(PO-116) Not Always Alcohol: A Case of Restriction-Induced Wernicke Encephalopathy
Background: Anorexia nervosa can result in complications across many organ systems with malnutrition and weight loss acting as the key etiologic factor (So, 2021). Poor dietary intake can lead to deficiencies of thiamine and the classical triad of encephalopathy, oculomotor dysfunction, and gait ataxia. Presented here is a case of a young patient suffering from anorexia nervosa who developed thiamine deficiency and a literature review regarding non-alcoholic Wernicke encephalopathy.
Case: A 15-year-old female with no medical history presented with a new diagnosis of anorexia nervosa, restricting type, at a BMI of 12.38. The patient was admitted for nutritional rehabilitation and refeeding syndrome monitoring. On hospital day 6, the patient was noted to have increased confusion. Overnight EEG was within normal limits. The next day, the patient was experiencing worsening agitation and hallucinations with nystagmus noted on exam. No gait disturbances were observed. MRI revealed mild diffuse parenchymal loss consistent with anorexia nervosa and mild cerebral hypoprofusion. The patient was managed with two days of IV thiamine 1500mg followed by five days of 250mg IV thiamine then 100mg oral thiamine daily. Mentation returned to baseline by time of discharge and the patient continued on thiamine upon discharge.
Discussion: In one autopsy study, non-alcoholics counted for nearly one-quarter of Wernicke encephalopathy (Lindboe, 1989). A retrospective observational cohort study found non-alcoholics took longer to diagnose over alcoholic patients (4 vs 1 days) and required longer hospitalizations (23 vs 13 days). They also found that in non-alcoholic patients, ocular signs were more common and cerebellar signs were less common (Chamorro, 2017). Fittingly, another retrospective autopsy study found that the classic triad was only recorded in 17% of patients (Harper, 1986). In this case, nystagmus was present and cerebellar gait ataxia was not observed. These key differences all contribute to the need for more attention to subtle clinical characteristics of Wernicke encephalopathy rather than seeking the classic triad.
Conclusions: Wernicke encephalopathy can present subtly, oftentimes not meeting all facets of the classical triad. The index of suspicion for this dangerous syndrome should remain high when assessing non-alcoholic patients with other causes of poor nutrition, including eating disorders. References:
So, YT. Wernicke encephalopathy. In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2021.
Lindboe CF, Løberg EM. Wernicke's encephalopathy in non-alcoholics. An autopsy study. J Neurol Sci. 1989 Apr;90(2):125-9. doi: 10.1016/0022-510x(89)90095-6. PMID: 2723677.
Chamorro AJ et al. Differences Between Alcoholic and Nonalcoholic Patients With Wernicke Encephalopathy: A Multicenter Observational Study. Mayo Clin Proc. 2017 Jun;92(6):899-907. doi: 10.1016/j.mayocp.2017.02.019. PMID: 28578781.
Harper CG, Giles M, Finlay-Jones R. Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy. J Neurol Neurosurg Psychiatry. 1986 Apr;49(4):341-5. doi: 10.1136/jnnp.49.4.341. PMID: 3701343; PMCID: PMC1028756.
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