Wernicke encephalopathy in a malnourished, depressed 16-year-old male

Wernicke encephalopathy (WE) is an acute neurological disorder characterized by a triad of confusion, ophthalmoplegia, and ataxia secondary to thiamine deficiency most commonly seen in adults with severe alcoholism. In the pediatric population, WE is rare though has been reported in patients with anorexia nervosa, malignancy, intensive care unit stays, and parenteral nutrition.[1] To describe a case of WE in a 16-year-old male patient with severe malnutrition in the setting of depression The patient and guardian/family were interviewed. Literature relevant to the case was reviewed prior to and after the diagnosis. In this report we present a 16-year-old male with depression in the setting of a 17-kilogram weight loss over a 2-month period. He reports not eating much after moving out of his guardian's home because he did “not want the other people he was living with to not have food.” He presented clinically with confusion, dysarthria, ophthalmoplegia, nystagmus, memory impairment and gait instability. Magnetic resonance imaging (MRI) demonstrated hyperintense signals along the margins of the third ventricle and cerebral aqueduct. Laboratory work confirmed low thiamine levels. This overall presentation was consistent with Wernicke's encephalopathy. Intravenous thiamine followed by parenteral thiamine replacement and nutritional support contributed to the recovery of his ataxia, nystagmus, confusion, dysarthria, and improvement of memory impairment over a 1 week hospitalization. The reported case of WE was likely secondary to severe depression and decreased food intake. WE should be considered in pediatric patients with depression. Initiation of thiamine therapy should be considered in cases of significant confusion after following a negative stroke protocol.