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N. E. Knox Cartwright, J. R. Tyrer, J. Marshall; Keratectasia Demystified: An Evidence-based Model Of The Corneal Response To Refractive Surgery.. Invest. Ophthalmol. Vis. Sci. 2008;49(13):662. doi: https://doi.org/.
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Despite an estimated 30 million keratorefractive surgical procedures having been performed the risk factors for post-operative keratectasia remain disputed. Not only is this because the mechanical properties of the cornea are poorly understood but it is also due to the fact that current models of the response to surgery are unable to integrate both the normal and ectatic response. By quantitatively analysing the corneal response to surgery this study aims to address these points.
A 60 kHz femtosecond laser was used to create 90 and 160 µm lamellar flap, circular trephine and tangential delamination incisions in organ cultured human corneas. Strain was measured before, immediately following and one week after surgery using a radial shearing speckle interferometer.
Flap creation resulted in an increase in corneal strain in both the central and peripheral cornea (p<0.05). A similar magnitude of strain increase was associated with side-cut creation but subsurface delamination did not cause significant strain change. The magnitude of strain increase correlated positively with vertical incision depth and did not recover during wound healing. Compared to 90 µm depth flaps, 160 µm flaps resulted in significantly less strain increase (10 % versus 33 %, p<0.05).
Central corneal elasticity increases following lamellar flap creation challenging the belief that the central corneal flattening associated with LASIK flap creation reflects the primary mechanical response of the cornea. Further analysis shows that the outwards force conjectured to cause this flattening is a mechanical impossibility. Instead it is suggested that the mechanical response of all corneas to keratorefractive surgery is steepening but that changes in stromal hydration result in the flattening and hyperopic shift seen clinically. It is argued that keratectasia develops when creep and fatigue damage caused by the intraocular pressure and its pulse accumulate more rapidly than can be repaired. Individual susceptibility is determined by genetic, mechanical, structural and cellular factors. It is shown that this model can resolve many of the enigmas and apparent paradoxes surrounding ectasia development including the regression of ectasia manifest as keratometric flattening seen following corneal collagen cross linking treatment.
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