Retinal Vein Occlusion:
Sudden Vision Loss —
Understanding BRVO, CRVO & Treatment

Retinal vein occlusion (RVO) is one of the most common serious retinal vascular emergencies. It occurs when a vein that drains blood from the retina becomes blocked by a blood clot or atherosclerotic plaque. The result is sudden vision loss — not painful, but unmistakable. Many patients report noticing a sudden blur, a dark shadow, or floaters in their vision that appeared without warning.

The good news: this is a medical emergency that, when recognized and treated promptly, can be managed effectively. The bad news: delay in diagnosis and treatment significantly worsens the outcome. This guide explains what happens in RVO, why prompt intervention matters, and what the treatment pathway looks like.

What Is a Retinal Vein Occlusion?

The retina is a thin, transparent tissue at the back of the eye containing millions of light-sensitive cells. Blood reaches the retina via the central retinal artery and drains back via the central retinal vein. This venous drainage system has a main trunk (the central retinal vein, or CRV) and tributary branches that empty into it.

An RVO occurs when one or more of these veins becomes blocked, preventing normal drainage. Blood and fluid back up behind the obstruction, causing swelling (oedema) and bleeding within the retinal tissue. The affected portion of the retina becomes starved of oxygen, and photoreceptors begin to die. The degree of permanent damage depends on how quickly flow is restored or alternative drainage pathways develop.

There are two main types of RVO, classified by the location of the obstruction:

Branch Retinal Vein Occlusion (BRVO) vs Central Retinal Vein Occlusion (CRVO)

Branch Retinal Vein Occlusion (BRVO): The blockage occurs in one of the tributary branches of the central retinal vein. This affects only a portion of the retina — typically the upper half, lower half, or a wedge-shaped sector. Because only part of the retina is affected, the macula (the central zone responsible for detailed vision) may be spared entirely, or affected only partially. BRVO accounts for approximately 60–70% of all RVO cases and generally carries a better visual prognosis than CRVO.

Central Retinal Vein Occlusion (CRVO): The blockage occurs in the main central retinal vein itself, blocking drainage from the entire retina. The entire retina becomes congested and swollen. CRVO is more serious than BRVO because it affects the whole eye and always involves the macula. Vision loss is typically more severe. CRVO accounts for 30–40% of RVO cases.

Within the category of CRVO, ophthalmologists further classify the condition as ischemic or non-ischemic based on the extent of retinal tissue that is oxygen-starved. Ischemic CRVO (where large areas of the retina have lost blood supply) carries a worse prognosis and higher risk of rubeotic glaucoma (abnormal blood vessel growth) than non-ischemic CRVO.

What Causes Retinal Vein Occlusion?

RVO results from a combination of factors — both local (at the site of the occlusion) and systemic (affecting the entire body). The occlusion itself may be caused by a blood clot, atherosclerotic plaque, or compression of the vein. What makes a patient susceptible to that blockage is usually a systemic risk factor.

Age and Hypertension: The single strongest risk factor for RVO is elevated blood pressure. Hypertension damages the vein wall, making it stiff and prone to atherosclerotic plaque formation. Age is also a major risk — RVO incidence rises sharply after age 60.

Diabetes: Diabetic patients have higher RVO risk, independent of blood pressure control. Hyperglycemia damages the vein endothelium, increases blood viscosity, and promotes thrombosis (clot formation).

Glaucoma: Elevated intraocular pressure (glaucoma) is associated with RVO, particularly in CRVO. The mechanism is thought to involve compression and ischemia of the optic nerve head, where the central retinal vein is vulnerable.

Blood Clotting Disorders: Thrombophilia — an inherited or acquired tendency to form blood clots — increases RVO risk. This includes Factor V Leiden, prothrombin gene mutation, antithrombin deficiency, and others. Testing for thrombophilia is recommended in younger patients with RVO (under 50) or those with a personal or family history of thromboembolism.

Atrial Fibrillation and Cardiac Disease: Irregular heartbeat increases the risk of clot formation. Any cardiac condition that predisposes to thrombus formation increases RVO risk.

