Neonatal Jaundice

1
Neonatal Jaundice

• Li weizhong

2
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.

3
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.

4
Metabolism of Bilirubin

• Increased bilirubin production
• Less effective binding and transportation
• Less efficient hepatic conjugation
• Enhanced absorption of bilirubin via the
  enterohepatic circulation

5
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.

6
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

7
Classifications

• Direct-reacting hyperbilirubinemia
• Hepatitis
• Cholestasis
• Inborn errors of metabolism
• Sepsis

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Classifications

• Indirect-reacting hyperbilirubinemia
• Hemolysis
• Reticulocytosis
• Evidences of red blood cell destruction
• A positive Coombs test
• Blood group incompatibility
• Positive results of specific examination

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Classifications

• Direct and indirect- reactin
• 
  hyperbilirubinemia
• Hepatitis
• Sepsis
• Liver damage complicated by Hemolysis

10
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
  lt12mg/dl (205.2 umol/L)
• Peak bilirubin concentration in Premature infant
  lt15mg/dl (257umol/L)
• Clinical jaundice is resolved by 2 weeks in the
  term infant by 3-4 weeks in the Preterm infant.

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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.

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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).

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Causes of Pathologic Jaundice

• Infective jaundice
• Neonatal hepatitis
• TORCH infection
• Neonatal sepsis

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Causes of Pathologic Jaundice

• Jaundice associated without infection
• Hemolytic disease of the newborn
• ABO incompatibility
• Rh incompatibility
• Biliary atresia
• Jaundice associated with breast- feeding

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Causes of Pathologic Jaundice

• Breast milk jaundice
• It is caused by prolonged increased enterohepatic
  circulation of bilirubin. (ß-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.

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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

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Hemolytic Disease of the Newborn

• Li weizhong

18
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.

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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

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Etiology and Pathogenesis

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

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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

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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.

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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

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Clinical Manifestations

• Jaundice
• Anemia
• Hydrops
• Massive enlargement of the liver and spleen
• Bilirubin encephalopathy (Kernicterus)

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Clinical Manifestations

• Clinical Features Of Hemolytic Disease

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Laboratory Diagnosis

• Laboratory Features Of Hemolytic Disease

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Diagnosis

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

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Diagnosis

• Antenatal Diagnosis
• History
• Expectant parents blood types
• Maternal titer of IgG antibodies to D or E
  (gt132)
• At 1216 wk
• At 2832 wk
• At 36 wk
• Fetal Rh and ABO status
• Fetal jaundice level

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Diagnosis

• Postnatal diagnosis
• Jaundice at lt 24 hr
• Anemia (Hematocrit and hemoglobin examination)
• Rh or ABO incompatibility
• Coombs test positive
• Examination for RBC antibodies in the mothers
  serum

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Differential Diagnosis

• Congenital nephrosis
• Neonatal anemia
• Physiological jaundice

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Treatment

• Main goals
• To prevent intrauterine or extrauterine death of
  fetal or infant form severe anemia and hypoxic
• To avoid neurotoxicity from hyperbilirubinemia

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Treatment

• Treatment of the unborn infant
• Utero transfusion
• Indication
• Hydrops
• Anemia (Hematocritlt30)
• Method
• Packed RBC matching with the mothers serum
• Umbilical vein transfusion

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Treatment

• Delivery in advance
• Indication
• Pulmonary maturity
• Fetal distress
• Maternal titer of Rh antibodies gt 132
• 3537 wk of gestation

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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

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Treatment

• Phototherapy
• Blue spectrum of 427-475 nm (or White or Green)
• Irradiance10-12µW/cm2
• Protection of eyes and genital
• Indication
• Bilirubin10mg/dl at lt12 hr
• Bilirubin12-14mg/dl at lt18 hr
• Bilirubin15mg/dl at 24 hr

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Treatment

• Side effect of phototherapy
• Diarrhea
• Dehydration
• Riboflavin destruction
• Hypocalcemia
• Bronze-baby syndrome

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Treatment

• Exchange transfusion
• Indication
• Hemoglobinlt120g/L
• Hydrops, hepatosplenomegaly and heart failure
• Bilirubin in the 1st 12 of lifegt0.75mg/dl/hr
• Bilirubin concentrationgt20mg/dl
• Factors supporting early exchange transfusion
• Previous kernicterus in a sibling,
  reticulocyte counts greater than 15, asphyxia of
  neonate and premature infant

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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

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Treatment

• Drug treatment
• Intravenous immune globulin (IVIG)
• Human albumin
• Protoporphyrins Sn-PP Zn-PP
• Glucocorticoids Dexamethasone
• Inducer of liver enzyme Luminal

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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