Occlusion of ocular or retinal arteries by an embolus traveling from a distant source or from local thrombosis. Other factors include vasospasm, necrosis, GCA (10%), and hyperhomocystinemia. It can affect the ophthalmic artery, cilioretinal arteries, and retinal arteries. Visible embolus known as a Hollenhorst plaque. Mortality rate over nine years is 3 times greater than that of age-matched normals.

• CRAO characterized by sudden, painless, profound loss of vision over several seconds. VA count fingers or worse in 90%.
• May or may not be preceded by episodes of amaurosis fugax.
• APD develops within seconds.
• Retina can appear normal for first hour or so.
• Emboli seen in only 20% of cases. Arise most frequently from the ipsilateral carotid artery or, more frequently, the heart valves (larger, calcific plaques).
• Within hours the retina becomes white and opacified due to ischemia. A "cherry red spot" remains in the fovea due to the thinness of the tissue and visibility of the underlying choroid which remains perfused.
• Over the course of about one month, the retinal appearance returns to normal except for optic atrophy with moderate nerve pallor and attenuated arteries.
• 25% of cases have some sparing of the macular area from perfusion by cilioretinal arteries which branch off the posterior ciliary arteries, not the central retinal artery. When this sparing occurs, vision can improve to 20/50 or better over the course of a few weeks if the fovea is perfused. Without cilioretinal vessel perfusion, VA does not make a meaningful recovery.
• Neovascularization of the iris, of the disc, and elsewhere (NVI, NVD, NVE) are very rare complications due to the rapid death of the retina.
• Other non-embolic associations with CRAO include giant cell arteritis, hypertension, and optic nerve head drusen.
• Treatment is notoriously ineffective. If seen early, paracentesis, massage, IOP lowering agents, and re-breathing may help dislodge the embolus. This usually has little to no effect on the final VA. The most effective treatment is hyperbaric oxygen chamber therapy if the patient is seen within a day or two of the event. This controversial treatment allows for super-oxygenated blood to perfuse the retinal tissue. It may, however, be counter-productive if applied before the embolus is dislodged.

• Branch retinal artery occlusions occur less frequently than do CRAOs. 68% have visible embolus.
• A smaller embolus makes it farther downstream before lodging in a branch retinal artery, usually temporal to the macula (80%).
• Appearance is similar but in a localized area.
• Susac syndrome: Encephalopathy, hearing loss, and bilateral, recurrent BRAOs. Greater occurence in females than males. Any race.
• Visual acuity is usually quite good unless the macula is involved and the presenting symptom is often a visual field defect.
• Underlying etiologies and treatment strategies are the same as those for CRAO but survival rates are actually lower.
• Cilioretinal and ophthalmic artery obstructions are also possible and are more common than retinal arterial occlusions in GCA.
• Ophthalmic artery obstruction mimics CRAO but vision is usually NLP; there is no cherry red spot; and the findings are more pronounced.

In all cases of suspected ocular artery occlusions, a systemic work-up is a must with special attention paid to the carotid arteries and the heart valves. In older patients, a stat ESR and C-reactive protein are warranted to rule out GCA.

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	Hollenhorst plaque (calcific) with BRAO
	Hollenhorst plaque
	Multiple Hollenhorst plaques
	Hollenhorst plaque (cholesterol) with BRAO