Vascular disorders that affect the eyes include central retinal artery occlusion, central retinal vein occlusion, ischemic optic neuropathy, amaurosis fugax, and occipital lobe vascular accident.

CENTRAL RETINAL ARTERY OCCLUSION
Occlusion of the central retinal artery produces sudden blindness in the affected eye. The typical cause in older patients is an atheroma, usually broken off the carotid artery wall. The atheroma occludes the central retinal artery in the deeper portion of the optic nerve head and thus cannot be seen. Within an hour after loss of vision, the arterial spasm ceases, and some blood flow is restored to the retina, giving the appearance of a relatively normal retina on ophthalmoscopy. However, within several hours, the retina becomes edematous and gray from the death of retinal ganglion cells. Because the retina in the foveal area contains no ganglion cells, the reddish underlying choroid remains visible, accounting for the characteristic central cherry-red spot surrounded by gray retina. In 2 to 3 wk, the cherry-red spot disappears, and as the ganglion cells and their axons die, the optic nerve becomes white, the hallmark of primary optic atrophy.
When an atheroma breaks off, passes through the central retinal artery, and lodges in a retinal artery branch, it can usually be seen as a retractile object in the branch and is referred to as a Hollenhorst plaque. This finding indicates embolic activity, usually from the carotid system. The portion of the retina supplied by the occluded vessel loses its function and a visual field defect, which may not affect central vision, results.
Intervention is needed within a few minutes of the occlusion to prevent retinal cell death. Acutely reducing intraocular pressure by paracentesis combined with vasodilators may occasionally prevent this complication.
CENTRAL RETINAL VEIN OCCLUSION
Retinal vein occlusion is probably the most common vascular accident in the eye. About 10% of patients having a central retinal vein occlusion in one eye will also develop one in the other eye. Even after the occlusion occurs, some vision remains.
Ophthalmoscopy reveals distended, tortuous veins with massive hemorrhages and edema throughout the retina. The margins of the optic nerve become blurred and the disk swollen. Complete resorption of the hemorrhages and edema may take months or even years. In the older patient, the prognosis for vision is poor. Also, about 25% of patients develop a fibrovascular membrane that seals the aqueous humor outflow channels in the anterior chamber, resulting in a painful neovascular glaucoma in 3 to 6 mo. If the intraocular pressure remains elevated, blindness results in weeks. Treatment is most often attempted with laser photocoagulation, but its effectiveness is still being assessed.
Branch vein occlusion is also seen when a branch of the central retinal vein becomes obstructed, most often the superior temporal branch. The characteristic exudates and hemorrhages are confined to the involved quadrant of the retina, which has an associated visual field defect. Vision is usually unaffected unless the retinal swelling impinges on the macula. A clinical trial has demonstrated that using laser photocoagulation to treat branch vein occlusion helps preserve vision. Fortunately, the development of neovascular glaucoma is much less common in branch vein occlusion.