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A 53-year-old male was referred for evaluation of a nonhealing corneal ulcer. He had not received medical care in 20 years and had no known medical diagnoses, but his social history was notable for consumption of approximately 12 alcoholic beverages per day. His ocular history was notable for left-eye enucleation from recent trauma. He initially presented to his local ophthalmologist with right eye redness, pain, and photophobia for 1 week. He was diagnosed with a corneal ulcer. Bacterial (aerobic and anaerobic) and fungal cultures were obtained, and the patient started receiving topical moxifloxacin. The cultures were negative after 1 week, but the patient did not demonstrate signs of clinical improvement. A complete blood cell count, metabolic panel, and serum test results (for antinuclear antibodies, peripheral antineutrophil cytoplasmic antibodies, cytoplasmic antineutrophil cytoplasmic antibodies, rheumatoid factor, and anti–cyclic citrullinated peptide) were unremarkable. On referral, his visual acuity was 20/100 OD, and his intraocular pressure was 16 mm Hg. Anterior examination revealed a diffusely hazy cornea with a blunted light reflex. A large, well-demarcated epithelial defect with substantial underlying stromal loss was seen in the inferonasal periphery (Figure). The stroma was 40% thinned without infiltrate. The epithelium was heaped up along the lesion borders. Corneal sensation was diminished. The conjunctiva demonstrated hyperemia, which was more prominent around the corneal lesion, although there was no discharge. A dilated ophthalmoscopic examination was unremarkable. Repeated bacterial and fungal cultures were obtained.
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D. Obtain serum vitamin A levels
The patient was sent to the emergency department for serum vitamin A testing (choice D), which revealed undetectable vitamin A levels (normal range, 30-80 μg/dL; to convert to micromoles per liter, multiply by 0.0349). The differential diagnosis for a nonhealing corneal ulcer may include inadequate antibiotic coverage, a nonbacterial infectious source, systemic autoimmune conditions, and epithelial wound-healing deficits.
The patient’s history and presentation is consistent with vitamin A deficiency–associated keratomalacia. Patients with alcoholism may have protein and vitamin deficiencies, including vitamin A,1 because of both low dietary intake and decreased absorption. Nyctalopia is often the initial finding in vitamin A deficiency,2 although it was not present in this case. Vitamin A deficiency may also lead to ocular surface disease, such as conjunctival and corneal xerosis, and diffuse or focal keratin accumulation with a foamy appearance (Bitôt spots). There is a lack of mucin because goblet cells in the mucosal surface are greatly reduced.3 In advanced stages, keratomalacia may develop, with severe corneal ulceration and thinning, and this may ultimately result in diffuse corneal necrosis.
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Corresponding Author: Daniel J. Oh, MD, 1855 W Taylor St, Ste 1.145 (MC 648), Chicago, IL 60612 (email@example.com).
Published Online: March 14, 2019. doi:10.1001/jamaophthalmol.2019.0115
Conflict of Interest Disclosures: None reported.
Additional Contributions: We thank the patient for granting permission to publish this information.
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