JAUNDICE IN

NEWBORN

DEPT OF PEDIATRICS
CHRI
WHAT IS JAUNDICE ?
 INTRODUCTION
• JAUNDICE IS THE VISIBLE MANIFESTATION OF CHEMICAL
BILIRUBINEMIA.

• CLINICAL ICTERUS- ADULTS AT BIL > 2MG/DL

NEONATES AT BIL > 5MG/DL

• ALMOST ALL NEONATES- 60% TERM AND 80% PRETERM WILL

HAVE BILIRUBIN GREATER THAN 5 MG/ DL IN 1 ST WEEK OF LIFE

• 3% OF TERM BABIES WILL HAVE LEVELS EXCEEDING 15 MG/

DL.
HOW IS BILIRUBIN FORMED ?
 BILIRUBIN PHYSIOLOGY
Bilirubin formation
Bilirubin Excretion
 CLASSIFICATION OF JAUNDICE

1. BASED ON PATHOLOGY- PHYSIOLOGIC

PATHOLOGIC

2. BASED ON TYPE OF BILIRUBIN- INDIRECT

DIRECT
PHYSIOLOGIC JAUNDICE ?
 CHARACTERISTICS OF PHYSIOLOGIC
JAUNDICE

• FIRST APPEARS BETWEEN 24-72 HOURS OF AGE

• MAXIMUM INTENSITY ON 4-5TH DAY IN TERM AND 7TH DAY IN PRETERM

• DOES NOT EXCEED 15 MG/ DL

• CLINICALLY UNDETECTABLE AFTER 14 DAYS.

• NO TREATMENT , ONLY CLOSE OBSERVATION FOR SIGNS OF WORSENING

JAUNDICE.
 MECHANISM OF PHYSIOLOGIC JAUNDICE
Immaturity in bilirubin metabolism at multiple steps

1. Increased rbc’s

2. Shortened rbc lifespan

3.Immature
hepatic uptake &
conjugation

4. Increased enterohepatic
Circulation
PATHOLOGICAL JAUNDICE ?
 CHARACTERISTICS OF PATHOLOGIC
JAUNDICE

• CLINICAL JAUNDICE BEFORE 24 HOURS OF AGE

• RISE IN SERUM BILIRUBIN > 5 MG/ DL/ DAY

• SERUM BILIRUBIN MORE THAN 15 MG/ DL

• CLINICAL JAUNDICE PERSISTING BEYOND 14 DAYS OF LIFE

• CLAY/WHITE COLOURED STOOL AND/OR DARK URINE STAINING THE

CLOTHES YELLOW

• DIRECT BILIRUBIN >2 MG/ DL

 CAUSES OF JAUNDICE

ONSET < 24 HOURS

• HEMOLYTIC DISEASE OF NEWBORN: RH, ABO AND MINOR GROUP

INCOMPATIBILITY

• INFECTIONS: TORCH ; MALARIA

• G-6PD DEFICIENCY
BETWEEN 24-72 HOURS OF LIFE

• PHYSIOLOGICAL
• SEPSIS NEONATORUM
• POLYCYTHEMIA
• CONCEALED HEMORRHAGES: CEPHALHEMATOMA,
SUBARACHNOID BLEED, IVH.
• INCREASED ENTEROHEPATIC CIRCULATION
AFTER 72 HOURS

• NEONATAL SEPSIS
• NEONATAL HEPATITIS
• EXTRA HEPATIC BILIARY ATRESIA
• BREAST MILK JAUNDICE
• METABOLIC DISORDERS
 RISK FACTORS FOR JAUNDICE

• A SIMPLE PNEUMONIC FOR RISK FACTORS IS JAUNDICE

• J - JAUNDICE WITHIN FIRST 24 HRS OF LIFE

• A - A SIBLING WHO WAS JAUNDICED AS NEONATE
• U - UNRECOGNIZED HEMOLYSIS
• N – NON-OPTIMAL SUCKING/NURSING
• D - DEFICIENCY OF G6PD
• I - INFECTION
• C – CEPHALHEMATOMA /BRUISING
• E - EAST ASIAN/NORTH INDIAN
 COMMON CAUSES IN INDIA

