Imaging interface fluid after laser in situ keratomileusis with corneal optical coherence tomography

Abstract

A 41-year-old myopic patient who had laser in situ keratomileusis 6 months earlier was treated for a complete retinal detachment (RD) with proliferative vitreoretinopathy. Surgical treatment consisted of an encircling band, pars plana vitrectomy, and silicone oil filling. Postoperatively, the patient developed marked corneal edema with no increase in intraocular pressure (IOP) as measured by applanation tonometry. Interface fluid was confirmed by corneal optical coherence tomography. Quantification of the corneal structures revealed that corneal edema was in the residual posterior stroma predominantly. The epithelial and flap thickness did not change significantly. The case demonstrated that after vitreoretinal surgery for RD repair, transient corneal endothelial cell dysfunction developed, causing marked edema of the posterior corneal stroma and interface fluid accumulation. However, an increase in IOP cannot be excluded.

Interface Fluid Syndrome Induced by Uncontrolled Intraocular Pressure Without Triggering Factors After LASIK in a Glaucoma Patient

“…IFS, which is associated with inaccurately low measurements of central IOP 1 – 3 , 5 – 8 because of cushioning of the fluid-filled pocket, 5 can result from increased IOP secondary to postoperative steroid use 1 – 6 , 10 or corneal endothelial dysfunction after vitreous surgery 7 , 8 or trabeculectomy. 9 A study of human eye bank corneas reported 2 mechanisms of IFS: increased IOP (the high-IOP form of IFS) and corneal endothelial dysfunction (the endothelial cell damage form of IFS).…”

“…Reports have described IFS cases resulting from increased IOP secondary to postoperative steroid administration 1 – 6 , 10 or to corneal endothelial dysfunction triggered by scleral buckling surgery for retinal detachment, 7 , 8 a shallow anterior chamber after trabeculectomy, 9 or uveitis. 11 To our knowledge, no reports have described the development of IFS because of uncontrolled IOP after LASIK during glaucoma management in the absence of these triggering factors.…”

Interface Fluid Syndrome (IFS) following Toxic Anterior Segment Syndrome (TASS): not related to high intraocular pressure but to endothelial failure

“…They confirmed that the condition had a spectrum of manifestations classified in 3 stages which include interface swelling, stromal haze [condition also known as Pressure Induced Interlamellar Stromal Keratitis (PISK)] and finally interface fluid deposition [2], [3]. Based on the experimental study of Dawson et al, and since some cases of both IFS and PISK had been reported without the presence of high IOP in 2012 Galvis et al proposed the name Post LASIK edema-induced keratopathy (PLEK) to the condition, in order to exclude the words “pressure induced”, as evidently this is not the etiology in all cases [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17]. Recently Luceri et al and Shajari et al reported the first two cases of Descemet Membrane Endothelial Keratoplasty (DMEK) performed to solve and IFS secondary to corneal edema in two patients with Fuchs endothelial dystrophy who developed corneal edema after phacoemulsification without an increase in IOP [16], [17]…”

Misleading Goldmann applanation tonometry in a post-LASIK eye with interface fluid syndrome

“…Interface fluid accumulation and posterior stromal edema after RD surgery has been reported due to transient endothelial decompensation in the immediate postoperative period. [6]…”

“…Temporary or permanent corneal endothelial cell dysfunction can lead to IFS. [6] When the corneal endothelium is damaged, aqueous humor typically diffuses into the corneal stroma resulting in corneal swelling predominantly in the posterior two-thirds of the corneal stroma, and diffusion of fluid into the interface creates a fluid pocket in the lamellar interface. The high-resolution images provided by the cornea anterior segment module of the Fourier domain OCT can be useful in visualizing the exact location, extent and height of fluid collection, epithelial ingrowth and noncellular reflective deposits which cannot be differentiated clinically.…”