Understanding Branch Retinal Artery Occlusion (BRAO)

What Is Branch Retinal Artery Occlusion?

A branch retinal artery occlusion (BRAO) occurs when one of the arterial branches supplying the retina becomes blocked, cutting off oxygenated blood flow to the corresponding retinal sector. Without arterial blood supply, photoreceptors and retinal ganglion cells in that sector begin to infarct within minutes — a process essentially identical to what happens in a cerebral stroke, but localised to the eye.

Because only a branch artery is occluded (rather than the central retinal artery), the ischaemia is sectoral rather than global. Visual acuity may be fully preserved if the fovea lies outside the affected retinal territory, though the patient will still have a fixed visual field defect.

Causes

The vast majority of BRAOs are caused by emboli — small particles that travel in the bloodstream and lodge at arterial bifurcations. Three main types of emboli are responsible:

• Cholesterol emboli (Hollenhorst plaques)— The most common. Bright, refractile, yellow-orange deposits at arterial bifurcations, visible on fundoscopy. They originate from atheromatous plaques in the carotid artery or aortic arch.
• Calcific emboli— White, non-refractile particles from calcified cardiac valves (particularly aortic stenosis). Associated with more complete occlusion.
• Platelet-fibrin emboli— Dull, grey-white and often temporary; may be associated with cardiac arrhythmias, particularly atrial fibrillation, or carotid artery disease.

Less common causes include vasculitis, coagulation disorders, sickle cell disease, and intravenous drug use.

Symptoms and Signs

BRAO presents as a sudden, painless, fixed visual field defect— a dark or absent area in part of the vision that does not recover spontaneously. Unlike floaters or flashes, which move with eye movement, this defect is stationary. Many patients first notice it when one eye is accidentally covered.

• • Visual acuity may be normal if the fovea is uninvolved; otherwise, reduced to varying degrees
• • On fundoscopy: a pale or white opacity in the affected retinal sector (ischaemic oedema of the inner retina), with the embolus often visible at the site of occlusion
• • The opacity typically fades over weeks as the oedema resolves, but the visual field defect from cell death remains permanent

Investigations

BRAO is a cardiovascular event. Ocular investigations (OCT, fluorescein angiography) confirm the diagnosis, but the priority is identifying the embolic source to prevent a future stroke:

• • Carotid Doppler ultrasound — to detect carotid stenosis or atheromatous plaques as the embolic source
• • Cardiac investigations — ECG, 24-hour Holter monitor (to detect paroxysmal AF), transthoracic or transoesophageal echocardiogram (to detect valve disease, intracardiac thrombus or patent foramen ovale)
• • Blood pressure — measured immediately
• • Fasting lipid profile and blood glucose
• • Full blood examination and coagulation profile
• • In younger patients: thrombophilia screen and inflammatory markers

Treatment

There is currently no proven treatment that directly restores vision once retinal ischaemia has occurred. Acute interventions — if the event is within 24 hours — include:

• • Ocular massage — rhythmic digital pressure on the globe to lower IOP and potentially dislodge the embolus distally
• • IOP-lowering agents (topical or systemic) — to reduce pressure and improve perfusion pressure gradient

The primary treatment focus is systemic secondary prevention:

• • Antiplatelet therapy (aspirin or clopidogrel) — to reduce the risk of further embolic events
• • Statin therapy — for lipid lowering and plaque stabilisation
• • Antihypertensive therapy if blood pressure is elevated
• • Anticoagulation if atrial fibrillation or a cardioembolic source is identified
• • Carotid endarterectomy if significant carotid stenosis (>70%) is present

Anti-VEGF injections are not typically needed in BRAO, as the pathology is ischaemic rather than VEGF-driven oedema.

Prognosis

Visual prognosis in BRAO depends primarily on foveal involvement. When the fovea is outside the occluded territory, central acuity is often preserved and the patient may function well despite a peripheral visual field defect. When the fovea is involved, central visual acuity loss is likely, though some patients experience partial spontaneous improvement over weeks as ischaemic oedema resolves.

The systemic prognosis is the more important consideration: BRAO patients face a meaningfully elevated risk of future stroke and myocardial infarction, underscoring the critical importance of identifying and treating the underlying cardiovascular cause.

Conclusion

BRAO is more than an eye problem — it is a signal from the cardiovascular system that demands urgent attention. While visual recovery may be limited, identifying the embolic source and instituting appropriate secondary prevention can be life-saving. Any patient with sudden, fixed sectoral vision loss should seek same-day assessment from an ophthalmologist and undergo prompt cardiovascular investigation.

Frequently Asked Questions