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Germán A. Rocha, MD; Arantxa Acera, DSc; Juan A. Durán, MD

Arch Ophthalmol. 2007;125(10):1423-1425.

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

Laser in situ keratomileusis (LASIK) surgery can induce changes in the corneal epithelium owing to a neurotrophic phenomenon as a consequence of the sectioning of nerves during flap cutting.¹ More profound alterations have been reported with a superior hinge, compared with a nasal hinge, and the associated effects tend to normalize over approximately 6 months,² although it is possible that complete reinnervation and recovery of the basal state may not occur.³ Epithelial damage has also been associated with a reduced blinking rate, which favors corneal exposition.⁴

To date, various cases of post-LASIK neurotrophic epitheliopathy have been reported, characterized by symptoms and signs of dry eye and a spotted distribution of rose bengal dye. Recommended treatments include artificial tears, tear plug, and autologous serum,⁵ among others. Herein, we report a case of severe corneal flap necrosis that occurred after formation . . . [Full Text of this Article]

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