1. ‫الرحيم‬ ‫الرحمن‬ ‫ال‬ ‫بسم‬‫الرحيم‬ ‫الرحمن‬ ‫ال‬ ‫بسم‬
Jaundice in the newbornJaundice in the newborn
DR.TOSIF AHMADDR.TOSIF AHMAD
TMO-PAEDSTMO-PAEDS

2. HISTORYHISTORY
 A neonate of 5 days age presented toA neonate of 5 days age presented to
nursery with fever, jaundice, reluctant tonursery with fever, jaundice, reluctant to
take feed and fits.take feed and fits.
 Baby was delivered in home at full termBaby was delivered in home at full term
pregnancy and uneventful labour.pregnancy and uneventful labour.
 One of the elder brother of the baby diedOne of the elder brother of the baby died
of jaundice at the age of 7 days.of jaundice at the age of 7 days.

3. EXAMINATIONEXAMINATION
 The baby is deeply jaundiced, pale, andThe baby is deeply jaundiced, pale, and
has hypertonia and decorticate posture,has hypertonia and decorticate posture,
although there are no fits at the moment.although there are no fits at the moment.

4. INVESTIGATIONSINVESTIGATIONS
 HB 12gHB 12g
 SBR 27mgSBR 27mg
 Blood group of baby B +veBlood group of baby B +ve
 Blood group of mother B –veBlood group of mother B –ve
 The mother has not received any injectionThe mother has not received any injection
after deliveryafter delivery

5. DIAGNOSISDIAGNOSIS
 Rh incompatibility leading to neonatalRh incompatibility leading to neonatal
jaundice and kernicterusjaundice and kernicterus

6. 

7. Jaundice in the newbornJaundice in the newborn
 ClinicalClinical jaundicejaundice
appear at SBr 5 mg/dlappear at SBr 5 mg/dl
 25% to 50% of term25% to 50% of term
newborns have clinicalnewborns have clinical
jaundice.jaundice.
 Jaundice may beJaundice may be
caused by seriouscaused by serious
illness & lead toillness & lead to
keriniectrus.keriniectrus.
 75% of bilirubin comes75% of bilirubin comes
from haemoglobin andfrom haemoglobin and
25% from other sources25% from other sources

8. Neonatal jaundiceNeonatal jaundice
Neonatal jaundice
physiological pathological
unconjugatedconjugated
Intrahepatic
Hepatic injures
Extrahepaitc
infectious
metabolic
Neonatal hepatitis
Paucity of hepatic
ducts

9. Physiological jaundicePhysiological jaundice
 Start after the first 24hours.Start after the first 24hours.
 Peak in the fourth or fifth day {not >12Peak in the fourth or fifth day {not >12
mg/dl} in term babies and not more thanmg/dl} in term babies and not more than
15 mg/dl in premature15 mg/dl in premature
 The baby is well.The baby is well.
 Clear in 2 weeks in term and 3 weeks inClear in 2 weeks in term and 3 weeks in
premature.premature.
 Bilirubin is unconjucated.Bilirubin is unconjucated.
 The rise is not more than 0.5 mg /hThe rise is not more than 0.5 mg /h

10. Causes of physiological jaundiceCauses of physiological jaundice
 High haemoglobinHigh haemoglobin
 Decrease RBC lifeDecrease RBC life
span due to HbFspan due to HbF
 IncreaseIncrease
enterohepaticenterohepatic
circulation.circulation.
 Defective conjugation.Defective conjugation.
 Decrease hepaticDecrease hepatic
excretionexcretion

11. Pathological jaundicePathological jaundice
 Jaundice is pathological if:Jaundice is pathological if:
 PrePresent on 1sent on 1stst
day of life.day of life.
 SBr level increases more thenSBr level increases more then
0.5mg/dl/hr.0.5mg/dl/hr.
 Peak SBr is greater than13mg/dl inPeak SBr is greater than13mg/dl in
term infant or 15mg/dl in pretermterm infant or 15mg/dl in preterm
infant.infant.

