Neonatal jaundice l.jpg
Sponsored Links
This presentation is the property of its rightful owner.
1 / 40

Neonatal Jaundice PowerPoint PPT Presentation

  • Updated On :
  • Presentation posted in: General

Neonatal Jaundice. Li weizhong . Introduction. Neonatal Jaundice is known as the visible clinical manifestation of dying skin and sclera yellow during the neonatal period, resulting from deposition of bilirubin in the neonatal bodies. Introduction.

Download Presentation

Neonatal Jaundice

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -

Presentation Transcript

Neonatal Jaundice

Li weizhong


  • Neonatal Jaundice is known as the visible clinical manifestation of dying skin and sclera yellow during the neonatal period, resulting from deposition of bilirubin in the neonatal bodies.


  • Jaundice is observed during the 1st wk in approximately 60% of term infant and 80% of preterm infant.

  • Hyperbilirubinemia can be toxic, with high levels resulting in an encephalopathy known as kerni-cterus.

Metabolism of Bilirubin

  • Increased bilirubin production

  • Less effective binding and transportation

  • Less efficient hepatic conjugation

  • Enhanced absorption of bilirubin via the enterohepatic circulation

Clinical Manifestation

  • Jaundice may be present at birth or at any time during the neonatal period.

  • Jaundice usually begins on the face and, as the serum level increases, progresses to the chest and abdomen and then the feet.

  • Jaundice resulting from deposition of indirect bilirubin in the skin tends to appear bright yellow or orange; jaundice of the obstructive type (direct bilibrubin), a greenish or muddy yellow.

Methods of Diagnosis

  • A complete diagnostic evaluation

    • Determination of direct and indicrect bilirubin fractions

    • Determination of hemoglobin

    • Reticulocyte count

    • Blood type

    • Coombs’ test

    • Examination of the peripheral blood smear


  • Direct-reacting hyperbilirubinemia

    • Hepatitis

    • Cholestasis

    • Inborn errors of metabolism

    • Sepsis


  • Indirect-reacting hyperbilirubinemia

    • Hemolysis

      • Reticulocytosis

      • Evidences of red blood cell destruction

      • A positive Coomb’s test

      • Blood group incompatibility

      • Positive results of specific examination


  • Direct and indirect- reactin


    • Hepatitis

    • Sepsis

    • Liver damage complicated by Hemolysis


  • Physiologic jaundice

    • Clinical jaundice appears at 2-3 days.

    • Total bilirubin rises by less than 5 mg/dl (86 umol/L) per day.

    • Peak bilirubin occurs at 3-5 days of age.

      • Peak bilirubin concentration in Full-term infant <12mg/dl (205.2 umol/L)

      • Peak bilirubin concentration in Premature infant <15mg/dl (257umol/L)

    • Clinical jaundice is resolved by 2 weeks in the term infant by 3-4 weeks in the Preterm infant.


  • Pathologic jaundice

    • Clinical jaundice appears in 24 hours of age.

    • Total bilirubin rises by higher than 5 mg/dl (86 umol/L) per day.

    • Peak concentration of total bilirubin is more than 12 mg/dL in the term infant and 15 mg/ dL in the preterm infant.


  • Pathologic jaundice

    • Clinical jaundice is not resolved in 2 weeks in the term infant and in 4 weeks in the Preterm infant.

    • Clinical jaundice appears again after it has been resolved.

    • Direct bilirubin concentration is more than 1.5 mg/dL (26umol/L).

Causes of Pathologic Jaundice

  • Infectivejaundice

    • Neonatal hepatitis

      • TORCH infection

    • Neonatal sepsis

Causes of Pathologic Jaundice

  • Jaundice associated without infection

    • Hemolytic disease of the newborn

      • ABO incompatibility

      • Rh incompatibility

    • Biliary atresia

    • Jaundice associated with breast- feeding

Causes of Pathologic Jaundice

  • Breast milk jaundice

    • It is caused by prolonged increased enterohepatic circulation of bilirubin. (β-GD↑)

    • The hyperbilirubinemia peaks at 10-15 days of age.

    • The level of unconjugated hyperbilirubinemia is at 10-30 mg/dL (172-516 umol/L).

    • If nursing is interrupted for 72 hours, the bilirubin level falls quickly.

Causes of Pathologic Jaundice

  • Genetic disease

    • Congenital deficiencies of the enzymes

      • glucose-6-phosphate dehydrogenase (G-6-PD)

    • Thalassemia

    • Cystic fibrosis

  • Drug

    • Vitamin k

    • Novobiocin

Hemolytic Disease of the Newborn

Li weizhong


  • Hemolytic disease of the newborn

    • It is an isoimmunity hemolysis associated with ABO or Rh incompatibility.

    • It results from transplacental passage of maternal antiboddy active against RBC antigens of the infant, leading to an increased rate of RBC destruction.

    • It is an important cause of anemia and jaundice in newborn infant.

