PURPOSE: To describe interface corneal edema secondary to steroid-induced elevation of intraocular pressure (IOP) following LASIK. METHODS: Retrospective observational case series. Diffuse interface edema secondary to steroid-induced elevation of IOP was observed after LASIK simulating diffuse lamellar keratitis (DLK) in 13 eyes. Mean patient age was 31.4 +/- 5.3 years. Patients were divided into two groups according to provisional misdiagnosis: DLK group (group 1) comprised 11 eyes and infection group (group 2) comprised 2 eyes (microbial keratitis). Mean follow-up was 8.1 +/- 0.5 weeks. RESULTS: In the DLK group, typical diffuse haze was confined to the interface and extended to the visual axis, impairing vision in all eyes. Provisional diagnosis was late-onset DLK and topical steroids were started. Repeat examination showed elevated IOP as measured at the corneal center and periphery using applanation tonometry (mean 19.1 mmHg and 39.5 mmHg, respectively), causing interface edema with evident interface fluid pockets. Steroids were stopped and topical anti-glaucoma therapy was started. The interface edema decreased and at the end of follow-up the corneal transparency was restored and IOP dropped to normal values. The infection group demonstrated a microbial keratitis-like reaction and underwent flap lifting and interface wound debridement and biopsy with administration of fortified antibiotics and steroids. After elevated IOP was detected, steroids and antibiotics were stopped and topical anti-glaucoma therapy was started, resulting in the resolution of the interface edema. CONCLUSIONS: Interface fluid syndrome secondary to steroid-induced elevation of IOP might develop in steroid responders after LASIK with a misleading clinical picture simulating DLK or infectious keratitis. Management includes stopping topical steroids and starting topical antiglaucoma therapy.
PURPOSE: To describe interface corneal edema secondary to steroid-induced elevation of intraocular pressure (IOP) following LASIK. METHODS: Retrospective observational case series. Diffuse interface edema secondary to steroid-induced elevation of IOP was observed after LASIK simulating diffuse lamellar keratitis (DLK) in 13 eyes. Mean patient age was 31.4 +/- 5.3 years. Patients were divided into two groups according to provisional misdiagnosis: DLK group (group 1) comprised 11 eyes and infection group (group 2) comprised 2 eyes (microbial keratitis). Mean follow-up was 8.1 +/- 0.5 weeks. RESULTS: In the DLK group, typical diffuse haze was confined to the interface and extended to the visual axis, impairing vision in all eyes. Provisional diagnosis was late-onset DLK and topical steroids were started. Repeat examination showed elevated IOP as measured at the corneal center and periphery using applanation tonometry (mean 19.1 mmHg and 39.5 mmHg, respectively), causing interface edema with evident interface fluid pockets. Steroids were stopped and topical anti-glaucoma therapy was started. The interface edema decreased and at the end of follow-up the corneal transparency was restored and IOP dropped to normal values. The infection group demonstrated a microbial keratitis-like reaction and underwent flap lifting and interface wound debridement and biopsy with administration of fortified antibiotics and steroids. After elevated IOP was detected, steroids and antibiotics were stopped and topical anti-glaucoma therapy was started, resulting in the resolution of the interface edema. CONCLUSIONS: Interface fluid syndrome secondary to steroid-induced elevation of IOP might develop in steroid responders after LASIK with a misleading clinical picture simulating DLK or infectious keratitis. Management includes stopping topical steroids and starting topical antiglaucoma therapy.