Interface Fluid Syndrome in Human Eye Bank Corneas after LASIK: Causes and Pathogenesis
Presented at: American Academy of Ophthalmology Annual Meeting, October 2005, Chicago, Illinois.
Received 17 October 2006; received in revised form 6 January 2007; accepted 9 January 2007.
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 μm) total corneal thickness relative to controls (52.3±33.7 μm), whereas high pressure resulted in a decreased thickness (24.8±14.1 μm) 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.
1Emory Eye Center, Emory University School of Medicine, Atlanta, Georgia.
2Bascom Palmer Eye Institute, University of Miami School of Medicine, Miami, Florida.
3Department of Ophthalmology, Ruprecht-Karls-University, Heidelberg, Germany.
Correspondence and reprint requests to Henry F. Edelhauser, PhD, Emory Eye Center, 1365-B Clifton Road, NE, Atlanta, GA 30322.
Manuscript no. 2006-1170.
Supported in part by the National Eye Institute, Bethesda, Maryland (grant nos. EY-00933, P30-EY06360, T32-EY07092); Research to Prevent Blindness, New York, New York (unrestricted departmental grant); and Gertrud-Kusen Foundation, Hamburg, Germany (grant no. Sch-05/06).
The authors have no financial or proprietary interest in any products mentioned in the article.
1 Drs Dawson and Schmack contributed equally to the work.
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