OBJECTIVE: To report a case with late-onset interface inflammation associated with traumatic flap injury at 7 months after laser in situ keratomileusis (LASIK) and to describe the type of infiltrating cells in the tears of the patient. METHODS: Interventional case report. A 24-year-old male patient who underwent uneventful LASIK on both eyes received blunt trauma from the tip of a shoe in the left eye 7 months after surgery. The corneal flap of his left eye was lacerated across the pupillary area. Inflammatory cells were observed under the lacerated flap segment. Tear fluid was collected from his left eye 3 days after the injury and assessed by tear cytology. For controls, tears of 2 patients who underwent LASIK and developed no interface inflammation were collected the next day after their surgeries and examined. RESULTS: Tear fluid of the patient with interface inflammation contained numerous neutrophils. Tears of control patients contained only a few epithelial cells and cell debris but no inflammatory cells. The inflammation was decreased by systemic and topical steroids. However, irregular astigmatism caused by stromal scarring remained, resulting in decreased best-corrected visual acuity. CONCLUSIONS: Interface inflammation can be caused by late-onset flap injury. Neutrophils detected in the tears may reflect a major component of cells infiltrating the interface after LASIK.
OBJECTIVE: To report a case with late-onset interface inflammation associated with traumatic flap injury at 7 months after laser in situ keratomileusis (LASIK) and to describe the type of infiltrating cells in the tears of the patient. METHODS: Interventional case report. A 24-year-old male patient who underwent uneventful LASIK on both eyes received blunt trauma from the tip of a shoe in the left eye 7 months after surgery. The corneal flap of his left eye was lacerated across the pupillary area. Inflammatory cells were observed under the lacerated flap segment. Tear fluid was collected from his left eye 3 days after the injury and assessed by tear cytology. For controls, tears of 2 patients who underwent LASIK and developed no interface inflammation were collected the next day after their surgeries and examined. RESULTS: Tear fluid of the patient with interface inflammation contained numerous neutrophils. Tears of control patients contained only a few epithelial cells and cell debris but no inflammatory cells. The inflammation was decreased by systemic and topical steroids. However, irregular astigmatism caused by stromal scarring remained, resulting in decreased best-corrected visual acuity. CONCLUSIONS: Interface inflammation can be caused by late-onset flap injury. Neutrophils detected in the tears may reflect a major component of cells infiltrating the interface after LASIK.
Authors: Timothy D Blalock; Sandra J Spurr-Michaud; Ann S Tisdale; Ilene K Gipson Journal: Invest Ophthalmol Vis Sci Date: 2008-05 Impact factor: 4.799