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
- 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
- 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.
- It is done by Modified Kramer’s Rule.
What is Modified Kramer’s Rule/Zones?
|Zone||Serum Bilirubin (mg//dl)|
* 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)
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.
- 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.
- 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.
- ↑ nosocomial sepsis
- Risk of HIV, HBV, HCV etc.
- Shock or Volume overload (Hemodynamic changes)
- Hypocalcemia (Citrate → Chelates ionized calcium)
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