1. MANAGEMENT OFMANAGEMENT OF
HYPERBILIRUBIC INFANTHYPERBILIRUBIC INFANT

2.  WHAT IS HYPERBILIRUBIC INFANT?WHAT IS HYPERBILIRUBIC INFANT?
 FORMATION OF BILIRUBIN.FORMATION OF BILIRUBIN.
 CAUSES OF NEONATAL JAUNDICE.CAUSES OF NEONATAL JAUNDICE.
 BURDEN OF THE DISEASE.BURDEN OF THE DISEASE.
 CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS
 WHY PHOTOTHERAPY.? DO’S AND DON’T’S .WHY PHOTOTHERAPY.? DO’S AND DON’T’S .
 TREATMETN & NORWEGIAN GUIDLINE.TREATMETN & NORWEGIAN GUIDLINE.
 TAKE HOME MESSAGE.TAKE HOME MESSAGE.
We Are Going To Learn…We Are Going To Learn…

3.  When a new born baby suffers fromWhen a new born baby suffers from yellow discolorationyellow discoloration
ofof skinskin andand sclerasclera (white part) of eyes it is called as(white part) of eyes it is called as
neonatal jaundice or hyperbilirubinemia.neonatal jaundice or hyperbilirubinemia.
 It is a result of accumulation ofIt is a result of accumulation of conjugated bilirubinconjugated bilirubin ..
 In most infant, hyperbilirubinemia is a normal transitionalIn most infant, hyperbilirubinemia is a normal transitional
phenomenon.phenomenon.
 But in some infants serum bilirubin levels riseBut in some infants serum bilirubin levels rise
excessively.excessively.
This unconjugated bilirubin is highlyThis unconjugated bilirubin is highly neurotoxicneurotoxic andand
causescauses deathdeath in infant and lifelong neurologic sequela inin infant and lifelong neurologic sequela in
infants those who survive.infants those who survive.
What isWhat is Neonatal Jaundice?Neonatal Jaundice?

4.  Jaundice is observed during theJaundice is observed during the first weekfirst week inin
approximately 60% ofapproximately 60% of term infantterm infant and 80% ofand 80% of
preterm infantpreterm infant..
 Hyperbilirubinemia can be toxic, with highHyperbilirubinemia can be toxic, with high
levels resulting in anlevels resulting in an encephalopathyencephalopathy known asknown as
kernicterus.kernicterus.
What isWhat is Neonatal Jaundice?Neonatal Jaundice?

5. What isWhat is Bilirubin?Bilirubin?
 Bilirubin is a on-polar, water insoluble
compound requiring conjugation with
glucuronic acid to form a water soluble
product that can be excreted.
 It circulates to the liver reversibly bound to
albumin

6.  In everybody bilirubin is present in blood.
 From where does this bilirubin comes from?
75%
from
hemoglobin
degradation
Myoglobin
Cytochrome
catalase
Heme
catabolism
Bilirubin is the end product of all these three
resources and is produced in reticulo-endothelial system
Bilirubin PhysiologyBilirubin Physiology

7. HemeHeme BiliverdinBiliverdin
Heme oxygenaseHeme oxygenase
((OxidationOxidation))
BilirubinBilirubin
Biliverdin reductaseBiliverdin reductase
((ReductionReduction))
Bilirubin PhysiologyBilirubin Physiology
Pathway of Heme - Biliverdin - BilirubinPathway of Heme - Biliverdin - Bilirubin

8.  Increased production in neonate due to larger red cellIncreased production in neonate due to larger red cell
volume, which producesvolume, which produces bilirubinbilirubin as red cells areas red cells are
broken down and shorter RBC life span, so broken downbroken down and shorter RBC life span, so broken down
faster.faster.
 HemeHeme is catabolized within the reticuloendothelial (RE)is catabolized within the reticuloendothelial (RE)
system bysystem by heme oxygenaseheme oxygenase to formto form biliverdinbiliverdin..
 BiliverdinBiliverdin is metabolized tois metabolized to bilirubinbilirubin in the presencein the presence
ofof biliverdin reductase.biliverdin reductase.
Bilirubin PhysiologyBilirubin Physiology

9.  Increased bilirubin production,
 Less effective binding and transportation,
 Less efficient hepatic conjugation,
 Enhanced absorption of bilirubin via the
enterohepatic circulation.
Metabolism of BilirubinMetabolism of Bilirubin

