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Branch Retinal Artery Occlusion

URGENT — Retina

Symptoms

Presentation

  • Abrupt, unilateral, painless visual change.
  • Sectoral visual field loss corresponding to the affected area.
  • May report preceding episodes of amaurosis fugax.

Clinical Findings

Retinal appearance

  • Superficial whitening and opacification along the distribution of the affected branch artery.
  • Retinal edema within the ischemic sector.
  • Possible cotton-wool spots in the involved area.

Vascular changes

  • Narrowed branch retinal artery with "boxcarring" or segmentation of the blood column.
  • Presence of emboli: Hollenhorst (bright, yellow-white cholesterol crystals), calcific, or platelet-fibrin.

Etiology

Primary mechanism

  • Embolic occlusion of a retinal arteriole branch.

Source of emboli

  • Carotid atherosclerosis: The most common source.
  • Cardiac sources: Valvular disease, endocarditis, or atrial fibrillation.
  • Aortic arch atherosclerosis.

Systemic risk factors

  • Hypertension, diabetes mellitus, hyperlipidemia, and smoking.
  • Less common: Vasculitis (GCA, SLE), hypercoagulable states, or sickle cell disease.

Red Flags

Stroke equivalency

  • BRAO is a retinal stroke equivalent; mandates immediate investigation for an embolic source.
  • Hollenhorst plaque at a bifurcation strongly indicates a carotid source; requires urgent Doppler.
  • Bilateral or recurrent BRAOs suggest cardiac embolism or Susac syndrome.
  • Patients age ≥55: Must rule out giant cell arteritis (GCA) with stat labs.

Investigations

Clinical exam

  • Dilated fundus exam to identify sectoral retinal whitening and emboli.
  • Macular OCT: Focal inner retinal hyperreflectivity (acute) followed by inner layer thinning (chronic).
  • Fluorescein angiography (FA): Shows delayed arterial filling in the affected branch.

Systemic workup

  • Carotid Doppler/CTA and echocardiography to identify the embolic source.
  • Cardiovascular risk assessment: Blood pressure, lipids, and HbA1c.
  • If age ≥55: Stat ESR, CRP, and platelet count.
  • Consider hypercoagulability panel in young or recurrent cases.

Treatment

Systemic management

  • No proven acute ocular treatment; focus is on systemic workup and secondary stroke prevention.
  • Optimize cardiovascular risk factors (BP, lipids, glucose control).

Complication care

  • Anti-VEGF therapy for macular edema if vision is affected.
  • Sector laser photocoagulation if retinal neovascularization develops (rare).
  • Low-vision rehabilitation for persistent visual field defects.

Clinical Pearl

BRAO = embolic stroke until proven otherwise. Hollenhorst plaques (bright, yellow-white cholesterol crystals at vessel bifurcations) are pathognomonic for carotid emboli. Full cardiovascular workup is mandatory — same risk of stroke as CRAO.

Differential Diagnosis

  • Branch retinal vein occlusion (BRVO)
  • Commotio retinae (history of trauma)
  • Diabetic retinopathy (isolated cotton-wool spot)
  • Acute retinal necrosis (ARN)
  • Choroidal infarct

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