Neonatal Jaundice (NNJ) : Cause, Types, Symptoms, Diagnosis, Treatment

Neonatal Jaundice (NNJ) : Definition, Etiology, Types, Pathophysiology, Signs & Symptoms, Chart, Diagnosis, Care Plan, & Management


  • Neonatal Jaundice is defined as yellow discoloration of body parts because of high bilirubin level.
  • Within first 1-2 weeks of life, upto 60% of all term neonates & upto 80% of all preterm neonates develop neonatal jaundice.


A. Physiological NNJ

  • Very common
  • Self limiting
  • Never needs therapy
  • Always due to ↑ unconjugated bilirubin
  • No CNS complications are seen

Cause: Increased production of unconjugated bilirubin & decreased hepatic conjugation.


Normal RBC life span

  • Adults RBC: 120 days
  • Term neonate RBC: ∼ 70 days
  • Preterm neonate RBC: ∼ 30-50 days

B. Pathological


  • Visible jaundice in first 24 hours of life
  • Rapid rise in serum bilirubin (i.e. >0.5 mg/dl/hr OR >5 mg/dl/24 hr)
  • Any neonatal jaundice which needs therapy
  • Persistent or prolonged jaundice (i.e. beyond 2 week in term OR beyond 3 week in preterm)
  • Any conjugated hyperbilirubinemia
  • Neonatal jaundice with encephalopathy
  • Yellow staining of palms & soles


  • Hemolysis (Most common cause overall): Rh incompatibility (Single most common cause), ABO incompatibility, Minor blood group incompatibility, G6PD deficiency, Hereditary spherocytosis
  • Sepsis
  • Cephalhematoma
  • Breast milk jaundice
  • Inherited unconjugated hyperbilirubinemia e.g. Crigler Najjar Syndrome (1 & 2), Gilbert syndrome
  • Congenital hypothyroidism
  • Neonatal cholestasis e.g. Neonatal hepatitis, Biliary atresia etc.

Note: Sickle cell anemia doesn’t lead to pathological jaundice because there will be no hemolysis in neonates since Hb-F is still present.

Clinical Assessment

  • It is done by Modified Kramer’s Rule.

What is Modified Kramer’s Rule/Zones?

Neonatal Jaundice
Zone Serum Bilirubin (mg//dl)
1 5-8
2 8-10
3 10-12
4 12-15
5 > 15


* 1st Line Investigation : Total Serum Bilirubin (TSB)

* 2nd Line Investigations

  • Complete hemogram
  • ABO, Rh grouping
  • Direct coomb’s test (DCT)
  • G6PD deficiency
  • Liver function test (including direct function)


A. Acute 

Acute bilirubin encephalopathy

  • Stage 1: Hypotonia
  • Stage 2: Hypertonia → Retrocollis → Opisthotonus posture
  • Stage 3: Hypotonia → Posturing → Death may occur

B. Long term (Sequelae)


  • Most common site: Basal ganglia
  • Produces deafness, cerebral palsy (extrapyramidal), dental dysplasia.


1. Phototherapy

  • Safe, effective, usually initial therapy.
  • Efficacy does not depend upon color of child.
  • Most important mechanism: Structural Isomerism (Unconjugated bilirubin → Lumirubin)


  • It can’t reverse stage 1 encephalopathy.
  • Dehydration
  • Bronze baby syndrome 〈Patient → Conjugated bilirubin → Porphyrin pigments (1-3 months) 〉

2. Exchange Transfusion (Double Volume Exchange Transfusion DVET)

  • It is more effective than phototherapy & can reverse the stage  1 encephalopathy.

Principle: Exchange baby’s blood with fresh, cross matched blood

  • Acutely: Remove unconjugated bilirubin → Decrease in serum bilirubin levels rapidly
  • Long term: Stops ongoing hemolysis

It is done by Push-Pull Technique.


  • Invasive
  • ↑ nosocomial sepsis
  • Risk of HIV, HBV, HCV etc.
  • Shock or Volume overload (Hemodynamic changes)
  • Hypocalcemia (Citrate → Chelates ionized calcium)
  • Hyperkalemia

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