Wernicke Encephalopathy Secondary to Cannabinoid Hyperemesis Syndrome in a 15-Year-Old Male Patient: A Case Report.

The use of cannabis and high-potency tetrahydrocannabinol (THC) products has risen substantially among adolescents, and cannabinoid hyperemesis syndrome (CHS) is now an increasingly recognized complication of chronic use. CHS is characterized by recurrent episodes of intractable nausea, vomiting, and abdominal pain that resolve with cannabis cessation. Wernicke encephalopathy (WE), a neurologic syndrome caused by thiamine deficiency, is classically associated with chronic alcohol use but is increasingly reported in nonalcoholic and pediatric patients, in whom atypical presentations complicate timely diagnosis. We report the case of a 15-year-old male patient with no significant past medical history and chronic cannabis use who developed WE in the setting of CHS. He initially presented with several days of intractable nausea, vomiting, and headache and was diagnosed with CHS. Symptoms persisted, and he returned weeks later with a 25- to 30-pound weight loss along with headache and dizziness. Repeat laboratory studies revealed worsening transaminitis and progressive hyponatremia, which was treated with fluid restriction and oral sodium supplementation. He was admitted for management of presumed CHS, and on admission demonstrated slowed speech, mild confusion, and episodes of unresponsiveness. Nephrology and gastroenterology were consulted. Several days into admission, he showed little cognitive improvement, remained bedbound, and developed an ataxic gait once movement was initiated. This was followed by new-onset horizontal nystagmus with blurred vision. Brain magnetic resonance imaging and electroencephalography were unremarkable, and a workup for encephalopathy was unrevealing. Given the constellation of nystagmus, ataxia, altered mentation, and protracted vomiting with significant weight loss, WE was suspected; a vitamin panel was ordered, and empiric thiamine was initiated. The vitamin panel subsequently confirmed thiamine deficiency. Within one day of thiamine supplementation, the patient's nystagmus, gait, and cognitive function improved, consistent with a clinical diagnosis of WE likely secondary to CHS-induced thiamine deficiency. At follow-up, he reported cessation of cannabis, demonstrated adequate weight gain, and full neurologic recovery. To our knowledge, this is among the few reported cases of WE associated with CHS and highlights that normal MRI findings do not exclude the diagnosis. As adolescent THC use continues to rise, clinicians should maintain a low threshold for empiric thiamine supplementation in adolescents with prolonged CHS and any new neurologic findings, regardless of imaging results.