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A Nonhealing Epithelial Defect in a Patient Experiencing Alcohol Use Disorder

Educational Objective
Based on this clinical scenario and the accompanying image, understand how to arrive at a correct diagnosis.
1 Credit CME

A 50-year-old man with a history of type 2 diabetes, hypertension, heroin use, and alcohol use disorder presented with a new epithelial defect in the setting of a healing right corneal ulcer. Six days prior, he had presented with an inferior stromal infiltrate with an overlying epithelial defect, diffuse corneal edema, and a small hypopyon with no hemorrhage in the anterior chamber (Figure 1A). He also had patchy iris hemorrhages with no transillumination defects and areas of conjunctival ulceration nasally and temporally. He denied contact lens use. Given these findings, a presumed herpes zoster sine herpete1 with secondary bacterial infection was suspected. Treatment with hourly topical vancomycin at 14 mg/mL and tobramycin at 25 mg/mL, as well as 1000 mg of oral valacyclovir 3 times a day, was initiated. Corneal cultures grew Streptococcus pneumonia. He initially responded well with improvement of the stromal infiltrate and overlying epithelial defect. However, on day 6 of treatment, he had a new larger epithelial defect and subepithelial bullae in an adjacent location but no infiltrate. While evaluating the new defect, the patient was also noted to have dull conjunctival reflexes and bulbar conjunctival lesions in both eyes (Figure 1B). Additionally, both eyes had patchy interpalpebral results on lissamine green staining of the conjunctiva and clinically significant punctate epithelial erosions of the cornea with fluorescein staining.

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Nonhealing corneal ulcer because of xerophthalmia

D. Obtain serum vitamin levels.

Further questioning revealed that the patient had been experiencing dysphagia and had a 6.8-kg weight loss recently. Vitamin A serum levels were less than 5 μg/dL (reference range, 38-98 μg/dL; to convert to micromoles per liter, multiply by 0.0349). Conjunctival findings were consistent with Bitot spots (Figure 2), and the cornea bullae were thought to be attributable to herpes zoster sine herpete. A gastroenterology assessment revealed severe esophagitis and chronic pancreatitis secondary to alcohol use. He started receiving oral vitamin A at 10 000 units daily.

Continuing treatment with topical antibiotics (choice A) is not recommended, because the patient no longer had an infiltrate and the new findings occurred with appropriate antibiotic treatment. Nontuberculous mycobacteria, which is cultured with Lowenstein-Jensen media (choice B), can cause nonhealing corneal ulcers; however, this patient did not have risk factors for nontuberculous mycobacteria, such as steroid use, contact lenses, or a history of ocular surgery.2 Sjögren syndrome, which is tested with anti-Ro and anti-La tests (choice C), can cause severe dry eye and corneal ulceration, but it is not associated with Bitot spots.

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Article Information

Corresponding Author: Ariel Chen, MD, Wilmer Eye Institute, Johns Hopkins University School of Medicine, 600 N Wolfe St, Baltimore, MD 21287 (achen113@jhmi.edu).

Published Online: December 30, 2020. doi:10.1001/jamaophthalmol.2020.4651

Conflict of Interest Disclosures: Dr Akpek reported grants from Gore & Associates, the US Department of Defense, and the National Eye Institute and personal fees from CorneaGen, Dompe, EpiTech, FirstString, Novalique, Novartis Pharma AG, Regeneron, and Up-To-Date (royalties), as well as nonfinancial support from the Sjögren’s Syndrome Foundation, outside the submitted work. No other disclosures were reported.

Additional Contributions: We thank the patient for granting permission to publish this information.

References
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2.
Girgis  DO , Karp  CL , Miller  D .  Ocular infections caused by non-tuberculous mycobacteria: update on epidemiology and management.   Clin Exp Ophthalmol. 2012;40(5):467-475. doi:10.1111/j.1442-9071.2011.02679.xPubMedGoogle ScholarCrossref
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World Health Organization. Global prevalence of vitamin A deficiency in populations at risk 1995–2005. Published 2009. Accessed March 19, 2020. https://apps.who.int/iris/bitstream/handle/10665/44110/9789241598019_eng.pdf;jsessionid=5896FF1CB97C08664A7A0431AA729B55?sequence=1
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Stevens  GA , Bennett  JE , Hennocq  Q ,  et al.  Trends and mortality effects of vitamin A deficiency in children in 138 low-income and middle-income countries between 1991 and 2013: a pooled analysis of population-based surveys.   Lancet Glob Health. 2015;3(9):e528-e536. doi:10.1016/S2214-109X(15)00039-XPubMedGoogle ScholarCrossref
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Smith  J , Steinemann  TL .  Vitamin A deficiency and the eye.   Int Ophthalmol Clin. 2000;40(4):83-91. doi:10.1097/00004397-200010000-00007PubMedGoogle ScholarCrossref
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Clugston  RD , Blaner  WS .  The adverse effects of alcohol on vitamin A metabolism.   Nutrients. 2012;4(5):356-371. doi:10.3390/nu4050356PubMedGoogle ScholarCrossref
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World Health Organization. WHO model formulary 2008. Published 2009. Accessed March 19, 2020. https://apps.who.int/medicinedocs/documents/s16879e/s16879e.pdf
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