Neonatal jaundice

Last updated: July 27, 2023

Summarytoggle arrow icon

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). The most common cause of neonatal jaundice is a physiological rise in unconjugated bilirubin, which results from hemolysis of fetal hemoglobin and an immature hepatic metabolism of bilirubin. Physiological neonatal jaundice is harmless and occurs in most infants between the second and the eighth day of life. Pathologic neonatal jaundice can be conjugated or unconjugated and is typically a symptom of an underlying disease. Possible conditions include hemolytic anemias, blood group incompatibilities, Gilbert syndrome and Crigler-Najjar syndrome, G6PD deficiency, and congenital biliary flow obstructions. 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). The degree of hyperbilirubinemia can be measured by transcutaneous and/or serum bilirubin measurements. Treatment modalities include phototherapy, intravenous immune globulin (IVIG), and exchange transfusion, in addition to specific therapies for the respective underlying conditions. Treatment is targeted at reducing the risk of kernicterus and hence permanent neurological sequelae.

Classificationtoggle arrow icon

Types of neonatal jaundice
Features Physiological neonatal jaundice Pathological neonatal jaundice
Type of hyperbilirubinemia
  • Can present < 24 hours after birth
Peak total serum bilirubin
  • May rise > 15 mg/dL
Daily rise in bilirubin levels
  • < 5 mg/dL/day
  • > 5 mg/dL/day
  • See “Etiology” below.

Etiologytoggle arrow icon

Overview of mechanisms of neonatal jaundice [1][2]
Type of hyperbilirubinemia Mechanism Etiology
Pathological unconjugated hyperbilirubinemia
Pathological conjugated hyperbilirubinemia
  • Intrahepatic
  • Extrahepatic
Mixed hyperbilirubinemia
  • Combined

Pathophysiologytoggle arrow icon

Physiological neonatal jaundice [5]

Pathological neonatal jaundice [5]

Subtypes and variantstoggle arrow icon

Breastfeeding jaundice [5]

Breast milk jaundice [5]

Clinical featurestoggle arrow icon

Diagnosticstoggle arrow icon

Physiological neonatal jaundice is a diagnosis of exclusion. Laboratory tests should first rule out all pathological causes of neonatal jaundice.

Jaundice in a term newborn less than 24 hours old is always pathologic.

Treatmenttoggle arrow icon

Phototherapy [2][7][9]

Phototherapy is the primary treatment in neonates with unconjugated hyperbilirubinemia.

Newborns with TSB levels below the phototherapy threshold usually do not require treatment. [11]

Exchange transfusion

Most rapid method for lowering serum bilirubin concentrations

IV immunoglobulin

  • Indications: used in cases with immunologically mediated conditions, or in the presence of Rh, ABO, or other blood group incompatibilities that cause significant neonatal jaundice
  • Dose range for IVIG: 500–1000 mg/kg

Complicationstoggle arrow icon

Acute bilirubin encephalopathy

Kernicterus (chronic bilirubin encephalopathy)

We list the most important complications. The selection is not exhaustive.

Prognosistoggle arrow icon

  • Favorable in most cases
  • In rare cases, kernicterus may occur, resulting in permanent neurological sequelae.

Preventiontoggle arrow icon

Interruption of enterohepatic circulation with adequate enteral nutrition [7]

  • Frequent feeds with breast milk
  • Protein-rich nutrition in the form of breast milk or special formula feeds
  • In the case of dehydration, protein-rich feeding solutions are preferred over glucose or water.

Referencestoggle arrow icon

  1. Joseph A, Samant H. Jaundice. StatPearls. 2020.
  2. Porter ML, Dennis BL. Hyperbilirubinemia in the term newborn. Am Fam Physician. 2002; 65 (4): p.599-606.
  3. Memon N, Weinberger BI, Hegyi T, Aleksunes LM. Inherited disorders of bilirubin clearance. Pediatr Res. 2015; 79 (3): p.378-386.doi: 10.1038/pr.2015.247 . | Open in Read by QxMD
  4. Singh SP, Pati GK. Alagille Syndrome and the Liver: Current Insights. Euroasian Journal of Hepato-Gastroenterology. 2018; 8 (2): p.140-147.doi: 10.5005/jp-journals-10018-1280 . | Open in Read by QxMD
  5. Neonatal Hyperbilirubinemia. Updated: January 1, 2018. Accessed: January 27, 2018.
  6. Chen CY, Shiesh SC, Tsao HC, Lin XZ. Human biliary beta-glucuronidase activity before and after relief of bile duct obstruction: is it the major role in the formation of pigment gallstones?. J Gastroenterol Hepatol. 2000; 15 (9): p.1071-5.doi: 10.1046/j.1440-1746.2000.02292.x . | Open in Read by QxMD
  7. American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. 2004; 114 (1): p.297-316.
  8. Maisels MJ, Kring E. Transcutaneous bilirubin levels in the first 96 hours in a normal newborn population of > or = 35 weeks' gestation. Pediatrics. 2006; 117 (4): p.1169-1173.doi: 10.1542/peds.2005-0744 . | Open in Read by QxMD
  9. Woodgate P, Jardine LA. Neonatal jaundice: phototherapy. BMJ Clin Evid. 2015; 2015.
  10. Sawyer TL. Phototherapy for Jaundice. In: Rosenkrantz T, Phototherapy for Jaundice. New York, NY: WebMD. Updated: December 6, 2015. Accessed: May 11, 2017.
  11. Kemper AR, Newman TB, Slaughter JL, et al. Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics. 2022; 150 (3).doi: 10.1542/peds.2022-058859 . | Open in Read by QxMD

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