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A pocket of fluid developing in the lamellar interface is a new complication that has previously been described in patients with steroid-induced intraocular hypertension after laser in situ keratomileusis (LASIK). The first case of interface fluid collection following LASIK was reported in 1999. Steroid-induced intraocular pressure (IOP) elevation and epithelial ingrowth were notable features in this case.1 Subsequently, more cases of interface fluid and steroid-induced elevation of IOP have been reported.2-5 The pathophysiologic mechanism behind the fluid collection in these cases is presumably the high IOP, which causes diffusion of aqueous humor across the endothelium into the interface, creating a fluid pocket in the lamellar interface. Clinically, this is usually associated with a fluid pocket visible on slitlamp examination in the lamellar interface, decreased visual acuity, a myopic shift in refraction, the presence of microcystic epithelial edema peripheral to the lamellar flap, an increase in central corneal thickness, steepening of corneal topography, and paradoxical hypotony when measuring IOP over the area of the fluid. It usually resolves by treating the high IOP. We report a case of lamellar interface fluid caused by graft failure from endothelial decompensation, without any evidence of intraocular hypertension. To our knowledge, this is the first histopathologic demonstration of a pocket of fluid in the lamellar interface and the first such case caused by endothelial decompensation.
Dawson DG, Hardten DR, Albert DM. Pocket of Fluid in the Lamellar Interface After Penetrating Keratoplasty and Laser In Situ Keratomileusis. Arch Ophthalmol. 2003;121(6):894–896. doi:10.1001/archopht.121.6.894
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