Contributor: Gordon K. Klintworth
The many causes of a vitreous hemorrhage include vitreoretinal neovascularization [neovascularization - vitreoretinal] (as in proliferative diabetic retinopathy, central retinal vein occlusion [retinal vein occlusion - central], branch retinal vein occlusion [retinal vein occlusion - branch] and sickle cell retinopathy [retinopathy - sickle cell]), trauma, a retinal tear, retinal detachment, age-related macular degeneration, ocular ischemic syndrome, Eales disease, intracranial hemorrhage [hemorrhage - intracranial](such as subarachnoid hemorrhage [hemorrhage - subarachnoid] and subdural hemorrhage [hemorrhage - subdural]), posterior vitreous detachments [vitreous detachment - posterior], congenital retinal vascular disease, macular lesions and rarely a malignant melanoma of the choroid [melanoma - choroid] and other intraocular tumors. Vitreous hemorrhage is a component of Terson syndrome. Vitreous hemorrhage is a common cause of vitreal liquefaction and membrane formation. In longstanding vitreous hemorrhage, white opaque masses may form and be confused with endophthalmitis, inflammatory exudates, or an intraocular tumor.Vision may be reduced in severe hemorrhages. Mild to moderate amounts of vitreous hemorrhage usually resolve over week to months. During the resolution of a vitreous hemorrhage erythrocytes release hemoglobin, but the cells may retain their cell membrane and remain as ghost cells. Macrophage may ingest the cellular products. Erythroclasts, hemoglobin spherulosis, macrophages laden with hemosiderin and other blood-breakdown products of blood are abundant in chronic vitreous hemorrhage. Degenerated blood in chronic vitreous hemorrhage develops a yellow-ochre color. Syneresis and an accumulation of highly refractile cholesterol crystals occurs when an extensive vitreous hemorrhage fails to resolve. Following vitreous hemorrhage other vitreous opacities may be evident clinically from aggregates of hemoglobin spherulosis. Vitreous hemorrhage may complicate a subretinal hemorrhage. The opacities may result from eosinophilic spherules of hemoglobin (10-20 μm in diameter) occasional associated macrophages. Persistent hemorrhage or recurrent hemorrhage may lead to organization of the hemorrhage and contraction in conjunction with proliferation of fibrovascular tissue arising from the retina. With time the hemoglobin derived from the hemorrhage can result in hemosiderosis bulbi.