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The incidence of spontaneous vitreous hemorrhage is approximately 7 cases per 100,000 population. Proliferative diabetic retinopathy (32%), retinal tear (30%), proliferative retinopathy after retinal vein occlusion (11%) and posterior vitreous detachment without retinal tear (8%) are the most common causes of spontaneous vitreous hemorrhage. Vitreous hemorrhage can be caused by the pathologic mechanisms of disruption of normal retinal vessels, bleeding from diseased retinal vessels or abnormal new vessels, and extension of hemorrhage through the retina from other sources. Hemorrhage into the vitreous gel results in rapid clot formation and is followed by slow clearance of approximately 1% per day. The cellular response to vitreous hemorrhage is unusual with regard to hemorrhage in any tissue outside the vitreous cavity and has been compared to a "low-turnover" granuloma. Unique clinicopathologic features of long-standing vitreous hemorrhage include cholesterolosis bulbi (synchysis scintillans), hemoglobin spherulosis, and vitreous cylinders. Complications of nonclearing vitreous hemorrhage are hemosiderosis bulbi and glaucoma. Ghost cell glaucoma, hemolytic glaucoma, and hemosiderotic glaucoma may result from vitreous hemorrhage. The established treatment option for nonclearing vitreous hemorrhage is pars plana vitrectomy. Experimental nonsurgical treatment options involve improvement of physiologic clearance mechanisms in order to accelerate fibrinolysis, liquefaction, hemolysis and phagocytosis.

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Eyes with advanced glaucomatous damage after long standing primary open-angle glaucoma exhibit several changes including decreased density of capillaries of the choriocapillaris and decreased density of large choroidal vessels. We cannot conclude from our study whether the observed vascular changes in the choroid are primary pathogenic factors or secondary phenomena.