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Diseases

Neonatal Hepatitis

Neonatal hepatitis refers to damage (inflammation) in the liver that occurs in early infancy, about 1-2 months after birth. The liver is very small and still immature at birth. It has been suggested that any stress on the liver caused by other health issues in infancy can also cause neonatal hepatitis.

Nearly 20% of neonatal hepatitis is caused by a virus that caused the inflammation before birth by their mother or at the time of delivery. These include cytomegalovirus, rubella (measles) and hepatitis A, B, or C virus infections. Rare genetic abnormalities and certain non-viral infections can also cause neonatal hepatitis including congenital syphilis and toxoplasmosis infection. In the remaining 80% of infants with neonatal hepatitis, no specific virus can be identified as the cause (idiopathic neonatal hepatitis).

If neonatal hepatitis resolves fully, infants are not at increased risk for developing liver disease as they become children and adults. Neonatal hepatitis caused by the hepatitis A virus usually resolves itself within six months, but infections with the hepatitis B or C viruses most likely will result in chronic liver disease. Infants who develop extensive liver damage (cirrhosis) will ultimately need a liver transplant. Most newborns that have hepatitis B virus infection have no symptoms at birth but continue to carry the infection.

    Symptoms

    • Yellow discoloration of the skin and whites of the eye (jaundice)
    • Lack of weight gain
    • Failure to thrive, and grow normally, inability to absorb vitamins for normal growth
    • May be irritable because of excessively itchy skin
    • Enlarged liver and spleen
    • Clay colored stools
    • Dark urine

    In the more serious forms of neonatal hepatitis, additional symptoms can occur:

    • Tendency to bruise easily
    • Serious infection (sepsis)
    • Accumulation of body fluids within the abdomen (ascites) in the later stages of chronic liver damage Liver failure may eventually develop in some infants

    Diagnosis

    Since many causes of liver disease occur in in infancy presenting with the same symptoms, the cause for neonatal hepatitis must be evaluated since the mode of treatments differ.

    Any infant that has jaundice for more than 2 weeks of life should have blood tests done to determine the cause. Blood tests will include all tests for the cause of jaundice including viral infections, metabolic diseases and genetic conditions causing liver disease.

    Bilirubin is formed when the liver processes old red blood cells by removing it from the blood. The immature liver is unable to remove bilirubin from the bloodstream resulting in increased bilirubin levels:

    • Increased unconjugated bilirubin levels is considered normal (“physiologic jaundice”) and is the most common form of newborn As the breakdown of red blood cells slows down, and the liver matures, this type of jaundice rapidly disappears. This type of jaundice is particularly seen in babies born before 38 weeks’ gestation (preterm babies) and it typically appears on the second or third day of life
    • Increased conjugated bilirubin level (hyperbilirubinemia) indicates impaired flow of bile at any point from the liver cells into the intestine (cholestasis)

    Imaging

    Abdominal ultrasound imaging can indicate the likely cause such as structural abnormalities of the liver and biliary system but a confirmatory test is the liver biopsy.

    Treatment

    There is no specific treatment for neonatal hepatitis. The goal is to identify treatable disorders.

    Physiological jaundice can be prevented by adequate feeding. Breast-fed infants should have eight to 12 feedings a day for the first several days of life. Formula-fed infants usually should have 1 to 2 ounces (about 30 to 60 ml) of formula every two to three hours for the first week.

    Phototherapy

    The key is the early recognition of neonatal jaundice – hyperbilirubinemia. True neonatal hepatitis resolves on its own over time – usually over weeks to several months – and does not require follow up once there is no longer any evidence of jaundice and inflammation of the liver. Significant jaundice is often treated with phototherapy. This involves placing the baby on a warmer beneath special lights that penetrate a baby’s skin changing bilirubin into lumirubin, which is cleared easily out of the body thereby reducing bilirubin levels in the body. Special goggles’ covering the baby’s eyes for protection from the lights is used. If standard phototherapy fails other treatments for a more serious condition that is causing jaundice is explored. Physiologic jaundice almost never requires treatment beyond phototherapy.

    Reducing the bilirubin level may require an exchange transfusion, which involves the infants blood is exchanged with donated blood. This is a very specialized procedure and can only be carried out in centres for critically ill children. The jaundice may be related to blood type differences between mother and baby resulting in a rapid breakdown of the baby’s red blood cells.

    Intravenous transfusion of an immunoglobulin, a blood protein that can reduce levels of antibodies, may decrease jaundice and lessen the need for an exchange transfusion

    The nutritional needs and diet are essential for infants with neonatal jaundice and the following is advised:

    • Vitamin supplements are usually prescribed since Infants who are jaundiced have impaired bile flow from the liver; bile is required to absorb fats and fat-soluble vitamins (A, D, E and K).
    • Many infants are given phenobarbital, a drug used to control seizures, but which also stimulates the liver to excrete additional bile
    • Formula milk powders containing more easily digested fats are also given to ensure proper growth and development