Wernicke Encephalopathy in a Child With Acute Lymphoblastic Leukemia: A Case Report

Abstract

Background: Wernicke encephalopathy (WE) is a life-threatening neurological disorder caused by thiamine deficiency, commonly associated with alcoholism but also observed in malnourished pediatric cancer patients undergoing intensive chemotherapy. WE remains underdiagnosed in children, with many cases only confirmed postmortem. We report a 6-year-old girl with acute lymphoblastic leukemia (ALL) who developed WE secondary to treatment-resistant nausea and vomiting.

Case: The patient presented with acute gait disturbance, ophthalmoparesis, and paraparesis following persistent vomiting and significant weight loss. Initial diagnostic evaluations, including cerebrospinal fluid analysis and neuroimaging, suggested alternative diagnoses such as cerebellitis and Guillain-Barré Syndrome. However, progressive neurological deterioration, the emergence of encephalopathy, and follow-up magnetic resonance imaging (MRI) findings of hyperintense lesions in the periventricular, periaqueductal, and cerebellar regions supported the diagnosis of WE. The overlapping features with other neurological conditions contributed to a delay in recognizing WE and initiating thiamine therapy. Despite initiating high-dose intravenous thiamine, symptom resolution was significant but partial. Unfortunately, the patient later developed lymphomatous meningitis and sepsis and ultimately succumbed to complications.

Conclusion: This case highlights the importance of early clinical recognition of WE in pediatric leukemia patients with prolonged vomiting, as delayed diagnosis can lead to irreversible neurological damage or death. Given the limitations of early neuroimaging findings, clinical suspicion should prompt immediate thiamine supplementation. The report points out the need for heightened awareness of thiamine deficiency in pediatric oncology, emphasizing the role of prophylactic supplementation in high-risk patients.

Keywords: Wernicke encephalopathy; acute lymphoblastic leukemia; pediatric oncology; thiamine deficiency.

FIGURE 1

First MRI: Fluid attenuated inversion recovery (FLAIR). MRI showing hyperintensities in cerebellum (A, B). Restricted diffusion in cerebellum (C–F).

FIGURE 2

Second MRI: Fluid‐attenuated inversion recovery (FLAIR). MRI showing hyperintensities in the cerebellum, peri‐aqueductal region, and medial thalamic region (A–D). Restricted diffusion more evident in cerebellum (E, F).

FIGURE 3

Timeline of the patient's hospitalization and key clinical events.