Neonatal Jaundice
Basics
Produced by an imbalance between rates of bilirubin production and bilirubin elimination:
- Newborns have higher rate of bilirubin production than adults because of increased RBC mass and shorter RBC life span
- Newborns, especially preterm infants, have rate limitations in hepatic conjugation and biliary excretion of bilirubin, increased enterohepatic circulation, and diminished bilirubin binding to albumin- and bilirubin-binding protein
Description
Description
- In most newborns, this represents physiologic jaundice and is not pathologic:
- Bilirubin normally increases from 1.5 mg/dL in cord blood to a mean of 6.5 mg/dL on day 3, followed by a gradual decline to levels of <1.5 mg/dL by day 10 or 12 of life
- Serum bilirubin may rise to levels exceeding neuroprotective defenses, causing bilirubin tissue binding in basal ganglia, hippocampus, brainstem nuclei, and cerebellum:
- Bilirubin-induced neurologic dysfunction (BIND) caused by increasingly severe hyperbilirubinemia from mild dysfunction to acute bilirubin encephalopathy (ABE) and kernicterus
- ABE describes the acute manifestations of bilirubin toxicity seen in the first wk after birth
- Kernicterus: Chronic form of BIND, with significant mortality or permanent sequelae including choreoathetoid type of cerebral palsy, gaze abnormalities, hearing loss, and dental dysplasia
- Rate of progression of BIND depends on rate of increase of bilirubin levels, duration of hyperbilirubinemia, albumin-binding reserves, unbound bilirubin level, host susceptibility, and comorbidities
- Death is due to respiratory failure and progressive coma or intractable seizures
- Bilirubin-induced neurologic dysfunction (BIND) caused by increasingly severe hyperbilirubinemia from mild dysfunction to acute bilirubin encephalopathy (ABE) and kernicterus
- Risk factors for severe hyperbilirubinemia:
- Jaundice observed in first 24 hr
- Predischarge total serum bilirubin (TSB) or transcutaneous bilirubin (TcB) (see Diagnosis) in high-risk or high–intermediate-risk zone
- Lower gestational age, 35–38 wk
- Exclusive breastfeeding, esp if inadequate with excessive weight loss
- Isoimmune or other hemolytic disease
- Sibling with neonatal jaundice
- Cephalohematoma or excessive bruising
- Ethnicity: East Asian
- Maternal obesity, primiparity
- SGA (small for gestational age), LGA (large for gestational age)
- Severe hyperbilirubinemia is associated with perinatal factors: Low birth weight, macrosomia from maternal diabetes, infection, polycythemia
- Hyperbilirubinemia neurotoxicity risk factors:
- Isoimmune hemolytic disease
- G6PD deficiency
- Asphyxia
- Sepsis
- Acidosis
- Albumin <3 mg/dL
- Postphototherapy (post-PT) bilirubin rebound to bilirubin levels of concern may occur:
- At high risk are newborns <37 wk gestation, patients with hemolytic disease, patients treated for <72 hr
Etiology
Etiology
- Unconjugated hyperbilirubinemia:
- Physiologic jaundice
- Jaundice in breastfed infants:
- Breastfeeding failure jaundice: Exaggeration of physiologic jaundice due to inadequate ingestion/production of sufficient volume of breast milk in the first wk of life. Neonates dehydrated
- Breast milk jaundice: Begins days 3–5, peaks within 2 wk but lasts up to 8 wk; caused by increased β-glucuronidase in breast milk
- 20–30% of predominately breastfed newborns may be jaundiced at 3–4 wk of age; 30–40% of these infants may have bilirubin levels ≥5 mg/dL
- May be exacerbated by dehydration
- Specific hemolytic conditions:
- Blood group isoimmunization due to ABO, Rh, and minor blood group incompatibility; ABO is most common: Rh disease is unusual (RhoGAM prevents)
- Red cell enzyme deficiencies: G6PD deficiency
- Red cell membrane defects: Hereditary spherocytosis and elliptocytosis
- Sepsis: Bacterial, viral, or protozoal
- Birth trauma:
- Increased heme load from resolving cephalohematoma or ecchymosis
- Polycythemia:
- Caused by maternal–fetal transfusion
- Fetal–fetal transfusion
- Infants of diabetic mothers
- Congenital hypothyroidism
- Defective hepatic conjugation:
- Gilbert syndrome (familial partial defect in glucuronyltransferase activity) is benign
- Crigler–Najjar syndrome (congenital absence of glucuronyltransferase), lifelong unconjugated hyperbilirubinemia
- Intestinal obstruction such as ileus, functional or anatomic, increases enterohepatic circulation
- Conjugated hyperbilirubinemia:
- Failure of hepatic excretion of conjugated bilirubin
- Causes include neonatal hepatitis, congenital biliary atresia, extrahepatic biliary obstruction, shock liver from neonatal asphyxia, neonatal hemosiderosis
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Citation
Schaider, Jeffrey J., et al., editors. "Neonatal Jaundice." 5-Minute Emergency Consult, 6th ed., Lippincott Williams & Wilkins, 2020. Emergency Central, emergency.unboundmedicine.com/emergency/view/5-Minute_Emergency_Consult/307035/0.1/Neonatal_Jaundice.
Neonatal Jaundice. In: Schaider JJJ, Barkin RMR, Hayden SRS, et al, eds. 5-Minute Emergency Consult. Lippincott Williams & Wilkins; 2020. https://emergency.unboundmedicine.com/emergency/view/5-Minute_Emergency_Consult/307035/0.1/Neonatal_Jaundice. Accessed December 3, 2024.
Neonatal Jaundice. (2020). In Schaider, J. J., Barkin, R. M., Hayden, S. R., Wolfe, R. E., Barkin, A. Z., Shayne, P., & Rosen, P. (Eds.), 5-Minute Emergency Consult (6th ed.). Lippincott Williams & Wilkins. https://emergency.unboundmedicine.com/emergency/view/5-Minute_Emergency_Consult/307035/0.1/Neonatal_Jaundice
Neonatal Jaundice [Internet]. In: Schaider JJJ, Barkin RMR, Hayden SRS, Wolfe RER, Barkin AZA, Shayne PP, Rosen PP, editors. 5-Minute Emergency Consult. Lippincott Williams & Wilkins; 2020. [cited 2024 December 03]. Available from: https://emergency.unboundmedicine.com/emergency/view/5-Minute_Emergency_Consult/307035/0.1/Neonatal_Jaundice.
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