Approach To Neonatal Jaundice

APPROACH TO
NEONATAL
JAUNDICE
DR. USHNA RAHMAN

DCH TRAINEE.
NEONATAL HYPERBILIRUBINEMIA
 Bilirubin is a yellow pigment derived from the
breakdown of hemoglobin. Accumulation of bilirubin in
body tissues leading to visible yellowness of skin, sclera
and mucosa is known as Jaundice.
WHEN IT IS VISIBLE ?
 It becomes clinically apparent when serum bilirubin
concentration of >5mg/dl. Jaundice usually becomes
apparent in a cephalocaudal progression, starting on the
face, progressing to the abdomen and then the feet, as
serum bilirubin levels increase. (face approx: 5mg/dl;
mid-abdomen 15mg/dl; soles 20mg/dl)
INCIDENCE:
 60% in term baby
 80% in preterm baby
TYPES OF BILIRUBIN:
 UNCONJUGATED  CONJUGATED
 Present normally in plasma  Present normally in bile
 Bind to albumin  Bind to glucoronic acid
 Fat soluble  Water soluble
 Can cross blood brain  Cannot cross blood brain

barrier barrier
 High molecular weight &  Small molecular weight &
cannot be excreted through can be excreted through
kidney kidney
ETIOLOGY OF JAUNDICE:
 1st 24 Hours Jaundice:
 1. Hemolytic jaundice (G6PD, RH isoimmunization, ABO
incompatibility)
 2. TORCH (congenital infections)
 3. Polycythemia
 2nd Day to 3rd Week:

 1. Physiological
 2. Breast milk
 3. Sepsis
 4. Polycythemia
 5. Cephalhematoma
 6. Crigler najjar syndrome
 7. Hemolytic disorders
 Persistance after 3rd Week:
 1. Breast milk
 2. Hypothyroidism
 3. Pyloric stenosis
 4. Cholestasis
PHYSIOLOGICAL JAUNDICE:
 Appears after 24 hours of life
 Unconjugated hyperbilirubinemia
 Total bilirubin rises by less than 5mg/dl per day
 Jaundice appears by 2-3 days of age in term and 3-4 days

of age in preterm
 It disappears by 4-5 days of age in term and 7-9 days of
age in preterm
 Serum bilirubin levels do not exceed 12mg/dl in term
and 15mg/dl in preterm
 Increase in serum bilirubin by <5mg/dl/day or
<0.2mg/dl/hour
 Clinically not detected after 14 days of life
WHY DOES PHYSIOLOGIC JAUNDICE
DEVELOP (PATHOPHYSIOLOGY)
1. Increased Bilirubin Synthesis
2. Decrease Binding and Transport
3. Impaired Bilirubin Conjugation and Excretion
4. Enhanced Enterohepatic Circulation

Breast milk jaundice: Breast milk jaundice
most often occurs in the second or later weeks of life and
can continue for several weeks. While the exact
mechanism leading to breast milk jaundice is unknown,
it is believed that substances in the mother’s milk inhibit
the ability of the infant’s liver to process bilirubin.
Beta-glucuronidase resulting in deconjugation of
bilirubin
Breast feeding jaundice: Caloric

deprivation (i.e, starvation and increased enterohepatic
circulation), occurs in 1st week after birth in breastfed
infants. Lower milk intake can result in dehydration,
which hemoconcentrates bilirubin
PATHOLOGICAL JAUNDICE:
 Appears within first 24 hours of life
 Conjugated Hyperbilirubinemia
 Bilirubin level Increasing at rate >0.2mg/dl/hour or

>5mg/dl/day
 Jaundice persisting after 14 days
 Prolonged jaundice: Jaundice persisting beyond 2 weeks

in term and 3 weeks in preterms
 Serum bilirubin >15mg/dl
 Stool clay/ white colored and urine staining yellow,

staining clothes.
CAUSES OF UNCONJUGATED
(INDIRECT) HYPERBILIRUBINEMIA:
 Physiologic jaundice
 ABO or Rh incompatibility
 G6PD deficiency
 Infections (sepsis)
 Drugs
 Infant of diabetic mother
 Delayed cord clamping
 Feto-maternal or feto-fetal transfusion
 Cephalhematoma/Subdural hematoma
 Bruises
 Breast milk + breast feeding jaundice
 Crigler najjar syndrome I + II
 Galactosemia
 Hypothyroidism
 Pyloric stenosis
CAUSES OF CONJUGATED (DIRECT)
HYPERBILIRUBINEMIA:
 BILE FLOW OBSTRUCTION:
 Extra hepatic biliary atresia
 Intrahepatic cholestasis
 Choledochal cyst
 Stenosis of bile duct
 Inspissated bile syndrome
 Cystic fibrosis
 LIVER CELL INJURY:

