Visual Recovery and Endothelial Cell Survival After Descemet Stripping Automated Endothelial Keratoplasty for Failed Penetrating Keratoplasty Grafts­A Cohort Study.

PURPOSE: To assess visual recovery and donor cell survival after Descemet stripping automated endothelial keratoplasty (DSAEK) for the repair of failed penetrating keratoplasty (PK) grafts. METHODS: Best spectacle-corrected Snellen visual acuity results after DSAEK were compared with best-ever documented visual acuity (BDVA) results obtained with the previous PK graft in a prospective cohort study. Donor cell survival after DSAEK for PK repair was compared with cell survival after DSAEK for Fuchs endothelial dystrophy and pseudophakic bullous keratopathy. Differences in the logMAR best spectacle-corrected Snellen visual acuity and endothelial cell loss rates were calculated. RESULTS: Twenty-eight eyes with DSAEK for PK repair were identified, 21 of which lacked vision-limiting comorbidities. The mean follow-up was 18.4 ± 10.6 months. At 3 months postoperatively, 10/21 eyes (48%) regained their BDVA. By 24 months, only 14% remained with 0.2 logMAR below their BDVA. Endothelial cell counts decreased significantly faster in patients with DSAEK for failed PK (P = 0.024) or pseudophakic bullous keratopathy (P = 0.018) than in patients with DSAEK for Fuchs endothelial dystrophy. CONCLUSIONS: DSAEK for the restoration of failed PK grafts promotes rapid visual recovery within the visual limits of the previous PK graft. Increased endothelial cell loss is noted relative to other DSAEK indications, which may result in earlier endothelial graft failure in renovated PK.

Changes in intraocular pressure after descemet stripping automated endothelial keratoplasty: a retrospective analysis.

PURPOSE: To analyze the occurrence of postoperative intraocular pressure (IOP) elevation and types of pressure-lowering treatment in patients after Descemet stripping automated endothelial keratoplasty (DSAEK) with and without previous diagnoses of glaucoma and/or pseudoexfoliation (PXF) syndrome. METHODS: This retrospective assessment considered 211 consecutive DSAEK cases (176 patients) performed by 1 surgeon between January 2007 and November 2010 with at least 1-year follow-up. Salient patient characteristics, IOP, and type of antiglaucoma treatment registered in postoperative visits up to 36 months were extracted from medical records. IOP elevation and its association with glaucoma, PXF, and combination of the 2 were assessed using multivariate ordinal logit models. RESULTS: Of 211 eyes, 97 eyes (45%) showed at least 1 increase in IOP >25 mm Hg after DSAEK. Of these 97 eyes, 17 eyes (17.5%) had a history of glaucoma alone, another 17 eyes (17.5%) had a history of glaucoma combined with PXF, 10 eyes (9.7%) had PXF alone, and 53 eyes (54.6%) were steroid responders only. To control IOP elevation, steroid reduction alone was performed in 6 eyes (6.2%) and IOP-lowering medication as the only measure was performed in 26 eyes (26.8%). In 46 eyes (47.4%), steroids were reduced in combination with IOP-lowering medication and 16 eyes (16.5%) required surgery. In 3 eyes (3.1%), no action was required. Presence of PXF (odds ratio, 1.71; 95% confidence interval, 0.62-2.81; P = 0.002) and PXF glaucoma (1.14; 95% confidence interval, 0.06-2.21; P = 0.038) required a more intensive IOP-lowering management than patients without PXF with IOP problems. CONCLUSIONS: Increased IOP is common after DSAEK, and a significant number of patients need IOP-lowering treatment. PXF syndrome and PXF glaucoma are risk factors for significant IOP elevation after DSAEK. In most cases, IOP remains controlled with conservative management, but some patients require glaucoma surgery.