Acute retinal arterial ischemia

Abstract

Acute retinal arterial ischemia, which includes transient monocular vision loss (TMVL), branch retinal artery occlusion (BRAO), central retinal artery occlusion (CRAO) and ophthalmic artery occlusion (OAO), is most commonly the consequence of an embolic phenomenon from the ipsilateral carotid artery, heart or aortic arch, leading to partial or complete occlusion of the central retinal artery (CRA) or its branches. Acute retinal arterial ischemia is the ocular equivalent of acute cerebral ischemia and is an ophthalmic and medical emergency. Patients with acute retinal arterial ischemia are at a high risk of having further vascular events, such as subsequent strokes and myocardial infarctions (MIs). Therefore, prompt diagnosis and urgent referral to appropriate specialists and centers is necessary for further work-up (such as brain magnetic resonance imaging with diffusion weighted imaging, vascular imaging, and cardiac monitoring and imaging) and potential treatment of an urgent etiology (e.g., carotid dissection or critical carotid artery stenosis). Since there are no proven, effective treatments to improve visual outcome following permanent retinal arterial ischemia (central or branch retinal artery occlusion), treatment must focus on secondary prevention measures to decrease the likelihood of subsequent ischemic events.

Keywords: Central retinal artery occlusion (CRAO); ischemia; management; stroke; thrombolysis; treatment.

Figure 1

Left central retinal artery occlusion (CRAO) with sparing of the cilioretinal artery. (A) Color fundus photograph of the normal right eye; (B) normal Humphrey visual field from the right eye; (C) color fundus photograph of the left eye showing a CRAO with a perfused cilioretinal artery (blue arrows). The remainder of the retinal arterioles is attenuated. There is a small retinal hemorrhage near the end of the superotemporal arcade (yellow arrow). Compared to the right eye, the fundus of the left eye has a white hue, indicative of inner retinal edema. Visual acuity in the left eye was 20/40. (D) Left eye Humphrey visual field showing marked visual field deficits despite near normal visual acuity, due to the patent cilioretinal artery, in the left eye.

Figure 2

Left central retinal artery occlusion (CRAO) with sparing of the cilioretinal artery. Color fundus photographs (A,B) and retinal fluorescein angiography (C,D,E,F) in acute left CRAO with cilioretinal artery sparing (same patient as Figure 1). A. Color fundus photograph of the left eye showing a CRAO with cilioretinal artery sparing. The papillomacular bundle is perfused by a patent cilioretinal artery. (B) Same photograph as in (A) outlining the area perfused by the cilioretinal arteries (area contained within the yellow lines). Retinal edema is seen outside of the area perfused by the cilioretinal arteries. (C,D,E,F) Fluorescein angiogram of the left eye taken 21 seconds (C), 24 seconds (D), 28 seconds (E), and 1 minute and 5 seconds (F) after injection of fluorescein dye. There is minimal fluorescent signal in the papillomacular bundle (C, area outlined by yellow arrows) and no appreciable fluorescent signal outside of the papillomacular bundle 21 seconds after fluorescein dye injection. One minute after injection of fluorescein dye (F), there continue to be large vascular segments without fluorescent signal (black segments of retinal vessels) and almost no retinal perfusion outside of the papillomacular bundle.