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Chapter 25: Obstetrics
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A 29-year-old woman at 8 weeks age of gestation has been having intractable nausea and vomiting for the last 2 weeks and was admitted to the hospital. She was started on antiemetic medications and dextrose ½ normal saline for intravenous fluids. After 2 weeks, she failed to improve and her neurologic status appeared to change. Her cognition appeared to have slowed down and she was noted to have vertical and horizontal nystagmus. Her labs show the following:
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Her CT head was negative. Her video electroencephalography (VEEG) is pending. What is the likely diagnosis?
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A. Wernicke encephalopathy from hyperemesis gravidarum
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B. Subclinical status epilepticus from HELLP syndrome
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C. Hepatic encephalopathy from intrahepatic cholestasis of pregnancy
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A. Wernicke encephalopathy from hyperemesis gravidarum
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When evaluating liver function tests during pregnancy, the physiologic hepatic changes must be taken into account. Physiologic hepatic changes include (1) serum albumin, which may be lowered due to dilutional effects of increased plasma volume; (2) serum alkaline phosphatase, which may be produced in the bone, liver, intestine, kidney, and leukocytes, can be elevated up to 2-15 times due to placental production, particularly during the third trimester; and (3) decreased bile salts, increased biliary cholesterol, and decreased gallbladder emptying. Elevated levels of AST, ALT, γ-glutamyl transferase, and bilirubin would warrant further investigation.
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Hyperemesis gravidarum (HG) is defined as persistent vomiting that is associated with a 5% weight loss and ketosis. It can lead to Wernicke encephalopathy, central pontine myelinolysis, and death. The direct correlation between levels of HCG and severity of vomiting has suggested a causal relationship, although other theories include starvation, placenta cytokines, and abnormal mitochondrial fatty acid oxidation. Hyperemesis gravidarum begins in the first trimester, peaks at 8 to 12 weeks, and usually resolves by 20 weeks’ age of gestation. Labs may show hemoconcentration, hypokalemia, metabolic alkalosis, transaminitis of 100 to 1600 U/L, and total bilirubin less than 4 mg/dL, and amylase and lipase may be elevated 5-fold as opposed to 5- to 10-fold in acute pancreatitis. Biopsy shows necrosis, steatosis, and bile plugs. Risk factors include multiple gestations, molar pregnancies, hydrops fetalis, and trisomy 21. Treatment includes hydration, thiamine supplementation, antiemetics, small meals, and psychotherapy. If refractory, then hydrocortisone and total parenteral nutrition may be ...