Central and branch retinal-vein occlusion

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Retinal vein occlusion obstructs drainage from part or all of the retina. Central occlusion affects the main venous outflow, while a branch occlusion usually develops where an artery and vein share a crossing. The resulting increase in venous and capillary pressure produces haemorrhage and fluid leakage. The fundus often looks striking, but clinical decisions should follow macular function, perfusion and complications rather than the amount of visible blood alone.

Two questions continue throughout follow-up: is fluid causing treatable visual impairment, and is retinal ischaemia creating a risk of neovascular complications? Their answers may diverge. Anti-VEGF can improve oedema and acuity without restoring perfusion, and its suppression of new vessels can delay their appearance. A patient whose reading vision improves therefore still needs the surveillance appropriate to the ischaemic risk.

Key points

Central retinal vein occlusion usually causes widespread venous dilatation and haemorrhage; branch occlusion follows the territory of an affected venous branch.
Macular oedema is a major reversible contributor to reduced acuity, whereas macular ischaemia can limit recovery despite a drier retina.
OCT assesses macular fluid; angiographic assessment and clinical findings establish the extent of non-perfusion.
Intravitreal anti-VEGF or a dexamethasone implant may treat venous-occlusion macular oedema, with different visit and adverse-effect burdens.
Ischaemic central occlusion requires surveillance for iris and angle new vessels even when anti-VEGF treatment suppresses visible activity.
Investigate ordinary vascular risk factors; a retinal venous occlusion alone is not an indication for routine anticoagulation or thrombophilia panels.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Venous outflow obstruction

Central occlusion occurs around the passage of the retinal vein through the optic-nerve head. Branch occlusion commonly develops at a shared arteriovenous crossing where vascular changes compromise the venous lumen.

Associated vascular risk

Hypertension, dyslipidaemia, increasing age and glaucoma are relevant associations. Diabetes should be identified and managed, while selected atypical presentations may justify investigation for blood or inflammatory disorders.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Raised capillary pressure
Obstructed venous drainage increases capillary pressure and encourages blood and fluid to escape into the retinal tissue. Macular involvement produces central blur and distortion that may respond to leakage-directed treatment.
2
Non-perfusion and signalling
Reduced capillary perfusion increases retinal hypoxia and VEGF release. VEGF contributes both to oedema and to abnormal vessel growth, linking two complications that still require separate clinical assessment.
3
Anterior and posterior new vessels
The ischaemic stimulus can produce iris and angle neovascularisation in central occlusion or retinal neovascularisation in branch occlusion. Subsequent angle closure or bleeding can damage vision beyond the original vascular event.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Central distribution

Central occlusion commonly produces dilated tortuous veins, retinal haemorrhages across multiple quadrants, disc swelling and variable cotton-wool lesions. The acuity can range from mildly affected to profoundly reduced. A marked RAPD and severe visual loss increase concern for ischaemia but do not quantify it alone.

Branch distribution

Haemorrhage and venous changes occupy a sector corresponding to the obstructed branch, often beginning near an arteriovenous crossing. Vision may be preserved if the macula is spared. Hemiretinal occlusion affects a larger superior or inferior territory and requires careful classification.

Macular leakage

Patients report blur, distortion or reduced contrast rather than pain. OCT may reveal central thickening and intraretinal cysts. Explain that the purpose of injections is to control this leakage and improve or preserve function, not to mechanically extract the original venous thrombus.

Late ischaemic complications

New vessels can grow on the iris or drainage angle after central occlusion, or on the retina after branch occlusion. Pain may occur only after pressure has risen. Examine the anterior segment rather than relying on posterior-pole imaging to identify this risk.

