Nausea and vomiting are common symptoms in pregnancy, with an incidence of nausea from 50% to 80% and vomiting of 50%. Hyperemesis gravidarum is much less common, complicating approximately 1% of pregnancies. There is no universally accepted definition of hyperemesis gravidarum, but diagnostic criteria include a combination of the following: exclusion of alternative etiologies for nausea and vomiting (Table 5-1), acute starvation (eg, ketonuria), and weight loss (eg, 5% from pregravid weight) and may also include electrolyte, thyroid, and hepatic function testing abnormalities. Hyperemesis gravidarum, which peaks around 9 weeks, is generally viewed as a severe manifestation of nausea and vomiting of pregnancy, rather than a separate disorder (see chapter 15).
The etiology of nausea and vomiting of pregnancy is poorly understood. Increased levels of human chorionic gonadotropin (such as is produced by multiple gestations and molar pregnancy) and estradiol are associated with worsened symptoms, although the exact mechanism is unclear. Theories that nausea and vomiting of pregnancy are driven by a psychological predisposition to the condition are less helpful in understanding and managing the condition. Other risk factors include history of motion sickness, migraine headaches, family or personal history of the condition, and female fetus.
Serious complications of nausea and vomiting in pregnancy (such as Boerhaave syndrome or Wernicke encephalopathy) are rare in modern obstetric practice, but the disorder remains the second most common reason for antepartum hospitalization (after preterm labor) in the United States and has a considerable impact on maternal quality of life. Mild to moderate nausea and vomiting in pregnancy has not been associated with fetal or neonatal impacts. Severe nausea and vomiting and hyperemesis may be associated with higher rates of low birthweight and preterm birth, but there has been no association between hyperemesis and either perinatal or neonatal mortality in large cohorts.
Management: Preventative efforts include recommending patients start prenatal vitamins at least 1 month prior to conception, and for women with a history of hyperemesis, starting antiemetic treatment prior to onset of symptoms. For management of nausea and vomiting once it manifests, current American College of Obstetrics and Gynecologists (ACOG) guidance recommends nonpharmacologic therapies as first-line management, starting with transition from prenatal vitamins to only folic acid supplementation, ginger capsules, and consideration of P6 acupressure wrist bands. See Table 5-2. Counseling regarding small frequent meals and avoidance of foods that trigger symptoms are reasonable, albeit non–evidence-based interventions. In the event nonpharmacologic management is unsuccessful, ACOG recommends products containing a combination of vitamin B6 (pyridoxine) and doxylamine as the first-line pharmacotherapeutic option. For patients with persistent symptoms, escalation to a sedating antihistamine (eg, dimenhydrinate or diphenhydramine) or phenothiazine derivative (eg, prochlorperazine or promethazine) is suggested. Further escalation in the absence of dehydration could include metoclopramide, ondansetron, promethazine, or trimethobenzamide. In escalating therapy, it is important to consider that combinations of dopamine antagonists and phenothiazines increase the risk of extrapyramidal side effects and neuroleptic malignant syndrome, whereas combinations of ondansetron and phenothiazines may lead to excessive QTc prolongation.
For patients who present with dehydration or who cannot tolerate oral rehydration, current ACOG guidance recommends the use of parenteral hydration as first-line therapy. Patients who require intravenous (IV) hydration, or who have been vomiting for more than 3 weeks, should receive 100 mg of thiamine with her first bag of IV fluids, and an additional 100 mg daily for the next 2 to 3 days to prevent Wernicke encephalopathy. Dextrose-containing fluids should be deferred until the first dose of thiamine is delivered. For patients whose vomiting is refractory to these management efforts, a corticosteroid is a further management option, which has been shown to reduce the risk of readmission. However, corticosteroids have been shown to increase the risk of oral cleft defects when given before 10 weeks of gestation, and given the potential risks of prolonged steroid use for both fetus and mother, should be limited to 6 weeks of therapy during pregnancy per ACOG guidelines as a last-resort therapy.
While management of the patient's symptoms is in progress, it is important to also manage her nutritional status. For patients whose symptoms preclude oral intake or who cannot maintain weight despite pharmacotherapy, enteral feeding using a nasogastric or nasoduodenal tube should be first-line management. Prolonged use of central catheters, even peripherally inserted central catheters, are associated with significant morbidity in pregnancy, and for this reason, the use of total parenteral nutrition should be reserved for those patients who are not able to tolerate enteral feeding despite maximum pharmacologic management of nausea and vomiting.
Gestational transient thyrotoxicosis is a common complication of nausea and vomiting of pregnancy. Abnormal thyroid function studies diagnosed in the setting of nausea and vomiting of pregnancy should not automatically be treated with antithyroid medication because the thyroid function abnormalities will resolve as the symptoms improve.