Gastrointestinal disorders in pregnancy

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Chapter 51 Gastrointestinal disorders in pregnancy

Michael Flynn

Abdominal pain in pregnancy

Pain arises either from inside an organ or the covering visceral peritoneum or, later, involvement of parietal peritoneum. Visceral pain is poorly localised, as it is mediated by the autonomic nervous system. With parietal peritoneum, localisation is more specific.

Pain pathways of pelvic organs

• Sensory afferent pathways from the body of the uterus travel via sympathetic nerves to T10–L1.
• The cervix is supplied by sympathetic nerves to T10–L1 and parasympathetic nerves to S2–S4.
• Pain pathways from the ovary travel via sympathetic nerves to T10.

Causes of abdominal pain in early pregnancy

• abortion
• impacted retroverted uterus at 10–14 weeks gestation, with the pain caused by urinary retention (management is by draining the urine and laying the woman prone or lateral)
• fibroids (torsion tends to occur in the puerperium; red degeneration is most common at 12–18 weeks gestation; presenting complaint is of tenderness over a mass, with mild fever and nausea/vomiting; management is with rest and analgesia)
• fallopian tube: ectopic pregnancy, torsion, salpingitis
• ovary: ovarian tumour/mass; complications: rupture, haemorrhage or torsion
• pelvic soft tissue (round ligament pain may commence from early second trimester; management is with rest, analgesia and warm packs)
• others: gastrointestinal (e.g. appendicitis) and urinary tract (e.g. infection, stone)

Causes of abdominal pain in late pregnancy

• uterine: contractions, placental abruption
• gastrointestinal tract: heartburn (occurs in 70%–80% of pregnant women), constipation, peptic ulcer disease, cholelithiasis (occurs in 3%–5% of pregnant women, but is mostly asymptomatic), pancreatitis, acute appendicitis (incidence of about 1 in 2500 pregnancies; has a significant association with premature labour), acute obstruction (from bands/adhesions, volvulus, hernia), inflammatory bowel disease
• other causes: renal (pyelonephritis, calculus), malignancy

Gastro-oesophageal disorders

Gastro-oesophageal reflux

• This is due to a combination of changes in lower oesophageal pressure, raised intragastric pressure and failure of acid clearance. The incidence is up to 80% in the third trimester.
• Initial management of reflux is with dietary change, upright posture and antacids.
• In established gastro-oesophageal reflux, the use of proton pump inhibitors (esomeprozole) is indicated.

Nausea and vomiting

• This is present in up to 85% of early normal pregnancies. Women with hyperemesis often have higher levels of serum human chorionic gonadotrophin (hCG).
• The nausea and vomiting commonly occurs at 6–16 weeks gestation, but 20% persist beyond this time.
• Hyperemesis does not affect birthweight. The incidence of abortion, stillbirths and premature delivery is lower in these women.

Management of hyperemesis gravidarum

• between 7 and 11 weeks; rarely severe
• fluid resuscitation and electrolyte restoration
• avoidance of trigger events
• ginger and vitamin B6 have some effect
• antiemetics, including metoclopramide and prochlorpromazine, and antihistamines, have been used as first-line management safely
• ondansetron: used successfully as second-line management
• glucocorticoids: used in severe hyperemesis, especially after the fetal palate has been formed
• investigations: mid-stream urine for urinary infection; pelvic ultrasound scan to exclude gestational trophoblastic disease and multiple pregnancy; full blood examination and electrolytes; liver function tests and thyroid function tests looking for hypochloraemic alkalosis
• differential diagnosis of persistent hyperemesis: includes hepatitis, pancreatitis, gastrointestinal obstruction, peptic ulcer disease, thyroid disease and adrenocortical insufficiency

Gastrointestinal disorders

Peptic ulcer disease

Incidence. Incidence is 1 in 4000.

Peptic ulcer disease rarely occurs for the first time in pregnancy. If it is present before pregnancy, there is often a reduction in symptoms. Peptic ulceration can increase in severity with pre-eclampsia and during the puerperium.

Management of peptic ulcer disease is similar to that in non-pregnant patients, with proton pump inhibitors forming the mainstay of treatment.

Coeliac disease

Gluten-sensitive enteropathy is often associated with subfertility in those with untreated coeliac disease. Untreated disease in pregnancy has an increased risk of recurrent abortion, intrauterine growth restriction (IUGR) and megaloblastic anaemia.

Management of coeliac disease in pregnancy includes a gluten-free diet, iron and folate supplementation, and fetal monitoring.

Inflammatory bowel disease

Fertility correlates with disease activity. Pregnancy itself does not increase the risk of relapse of inflammatory bowel disease.

Acute exacerbations are managed by admission to hospital, stool cultures, rest, withholding food and drink, corticosteroids and salazopyrine.

Hepatic disorders in pregnancy

Liver function tests in pregnancy

• There is no change in serum bilirubin and transaminase levels, although reduced total protein and albumin levels are normal.
• The increase in serum alkaline phosphatase is secondary to placental production.

Intrahepatic cholestasis of pregnancy

Incidence. Intrahepatic cholestasis affects up to 2% of pregnancies.