Smoking: Active smoking increases blood viscosity and promotes thrombosis, significantly raising RVO risk.

Hyperlipidemia: Elevated cholesterol and triglycerides contribute to atherosclerosis and increase RVO incidence.

Other Risk Factors: Obstructive sleep apnea, vasculitis (inflammation of blood vessels), oral contraceptive use in women, and recent surgery or immobility all increase RVO risk.

Symptoms of Retinal Vein Occlusion

The hallmark symptom of RVO is sudden, painless vision loss. The onset is the key distinguishing feature — it can happen over minutes to hours, occasionally over a day. Patients typically notice one or more of the following:

• Sudden blurring or haziness of vision in the affected area
• Dark shadow or scotoma — a blank area in the visual field that corresponds to the blocked vein's territory (more common in BRVO)
• Floaters — sudden increase in floating spots, which represent retinal hemorrhage (blood in the vitreous)
• Peripheral vision loss — the patient may not notice if the blockage affects the peripheral retina, as long as the macula is spared
• Distortion (metamorphopsia) — straight lines may appear wavy, though this is more common with macular edema

Importantly, RVO is painless. If a patient reports eye pain along with vision loss, the diagnosis is likely something else (acute angle-closure glaucoma, uveitis, optic neuritis).

The severity of vision loss varies. Some patients with peripheral BRVO notice only a subtle visual field defect. Others with CRVO experience severe central vision loss, reducing visual acuity to hand motions or light perception. Most patients with BRVO have better initial vision than those with CRVO.

How Is Retinal Vein Occlusion Diagnosed?

RVO diagnosis requires specialized imaging. Clinical examination and history alone are not sufficient — you need imaging evidence of the blockage and its consequences.

Dilated Retinal Examination

The eye is dilated with eye drops, and the ophthalmologist examines the retina using a microscope (slit lamp with a magnifying lens or indirect ophthalmoscope). In RVO, the findings are characteristic: retinal hemorrhages (bleeding) are present in a wedge-shaped distribution (for BRVO) or throughout the retina (for CRVO). Cotton-wool spots may be visible. The vein beyond the site of occlusion is dilated and tortuous, while the artery may appear narrowed.

Optical Coherence Tomography (OCT)

OCT is a cross-sectional imaging tool that shows the thickness and architecture of the retina in exquisite detail. In RVO, OCT reveals retinal thickening (oedema) due to fluid accumulation. The OCT is particularly valuable for measuring macular oedema — swelling in the central retina — which is the primary cause of vision loss in many RVO cases. OCT is repeated at follow-up visits to monitor response to treatment.

Fluorescein Angiography (FA)

Fluorescein angiography is an imaging technique in which dye is injected intravenously and photographed as it circulates through the retinal blood vessels. In RVO, FA reveals areas where the dye fails to perfuse (ischemic zones) and areas of retinal leakage. Ischemic CRVO shows large zones of non-perfusion and carries a worse prognosis than non-ischemic CRVO, where leakage dominates. FA helps guide treatment decisions and monitors response to therapy.

Fundus Autofluorescence (FAF)

This imaging modality detects natural fluorescence from retinal pigment epithelium. FAF may reveal areas of retinal damage and helps in prognosis assessment.

Treatment Options for Retinal Vein Occlusion

Anti-VEGF Injections — The Primary Treatment

Anti-vascular endothelial growth factor (anti-VEGF) therapy is now the first-line treatment for RVO, particularly when macular oedema is present. VEGF is a growth factor that promotes abnormal blood vessel growth and increases vascular permeability (leakiness). In RVO, VEGF levels rise rapidly, contributing to macular oedema and vision loss.

Anti-VEGF drugs work by blocking VEGF, thereby reducing fluid leakage and promoting resolution of oedema. Several anti-VEGF agents are available: bevacizumab (Avastin), ranibizumab (Lucentis), aflibercept (Eylea), and faricimab (Vabysmo). These are injected directly into the vitreous (the gel-filled space in the back of the eye) every 4 weeks initially, though the interval may be adjusted based on response.

