APPROCH TO

NEONATAL JAUNDICE

Dr prinka
Peads pg1
CASE REPORT
A 4 day old 36 gestation male presents to his
primary care physician with worsening
jaundice , maternal blood is O+ve , he was
discharged on 2nd day of life after successful
breastfeeding for 24 hours periods, at time of
discharge his physical exam was remarkable
for jaundice n cephalhematoma.
 At today's visit there is 8% weight loss from
birth , Hx of fair urine output n yellow color
stools. He is markedly jaundiced n resolving
cephalhematoma,
other physical finding are unremarkable for normal cry,
flat anterior fontanele, moist oral mucosa n normal
neurological examination.
Total bilirubin 27mg/dl with direct fraction 2mg/dl. He
is admitted to hospital where photo therapy initiated,
his blood group is A +ve with positive coombs test,
his hematocrit 42% with retic count 12% n
pathologist identify spherocytes in blood smear.
 G6PD is pending , after 12 hours of photo
therapy total bili is 25% n G6PD is normal. The
decision is made to perform double volume
exchange transfusion. The infant was reamin on
photo therapy for 2days more n discharged for
home after being off on photo therapy for 1day..
The serum bilirubin is 12mg on discharge day, n
he passes auditory brainstem test.

 Watare D/D
 Most likely?
CONTENTS
Defination of jaundice
Metabolism of billirubin
Types of jaundice
Causes of neonatal jaundice
Management of neonatal jaundice
JAUNDICE
 NEONATAL
HYPERBILLIRUBINEMIA

Jaundice is yellow discoloration of scelra , skin

and mucosa due to deposition of billirubin
( yellow-orange pigment).
INCIDENCE
 60-70% of term baby

 80% of preterm baby

When it is visible?
 Itbecomes clinically apparent when serum
billirubin conc: of >5mg/dl.
TYPES OF BILLIRUBIN
Unconjugated Conjugated
 Bind to albumin  Bind to glucoronic acid
 Water soluble

 Fat soluble
 Excreted in urine and
 can cross blood brain stool
barrier
 Non toxic
 Toxin in heigher level to
brain
 Etiology of jaundice
IN 1ST 24 HOURS JAUNDICE

 1-Hemolytic jaundice ( like G6PD , RH isoimmunization

, ABO incompatibility

 2- TORCH (congenital infection)

 3- polycythemia
2ND DAY – 3RD WEEK
 1. physiological (disappear after 1st week
 2. breast milk

 3. sepsis

 4. polycythemia

 5.cephalhematoma

 6. crigler najjer sydrome

 7.hemolytic disorders
PERSISTANCE AFTER 3 WEEK
 1. breast milk

 2 hypothyrodism

 3 pyloric stenosis

 4 cholestasis
PHYSIOLOGIC JAUNDICE
 Appears after 24 hours of life
 Total bilirubin rises by less 5mg/dl per day

 Maximum intensity by 4-5th day in term n 7th day in

preterm
 TSB is less than 15mg/dl

 Clinically not detected after 14 days of life.

WHY DOES PHYSIOLOGIC JAUNDICE
DEVELOP ( PATHOPHYSIOLOGY)
1.Increased bilirubin load – due to high hemoglobin
concentration
 Hemolysis

 Cephalhematoma, brusing, polycythemi a.

2. decrease binding and transport – due to dec

plasma albumin , liver transfer protein , ligandin

3. Decreased bilirubin conjugation in liver

 Decrease Uridine glucoronyl transfrase activity

4. defective bilirubin excretion

BREAST MILK JAUNDICE
 It is caused by prolonged increased
enterohepatic circulation of bilirubin .

 prolonged indirect hyperbilirubinemia beyond

3rd week of life,
 has been reported in 10-30% of breast fed
infants
 may persist up to 3 months of age
 It is not totally benign bcz kernicterus has been
reported in healthy term n late preterm infants…
PATHOLOGICAL JAUNDICE
 Appears within 24 hours
 bilirubin level Increasing at rate
>0.2mg/dl/h or >5mg/dl/d
 Direct serum bilirubin level >1.5-2.0mg/dl
or 20% of TSB
 TSB level >95th percentile that is > 15mg/dl
 Jaundice persisting after 14 days
 Stool clay/ white colored and urine staining
yellow, staining clothes.
PATHOLOGIC UNCONJUGATED
HYPERBILIRUBINEMIA
1-hemoltic

 Rh , ABO incompatibilities
 G6PD ,

 alpha thalasemia

 sepsis (DIC)

 Polycythemia

 blood sequestration ( catabolism of 1gm of HB give

 35mg of bilirubin)
2- Non-hemolytic
 Crigler najjar syndrome (CNS) type 1 n 2
 Gilbert syndrome

 Metabolic disorders ( galatcosemia,

tyrosenemia)
 Endocrine (hypothyrodism)

 Conditions causing GI obstructions like pyloric

stenosis, doudonal atresia.
 Breast milk jaundice
CONJUGATED HYPERBILIRUBINEMIA
( ITS ALWAYS PATHOLOGICAL)

extra hepatic –biliary atresia, bile duct stenosis,

cholelithiasis
Intra hepatic -progressive intra hepatic cholestasis
Infections- TORCH ,sepsis
Metabolic – dubin johsin syndrome, rotor syndrome,
cystic fibrosis, alpha 1 anti trypsin deficiency
Other- TPN, neonatal hemochromatosis, congenital
neonatal hepatitis
APPROACH TO NEONATAL JAUNDICE

HISTORY ( antenatal n post natal )

PHYSHICAL EXAM
LABS
Antenatal =
PROM, DM ,APH, Drugs , trauma , family H/O jaundice ,
liver disease, sepsis, sibling jaundice, anemia n
splenectomy in family
Post natal =
Gestational age, age of onset of jaundice , Hx of birth
asphyxia urine n stool color, Hx of convlsions, Hx of
weak cry , Hx about weight gain, Hx of feeding ,
irritiblity, lethargic.

