Retinal Vein Occlusion (RVO)
Retinal vein occlusion (RVO) includes central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO).
This updated UKMLA guide to retinal vein occlusion is based on RCOphth guidance, which covers causes, risk factors, symptoms, diagnosis, and management.
Types and Causes
| Central retinal vein occlusion (CRVO) | Most often occurs when the central retinal vein is compressed by an adjacent atherosclerotic central retinal artery → thrombosis inside the vein |
| Branch retinal vein occlusion (BRVO) | Thrombosis takes place in an arteriovenous crossing in the retina, where a retinal artery and vein physically share a common vascular sheath |
Causes and Risk Factors
Most common contributing factor: atherosclerosis
Risk factors:
- Hypertension – major risk factor
- Diabetes
- Hyperlipidaemia
Despite the term “vein occlusion”, retinal vein occlusion is NOT significantly associated with the standard risk factors for systemic VTE (e.g. immobilisation, cancer, pregnancy)
Rarely, retinal vein occlusion can be caused by external retrobulbar compression (e.g. from thyroid eye disease, an orbital tumour) or by vasculitis.
Clinical Features
Typical presentation: sudden, painless, unilateral vision loss
| CRVO | BRVO |
|---|---|
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Investigation and Diagnosis
CRVO can be diagnosed if there are typical clinical features (see above) + dilated fundoscopic examination
Typical fundoscopic findings of CRVO:
- Blood-shot retina – diffuse retinal haemorrhages (across all 4 quadrants)
- Increased tortuosity and dilated retinal veins (global)
- Cotton wool spots (from infarction)
- Optic disc swelling
In BRVO, the classic CRVO findings are localised / segmental rather than diffuse, because only one branch of the central retinal vein is occluded.
If the fundoscopy is inconclusive, consider:
- Optical coherence tomography (OCT) to detect macular oedema
- Fluorescein angiography
Management
All suspected cases of CRVO should be referred directly to the nearest Eye Centre (aim: treatment to be started by an ophthalmologist within 2-4 weeks).
1st line therapy (to manage macular oedema):
- Anti-VEGF intravitreal injections (e.g. ranibizumab, aflibercept, bevacizumab), or
- Dexamethasone steroid implant
Long-term management: address concurrent cardiovascular risk factors (e.g. hypertension, diabetes, dyslipidaemia)
Complications
Acute complications:
- Macular oedema – leading cause of visual impairment
- Retinal ischaemia – fovea ischaemia is the 2nd most common cause of visual impairment
Chronic complications arise from oxygen-starved tissue producing high levels of VEGF:
- Anterior segment neovascularisation
- Most commonly occurs on the iris (rubeosis iridis) and in the iridocorneal angle
- The new vessels can obstruct the drainage angle and cause neovascular glaucoma
- Retinal neovascularisation
Both retinal neovascularisation or anterior segment neovascularisation can bleed (vitreous haemorrhage) and potentially cause retinal detachment
Due to the risk of anterior segment neovascularisation, patients require monitoring with gonioscopy under slit lamp for the first 6 months (esp. in ischaemic CRVO)
If neovascularisation develops → panretinal photocoagulation