Nausea (with or without vomiting) occurs in up to 80% of pregnancies at any time of day, despite the general term morning sickness. Mean onset of symptoms is 5 to 6 weeks' gestation. Although symptoms typically abate by 16 to 18 weeks of gestation, they continue into the third trimester in 15% to 20% of pregnant women and until delivery in 5%.
Hyperemesis gravidarum is a severe form of nausea and vomiting in pregnancy, characterized by intractable vomiting, dehydration, alkalosis, hypokalemia, and weight loss usually exceeding 5% of prepregnant body weight. It affects 0.3% to 2% of pregnancies and peaks between the 8th and 12th weeks of pregnancy. The etiology may be multifactorial, involving hormonal, neurologic, metabolic, toxic, and psychosocial factors.
In true hyperemesis gravidarum, persistent vomiting leads to plasma volume depletion and elevated hematocrit, and metabolic derangements that include increased blood urea nitrogen, hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis. A complete workup includes a pelvic sonogram to identify multiple gestation or molar pregnancy and thyroid function tests to evaluate for hyperthyroidism. Some patients with hyperemesis gravidarum have transient benign hyperthyroidism most likely due to thyroid stimulation by the human chorionic gonadotropin (hCG) molecule, which is structurally similar to TSH and has been shown in animal studies to be a weak thyrotropin. This usually resolves spontaneously as pregnancy continues.
Treatment depends on the severity of symptoms. Usually, intravenous (IV) hydration and antiemetic therapy are sufficient. Patients may require hospitalization for intractable emesis, electrolyte abnormalities, and severe hypovolemia. Thiamine supplementation (100 mg daily intramuscularly or intravenously) is given prior to administration of glucose to prevent Wernicke encephalopathy. Oral feeding with a bland diet should be introduced slowly as tolerated.
There are no drugs approved specifically for the treatment of nausea and vomiting in pregnancy; however, the following medications have been shown to be clinically effective (see chapter 5, Figure 5-1):
Pyridoxine (vitamin B6) 10 to 25 mg orally 3 to 4 times daily
Doxylamine succinate 20 mg with pyridoxine 20 mg orally at bedtime. A recent formulation consisting of delayed release tablets of 10 mg of doxylamine and 10 mg of pyridoxine has recently become available in the United States, which may be taken as needed, up to four tablets daily: one in the morning, one in the afternoon, and two in the evening.
Promethazine hydrochloride (Phenergan) 12.5 to 25 mg orally or rectally every 4 to 6 hours
Prochlorperazine (Compazine) 25 mg rectally twice daily or 5 to 10 mg orally, IV, or intramuscularly 4 times daily
Metoclopramide hydrochloride (Reglan) 5 to 10 mg orally or intramuscularly 3 times daily
Ondansetron hydrochloride (Zofran) 4 mg orally or IV 3 times daily
Methylprednisolone (Medrol) 16 mg orally or IV every 8 hours for 3 days may be used for refractory cases after 10 weeks' gestation. There is a theoretical risk of cleft lip and palate when steroids are administered in the early- to mid-first trimester.
In severe cases requiring prolonged IV hydration and poor nutritional status, enteral feeds via nasogastric tube is first-line management. Complications from parenteral nutrition, even peripherally inserted central catheters, are common and severe; therefore, parenteral feeding should be used only for the most refractory of patients who cannot tolerate enteral feeding.
Gastroesophageal reflux disease (GERD) and the resulting symptom of pyrosis (“heartburn”) are common during pregnancy secondary to the altered position of the stomach, decreased lower esophageal sphincter tone (due to elevated progesterone levels), and lower intraesophageal pressures. The incidence is 30% to 50% but may approach 80% in selected populations. Symptoms begin late in the first trimester and become more frequent and severe with increasing gestational age. Risk factors include multiparity and history of GERD before pregnancy.
Treatment is aimed at neutralizing acid or decreasing reflux.
Lifestyle modification is key in treating mild disease. Elevating the head of the bed at night, avoiding meals within 3 hours of bedtime, and consuming smaller but more frequent meals can help. Dietary modification is recommended, including reduced consumption of fatty or acidic foods, chocolate, and caffeine. Cigarette smoking and alcohol consumption can exacerbate GERD.
Mild intermittent symptoms can be treated with over-the-counter antacids (eg, calcium carbonate). More persistent and severe symptoms can be treated with H2 blockers (eg, ranitidine) or proton pump inhibitors (eg, omeprazole).
Peptic ulcer disease (PUD) is not common in pregnancy, and the hormonal changes of pregnancy usually decrease PUD severity and symptoms.
Treatment during pregnancy is similar to treatment for GERD and consists of diet modification, avoiding nonsteroidal anti-inflammatory drugs, and starting a proton pump inhibitor. Indomethacin for tocolysis in patients with PUD should be avoided. Testing for Helicobacter pylori infection is recommended for those with PUD; treatment regimens for H pylori should not include tetracycline or levofloxacin during pregnancy.