10. Metabolism of BilirubinMetabolism of Bilirubin

11.  Neonatal jaundice can occasionally become moreNeonatal jaundice can occasionally become more
pronounced. Blood group incompatibilities (e.g., Rh,pronounced. Blood group incompatibilities (e.g., Rh,
ABO) may increase bilirubin production throughABO) may increase bilirubin production through
increasedincreased hemolysishemolysis. Historically, Rh isoimmunization. Historically, Rh isoimmunization
was an important cause of severe jaundice .was an important cause of severe jaundice .
 Therefore Rh prophylaxis in Rh-negative women,Therefore Rh prophylaxis in Rh-negative women,
Rh isoimmunization remains common in developingRh isoimmunization remains common in developing
countries.countries.
Causes of Neonatal JaundiceCauses of Neonatal Jaundice

12.  Out of 4-millions new born at least 60% of the babies getOut of 4-millions new born at least 60% of the babies get
infected.infected.
 In these babies serum levels are elevated therefore it isIn these babies serum levels are elevated therefore it is
must to measure TSB or TCB if jaundice occurs in babymust to measure TSB or TCB if jaundice occurs in baby
within 1within 1stst
24 hours of birth.24 hours of birth.
 Disease occur pertaining to the weight of the baby .i.eDisease occur pertaining to the weight of the baby .i.e
birth weight > OR =2500gms.birth weight > OR =2500gms.
 High chances of disease occurs after 37 complete weeksHigh chances of disease occurs after 37 complete weeks
of gestation.of gestation.
Burden of DiseaseBurden of Disease

13.  Jaundice may be present at birth or at any time during the
neonatal period.
 Jaundice usually begins on the face and, as the serum
level increases, progresses to the chest and abdomen and
then the feet.
 Jaundice resulting from deposition of indirect bilirubin in
the skin tends to appear bright yellow or orange;
 Jaundice of the obstructive type (direct bilibrubin), a
greenish or muddy yellow.
Clinical ManifestationClinical Manifestation

14. – Determination of direct and indicrect bilirubin fractions
– Determination of hemoglobin
– Reticulocyte count
– Blood type
– Coombs’ test
– Examination of the peripheral blood smear
DiagnosisDiagnosis

15.  Direct-reactingDirect-reacting
hyperbilirubinemiahyperbilirubinemia
HepatitisHepatitis
CholestasisCholestasis
Inborn errors ofInborn errors of
metabolismmetabolism
SepsisSepsis
Classifications - IClassifications - I
 Indirect-reactingIndirect-reacting
hyperbilirubinemiahyperbilirubinemia
– Hemolysis:Hemolysis:
Reticulocytosis,Reticulocytosis,
Evidences of redEvidences of red
blood cellblood cell
Destruction,Destruction,
A positiveA positive
Coomb’sCoomb’s
test, Blood grouptest, Blood group
incompatibility,incompatibility,
Positive resultsPositive results
ofof
specificspecific
 Direct andDirect and
Indirect- reactingIndirect- reacting
HyperbilirubinemiaHyperbilirubinemia
Hepatitis,Hepatitis,
Sepsis,Sepsis,
Liver damageLiver damage
complicated bycomplicated by
Hemolysis.Hemolysis.

16.  Physiologic Jaundice:Physiologic Jaundice:
Clinical jaundice appearsClinical jaundice appears
atat
2-3 days.2-3 days.
Total bilirubin rises < 5Total bilirubin rises < 5
mg/dlmg/dl
(86 umol/L) per day.(86 umol/L) per day.
Peak bilirubin occurs at 3-Peak bilirubin occurs at 3-
55
days of age.days of age.
Peak bilirubinPeak bilirubin
concentration inconcentration in
Classifications – II…cont.Classifications – II…cont.
 Pathologic Jaundice:Pathologic Jaundice:
Clinical jaundice appears inClinical jaundice appears in
2424
hours of age.hours of age.
Total bilirubin rises by higherTotal bilirubin rises by higher
than 5 mg/dl (86 umol/L) perthan 5 mg/dl (86 umol/L) per
day.day.
Peak concentration of totalPeak concentration of total
bilirubin is more than 12bilirubin is more than 12
mg/dL in the term infant andmg/dL in the term infant and
15 mg/ dL in the preterm15 mg/ dL in the preterm
infant.infant.

