Michael L Nordlund1, Sara Grimm, Stephen Lane, Edward J Holland. 1. Cincinnati Eye Institute and Department of Ophthalmology, University of Cincinnati College of Medicine, Cincinnati, OH 45242, USA. mnordlund@cincinnatieye.cin
Abstract
PURPOSE: Interface inflammation is a common complication of laser in situ keratomileusis (LASIK). The most well-described presentation is diffuse lamellar keratitis (DLK), which typically develops early after LASIK and responds quickly to topical steroids. In this report, we describe a novel presentation of interface inflammation that resembles DLK in appearance but presents late in the postoperative period, is associated with increased intraocular pressure, and is exacerbated by steroid treatment. METHODS: A retrospective case series and chart review of all patients treated in our tertiary care private practice for late-onset interface inflammation associated with elevated intraocular pressure. RESULTS: Ten eyes in 6 patients with late-onset interface inflammation and increased intraocular pressure were identified. At presentation, all patients were presumed to have classic DLK and were treated initially with aggressive topical steroids. Eight of the 10 eyes were receiving topical steroids at the time of presentation. The average time of presentation was 17 days after LASIK (range, 7-34). Elevated intraocular pressure was noted on average 28 days after presentation (range, 8-69). Lamellar inflammation was exacerbated by topical steroids. Resolution of the interface inflammation did not occur until intraocular pressure was controlled. CONCLUSIONS: This case series describes a clinically distinct form of interface inflammation that presents late and is associated with elevated intraocular pressure. The lamellar inflammation was refractory to topical steroids and only resolved when pressure was controlled. These findings suggest that elevated intraocular pressure can contribute to interface inflammation. Postoperative assessment of intraocular pressure is essential in patients presenting with flap inflammation.
PURPOSE: Interface inflammation is a common complication of laser in situ keratomileusis (LASIK). The most well-described presentation is diffuse lamellar keratitis (DLK), which typically develops early after LASIK and responds quickly to topical steroids. In this report, we describe a novel presentation of interface inflammation that resembles DLK in appearance but presents late in the postoperative period, is associated with increased intraocular pressure, and is exacerbated by steroid treatment. METHODS: A retrospective case series and chart review of all patients treated in our tertiary care private practice for late-onset interface inflammation associated with elevated intraocular pressure. RESULTS: Ten eyes in 6 patients with late-onset interface inflammation and increased intraocular pressure were identified. At presentation, all patients were presumed to have classic DLK and were treated initially with aggressive topical steroids. Eight of the 10 eyes were receiving topical steroids at the time of presentation. The average time of presentation was 17 days after LASIK (range, 7-34). Elevated intraocular pressure was noted on average 28 days after presentation (range, 8-69). Lamellar inflammation was exacerbated by topical steroids. Resolution of the interface inflammation did not occur until intraocular pressure was controlled. CONCLUSIONS: This case series describes a clinically distinct form of interface inflammation that presents late and is associated with elevated intraocular pressure. The lamellar inflammation was refractory to topical steroids and only resolved when pressure was controlled. These findings suggest that elevated intraocular pressure can contribute to interface inflammation. Postoperative assessment of intraocular pressure is essential in patients presenting with flap inflammation.