Etiology and Pathogenesis

  • ABO hemolytic disease

    • ABO incompatibility

      • Type O mothers

      • Type A or B fetuses

      • Presence of IgG anti-A or Anti-B antibodies in type O mother

      • Frequently occurring during the first pregnancy without prior sensitization

Etiology and Pathogenesis

  • Rh hemolytic disease

    • Rh blood group antigens (C, c, D, d, E, e)

      • D>E>C>c>e

    • Pathophysiology of alloimmune hemolysis resulting from Rh incompatibility

      • An Rh-negative mother

      • An Rh-positive fetus

      • Leakage of fetal RBC into maternal circulation

      • Maternal sensitization to D antigen on fetal RBC

Etiology and Pathogenesis

  • Production and transplacental passage of maternal anti-D antibodies into fetal circulation

  • Attachment of maternal antibodies to Rh-positive fetal RBC

  • Destruction of antibody-coated fetal RBC

Etiology and Pathogenesis

  • Rh hemolytic disease was rare during the first pregnancy involving an Rh-positive fetus.

  • Once sensitization has occurred, re-exposure to Rh D RBC in subsequent pregnancies leads to an anamnestic response, with an increase in the maternal anti-Rh D antibody titer.

  • The likelihood of an infant being affected increased significantly with each subsequent pregnancy.

Etiology and Pathogenesis

  • Significant hemolysis occurring in the first pregnancy indicates prior maternal exposure to Rh-positive RBC.

    • Fetal bleeding associated with a previous spontaneous or therapeutic abortion

    • Ectopic pregnancy

    • A variety of different prenatal procedures

    • Transfusion of some other blood product containing Rh D RBC in an Rh-negative mother

Clinical Manifestations

  • Jaundice

  • Anemia

  • Hydrops

  • Massive enlargement of the liver and spleen

  • Bilirubin encephalopathy (Kernicterus)

Clinical Manifestations

Clinical Features Of Hemolytic Disease

Laboratory Diagnosis

Laboratory Features Of Hemolytic Disease


  • The definitive diagnosis requires demonstration of blood group incompatibility and of corresponding antibody bound to the infant’s RBC.


  • Antenatal Diagnosis

    • History

    • Expectant parents’ blood types

    • Maternal titer of IgG antibodies to D or E (>1:32)

      • At 12~16 wk

      • At 28~32 wk

      • At 36 wk

    • Fetal Rh and ABO status

    • Fetal jaundice level


  • Postnatal diagnosis

    • Jaundice at < 24 hr

    • Anemia (Hematocrit and hemoglobin examination)

    • Rh or ABO incompatibility

    • Coomb’s test positive

    • Examination for RBC antibodies in the mother’s serum

Differential Diagnosis

  • Congenital nephrosis

  • Neonatal anemia

  • Physiological jaundice


  • Main goals

    • To prevent intrauterine or extrauterine death of fetal or infant form severe anemia and hypoxic

    • To avoid neurotoxicity from hyperbilirubinemia


  • Treatment of the unborn infant

    • Utero transfusion

      • Indication

        • Hydrops

        • Anemia (Hematocrit<30%)

      • Method

        • Packed RBC matching with the mother’s serum

        • Umbilical vein transfusion


  • Delivery in advance

    • Indication

      • Pulmonary maturity

      • Fetal distress

      • Maternal titer of Rh antibodies > 1:32

      • 35~37 wk of gestation


  • Treatment of the liveborn infant

    • Immediate resuscitation and supportive therapy

      • Temperature stabilization

      • Correction of acidosis: 1-2mEq/kg of sodium bicarbonate

      • A small transfusion compatible packed RBC

      • Volume expansion for hypotension

      • Provision of assisted ventilation for respiratory failure


  • Phototherapy

    • Blue spectrum of 427-475 nm (or White or Green)

    • Irradiance:10-12μW/cm2

    • Protection of eyes and genital

    • Indication

      Bilirubin≥10mg/dl at <12 hr

      Bilirubin≥12-14mg/dl at <18 hr

      Bilirubin≥15mg/dl at ≥24 hr


  • Side effect of phototherapy

    • Diarrhea

    • Dehydration

    • Riboflavin destruction

    • Hypocalcemia

    • Bronze-baby syndrome


  • Exchange transfusion

    • Indication

      • Hemoglobin<120g/L

      • Hydrops, hepatosplenomegaly and heart failure

      • Bilirubin in the 1st12 of life>0.75mg/dl/hr

      • Bilirubin concentration>20mg/dl

      • Factors supporting early exchange transfusion:

        Previous kernicterus in a sibling, reticulocyte counts greater than 15%, asphyxia of neonate and premature infant


  • Blood volume of exchange transfusion

    • Double-volume exchange transfusion :150-180ml/kg

  • Blood choose of Rh incompatibility

    • Rh in accordance with mother

    • ABO in accordance with neonate

  • Blood choose of ABO incompatibility

    • Plasm of AB type

    • RBC of O type


  • Drug treatment

    • Intravenous immuneglobulin (IVIG)

    • Human albumin

    • Protoporphyrins : Sn-PP; Zn-PP

    • Glucocorticoids: Dexamethasone

    • Inducerof liver enzyme: Luminal


  • Intramuscular injection of 300ug of human anti-D globulin to an Rh-negative mother

    • Within 72 hr of delivery of an ectopic pregnancy

    • Abdominal trauma in pregnancy

    • Amniocentesis

    • Chorionic villus biopsy

    • Abortion

  • Login