Bariatric surgery can be either restrictive (gastric banding or sleeve) or a combination of restrictive and malabsorptive (Roux-en-Y). Rapid weight loss is common following surgery and has been shown to decrease rates of pregestational diabetes, hypertension, gestational diabetes, and preeclampsia. It is recommended that pregnancy after bariatric surgery be delayed for at least 12 to 24 months. Although there is decreased average weight gain during pregnancy, rates of obesity can remain as high as 80% in patients who become pregnant following bariatric surgery. Compared to the general population, obese patients, including those who have had bariatric surgery, are more likely to deliver via cesarean delivery. However, bariatric surgery alone should not be an indication for cesarean delivery. Rates of fetal macrosomia are decreased following Roux-en-Y gastric bypass.
Nutritional deficiencies following Roux-en-Y gastric bypass may include protein, iron, vitamin B12, folate, vitamin D, and calcium, and individual micronutrient deficiencies should be identified and corrected. Oral multivitamin supplementation should be initiated; however, continued deficiency may require parental supplementation due to malabsorption. An excess of vitamin A can lead to birth defects, and supplementation should not exceed 5000 IU/d during pregnancy. Monitoring the blood count, iron, ferritin, calcium, and vitamin D levels can be considered in each trimester. Nutritional deficiencies can develop in infants who are breastfed by patients who have undergone bariatric surgery.
Anastomotic leaks, bowel obstruction, internal hernias, ventral hernias, band erosion, and band migration are bariatric-related surgical complications that can occur during pregnancy. Common gastrointestinal complaints during pregnancy like nausea, vomiting, and abdominal pain should be thoroughly evaluated in patients who have had prior bariatric surgery. Abdominal bloating, cramps, nausea, and vomiting can be signs of dumping syndrome, which can occur following the ingestion of refined sugars or high glycemic carbohydrates and result in rapid stomach emptying and small bowel distention. Hyperinsulinemia and consequent hypoglycemia can follow, resulting in tachycardia, palpitations, anxiety, and diaphoresis. Patients who have undergone gastric bypass surgery may not tolerate the 28-week glucose screen used to test gestational diabetes. One week of home glucose monitoring (fasting and 2-hour post prandial) at 24 to 28 weeks of gestation can be considered as an alternative. Extended release preparations of many medications are not recommended in patients who have undergone Roux-en-Y gastric bypass given the decreased intestinal absorptive area. A smaller gastric pouch can lead to gastric ulceration with nonsteroidal anti-inflammatory drug use postpartum in patients who have undergone gastric bypass surgery.
Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn disease, often presents in reproductive age women. An IBD increases the risk for preterm birth, low birth weight, and fetal growth restriction, particularly if remission is not achieved before or during pregnancy. There is no evidence that pregnancy influences disease activity; however, patients with active disease around the time of conception often fail to achieve remission during the pregnancy.
Treatment is largely pharmacologic. If a patient is well controlled on medications prior to pregnancy, we typically continue treatment, with the few exceptions outlined in the following text. Common medications include 5-ASA formulations and corticosteroids. Because sulfasalazine may interfere with folate absorption, supplemental folate (2 mg orally daily) should be prescribed. Immunosuppressive agents, such as azathioprine, 6-mercaptopurine, cyclosporine, or infliximab, are used for more severe disease. Limited experience shows that all these medications are safe during pregnancy. Methotrexate and mycophenolate are avoided in pregnancy. Antibiotics, particularly metronidazole and cephalosporins, are used for perirectal abscesses/fistulae. There is limited data regarding the safety of antidiarrheal medications such as Kaopectate, Lomotil, and Imodium in pregnancy, but significant teratogenicity is unlikely. Surgical intervention is indicated only for severe complications of IBD.
The mode of delivery may be affected by IBD depending on disease activity and past surgical history. Vaginal delivery can usually be attempted unless there is severe perianal disease or previous colorectal surgery. Operative vaginal delivery or episiotomy should be avoided if possible to prevent excessive perineal trauma. Cesarean delivery may be considered in patients with active perianal disease due to the risk of wound complications and fistulae formation.
Pancreatitis is an uncommon cause of abdominal pain in pregnancy, with an incidence of 1 in 1000 to 1 in 10 000 pregnancies.
The presentation is usually midepigastric or left upper quadrant pain with radiation to the back, nausea, vomiting, ileus, and low-grade fever. Cholelithiasis is the most common cause of pancreatitis during pregnancy. Other causes include alcohol abuse, hyperlipidemias, drugs, and autoimmune pancreatitis. Ultrasound is of limited use for acute pancreatitis in pregnancy because of the enlarged uterus and overlying bowel gas. Serum amylase and lipase levels are usually markedly elevated. However, degree of enzyme elevation and disease severity do not reliably correlate.
Management is supportive and consists of IV hydration, analgesics, antibiotics when appropriate, and bowel rest. Most cases of gallstone pancreatitis can be managed medically. In women with gallstone-induced pancreatitis, cholecystectomy should be considered after an acute infection to prevent recurrence.
Appendicitis can be a challenging diagnosis in the gravid patient due to the changes of pregnancy (see chapter 23).