• PHYSIOLOGICAL
• BLOOD GROUP INCOMPATIBILITY
• INTRAUTERINE AND POSTNATAL INFECTIONS
• G-6PD DEFICIENCY
• BRUISING AND CEPHALHEMATOMA
• BREAST MILK JAUNDICE
 WHY ARE WE WORRIED ABOUT
JAUNDICE?
• INCREASED RISK FOR BILIRUBIN-INDUCED NEUROLOGIC DYSFUNCTION
(BIND)
• BILIRUBIN CROSSES THE BLOOD-BRAIN BARRIER AND BINDS TO BRAIN
TISSUE

• ACUTE MANIFESTATIONS OF BIND

• “ACUTE BILIRUBIN ENCEPHALOPATHY" (ABE)

FEATURES- LETHARGY , POOR FEEDING, POOR OR ABSENT MORO'S

REFLEX, OPISTHOTONUS OR CONVULSIONS.
• CHRONIC AND PERMANENT SEQUELAE
• “KERNICTERUS
FACTORS THAT INCREASE THE RISK
OF KERNICTERUS
(I)INCREASE FREE BILIRUBIN: TSB
 ALBUMIN
 ALBUMIN BINDING
 ALBUMIN : BIL RATIO
DRUGS, ACIDOSIS, FFA, VITAMIN A, E.

(II)DEFECTIVE BLOOD BRAIN BARRIER:

ASPHYXIA, MENINGITIS, ACIDOSIS, ANY SICKNESS
.
(III)  SUSCEPTIBILITY OF BRAIN : RACIAL, ACIDOSIS,
MENINGITIS
 APPROACH TO A JAUNDICED
BABY
FOLLOWING MUST BE ASSESSED

• WHAT IS THE EXTENT OF JAUNDICE?

• WHAT IS THE BIRTH WEIGHT?
• WHAT IS THE GESTATION?
• WHAT IS THE POSTNATAL AGE IN HOURS?
• IS THE JAUNDICE PHYSIOLOGICAL OR PATHOLOGICAL?
• ARE FEATURES OF BIND PRESENT?
KRAMER’S RULE

Dermal zone Bilirubin (mg/dL)

1 4- 8
2 5-12
3 8- 16
4 11-18
5 >15
 MATERNAL AND PERINATAL
HISTORY

• FAMILY HISTORY OF JAUNDICE, LIVER DISEASE

• PREVIOUS SIBLING WITH JAUNDICE FOR BLOOD GROUP
INCOMPATIBILITY
• MATERNAL ILLNESS DURING PREGNANCY
• PREVIOUS HISTORY OF MALARIA
• TRAUMATIC DELIVERY, DELAYED CORD CLAMPING, OXYTOCIN USE
• BIRTH ASPHYXIA, DELAYED FEEDING, DELAY IN MECONIUM PASSAGE
• BREAST FEEDING
 PHYSICAL EXAMINATION

• PREMATURITY
• SMALL FOR GESTATION: POLYCYTHEMIA, HEPATO-SPLENOMEGALY,
CATARACT, RASH.
• EXTRAVASCULAR BLEED: CEPHALHEMATOMA
• PALLOR: HEMOLYSIS, BLOOD LOSS
• PETECHIAE: SEPSIS, TORCH INFECTIONS
• HEPATOSPLENOMEGALY: RH-ISOIMMUNIZATION, SEPSIS, TORCH
INFECTIONS
 LABORATORY TESTS

• SERUM BILIRUBIN TOTAL AND DIRECT

• BLOOD GROUP AND RH FOR MOTHER AND BABY
• DIRECT COOMB’S TEST ON INFANT
• HEMATOCRIT
• PERIPHERAL SMEAR FOR RBC MORPHOLOGY, EVIDENCE OF HEMOLYSIS AND,
RETICULOCYTE COUNT
• SEPSIS SCREEN
• LIVER AND THYROID FUNCTION TESTS IN CASES WITH PROLONGED JAUNDICE
• TORCH TITRES
 MANAGEMENT
AIMS

1. PREVENTION OF HYPERBILIRUBINEMIA

• EARLY AND FREQUENT FEEDING

• ADEQUATE HYDRATION

2. REDUCTION OF BILIRUBIN:

• PHOTOTHERAPY

• EXCHANGE TRANSFUSION.

• PHENOBARBITONE

• IVIG

• METALLOPORPHYRINS- ZN, TN
 PHOTOTHERAPHY

• EXPOSURE OF THE NAKED BABY TO BLUE, COOL WHITE LIGHT

OF WAVE LENGTH 400-520 NM.

