Hepatitis in Pregnancy

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Chapter 211 Hepatitis in Pregnancy

INTRODUCTION

Description: Hepatitis is one of the most serious infections that occurs during pregnancy.
Prevalence: Hepatitis—0.1% to 1.5% of pregnancies (one third of Americans have antibodies to hepatitis A). The prevalence of hepatitis in pregnancy has declined in the past 15 years.
Predominant Age: Reproductive.
Genetics: No genetic pattern.

ETIOLOGY AND PATHOGENESIS

Causes: Five different forms of hepatitis may be involved. Hepatitis A is caused by a ribonucleic acid (RNA) virus that is transmitted by fecal–oral contamination and accounts for 30% to 50% of acute disease. Hepatitis B is caused by a small DNA virus that accounts for 40% to 45% of occurrences. It is estimated that acute hepatitis B occurs in 1 to 2 of 1000 pregnancies and that chronic infections are present in 5 to 15 of 1000 pregnancies. Hepatitis B is transmitted by parenteral and sexual contact. Hepatitis B is easily transmitted sexually: 25% of people who have sexual contact with an infected person become infected. Hepatitis C (non-A, non-B) accounts for 10% to 20% of cases and is caused by a single-stranded RNA virus spread by parenteral exposure. Hepatitis D is caused by an RNA virus that requires coinfection with the hepatitis B virus. Significant mortality and long-term consequences may occur from this less common infection. Hepatitis E, G and other forms of non-A, non-B hepatitis are uncommon but may occur during pregnancy as well.
Risk Factors: Groups at greatest risk for hepatitis B are intravenous drug users, hemophiliacs, homosexuals, and health care workers. Poor handwashing habits, multiple sexual partners, a history of sexually transmitted disease, tattoos, and multiple blood transfusions (hepatitis C) increase the risk of infection as well.

CLINICAL CHARACTERISTICS

Signs and Symptoms

(Unchanged by pregnancy)

• Fever (60%), malaise (70%), fatigue, anorexia (50%), nausea (80%)
• Variable right upper quadrant pain (50%)
• Upper abdominal tenderness with hepatomegaly
• Dark urine (85%) and acholic stools
• Jaundice a possibility in up to 60%
• Coagulopathy or encephalopathy (fulminant infections only)

DIAGNOSTIC APPROACH

Differential Diagnosis

• Acute fatty liver of pregnancy
• Toxic hepatic injury
• Cholestasis of pregnancy
• Severe pre-eclampsia
• Mononucleosis
• Cytomegalovirus hepatitis
• Lupoid hepatitis
• Viral enteritis

Associated Conditions: Jaundice, cirrhosis, pancreatitis, nephritis, ileus, and premature labor.

Workup and Evaluation

Laboratory: Hepatitis during pregnancy is diagnosed in the same manner as for nonpregnant patients; serum chemistry abnormalities indicate active hepatic disease (marked elevation of alanine aminotransferase, aspartate aminotransferase, and bilirubin), and immunochemical analysis indicates the presence of infection and the phase of the clinical course. In severe cases, coagulation studies should be performed. Routine screening of all pregnant patients is recommended.
Imaging: None indicated.
Special Tests: Percutaneous liver biopsy may be helpful but is generally not required.
Diagnostic Procedures: History, physical examination, ultrasonography (limited value), and laboratory investigation.

Pathologic Findings

Viral hepatitis is distinguished from other hepatic injuries by the characteristic pattern of injury and infiltrate.

MANAGEMENT AND THERAPY

Nonpharmacologic

General Measures: Patients with encephalopathy or coagulopathy or who are severely debilitated should be hospitalized. Nutritional support is generally required. Fluid intake and electrolyte levels must be maintained. The upper abdomen should be protected from trauma. Sexual contact should be avoided until the partner(s) receive prophylaxis.
Specific Measures: No specific measures have been shown to alter the natural course of these infections. Prophylaxis should be considered for anyone at risk (e.g., travel to endemic area, sexual partners). Acute exposure should be treated with immune globulin (see Follow-up).
Diet: Maintain good nutrition.
Activity: The upper abdomen should be protected from trauma.
Patient Education: Patients should be instructed regarding risk factors and modes of spread to limit risk for family contacts and future recurrences; American College of Obstetricians and Gynecologists Patient Education Pamphlet AP125 (Protecting Yourself Against Hepatitis B).

Drug(s) of Choice

Those necessary for support only; others of limited or unproved value.

