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.