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March 1982

Corneal Xerophthalmia and Keratomalacia

Author Affiliations

From the International Center for Epidemiologic and Preventive Ophthalmology, Wilmer Ophthalmological Institute, The Johns Hopkins Medical Institutions, Baltimore, and Helen Keller International, New York (Dr Sommer); and the Nutritional Blindness Prevention Project, Bandung, Indonesia (Drs Sommer and Sugana).

Arch Ophthalmol. 1982;100(3):404-411. doi:10.1001/archopht.1982.01030030406003

• Detailed examinations were conducted on 162 consecutive children with nutritional keratopathy. Surface changes ranged from mild haziness through generalized xerosis and formation of thickened keratinized plaques. Diffuse stromal edema occurred early in the disease. Stromal loss took two forms: relatively small, sharply demarcated, eccentric, noninfiltrated cylindrical ulcers of varying depth; and localized or generalized, usually full-thickness necrosis. All forms of involvement were sometimes present in the same individual or even the same eye. Traumatic separation of a keratinized plaque, or decompensation of a dellen, accounted for some instances of stromal baring. In other cases, stromal melting appeared to progress below an intact epithelium. Focal areas of necrosis healed rapidly, as adherent leukomas; larger lesions sloughed, forming extensive descemetoceles. With therapy, the vast majority of children retained central corneal clarity.

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