The elevated and everted margins of macular holes represent slope, step, and gap-like obstacles to the migration of glial cells and hence to the healing of defects. The defect allows extension of extracellular matrix into it and the subretinal space. Our results indicate that gaps in the migratory surface caused and aggravated by eversion and the presence of vitreous present obstacles to glial migration and closure of macular holes.
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.
With the advent of phacoemulsification and foldable intraocular lenses, there is renewed interest in sutureless cataract wound. We report the use of laser activated tissue glues for the closure of scleral tunnel cataract incisions. Two glue mixtures were tested in enucleated porcine eyes. Glue A was composed of hyaluronic acid, human albumin, and indocyanine green dye. Glue B contained hyaluronic acid, chondroitin sulfate, human albumin, and indocyanine green dye. A Spectra Physics diode laser (808 nm) with a power density of 7-1 1 watts/cm2 was used for glue activation. Wound bursting pressures, as determined by the presence of fluid at the wound margin, was significantly higher with both glue combinations than without the glue (P
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