Professional Documents
Culture Documents
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
preterm infant.
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
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
Sepsis 15
Classifications
Indirect-reacting hyperbilirubinemia
Hemolysis
Reticulocytosis
Hepatitis
Sepsis
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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.
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
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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
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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
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Diagnosis
The definitive diagnosis requires
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
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
Amniocentesis
Abortion 49
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