Abstract
AbstractPurpose: To present a case of persistent corneal edema after endothelial disease of unknown cause and with a severe decrease in the endothelial count and clinical improvement after DWEK (descemetorhexis without endothelial keratoplasty).Methods: A 61‐year‐old immunocompetent male patient, with no relevant ophthalmological or systemic history, who after multiple episodes of subacute endotheliitis with retrokeratic precipitates and diffuse iridian atrophy in his right eye, showed central persistent corneal edema, secondary to a marked decrease in endothelial count and severe decrease in best‐corrected visual acuity (0.2) after several months of inflammatory stability.Results: During flare‐ups of inflammation, treatment with corticosteroids, topical ganciclovir and oral acyclovir was prescribed, with a good clinical response. Aqueous humour samples were taken during the outbreaks without yielding results for herpesviruses. The endothelial count remained low at the central level several months later, although the peripheral count was good. The fellow eye showed a normal count. It was decided to perform DWEK in the endothelial zone of retrokeratic precipitates as a diagnostic measure. The analyses of the endothelial sample FOR THE HERPESVIRIDAE FAMILY do not show results, however, a progressive improvement in corneal edema and visual acuity was observed from the first month after DWEK. He is currently stable, with mild paracentral edema and a best‐corrected visual acuity of 0.7.Conclusions: DWEK is reserved for cases of slightly advanced endothelial dystrophy, in which the central endothelial denudation causes a centripetal migration of the peripheral endothelial reserve. In this case, the clinical findings suggest a viral aetiology of the endothelial loss, therefore, DWEK was considered as a diagnostic procedure, to obtain samples for PCR and as a first step prior to DMEK. The improvement after DWEK in the area of retrokeratic precipitates without the need for a subsequent transplant suggests localized endothelial involvement in cases of endothelial loss associated with localized inflammatory precipitates.
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