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D.S. Chu, B.D. Ayres, K. La Perle, P.S. Hersh; Inflammatory Response at the Corneal Flap–Stromal Interface After Mechanical and Chemical Injuries in White New Zealand Rabbit Corneas . Invest. Ophthalmol. Vis. Sci. 2004;45(13):129.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To propose a model of late onset diffuse lamellar keratitis(DLK) that is observed after chemical or mechanical corneal injury in patients with previous laser in situ keratomileusis (LASIK). Methods: Corneal flaps were created in eight eyes from four White New Zealand Rabbits. The flaps were reflected and then repositioned and allowed to heal for two weeks. One eye of each rabbit was then given either a chemical (0.5N NaOH) or mechanical epithelial injury with the contralateral eye serving as control. Corneas were then harvested one day after the injury was created for microscopic analysis. Results: Histopathalogical analysis of sections from corneas that sustained mechanical injury show focal aggregates of heterophils, macrophages, and mild corneal edema at the flap–stromal interface. After chemical injury, in addition to heterophils and macrophages, focal and subepithelial aggregates of fibroblasts and myxomatous stromal changes were observed at the flap–stromal interface. Control corneas show only myxomatous stromal changes. Discussion: Late DLK is an inflammatory condition of corneas observed in patients with previous LASIK and subsequent corneal injury or associated corneal epithelial defect. In our rabbit model, histopathologic analysis shows an inflammatory response at the flap–stromal interface, incited by either chemical or mechanical injury. This may serve as a possible model of late onset DLK.
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