Neonatal jaundice
1 / 40

- PowerPoint PPT Presentation

  • Updated On :

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.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about '' - ghita

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 l.jpg

Neonatal Jaundice

Li weizhong

Introduction l.jpg

  • 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.

Introduction3 l.jpg

  • 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 l.jpg
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 l.jpg
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 l.jpg
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

Classifications l.jpg

  • Direct-reacting hyperbilirubinemia

    • Hepatitis

    • Cholestasis

    • Inborn errors of metabolism

    • Sepsis

Classifications8 l.jpg

  • Indirect-reacting hyperbilirubinemia

    • Hemolysis

      • Reticulocytosis

      • Evidences of red blood cell destruction

      • A positive Coomb’s test

      • Blood group incompatibility

      • Positive results of specific examination

Classifications9 l.jpg

  • Direct and indirect- reactin


    • Hepatitis

    • Sepsis

    • Liver damage complicated by Hemolysis

Classifications10 l.jpg

  • 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.

Classifications11 l.jpg

  • 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.

Classifications12 l.jpg

  • 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 l.jpg
Causes of Pathologic Jaundice

  • Infectivejaundice

    • Neonatal hepatitis

      • TORCH infection

    • Neonatal sepsis

Causes of pathologic jaundice14 l.jpg
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 jaundice15 l.jpg
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 jaundice16 l.jpg
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

Introduction18 l.jpg

  • 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 l.jpg
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 pathogenesis20 l.jpg
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 pathogenesis21 l.jpg
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 pathogenesis22 l.jpg
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 pathogenesis23 l.jpg
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 l.jpg
Clinical Manifestations

  • Jaundice

  • Anemia

  • Hydrops

  • Massive enlargement of the liver and spleen

  • Bilirubin encephalopathy (Kernicterus)

Clinical manifestations25 l.jpg
Clinical Manifestations

Clinical Features Of Hemolytic Disease

Laboratory diagnosis l.jpg
Laboratory Diagnosis

Laboratory Features Of Hemolytic Disease

Diagnosis l.jpg

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

Diagnosis28 l.jpg

  • 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

Diagnosis29 l.jpg

  • 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 l.jpg
Differential Diagnosis

  • Congenital nephrosis

  • Neonatal anemia

  • Physiological jaundice

Treatment l.jpg

  • Main goals

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

    • To avoid neurotoxicity from hyperbilirubinemia

Treatment32 l.jpg

  • Treatment of the unborn infant

    • Utero transfusion

      • Indication

        • Hydrops

        • Anemia (Hematocrit<30%)

      • Method

        • Packed RBC matching with the mother’s serum

        • Umbilical vein transfusion

Treatment33 l.jpg

  • Delivery in advance

    • Indication

      • Pulmonary maturity

      • Fetal distress

      • Maternal titer of Rh antibodies > 1:32

      • 35~37 wk of gestation

Treatment34 l.jpg

  • 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

Treatment35 l.jpg

  • 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

Treatment36 l.jpg

  • Side effect of phototherapy

    • Diarrhea

    • Dehydration

    • Riboflavin destruction

    • Hypocalcemia

    • Bronze-baby syndrome

Treatment37 l.jpg

  • 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

Treatment38 l.jpg

  • 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

Treatment39 l.jpg

  • Drug treatment

    • Intravenous immuneglobulin (IVIG)

    • Human albumin

    • Protoporphyrins : Sn-PP; Zn-PP

    • Glucocorticoids: Dexamethasone

    • Inducerof liver enzyme: Luminal

Prevention l.jpg

  • 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