 Infections (sepsis, hepatitis, TORCH)
 Metabolic (galactosemia, alpha 1 antitrypsin deficiency)
 Hyperalimentation (TPN induced cholestasis)
 Genetic disorders (Dubin-Johnson syndrome, Rotor’s syndrome)

RISK FACTORS:
 Blood group incompatibility
 Hemolytic diseases
 Gestational age <34-35 or >41 weeks
 Previous sibling received phototherapy
 Cephalohematoma and bruising
 Exclusive breastfeeding
 Macrosomic infant of diabetic mother
 Sepsis/Infections
 East Asian race/Black race

CLINICAL ASSESSMENT OF
JAUNDICE!
(KRAMER’S STAGING)
KERNICTERUS
(BILIRUBIN ENCEPHALOPATHY)
 Neurological syndrome resulting from the deposition of
unconjugated (indirect) bilirubin in basal ganglia and
brainstem
APPROACH:
 History
 Examination
 Investigations
 Management
HISTORY:
1. Gestational age
2. Maternal age
3. Mother blood group
4. Maternal diabetes
5. PROM/APH
6. Antenatal infections
7. Drugs
8. Birth trauma (Bruising)
9. Birth asphaxia
10. Family history (G6PD, TORCH, Hypothyroidism)
11. Previous sibling hx of jaundice
12. Breastfeeding
13. Constipation (Delayed bowel movement)
14. Polycythemia
CLINICAL EXAMINATION:
1.Pallor
2.Plethora
3.Petechiaes/Ecchymoses/Purpuric Lesions
4.Bruises
5.Polycythemia
6.Cephalohematoma
7.Signs of dehydration
8.Abdominal distention
9.Hepatospleenomegaly
Chorioretinitis
10.
11.Microcephaly
Large infants of diabetic mother
12.
Clay color stools
13.
Dysmorphism
14.
NEUROLOGICAL FEATURES: Lethargy, Poor feeding,

Seizures, Vomiting, Hearing loss, Hypotonia.
INVESTIGATIONS:
Total serum bilirubin level (Direct + Indirect)
Blood group Rh status
Direct antibody test (Direct antiglobulin test [DAT]) also known as Direct Coombs
test
CBC, ESR
Retic count
Liver enzyme (AST, ALT, GGT)
PT , APTT
Serum Albumin
Ammonia level
Serum glucose level
TSH level
Hb electrophoresis
G6PD screening
Blood n Urine C/S
Metabolic screening of blood and urine
TORCH antibody titers
Alpha 1 antitrypsin
Abdominal USG
Liver Biopsy
TRANSCUTANEOUS BILIRUBINOMETRY
MANAGEMENT:
 General Measures and Pharmacological Therapy
 Phototherapy
 Exchange Transfusion
 Surgery
GENERAL MEASURES AND
SUPPORTIVE TREATMENT:
 Breastfeeding should be encouraged
 MCT oil administration in a dose of 1-2ml/kg/dose in 2-
4 divided doses in expressed milk
 Intravenous fluids
 Give antibiotics if septicemia is present
 Ensure good caloric intake.
 Intravenous immunoglobulins: It is recommended when serum bilirubin is
approaching exchange levels, despite maximal interventions including
phototherapy. It works by blockage of Fc receptors in neonatal
reticuloendothelial system. IVIG (0.5-1g/kg/dose; repeat in 12 hours).
 Albumin: It is helpful because an increased reserve of albumin provides more

binding sites for free bilirubin and protect against bilirubin toxicity. (1g/kg
over 2 hours).
 Metalloporphyrins: It is a synthetic heme analog, SnMP is a potent HO

inhibitor given as a single intramuscular dose (6mmol/kg) on the 1 st DOL
particularly in pts with ABO incompatibility or G6PD deficiency.
 Phenobarbitone: Affecting on bilirubin metabolism by increasing conc: of

ligandin in liver cell, induce production of glucuronyl transferase
(2.5mg/kg/day).
 Ursodeoxycholic acid: Improves biliary secretion of bile acids, may improve

bile flow, use in the treatment of cholestatic liver disease (20-30mg/kg/day,
thrice a day and syrup URSO 250mg/5ml).
PHOTOTHERAPY:
 Reduces serum bilirubin level through
Photoisomerization and Photooxidation of bilirubin to an
excretable form. Bilirubin is absorbs maximally in the
blue light range (420-470nm).
 INDICATIONS: COMPLICATIO
NS:
1. TSB level is greater than 5
times the body weight
2. Jaundice on 1st DOL 1. Overheating
3. When serum bilirubin
below the exchange level
2. Dehydration
4. Hemolytic diseases of 3. Hypothermia
newborn during the wait for 4. Skin rashes/lesions
exchange transfusion (associated with
5. Following the exchange transient prophyrinemia)
transfusion to prevent
further rise 5. Eye injury (Corneal
6. Extremely low birth weight abrasion, conjunctivitis,
infants retinal damage)
7. Severely bruised infants 6. Bronze baby syndrome
EXCHANGE TRANFUSION:
 Exchange transfusion is used when risk of kernicterus
for infant is significant.
 A double volume exchange method in infants, which

