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Arch Ophthalmol. 2005;123:1604-1607.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Keratectasia, an acquired, noninflammatory, outward bulging of the cornea, is associated with a progressive myopic shift in refraction, irregular astigmatism, corneal thinning, and scarring. It generally occurs in the thinnest portions of the cornea, with a central or inferonasal paracentral predilection; however, it may occur elsewhere. Ocular surgical procedures, particularly lamellar refractive surgery (eg, laser-assisted in situ keratomileusis [LASIK]), have been known to induce corneal ectasia. Because the flap produced by LASIK never completely heals, the residual bed likely provides most of the support to maintain corneal shape and function, and keratectasia occurs when the residual bed is unable to provide this support. The 2 main risk factors for post-LASIK keratectasia are a residual corneal bed of 250 µm or less¹ and keratoconus.²

Although post-LASIK corneal ectasia may be managed conservatively with rigid gas-permeable lenses, this nonsurgical treatment option may fail or may represent an unacceptable alternative for patients who . . . [Full Text of this Article]

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AUTHOR INFORMATION
Marc J. Spirn, MD; Daniel G. Dawson, MD; Roy S. Rubinfeld, MD; Christine Burris, OD; Jonathan Talamo, MD; Henry F. Edelhauser, PhD; Hans E. Grossniklaus, MD