To examine the histologic and ultrastructural features of human corneas after successful laser in situ keratomileusis (LASIK).
Corneas from 48 eyes of 25 postmortem patients were processed for histology and transmission electron microscopy (TEM). The 25 patients had LASIK between 3 months and 7 years prior to death. Evaluation of all 5 layers of the cornea and the LASIK flap interface region was done using routine histology, periodic acid–Schiff (PAS)-stained specimens, toluidine blue–stained thick sections, and TEM.
In patients for whom visual acuity was known, the first postoperative day uncorrected visual acuity was 20/15 to 20/30. In patients for whom clinical records were available, the postoperative corneal topography was normal and clinical examination showed a semicircular ring of haze at the wound margin of the LASIK flap. Histologically, the LASIK flap measured, on average, 142.7 μm (range, 100–200). A spectrum of abnormal histopathologic and ultrastructural findings was present in all corneas. Findings at the flap surface included elongated basal epithelial cells, epithelial hyperplasia, thickening and undulations of the epithelial basement membrane (EBM), and undulations of Bowman’s layer. Findings in or adjacent to the wound included collagen lamellar disarray; activated keratocytes; quiescent keratocytes with small vacuoles; epithelial ingrowth; eosinophilic deposits; PAS-positive, electron-dense granular material interspersed with randomly ordered collagen fibrils; increased spacing between collagen fibrils; and widely spaced banded collagen. There was no observable correlation between postoperative intervals and the severity or type of pathologic change except for the accumulation the electron-dense granular material.
Permanent pathologic changes were present in all post-LASIK corneas. These changes were most prevalent in the lamellar interface wound. These changes along with other pathologic alterations in post-LASIK corneas may change the functionality of the cornea after LASIK.
From the Emory Eye Center, Emory University, Atlanta, GA.
Received for publication February 23, 2004; revision received May 4, 2004; accepted May 9, 2004.
Supported in part by NEI grants R01-EY00933 and P30-EY06360 and Research to Prevent Blindness, Inc.
Reprints: Theresa R. Kramer, MD, Emory Eye Center, 1365-B Clifton Road, N.E., Atlanta, GA 30322 (e-mail: Theresa_Kramer@emoryhealthcare.org).