replaces 85% of circulating RBCs and decrease bilirubin
level to about half of pre-exchange level.
 2 x blood volume of body (85ml/kg).
 There is no specific level of bilirubin can be considered

safe or dangerous for all infants because patient to
patient variations exist for permiability of blood brain
barrier.
 INDICATIONS:
1. Evidence of ongoing hemolytic process and TSB level

failed to decline by 1-2mg/dl with 4-6 hours of intensive
phototherapy
2. RH , ABO incompatibility
3. Unconjugated bilirubin 20-25mg/dl in term, 15-28mg/dl
in preterm
4. Early signs of bilirubin encephalopathy
5. Severe anemia due to hemolysis
6. Hydrops fetalis
GENERAL GUIDELINES FOR
EXCHANGE TRANSFUSION:
1. Generally type O Rh-negative blood is used for ABO or Rh

incompatibility, if the infant is type A or B and the mother
of the same blood type, type-specific, Rh-negative blood
can be used
2. Obtain parental consent
3. Donor blood always must be crossmatched with maternal
serum
4. Use fresh blood (no more than 4 days old)
5. Donor blood should be warmed to 37C
6. Calcium gluconate infusion because citrate chelates calcium
7. Monitor RBS every 30-60 minutes during procedure.
COMPLICATIONS OF EXCHANGE TRANSFUSION:
1. Cardiac arrhythmias or arrest

2. Respiratory distress
3. Reactions due to blood group incompatibilities
4. Shock
5. Infection
6. Hypervolemia
7. Electrolyte abnormalities
8. Hypoglycemia
9. Hypocalcemia
10. Air embolism
11. Portal vein thrombosis
12. Anemia
13. NEC
14. Thrombocytopenia
15. Metabolic acidosis
SURGICAL MANAGEMANT:
 KASAI Procedure (Biliary atresia)
 Liver Transplant
 Laparotomy
PROGNOSIS:
 Early recognition and treatment of hyperbilirubinemia
prevents severe brain damage.
 But brain damage due to kernicterus (bilirubin
encephalopathy) remain devastating event

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APPROACH TO

DR. USHNA RAHMAN

 Fat soluble  Water soluble

 Can cross blood brain  Cannot cross blood brain

 2nd Day to 3rd Week:

 6. Crigler najjar syndrome

 Total bilirubin rises by less than 5mg/dl per day

 Jaundice appears by 2-3 days of age in term and 3-4 days

2. Decrease Binding and Transport

3. Impaired Bilirubin Conjugation and Excretion

4. Enhanced Enterohepatic Circulation

Breast feeding jaundice: Caloric

 Bilirubin level Increasing at rate >0.2mg/dl/hour or

 Prolonged jaundice: Jaundice persisting beyond 2 weeks

 Stool clay/ white colored and urine staining yellow,

 Infant of diabetic mother

 Delayed cord clamping

 Feto-maternal or feto-fetal transfusion

 Breast milk + breast feeding jaundice

 Crigler najjar syndrome I + II

 Stenosis of bile duct

 Inspissated bile syndrome

 LIVER CELL INJURY:

 Metabolic (galactosemia, alpha 1 antitrypsin deficiency)

 Hyperalimentation (TPN induced cholestasis)

 Genetic disorders (Dubin-Johnson syndrome, Rotor’s syndrome)

 Gestational age <34-35 or >41 weeks

 Previous sibling received phototherapy

 Cephalohematoma and bruising

 Macrosomic infant of diabetic mother

 East Asian race/Black race

NEUROLOGICAL FEATURES: Lethargy, Poor feeding,

 Albumin: It is helpful because an increased reserve of albumin provides more

 Metalloporphyrins: It is a synthetic heme analog, SnMP is a potent HO

 Phenobarbitone: Affecting on bilirubin metabolism by increasing conc: of

 Ursodeoxycholic acid: Improves biliary secretion of bile acids, may improve

 A double volume exchange method in infants, which

 There is no specific level of bilirubin can be considered

1. Evidence of ongoing hemolytic process and TSB level

1. Generally type O Rh-negative blood is used for ABO or Rh

1. Cardiac arrhythmias or arrest

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