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Purpose: To evaluate the effects of corneal edema on human donor corneas that had previous LASIK using a laboratory model with histologic and ultrastructural correlations., Design: Experimental study., Participants: Thirty human eye bank corneas from 15 donors (mean age +/- standard deviation, 49.9+/-8.9 years) who had had previous LASIK surgery (2-8 years before death)., Methods: The corneas were mounted in an artificial anterior chamber and the corneal endothelium was perfused for up to 5.0 hours with 0.9% saline solution (endothelial cell damage group) or BSS Plus at a pressure of 15 mmHg (control group), or BSS Plus at a pressure of 55 mmHg (high-pressure group). The corneas were evaluated by confocal and specular microscopy before, during, and at the end of the experimental period. Subsequently, the specimens were evaluated by light and electron microscopy., Main Outcome Measures: Corneal thickness, reflectivity, histology, and ultrastructure., Results: Endothelial cell damage resulted in an increased (141.5+/-38.8 microm) total corneal thickness relative to controls (52.3+/-33.7 microm), whereas high pressure resulted in a decreased thickness (24.8+/-14.1 microm) relative to controls. This ultimately was due to swelling of the LASIK interface in both groups and swelling of the residual stromal bed (RSB) in the endothelial cell damage group or compression of the RSB and, possibly, the flap in the high-pressure group. A significant increase in corneal reflectivity at the LASIK interface occurred in both groups, primarily due to varying degrees of fluid accumulation and associated hydropic keratocyte degeneration, as well as increased corneal reflectivity in the RSB only in the endothelial cell damage group., Conclusions: After LASIK surgery, edematous corneas preferentially hydrate and swell in the paracentral and central interface wound, commonly resulting in a hazy corneal appearance primarily due to keratocyte hydropic degeneration. More severe corneal edema is characterized by the formation of an optically empty space corresponding to an interface fluid pocket. The spectrum of interface fluid syndrome can be described in 3 stages.

Purpose: To report two cases of corneal pathology associated with anterior uveitis after laser in situ keratomileusis (LASIK)., Design: Observational case report., Methods: A 47-year-old man and a 50-year-old woman who experienced vision loss and corneal changes associated with acute anterior uveitis after LASIK were examined., Results: The 47-year-old man, who had undergone LASIK for low myopia developed an interlamellar fluid pocket at the level of the flap interface, whereas the 50-year-old woman, who underwent LASIK for hyperopia, developed marked flap edema without interface fluid collection., Conclusions: These two cases demonstrated acute corneal fluid accumulation associated with episodes of acute anterior uveitis in eyes that had undergone LASIK. Uveitis should be considered a risk factor for vision threatening corneal complications after LASIK.

A 41-year-old man with myopic astigmatism had laser in situ keratomileusis (LASIK) in each eye in April 2002. Ten months later, he sustained a central perforating corneal injury to the right eye. One day following repair of the corneal wound, he presented with diffuse corneal epithelial microcystic edema, lamellar interface fluid accumulation, and 20/400 visual acuity. Additional sutures were placed to close a presumed posterior wound gape with complete resolution of the corneal edema and lamellar interface fluid collection. One year later, his best corrected visual acuity measured 20/20+ in the right eye. This case is the first to document lamellar interface fluid accumulation following LASIK owing to traumatic disruption of the corneal endothelium.

Purpose: To describe a case of interface fluid after laser in situ keratomileusis (LASIK) and review the literature on this rare complication after LASIK., Methods: We present a case report and literature review. Articles for this review were chosen from electronic database and manual literature searches. MEDLINE searches were made from 1990 to April 2002, using the key words "interface fluid" and "LASIK.", Results: A 40-year-old man had uneventful LASIK for residual refractive error from previous penetrating keratoplasty in his right eye. Diffuse lamellar keratitis began 1 day postoperatively. Topical corticosteroids were administered. Six weeks after LASIK, a layer of interface fluid developed. Intraocular pressure was 9 mmHg when measured centrally by Goldmann applanation tonometry and 30 mmHg by Tono-pen tonometry. The interface fluid resolved with antiglaucoma agents and corticosteroids combined with cyclosporine., Conclusions: This case, along with other reported cases, demonstrate the clinical features of interface fluid after LASIK.

Purpose: To report a new complication of interface fluid accumulation and corneal edema in an uneventful laser in situ keratomileusis (LASIK) procedure., Methods: Uncomplicated bilateral LASIK for myopia using the Hansatome microkeratome was performed. One day postoperatively, the patient noted decreased visual acuity. The topical corticosteroid was changed from dexamethasone to prednisolone acetate 1% every 2 hours. Two weeks later the patient reported worsening visual acuity in both eyes. Uncorrected visual acuity was 20/200 in the right eye and 20/100 in the left. Slit-lamp biomicroscopy indicated significant fluid build-up in the interface. Intraocular pressure (IOP) by Goldmann applanation tonometry was 15 mmHg in the right eye and 14 mmHg in the left., Results: After 4 weeks, intraocular pressure by bidigital pressure was increased and high. The corticosteroid was discontinued and antiglaucoma medication lowered the intraocular pressure, which resulted in corneal clearing and disappearence of interface fluid in both eyes., Conclusions: Early recognition of this new complication of LASIK is necessary. The falsely low reading of IOP in the setting of interface fluid was the result of easy compressibility of the fluid-filled space and reflects the pressure of the interface fluid. This apparently low IOP reading can be an additional sign of the existence of interface fluid. The corticosteroid should be discontinued and antiglaucoma medication instituted. This should lead to a lowering of intraocular pressure and result in corneal clearing and disappearence of the interface fluid with improvement in visual acuity.