12. Pathological jaundicePathological jaundice
 Direct bilirubin fraction is greater than 1.5-Direct bilirubin fraction is greater than 1.5-
2mg/dl2mg/dl
 Hepatosplenomegaly and anemia areHepatosplenomegaly and anemia are
present.present.

13. Causes of unconjucatedCauses of unconjucated
hyperbiliruniemiahyperbiliruniemia
 Glucuronyl transferase defect.(CriglerGlucuronyl transferase defect.(Crigler
Najjar syndrome,Gilbert syndrome)Najjar syndrome,Gilbert syndrome)
 Defective conjugation.Defective conjugation.
Jaundice of prematurity.Jaundice of prematurity.
Breast milk jaundice.Breast milk jaundice.
Hypothyroidism.Hypothyroidism.
Other conditions Pyloric stenosis,infant ofOther conditions Pyloric stenosis,infant of
diabetic mother, down's syndromediabetic mother, down's syndrome
G6PD deficiencyG6PD deficiency

14. Investigation of unconj-Investigation of unconj-
hyberbilirubinneamiahyberbilirubinneamia
 Split biliurubin.Split biliurubin.
 Blood groups and Rh of mother and baby.Blood groups and Rh of mother and baby.
 coomb’s test of mother and baby.coomb’s test of mother and baby.
 CBC and reticulocyte.CBC and reticulocyte.
 G-6-P-D estimationG-6-P-D estimation
 Blood film and osmotic fragility test.Blood film and osmotic fragility test.
TFT and urine for reducing substance.TFT and urine for reducing substance.

15. Causes of conjugatedCauses of conjugated
hyberbilirubineamiahyberbilirubineamia
 Hepatitis:Hepatitis:
CMV.toxoplasmosis.rubella.herpes.Hep A andCMV.toxoplasmosis.rubella.herpes.Hep A and
b,syphilis,E coli.b,syphilis,E coli.
 Metabolic:Metabolic:
Galctosemia,Tyroseanemia,Fructoseamia.Galctosemia,Tyroseanemia,Fructoseamia.
 Cystic fibrosis.Cystic fibrosis.
 Alpha one anti trypsin deficiency.Alpha one anti trypsin deficiency.
 Gauchers and neimman pickGauchers and neimman pick
 Biliary Artesia (intrahepatic and extrahepatic)Biliary Artesia (intrahepatic and extrahepatic)
 Choldoccal cyst.Choldoccal cyst.
 T.P.NT.P.N

16. Investigation of conjugatedInvestigation of conjugated
hyperbiliruniemiahyperbiliruniemia
 L.F.TL.F.T
 PT.PTT.PT.PTT.
 Urine for glucose andUrine for glucose and
reducing substance.reducing substance.
 Serum and urine aminoSerum and urine amino
acid determinations.acid determinations.
 TORCH serology.TORCH serology.
 Ultrasound.Ultrasound.
 Liver scanLiver scan
 Duodenal aspiration.Duodenal aspiration.
 Liver biopsy.Liver biopsy.

17. ManagementManagement
 Prevention:Prevention:
 Rh incompatibility----- Anti DRh incompatibility----- Anti D
 Syphlis---PencillineSyphlis---Pencilline
 Specific therapy:Specific therapy:
 PhototherapyPhototherapy
 Exchange transfusionExchange transfusion
 Septicaemia---- Antibiotic.Septicaemia---- Antibiotic.
 Surgery------------ Ex hepatic biliary Artesia.Surgery------------ Ex hepatic biliary Artesia.
 Lactose free formula for galactosemia.Lactose free formula for galactosemia.