• LIGHT SOURCES

1. HALOGEN BULBS
2. COMPACT FLORESCENT TUBES
3. FIBRE-OPTIC PADS
4. LED
 PHOTOTHERAPHY DEVICES

CFL lamps

Biliblanket LED
 PHOTOTHERAPHY

• MECHANISM OF ACTION

UNCONJUGATED BILIRUBIN IN SKIN GETS CONVERTED INTO WATER-

SOLUBLE PHOTO-PRODUCTS ON EXPOSURE TO LIGHT OF A
PARTICULAR WAVELENGTH (400-520 MM).
• INVOLVES- CONFIGURATIONAL ISOMERIZATION

STRUCTURAL ISOMERIZATION
PHOTO OXIDATION
• THESE PHOTO-PRODUCTS ARE WATER SOLUBLE, NONTOXIC AND
EXCRETED THROUGH THE INTESTINE AND IN THE URINE.
PHOTOTHERAPY
 PHOTOTHERAPHY- INDICATIONS
AND CONTRA INDICATIONS
• FOR TERM HEALTHY BABIES, AMERICAN ACADEMY OF
PEDIATRICS GUIDELINES CAN BE FOLLOWED.
• FOR PRETERM BABIES < 35 WEEKS MEISEL’S CHART/ NICE
GUIDELINES CAN BE USED.
• EARLY PHOTOTHERAPY- IN HEMOLYSIS,
IN ACIDOSIS, ASPHYXIA, HYPOGLYCEMIA OR SEPSIS

• PHOTOTHERAPY IS CONTRAINDICATED IN THE PRESENCE

OF CONJUGATED HYPERBILIRUBINEMIA ( 2MG/DL) BECAUSE
IT MAY RESULT IN BRONZE BABY SYNDROME
PHO
TOT
HER
APY
 WHEN TO STOP?

• ONCE BILIRUBIN LEVELS REDUCE BELOW THE CUT OFF

ACCORDING TO THE CHART.
• REBOUND IS CHECKED AFTER 12 TO 24 HRS.
 EXCHANGE TRANSFUSION

• DOUBLE VOLUME EXCHANGE IS NORMALLY DONE.

• BABY’S BLOOD IS REPLACED WITH RECONSTITUTED
DONOR WHOLE BLOOD .
• IT REMOVES- ANTIBODY COATED RBCS, ANTIBODIES,
BILIRUBIN
• TECHNIQUE – PUSH AND PULL METHOD VIA UMBILICAL
VEIN
EXCHANGE TRANSFUSION
 EXCHANGE TRANSFUSION -
INDICATIONS

• RISING BILIRUBIN DESPITE PHOTOTHERAPHY

• BILIRUBIN LEVELS ABOVE THE CUT OFF ( AAP CHARTS)

• TO CORRECT ANEMIA AND HEART FAILURE IN HYDROPS

• IN RH/ ABO ISO IMMUNISATION

EXCH
ANGE
TRAN
SFUSI
ON
 CONJUGATED
HYPERBILIRUBINEMIA
• DEFINED AS A DIRECT BILIRUBIN LEVEL OF > 2MG/DL.
• IT IS NEVER PHYSIOLOGICAL.

ENQUIRE IF
• THE BABY IS SYMMETRIC SGA?
• STOOL IS WHITE OR CLAY COLORED?
• URINE HIGH COLORED?
• LIVER AND SPLEEN ARE ENLARGED?
• BABY IS ON TOTAL PARENTERAL NUTRITION?
 CONJUGATED
HYPERBILIRUBINEMIA- CAUSES
1. IDIOPATHIC NEONATAL HEPATITIS
2. INFECTIONS -HEPATITIS B, TORCH, SEPSIS
3. MALFORMATIONS –
• BILIARY ATRESIA (EXTRA AND INTRAHEPATIC),
• CHOLEDOCHAL CYST, BILE DUCT STENOSIS.
4. METABOLIC DISORDER –
• GALACTOSEMIA
• HEREDITARY FRUCTOSE INTOLERANCE
• ALPHA-L ANTITRYPSIN DEFICIENCY
• TYROSINEMIA
• GLYCOGEN STORAGE DISEASE TYPE IV
• HYPOTHYROIDISM
5. TOTAL PARENTERAL NUTRITION