PURPOSE
To investigate the impact of corneal elasticity on
corneal shape changes before and after simulated LASIK with and without
consideration of whole-eye biomechanics.
METHODS
A finite element whole-eye model of a human eye was
constructed. The cornea was modeled as hyperelastic and incompressible using
experimental data representing a range of corneal stiffness. The corneal
response to intraocular pressure loading and LASIK for 2.00, 4.00, and 6.00
diopters of spherical myopia was analyzed as a function of corneal stiffness
and limbal boundary conditions.
RESULTS
Myopic LASIK produced different degrees of central
flattening and postoperative ametropia in low-stiffness and high-stiffness
corneas. Although a cornea-only model demonstrated maximum stresses and
displacements in the central cornea and predicted residual myopia, a whole-eye
model with equivalent corneal stiffness predicted greater paracentral
displacements and less myopic undercorrection. In a whole-eye model with a
stiffer cornea, maximum displacements shifted further toward the limbus,
favoring additional mechanically mediated central flattening and refractive
overcorrection (hyperopia). In postoperative LASIK models thinned by high
myopic corrections, corneal stiffening caused central cornea flattening.
CONCLUSIONS
Differences in the corneoscleral stiffness
relationship affect simulated refractive outcomes after LASIK and may be a
source of individual variation in refractive surgery outcomes. A whole-eye
model allowing limbal motion illustrates a stiffness-dependent biomechanical
balance between central corneal flattening and pre-ectatic weakening of the
corneal apex not demonstrated in previous computational models and provides
insight into under- and overcorrection in myopic LASIK and the previously
unexplained phenomenon of corneal flattening after therapeutic collagen
cross-linking for keratoconus. [J Refract Surg. 2009;25:875-887.]
doi:10.3928/1081597X-20090917-09
AUTHORS
From Cole Eye Institute (Roy, Dupps), and the Department of
Biomedical Engineering, Lerner Research Institute, Cleveland Clinic (Dupps),
Cleveland, Ohio.
Supported in part by grant 1KL2RR024990 from the National
Center for Research Resources (NCRR), a component of the National Institutes of
Health (NIH) and NIH Roadmap for Medical Research, a Cleveland Clinic
Foundation Innovations Grant, and a Research to Prevent Blindness Challenge
Grant to the Department of Ophthalmology, Cleveland Clinic Lerner College of
Medicine and Case Western Reserve University. Dr Dupps is a recipient of a
Research to Prevent Blindness Career Development Award.
The authors have no financial interest in the materials
presented herein.
Correspondence: William J. Dupps, Jr, MD, PhD, Cole Eye
Institute, Cleveland Clinic, 9500 Euclid Ave, i-32, Cleveland, OH 44195. Tel:
219.444.8396; E-mail: bjdupps@sbcglobal.net
Received: June 30, 2008; Accepted: November 20, 2008
Posted online: January 30, 2009
