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Neonatology Neonatal Jaundice

Neonatology Neonatal Jaundice. Contents. Billirubin metabolism in normal neonates Special problems in neonates The diseases in relation with Neonatal Jaundice Dangerous of the Hyperbillirubinemia. Normal Billirubin Metabolism in neonates. ineffective erythropoiesis. liver.

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Neonatology Neonatal Jaundice

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  1. NeonatologyNeonatal Jaundice

  2. Contents • Billirubin metabolism in normal neonates • Special problems in neonates • The diseases in relation with Neonatal Jaundice • Dangerous of the Hyperbillirubinemia

  3. Normal Billirubin Metabolism in neonates ineffective erythropoiesis liver Reticulo- endothelial system breakdown of hemoglobin80% Intrahepatic hemachrome Tissue hemachrome breakdown of hemoproteins Billirubin +plasm albumin---in blood Bilirubin+ProteinY、Z Hepato- enteral circulation Smooth endoplasmic reticulum conjugative —Hepatic cells Reabsoption:90% conjugated Bi Capillary bile duct Kidney 10% intestine lumen Glucuronic acid90% Glucose conjugates Xylose conjugates Urine ：urobilinogen （0-4mg/d） Bacteria conjugated Bi Portal vein urobilinogen 80%excrete Fecal:urobilinogen(40-280mg/d)

  4. Specificity of Billirubin Metabolism in newborns • Increased bilirubin formation • Excesive RBCs after birth • Shorter half life of fetal hemoglobin • Heme oxygenase • Increased bilirubin originated from bypass

  5. Specificity of Billirubin Metabolism in newborns • Insufficient in transiting bilirubin • albumin linking/transporting bilirubin 

  6. Specificity of Billirubin Metabolism in newborns • Insufficient in treatingbilirubin by liver • Y. Z protein  • Hepatic Enzyme under developed • Activity of hepatic enzymeeasily being undermined • Serums glucose rapidly 

  7. Specificity of Billirubin Metabolism in newborns • Load of hepatoenteral circulation • Intestine flora • Activity ofβ-Glucuronidase within mesocaval  • High quantity of bilirubin in meconium

  8. Physiological Jaundice

  9. Pathological Jaundice • Presenting earlier, <24-48 h after birth • Higher Serum Billirubin level • TBI >12mg/dl • increasing rapidly, >5mg/dl/d • Longer duration: • Term:>2 w preterm:>4 w • Persistently progressing, or re-presence after disappearing

  10. Etiology of Pathological Jaundice • Unconjugated • Hemolytic Disease of the Newborn • alloimmune hemolytic (ABO and Rh types) • deformity of RBC • RBC Enzyme deficiency • Extravascular Hemolysis • BreastfeedingJaundice • Erythrocytosis

  11. Etiology of Pathological Jaundice • Conjugated • Neonatal Hepatic diseases • Congenital bile duct disorders • Congenital metabolic disorders

  12. Etiology of Pathological Jaundice • Mixed by Unconjugated with Conjugated • Infectious

  13. Hemolytic disease of newborn • ABO type incompatability alloimmune hemolytic disease • 50% happened in first pregnancy • 20％ ABO type incompatability，incidence 10％ • majority maternal type O and infant type A or B • RH type incompatability alloimmune hemolytic disease • No Occurrence in first pregnancy, except the one had history of abortion and transfusion • Antigenic: D>E>C>c>e • RH D most commonly seen

  14. Hemolytic disease of newborn Clinical manifestation • Jaundice • Present at different time: ABO 2-3d. RH<24H • Level of TBi: ABO: light elevated RH: severely elevated and progressing • Anemia: severe in RH and may complicated with heat failure • Hepatosplenomegaly • Hydrops fetalis (universal edema of the fetus)

  15. Hemolytic disease of newborn Laboratory investigation • Prompt hemolysis indicators • RBC Hb • Reticulocyte • Nuclear RBC> 10% • blood type incompatibility • Maternal: O, newborn: A,B • Maternal: Rh-, newborn: Rh+

