A patient with amaurosis fugax presents with yellow, refractive cholesterol emboli. What is the most likely arterial source?

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Multiple Choice

A patient with amaurosis fugax presents with yellow, refractive cholesterol emboli. What is the most likely arterial source?

Explanation:
This scenario hinges on recognizing that amaurosis fugax is transient ischemia of the retina caused by an embolus. The yellow, refractile cholesterol emboli seen in the retina are classic for cholesterol crystal emboli that originate from atherosclerotic plaques. The retina’s blood supply comes from the central retinal artery, which branches off the ophthalmic artery from the internal carotid. Emboli shed from an atherosclerotic plaque in the carotid arteries can travel into the ophthalmic/retinal circulation and lodge in small retinal arterioles, producing transient monocular vision loss—amaurosis fugax. Those emboli appear as yellow, refractile plaques on fundoscopic exam, known as Hollenhorst plaques. While other arteries can contribute emboli to the systemic circulation, the retinal findings in this context point most strongly to the carotid arteries as the source. Emboli from the aorta are less likely to present specifically as retinal cholesterol emboli, and emboli to the renal arteries would cause renal symptoms, not vision changes. Cerebral veins are not involved in this arterial embolic process targeting the retina. This situation also signals a need to evaluate for carotid stenosis to reduce stroke risk.

This scenario hinges on recognizing that amaurosis fugax is transient ischemia of the retina caused by an embolus. The yellow, refractile cholesterol emboli seen in the retina are classic for cholesterol crystal emboli that originate from atherosclerotic plaques. The retina’s blood supply comes from the central retinal artery, which branches off the ophthalmic artery from the internal carotid. Emboli shed from an atherosclerotic plaque in the carotid arteries can travel into the ophthalmic/retinal circulation and lodge in small retinal arterioles, producing transient monocular vision loss—amaurosis fugax. Those emboli appear as yellow, refractile plaques on fundoscopic exam, known as Hollenhorst plaques.

While other arteries can contribute emboli to the systemic circulation, the retinal findings in this context point most strongly to the carotid arteries as the source. Emboli from the aorta are less likely to present specifically as retinal cholesterol emboli, and emboli to the renal arteries would cause renal symptoms, not vision changes. Cerebral veins are not involved in this arterial embolic process targeting the retina. This situation also signals a need to evaluate for carotid stenosis to reduce stroke risk.

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