Confocal assessment of the corneal response to intracorneal lens insertion and laser in situ keratomileusis with flap creation using IntraLase

W. Matthew Petroll, Damien Goldberg, Sara S. Lindsey, Patrick S. Kelley, H. Dwight Cavanagh, R. Wayne Bowman, Dipak N. Parmar, Steven M. Verity, James P. McCulley

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Abstract

Purpose: To assess the response of the cornea to hydrogel intracorneal lens (ICL) insertion or laser in situ keratomileusis (LASIK) with IntraLase (IntraLase Corp.) at the cellular level. Setting: Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Methods: Twenty patients (29 eyes) were evaluated by in vivo confocal microscopy 1 to 6 months postoperatively: 20 eyes had LASIK with flap creation by IntraLase, and 9 eyes had ICL insertion (8 following IntraLase). Results: For LASIK with IntraLase, keratocyte activation and/or interface haze was detected in 8 of 20 eyes. The remaining eyes had interface particles but no cell activation. Keratocyte activation was generally limited to a few cell layers adjacent to the interface. However, 2 patients exhibited multiple layers of activation and increased extracellular matrix (ECM) reflectivity (haze) surrounding the interface by confocal microscopy. Both patients also had clinical haze and photophobia. For ICLs, following insertion, 5 of 9 eyes had activated keratocytes adjacent to the implant surfaces. The largest amount of cell activation and ECM haze detected by confocal microscopy was in 2 patients with significant clinical haze. Structures with an epithelioid morphology were detected on some implant surfaces. Epithelial thickness was 33.3 μm ± 2.3 (SD) in the ICL eyes and 49.2 ± 6.5 μm in the LASIK with IntraLase eyes. Conclusions: Both LASIK with IntraLase and ICL insertion following IntraLase induced keratocyte activation, which may underlie clinical observations of haze in some patients. Intracorneal lens implant also induced thinning of the overlying corneal epithelium.

Original languageEnglish (US)
Pages (from-to)1119-1128
Number of pages10
JournalJournal of Cataract and Refractive Surgery
Volume32
Issue number7
DOIs
StatePublished - Jul 2006

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Laser In Situ Keratomileusis
Lenses
Confocal Microscopy
Extracellular Matrix
Photophobia
Corneal Epithelium
Crystalline Lens
Hydrogel
Ophthalmology
Cornea

ASJC Scopus subject areas

  • Ophthalmology

Cite this

@article{23db0da2e5ea4f72ba3df316efbc23b0,
title = "Confocal assessment of the corneal response to intracorneal lens insertion and laser in situ keratomileusis with flap creation using IntraLase",
abstract = "Purpose: To assess the response of the cornea to hydrogel intracorneal lens (ICL) insertion or laser in situ keratomileusis (LASIK) with IntraLase (IntraLase Corp.) at the cellular level. Setting: Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Methods: Twenty patients (29 eyes) were evaluated by in vivo confocal microscopy 1 to 6 months postoperatively: 20 eyes had LASIK with flap creation by IntraLase, and 9 eyes had ICL insertion (8 following IntraLase). Results: For LASIK with IntraLase, keratocyte activation and/or interface haze was detected in 8 of 20 eyes. The remaining eyes had interface particles but no cell activation. Keratocyte activation was generally limited to a few cell layers adjacent to the interface. However, 2 patients exhibited multiple layers of activation and increased extracellular matrix (ECM) reflectivity (haze) surrounding the interface by confocal microscopy. Both patients also had clinical haze and photophobia. For ICLs, following insertion, 5 of 9 eyes had activated keratocytes adjacent to the implant surfaces. The largest amount of cell activation and ECM haze detected by confocal microscopy was in 2 patients with significant clinical haze. Structures with an epithelioid morphology were detected on some implant surfaces. Epithelial thickness was 33.3 μm ± 2.3 (SD) in the ICL eyes and 49.2 ± 6.5 μm in the LASIK with IntraLase eyes. Conclusions: Both LASIK with IntraLase and ICL insertion following IntraLase induced keratocyte activation, which may underlie clinical observations of haze in some patients. Intracorneal lens implant also induced thinning of the overlying corneal epithelium.",
author = "Petroll, {W. Matthew} and Damien Goldberg and Lindsey, {Sara S.} and Kelley, {Patrick S.} and Cavanagh, {H. Dwight} and Bowman, {R. Wayne} and Parmar, {Dipak N.} and Verity, {Steven M.} and McCulley, {James P.}",
year = "2006",
month = "7",
doi = "10.1016/j.jcrs.2006.01.093",
language = "English (US)",
volume = "32",
pages = "1119--1128",
journal = "Journal of Cataract and Refractive Surgery",
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}