  16. Hemolytic disease of newborn Laboratory investigation • Coomb’s test • Rh: • Direct: positive • Indirect: positive (Ab. present and the type) • ABO: • Direct: positive • Free antibody present • Ab. Release test: positive

  17. Hemolytic disease of newborn • Diagnosis • History: • Past production history of the mother • Newborn with hyperbilirubinemia, anemia • Stillbirth • Hydrops fetalis • Clinical manifestation • Laboratory evidences

  18. Hemolytic disease of newborn • Prenatal diagnosis • Mother with Rh-negative: measure Rh Ab in GA 28,32,36 w • Examining amniotic fluid: bilirubine level

  19. Hemolytic disease of newborn • Prevention • Mother with Rh-negative delivering the first fetus given anti-D Ab.

  20. Neonatal Hepatitis • Intrauterine, intrapartum and during delivering infected • Virus: common: CROTCHS/CMV • Pathogenesis • Cholestasis: Capillary bile duct and hepatic duct obstruction • Liver cells and mesenchymal inflammatory change • portal area hyperplasia

  21. Neonatal hepatitis Clinical manifestation • Obstructive jaundice • Jaundice represent following the fading of physiological jaundice • Dark yellow urine and grey-white stool • Gastrointestinal symptoms: • anorexia, hyperphagia, vomiting, diarrhea • Anemia • hepatosplenomegaly

  22. Neonatal hepatitis Laboratory investigation • TBi , VDB: direct and indirect positive • Hepatic function: • ALT , serum proteins , albumin  • Serous virology • Positive: CMV IgG/M, TOXO IgG/M • HBV: antigens and antibodies

  23. Biliary atresia cholestasis • Severe obstructive jaundice with high Conjugated Bi • Persistent grey-white stool • Severe hepatosplenomegaly • Progressive worsening in hepatic function • Diagnosis based on ultrasound, CT and MRI Isotope ECT may helpful

  24. Jaundice with Infection • When there are no find in particular • General manifestation of the infection • Blood stream infection or organ infection • Both conjugated and unconjugated Bi • Jaundice subsided when infection controled

  25. BreastfeedingJaundice • Babies with exclusive breast feeding • Jaundice persists • Unconjugated Bi predominant • Without hepatosplenomegaly and injury of hepatic function • Jaundice fading or disappearing after suspending breast feeding • Good outcome

  26. Kernicterus • Pathology • staining and necrosis of neurons in the basal ganglia, hippocampus, and subthalamic nucleus of the brain

  27. Kernicterus • For a healthy term infant with a STB concentration less than 30mg/dl (513μmol/L) will usually not suffer neurologic damage • No certainty that lower STB levels under some circumstances eliminates the possibility of permanent injury, in particular with respect to auditory function. • The neurologic consequences of prolonged exposure to moderate hyperbilirubinemia are uncertain.

  28. Kernicterus • Major risk factor • Albumin binding of bilirubin. • 1 gram of albumin can bind 8.2mg of bilirubin • A serum albumin concentration of 3g/dl could theoretically bind approximately 25mg/dl of bilirubin • Not cross the blood-brain barrier • Albumin-bound bilirubin • Conjugated bilirubin • Premature • low serum albumin concentrations • frequency of acidosis

  29. Kernicterus • Clinical manifestation • First 1 to 2 d: poor sucking, stupor, hypotonia, seizures • In the middle of the first week: hypertonia of extensor muscles, opisthotonus，retrocollis, and fever • After the first week: hypertonia • Survivors: appeared with hypotonia, active deep tendon reflexes, obligatory tonic neck reflexes, delayed motor skills and after the first year, movement disorder

  30. Clinical management • Phototherapy • Plasma or albumin • Exchange transfusion • Enzyme inducer: phenobarbital • Original diseases treatment • The other symptomatic treatment

  31. Summery • Almost all newborns have jaundice and the majority are transient or physiological • Certain diseases causing neonatal jaundice have prolong and serious presentation • Kernicterus is the most severe complication and has very poor outcome and sequelae

  32. Thanks and questions?

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