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

positive Coombs test

group incompatibility results of specific examination

Blood

Positive

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 Peak

bilirubin concentration in Full-term infant <12mg/dl (205.2 umol/L) 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

Infective

jaundice

Neonatal hepatitis
TORCH infection

Neonatal sepsis

Causes of Pathologic Jaundice

Jaundice associated without infection

Hemolytic disease of the newborn
ABO Rh

incompatibility

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. (-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 k

Drug
Vitamin 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 Type

O mothers A or B fetuses of IgG anti-A or Anti-B antibodies in occurring during the first pregnancy

Presence

type O mother
Frequently

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 An

Rh-negative mother Rh-positive fetus of fetal RBC into maternal circulation sensitization to D antigen on fetal RBC

Leakage Maternal

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 pregnancy variety of different prenatal procedures

Ectopic A

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 Clinical Features
Frequency Anemia Jaundice Hydrops

Rh
Unusual Marked Marked Common

ABO
Common Minimal Minimal to moderate Rare Minimal Rare

Hepatosplenomegaly Marked Kernicterus Common

Laboratory Diagnosis
Laboratory Features Of Hemolytic Disease
Laboratory Features
blood type of Mother blood type of Infant

Rh
Rh negative Rh positive

ABO
O A or B

Anemia
Direct Commbs test Indirect Commbs test

Marked
Positive Positive

Minimal
Negative Usually positive

Hyperbilirubinemia
RBC morphology

marked
Nucleated RBC

Variable
Spherocytes

Diagnosis
The

definitive diagnosis requires

demonstration of blood group incompatibility and of corresponding

antibody bound to the infants RBC.

Diagnosis

Antenatal Diagnosis
History Expectant parents blood types Maternal titer of IgG antibodies to D or E

(>1:32)
At

1216 wk At 2832 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
Coombs test positive Examination for RBC antibodies in the

mothers serum

Differential Diagnosis
Congenital Neonatal

nephrosis

anemia jaundice

Physiological

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 mothers

serum
Umbilical vein transfusion

Treatment
Delivery in advance
Indication
Pulmonary maturity
Fetal distress

Maternal titer of Rh antibodies > 1:32

3537 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:10-12W/cm2 Protection of eyes and genital Indication
Bilirubin10mg/dl at 12 hr Bilirubin12-14mg/dl at 18 hr Bilirubin15mg/dl at 24 hr

Treatment
Side

effect of phototherapy

Diarrhea

Dehydration
Riboflavin destruction

Hypocalcemia
Bronze-baby syndrome

Treatment Exchange transfusion

Indication
Hemoglobin120g/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 transfusion Blood volume of exchange

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) : Sn-PP; Zn-PP

Human

albumin Dexamethasone

Protoporphyrins Glucocorticoids:

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