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IW McLean, M Pontigo; Histopathological Findings In Bullous Keratopathy . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1093.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:To better understand the mechanism of bullous keratopathy formation, we reviewed the histopathological findings in cases of bullous keratopathy from the Ophthalmic Pathology Registry. Methods:We examined 202 cases diagnosed as bullous keratopathy and 21 normal corneas. All patients were treated between 1980 to 1990. We divided the cases based on the main ophthalmic disease in three different groups: 20 cases of glaucoma, 100 cases of pseudophakic bullous keratopathy (PBK), and 82 others. Thirteen cases of pseudophakic bullous keratopathy that had gutatta indicative of Fuchs corneal dystrophy (PBKF) were analyzed as a separate group. The others group was composed mostly of inflammatory cases but it was very heterogeneous and not further analyzed. By light microscopy four pathological findings were determined: thickness of Descemet's membrane (TDM) and the presence or absence of edema, bullae and endothelial cell loss (ECL). We compared the pathological findings using discriminant statistical analysis. Results:By univariate analysis ECL was the most significant variable present in none of the normal cases, 60% of the glaucoma cases, 98% of the PBK cases, and 92% of the PBKF cases. By multivariate analysis, the most significant finding was the TDM. In the normal group the mean TDM was 5.14 µ, compared with the glaucoma group (5.73 µ), PBK group (10.21 µ), and PBKF group (15.75 µ). Stromal edema and ECL were significant in the multivariate analysis but the presence of bullae had no statistical significance. Conclusion:Our histopathological findings suggest that the physiopathologic mechanisms of bullous keratopathy are different in glaucoma compared with pseudophakic bullous keratopathy with or without Fuchs' dystrophy. In the glaucoma group, high intraocular pressure can drive aqueous humor into the cornea causing bullous keratopathy without killing or chronically injuring the endothelium in many of the cases. In the PBK and PBKF groups the thickening of Descemet's membrane suggests that chronic injury stimulates the endothelial cells to produce basal membrane prior to the loss of the endothelial cells population. This injury is probably more chronic in the PBKF group.
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