PRK and LASIK--their potential risk of cataractogenesis: lipid peroxidation changes in the aqueous humor and crystalline lens of rabbits.

PURPOSE: There are insufficient data on the possible cataractogenic side effects of excimer laser corneal surgery. Higher malondialdehyde (MDA) levels could indicate oxidative events related to the cataractogenic process. We therefore examined MDA levels after refractive laser surgery. METHODS: Six white Russian rabbits received laser in situ keratomileusis (LASIK) (Schwind keratome) in the right eye and a 250-microm-deep microkeratome cut (Schwind microkeratome) in the left eye. Six others underwent photorefractive keratectomy (PRK) in the right eye; the left eye remained untreated. The 180 mJ/cm2 fluence applied at a rate of 10 Hz with an optical zone diameter of 5 mm in all rabbits (438 pulses) resulted in an estimated central photoablation depth of 116 microm. Two weeks later, lenses and aqueous were taken immediately after death. MDA was detected in aqueous and homogenate of lenses after reacting with thiobarbituric acid (TBA). MDA bound to TBA (MDA-TBA) was specifically analyzed by high-performance liquid chromatography (HPLC) (excitation, 525 nm; emission, 551 nm) using phosphate-buffered methanol as eluent. RESULTS: No significant laser-induced MDA alteration was found in either the aqueous or the lens. The microkeratome group, however, had two to three times higher MDA levels in the lenses than the control group (p = 0.12) or the PRK (p = 0.03) group. CONCLUSION: Elevation of MDA in the lens of the microkeratome group indicates that LASIK, but not PRK, may be a risk factor in cataractogenesis. The increased MDA levels in the LASIK group are probably caused by the microkeratome incision rather than the secondary radiation of the excimer laser. Postoperative inflammation may explain the surprising results.

Immunohistology of corneal wound healing after photorefractive keratectomy and laser in situ keratomileusis. wachtlin@ukbf.fu-berlin.de.

PURPOSE: The aim of the study was to compare corneal wound healing after photorefractive keratectomy (PRK) and laser in situ keratomileusis (LASIK) using conventional, immuno- and enzymohistologic methods. METHODS: Sixteen white Russian rabbits in each group underwent PRK or LASIK. Keratocyte density was recorded from 1 week to 6 months post-operatively on conventional histological sections. Immunohistologic cellular fibronectin and tenascin were used as markers of early epithelial and stromal wound healing in the cornea. The cell damage was demonstrated enzymohistologically using alkaline phosphatase. RESULTS: The reaction was similar in quality with both methods and occurred at sites of simultaneous epithelial and stromal injury. Mild scarring was found around the edge of the flap after LASIK; PRK-treated corneas developed a central subepithelial haze and scarring. A hypocellular region was found in the anterior part of the ablation zone shortly after PRK. Fibroblast migration later led to hypercellularity and subsequent clinical haze formation. After LASIK this reaction was limited to the peripheral entry point of the microkeratome blade around the edge of the corneal flap, where cellular fibronectin and tenascin reactions were positive. An acellular zone was found anterior to the interface after LASIK. The keratocyte damage visualized by alkaline phosphatase was more extensive after PRK than after LASIK. CONCLUSION: The stromal reaction to surgery was more extensive after PRK than after LASIK. A cytokine-mediated interaction between the epithelium and stroma was suggested as the cause of keratocyte cell migration and scar formation.