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Neonatal hyperbilirubinemia
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Neonatal hyperbilirubinemia

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features of hyperbilirubinemia ,differential diagnosis ,management

features of hyperbilirubinemia ,differential diagnosis ,management

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  • .*Uptake of bilirubin by the liver is mediated by a carrier protein (receptor) * Uptake may be competitively inhibited by other organic anions *On the smooth ER, bilirubin is conjugated with glucoronic acid, xylose, or ribose * Glucoronic acid is the major conjugate - catalyzed by UDP glucuronyl tranferase “ Conjugated” bilirubin is water soluble and is secreted by the hepatocytes into the biliary canaliculi * Converted to stercobilinogen (urobilinogen) (colorless) by bacteria in the gut * Oxidized to stercobilin which is colored * Excreted in feces * Some stercobilin may be re-adsorbed by the gut and re-excreted by either the liver or kidney
  • Prehepatic (hemolytic) jaundice *Results from excess production of bilirubin (beyond the livers ability to conjugate it) following hemolysis *Excess RBC lysis is commonly the result of autoimmune disease; hemolytic disease of the newborn (Rh- or ABO- incompatibility); structurally abnormal RBCs (Sickle cell disease); or breakdown of extravasated blood *High plasma concentrations of unconjugated bilirubin (normal concentration ~0.5 mg/dL)
  • Intrahepatic jaundice *Impaired uptake, conjugation, or secretion of bilirubin *Reflects a generalized liver (hepatocyte) dysfunction *In this case, hyperbilirubinemia is usually accompanied by other abnormalities in biochemical markers of liver function
  • Posthepatic jaundice *Caused by an obstruction of the biliary tree *Plasma bilirubin is conjugated, and other biliary metabolites, such as bile acids accumulate in the plasma *Characterized by pale colored stools (absence of fecal bilirubin or urobilin), and dark urine (increased conjugated bilirubin) *In a complete obstruction, urobilin is absent from the urine

Transcript

  • 1. Prof. Saad Sal-Ani Senior Pediatric Consultant Head Of Pediatric department Khorfakkan Hospital Notes on Neonatal Hyperbilirubinemia
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  • 8. Copyright ©2004 American Academy of Pediatrics Subcommittee on Hyperbilirubinemia, Pediatrics 2004;114:297-316 Guidelines for phototherapy in hospitalized infants of 35 or more weeks' gestation
  • 9. ASSESSING THE RISK OF JAUNDICE BY THE NUMBERS
    • Bhutani curve
  • 10. KERNICTERUS
    • Why we care about indirect hyperbilirubinemia
    • Staining of the brain by bilirubin
    • Early symptoms-acute bilirubin encephalopathy-poor feeding, abnormal cry, hypotonia,
    • Intermediate phase-stupor, irritability, hypertonia
    • Late – shrill cry, no feeding, opisthotonus, apnea, seizures, coma, death
  • 11. KERNICTERUS
    • Late sequelae can include
    • gaze abnormalities
    • feeding difficulties
    • dystonia
    • incoordination
    • choreoathetosis
    • sensorineural hearing loss
    • painful muscle spasms
  • 12. RISK FACTORS FOR SIGNIFICANT JAUNDICE
    • Gestational Age
    • Race
    • Family history of jaundice requiring phototherapy
    • Hemolysis (ABO or other)
    • Severe bruising
    • Breastfeeding
  • 13. RISK FACTORS-RACE
    • Asians-highest risk
    • Levels peak at 16-18 as opposed to average Caucasian levels of 6-8. There is also a later peak which can occur at 5-7 days.
    • Black infants have a lower peak, rarely exceeding 12. (but they have a much higher incidence of G6PD deficiency)
    • Caucasians are in the middle.
  • 14. RISK FACTORS-GESTATIONAL AGE
    • The younger the gestation, the higher the risk of jaundice.
    • 37 weeks more prone to jaundice than 40 weeker who is more prone than a 42 weeker.
    • 35 and below is much more prone
    • Extreme preemies also more prone to kernicterus and are treated at much lower levels.
  • 15. RISK FACTORS-FAMILY HX
    • A child whose sibling needed phototherapy is 12 times more likely to also have significant jaundice.
    • Frequently peak bilirubin levels correlate between siblings.
  • 16. RISK FACTORS-HEMOLYSIS
    • ABO Incompatibility is the most common cause of hemolysis causing jaundice.
    • Only 10-20% of infants with ABO mismatch develop significant jaundice.
    • Some of these infants, however, develop very significant jaundice quickly.
    • Coombs positive ABO is more likely to cause hemolysis, but many babies will be asymptomatic. Conversely, Coombs negative ABO mismatch does occasionally cause significant hemolysis, but this is rather rare.
  • 17. RISK FACTORS-PATHOLOGIC
    • G6PD Deficiency
    • Hereditary Spherocytosis
    • Glucuronyl Transferase Deficiency Type 1 (Crigler Najar Syndrome)
    • GT deficiency Type 2 (Arias Syndrome)
    • Polycythemia
  • 18. Thank you