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Harvey Lincoff, MD; Bogidar Madjarov, MD; Norah Lincoff, MD; Alexander Movshovich, MD; Sandeep Saxena, MD; D. Jackson Coleman, MD; Herman Schubert, MD; Daniel Rosberger, MD; Stephen McCormack, MD

Arch Ophthalmol. 2003;121:91-96.

Objective  To determine the cellular mechanism that allows subretinal hemorrhage to cloud the vitreous.

Methods  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.

Results  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.

Conclusions  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.

Clinical Relevance  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.

From the New York Presbyterian Hospital–Cornell Weill Medical Center (Drs H. Lincoff, Madjarov, Movshovich, Saxena, Coleman, and Rosberger), New York; Department of Neurology, University of Buffalo, Buffalo, NY (Dr N. Lincoff); Columbia Presbyterian Hospital, Columbia University Medical College (Dr Schubert), and the Department of Pathology and Laboratory Medicine, New York Eye & Ear Infirmary (Dr McCormack), New York.

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