Central and branch retinal-artery occlusion

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

Retinal artery occlusion interrupts oxygen delivery to the inner retina and can produce permanent tissue loss over a short period. Central occlusion usually causes a major monocular deficit; branch occlusion affects the field supplied by the involved artery. The patient may describe a missing patch rather than total blindness. Preserved central acuity in a branch event therefore does not make the vascular mechanism unimportant.

Initial management has two parallel purposes: evaluate the threatened eye and identify a vascular process that may also endanger the brain or fellow eye. Emergency assessment remains appropriate even when useful visual recovery is uncertain. An incidental retinal embolus without symptoms is a different presentation from acute retinal infarction, but it still warrants assessment of the clinical context and vascular risk rather than an unsupported assumption of benignity.

Key points

Central occlusion threatens much of the inner retina; a branch occlusion causes a territorial defect and can leave central acuity deceptively good.
An early retina may lack the full classic appearance, so a missing cherry-red spot does not exclude acute arterial ischaemia.
Evaluate for embolic sources and systemic vascular disease while ophthalmology confirms the ocular diagnosis.
Separate arteritic from non-arteritic disease promptly, because strongly suspected giant cell arteritis needs immediate glucocorticoids to protect remaining sight.
Resolved retinal ischaemic symptoms follow a suspected-TIA pathway; persistent symptoms require an acute stroke and ophthalmic assessment.
The 2026 TenCRAOS trial did not establish a visual benefit from routine intravenous tenecteplase and identified serious safety concerns.

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

Embolic and thrombotic disease

Emboli may arise from carotid atherosclerosis or the heart, while local thrombosis and systemic vascular disease also contribute. Investigation seeks a cause that may endanger other vascular territories.

Arteritis and less common mechanisms

Giant cell arteritis is an important treatable inflammatory cause in older adults. Dissection, vascular procedures, inflammatory disease or other unusual mechanisms require consideration when the age, history or examination is atypical.

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

1
Loss of arterial oxygen delivery
Interruption of inner-retinal blood supply rapidly impairs neuronal function. Persistent ischaemia can progress to infarction, leaving structural thinning and permanent loss of acuity or visual field.
2
Central and territorial injury
Central occlusion affects a broad inner-retinal area, whereas branch obstruction damages its downstream territory. The location of foveal involvement and any alternative arterial supply strongly influence the measured acuity.
3
A visible systemic vascular event
Retinal infarction may be the first recognised manifestation of embolic or inflammatory vascular disease. Preventing a further eye or brain event therefore remains a major goal even when retinal recovery is limited.

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

Central arterial pattern

Sudden painless monocular loss, poor colour perception and a RAPD support a major retinal or optic-nerve lesion. Retinal pallor and narrowed arteries may develop, sometimes with a contrasting red fovea. A visible embolus can suggest a source but is neither necessary nor sufficient for diagnosis.

Branch arterial pattern

A sector of retinal whitening corresponds to the affected arterial territory and produces the opposite area of field loss. Central acuity may remain good when the fovea is spared. Ask specifically about a fixed missing area because a patient may not volunteer it as visual loss.

Arteritic warning history

In an older adult, new headache, scalp tenderness, jaw or tongue pain with chewing, systemic symptoms and polymyalgic symptoms raise concern for giant cell arteritis. Transient visual episodes or diplopia can precede permanent loss. No single absent symptom safely excludes the disease.

Neurological and vascular context

Check speech, face and limb function, gait where safe, pulse rhythm and other neurological symptoms. Ask about previous TIA, atrial fibrillation, carotid disease, vascular procedures and neck trauma or pain. A normal standard stroke screen does not exclude isolated retinal ischaemia.

Red flags requiring action

Sudden persistent monocular loss, a marked RAPD or new focal visual-field loss requires immediate assessment for retinal arterial occlusion and associated vascular disease.
Visual loss in someone over fifty with jaw or tongue claudication, new headache or scalp tenderness needs immediate treatment consideration for giant cell arteritis without waiting for confirmatory tests.

