2020–2021 BCSC Basic and Clinical Science Course™
4 Ophthalmic Pathology and Intraocular Tumors
Part I: Ophthalmic Pathology
Chapter 10: Vitreous
Degenerations
Hemorrhage
A constellation of pathologic features may develop in the vitreous following vitreous hemorrhage. After 3–10 days, red blood cell clots undergo fibrinolysis, and red blood cells may diffuse throughout the vitreous cavity. At this time, red blood cell breakdown may also occur. Denaturation of hemoglobin in the red blood cells produces ghost cells (see Chapter 7, Fig 7-12) and hemoglobin spherules. Obstruction of the trabecular meshwork by these cells may lead to ghost cell glaucoma. See also BCSC Section 10, Glaucoma.
The process of red blood cell dissolution attracts histiocytes, which phagocytose the degenerate red blood cells. Ferric iron (Fe3+) is released during hemoglobin breakdown. This can occur intracellularly in histiocytes with iron storage as ferritin or hemosiderin, or extracellularly with iron binding to vitreous proteins such as lactoferrin and transferrin. In massive hemorrhages, cholesterol may deposit in the vitreous in the form of cholesterol crystals, which result from the breakdown of red blood cell membranes. Clinically, cholesterol appears as refractile crystals in the vitreous cavity (synchysis scintillans); the crystals are typically not attached to vitreous fibrils. Syneresis of the vitreous and PVD are common after vitreous hemorrhage.
Excerpted from BCSC 2020-2021 series: Section 4 - Ophthalmic Pathology and Intraocular Tumors. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.