SUN-521 Hyperemesis Gravidarum Resulting in Wernicke’s Encephalopathy and Abnormal Thyroid Function Tests

Abstract

Background: Wernicke’s encephalopathy (WE) is a potentially fatal consequence of thiamine deficiency that must be considered in patients with poor nutrition and altered mentation. We report a case of a female with hyperemesis gravidarum (HG), nystagmus, clonus, and abnormal thyroid function tests associated with WE. Clinical Case: A 23 year-old healthy G2P0010 woman was admitted for rehydration at 15 weeks gestation after four weeks of intractable vomiting. She denied medications, supplements and alcohol use. Vitals were normal. Exam showed a fatigued ill appearing female with no thyromegaly, tremor, lid lag, or stare. She had a gravid uterus but otherwise normal exam. Fetal heart rate was normal. Laboratory findings included hyponatremia, hypokalemia, elevated creatinine and transaminases, and normocytic anemia. Hepatitis panel, vitamin B12, ammonia, urinalysis and ultrasound of the appendix and gallbladder were unremarkable. She was treated with intravenous fluids and potassium. Electrolyte abnormalities and renal dysfunction resolved. On hospital day three, she became lethargic, tachycardic, unable to follow commands, and exhibited nystagmus and clonus. Thyroid studies showed TSH 0.06 uIU/mL (0.34 - 5.66 µIU/mL), and free T4 3.59 ng/dL (0.52 - 1.21 ng/dL). Methimazole and propranolol were started while awaiting repeat thyroid studies. MRI brain was not obtained due to aspiration risk. EEG showed diffuse slowing but no epileptiform activity. She returned to baseline mentation within hours of intravenous thiamine, with resolution of dysphagia and nystagmus. Thiamine level returned low (51 nmol/l; normal 67–200 nmol/L). Methimazole and propranolol were stopped and thyroid function tests normalized. She was discharged and delivered a healthy baby at term. Conclusion: WE is an acute neuropsychiatric condition caused by thiamine deficiency. Early recognition and treatment are critical to prevent irreversible damage; the classic signs are ataxia, ophthalmoplegia, and encephalopathy. Historically considered in patients with a history of alcohol use, WE is increasingly recognized in other conditions associated with dietary deficiency, since body stores of thiamine last only 18 days. WE has been reported in HG due to prolonged vomiting and increased thiamine requirements in pregnancy. WE has been associated with thyrotoxicosis, possibly due to increased metabolic demands. Both gestational transient thyrotoxicosis and HG are associated with markedly elevated HCG and present in the first 16 weeks of pregnancy. Initial thyroid studies were concerning for thyrotoxicosis, but normal repeat studies argue against that as a contributor. WE is a life threatening complication of poor oral intake, which should be empirically treated with thiamine prior to glucose. WE may be associated with thyrotoxicosis.