A Branch Retinal Artery Occlusion (BRAO) is a sudden visual event occurring when a smaller artery supplying the retina becomes blocked. This blockage cuts off blood flow and oxygen to the delicate, light-sensitive tissue of the inner retina, causing immediate damage. Since the brain’s visual processing relies entirely on the retina’s function, this lack of blood flow results in a sudden, painless loss of vision.
Defining Branch Retinal Artery Occlusion
A BRAO is a specific type of retinal vascular occlusion where one of the branching arterioles in the retina is obstructed, usually by a small particle traveling through the bloodstream. The retina is a thin layer of nerve tissue lining the back of the eye, nourished by the central retinal artery and its subdivisions. When an occlusion occurs in a branch, the resulting damage is confined to a specific area of the retina, unlike a Central Retinal Artery Occlusion (CRAO), which affects the entire retina.
The defining symptom is a sudden, painless defect in the visual field of one eye, often described as a shadow or a curtain blocking a specific wedge-shaped area. The severity of vision loss depends on which branch is blocked and whether the blockage affects the macula, the central part of the retina responsible for detailed vision. If the macula is spared, central vision remains clear, but peripheral vision is lost. The sudden interruption of blood flow leads to a whitening of the affected retinal tissue, visible upon examination.
The Connection to Systemic Strokes
Branch Retinal Artery Occlusion is frequently referred to as an “eye stroke” or “ocular stroke.” This term is used because the underlying pathology is identical to that of an ischemic stroke in the brain: a blockage interrupts blood flow, causing tissue death. The retina is an extension of the central nervous system, making the event a form of localized stroke.
While a traditional brain stroke affects motor function, speech, or cognition, a BRAO is confined to the visual pathway. The American Heart Association and American Stroke Association consider retinal arterial ischemia, including BRAO, to be the equivalent of acute cerebral ischemia. This highlights the shared mechanism and the significant systemic warning that a BRAO represents. Having a BRAO substantially increases the risk of experiencing a future brain stroke.
Underlying Causes of Retinal Artery Blockages
The majority of BRAO cases occur because an embolus, a tiny piece of debris, breaks off from a larger blood vessel or the heart and travels to the eye. The retinal arteries are narrow, and the embolus typically lodges where the artery branches. Cholesterol plaques, often called Hollenhorst plaques, are the most common emboli, originating from atherosclerotic disease in the carotid arteries.
Platelet-fibrin clots from the carotid arteries or calcific emboli from diseased heart valves, particularly in patients with atrial fibrillation, are also frequent sources. These blockages signal a widespread vascular problem, indicating systemic vascular disease. Risk factors for this condition are the same as those for heart attack and brain stroke, including high blood pressure, elevated cholesterol levels, diabetes, and smoking.
Urgent Diagnosis and Treatment
A BRAO is a time-sensitive medical emergency requiring immediate evaluation to maximize the chance of vision recovery and prevent a subsequent brain stroke. Since irreversible damage to the retina can occur quickly, patients must be urgently transferred to an emergency department or stroke center. The initial diagnosis involves a thorough eye examination to confirm the occlusion and visualize the embolus.
The immediate priority is a comprehensive systemic workup to find the source of the embolus. This workup typically includes an ultrasound of the carotid arteries to check for plaques and an electrocardiogram (EKG) or prolonged heart monitoring to rule out an irregular heart rhythm like atrial fibrillation. While acute treatments may be attempted to dislodge the clot, the long-term management focuses on aggressive risk factor modification—such as controlling blood pressure, lowering cholesterol, and prescribing antiplatelet therapy—to prevent further ischemic events.