![]() Decreased stool passage → ↑ Enterohepatic circulation of bilirubin.Deficiency of UDP-glucuronosyltransferase.Infection/ sepsis (see “ Neonatal infection”).Hematomas (e.g., vacuum-assisted delivery, vitamin K deficiency bleeding).Hemoglobinopathies (e.g., sickle cell anemia, thalassemias).Erythrocyte membrane defects (e.g., hereditary spherocytosis).Erythrocyte enzyme defects (e.g., G6PD deficiency, pyruvate kinase deficiency).Hemolytic disease of the newborn (e.g., ABO incompatibility, Rh incompatibility ).Pathological unconjugated hyperbilirubinemia Overview of mechanisms of neonatal jaundice Treatment is targeted at reducing the risk of kernicterus and hence permanent neurological sequelae. ![]() Treatment modalities include phototherapy, intravenous immune globulin (IVIG), and exchange transfusion, in addition to specific therapies for the respective underlying conditions. The degree of hyperbilirubinemia can be measured by transcutaneous and/or serum bilirubin measurements. Hyperbilirubinemia can cause drowsiness and poor feeding in the newborn, and in severe cases, unconjugated bilirubin can cross the blood-brain barrier and cause permanent neurological damage ( kernicterus). Possible conditions include hemolytic anemias, blood group incompatibilities, Gilbert syndrome and Crigler-Najjar syndrome, G6PD deficiency, and congenital biliary flow obstructions. Pathologic neonatal jaundice can be conjugated or unconjugated and is typically a symptom of an underlying disease. Physiological neonatal jaundice is harmless and occurs in most infants between the second and the eighth day of life. The most common cause of neonata l jaundice is a physiological rise in unconjugated bilirubin, which results from hemolysis of fetal hemoglobin and an immature hepatic metabolism of bilirubin. Neonatal jaundice is one of the most common conditions occurring in newborn infants and is characterized by elevated levels of bilirubin in the blood (total serum bilirubin concentration > 5 mg/dL or > 85.5 μmol/L).
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