Jaundice (cont.)

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What is neonatal jaundice (jaundice in newborn infants)?

Neonatal jaundice is jaundice that begins within the first few days after birth. (Jaundice that is present at the time of birth suggests a more serious cause of the jaundice.) In fact, bilirubin levels in the blood become elevated in almost all infants during the first few days following birth, and jaundice occurs in more than half of newborns. For all but a few infants, the elevation and jaundice represents a normal physiological phenomenon and does not cause problems.

The cause of normal, physiological jaundice is well understood. During life in the uterus, the red blood cells of the fetus contain a type of hemoglobin that is different from the hemoglobin that is present after birth. When an infant is born, the infant's body begins to rapidly destroy the red blood cells containing the fetal-type hemoglobin and replaces them with red blood cells containing the adult-type hemoglobin. This overloads the liver with bilirubin derived from the fetal hemoglobin from the destroyed red blood cells. The liver in a newborn infant is not significantly mature, and its ability to process and eliminate bilirubin is limited. As a result of both the influx of large amounts of bilirubin and the immaturity of the liver, bilirubin accumulates in the blood. Within two or three weeks, the destruction of red blood cells comes to an end, the liver matures, and the bilirubin levels return to normal.

There is another uncommon syndrome associated with neonatal jaundice, referred to as breast-milk or breastfeeding jaundice. In this syndrome, jaundice appears to be caused by or at least accentuated by breastfeeding. Although the cause of this type of jaundice is unknown, it has been hypothesized that there is something in breast milk that reduces the ability of the liver to process and eliminate bilirubin. With breast-milk jaundice, the bilirubin levels rise and reach peak levels in approximately two weeks, remain elevated for a week or so, and then decline to normal over several weeks or months. This timing of the elevation in bilirubin and jaundice is different from normal physiological jaundice described previously, and allows the two causes of jaundice to be differentiated. The real importance of the more prolonged jaundice associate with breast-milk jaundice is that it raises the possibility that there is a more serious cause for the jaundice that needs to be sought, for example, biliary atresia (destruction of the bile ducts). Breast-milk jaundice alone usually does not cause problems for the infant.

Physiologic jaundice and breast-milk jaundice usually do not cause problems for the infant; however, there is a concern that high or prolonged elevation in the levels of unconjugated bilirubin (the type of bilirubin that is not attached to glucuronic acid and the main type of bilirubin that is present in physiologic and breast-milk jaundice) will cause brain (neurologic) damage in the infant. Therefore, when unconjugated bilirubin levels are high or prolonged, treatment usually is started to lower the levels of bilirubin. Treatment may be started earlier in infants who are born prematurely since their livers take longer to mature, and the risk of higher and more prolonged elevations of bilirubin is greater. Treatment involves phototherapy with artificial or natural sunlight and, if phototherapy is not successful, exchange transfusion in which the infant's blood is exchanged with normal blood from blood donors.

The benign nature of physiologic and breast-milk jaundice needs to be distinguished from hemolytic disease of the newborn, a much more serious, even life-threatening cause of jaundice in newborns that is due to blood group incompatibilities between mother and fetus, for example Rh incompatibility. The incompatibility results in an attack by the mother's antibodies on the babies red blood cells leading to hemolysis. Fortunately, because of modern management of pregnancy, this cause of jaundice is rare.


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