Neonatal Jaundice Li weizhong. Introduction Neonatal Jaundice is known as the visible clinical manifestation of dying skin and sclera yellow during.

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

ClassificationsDirect 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.

ClassificationsPathologic 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.

ClassificationsPathologic 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

Infective jaundice

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 incompatibilityAn Rh-negative motherAn Rh-positive fetusLeakage of fetal RBC into maternal circulationMaternal sensitization to D antigen on fetal RBC

Etiology and PathogenesisProduction 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 abortionEctopic pregnancyA variety of different prenatal proceduresTransfusion 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

Clinical Features Rh ABO

Frequency Unusual Common

Anemia Marked Minimal

Jaundice Marked Minimal to moderate

Hydrops Common Rare

Hepatosplenomegaly Marked Minimal

Kernicterus Common Rare

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

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 wkAt 28 ～ 32 wkAt 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 therapyTemperature stabilizationCorrection of acidosis: 1-2mEq/kg of sodium

bicarbonateA small transfusion compatible packed RBCVolume expansion for hypotensionProvision of assisted ventilation for respiratory

failure

Treatment Phototherapy

Blue spectrum of 427-475 nm (or White or Green)

Irradiance:10-12μW/cm2Protection 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 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

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 immune globulin

(IVIG)

Human albumin

Protoporphyrins : Sn-PP; Zn-PP

Glucocorticoids: Dexamethasone

Inducer of 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