P2.257: Think Thiamine: Wernicke’s Encephalopathy in an Unexpected Pediatric Case

Introduction: Wernicke’s Encephalopathy (WE) is a diagnosis classically associated with severe vitamin B1 (thiamine) deficiency often secondary to alcoholism, metabolic syndromes, and severe malnutrition. Symptoms include changes in memory, nystagmus, ataxia and ophthalmoplegia. Although often taught as a disease of adults, we report a case of WE in a 12-year-old male with acute onset of blurry vision and altered mental status.

Case Description: 12 year old male with a history of autism and ADHD presented to the ED with altered mental status, eye pain and blurry vision. Two months prior, the patient had choked on his lisdexamfetamine pill and since then has had severe oral aversion and inability to eat food or drink without self-induced postprandial emesis. Notably he lost 14 kilograms since the incident. One week prior to admission, the patient started acting strange, appearing disoriented and reported blurry vision, hallucinations, and ataxia. Brain MRI with contrast showed hyperintensity of bilateral thalami, mamillary bodies and periaqueductal gray. Lumbar puncture with CSF studies showed no abnormalities. Spine MRI and brain venogram were unremarkable. Due to possible infectious etiology, IV ceftriaxone, acyclovir, and azithromycin were initiated on day 1 after blood and CSF cultures were obtained. Although rare, WE was on the differential, and IV thiamine was started on admission in addition to antimicrobials. Within 24 hours of administration of IV thiamine 200mg TID, the patient showed improvement of symptoms. Antimicrobials were discontinued after negative blood and CSF cultures.

Discussion: This case highlights a rare presentation of WE in a pediatric patient without a history of alcohol use or traditional risk factors. While WE is classically associated with chronic alcoholism in adults, it is increasingly recognized in children with malnutrition, prolonged vomiting, or restrictive diets. In this case, the patient’s severe oral aversion and self-induced postprandial emesis led to rapid and significant weight loss, ultimately resulting in thiamine deficiency. The patient’s clinical presentation, combined with MRI findings of hyperintensity in the bilateral thalami, mammillary bodies, and periaqueductal gray, was consistent with WE. Early recognition and empiric treatment with high-dose IV thiamine were critical, as evidenced by the rapid neurological improvement within 24 hours. This case reinforces the importance of considering WE in pediatric patients presenting with encephalopathy, especially when there is a history of malnutrition or prolonged vomiting. Additionally, this case underscores the diagnostic challenges of WE in children. Although the patient’s clinical course initially prompted an infectious workup with broad-spectrum antimicrobials, the prompt addition of thiamine likely prevented further neurological deterioration.

Conclusion: Ultimately, this case emphasizes the need for early recognition of WE in pediatric patients with atypical risk factors. Timely thiamine supplementation can lead to significant clinical improvement and prevent long-term neurological sequelae.