Central toxic keratopathy: description of a syndrome in laser refractive surgery.

PURPOSE

To describe the clinical spectrum of a syndrome in laser refractive surgery, which we call central toxic keratopathy, and to present cases that illustrate the range of this syndrome.

DESIGN

Retrospective observational case series.

METHODS

Eyes with noninflammatory central corneal opacification in the immediate postoperative period after photorefractive keratectomy (PRK) or laser in situ keratomileusis (LASIK) were identified, and the charts abstracted.

RESULTS

Twenty-three eyes of 14 patients were identified who developed central corneal opacification three to nine days after laser refractive surgery. Nineteen of these eyes had LASIK and four had PRK. All eyes had central corneal opacification in the area of laser treatment that extended posteriorly from the interface into the stromal bed (in the case of LASIK eyes). The opacification persisted a minimum of two months to a maximum of 18 months before clearing. Nine eyes developed postoperative hyperopia of greater than 2 diopters. Pre- and postoperative best-spectacle corrected acuity was available on 19 eyes; one of these eyes lost two lines of corrected acuity, and two other eyes lost one line. Eighteen of 19 LASIK eyes had diffuse lamellar keratitis preceding the onset of corneal opacification.

CONCLUSIONS

Central toxic keratopathy is characterized by noninflammatory central corneal opacification with a significant hyperopic shift. The opacification gradually clears over a period of months, leaving the eye hyperopic. Enhancement is indicated to treat residual hyperopia and remove residual striae. Topical or oral corticosteroid treatment is not indicated. The cause of central toxic keratopathy is unknown.