Red flags requiring action

New iris vessels, pain, redness or nausea after an ischaemic retinal vein occlusion requires urgent assessment for neovascular glaucoma.
A sudden profound visual deficit with little retinal haemorrhage should prompt reconsideration of arterial occlusion and its emergency vascular pathway.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Baseline visual and ocular examinationFirst step
Why
Classify the distribution and assess functional loss, pressure and anterior-segment risk.
Interpretation and limitations
Measure corrected monocular acuity, pupils and pressure; examine iris, angle when indicated, vitreous and retina. Record glaucoma and previous retinal treatment. An atypical presentation needs reconsideration of arterial occlusion, ocular ischaemia or another cause.
02
OCT of the macula
Why
Quantify fluid and identify structural reasons for reduced central vision.
Interpretation and limitations
Compare serial scans with acuity and symptoms. A reduction in thickness supports an anatomical response but does not prove recovery of perfusion. Persistent poor vision after oedema resolves may reflect ischaemia or irreversible foveal injury.
03
Fluorescein angiography or OCT angiography
Why
Assess retinal non-perfusion and distinguish leakage, collateral vessels and neovascularisation.
Interpretation and limitations
The choice depends on the clinical question and image quality; dense haemorrhage can obscure perfusion assessment. Angiography complements examination, and an initially uncertain ischaemic classification may need revision when blood clears.
04
Medical risk-factor assessment
Why
Identify modifiable contributors and clinically indicated systemic disease.
Interpretation and limitations
Check blood pressure, glucose, full blood count and relevant inflammatory or biochemical tests, with GP coordination. RCOphth does not recommend antiphospholipid testing solely for an isolated RVO without other suggestive features, and indiscriminate thrombophilia results rarely change ocular management.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Retinal arterial occlusion

An arterial event more often produces sudden profound loss with a pale retina rather than a heavily haemorrhagic venous pattern. It requires immediate emergency vascular assessment and consideration of arteritis.

Diabetic retinal disease

Diabetic retinopathy may be bilateral and distributed beyond a single venous territory. Coexisting diabetes does not exclude a superimposed vein occlusion, particularly when the change is sudden and asymmetric.

Ocular ischaemic syndrome

Reduced arterial inflow from carotid disease can produce retinal haemorrhage with ocular hypoperfusion. Pain, arterial abnormalities and the pattern of perfusion should prompt assessment for a different vascular mechanism.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Initial careConfirm the occlusion and arrange retinal accessFirst stepNew painless monocular visual loss has a venous haemorrhagic pattern.

1EscalationRefer directly through an urgent eye pathway, with same-day escalation if the diagnosis is uncertain or pain, severe pressure elevation or an arterial pattern is present.
2Record corrected acuity and obtain retinal examination, OCT and perfusion assessment as required to define oedema and ischaemia.
3Initiate treatment for clinically important macular oedema promptly after specialist assessment and explain the expected need for repeated visits.

02Macular treatmentSelect anti-VEGF or steroid therapyMacular oedema is contributing to visual impairment after central or branch occlusion.

1Discuss licensed intravitreal anti-VEGF treatment or a dexamethasone implant, balancing likely benefit, visit burden, pressure risk and cataract formation.
2Assess response with both acuity and OCT and individualise retreatment; severe ischaemia does not automatically exclude a potentially useful treatment trial.
3If oedema improves without useful functional benefit, reassess ischaemia and structural damage before continuing indefinitely or switching agents.
4Maintain surveillance for neovascularisation when injections are extended or stopped; a dry scan is not a reason to discharge an ischaemic eye.

03Neovascular treatmentControl the ischaemic stimulus and pressureIris, angle, retinal or disc neovascularisation develops after venous occlusion.

1In ischaemic central occlusion with iris or angle new vessels, arrange prompt anti-VEGF as an adjunct and sufficient panretinal photocoagulation.
2Laser can be delivered on the same day before anti-VEGF or within one to two weeks; pressure treatment and glaucoma expertise are needed when the angle is compromised.
3For branch occlusion with retinal or disc new vessels, apply sector laser to the relevant ischaemic territory rather than treating macular oedema as the only problem.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Suppresses VEGF-mediated leakage responsible for treatable macular oedema following a venous occlusion.

Ranibizumab for RVO-related macular oedema

Lucentis is administered intravitreally at 0.5 mg, equivalent to 0.05 mL, per treated adult eye. Start with one dose monthly until stable maximum vision and/or inactivity; initially at least three monthly treatments may be required. Doses to the same eye must be separated by at least four weeks. The retinal clinician then adjusts the interval and discontinues treatment when meaningful benefit is absent.

