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Neonatal Jaundice

Jaundice is defined by a serum bilirubin concentration greater than 5 mg/dL. Clinical jaundice develops in 50% of newborns, and breast-feed infants have an increased incidence of jaundice. Differentiation between physiologic jaundice, which is seen in many infants during the first week of life, and pathologic jaundice is essential because pathologic jaundice is a sign of a more serious condition.


Physiologic versus pathologic jaundice

Physiologic jaundice is characterized by unconjugated hyperbilirubinemia that peaks by the third or fourth day of life in full-term newborns and then steadily declines by 1 week of age.

Pathologic jaundice usually appears within the first 24 hours after birth and is characterized by a rapidly rising serum bilirubin concentration (>5 mg/dL per day), prolonged jaundice (>7 to 10 days).

Differential diagnosis of unconjugated hyperbilirubinemia

Increased bilirubin production

Fetal-maternal blood group incompatibility is one cause of increased bilirubin production. Rh sensitization occurs when an Rh-negative mother is exposed to Rh-positive blood cells. Subsequent Rh-positive fetuses may develop hemolysis. Other minor blood group incompatibilities also can cause hemolysis and jaundice.

ABO incompatibility is the most common type of isoimmune hemolytic disease. It can occur when the mother's blood group is O and the baby’s is A or B. This type of hemolysis is relatively mild.

G6PD deficiency, a sex-linked disease, is an important cause of hyperbilirubinemia and anemia in infants of Greek and Asian descent.

Abnormalities of the red blood cell membrane, such as spherocytosis and elliptocytosis, may cause hyperbilirubinemia. Alpha thalassemia may occur in the neonatal period.

Hematoma, occult hemorrhage, or polycythemia (fetomaternal or twin-to-twin transfusion, delayed cord clamping, intrauterine growth retardation, or maternal diabetes) may lead to hyperbilirubinemia.

Decreased bilirubin excretion

Delay in intestinal transit time, because of decreased motility or bowel obstruction, increases the enterohepatic circulation. Relief of the obstruction results in a decline in bilirubin concentration.

Crigler-Najjar syndrome is a rare, inherited, lifelong deficiency of bilirubin excretion. Type I is autosomal recessive. Patients present with extreme jaundice (bilirubin concentration $25 mg/dL) and have a very high risk of bilirubin encephalopathy. Type II is autosomal dominant, and it can effectively be treated with phenobarbital.

Neonatal hypothyroidism is another cause of prolonged indirect hyperbilirubinemia.

Increased bilirubin production and decreased excretion

Sepsis often causes increased breakdown of red blood cells and decreased hepatic excretion of bilirubin.

Certain drugs given to the newborn may also induce hemolysis or decrease bilirubin excretion.

Breast feeding

Feeding with breast milk is associated with neonatal hyperbilirubinemia.

In healthy newborns, the danger of an elevated bilirubin concentration is minimal, and switching to formula feeding is unnecessary.

Consequences of unconjugated hyperbilirubinemia. Bilirubin encephalopathy (kernicterus) is defined as the acute and often fatal syndrome characterized by opisthotonos, hypotonia, a high-pitched cry.


Low-risk infants with minimal jaundice are observed for an increase in the jaundice intensity or a spread to the baby’s feet (jaundice advances from head-to-foot).

Phototherapy with blue light causes photoconversion of bilirubin to a water-soluble product that is excreted in urine and stool. Bilirubin concentrations are measured once or twice a day.

Exchange transfusion therapy. Exchange transfusion is used for emergent treatment .