Contributor: Gordon K. Klintworth
Ocular occlusovascular disease results from thrombosis (as in atherosclerosis and giant cell arteritis), embolism, stenosis (as in atherosclerosis), vascular compression, intravascular sludging or coagulation, and vasoconstriction (as in hypertensive retinopathy [retinopathy - hypertensive] and migraine). Occlusovascular disease of the carotid arteries results in carotid artery insufficiency, which can affect the eye. The most frequently involved parts of the eye in occlusovascular disease are the retina [retinal artery occlusion, retinal vein occlusion], and optic nerve, but the anterior segment may also be affected [anterior segment ischemia]. The effect of retinal arterial occlusion depends upon the size of the vessel involved, the degree of resultant ischemia, and the cause of the vascular occlusion. Retinal and other neurons are extremely susceptible to hypoxia. Coagulative necrosis of the inner retinal layers (supplied by the central retinal artery) often follows acute central retinal artery occlusion. Initially intracellular edema (manifest by retinal pallor) is prominent, particularly in the macula. Cellular dissolution and nuclear pyknosis of the affected retinal layers are common. Occluded short posterior ciliary arteries cause infarction of the optic nerve mainly at or immediately posterior to the lamina cribrosa. With an acute infarct the affected tissue undergoes liquefaction necrosis of the axons and the necrotic debris becomes phagocytosed. When the infarct affects the optic nerve head anterior to the lamina cribrosa hyaluronic acid may be present in the area of necrosis. The hyaluronic acid is presumably from vitreous that is displaced through defects in the prelaminar glial membrane and this lesion resembles the cavernous optic atrophy [optic atrophy - cavernous] of glaucoma.