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Jaundice is the most common condition that requires medical attention in newborns. The yellow coloration of
the skin and sclera in newborns with jaundice is the result of accumulation of unconjugated bilirubin. In most
infants, unconjugated hyperbilirubinemia reflects a normal transitional phenomenon. However, in some infants,
serum bilirubin levels may rise excessively, which can be cause for concern because unconjugated bilirubin is
neurotoxic and can cause death in newborns and lifelong neurologic sequelae in infants who survive
(kernicterus). For these reasons, the presence of neonatal jaundice frequently results in diagnostic evaluation.
Neonatal physiologic jaundice results from simultaneous occurrence of the following two phenomena [1] :
Bilirubin production is elevated because of increased breakdown of fetal erythrocytes. This is the result
of the shortened lifespan of fetal erythrocytes and the higher erythrocyte mass in neonates.
Hepatic excretory capacity is low both because of low concentrations of the binding protein ligandin in
the hepatocytes and because of low activity of glucuronyl transferase, the enzyme responsible for binding
bilirubin to glucuronic acid, thus making bilirubin water soluble (conjugation).
Etiologi : In mother-infant who are experiencing difficulties with the establishment of breast feeding, inadequate
fluid and nutrient intake often leads to significant postnatal weight loss in the infant. Such infants have an
increased risk of developing jaundice through increased enterohepatic circulation, as described above. This
phenomenon is often referred to as breastfeeding jaundice and is different from the breast milk
jaundice described below.
Neonatal jaundice, although a normal transitional phenomenon in most infants. Blood group incompatibilities
(eg, Rh, ABO) may increase bilirubin production through increased hemolysis..Nonimmune hemolytic disorders
(spherocytosis, G-6-PD deficiency) may also cause increased jaundice, and increased hemolysis appears to
have been present in some of the infants reported to have developed kernicterus in the United States in the
past 15-20 years.
Race: Incidence is higher in East Asians and American Indians and is lower in Africans/African
Americans.
Bowel atresia
Choledochal cyst
Conjugated hyperbilirubinemia
Crigler-Najjar syndrome
Immune hemolytic anemia
Nonimmune hemolytic anemia
Congenital infections with cytomegalovirus or toxoplasmosis
Differential Diagnoses
Biliary Atresia
Breast Milk Jaundice
Cholestasis
Cytomegalovirus Infection
Duodenal Atresia
Galactose-1-Phosphate Uridyltransferase Deficiency (Galactosemia)
Hemolytic Disease of Newborn
Hepatitis B
Hypothyroidism
Treatment : Phototherapy, intravenous immune globulin (IVIG), and exchange transfusion are the most widely
used therapeutic modalities in infants with neonatal jaundice.
Phototherapy
Phototherapy is the primary treatment in neonates with unconjugated hyperbilirubinemia.
Exchange transfusion
Early exchange transfusion has usually been performed because of anemia (cord hemoglobin < 11 g/dL),
elevated cord bilirubin level (>70 mol/L or 4.5 mg/dL), or both. A rapid rate of increase in the serum bilirubin
level (>15-20 mol/L /h or 1 mg/dL/h) was an indication for exchange transfusion, as was a more moderate rate
of increase (>8-10 mol/L/h or 0.5 mg/dL/h) in the presence of moderate anemia (11-13 g/dL).
The serum bilirubin level that triggered an exchange transfusion in infants with hemolytic jaundice was 350
mol/L (20 mg/dL) or a rate of increase that predicted this level or higher. Strict adherence to the level of 20
mg/dL has been jocularly referred to as vigintiphobia (fear of 20).