Clinical trials have shown that anti-VEGF therapy significantly improves visual outcomes in both BRVO and CRVO compared to no treatment or sham injection. Most patients show improvement in macular oedema and vision within the first month of treatment.

Corticosteroid Implants

In patients who have had a poor response to anti-VEGF therapy or who have contraindications to anti-VEGF, a sustained-release corticosteroid implant may be considered. The most commonly used implant is dexamethasone (Ozurdex), which is injected into the vitreous and releases steroid gradually over several months. Corticosteroids reduce inflammation and suppress VEGF production, thereby reducing oedema.

Corticosteroid implants are also used as adjunctive therapy alongside anti-VEGF in cases of treatment-resistant oedema.

Laser Photocoagulation

Laser treatment is no longer first-line for RVO, having been largely replaced by anti-VEGF therapy. However, laser still plays a role in specific scenarios:

• Grid laser: Applied to areas of retinal thickening to reduce oedema. Now used mainly as adjunctive therapy when oedema persists despite anti-VEGF injections.
• Panretinal photocoagulation (PRP): Used in ischemic CRVO to treat areas of non-perfusion and reduce the risk of rubeotic glaucoma (abnormal vessel growth).
• Scatter laser: May be applied in branch RVO at arteriovenous crossing sites to prevent propagation of the thrombus.

Observation and Supportive Care

In some cases of mild BRVO with minimal symptoms and no macular involvement, observation may be appropriate initially, with close follow-up to ensure the condition does not progress. If vision remains good and macular oedema does not develop, active treatment may not be necessary.

Optimal control of blood pressure, diabetes, and glaucoma is essential in all RVO cases. These are not secondary — they are central to treatment and prevention of progression.

What to Expect with Treatment

The Loading Phase

Most anti-VEGF protocols begin with a loading phase: 3 injections given 4 weeks apart. This rapid loading achieves maximum drug levels and gives the retina the best chance at rapid oedema resolution. During this phase, close monitoring with OCT imaging is essential to assess response.

Ongoing Monitoring and Maintenance

After the loading phase, the frequency of injections depends on response. Some patients achieve stable oedema resolution and can be moved to less frequent intervals (every 8 weeks, then every 12 weeks). Others may require ongoing monthly injections. The schedule is individualized, guided by OCT findings and clinical examination.

Visual Recovery Timeline

Vision improvement typically follows this pattern:

• Weeks 1–4: Oedema begins to resolve; some patients notice early improvement in blur or field defect
• Months 1–3: The period of most rapid visual recovery. Many patients regain functional vision during this window
• Months 3–6: Continued gradual improvement in most cases
• Months 6–12: Slower improvement, with final visual outcome typically reached by 12 months post-treatment

Importantly, not all vision loss is recoverable. Eyes with large areas of retinal infarction (ischemic damage) will not recover vision in those zones. However, reducing macular oedema still improves vision by clarifying the remaining functioning retina.

Prognosis

BRVO: With prompt anti-VEGF treatment, approximately 60–70% of patients with macular oedema achieve visual acuity of 6/12 or better. Some recover near-normal vision. Peripheral BRVO that does not involve the macula often has minimal long-term visual impact.

CRVO: Prognosis is more guarded. Non-ischemic CRVO responds better to treatment; approximately 40–50% of patients achieve visual acuity of 6/12 or better with treatment. Ischemic CRVO has worse outcomes — only 10–15% achieve 6/12 or better — because irreversible photoreceptor death occurs in large retinal areas.

In all cases, early treatment leads to better outcomes. Delays of even a few weeks result in worse final vision.

Cost, MediSave & Insurance

Anti-VEGF injections are expensive. A single injection typically costs between SGD 1,200–2,500, depending on the agent used and facility. A loading phase of 3 injections represents a significant cost, and ongoing maintenance may extend that further.

