Lincoff Harvey, Madjarov Bogidar, Lincoff Norah, Movshovich Alexander, Saxena Sandeep, Coleman D Jackson, Schubert Herman, Rosberger Daniel, McCormick Stephen
New York Presbyterian Hospital-Cornell Weill Medical Center, Suite F-832, 525 E 68th St, New York, NY 10021, USA.
Arch Ophthalmol. 2003 Jan;121(1):91-6. doi: 10.1001/archopht.121.1.91.
To determine the cellular mechanism that allows subretinal hemorrhage to cloud the vitreous.
We simulated subretinal hemorrhage in a rabbit model by injecting autologous blood beneath the retina. At the first appearance of a cloud in the vitreous a vitrectomy was performed and using a surgical microscope, the retina was searched for breaks. After enucleation and fixation, the retina was searched for microscopic breaks using light and electron microscopy. The vitreous was then examined to determine the character of the cell population in the cloud. In a related study, we sampled and examined the vitreous for its cellular content in patients undergoing vitrectomy to clear cloudy vitreous emanating from subretinal hemorrhage.
We found no breaks in the living retina of the animal models or the patients. Microscopic examination of serial sections of the rabbit retina revealed necrosis except for the internal limiting membrane. Fragments of the erythrocytes were seen within the damaged retina and on both sides of the internal limiting membrane. Electron microscopy suggested that the erythrocytic fragments had migrated across the internal limiting membrane. The vitreous cloud in both rabbits and patients contained only fragments of erythrocytes.
Thick subretinal hemorrhage causes necrosis of the overlying retina. Fragments of the erythrocytes infiltrate the retina and cross an intact internal limiting membrane to cloud the vitreous.
Rapid necrosis of the retina occurs over thick subretinal hemorrhage and indicates the need for early displacement of the hemorrhage from the macula if function is to be preserved and breakthrough prevented.
