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Neonatal Jaundice

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Intro & Metabolism - Yellow Fellow Intro

  • Neonatal Jaundice (NNJ): Yellow sclera/skin; Total Serum Bilirubin (TSB) > 5 mg/dL.
  • Bilirubin Source: Breakdown of heme from Red Blood Cells (RBCs).
    • Heme $\xrightarrow{Heme\ Oxygenase}$ Biliverdin $\xrightarrow{Biliverdin\ Reductase}$ Unconjugated Bilirubin (UCB)
  • UCB (lipid-soluble, neurotoxic) binds albumin $\rightarrow$ transported to liver.
  • Liver Conjugation: UCB $\xrightarrow{UDPGT\ (Uridine\ Diphosphate\ Glucuronosyltransferase)}$ Conjugated Bilirubin (CB; water-soluble).
  • CB Excretion: Into bile $\rightarrow$ gut. Some CB deconjugated by β-glucuronidase $\rightarrow$ UCB reabsorbed (enterohepatic circulation).

⭐ Fetal RBCs have a shorter lifespan (approx. 70-90 days vs. adult 120 days), contributing to an increased bilirubin load in neonates.

Causes & Types - Code Yellow Causes

Pathological Jaundice if:

  • Onset <24h life

  • TSB ↑ >5 mg/dL/day (or >0.2 mg/dL/hr)

  • Direct Bilirubin >1 mg/dL

  • Persists >2wks (term), >3wks (preterm)

  • Unconjugated Hyperbilirubinemia:

    • ↑ Production (Hemolysis):
      • Isoimmune: ABO/Rh incompatibility (Coombs' +ve)
      • RBC defects: G6PD def., spherocytosis
      • Sepsis, bruising/cephalohematoma
    • ↓ Conjugation:
      • Crigler-Najjar, Gilbert syndrome
      • Hypothyroidism, Breast milk jaundice (late)
  • Conjugated Hyperbilirubinemia (Cholestasis):

    • Biliary atresia
    • Neonatal hepatitis (TORCH)
    • Metabolic: Galactosemia, α1-antitrypsin def.

⭐ Jaundice in first 24 hours is ALWAYS pathological; suspect hemolysis (e.g., ABO/Rh).

Assessment & Diagnosis - Spot the Yellow Alert

  • Clinical Assessment:
    • History: Onset, feeding, family hx (G6PD, jaundice).
    • Examine: Cephalo-caudal progression (Kramer’s zones), signs of kernicterus, pallor, hepatosplenomegaly.
  • Bilirubin Measurement:
    • Transcutaneous Bilirubin (TcB): Screening if GA ≥35 wks & age >24 hrs.
    • Total Serum Bilirubin (TSB): Gold standard; if TcB high, <24 hrs old, or unwell.
  • Investigations:
    • Essential: Blood group (mother, baby), Direct Coombs Test (DCT), TSB (Total & Direct).
    • Further (if indicated): CBC, reticulocytes, peripheral smear, G6PD, sepsis screen, LFTs.

Bhutani Nomogram for Neonatal Jaundice Risk

⭐ Bhutani nomogram plots TSB against postnatal age (hours) to define risk zones for hyperbilirubinemia.

Management & Complications - Light & Might Fight 📌

  • Goal: Prevent Kernicterus (bilirubin neurotoxicity).
  • Phototherapy (Light):
    • Converts bilirubin to lumirubin (water-soluble).
    • Indications: Total Serum Bilirubin (TSB) thresholds per AAP nomograms (gestational age, risk factors).
    • Side effects: Bronze baby syndrome, loose stools, dehydration. (Eye protection essential).
  • Exchange Transfusion (Might):
    • Indications: High TSB despite intensive phototherapy (PT), or signs of Acute Bilirubin Encephalopathy (ABE).
    • Procedure: Double volume exchange (~160 mL/kg).
  • Complications:
    • Acute Bilirubin Encephalopathy (ABE): Early: lethargy, hypotonia. Late: hypertonia (opisthotonus, retrocollis), seizures.
    • Kernicterus (Chronic Bilirubin Encephalopathy - CBE): Irreversible. Classic tetrad: choreoathetoid cerebral palsy, sensorineural hearing loss (SNHL), upward gaze palsy, dental enamel dysplasia.

![Image: Neonate under blue light phototherapy with eye protection]

⭐ Unconjugated bilirubin is lipid-soluble and readily crosses the blood-brain barrier, leading to neurotoxicity if levels are excessively high or protective mechanisms are compromised.

High‑Yield Points - ⚡ Biggest Takeaways

  • Physiological jaundice: Appears after 24 hrs, peaks 3-5 days, resolves 1-2 wks.
  • Pathological jaundice: <24h onset, TSB >15 mg/dL, D.Bili >2 mg/dL or >20% TSB, rapid rise >5 mg/dL/day.
  • Breastfeeding jaundice (early, ↓intake); Breast milk jaundice (late, prolonged).
  • Kernicterus: Bilirubin encephalopathy (basal ganglia); most feared complication.
  • Treatment: Phototherapy (mainstay); Exchange transfusion (severe/encephalopathy).
  • Common hemolytic causes: ABO incompatibility, Rh isoimmunization.
  • G6PD deficiency: Can cause severe jaundice with oxidant stress.

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