īRAO has been reported to occur following retrobulbar anesthesia for intraocular sugery. Endothelial cell injury, the accumulation of thrombotic material, and narrowing of the vessel lumen is thought to result in BRAO. This particular cause of BRAO possesses an auto-immune etiology, with antiendothelial cell antibodies playing an important role. Susac syndrome is a rare disease with clinical features including encephalopathy, sensorineural hearing loss, and BRAO. Nonembolic causes of BRAO include vasospasm secondary to migraines, cocaine abuse and sildenafil, vasculitidies such as Behcets Disease, coagulopathies, and inflammatory/infectious conditions such as Toxoplasmosis, Herpes Zoster, Lyme disease and Giant Cell Arteritis. Other less common forms of embolic sources include calcified cardiac valves, fat emboli from long bone fractures, air emboli from trauma or surgery, talc emboli from IV drug use and synthetic emboli from interventional procedures. The embolus may be composes of cholesterol or fibrin. They often occur at the bifurcation of vessels, and the temporal retinal arteries are involved in 98% of cases. On funduscopic examination, emboli are visualized in 62% of cases. Typically, this hypoperfusion results from emboli to a branch of the central retinal artery. Transient BRAO bears a better visual prognosis.Īny condition which causes decreased perfusion in a branch retinal artery can result in BRAO. More permanent occlusion typically results in more severe visual losses. While frequently described under one heading, two distinct subtypes comprise the condition: permanent BRAO and transient BRAO. The resultant hypoperfusion of retinal tissue may result in vision loss. BRAO represent 38% of all acute retinal artery obstructions.
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