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
Immediate visual and neurological assessmentFirst step
Why
Define the deficit and establish the timeline needed for emergency decisions.
Interpretation and limitations
Record last known normal vision, discovery time and whether symptoms have fully resolved. Measure acuity in each eye, pupils and a rapid field assessment. Do not spend prolonged time obtaining a perfect retinal image before activating emergency services.
02
Ophthalmic examination and OCT
Why
Confirm retinal hypoperfusion and exclude other ocular causes of sudden loss.
Interpretation and limitations
Dilated examination can show territorial pallor or an embolus. OCT may demonstrate acute inner-retinal changes, with later thinning. Angiography can clarify perfusion in selected cases, but specialist imaging should complement rather than delay the vascular assessment.
03
Blood tests for arteritis when indicated
Why
Support rapid evaluation of giant cell arteritis and establish a treatment baseline.
Interpretation and limitations
Obtain full blood count, platelets, ESR and CRP before or immediately after glucocorticoids if readily possible. Strong suspicion with ischaemic visual symptoms must not wait for results, ultrasound or biopsy. Inflammatory markers are supportive rather than a stand-alone exclusion test.
04
Stroke and embolic-source investigations
Why
Identify cerebral involvement and a treatable cause of retinal embolism or hypoperfusion.
Interpretation and limitations
The acute service selects brain and vascular imaging, ECG or rhythm monitoring, carotid assessment and cardiac testing as appropriate. Blood pressure, glucose and lipid assessment inform secondary prevention. Investigations should be guided by the clinical mechanism rather than a blanket identical panel for every patient.

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

Retinal detachment

Flashes, floaters and a spreading curtain suggest detachment, although severe arterial field loss can also be described as a curtain. Retinal examination and urgent specialist assessment distinguish the mechanisms.

Optic neuropathy

Ischaemic or inflammatory optic-nerve disease can cause reduced acuity, colour loss and RAPD. Disc appearance, pain, field pattern and retinal imaging help localise the lesion while arteritis remains a shared concern.

Retinal vein occlusion

Venous engorgement and extensive haemorrhage favour a venous event. The distinction matters because venous-occlusion oedema treatment is different from acute retinal arterial and systemic stroke assessment.

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

01Emergency accessActivate eye and stroke pathways togetherFirst stepA sudden monocular or territorial visual deficit is ongoing or acute retinal arterial occlusion is suspected.

1Arrange immediate emergency assessment and provide onset, last-known-well time, acuity, pupil findings and the possibility of arteritis.
2Ensure ophthalmology and the stroke team coordinate diagnostic confirmation, vascular investigation and any time-sensitive specialist decision.
3Do not delay transfer with ocular massage, anterior-chamber paracentesis or an attempt to normalise pressure; these historical manoeuvres have no established routine benefit and may cause harm.

02Arteritic diseaseProtect the fellow eye without diagnostic delayThe presentation suggests giant cell arteritis with acute or intermittent ischaemic visual symptoms.

1Take readily available baseline bloods and immediately discuss high-dose glucocorticoid treatment with the responsible acute specialist.
2Arrange ophthalmologist assessment as soon as possible on the same calendar day and coordinate rheumatology or the local GCA service.
3If intravenous glucocorticoids cannot be delivered immediately, begin the appropriate oral regimen rather than waiting for transfer or imaging.
4ConfirmatoryContinue confirmatory vascular ultrasound or biopsy and a specialist-directed long-term treatment and safety plan after emergency treatment has begun.

03Non-arteritic careUse current evidence and prevent further eventsSpecialists consider embolic or non-arteritic retinal infarction the likely diagnosis.

1Keep any reperfusion decision within the acute specialist service; do not present a retinal arterial occlusion as an automatic indication for systemic thrombolysis.
2For fully resolved suspected TIA, start aspirin when appropriate under NICE guidance and obtain urgent specialist assessment; ongoing stroke symptoms require the relevant imaging and treatment sequence.
3Select secondary prevention according to the demonstrated vascular mechanism, including antithrombotic choice, carotid management, lipid treatment and risk-factor control.
4Arrange retinal and functional follow-up even when the visual prognosis is poor, because recurrent vascular events and ocular complications remain clinically important.

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

Urgent suppression of arteritic vascular inflammation when acute or intermittent visual loss threatens remaining vision.

