Emergency physicians frequently treat hyperemesis gravidarum and should be aware of possible complications. Wernicke encephalopathy secondary to thiamine deficiency should be considered in the differential diagnosis of acute encephalopathy in pregnant women. A seventeen-week pregnant 27-year-old woman presented to the Emergency Department with nausea, emesis, and right upper quadrant abdominal pain. Ultrasound diagnosed gallbladder sludge. Surgical consultant offered cholecystectomy versus expectant management. She improved with IV hydration, ondansetron, and was discharged on hospital day 3 with a diagnosis of hyperemesis gravidarum and gallbladder sludge. Three days later she presented with continued emesis and altered mental status. She and family members denied alcohol or illicit drug use. Vital signs were pulse 99/min, blood pressure 115/70, temperature 36.4 °C, respiratory rate 18, and oxygen saturation 99%. Neurological examination was delirium, variable mentation, and inability to follow commands. She had internuclear opthalmoplegia with bilateral nystagmus. CT scan of brain was negative. MRI found abnormal T2-weighted signal in the central pons and medial thalami. Radiographic differential included central pontine myelinolysis, dysmyelinating conditions from malnutrition, toxic encephalopathy, and Wernicke encephalopathy. Thiamine level was below the limits of detection. Alcohol and urine drug screen were negative. Diagnosis was thiamine deficiency secondary to hyperemesis gravidarum with Wernicke encephalopathy. Emergency physicians frequently treat hyperemesis gravidarum. Nutritional status should be evaluated in patients who are unable to take neonatal vitamins. Awareness should exist of possible complications, including Wernicke encephalopathy secondary to thiamine deficiency.