Retinal artery occlusions can be categorized into branch retinal artery occlusion (BRAO), hemiretinal artery occlusion (HRAO), central retinal artery occlusion (CRAO) or cilioretinal artery occlusion (CLRAO). The underlying pathophysiology is usually secondary to blockage of the retinal artery from a retinal emboli. The most common retinal emboli types are calcific, platelet-fibrin or cholesterol, also commonly referred to as Hollenhorst plaques. The occlusion can be transient or permanent leading to symptoms of amaurosis fugax, visual field defects or complete monocular blindness. Other causes of a CRAO includes, inflammation from temporal arteritis in older patients and a hemodynamic block secondary to a CRVO.
In an acute retinal artery occlusion, the retinal whitening seen on examination is secondary to significant swelling of the inner retinal layers from the ischemic event. The classic text book description of a “cherry red spot” in a CRAO describes the retinal whitening and thickening of the inner retinal layers and a normal fovea appearance. The fovea appears normal because there are no ganglion cell swelling to obscure the fovea. OCT is able capture the thickening/swelling of the inner retinal layers.
Figure 1: Acute branch retinal artery occlusion (BRAO) with retinal whitening. SD-OCT scan from left to right over the area of normal retina and the area involved. The inner retinal layers are significantly thicker and hyperreflective from the acute infaract.
After the initial acute phase of the retina artery occlusion, the swollen inner retinal layers will start to atrophy. OCT scans will display thin inner retinal layers with fairly normal outer retinal layers. On clinical examination, the area of retinal artery occlusion will sometimes be difficult to appreciate without the aid of OCT or fluorescein angiography. The macular cube 512x128 ILM-RPE layer map is useful at detecting areas of thinning outside the fovea.
Figure 2: Large branch retinal artery occlusion vs hemiretinal artery occlusion. The inferior of the retina was involved resulting in thinning of the inner retinal layers. Cirrus macular cube 512x128 scans reveal inner retinal thinning temporal to the fovea on the horizontal scan and severe thinning inferiorly on the vertical scan. The ILM-RPE layer map on the right of the scan reveals inferior thinning of the entire posterior pole.
Figure 3: Small branch retinal artery occlusion involving inferior to the fovea. Cirrus macular cube 512x128 reveals thinning on the ILM-RPE layer map. On clinical examination, the area of the BRAO was difficult to appreciate without the aid of the OCT.
Figure 4: Central retinal artery occlusion 3 months after initial onset with light perception vision. Cirrus HD 5-line raster scan revealing loss/thin of inner retinal layers (RNFL/GCC/IPL/INL) with minimal foveal contour. The outer retinal layers remain intact including the EPIS line.
Figure 5: Comparison of the inner retinal layers of the right eye and left eye. The right eye had the CRAO and loss the inner retinal layers.
Figure 6: Cirrus RNFL analysis with optic disc cube scan. The right eye had severely thin RNFL layer in all sectors and quadrants compared to the left eye. Comparison of the asymmetric average thickness correlates with clinical findings of a relative afferent pupillary defect in the right eye. Even with light perception, the right eye had RNFL thickness of ~30 microns.
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