Neonatal jaundice

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  • 1. Neonatal Jaundice. Valmiki Seecheran. Year V MBBS.
  • 2. Introduction. • A bilirubin level of more than 5mg/dl manifests clinical jaundice in neonates. • Cranio-caudal progression. • 50-60% of babies affected in the first week of life.
  • 3. Physiological • Most infants develop visible jaundice due to elevation of unconjugated bilirubin concentration during their first week. • Phase I. – Term infants – lasts up to 10 days with rapid rise of serum bilirubin up to (12mg/dL). – Preterm infants – lasts up to two weeks with rapid rise of serum bilirubin up to (15mg/Dl). • Phase II – bilirubin levels decline to 2mg/Dl for 2 weeks. – Preterm infants – phase II can last more than 1 month. – Breastfed infants – phase I can last more than 1 month.
  • 4. Causes. • Low enzymatic activity of glucruonosyltransferase. (converts unconjugated to conjugated bilirubin). • Shorter life span of fetal red blood cells. (90days). • Low conversion of bilirubin to urobilinogen by intestinal flora.
  • 5. Pathological. • Clinical jaundice appearing in the 1st 24 hours or greater than 14 days of life. • Increases in the level of total bilirubin by more than (0.5 mg/dL) per hour or 5 mg/dL per 24 hours. • Total bilirubin more than (19.5 mg/dL) • Direct bilirubin more than (2.0 mg/dL).
  • 6. Pathological vs. Physiological. • Presence of intrauterine growth restriction. • Family history of jaundice and anemia. (Neonatal or early infant death.) • Maternal drugs (sulphanoamides, anti- malarials). • Stigma of intrauterine infections – Cataracts, microcephaly, cephalohematomas.
  • 7. Causes of jaundice. • Breakdown of fetal hemoglobin. • Immature hepatic metabolic pathways. • In the event if neonatal jaundice is not alleviated with phototherapy, biliary atresia, progressive familial intrahepatic cholestasis and other pediatric liver diseases should be considered.
  • 8. Causes of jaundice. • Unconjugated bilirubin. – Pathologic. • Hemolytic. – G6PD, spherocytosis, sickle cell, sepsis, ABO. • Non-hemolytic. –Breast milk, UTI, Sepsis. – Physiological • Conjugated bilirubin. – Hepatic. – Sepsis, Hep A & B, Alpha 1 antitrypsin deficieny. – Post-hepatic. – Bile duct obstruction.
  • 9. Causes of jaundice. • Breast milk jaundice is a biochemical occurrence. Bilirubin levels peaks 6-14days of life. • Enzymes such as 3 alpha 20 beta pregnanediol and lipoprotein lipase prevents conjugation leading to higher levels of bilirubin in blood.
  • 10. Clinical assessment. • Ingram icterometer. – 5 transverse strips of graded yellow lines. – Pressed against the nose and the corresponding yellow colour of the blanched skin is match and level is assigned. • Transcutaneous bilirubinometer. – Pressure applied to photoprobe, generates light, the intensity of the yellow colour in the light is measured and displayed.
  • 11. Treatment. • Phototherapy – Discovered in Essex, England by a nurse. – Process of isomerization that changes trans- bilirubin into water soluble bilirubin isomer. – Blue light more effective at breaking down bilirubin. – Biliblanket. • Exchange transfusions. – Indicated for a total serum bilirubin >25mg/Dl.
  • 12. Complications. • Kernicterus – chronic bilirubin encephalopathy. – Neurotoxic. – Gray matter of the brain. – Brain damage/death. • Fever/ Seizures.
  • 13. Thank you.