HAVE YOU SEEN MY THIAMINE?

Case Presentation: A 26-year-old woman with a past medical history of obesity presented with four weeks of intractable nausea and vomiting associated with poor oral intake and a 60-pound unintentional weight loss. She also complained of lightheadedness and difficulty ambulating. Three months prior to presentation, the patient underwent an uneventful elective laparoscopic sleeve gastrectomy. Because the surgery was performed in Mexico, the patient had poor nutritional follow up and started to develop symptoms shortly thereafter.
Physical examination was notable for deficits in her short-term memory. She also had an unsteady gait and bilateral horizontal end gaze nystagmus. An MRI of the brain showed increased signal intensity and enhancement in the mammillary bodies suggestive of Wernicke’s Encephalopathy (WE). Additionally, she was found to have a serum thiamine level of 30.4 nmol/L (normal 66.5-200 nmol/L). The patient was subsequently initiated on a three-day regimen of 500mg IV thiamine three times per day followed by 100mg IV daily. The patient’s nausea and vomiting dramatically improved on the second day of parenteral thiamine treatment, and she was discharged 9 days after admission with complete resolution of her symptoms. The patient was discharged with oral thiamine supplementation.

Discussion: Thiamine is a water-soluble vitamin that plays an essential role in regulating neurological function as well as carbohydrate metabolism. Thus, thiamine deficiency can cause neuronal injury as the high metabolic demands of the brain can longer be compensated. Deficiencies are commonly seen in chronic alcoholism, malnutrition, and as in our case, post-bariatric surgery. WE, a complication of thiamine deficiency, typically manifests as a triad of unsteady gait, altered mental status, and abnormal eye movements.

A diagnosis of WE can be challenging, as a serum thiamine level and imaging results may be normal. In some patients such as ours, MRI of the head may show enhancement involving the mammillary bodies, dorsomedial thalami, periaqueductal area and third ventricle. Nevertheless, WE remains primarily a clinical diagnosis.

Conclusions: We present one of the few reported cases of WE secondary to complications of sleeve gastrectomy. Because most community providers are not frequently exposed to patients who have undergone bariatric surgery, we aim to increase awareness and suspicion of WE, as it is a preventable cause of neurological deterioration. A timely diagnosis is crucial, since early WE can be readily reversed by simple serum repletion of thiamine.