18. PhototherapyPhototherapy
 Wave length 450-460Wave length 450-460
---- Reduce bilirubinReduce bilirubin
To harmlessTo harmless
compound excreted incompound excreted in
the urine.the urine.
 Side effects:Side effects:
Retinal damage, NasalRetinal damage, Nasal
obstruction, Mildobstruction, Mild
diarrhea,Dehydration,diarrhea,Dehydration,
Bronze babyBronze baby
syndromesyndrome

19. Exchange TransfusionExchange Transfusion
 Indicated whenIndicated when
bilirubin reach toxicbilirubin reach toxic
level.level.
 Mortality1%Mortality1%
 Remove bilirubinRemove bilirubin
,antibodies ,correct,antibodies ,correct
anaemia.anaemia.
 Double blood volumeDouble blood volume
is used 85 ml /kgis used 85 ml /kg

20. Exchange TransfusionExchange Transfusion
Side effectsSide effects::
 HypervolemiaHypervolemia
 HypothermiaHypothermia
 Skin rashesSkin rashes
 Cardiac failureCardiac failure
 HypocalcemiaHypocalcemia
 Air embolismAir embolism

21. PhenobarbitonePhenobarbitone
 This act as enzyme inducer whichThis act as enzyme inducer which
increase amount of glucoreny transferaseincrease amount of glucoreny transferase
and protein z.and protein z.
 Used in Crigler Najjar syndrome ,GilbertUsed in Crigler Najjar syndrome ,Gilbert
syndrome.syndrome.

22. KernicterusKernicterus
 Yellow staining ofYellow staining of
nuclear centres of thenuclear centres of the
brainbrain
 Due to high level ofDue to high level of
indirect bilirubin.indirect bilirubin.
 Bilirubin cause neuralBilirubin cause neural
loss.loss.
 Bilrubin inhibit cellBilrubin inhibit cell
respiration, proteinrespiration, protein
synthesis,glucousesynthesis,glucouse
metabolism.metabolism.

23. KERNICTERUSKERNICTERUS
 Poor feeding and lethargy-Poor feeding and lethargy-
fits,rigidityfits,rigidityspasticityspasticity deafnes,athetosisdeafnes,athetosis

24. PathophysiologyPathophysiology
 UCB is lipophilic and crosses the Blood-UCB is lipophilic and crosses the Blood-
Brain BarrierBrain Barrier
 UCB has an affinity for the basal ganglia,UCB has an affinity for the basal ganglia,
hippocampus, cranial nerve nucleihippocampus, cranial nerve nuclei
 UCB interrupts metabolism in glial cellsUCB interrupts metabolism in glial cells
and causes apoptosis of neuronsand causes apoptosis of neurons

25. Clinical ManifestationsClinical Manifestations
Bilirubin EncephalopathyBilirubin Encephalopathy
 Acute Bilirubin EncephalopathyAcute Bilirubin Encephalopathy
11stst
phase: hypotonia, poor suck-present in thephase: hypotonia, poor suck-present in the
first few daysfirst few days
22ndnd
phase: Hypertonia (retrocollis andphase: Hypertonia (retrocollis and
opisthotonos), feveropisthotonos), fever
33rdrd
phase: Gradual disappearance of thephase: Gradual disappearance of the
hypertonia-Up to years after the first weekhypertonia-Up to years after the first week

26. Clinical Manifestations:Clinical Manifestations:
Bilirubin EncephalopathyBilirubin Encephalopathy
 Chronic Encephalopathy:Chronic Encephalopathy:
 Extrapyramidal abnormalities: Facial grimacing,Extrapyramidal abnormalities: Facial grimacing,
drooling, dysarthria, and athetosis--may develop bydrooling, dysarthria, and athetosis--may develop by
18mo or delayed to 8or9 years.18mo or delayed to 8or9 years.
 Hearing loss is usually due to injury of the cochlearHearing loss is usually due to injury of the cochlear
nuclei in the brainstem. It may be the onlynuclei in the brainstem. It may be the only
manifestationmanifestation
 Gaze abnormalities: Limitation of upward gaze,Gaze abnormalities: Limitation of upward gaze,
palsiespalsies
 Cerebral cortex is relatively spared, so intelligence isCerebral cortex is relatively spared, so intelligence is
often close to normaloften close to normal

27. PreventionPrevention
 Treatment of Hyperbilirubinemia by:Treatment of Hyperbilirubinemia by:
 PhototherapyPhototherapy
 Exchange transfusionExchange transfusion

28. Thank youThank you