Biomechanics of corneal ectasia and biomechanical treatments

Abstract

Many algorithms exist for the topographic/tomographic detection of corneas at risk for post-refractive surgery ectasia. It is proposed that the reason for the difficulty in finding a universal screening tool based on corneal morphologic features is that curvature, elevation, and pachymetric changes are all secondary signs of keratoconus and post-refractive surgery ectasia and that the primary abnormality is in the biomechanical properties. It is further proposed that the biomechanical modification is focal in nature, rather than a uniform generalized weakening, and that the focal reduction in elastic modulus precipitates a cycle of biomechanical decompensation that is driven by asymmetry in the biomechanical properties. This initiates a repeating cycle of increased strain, stress redistribution, and subsequent focal steepening and thinning. Various interventions are described in terms of how this cycle of biomechanical decompensation is interrupted, such as intrastromal corneal ring segments, which redistribute the corneal stress, and collagen crosslinking, which modifies the basic structural properties.

Financial disclosures: Proprietary or commercial disclosures are listed after the references.

Figure 1

Stress (σ) on the y-axis is defined as force over cross-sectional area and strain (ε) on the x-axis is defined as percent change in length. A constant stress horizontal dashed line is shown. A higher elastic modulus material (black) will have less strain or less deformation than a lower elastic modulus material (red) at the same stress, as shown by the vertical dashed lines.

Figure 2

Cornea with a focally weak area of lower elastic modulus (red) surrounded by areas of higher elastic modulus (black) will strain to a greater extent when placed under the same intraocular pressure load. Greater deformation occurs in the weaker region, which is exaggerated for illustration.

Figure 3

Proposed schematic for a biomechanical cycle of decompensation in ectasia. The cycle is initiated by asymmetry in the distribution of biomechanical properties, which causes the cornea to thin, which causes an increase in stress, which causes the cornea to deform or redistribute curvature in a compensatory fashion.

Figure 4

Example of mesh from a 3-dimensional whole-eye finite element model that has been modified to evaluate progression in keratoconus.

Figure 5

Finite element model-generated tangential curvature maps of the anterior corneal surface of the less affected eye of an asymmetric keratoconus patient after elastic modulus reductions of (A) 10%, (B) 30%, and (C) 45%. D to F: Associated tangential curvature difference maps for each elastic modulus decrement (Reprinted with permission of Investigative Ophthalmology & Visual Science)

Figure 6

A: Modified artificial anterior chamber to hold 8 mm corneal button with 6 mm of exposed tissue. B: Preoperative topographic mires measured with Keratron. C: Topographic mires of thawed keratoconic button of same patient in mount for cone localization with pressure of 10 mm Hg measured with a Keratron Scout.

Figure 7

Axial stretch ratio under a change in pressure of 10 mm Hg. The tissue above the label A was identified as the cone on the Keratron scout and the optical coherence tomography images. Portions of the stroma and tissue with low cross-correlation coefficients are not shown. The cone demonstrates the highest concentration of strain and the lowest resistance to deformation.