20.1 Features
Retinal artery occlusion (RAO) typically occurs due to embolism or thrombosis, resulting in either branch retinal artery occlusion (BRAO) or central retinal artery occlusion (CRAO). Vision loss is often severe in the areas impacted by the RAO. Central visual acuity can be maintained if the fovea is not involved.
20.1.1 Common Symptoms
Branch Retinal Artery Occlusion
Occasionally asymptomatic. Symptoms include sudden, acute, unilateral, painless, and partial vision loss. Possible prior history of amaurosis fugax (transient vision loss). Visual acuity varies widely.
Central Retinal Artery Occlusion
Sudden, painless, and typically profound unilateral vision loss. Possible prior history of amaurosis fugax. Vision loss typically involves entire visual field. Associated symptoms of jaw claudication, scalp hyperalgesia, and temporal headaches are concerning for concurrent giant cell arteritis (GCA).
20.1.2 Exam Findings
Branch Retinal Artery Occlusion
Fundus findings if examined at time of symptom onset may be absent. Within hours classic findings appear, including retinal whitening in the distribution of occluded arteriole (▶ Fig. 20.1), arteriolar attenuation, and possible Hollenhorst plaque (i.e., platelet–fibrin–cholesterol intravascular emboli). Relative afferent pupillary defect may be present.
Fig. 20.1 (a) Fundus photograph demonstrating inferior branch retinal artery occlusion (BRAO). (b) Optical coherence tomography demonstrating increased inner retinal thickening with associated increased hyperreflectivity consistent with acute BRAO. A follow-up after four weeks demonstrates persistent though less hyperreflectivity and early inner retinal atrophy consistent with previous BRAO. (c) The regional atrophy is consistent with a BRAO.
Central Retinal Artery Occlusion
Findings include retinal whitening, cherry red spot, arteriolar attenuation, boxcarring (segmental stagnant blood flow), and Hollenhorst plaque. About 15 to 25% of eyes have cilioretinal artery that perfuses part of the macula, which preserves central vision (▶ Fig. 20.2). For the majority of cases, however, presenting visual acuity ranges from 20/200 to counting fingers. Relative afferent pupillary defect frequently presents.
Fig. 20.2 (a) Ultra-widefield fundus photo shows disc pallor, macular whitening with sparing of fovea, and temporal wedge supplied by cilioretinal artery. No visible plaques are present. (b) Ultra-widefield fluorescein angiography shows patchy and delayed choroidal filling, delayed central retinal artery filling, and profound peripheral nonperfusion. Cilioretinal artery to the macula and inferotemporal arcade was spared.
20.2 Key Diagnostic Tests and Findings
20.2.1 Optical Coherence Tomography
Branch Retinal Artery Occlusion
Acute BRAO has inner retina thickening and hyperreflectivity; chronic has inner retina thinning and atrophy (▶ Fig. 20.1).
Central Retinal Artery Occlusion
Acute CRAO has inner retina thickening and hyperreflectivity (▶ Fig. 20.3); chronic has inner retina thinning and atrophy. Rarely, may be associated with intraretinal fluid that may reflect combined vein occlusion (▶ Fig. 20.3). Some cases show patchy areas of increased reflectivity from deep capillary bed ischemia, referred to as paracentral acute middle maculopathy.
Fig. 20.3 Optical coherence tomography (OCT) demonstrating scattered multifocal hyperreflective inner retinal paracentral middle maculopathy–like lesions consistent with inner retinal ischemia in a retinal artery occlusion (RAO). (a) Mild cystic changes are also present. (b) OCT with diffuse inner retinal hyperreflectivity consistent with central RAO.
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