TY - JOUR

T1 - Confocal assessment of the corneal response to intracorneal lens insertion and laser in situ keratomileusis with flap creation using IntraLase

AU - Petroll, W. Matthew

AU - Goldberg, Damien

AU - Lindsey, Sara S.

AU - Kelley, Patrick S.

AU - Cavanagh, H. Dwight

AU - Bowman, R. Wayne

AU - Parmar, Dipak N.

AU - Verity, Steven M.

AU - McCulley, James P.

PY - 2006/7

Y1 - 2006/7

N2 - Purpose: To assess the response of the cornea to hydrogel intracorneal lens (ICL) insertion or laser in situ keratomileusis (LASIK) with IntraLase (IntraLase Corp.) at the cellular level. Setting: Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Methods: Twenty patients (29 eyes) were evaluated by in vivo confocal microscopy 1 to 6 months postoperatively: 20 eyes had LASIK with flap creation by IntraLase, and 9 eyes had ICL insertion (8 following IntraLase). Results: For LASIK with IntraLase, keratocyte activation and/or interface haze was detected in 8 of 20 eyes. The remaining eyes had interface particles but no cell activation. Keratocyte activation was generally limited to a few cell layers adjacent to the interface. However, 2 patients exhibited multiple layers of activation and increased extracellular matrix (ECM) reflectivity (haze) surrounding the interface by confocal microscopy. Both patients also had clinical haze and photophobia. For ICLs, following insertion, 5 of 9 eyes had activated keratocytes adjacent to the implant surfaces. The largest amount of cell activation and ECM haze detected by confocal microscopy was in 2 patients with significant clinical haze. Structures with an epithelioid morphology were detected on some implant surfaces. Epithelial thickness was 33.3 μm ± 2.3 (SD) in the ICL eyes and 49.2 ± 6.5 μm in the LASIK with IntraLase eyes. Conclusions: Both LASIK with IntraLase and ICL insertion following IntraLase induced keratocyte activation, which may underlie clinical observations of haze in some patients. Intracorneal lens implant also induced thinning of the overlying corneal epithelium.

AB - Purpose: To assess the response of the cornea to hydrogel intracorneal lens (ICL) insertion or laser in situ keratomileusis (LASIK) with IntraLase (IntraLase Corp.) at the cellular level. Setting: Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas, USA. Methods: Twenty patients (29 eyes) were evaluated by in vivo confocal microscopy 1 to 6 months postoperatively: 20 eyes had LASIK with flap creation by IntraLase, and 9 eyes had ICL insertion (8 following IntraLase). Results: For LASIK with IntraLase, keratocyte activation and/or interface haze was detected in 8 of 20 eyes. The remaining eyes had interface particles but no cell activation. Keratocyte activation was generally limited to a few cell layers adjacent to the interface. However, 2 patients exhibited multiple layers of activation and increased extracellular matrix (ECM) reflectivity (haze) surrounding the interface by confocal microscopy. Both patients also had clinical haze and photophobia. For ICLs, following insertion, 5 of 9 eyes had activated keratocytes adjacent to the implant surfaces. The largest amount of cell activation and ECM haze detected by confocal microscopy was in 2 patients with significant clinical haze. Structures with an epithelioid morphology were detected on some implant surfaces. Epithelial thickness was 33.3 μm ± 2.3 (SD) in the ICL eyes and 49.2 ± 6.5 μm in the LASIK with IntraLase eyes. Conclusions: Both LASIK with IntraLase and ICL insertion following IntraLase induced keratocyte activation, which may underlie clinical observations of haze in some patients. Intracorneal lens implant also induced thinning of the overlying corneal epithelium.

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