By Karina Luise Glaser
From Medstudents'Homepage

Jaundice is present during the first week of life in 60 percent of term infants and 80 percent of pre-term infants. There is usually accumulation of unconjugated bilirubin, but there may also be deposition of direct-reacting bilirubin.

The unconjugated bilirubin may be neurotoxic for infants, and the conjugated form indicates a potentially serious disorder.

During the fetal life, the placenta is the principal route of elimination of unconjugated bilirubin. In the newborn infant, the hepatic cells excrete the conjugated, water soluble bilirubin into the biliary system, then into the gastrointestinal tract.


  • Increased production of bilirubin (hemolytic anemias, shortened red cell life due to immaturity or transfused cells, increased enterohepatic circulation, infection).

  • Decreased activity of the transferase enzyme (hypoxia, infection, hypothermia, thyroid deficiency).

  • Block of the transferase enzyme (drugs, substances which require glucuronic acid conjugation for excretion).

  • Decreased amounts or absence of the enzyme (genetic defect, prematurity).

  • Reduction of bilirubin uptake by the hepatic cell.

  • The unconjugated bilirubin toxic effects are increased by hypoproteinemia, drugs, acidosis, hypoglycemia, starvation and hypothermia, which reduce the retention of bilirubin in the circulation. Toxic effects are also increased by factors that increase the permeability of the blood-brain barrier and nerve cells membrane such as asphyxia, prematurity, hyperosmolality and infection.

    Other factors which increase unconjugated, lipid soluble bilirubin levels include breast feeding, dehydration, meconium, oxytocin and phenolic detergents.

    Jaundice usually begins on the face (serum bilirubin - 5 mg/dL), progressing to the mid-abdomen (15 mg/dL) and feet (20 mg/dL). It may be present at birth or appear during the neonatal period. Unconjugated bilirubin jaundice is bright yellow or orange, while direct bilirubin jaundice is greenish or muddy yellow. The infant appears lethargic, feeding poorly.


    Jaundice appearing at birth or within 24 hours: sepsis, erythroblastosis fetalis, concealed hemorrhage, cytomegalic inclusion disease, rubella, congenital toxoplasmosis.

    Jaundice appearing on the 2nd or 3rd day: physiologic, hyperbilirubinemia of the newborn (severe form of jaundice), Crigler Najjar syndrome (familial non-hemolytic icterus).

    Jaundice appearing after the 3rd day, within the 1st week: septicemia, syphilis, toxoplasmosis, cytomegalic inclusion disease.

    Other causes of early jaundice: intrauterine transfusions, extensive ecchymosis or hematomas, polycythemia.

    Jaundice appearing after the 1st week: breast milk jaundice, septicemia, congenital atresia of the bile ducts, hepatitis, rubella, herpetic hepatitis, galactosemia, hypothyroidism, spherocytosis (congenital hemolytic anemia), other hemolytic anemias (G6PD deficiency, glutathione synthetase, reductase, peroxidase, pyruvate kinase deficiencies).

    Jaundice persisting during the 1st month: inspissated bile syndrome, hyperalimentation associated cholestasis, hepatitis, cytomegalic inclusion disease, syphilis, toxoplasmosis, familial non-hemolytic icterus, congenital atresia of bile ducts, galactosemia, rarely physiologic jaundice (pyloric stenosis, hypothyroidism).

    The diagnostic evaluation should include determinations of bilirubin levels (direct and indirect reacting levels), hemoglobin, reticulocyte count, blood type, Coombs test, examination of peripheral blood smear.

    Indirect reacting hyperbilirubinemia, reticulocytosis and red blood cell destruction indicate hemolysis. Direct reacting hyperbilirubinemia suggests hepatitis, cholestasis, inborn errors of metabolism, cystic fibrosis, sepsis.


    Result of increased bilirubin production following breakdown of fetal red blood cells and limitation of liver bilirubin conjugation. It is usually visible by the 2nd to 3rd day and disappears by the 5th to 7th day.

    Risk factors for increased unconjugated bilirubinemia include maternal diabetes, race (Chinese, Japanese, Korean, Native American), prematurity, drugs (vitamin K, novobiocin), altitude, polycythemia, male sex, 21 trisomy, cutaneous bruising, cephalohematoma, oxytocin induction, breast feeding, weight loss (dehydration or calorie deprivation), delayed stooling. Bilirubin levels decline to adult levels within 10 to 14 days. After 2 weeks, hemolysis, hereditary glucuronyl transferase deficiency, breast milk jaundice, hypothyroidism or intestinal obstruction should be investigated (persistent indirect hyperbilirubinemia). Premature infants bilirubin levels rise slower and last longer.


    • 1st 24 hours of life.
    • Rise rate greater than 5 mg/dL/24 hours.
    • Bilirubin levels greater than 12 mg/dL in full-term infants and 10 to 14 mg/dL/24 hours in pre-term infants.
    • Persistence after the 2nd week of life.
    • Conjugated bilirubin greater than 1 mg/dL.
    Other important signs and symptoms include family history of hemolytic disease, pallor, hepatomegaly, splenomegaly, failure of phototherapy, vomiting, lethargy, poor feeding, excessive weight loss, apnea, bradycardia, abnormal vital signs (hypothermia), light colored stools, dark urine, signs of kernicterus.


    Risk related to the development of kernicterus (bilirubin encephalopathy). Jaundice may be considered pathologic when the time of appearance, duration and pattern varies from physiologic jaundice, or if the infants has risk factors.


    The milk of some of the mothers have non-esterified long chain fatty acids or other substances which inhibit glucuronyl transferase conjugation activity.

    It usually appears between the 4th and 7th days of life, peaking during the 2nd and 3rd weeks. Nursing may be discontinued, and bilirubin levels fall rapidly; then nursing is resumed. If breastfeeding is continued, bilirubin levels decrease more gradually.


    Characterized by the presence of glucuronyl transferase inhibiting factor, leading to kernicterus.

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