Neonatal Hyperbilirubinemia (Jaundice), continued
Causes of Jaundice
Clues to the etiology of neonatal hyperbilirubinemia may be obtained by reviewing the family, maternal, and neonatal history. Clues are also found in the course of jaundice.
Disorders of Overproduction
Excessive hemolysis with overproduction of bilirubin is the most common cause of neonatal hyperbilirubinemia. Jaundice that appears early suggests abnormally rapid destruction of red blood cells. Hemolytic disease in the newborn has two common causes:
- ABO incompatibility (dictionary): infants of blood type A or B born to mothers of blood type O received maternal type-specific anti-A or anti-B antibody across the placenta. The antibody binds to fetal red blood cells and causes hemolysis.
- Rh incompatibility (dictionary): Rh positive offspring of previously sensitized Rh negative mothers are exposed to anti-Rh antibody, usually anti-D, with consequent hemolysis.
Infants with ABO or Rh incompatibility may have anemia or progressively falling HCT with reticulocytosis. The direct Coombs test is usually positive.
Less frequently, neonatal hyperbilirubinemia may result from a inherited hemolytic disorder such as hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency or a hemoglobinopathy such as thalassemia.
Infants with a cephalohematoma or excessive bruising may develop hyperbilirubinemia from breakdown of the extravasated blood. Similarly, the infant with an unusually high HCT (venous HCT >65%) may have hyperbilirubinemia from the normal rate of destruction of an abnormally large red cell mass.
Hyperbilirubinemia may also result from increased enterohepatic circulation of bilirubin from delayed passage of meconium resulting from mechanical obstruction or reduced peristalsis.
More information on Jaundice
Disorders of Inadequate Conjugation or Secretion
These are uncommon and result from biliary obstruction or the impairment of hepatic uptake, conjugation, or canalicular transport of bilirubin. The hyperbilirubinemia may be unconjugated or conjugated, depending on whether the etiology is inadequate conjugation or inadequate biliary secretion. Examples include metabolic disorders such as Crigler-Najar syndrome (unconjugated), galactosemia and biliary atresia (conjugated). This type of disorder should be suspected if jaundice is prolonged beyond the first week of life.
Combined Disorders
These include bacterial sepsis, intrauterine infections such as syphilis, and metabolic disorders such as maternal diabetes mellitus. Note also that babies who are exclusively breastfed may have an exaggerated course of physiologic jaundice possibly related to increased enterohepatic recirculation of bilirubin.
