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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.

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Neonatal Jaundice

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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

  • 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


Classifications

  • Direct-reacting hyperbilirubinemia

    • Hepatitis

    • Cholestasis

    • Inborn errors of metabolism

    • Sepsis


Classifications

  • Indirect-reacting hyperbilirubinemia

    • Hemolysis

      • Reticulocytosis

      • Evidences of red blood cell destruction

      • A positive Coomb’s test

      • Blood group incompatibility

      • Positive results of specific examination


Classifications

  • Direct and indirect- reactin

    hyperbilirubinemia

    • Hepatitis

    • Sepsis

    • Liver damage complicated by Hemolysis


Classifications

  • 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.


Classifications

  • 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.


Classifications

  • 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


Introduction

  • 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


Diagnosis

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


Diagnosis

  • 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


Diagnosis

  • 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


Treatment

  • Main goals

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

    • To avoid neurotoxicity from hyperbilirubinemia


Treatment

  • Treatment of the unborn infant

    • Utero transfusion

      • Indication

        • Hydrops

        • Anemia (Hematocrit<30%)

      • Method

        • Packed RBC matching with the mother’s serum

        • Umbilical vein transfusion


Treatment

  • Delivery in advance

    • Indication

      • Pulmonary maturity

      • Fetal distress

      • Maternal titer of Rh antibodies > 1:32

      • 35~37 wk of gestation


Treatment

  • 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


Treatment

  • 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


Treatment

  • Side effect of phototherapy

    • Diarrhea

    • Dehydration

    • Riboflavin destruction

    • Hypocalcemia

    • Bronze-baby syndrome


Treatment

  • 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


Treatment

  • 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


Treatment

  • Drug treatment

    • Intravenous immuneglobulin (IVIG)

    • Human albumin

    • Protoporphyrins : Sn-PP; Zn-PP

    • Glucocorticoids: Dexamethasone

    • Inducerof liver enzyme: Luminal


Prevention

  • 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


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