Do not inject during active or suspected ocular infection or severe intraocular inflammation. Review pressure, recent arterial vascular events and the risks of repeated procedures. Warn about pain, redness, photophobia or falling vision after injection. Pregnancy, planned conception and breastfeeding require the product-specific discussion and specialist advice.

An alternative intravitreal approach to venous-occlusion macular oedema when its benefit and adverse-effect profile are suitable.

Dexamethasone, Ozurdex intravitreal implant

Administer one 700-microgram implant intravitreally into the affected adult eye. In RVO, consider another implant only after an initial response followed by loss of benefit when the likely gain outweighs risk; information on intervals shorter than six months is limited. Do not repeat while improvement persists or when deterioration was not slowed by treatment.

Exclude ocular infection and advanced glaucoma uncontrolled by medicines. Contraindications include aphakia with a ruptured posterior capsule, or an anterior-chamber, iris-fixated or transsclerally fixated intraocular lens with capsule rupture. Other capsule defects can still increase migration risk. Monitor pressure and cataract, assess post-injection pain or vision loss urgently, and note that concurrent treatment of both eyes is not recommended in this SmPC.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Persistent macular dysfunction

Leakage may respond to treatment while ischaemia and photoreceptor damage limit functional recovery. Discuss realistic goals using the clinical course rather than promising that a dry retina guarantees normal vision.

Neovascular glaucoma

Iris and angle new vessels can lead to obstructed aqueous drainage and a painful pressure rise. Early detection allows treatment before severe irreversible damage and persistent pain develop.

Vitreous haemorrhage

Fragile retinal new vessels may bleed into the vitreous and obscure vision. Haemorrhage should prompt renewed retinal assessment for ischaemia, neovascularisation and any associated tractional changes.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Ischaemic central occlusion needs close iris and angle surveillance, commonly monthly initially. RCOphth recommends monthly follow-up for the first six months with significant ischaemia, then three-monthly review for the following year, adjusted for treatment and complications.
After stopping anti-VEGF in an ischaemic central occlusion, RCOphth recommends one-to-two-monthly observation for neovascularisation during the first year. Explain why visits continue despite a decision that further oedema treatment is unlikely to help.
Branch occlusion with at least a quadrant of ischaemia generally warrants three-to-four-monthly review for retinal neovascularisation. New floaters or haemorrhage should trigger earlier assessment.
Track pressure and lens changes after steroid implants, cardiovascular risk management, fellow-eye status and functional goals. A single lower OCT thickness value is insufficient to judge the overall success or safety of care.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Venous is not arterial

RVO shares vascular risk factors with stroke and coronary disease, but it does not create an automatic indication for systemic anticoagulation. Prescribe antiplatelet or anticoagulant treatment only for a separate supported systemic indication, while the eye receives the appropriate oedema and ischaemia management.

A younger patient

Age below fifty does not exclude RVO or ensure a benign course. Take a careful history for systemic inflammatory disease, hyperviscosity or other unusual features and investigate selectively. Broad testing without a clinical question can produce incidental results that do not explain the occlusion.

Collateral vessels versus new vessels

Collateral channels may develop as an alternative drainage route and can indicate adaptation after occlusion. They must be distinguished from fragile neovascularisation that signals an ischaemic complication. Clinical appearance and angiographic behaviour guide this distinction when photography alone is uncertain.

Consent and treatment burden

Frequent injections can be difficult for a person with limited mobility or transport. Steroid treatment may reduce some visit burden but adds pressure and cataract risks. Shared selection should include the ability to return for safety monitoring rather than assuming fewer injections means no follow-up.

11Common pitfallsFrequent interpretation and management errors.

01
Do not treat a retinal vein occlusion as a leg DVT by automatically starting an anticoagulant; the ocular treatment targets its complications.
02
Do not label a retina non-ischaemic permanently from the first visit, because perfusion status and the ability to assess it can change.
03
Avoid ending anterior-segment surveillance because macular oedema has resolved during anti-VEGF treatment.
04
Do not use macular grid laser as a substitute for the indicated treatment of central-occlusion oedema or apply panretinal laser without defining its ischaemic indication.