Retinal artery occlusions may arise where atheromatous emboli break free, most often in the carotid artery, and travel in the bloodstream to cause a blockage downstream. Emboli may also be cholesterol (Hollenhorst’s plaques), calcifications, impurities injected into the blood from intravenous drug use, and many other factors. They show a strong association with systemic diseases, such as atherosclerosis and carotid artery disease, hypertension, diabetes, hyperlipidaemia, giant cell arteritis (GCA), and hypercoagulation or vasculitis disorders.


Retinal vascular occlusions are usually unilateral. Visual symptoms are more likely if a large area of retina is affected or is in close proximity to the macula. There may be a history of previous brief loss of vision (amaurosis fugax), transient ischemic attack fTIA) or stroke (cerebrovascular accident).


Arterial occlusions cause retinal infarction (whitening) rather than the hemorrhagic signs associated with venous occlusions. The arterioles and venules are narrowed and the retinal tissue whitens due to ischemia and edema of the tissue. BRAOs may be characterized in terms of the occlusion location – distance from the disc and proximity to the macula. The location of the occlusion dictates the size of the affected area of retina and the likelihood of macular edema, which in turn affects the visual prognosis.


Retinal vascular occlusions are the second most common vascular disease affecting the retina, after diabetic retinopathy.


BRAOs are not only potentially vision threatening; they are a harbinger of potentially life-threatening systemic conditions such as stroke, requiring prompt investigation and treatment.

Differential diagnosis

Branch retinal vascular disease;hypertensive retinopathy; commotio retinae; diabetic retinopathy.

See also



Management is principally systemic in nature.

Urgent treatment Urgent treatment of a BRAO may be initiated if the foveal circulation is affected and the occlusion is recent in onset (2 hours to 48 hours). However, most BRAOs are not treated, as there is no proven treatment for this condition (see Central retinal artery occlusion). Treatment of GCA (see below), if suspected, is also urgent.

Blood tests Erythrocyte sedimentation rate and C-reactive protein levels should be determined urgently in patients over sixty years of age, when a diagnosis of GCA cannot be excluded. Coagulation studies, full blood examination and screening tests for vasculitis are usually performed. In the longer term, cardiovascular risk assessment includes measurement of fasting blood sugar levels and a lipid profile.

Ocular investigations Fluorescein angiography may be conducted to confirm the diagnosis. It will demonstrate delayed arterial filling and masking of background fluorescence by retinal edema in the
affected area.


Occlusion of a superior branch retinal artery shovi/ing attenuation of the vessel calibre and a corresponding segment of retinal pallor from axoplasmic stasis.

Fig. 16.2

Arterial embolus located over the disc, causing infarction of superior retina. The retinal whitening will clear after a few weeks.

Surgery  Carotid endarterectomy is generally indicated for incomplete stenotic lesions of the carotid artery greater than 70 per cent. Lesser degrees of stenosis are treated non-surgically (i.e. medication and lifestyle adjustments).

Review Initial review is often conducted after an interval of several weeks.

Neovascular sequelae are uncommon in patients with arterial occlusions, unlike the bcase for venous occlusions, perhaps due to the complete ischemia in the affected retinal segment. The visual prognosis is good if the macula has been spared, although a visual field defect will usually remain.

Branch retinal artery occlusion