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Neonatal

Jaundice

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 Be able to differentiate
 between physio and patho
jaundice in the newborn

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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.

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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 kernicterus.
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胆红素代谢简图

RBC破坏

Indircted bilirubin
未结合胆红素

UDPGT
dircted bilirubin结合胆红素

肠道intestine
尿胆原urobilinogen
未结合胆红素 7
Metabolism of Bilirubin
 Increased bilirubin production

 Less effective binding and transportation

 Less efficient hepatic conjugation

 Enhanced absorption of bilirubin via the

enterohepatic circulation
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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.
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Methods of Diagnosis
 A complete diagnostic evaluation
Determination of direct and indirect
bilirubin fractions
Determination of hemoglobin
Reticulocyte count
Blood type
Coombs’ test
Examination of the peripheral blood smear
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Classifications
 Direct-reacting hyperbilirubinemia
Hepatitis

Cholestasis

Inborn errors of metabolism

Sepsis 15
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
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Classifications
 Direct and indirect- reactin
hyperbilirubinemia

Hepatitis

Sepsis

Liver damage complicated by Hemolysis

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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. 18
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 22


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.
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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 24
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Hemolytic
Disease of
the Newborn

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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. 27
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 28
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

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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
 Transfusionof some other blood product
containing Rh D RBC in an Rh-negative
mother 32
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

Clinical Features Rh ABO


Frequency Unusual Common
Anemia Marked Minimal
Jaundice Marked Minimal to moderate
Hydrops Common Rare
Hepatosplenomegaly Marked Minimal
Kernicterus Common Rare 34
Laboratory Diagnosis
Laboratory Features Of Hemolytic Disease
Laboratory Features Rh ABO
blood type of Mother Rh negative O
blood type of Infant Rh positive A or B
Anemia Marked Minimal
Direct Commb’s test Positive Negative
Indirect Commb’s test Positive Usually positive
Hyperbilirubinemia marked Variable
RBC morphology Nucleated RBC Spherocytes

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Diagnosis
 The definitive diagnosis requires

demonstration of blood group

incompatibility and of corresponding

antibody bound to the infant’s RBC.


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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 37
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 38
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 (Hematocrit<30%)
Method
Packed RBC matching with the mother’s
serum
Umbilical vein transfusion 41
Treatment
Delivery in advance

Indication

Pulmonary maturity

Fetal distress

Maternal titer of Rh antibodies > 1:32

35~37 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 43
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
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Treatment
Side effect of phototherapy
Diarrhea

Dehydration
Riboflavin destruction

Hypocalcemia

Bronze-baby syndrome 45
Treatment
Exchange transfusion
Indication
Hemoglobin<120g/L
Hydrops, hepatosplenomegaly and heart failure
Bilirubin in the 1st 12 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
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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 49
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