the eye treatment itself. An RVO is a vascular event. Blood pressure, diabetes, cholesterol, and cardiovascular risk should be assessed and optimised by a GP or physician. Patients with undiagnosed hypertension are frequently identified at the point of RVO diagnosis. Controlling these factors reduces the risk of a further RVO in either eye and addresses the broader cardiovascular risk that the RVO has revealed.

If you would like to learn more, the American Academy of Ophthalmology’s retinal vein occlusion page offers a clear patient-friendly overview of symptoms, causes, treatment, and what to expect if a retinal vein becomes blocked.