Case Presentation: Wernicke’s encephalopathy is the presence of neurological symptoms caused by lesions in the central nervous system due to a lack of thiamine (vitamin B1). The deficiency is seen in malnutrition due to excessive alcohol, malabsorption or decreased intake. Most symptoms will improve quickly if deficiencies are repleted; however, we present the case of a patient with Wernicke’s encephalopathy with an unusually long and complicated treatment course.A 24-year-old female with past medical history of morbid obesity status post sleeve gastrectomy six weeks prior presented to the emergency department for worsening mental status. She was found to have GCS 4 leading to intubation with a drop in blood pressures to the 50s/30s leading to the initiation of multiple pressors. The patient was admitted to the medical ICU for hypovolemic shock secondary to dehydration complicated by metabolic acidosis, hyperglycemia, and encephalopathy. After extensive work-up, she was found to have severe thiamine deficiency and head MRI showed lesions in the mamillary body indicating Wernicke’s encephalopathy secondary to vomiting and malabsorption from recent gastric surgery.The patient was given thiamine supplementation daily but continued to have encephalopathy and diffuse muscle weakness. Patient was extubated but reintubated for several more days due to post-extubation stridor. During this time, she was found to have ventilator acquired pneumonia and severe ileus requiring IV antibiotics and nasogastric decompression. The patient slowly became more alert after extubation with continued hypophonia, dysphagia and bilateral motor weakness with right side greater than left, even after aggressive correction of vitamin deficiencies. It was suspected that she had critical illness neuropathy due to her almost one month stay in the ICU. The patient was transitioned out of the ICU to a stepdown unit where more tests were conducted to find the cause of her motor weakness. An EMG showed asymmetric length-dependent axonal sensorimotor large fiber polyneuropathy and proximal irritable myopathy. Due to initial concerns of vasculitis, a trial of IVIG was given but a subsequent sural nerve biopsy showed generalized axonal neuropathy with no vasculitis. No specific findings including those on imaging could explain the patient’s lasting motor deficiencies though acute nutritional axonal neuropathy was not ruled out. The patient was discharged to a skilled nursing facility for rehabilitation after a two-month hospital stay.

Discussion: This case illustrates the lingering effects of thiamine deficiency long after the deficiency is corrected. Many case reports note that patients had full recovery after several weeks of thiamine repletion, but our case shows that thiamine deficiency induced Wernicke’s encephalopathy can produce unexpected motor complications with long recovery times even after correction of the vitamin deficiency.

Conclusions: Treatment of patients with thiamine deficiency should not be taken lightly more than a course of vitamin repletion may be need. The sequelae of thiamine deficiency can range from Wernicke’s encephalopathy to acute axonal neuropathy which can have lasting effects on patients requiring many months of rehabilitation for recovery.