Purpose. To examine the incidence of sporadic diffuse lamellar keratitis (DLK) in a large series of LASIK eyes and to suggest the hypothesis that the etiology of sporadic DLK differs from that of epidemic DLK.
Methods. The incidence and severity of DLK was noted in 1352 consecutive eyes that had primary LASIK for myopia or hyperopia and 217 consecutive eyes that had LASIK enhancement.
Results. Twelve of the eyes having primary LASIK had stage 1 DLK and 5 had stage 2 DLK (.9% total). No eyes had stage 3 or stage 4 DLK. Three of the 217 eyes (1.4%) that had LASIK enhancement had stage 1 DLK. The difference in the rate of DLK for primary LASIK compared with LASIK enhancement was not statistically significant (p = 0.69). All eyes responded to intensive corticosteroid therapy, with the addition of flap lifting and irrigation for the eyes with stage 2 DLK. Two of the eyes (one primary LASIK and one LASIK-enhancement) had implanted epithelial nests associated with the DLK. None of the cases of DLK occurred in eyes of patients who had surgery on the same operating day in this series. Two other eyes that had epithelial abrasions more than 3 months after LASIK or LASIK enhancement developed stage 1 DLK.
Conclusions. Many cases of sporadic DLK, including cases associated with epithelial trauma after LASIK, are likely attributable to endogenous factors that trigger inflammation. One trigger is the release of epithelium-derived cytokines such as interleukin-1 that stimulate keratocytes to produce chemokines that are chemotactic to inflammatory cells. Cells likely accumulate at the interface because it is potential space, representing a path of least resistance for cell movement. Some sporadic cases may also be related to exogenous factors such as Betadine. Epidemic DLK is likely associated with exogenous factors that stimulate inflammation, such as endotoxin contaminating sterilizer reservoirs or detergents on instruments.
From the Department of Ophthalmology (S.E.W., R.A.), University of Washington School of Medicine, Seattle, Washington and the Department of Ophthalmology (R.A.), University of São Paulo, São Paulo, Brazil.
Submitted December 19, 2001.
Revision received March 21, 2002.
Accepted March 29, 2002.
Supported in part by US Public Health Service grant EY10056 and EYO1730 from the National Eye Institute, National Institutes of Health, Bethesda, Maryland, and an unrestricted grant from Research to Prevent Blindness, New York, New York, U.S.A.
Address correspondence and reprint requests to Dr. S. Wilson, Department of Ophthalmology, University of Washington School of Medicine, Box 356485, Seattle, WA 98195-6485 U.S.A. E-mail: sewilson@u. Washington.edu