MediSave: RVO treatment is eligible for MediSave claims in Singapore, provided the condition meets criteria for serious eye disease. Patients may claim against their MediSave account for anti-VEGF injections. The amount claimable depends on the individual's MediSave balance and the specific condition classification.

Insurance: Some private insurance plans cover anti-VEGF injections for RVO. Coverage varies significantly by policy. Patients should check with their insurance provider regarding eligibility and coverage limits.

Subsidized Care: Government hospitals and restructured hospitals in Singapore offer subsidized rates for RVO treatment, significantly reducing out-of-pocket costs for those eligible.

For details on fees and payment options at Dr. Wong's clinic, please visit the Fees page or contact the clinic directly.

Frequently Asked Questions

Will my vision return to normal after RVO?

Vision recovery depends on the extent of retinal damage. Many patients with branch RVO (BRVO) recover good vision, especially with early treatment. Central RVO (CRVO) typically causes more permanent vision loss. Anti-VEGF injections and laser treatment have improved outcomes significantly in recent years. Most vision recovery occurs within the first 3–6 months of treatment, though improvement can continue for up to a year. The prognosis is better when treatment is started promptly.

How many injections will I need?

The number of injections varies based on the severity of your RVO and how your eye responds to treatment. Most patients require a loading phase of 3 monthly injections, followed by ongoing monitoring. Some may need continued injections every 4–8 weeks for several months or longer. Others may achieve stability and require fewer treatments. Your ophthalmologist will determine the frequency based on your OCT findings and clinical response. Many patients eventually need injections only every 2–3 months or can discontinue them if the condition stabilizes.

Can retinal vein occlusion happen in my other eye?

Yes, RVO can affect the other eye, though it is not guaranteed. Patients with RVO in one eye have an increased risk of RVO in the other eye, estimated at about 1–2% per year. This is why managing underlying risk factors — blood pressure, diabetes, and glaucoma — is critical. Regular monitoring of both eyes is essential. Some patients may benefit from preventive strategies if they have significant risk factors.

Is RVO related to stroke or heart disease?

RVO shares many risk factors with stroke and heart disease, including hypertension, diabetes, atrial fibrillation, and blood clotting disorders. However, RVO itself is an ocular vascular event and does not directly cause stroke. That said, patients with RVO should be evaluated for systemic vascular risk factors. Some patients with RVO may have underlying conditions like thrombophilia that increase cardiovascular risk. Coordination with your general physician or cardiologist is recommended to assess and manage these systemic risks.

What is the difference between BRVO and CRVO?

Branch RVO (BRVO) blocks a tributary of the main retinal vein, affecting only a portion of the retina — typically in the upper or lower half. CRVO blocks the main central retinal vein itself, affecting the entire retina. BRVO patients typically have better visual outcomes because less of the retina is affected. CRVO is more serious and causes more extensive retinal damage. Ischemic CRVO (where significant retinal tissue is starved of blood) has a worse prognosis than non-ischemic CRVO. The treatment approach is similar for both, but CRVO requires more vigilant monitoring for complications.

Can I drive after a retinal vein occlusion?

Driving ability depends on your visual acuity and visual field. Most countries require a minimum visual acuity (typically 6/12) in at least one eye to drive legally. Immediately after RVO, vision is often too blurred for safe driving. As treatment begins and vision improves, you may become eligible to drive again, but this must be assessed by your ophthalmologist. You should not drive until your vision has improved sufficiently and your ophthalmologist has cleared you. Discuss your specific situation with Dr. Wong to determine when it is safe to resume driving.

Should I see my GP or cardiologist after RVO?

Yes. RVO is a sign that something is affecting your vascular system. Your GP and cardiologist should be informed of the RVO so they can assess your cardiovascular risk. You may need further testing for thrombophilia, atrial fibrillation, or other systemic conditions. Optimal management of blood pressure, diabetes, and lipids is critical not only for your eye health but for your overall vascular health. Think of RVO as a warning signal from your body that deserves systemic evaluation.