Confocal assessment of the corneal response to intracorneal lens insertion and laser in situ keratomileusis with flap creation using IntraLase
Accepted 2 January 2006.
Purpose
To assess the response of the cornea to hydrogel intracorneal lens (ICL) insertion or laser in situ keratomileusis (LASIK) with IntraLase (IntraLase Corp.) at the cellular level.
Setting
Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Methods
Twenty patients (29 eyes) were evaluated by in vivo confocal microscopy 1 to 6 months postoperatively: 20 eyes had LASIK with flap creation by IntraLase, and 9 eyes had ICL insertion (8 following IntraLase).
Results
For LASIK with IntraLase, keratocyte activation and/or interface haze was detected in 8 of 20 eyes. The remaining eyes had interface particles but no cell activation. Keratocyte activation was generally limited to a few cell layers adjacent to the interface. However, 2 patients exhibited multiple layers of activation and increased extracellular matrix (ECM) reflectivity (haze) surrounding the interface by confocal microscopy. Both patients also had clinical haze and photophobia. For ICLs, following insertion, 5 of 9 eyes had activated keratocytes adjacent to the implant surfaces. The largest amount of cell activation and ECM haze detected by confocal microscopy was in 2 patients with significant clinical haze. Structures with an epithelioid morphology were detected on some implant surfaces. Epithelial thickness was 33.3 μm ± 2.3 (SD) in the ICL eyes and 49.2 ± 6.5 μm in the LASIK with IntraLase eyes.
Conclusions
Both LASIK with IntraLase and ICL insertion following IntraLase induced keratocyte activation, which may underlie clinical observations of haze in some patients. Intracorneal lens implant also induced thinning of the overlying corneal epithelium.
From the Department of Ophthalmology (Petroll, Goldberg, Kelley, Cavanagh, Bowman, Parmar, Verity, McCulley), and UT Southwestern Medical School (Lindsey), University of Texas Southwestern Medical Center, Dallas, Texas, USA
Reprint requests to W. Matthew Petroll, PhD, Department of Ophthalmology, Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9057, USA.
Presented in part at the ASCRS Symposium on Cataract, IOL and Refractive Surgery, Washington, DC, April 2005; the annual meeting of the Association for Research in Vision Science, Ft. Lauderdale, Florida, USA, May 2005; and the annual meeting of the American Academy of Ophthalmology, Chicago, Illinois, USA, October 2005.
Supported in part by NIH grants R01 EY013322 (W.M.P.), departmental infrastructure grant EY016664, a Lew R. Wasserman Merit award (W.M.P.), and an unrestricted grant from Research to Prevent Blindness, Inc.
No author has a financial or proprietary interest in any material or method mentioned.
ABSTRACT