Glucocorticoids for visually threatening suspected GCA

A specialist may give methylprednisolone 500 mg to 1 g intravenously daily for a maximum of three consecutive days before oral prednisolone. If intravenous treatment is unavailable immediately, do not delay oral treatment: BSR permits prednisolone 60–100 mg by mouth daily for up to three days as the initial bridge, followed by the agreed ongoing regimen and taper.

Obtain rapid senior input and same-day ophthalmic assessment. Check glucose, pressure, infection risk and mental state, and plan bone and other steroid protection for prolonged treatment. Do not wait for confirmatory tests when clinical suspicion is strong; subsequently reassess the diagnosis and individualise ongoing dosing.

Initial antiplatelet treatment for a clinically suspected transient retinal ischaemic episode after full symptom resolution.

Aspirin when the episode is a resolved suspected TIA

Give aspirin 300 mg orally once daily immediately, unless contraindicated, while arranging specialist assessment within twenty-four hours of symptom onset. Continue until the acute team establishes the diagnosis and specifies the definitive antithrombotic regimen; this is not a prescription for automatic indefinite high-dose aspirin.

Check allergy, active bleeding and existing anticoagulant or complex antithrombotic treatment. Persistent acute stroke follows its own pathway, including exclusion of intracerebral haemorrhage by imaging before routine aspirin. Do not let a dose of aspirin substitute for urgent specialist assessment.

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

Permanent monocular disability

Retinal infarction may leave poor acuity or an enduring field defect. Rehabilitation and practical adaptation are needed alongside a realistic explanation of prognosis and uncertainty.

Further vascular events

An untreated embolic source or inflammatory process can cause additional retinal or cerebral ischaemia. Completion of the systemic work-up is central to care rather than an optional extra.

Ocular neovascularisation

Persistent retinal ischaemia can sometimes stimulate new vessels and pressure-related complications. New pain, redness or deterioration after the initial event should prompt renewed ophthalmic assessment.

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

Confirm that vascular investigations and secondary prevention are completed, with a named team responsible for outstanding results. A referral that only addresses the eye can miss carotid or cardiac disease.
Monitor visual acuity and fields, retinal evolution and any new pain or redness. Neovascular complications are less prominent than after ischaemic venous occlusion but should still be considered when the course changes.
In arteritic disease, follow symptoms, inflammatory markers, fellow-eye function and treatment toxicity with the GCA team. A new visual event during treatment warrants urgent reassessment rather than waiting for the planned review.
Offer low-vision rehabilitation, mobility advice and support with driving decisions. Sudden loss can affect confidence and independence even when the fellow eye retains good acuity.

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

Interpreting the latest thrombolysis trial

TenCRAOS randomised seventy-eight people with non-arteritic central occlusion treated within four and a half hours. Tenecteplase did not significantly improve the defined thirty-day visual recovery outcome compared with aspirin, and adverse events included a fatal intracranial haemorrhage. This argues against assuming routine benefit; it does not remove the need for rapid assessment.

Limits of cross-condition extrapolation

Evidence supporting thrombolysis in selected cerebral stroke cannot be transferred unchanged to isolated retinal infarction. Retinal diagnosis, visual outcome measures, treatment delays and bleeding risk differ. Specialist protocols and research eligibility must be assessed separately, particularly when the patient also has cerebral symptoms.

Foveal sparing can mislead

A cilioretinal arterial supply or a branch distribution may preserve a central island of useful vision. A good letter-chart score can therefore coexist with major field loss and systemic vascular risk. Test the field and document functional limitations rather than describing the whole eye as unaffected.

A late presentation still matters

A patient presenting after several days may be beyond any proposed reperfusion window yet still need urgent investigation for arteritis or an embolic source. The question of recovering the affected retina is separate from preventing a fellow-eye or cerebral event.

11Common pitfallsFrequent interpretation and management errors.

01
Do not exclude arterial occlusion solely because the fundus lacks a cherry-red spot or the central acuity remains relatively good.
02
Do not allow a previous migraine diagnosis to explain away a new abrupt persistent monocular or territorial deficit without assessment.
03
Avoid describing ocular massage or paracentesis as proven sight-saving treatment, particularly if attempting them delays emergency transfer.
04
Do not equate initial aspirin, glucocorticoids or referral paperwork with completion of the diagnostic and secondary-prevention pathway.