BRAO

BRAO
Name	BRAO
Caption	Branch retinal artery occlusion affected retina
Field	Ophthalmology
Symptoms	Sudden, painless monocular visual field loss
Complications	Retinal ischemia, neovascularization, neovascular glaucoma
Onset	Sudden
Causes	Embolism, thrombosis, vasculitis
Risks	Hypertension, atherosclerosis, atrial fibrillation, carotid stenosis

BRAO

Branch retinal artery occlusion is an acute vascular event of the retina characterized by sudden, focal, painless loss of vision corresponding to an arterial distribution. It primarily affects the inner retinal layers supplied by a branch of the central retinal artery, producing sectoral visual field defects and retinal whitening on examination. BRAO is an ophthalmic emergency often associated with systemic vascular disease and embolic sources.

Signs and symptoms

Patients typically present with abrupt onset of monocular visual disturbance such as a sectoral scotoma, inferior or superior arcuate defect, or partial visual field loss. On funduscopic examination one finds localized retinal whitening or pallor in the area supplied by the occluded branch and a preserved foveal reflex if the macula is spared. Other signs may include a visible embolus within the retinal arteriole, attenuated arteries, and narrowed arteriolar segments; patients may have a relative afferent pupillary defect when a large sector of the retina is involved. Visual acuity ranges from near normal to severely reduced depending on macular involvement.

Causes and risk factors

The most frequent immediate cause is an embolus originating from cardiovascular or carotid sources. Common embolic materials include cholesterol plaques (Hollenhorst plaques) associated with atherosclerotic disease, calcific emboli often linked to valvular heart disease or prosthetic valves, and platelet-fibrin thrombi from atrial fibrillation or mural thrombus. Systemic risk factors include hypertension, hyperlipidemia, diabetes mellitus, smoking, carotid artery stenosis, ischemic heart disease, and atrial fibrillation. Inflammatory conditions such as giant cell arteritis and infectious or inflammatory vasculitides can produce arterial occlusion, as can hypercoagulable states, hematologic disorders (e.g., sickle cell disease), and iatrogenic causes following intraocular or systemic procedures.

Pathophysiology

Occlusion of a branch of the central retinal artery leads to abrupt cessation of blood flow to the inner retinal layers in that arterial territory, causing ischemia and intracellular edema. The ischemic cascade involves energy failure, ionic pump dysfunction, glutamate excitotoxicity, and eventual neuronal death if perfusion is not restored. Inner retinal neurons, particularly ganglion cells and bipolar cells, are highly susceptible to hypoxia. The retina supplied by the affected arteriole becomes opaque due to cytotoxic edema; the preserved choroidal circulation may maintain a normal-appearing fovea if the macular territory is spared. Chronic ischemia can induce angiogenic signaling with upregulation of vascular endothelial growth factor leading to neovascularization and secondary complications.

Diagnosis

Diagnosis relies on clinical history and ophthalmic examination supplemented by ancillary testing. Ophthalmoscopy reveals sectoral retinal whitening, emboli, and arterial attenuation; optical coherence tomography demonstrates inner retinal thickening and hyperreflectivity in acute stages and thinning in chronic stages. Fluorescein angiography can localize the site of occlusion by showing delayed or absent filling in the affected branch and may detect cilioretinal artery sparing. Visual field testing documents the defect pattern and extent. Systemic evaluation for embolic sources and risk stratification includes carotid duplex ultrasonography, cardiac rhythm monitoring (including telemetry or ambulatory Holter for atrial fibrillation), transthoracic or transesophageal echocardiography for valvular or intracardiac thrombus, and laboratory assessment for vasculitis or hypercoagulable disorders; giant cell arteritis screening with erythrocyte sedimentation rate and C-reactive protein is indicated in older patients.

Management and treatment

Immediate management aims to attempt reperfusion, reduce further embolic risk, and address underlying systemic causes. Ophthalmic acute measures that have been used include ocular massage, lowering intraocular pressure with topical or systemic agents (e.g., acetazolamide, intravenous mannitol), and anterior chamber paracentesis in select settings to improve retinal perfusion pressure; evidence for benefit is limited and time-dependent. Intra-arterial thrombolysis has been reported in select centers but carries procedural risk and is not standard. Identification and treatment of systemic sources is critical: antiplatelet therapy (aspirin) or anticoagulation for cardioembolic disease, carotid endarterectomy for significant carotid stenosis when indicated, and management of hypertension, hyperlipidemia, and diabetes in collaboration with cardiology, neurology, and primary care. Inflammatory causes require prompt corticosteroids or immunosuppression (e.g., giant cell arteritis management with high-dose steroids). Long-term ophthalmic follow-up monitors for ischemic complications such as neovascularization, which may require panretinal photocoagulation or intravitreal anti-VEGF therapy.

Prognosis and complications

Visual prognosis depends on the location and extent of ischemia and the presence of a cilioretinal artery or prompt reperfusion; many patients retain useful central acuity if the macula is spared, but persistent visual field defects are common. Complications include chronic retinal atrophy with inner retinal thinning, macular edema, neovascularization of the iris or angle, and neovascular glaucoma which can cause severe vision loss and ocular pain. Systemic prognosis relates to the underlying embolic source: BRAO can be a harbinger of cerebrovascular events such as ischemic stroke or transient ischemic attack, and identification of cardiovascular disease is essential to reduce morbidity and mortality.

Category:Retinal vascular diseases