‫بسم هللا الرحمن الرحيم‬

Jaundice in the newborn

DR Husain Alsaggaf
 Jaundice in the newborn
 Clinical jaundice
appear at SB 5 mg/dl
 25% to 50% of term
newborns have clinical
jaundice.
 Jaundice may caused
by serious illness or
lead to keriniectrus.
 75% of bilirubin comes
from haemoglobin and
25% from other sources
 Neonatal jaundice
Neonatal jaundice

physiological pathological

conjugated unconjugated

Intrahepatic

Hepatic injures

infectious

metabolic

Neonatal hepatitis

Paucity of hepatic
ducts
Extrahepaitc
 Physiological jaundice
 Start after the first 24hours.
 Peak in the fourth or fifth day {not >12
mg/dl} in term babies and not more than
15 mg/dl in premature
 The baby is well.
 Clear in week in term and two weeks in
premature.
 Bilirubin is unconjucated.
 The rise is not more than 0.5 mg /h
 Causes of physiological jaundice
 High haemoglobin
 Decrease RBC life
span.
 Increase
enterohepatic
circulation.
 Defective conjugation.
 Decrease hepatic
excretion
 Pathological jaundice
Unconjucated
 High Hg mass
 Haemolysis.
 Blood group
incompqatability.(RH.A
BO.)
 Red cell membrane
defect (spherocytosis)
 Heamoglobinopathy.
 Haemolytic agents (vit
k3.oxytocin)
 Infection E.coli
 Causes of unconjucated
hyperbiliruniemia
 Liver cell membrane defect (GILBRET).
 Defective conjugation.
 Jaundice of prematurity.
 Breast milk jaundice.
 Hypothyroidism.
 Hereditary(crigler-najjar).
 Other conditions Pyloric stenosis,infant of
diabetic mother, down's syndrome
 Investigation of unconj-
hyberbilirubinneamia
 Split biliurubin.
 Blood groups and Rh.
 coomb’s test.
 CBC and reticulocyte.
 G-6-P-D estimation
Blood film and osmotic fragility test.
TFT and urine for reducing substance.
 Causes of conjugated
hyberbilirubineamia
 Hepatitis:
CMV.toxoplasmosis.rubella.herpes.giant
cell,Hep A and b,syphilis,E coli.
 Metabolic:
Galctosemia,Tyroseanemia,Fructoseamia.
 Cystic fibrosis.
 Alpha one anti trypsin deficiency.
 Gauchers and neimman pick
 Biliary Artesia (intrahepatic and extrahepatic)
 Choldoccal cyst.
 T.P.N
 Investigation of conjugated
hyperbiliruniemia
 L.F.T
 PT.PTT.
 Urine for glucose and
reducing substance.
 Serum and urine amino
acid determinations.
 TORCH serology.
 Ultrasound.
 Liver scan
 Duodenal aspiration.
 Liver biopsy.
 Approach To neonatal jaundice

 History.  Infant history.

 FH of aneamia,spleenomegaly.
 Jaundice in other sibling  Feeding (breast milk
(breast milk jaundice.Rh
disease) jaundice).
 FH of liver disease
(galactoseamia,alpha-one-  Poor feeding.
antitrypsin difficiency,cystic
fibrosis, Gilbert and crigler-  Vomting(sepsis
najjar) pyloric
 Maternal illness during
pregnancy (TORCH and stenosis,galactosemia
diabetes).
 Maternal drugs.(sulfanomide
 Labour and
delivery(Truma,oxytocin,delaye
d clamping of the
cord,prematurity.
 Examination

 Small for date(polycythemia, in-utroinfection.

 Premature
 Extravagated blood(briuses
,cephaloheamatoma).
 Pallor(heamolytic anaemia and extravagated
blood)
 Cherioretinitis,cataract,(congenital
infection,galactoseamia)
 Petechia rash (congenital
infection,galactoseamia)
 Hepatospleenomegaly(heamolytic anaemia
,congenital infection, liver diseases)
 Management
 Prevention:
 Rh incompatibility----- Anti D
 Syphlis---Pencilline

 Specific therapy:
 Septicaemia---- Antibiotic.
 Surgery------------ Ex hepatic biliary Artesia.
 Galctose withdrawal for galactoseamia.
Management of unconjucated
hyberbilirubineamia
 Phototherapy
 Wave length 450-460
-- Reduce bilirubin
To harmless
compound excreted in
the urine.
 Complication:
 Retinal damage,
nasal obstruction,
mild
diarrhea,dehydration,
bronzed baby
syndrome
 Exchange Transfusion
 Indicated when
bilirubin reach toxic
level.
 Mortality1%
 Remove bilirubin
,antibodies ,correct
anaemia.
 Double blood volume
is used 85 ml /kg
 COMPLICATION.
 Infection,acidosis,Cad
 Phenobarbitone
 This act as enzyme inducer which
increase amount of glucoreny transferase
and protein z.
 Used in crigler najjar
 Kernicterus
 Yellow staining of
nuclear centres of the
brain
 Due to high level of
indirect bilirubin.
 Bilirubin cause neural
loss.
 Bilrubin inhibit cell
respiration, protein
synthesis,glucouse
metabolism.