May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Post–LASIK Interface Fluid Syndrome: Possible Pathogenesis and Causes Evaluated in a Laboratory Model
Author Affiliations & Notes
  • I. Schmack
    Ophthalmology, Emory Univ Eye Clinic, Atlanta, GA
    Ophthalmology, Ruprecht–Karls–University, Heidelberg, Germany
  • D.G. Dawson
    Ophthalmology, Emory Univ Eye Clinic, Atlanta, GA
  • G.P. Holley
    Ophthalmology, Emory Univ Eye Clinic, Atlanta, GA
  • H.E. Grossniklaus
    Ophthalmology, Emory Univ Eye Clinic, Atlanta, GA
  • H.F. Edelhauser
    Ophthalmology, Emory Univ Eye Clinic, Atlanta, GA
  • Footnotes
    Commercial Relationships  I. Schmack, None; D.G. Dawson, None; G.P. Holley, None; H.E. Grossniklaus, None; H.F. Edelhauser, None.
  • Footnotes
    Support  NIH Grants EY000933, P30–EY06360, T3–EY07092
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 2735. doi:
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      I. Schmack, D.G. Dawson, G.P. Holley, H.E. Grossniklaus, H.F. Edelhauser; Post–LASIK Interface Fluid Syndrome: Possible Pathogenesis and Causes Evaluated in a Laboratory Model . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2735.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : To examine the effects of corneal endothelial cell damage and elevated pressure on human LASIK corneas in a laboratory–induced model using confocal, light, and electron microscopy.

Methods: : Thirty Optisol–GS stored human eye bank LASIK corneas (range 2–8 yrs post–op) from 15 donors (mean±SD: 48.9±10.7; range 30 – 61 yrs) were perfused for up to 5 hrs with 0.9% NaCl (endothelial cell damage group) or BSS Plus (control group) at an intraocular pressure of 15 mm Hg, or with BSS Plus at an intraocular pressure of 55 mm Hg (pressure group) using an endothelial perfusion specular microscope. Corneal thickness measurements were taken throughout the experiment. The corneas were examined by ex–vivo confocal microscopy and submitted for histopathologic and ultrastructural evaluation.

Results: : All corneal specimens (test and control groups) demonstrated an increase in corneal thickness after 5 hours of perfusion due to various degrees of stromal edema. The increase in corneal thickness was more pronounced in the endothelial cell damage group (mean±SD: 147.5±37.3 µm) compared to the pressure group (mean±SD: 22.3±14.7 µm) and control group (mean±SD: 54.5±33.8 µm). Corneal edema occurred either at the central and paracentral areas of the hypocellular primitive LASIK interface scar and residual stromal bed (endothelial cell damage and control group) or predominantly only at the LASIK interface (high pressure group). No significant structural changes were observed in the LASIK flap and at the flap margin. A staging system (I–mild, II–moderate, III–severe) was developed to demonstrate the severity of interface fluid syndrome resulting from different degrees of corneal edema.

Conclusions: : Our laboratory model suggests that the central and paracentral hypocellular primitive stromal interface scar of human LASIK corneas preferentially hydrates and swells when the corneas become edematous. Endothelial cell damage affects the full–thickness of the LASIK cornea, whereas elevated pressure appears to affect primarily only the interface scar. Knowing the different stages of interface fluid syndrome should help clinicians in diagnosing this condition earlier and more accurately.

Keywords: wound healing • cornea: basic science • refractive surgery: complications 

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