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INTRODUCTION AND BACKGROUND
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KEY CLINICAL QUESTIONS
What is nausea and vomiting of pregnancy (NVP) and hyperemesis gravidarum (HG)?
What are the maternal and fetal risks of NVP and HG?
When is ambulatory treatment appropriate, and when is inpatient management recommended?
What are the treatment options for NVP and HG?
How would you counsel a patient on the potential side effects of treatment options and pharmacologic risks to the pregnancy, if any?
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CASE 30-1
A 27 y.o. G3 P1011 presents to the Emergency Department at 8 weeks gestation with persistent nausea and vomiting for two weeks. She vomits within 5 minutes of consuming both solids and liquids and has attempted rehydration with water and other electrolyte solutions. This also occurred in her first pregnancy, and it required hospitalization and further medical management in the first trimester. She denies fever, abdominal pain, diarrhea or constipation, recent travel, or close contacts with illness. Upon examination, her temperature is 37.0°C, pulse 110, blood pressure 96/64, oxygen saturation 98% on room air. She appears dehydrated. There is no abdominal tenderness. A transvaginal ultrasound reveals a live intrauterine pregnancy at 8 3/7 weeks gestation, with no uterine or adnexal pathology noted. Serum electrolytes reveal a potassium level of 2.5 mEq/L.
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Nausea and vomiting of pregnancy (NVP) is a common condition experienced in the early first trimester of pregnancy, with symptoms on a varied continuum from mild nausea to severe hyperemesis gravidarum (HG).1 Nearly three-quarters of women report nausea with or without vomiting in pregnancy, with mean onset of 5 weeks gestation, and with 90% of patients who will develop NVP experiencing symptom onset by 8 weeks gestation.2,3 Resolution occurs for 50% of patients by 14 weeks gestation, with up to 90% experiencing relief from symptoms by 22 weeks gestation.2 HG is the most severe form of NVP, with intractable nausea and vomiting, loss of more than 5% of prepregnancy weight, dehydration, and electrolyte imbalances.4–6 HG occurs at a mean rate of 1.1% worldwide.3,5
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Both NVP and HG are diagnoses of exclusion, with other pathologic causes of nausea and vomiting, such as peptic ulcer disease, cholecystitis, gastroenteritis, appendicitis, hepatitis, and genito-urinary, metabolic, and neurologic disorders, should be evaluated and considered in the differential diagnosis.5,7 Although instances are rare, women with NVP and HG are at risk for Wernicke's encephalopathy, splenic avulsion, Mallory-Weiss tears, bleeding, esophageal rupture, diaphragmatic rupture, pneumothorax, pneumomediastinum, pneumopericardium, hypoprothrombinemia due to vitamin K deficiency, acute kidney injury, and significant psychosocial morbidity.1,8 Of these complications, Wernicke's encephalopathy due to vitamin B1 deficiency is the most significant, as it is associated with permanent neurologic disability,1 particularly if it is not recognized or if dextrose is given prior to thiamine administration in patients with NVP and HG.1,6-9
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Recurrence rates of hyperemesis vary significantly, ...