FOLLOW-UP

Patient Monitoring: Normal prenatal care once the acute episode is resolved. Continued monitoring for chronic liver dysfunction or carrier state (where applicable).
Prevention/Avoidance: Active immunization of those at risk before a pregnancy is planned. Patients exposed to hepatitis A may be given γ-globulin in the same manner as that for nonpregnant patients. Patients exposed to hepatitis B or those found to be carriers may receive either active immunization with hepatitis vaccine or passive immunization with hepatitis B immune globulin (HBIG). To be effective, HBIG should be given within 48 hours of exposure. The infants of these mothers should receive both forms of immunization. Infants born to mothers with hepatitis B infection should be given HBIG 0.5 mL and hepatitis B vaccine (separate site) within 12 hours of birth, with follow-up vaccinations at 1 and 6 months of age.
Possible Complications: Mortality from acute hepatitis varies with the type of hepatitis and severity of infection but is generally in the range of 2 to 10 of 1000 cases. Serious complications of hepatitis A are uncommon. Vertical transmission of hepatitis B to the developing fetus can pose a significant risk. (Of women seropositive for hepatitis B surface antigen [HbsAg], 10% to 20% transmit the virus to their neonates in the absence of immunoprophylaxis. In women who are seropositive for both HBsAg and hepatitis B envelope antigen [HbeAg], vertical transmission is approximately 90%. In patients with acute hepatitis B, vertical transmission occurs in up to 10% of neonates when infection occurs in the first trimester and in 80% to 90% of neonates when acute infection occurs in the third trimester.) The majority of untreated infants become chronic carriers, capable of infecting others. These infants are also at increased risk of cirrhosis and hepatic cancer. Neonatal infection rates vary with gestation and are highest in the third trimester (exposure to blood and fluids at delivery). Patients with the envelope antigen have an 80% chance of vertical transmission of the infection. Hepatitis D leads to chronic hepatitis in 80% of patients with rapid appearance of cirrhosis in 15%; mortality approaches 25%. Chronic liver disease and liver failure may follow infection with hepatitis B, C, or D.
Expected Outcome: Of patients, 85% to 90% experience complete resolution of symptoms; 10% to 15% of patients with hepatitis B become chronic carriers (10% to 15% of these develop serious long-term liver problems including cirrhosis and hepatocellular carcinoma). Patients with hepatitis C or D have a >80% risk of chronic hepatitis with cirrhosis and liver failure in 20% to 25%.

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MISCELLANEOUS

ICD-9-CM Code: 647.6.

REFERENCES

Level II

European Paediatric Hepatitis C Virus Network. Effects of mode of delivery and infant feeding on the risk of mother-to-child transmission of hepatitis C virus. European Paediatric Hepatitis C Virus Network. BJOG. 2001;108:371.

Resti M, Azzari C, Galli L, et alItalian Study Group on Mother-to-Infant Hepatitis C Virus Transmission. Maternal drug use is a preeminent risk factor for mother-to-child hepatitis C virus transmission: results from a multicenter study of 1372 mother-infant pairs. J Infect Dis. 2002;185:567. Epub 2002 Feb 14

Level III

American College of Obstetricians and Gynecologists. Viral hepatitis in pregnancy. ACOG Educational Bulletin 248. Washington, DC: ACOG, 1992.

American College of Obstetricians and Gynecologists. Sexually transmitted diseases in adolescents. ACOG Committee Opinion 301. Obstet Gynecol. 2004;104:891.

American College of Obstetricians and Gynecologists. Hepatitis B and hepatitis C virus infections in obstetrician–gynecologists. ACOG Committee Opinion 332. Obstet Gynecol. 2005;106:1141.

Erdem G, Tekinalp G, Yurdakok M, et al. Perinatal transmission of hepatitis B virus infection. Lancet. 1994;343:289.

Euler GL, Wooten KG, Baughman AL, Williams WW. Hepatitis B surface antigen prevalence among pregnant women in urban areas: implications for testing, reporting, and preventing perinatal transmission. Pediatrics. 2003;111:1192.

Guntupalli SR, Steingrub J. Hepatic disease and pregnancy: an overview of diagnosis and management. Crit Care Med. 2005;33:S332.

Hadzic N. Hepatitis C in pregnancy. Arch Dis Child Fetal Neonatal Ed. 2001;84:F201.

Hunt CM, Carson KL, Sharara AI. Hepatitis C in pregnancy. Obstet Gynecol. 1997;89:883.

Lynch-Salamon DI, Combs CA. Hepatitis C in obstetrics and gynecology. Obstet Gynecol. 1992;79:621.

Poland GA, Jacobson RM. Clinical practice: prevention of hepatitis B with the hepatitis B vaccine. N Engl J Med. 2004;351:2832.

Riely CA. Hepatic disease in pregnancy. Am J Med. 1994;96:18S.

Snydman DR. Hepatitis in pregnancy. N Engl J Med. 1985;313:1398.

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