PURPOSE: To describe histopathological and immunohistochemical findings in human corneas after myopic laser in situ keratomileusis (LASIK) followed by iatrogenic keratectasia and after hyperopic LASIK. SETTING: Department of Ophthalmology, University of Innsbruck, Innsbruck, Austria. METHODS: Clinical, histological, and immunohistochemical investigations were performed of 1 human cornea with iatrogenic keratectasia following myopic LASIK and 1 human cornea with irregular astigmatism and central scar formation after hyperopic LASIK. Corneal buttons were obtained during penetrating keratoplasty in both patients. RESULTS: Histopathological examination showed thinning of the central stroma with a posterior residual thickness of 190 microm in the patient with iatrogenic keratectasia after myopic LASIK and significant midperipheral thinning in the patient who had hyperopic LASIK. However, this characteristic ablation profile of the stroma after hyperopic LASIK was partially mitigated and compensated by the epithelium, which was significantly thinned in the center and markedly thickened in the midperiphery. Traces of wound healing with minimal scar tissue were present at the flap margin after myopic and hyperopic LASIK. In a few sections of the cornea with keratectasia after myopia LASIK, only a few collagen lamellae were visible crossing between the posterior residual stroma and the superficial flap. Immunohistochemical examination revealed minimally increased staining of dermatan sulfate proteoglycan within the stroma adjacent to the interface of the microkeratome incision. Increased staining of hepatocyte growth factor was found on keratocytes/fibroblasts at the flap margin in both corneas. CONCLUSIONS: The wound-healing response is generally poor after LASIK, which may result in significant weakening of the tensile strength of the cornea after myopic LASIK, probably due to biomechanically ineffective superficial lamella. After LASIK in patients with high hyperopia, compensatory epithelial thickening in the annular midperipheral ablation zone might be partly responsible for regression.
PURPOSE: To describe histopathological and immunohistochemical findings in human corneas after myopic laser in situ keratomileusis (LASIK) followed by iatrogenic keratectasia and after hyperopic LASIK. SETTING: Department of Ophthalmology, University of Innsbruck, Innsbruck, Austria. METHODS: Clinical, histological, and immunohistochemical investigations were performed of 1 human cornea with iatrogenic keratectasia following myopic LASIK and 1 human cornea with irregular astigmatism and central scar formation after hyperopic LASIK. Corneal buttons were obtained during penetrating keratoplasty in both patients. RESULTS: Histopathological examination showed thinning of the central stroma with a posterior residual thickness of 190 microm in the patient with iatrogenic keratectasia after myopic LASIK and significant midperipheral thinning in the patient who had hyperopic LASIK. However, this characteristic ablation profile of the stroma after hyperopic LASIK was partially mitigated and compensated by the epithelium, which was significantly thinned in the center and markedly thickened in the midperiphery. Traces of wound healing with minimal scar tissue were present at the flap margin after myopic and hyperopic LASIK. In a few sections of the cornea with keratectasia after myopia LASIK, only a few collagen lamellae were visible crossing between the posterior residual stroma and the superficial flap. Immunohistochemical examination revealed minimally increased staining of dermatan sulfate proteoglycan within the stroma adjacent to the interface of the microkeratome incision. Increased staining of hepatocyte growth factor was found on keratocytes/fibroblasts at the flap margin in both corneas. CONCLUSIONS: The wound-healing response is generally poor after LASIK, which may result in significant weakening of the tensile strength of the cornea after myopic LASIK, probably due to biomechanically ineffective superficial lamella. After LASIK in patients with high hyperopia, compensatory epithelial thickening in the annular midperipheral ablation zone might be partly responsible for regression.
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