Gastrointestinal Disease in Pregnancy
Christopher C. DeStephano
Abimbola Aina-Mumuney
GASTROINTESTINAL PHYSIOLOGY AND ANATOMY IN PREGNANCY
During pregnancy, anatomic and physiologic changes undergone by the gastrointestinal tract can influence the diagnosis of gastrointestinal disorders. The displacement of the gastrointestinal organs by the gravid uterus changes the location, character, and intensity of gastrointestinal symptoms. This chapter summarizes the normal changes in pregnancy in contrast to pathologic conditions.
Liver Disorders
Hepatic Physiology in Pregnancy
As the gravid uterus expands into the upper abdomen, the liver is displaced posteriorly and to the right, decreasing its estimated size on physical examination. A palpable liver in pregnancy is abnormal and a workup is indicated. Table 17-1 summarizes the normal changes in liver function tests during pregnancy, some of which are considered abnormal in nonpregnant patients.
Hepatic Disorders Unique to Pregnancy
Cholestasis of Pregnancy
Intrahepatic cholestasis of pregnancy (ICP) occurs in about 1 in 1,000 pregnancies in the United States but has significant genetic and geographic variations. Risk factors include a personal or family history of ICP, multiple gestations, and chronic hepatitis C infection. The cause is postulated to be secondary to incomplete bile acid clearance. Complications include preterm labor, meconium ileus, and intrauterine fetal demise. These risks increase progressively with duration, regardless of symptoms. The cause of fetal demise is unknown and rarely happens before term.
Initial diagnosis is clinical, with confirmation by laboratory testing. The cardinal symptom is pruritus, especially of the palms and soles that worsens at night. Anorexia, malaise, steatorrhea, and dark urine are also common complaints. Jaundice develops in 15% of patients but resolves quickly after delivery. Fever, abdominal pain, hepatosplenomegaly, and stigmata of chronic liver disease are usually absent. Onset is typically late in pregnancy (80% after 30 weeks) but occasionally occurs in the second trimester.
Differential diagnosis includes preeclampsia, viral hepatitis, and gallbladder disease.
Laboratory findings include elevated total bilirubin, aminotransferases, and fasting serum total bile acids (>10 to 14 µmol/L). Cholic acid is raised more than chenodeoxycholic acid, which results in an elevation of the cholic/chenodeoxycholic
acid ratio compared to pregnant women without ICP. Lab abnormalities arise a mean of 3 weeks after the development of pruritus. Serum alkaline phosphatase and transaminase levels are modestly elevated. Serum gamma glutamyl transpeptidase, albumin, and prothrombin time remain normal.
Treatment is mainly for symptomatic relief until delivery, which is the definitive therapy. Diphenhydramine, topical emollients, and dexamethasone (12 mg/day for 7 days) can relieve pruritus. Ursodeoxycholic acid (8 to 10 mg/kg/day) is the most effective treatment and works by increasing bile flow, thereby decreasing serum bile acid levels and decreasing pruritus. Cholestyramine (8 to 16 g, two to four times per day) decreases intestinal absorption of bile salts and is effective for mild to moderate symptoms but does not improve lab values. Fat-soluble vitamins (A, D, E, and K) and prothrombin time should be checked periodically for patients taking cholestyramine for extended treatment. If the prothrombin time is elevated, 10 mg/day of oral vitamin K should be administered until the coagulation profile normalizes.
ICP at term is associated with 3% risk of fetal demise. Antepartum fetal testing is recommended, although intrauterine demise may occur despite reassuring testing. Delivery should be performed no later than 38 weeks’ gestation. When cholestasis is severe, delivery at 36 weeks with or without fetal lung maturity may be considered.
Recurrence risk in subsequent pregnancies is approximately 70% and is usually more severe. Estrogen-containing oral contraceptives can cause cholestasis in these patients.
TABLE 17-1 Liver Function Test Changes during Normal Pregnancy | ||||||||||||||||||
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Acute Fatty Liver of Pregnancy
Acute fatty liver of pregnancy (AFLP) is uncommon, occurring in 1 in 10,000 pregnancies. It typically occurs in primigravid women in the third trimester and is associated with multiple gestations, male fetuses, and with a fetal mitochondrial gene mutation causing long chain 3-hydroxylacyl-CoA-dehydrogenase deficiency. Patients present with nausea, vomiting, epigastric pain, anorexia, jaundice, and malaise. Intra-abdominal bleeding or altered mental status may indicate disease progression to disseminated intravascular coagulation (DIC) or hepatic failure. Laboratory tests may reveal hypoglycemia, elevated aminotransferases to 1,000 IU/L, leukocytosis, thrombocytopenia, coagulopathy, markedly reduced antithrombin III,
metabolic acidosis, hyperuricemia, and renal failure. Treatment includes maternal stabilization with intensive supportive care and prompt delivery, either with induction of labor with close maternal and fetal surveillance or cesarean delivery. Liver function usually normalizes within 1 week postpartum, and recurrence in subsequent pregnancy is uncommon.
Hepatic Disorders Not Directly Related to Pregnancy
