CORNEAL ENDOTHELIUM 5 YEARS AFTER TRANSPLANTATION

Citation
Wm. Bourne et al., CORNEAL ENDOTHELIUM 5 YEARS AFTER TRANSPLANTATION, American journal of ophthalmology, 118(2), 1994, pp. 185-196
Citations number
43
Categorie Soggetti
Ophthalmology
ISSN journal
00029394
Volume
118
Issue
2
Year of publication
1994
Pages
185 - 196
Database
ISI
SICI code
0002-9394(1994)118:2<185:CE5YAT>2.0.ZU;2-E
Abstract
We asked the recipients of 500 consecutive corneal transplants to retu rn for examination and endothelial photography at two months and at on e, three, and five years postoperatively. Thirty-six regrafts and 70 f ellow eyes of bilateral cases were excluded, leaving 394 eyes for anal ysis. We also recorded episodes of graft rejection and failure. In 129 grafts in patients who returned at each postoperative interval and ha d no rejection episodes, the mean endothelial cell density continued t o decrease 7.8% per year from three years to five years after keratopl asty, compared with approximately 0.5% per year in unoperated-on norma l corneas. The mean cell loss compared with the preoperative examinati on was 58.9% five years after keratoplasty. The percentage of hexagona l cells did not return to preoperative levels by five years after kera toplasty, suggesting that the endothelium continued to be unstable. Th e mean corneal thickness increased significantly with time. The Kaplan -Meier rates of rejection episodes and failure were 19% and 17%, respe ctively, five years after keratoplasty. Eyes with posterior chamber le ns implants lost more endothelial cells by five years after keratoplas ty than did eyes with open-looped anterior chamber lens implants. Low endothelial cell densities were statistically significantly associated with increased corneal thickness and with an increased risk of subseq uent failure. The Central endothelial cells of successful corneal tran splants five years after keratoplasty form an unstable monolayer with continued accelerated loss of cells and abnormal cellular morphologic features. This process results in fewer endothelial cells remaining on the central graft with an associated increase in stromal swelling and graft failure.