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Neonatal Hepatitis B Virus (HBV) Infection
(See also Overview of Acute Viral Hepatitis .)
Neonatal hepatitis B virus infection is usually acquired during delivery. It is usually asymptomatic but can cause chronic subclinical disease in later childhood or adulthood. Symptomatic infection causes jaundice, lethargy, failure to thrive, abdominal distention, and clay-colored stools. Diagnosis is by serology. Rarely, severe illness may cause acute liver failure requiring liver transplantation. Less severe illness is treated supportively. Active and passive immunization help prevent vertical transmission.
Of the recognized forms of primary viral hepatitis, only hepatitis B virus (HBV) is a cause of neonatal hepatitis. Infection with other viruses (eg, cytomegalovirus, herpes simplex virus) may cause liver inflammation along with other manifestations.
HBV infection occurs during delivery from an infected mother. The risk of transmission is 70 to 90% from women seropositive for hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg—see Overview of Acute Viral Hepatitis : Serology) at the time of delivery. Women without the e antigen or with anti-HBe transmit the infection only 5 to 20% of the time.
Mother–infant HBV transmission results primarily from maternofetal microtransfusions during labor or contact with infectious secretions in the birth canal. Transplacental transmission is identified in < 2% of infections. Postpartum transmission occurs rarely through exposure to infectious maternal blood, saliva, stool, urine, or breast milk. Up to 90% of infants infected perinatally will develop chronic infection, and perinatally acquired HBV infection may be an important viral reservoir in certain communities.
Most neonates with HBV infection are asymptomatic but develop chronic, subclinical infection characterized by persistent HBsAg antigenemia and variably elevated transaminase activity. Many neonates born to women with acute hepatitis B during pregnancy are of low birth weight, regardless of whether they are infected.
Infrequently, infected neonates develop acute hepatitis B, which is usually mild and self-limited. They develop jaundice, lethargy, failure to thrive, abdominal distention, and clay-colored stools. Occasionally, severe infection with hepatomegaly, ascites, and hyperbilirubinemia (primarily conjugated bilirubin) occurs. Rarely, the disease is fulminant and even fatal. Fulminant disease occurs more often in neonates whose mothers are chronic carriers of hepatitis B.
Diagnosis of neonatal HBV infection is by serologic testing, including measurement of HBsAg, HBeAg, antibody to hepatitis B e antigen (anti-HBe), and quantitation of HBV DNA in blood. Other initial tests include CBC with platelets, ALT and α-fetoprotein levels, and liver ultrasonography. Family history of liver cancer or liver disease is noted because of the long-term risk of hepatocellular carcinoma. If testing suggests HBV infection, consultation with a pediatric hepatologist is recommended.
Symptomatic care and adequate nutrition are needed. Neither corticosteroids nor hepatitis B immune globulin (HBIG) is helpful for acute infection. No therapy prevents the development of chronic, subclinical hepatitis once infection is acquired.
All children with chronic HBV infection should be immunized with hepatitis A vaccine. Children with chronic HBV infection may benefit from antiviral drugs (eg, interferon alfa, lamivudine, adefovir) but these should be used only in consultation with a pediatric hepatologist.
Pregnant women should be tested for HBsAg during an early prenatal visit. Failing that, they should be tested when admitted for delivery. Some women who are HBsAg-positive are treated with lamivudine or telbivudine during the 3rd trimester, which may prevent perinatal transmission of HBV.
Neonates whose mothers are HBsAg-positive should be given 1 dose of HBIG 0.5 mL IM within 12 h of birth. Recombinant HBV vaccine should be given IM in a series of 3 doses, as is recommended for all infants in the US. (Note: Doses vary among proprietary vaccines.) The first dose is given concurrently with HBIG but at a different site. The 2nd dose is given at 1 to 2 mo, and the 3rd dose is given 6 mo after the first. If the infant weighs < 2 kg, the first dose of vaccine may be less effective. Subsequent vaccine doses are given at age 30 days (or when discharged from the hospital), and then 2 other doses are given at 1 to 2 mo and 6 mo after the 30-day dose.
Neonates whose mothers have unknown HBsAg status at the time of delivery should also receive their first dose of vaccine within 12 h of birth. For infants < 2 kg, the first dose is given concurrently with HBIG (0.5 mL IM) at a different site. For infants ≥ 2 kg and whose mothers can be tested for HBsAg and in whom follow up is assured, HBIG (0.5 mL IM) can be delayed up to 7 days pending a positive maternal test for HBsAg. Testing for HBsAg and anti-HBs at 9 to 15 mo is recommended for all infants born to HBsAg-positive mothers.
Separating a neonate from its HBsAg-positive mother is not recommended, and breastfeeding does not seem to increase the risk of postpartum HBV transmission, particularly if HBIG and HBV vaccine have been given. However, if a mother has cracked nipples, abscesses, or other breast pathology, breastfeeding could potentially transmit HBV.
Only HBV is a major cause of neonatal hepatitis; it is typically transmitted during delivery.
Most neonates are asymptomatic but develop chronic, subclinical HBsAg antigenemia and elevated transaminase levels.
Some infants develop mild hepatitis, and a few have fulminant liver disease.
Do serologic testing of infant and mother.
Neonates whose mothers are HBsAg-positive should be given 1 dose of HBIG 0.5 mL IM and HBV vaccine within 12 h of birth.
HBV-infected children should be immunized with hepatitis A vaccine; anti-HBV drugs (eg, interferon alfa) may help but should be used only in consultation with a pediatric hepatologist.
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