A 30-year-old primigravida with a single intrauterine pregnancy at 16+1 weeks’ gestation based on last menstrual period (and consistent with an 11-week ultrasound) presented to the emergency department (ED) with protracted nausea and vomiting. Although the patient had not received prenatal care, she had been evaluated in the ED for nausea and vomiting at 11 and 14 weeks’ gestation. She was discharged home from the most recent ED visit after tolerating oral intake and receiving a combination of intravenous (IV) antiemetics and oral potassium repletion. During the current visit, the patient was found to have had a cumulative 60-lb weight loss (13.8% of prepregnancy weight), hypokalemia (2.0 mmol/L), hypomagnesemia (0.1 mmol/L), hypocalcemia (0.3 mmol/L), and elevated liver enzymes (aspartate transaminase [AST], 109 IU/L; alanine transaminase [ALT], 392 IU/L). She was admitted to the hospital for electrolyte repletion and IV fluids but was transferred to the labor and delivery unit after a second-trimester fetal demise was diagnosed and confirmed by ultrasonography.
The patient underwent medical termination of pregnancy, receiving vaginal and 400 μg oral misoprostol every 6 to 8 hours until delivery. She had a spontaneous vaginal delivery 23 hours after the first dose of misoprostol. Shortly after delivery, she developed diplopia, nystagmus, blurred vision, and ataxia. A specialist in maternal-fetal medicine was consulted because of the onset of neurologic symptoms and persistently elevated liver enzymes (AST, 562 IU/L and ALT, 139 IU/L). The diagnosis of Wernicke’s encephalopathy was entertained and the patient was transferred to an urban teaching hospital for further evaluation for suspected Wernicke’s encephalopathy. ,
A neurology consult was requested and they recommended brain magnetic resonance imaging. The images demonstrated symmetrical T2-weighted hyperintense signal and restricted diffusion in the medial thalami consistent with Wernicke’s encephalopathy ( Figures 1 and 2 ). The patient’s whole blood vitamin B 1 level was markedly decreased at 33.6 nmol/L (normal range, 66.5–200 nmol/L). After receiving electrolyte repletion with 500 mg IV thiamine every 8 hours for 3 days followed by 250 mg IV thiamine daily for 5 days, the patient was discharged on oral vitamin B 1 and outpatient physical therapy for gait instability. Three weeks after discharge, the patient continued to receive physical therapy for gait instability. After 3 weeks of therapy, the patient continued to experience nystagmus associated with bothersome blurred vision and was referred to the ophthalmology department for further evaluation.