On exam= color of skin, severity of jaundice, signs of

dehydration , hepatsplenomegaly cephalhematoma ,
brusing, pallor ( hemolytic anemia ) , petechiea, ,
neurological examination, abdominal distension..
INVESTIGATION ( UNCONJUGATED HYPER
BILIRUBINEMIA)
 TSB ,
 Blood type n RH status in mother n infant

 Direct coombs test

 Cbc with diffrentials, hematocrit n with periphral smear

 Retic count

 Other like urine for reducing substance, G6PD screening,

osmotic fragility test, thyroid profile.
 Serum albumin
INVESTIGATION ( IN CONJGATED HYPER
BILIRUBINEMIA)
 Bilirubin level ( direct n indirect)
 Liver enzyme ( AST, ALT,GGT)

 PT , APTT

 Cbc , CRP

 Blood n urine c/s

 Ammonia level

 Serum glucose level

 Urine testing for reducing substances

 TORCH titer n urine c/s for cytomegalovirus

 Alpha 1 antitrypsin
Ultrasonography – cholestasis in case of biliary atresia,
choledochal cyst.
Liver scan- in case of conjugated hyperbilirubinemia
ERCP- diagnostic n therapeutic in case of cholestasis caused by
bile duct stones.

Hearing tests (brainstem auditory –evoked potential) should

be obtained in aftermath after severe neonatal jaundice to
exclude SN hearing loss…
 Transcutaneous
Bilirubinometry-a
portable instrument that
use -
 to determine amount of
yellow color present in
skin
MANAGEMENT
 1- phototherapy

 2- intravenous immune globulin (IVIG)

 3-Albumin

 4- drugs

 5- exchange trasfusion
PHPTOTHERAPY
Reduces the serum bilirubin level through photo
isomerization and photo oxidation , n convert insoluble
into soluble exretable form…
Studies shows that blue high intensity light emitting diodes
are most effective in degrading bilirubin , range of
wavelength of light is 420 to 470nm..
Factors influencing therapy =
intensity of light, distance b/w light n infant (40cm),
surface area exposed, hydration
SIDE EFFECTS OF PHOTO THERAPY
 Increased insensible water loss
 Loose stools

 Skin rash

 Hyperthermia

 Retinal damage

 Low calcium (in preterm)

 Bronze baby syndrome – with conjugated

hyperbilirubinemia phtotherapy causes
photodestruction of copper porphyrin causing urine n
skin become bronze in color
EXCHANGE TRANSFUSION
 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 n 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 bcz patient to patient
variations exist for permiabilty of blood brain barrier…
INDICATIONS OF EXCHANGE
TRANFUSION
 RH , ABO incompatibility
 Unconjugated bilirubin 20-25mg/dl in term, 15-28mg/dl
in preterm
 Evedence of ongoing hemolysis n TSB level failed to
decline by 1-2 mg/dl with 4-6 hours of intensive PT
 Early kernicterus
GENERAL GUIDELINES FOR EXCHANGE
TRASFUSION
 Obtain parental consent
 Donor blood always must be crossmatched

 Use fresh blood (whole) ( no more than 4 day old)

 Donor blood should be warmed to 37C

 Calcium gluconate infusion via periphral vein bcz citrate

(pservative) chelates calcium (1mg/kg ).
 Monitor RBS every 30-60 minutes during procedure.
COMPLICATION OF EXCHANGE
TRASFUSION
 Cardiac m respiratory problems
 Shock

 Infection

 Clot formation

 Hypocalcemia

 Thrombocytopenia

 Metabolic acidosis
INTAVENOUS IMMUNE GLOBULIN

 IVIG in infants with RH or ABO isoimmunization can

significantly reduce need for exchange transfusions. It
inhibits hemolysis.

 Now IVIG has replaced exchange transfusion as the

second line treatment in infants with isoimmune jaundice

 1gm/kg/dose IV
Supportive treatment (specially in case CHB)
 Medium chain triglycerides- which can be
absorbed without action of bile acid
 Vitamin supplementation – fat soluble A D E K-

 Dietary restrictions - removal of galactose and

fructose from diet may prevent cirhosis n
galactosemia
SURGICAL TREATMENT FOR
CONJUGATED HYPER BILI

Kasai procedure ( biliary atresia)

Liver transplantation
 PHARMACOLOGICAL MANAGEMENT

 1-Ursodeoxycolic acid - it stimulates bile flow

 Dose 20mg/kg/d
 2-Cholestryramine ( dec entero hepatic
circulation)
 3-Phenobarbital (inc conjugation) 2.5mg//kg/day

 4-metalloporphyrin ( inhibit bili production)

 5- Albumin ( increase binding)
 PROGNOSIS
 Early recognition and treatment of
hyperbilirubinemia prevents severe brain
damage..
 But brain damage due to kernicterus
(bilirubin encephalopathy) remain
devasting event…