Presentation. Pruritus and mild jaundice present in the third trimester. Pruritus usually resolves within 48 hours of delivery. It starts at the soles and palms of the hands, and then spreads to the rest of the body.

Risk factors

• There is a family history in 45% of cases.
• It can recur with the use of the oral contraceptive pill and with future pregnancies.
• It is often worse with multiple pregnancies. Pre-eclampsia must be excluded.

Effect on pregnancy

• There is an increased risk of preterm delivery and perinatal mortality if not treated.
• In 10%–20% of cases, there is meconium liquor.

Investigations

• liver biochemistry (raised liver transaminase and bilirubin)
• raised fasting bile acids (this is the diagnostic feature of this disease)
• full blood count, urea/electrolytes and urate
• coagulation profile (raised prothrombin time may occur)
• hepatitis serology
• autoantibody screen
• antimitochondrial antibodies (primary biliary cirrhosis)
• ultrasound scan to exclude cholelithiasis

Pathophysiology

• altered bile acids and progesterone metabolism

Treatment

• coagulation monitoring
• vitamin K supplementation
• antihistamines
• ursodeoxycholic acid (UDCA) 10–16 mg/kg daily until delivery
• close monitoring (consider delivering early)

Acute fatty liver of pregnancy

Incidence. Incidence is 1 in 12,000 deliveries, with associated maternal and fetal mortality. It does not tend to recur.

Risk factors

• primiparity, obesity, pre-eclampsia and multiple pregnancy
• association with long-chain 3-hydroxyacyl CoA dehydrogenase (LCHAD)

Presentation

• abdominal pain, especially epigastric 50%
• nausea and vomiting in 75% of cases
• headache, pruritus
• jaundice in over 90% of cases
• hypertension in 50% of cases with oedema, proteinuria
• fever, ascites, pancreatitis
• progression to hepatic coma and renal failure possible

Investigation

• full blood examination (reveals a raised white cell count with neutrophilia, reduced platelets and haemolytic anaemia)
• coagulation profile (shows evidence of disseminated coagulopathy)
• electrolytes and renal function (elevated urea, creatinine and markedly raised urate)
• liver biochemistry (elevated bilirubin, but not markedly so; markedly elevated aspartate transaminase)
• hepatitis serology
• blood sugar levels (hypoglycaemia is common)
• ultrasound: microvascular fat deposits

Management

• Treat complications of hypoglycaemia and hypertension, and general supportive management.
• Exclude severe pre-eclampsia and prompt delivery required.
• 10% glucose and fresh frozen plasma/cryoprecipitate may be considered.
• Fetal morbidity is 90%, but with early recognition and treatment >70% survive.

Acute viral hepatitis

There does not appear to be an overall increase in congenital abnormalities if acute hepatitis occurs in pregnancy. Common causes are hepatitis A, B and C, herpes virus (simplex, varicella, cytomegalovirus) and Epstein-Barr virus.

Hepatitis A virus is usually self-limiting, with no increased fetal risks.

Chronic hepatitis

Chronic active hepatitis may be due to autoimmune diseases. In pregnancy, there is a risk of IUGR, fetal death, prematurity and pre-eclampsia. There does not appear to be an increased risk of fetal malformation.

Cirrhosis

• There may be a decrease in fertility secondary to oligomenorrhoea.
• Pregnancy is complicated by an increased incidence of abortion and intrauterine fetal death.
• Other complications of cirrhosis may also occur, such as bleeding oesophageal varices.
• Management: avoid increasing portal pressure, cease alcohol, increase carbohydrate consumption, lower protein and supplement with vitamins. In labour, shorten the second stage. Take precautions against the risk of postpartum haemorrhage. Avoid caesarean section because of large collateral circulation and adhesions.
• Primary biliary cirrhosis: antimitochondrial antibodies are present in over 95% of cases.
• There are no prospective studies to assess the effects of disease in pregnancy.

Causes of fulminant hepatic failure in pregnancy

• viral hepatitis
• acute fatty liver of pregnancy
• severe pre-eclampsia
• haemolytic uraemic syndrome
• paracetamol overdose

Gallbladder and biliary tract

Dilatation of the gallbladder is found in pregnancy. However, anecdotal evidence of an increased risk of developing cholesterol stones in pregnancy has not been substantiated.

Acute cholelithiasis and cholecystitis in pregnancy requiring cholecystectomy occurs in about 1 in 1000 deliveries. The prevalence of asymptomatic gallstones in pregnancy is 2%–10%, which is similar to the rate in non-pregnant women.

Further reading

Calhoun B.C. Gastrointestinal disorders in pregnancy. Obstetrics and Gynecology Clinics of North America. 1992;19:733-744.

Chamberlain G. Abdominal pain in pregnancy. British Medical Journal. 1991;302:1390-1394.

Mullaly B.A., Hansen W.F. Intraheptic cholestasis of pregnancy: review of the literature. Obstetrical and Gynecological Survey. 2001;57:47-52.

Samuels P., Cohen A. Pregnancies complicated by liver disease and liver dysfunction. Obstetrics and Gynecology Clinics of North America. 1992;19:745-763.

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