Neonatal Jaundice


  Physiological Pathological
Onset 2nd or 3rd day First 24 hrs
Disappearance Disappears by 5th or 7th day Persists for > 14 days (term) or

> 21 days (pre-term)

Rate of rise < 5 mg\dL\day > 5 mg\dL\day or

> 0.5 mg\dL\hr

Peak bilirubin < 13 mg\dL > 13 mg\dL
Direct bilirubin < 2 mg\dL (at any time) > 2 mg\dL (at any time)


Mechanism of physiological neonatal jaundice:

  • Breakdown of fetal RBCs -> ↑ bilirubin
  • Immaturity of hepatic conjugation of bilirubin and elimination (in the 1st wk)



  • Mechanism: ↑ Unconjugated (indirect) bilirubin -> crosses BBB (basal ganglia and brain stem nuclei)
  • Sx: hypotonia, seizures, opisthotonos, delayed motor skills, choreoathetosis, sensorineural hearing loss


Causes of neonatal hyperbilirubinemia:

1) RBC metabolism: 

a. Polycythemia (Hct > 65):

  • RBC production: chronic hypoxia (CHD), IUGR, IODM (insulin), maternal Grave’s ds
  • Extra RBCs entering the circulation: delayed cord clamping, twin-twin transfusion, maternal-fetal transfusion
  • Treatment -> partial exchange transfusion w\ NS (dilutional)

Neonatal jaundice 2b. Increased hemolysis:

  • Immune-mediated:
    • Labs: high unconjugated bilirubin, anemia, high reticulocyte count, + Coombs
      • Rh negative mother\Rh positive baby
      • ABO incompatibility
  • Non-immune mediated:
    • Labs: same as above, but – Coombs -> do blood smear
      • Abnormal-looking RBCs -> membrane defect (spherocytosis or elliptocytosis)
      • Normal-looking RBCs -> enzyme defect (G6PD deficiency)
      • Extravascular hemolysis: cephalohematoma or bruising


2) Uncoupling of bilirubin from albumin:

  • Due to neonatal sepsis, drugs (ceftriaxone), hypoxia, acidosis


3) Problems in the liver: 

  • Conjugation\glucuronyl transferate (GT):
    • Decreased enzymatic activity -> normal newborn in the 1st wk
    • No GT activity -> Crigler-Najjar syndrome type 1
  • Liver diseases (primary or secondary to systemic ds affecting the liver)
    • Cholestasis, sepsis, TORCH, metabolic ds, hypothyroidism


4) Problems in the transport of bilirubin: 

  • Biliary atresia: obstruction at birth due to fibrosis and atresia of extrahepatic ducts
    • Sx: direct hyperbilirubinemia, poor feeding, vomiting, hepatosplenomegaly, pale stool\dark urine
    • Initial test -> US (triangular cord sign)
    • Accurate test -> percutaneous liver biopsy
    • Tx (initial\palliative): hepatic portojejunosotmy (Kasai procedure)
    • Tx (definitive): liver transplant

Neonatal jaundice 3


5) Problems in intestinal transport and excretion: 

  • Intestinal enterohepatic circulation:
    • Intestinal obstruction
  • Decreased colonic bacteria:
    • 1st wk of life, prolonged Abx, severe diarrhea


6) Breast-feeding jaundice: 

  • Means baby is not nursing well -> not getting enough calories
  • Jaundice occurs in the first days of life
  • Common in first-time feeding mothers
  • Tx -> rehydrate baby + lactation consultation


7) Breast-milk jaundice: 

  • Due to glucoronidase present in some breast milk
  • Jaundice in 2nd wk of life
  • Stop breast feeding for 48 hrs to confirm
  • Tx -> phototherapy + continue breast feeding (jaundice will be gone in 2-3 mo)


Neonatal jaundice 5


Treatment of Hyperbilirubinemia:

  • Phototherapy:

    • Complications: loose stool, erythematous macular rash, overheating -> dehydration, bronze baby syndrome
  • Double volume exchange transfusion:

    • If phototherapy is not working, or kernicterus is a concern



Download the PDF version: here


  • Dr Awadallah’s lecture
  • Kaplan step 2 lecture notes

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