Latanoprost and clinically significant cystoid macular edema after uneventful phacoemulsification with intraocular lens implantation

Abstract

Purpose To elucidate an association between latanoprost and clinically significant cystoid macular edema (CME) in patients after uneventful phacoemulsification with intraocular lens implantation. Setting Bergman Eye Center, Department of Ophthalmology, The University of Chicago Hospitals, Chicago, Illinois, USA. Methods One hundred forty-five consecutive patients (162 eyes) who had phacoemulsification from July 1999 to December 2000 were retrospectively reviewed to determine which patients developed CME. Patients with a history of inflammation and pseudoexfoliation, previous intraocular procedures, or current intraoperative complications were excluded from the study. All cases of CME were diagnosed on the basis of a fundus examination showing typical CME accompanied by a decrease in visual acuity. Upon diagnosis, latanoprost was discontinued and ketorolac was prescribed. The data were analyzed using the Fisher exact test. Of the records reviewed, 134 patients (151 eyes) were included in the study; 11 eyes were excluded secondary to intraoperative complications, a history of ocular inflammation, or both. Among the patients included, 12 were receiving latanoprost preoperatively. Results Four cases of CME were identified; all 4 patients were taking latanoprost. Latanoprost was discontinued in 8 patients 1 week preoperatively, and none of them developed CME. Therefore, in this series, only patients receiving latanoprost developed CME after uneventful cataract surgery. This difference was statistically significant. In addition, all cases of CME resolved upon discontinuation of latanoprost and administration of ketorolac. Conclusions This retrospective study shows a clinical association between latanoprost use and postoperative CME after uneventful phacoemulsification. Given the absence of other coexisting risk factors for CME, this series suggests latanoprost is a significant etiologic factor for the development of postoperative CME.