Wernicke’s Encephalopathy (WE) is a well-discussed but rarely diagnosed disease state caused by a severe deficiency in Thiamine (Vitamin B1). Classically, WE is associated with chronic alcohol abuse, but it can also be associated with other states of poor nutrition, malabsorption, or increased metabolic requirements. The traditional clinical triad consists of ophthalmoplegia, ataxia, and confusion, however many other abnormalities such as autonomic dysregulation, seizures, and coma can also be associated. If not treated appropriately, WE can progress to severe neurological sequelae, including death. 

We present the case of a 25-year-old female with medical history of morbid obesity and recent elective second trimester abortion that presented to the emergency room complaining of 2-3 days of nausea, vomiting, and abdominal pain. On admission, she had a normal physical exam and was treated for colitis seen on CT scan. She initially improved and had good oral intake. However, shortly after improvement, her mentation quickly deteriorated into delirium and then into a coma-like state. Work up included EEG, CT head, transvaginal ultrasound, and toxicology labs, however, no etiology of her encephalopathy was identified. MRI revealed T2 FLAIR hyperintensity of the pulvinar nuclei, periaqueductal gray matter, and mammillary bodies. These findings were most concerning for pathology due to WE. A lumbar puncture was performed and revealed 0 WBC, 0 RBC, 54 protein, 112 glucose. All cultures returned negative. This patient had no history of alcoholism, but was discovered to have had severe vomiting for several weeks secondary to her pregnancy. The guideline-directed doses of thiamine were ordered but the patient went into PEA arrest shortly after diagnosis, and was unable to be resuscitated before initiation of the medication. 

Non-alcoholic Wernicke’s encephalopathy should remain on the neurological differential for any patient displaying worsening mentation with unexplainable physical exam signs.