In a CRAO, 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.
After the initial swelling and appearance of the "cherry red spot" in a CRAO, the inner retinal layers will become atrophy.
Figure 1: 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 2: 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 3: 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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