E. Infant's birthweight? Weight loss in the first few days of life is expected, but excessive weight loss may occur in the setting of dehydration and poor caloric intake. It is important to recognize dehydration in young infants to avoid life-threatening acidosis.
III. Differential Diagnosis. Indirect hyperbilirubinemia is much more common in neonates than in older children. When seen in an older infant or child, consider diagnoses of hemolytic anemia and hepatic disease.
A. Physiologic Jaundice. Jaundice that occurs in otherwise healthy term infants as a result of factors that include RBC turnover, liver immaturity (eg, low levels of uridine diphosphate [UDP]-glu-curonyl transferase), and increased enterohepatic circulation of bilirubin (due to delayed stooling, presence of bilirubin in meconium, and presence of glucuronidase in gut).
B. Breast-Feeding Jaundice. Distinct from breast-milk jaundice (which occurs at > 1 week of life). Breast-feeding jaundice occurs in first week of life among breast-fed infants and is believed to be due to relative lack of calories or dehydration, or both.
C. Breast-Milk Jaundice. Infant presents with indirect hyperbilirubinemia between 7 days and several months of life. Thought to be due to one or more ill-defined factors in breast milk that interfere with metabolism of bilirubin. Levels of indirect hyperbilirubinemia may be as high as 10-30 mg/dL. Temporary cessation of breastfeeding results in a drop in serum bilirubin level.
D. ABO Incompatibility. Occurs most commonly among infants born to mothers with O-type blood. Maternal antibodies (IgG) cross placenta and bind to surface of RBCs, which are subsequently destroyed in the spleen. Rh incompatibility, more severe than ABO incompatibility, is uncommon with the widespread use of Rh immunoglobulin.
E. G6PD Deficiency. An X-linked disorder that is seen in up to 10% of African-American males. G6PD helps to protect the rBc membrane from oxidant stresses. Although many cases of G6PD deficiency go undiagnosed, this diagnosis can be associated with severe hyperbilirubinemia.
F. Erythrocyte Structural Defects. Disorders such as spherocyto-sis and elliptocytosis are associated with RBC destruction in the spleen. Family history of splenectomy, gallbladder stones, or transfusions should raise suspicion of these disorders. Spherocytosis is due to a defect in the RBC membrane, often involving the protein spectrin.
G. Familial Disorders of Conjugation. Gilbert syndrome, associated with decreased UDP-glucuronyl transferase activity, affects up to 7% of the population and is typically diagnosed during adolescence.
Crigler-Najjar syndromes are very rare disorders, associated with structural abnormalities in UDP-glucuronyl transferase.
H. Other Causes. Hemolytic anemias, transfusions, and trauma associated with hematomas result in increased bilirubin load and are causes of indirect hyperbilirubinemia in any age group. Infants with galactosemia and hypothyroidism may present initially with indirect hyperbilirubinemia in the newborn period. Congenital infections (eg, cytomegalovirus, toxoplasmosis) that cause systemic illness may be associated with hemolysis and indirect hyperbilirubinemia, in addition to hepatitis and direct hyperbiliru-binemia. Indirect hyperbilirubinemia may be exaggerated in the presence of the following risk factors: Asian or Native American race, prematurity, polycythemia, male sex, Down syndrome, oxytocin induction, delayed stooling, and having a sibling with a history of neonatal jaundice.
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