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Arch Ophthalmol. 2002;120:215-217.

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

Impaired adhesion, migration, and/or mitosis can compromise corneal epithelial healing. Persistent epithelial defects can progress to ulceration, perforation, or endophthalmitis. Currently, our options are limited to methods that address the underlying cause of the epithelial defect. In addition to addressing exposure keratopathy, mechanical irritation to the eye, and systemic diseases, clinicians supplement the tear film, minimize the mechanical aspects of delayed wound healing, and use collagenolytic enzyme inhibitors. Specific therapy includes preservative-free artificial tears, pressure patching, bandage contact lens, and N-acetylcysteine. The more recent use of nerve growth factor,¹ amniotic membrane transplantation,^2-4 and scleral lens² has been reported. Nonsurgical therapeutic options have limited effect, and surgical procedures such as lamellar or penetrating keratoplasty become necessary to preserve the anatomic integrity of the globe. Vision-threatening procedures (Gunderson flap, tarsorrhaphy, evisceration, or enucleation) may also become necessary.

Recently, growth factors,^{1, 5-8} neuropeptides,^5-8 and fibronectin⁶ have promoted epithelial wound healing. Topical substance P . . . [Full Text of this Article]

Report of a Case


Comment
Corresponding author and reprints: Neal P. Barney, MD, Department of Ophthalmology and Visual Sciences, University of Wisconsin, 2870 University Ave, Suite 206, Madison, WI 53705 (e-mail: npbarney@facstaff.wisc.edu).

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