17.  Physiologic Jaundice:Physiologic Jaundice:
Peak bilirubin concentration inPeak bilirubin concentration in
Full-term infant <12mg/dlFull-term infant <12mg/dl
(205.2 umol/L).(205.2 umol/L).
Peak bilirubin concentration inPeak bilirubin concentration in
Premature infant <15mg/dlPremature infant <15mg/dl
(257umol/L).(257umol/L).
Clinical jaundice is resolvedClinical jaundice is resolved
by 2 weeks in the term infantby 2 weeks in the term infant
by 3-4 weeks in the Pretermby 3-4 weeks in the Preterm
infant.infant.
Classifications - IIClassifications - II
 Pathologic Jaundice:Pathologic Jaundice:
Clinical jaundice is notClinical jaundice is not
resolved in 2 weeks in theresolved in 2 weeks in the
termterm
infant and in 4 weeks in theinfant and in 4 weeks in the
Preterm infant.Preterm infant.
Clinical jaundice appearsClinical jaundice appears
againagain
after it has been resolved.after it has been resolved.
Direct bilirubin concentrationDirect bilirubin concentration
is more than 1.5 mg/dLis more than 1.5 mg/dL

18. InfectiveInfective
Jaundice:Jaundice:
Neonatal hepatitisNeonatal hepatitis
(TORCH(TORCH
infection),infection),
Neonatal sepsis.Neonatal sepsis.
Jaundice AssociatedJaundice Associated
Without Infection:Without Infection:
Hemolytic disease ofHemolytic disease of
The newbornThe newborn
(ABO incompatibility,(ABO incompatibility,
Rh incompatibility,Rh incompatibility,
BiliaryAtresia).BiliaryAtresia).
Jaundice associatedJaundice associated
With breast- feeding.With breast- feeding.
Breast Milk Jaundice:Breast Milk Jaundice:
Caused by prolongedCaused by prolonged
increased enterohepaticincreased enterohepatic
circulation of bilirubin.circulation of bilirubin.
((β-β-GD↑)GD↑)
The hyperbilirubinemiaThe hyperbilirubinemia
peaks at 10-15 days of age.peaks at 10-15 days of age.
The level of unconjugatedThe level of unconjugated
hyperbilirubinemia is at 10-30hyperbilirubinemia is at 10-30
mg/dL (172-516 umol/L).mg/dL (172-516 umol/L).
If nursing is interrupted for 72If nursing is interrupted for 72
hours, the bilirubin level fallshours, the bilirubin level falls
quickly.quickly.
Causes of Pathologic JaundiceCauses of Pathologic Jaundice

19. 1. Genetic Disease:1. Genetic Disease:
Congenital deficiencies of the enzymes:Congenital deficiencies of the enzymes:
glucose-6-phosphate dehydrogenase (G-6-PD)glucose-6-phosphate dehydrogenase (G-6-PD)
2. Thalassemia2. Thalassemia
3. Cystic fibrosis3. Cystic fibrosis
4. Drug:4. Drug: Vitamin kVitamin k
NovobiocinNovobiocin
Causes of Pathologic JaundiceCauses of Pathologic Jaundice

20.  Gestational Age
 Race
 Family history of
jaundice requiring
phototherapy
 Hemolysis (ABO or
other)
 Severe bruising
 Breastfeeding
Risk Factors forRisk Factors for
Neonatal JaundiceNeonatal Jaundice
 Pathologic by definition if
significant in first 24
hours
 Usually begins to peak by
48 hours and continues
until 96 hours
 In Asian infants and
preterm infants, peak can
continue out to 5-7 days.
Time Course of
Jaundice

21. Race
 Asians - highest risk
Levels peak at 16-18 as
opposed to average
Caucasian levels of 6-8.
There is also a later peak
which can occur at 5-7
days.
 Black infants have a lower
peak, rarely exceeding 12.
(but they have a much
higher incidence of G6PD
deficiency)
 Caucasians are in the
middle.
Risk Factors … cont.
Gestational Age
 The younger the gestation, the
higher the risk of jaundice.
 37 weeks more prone to
jaundice than 40 weeker who is
more prone than a 42 weeker.
 35 and below is much more
prone
 Extreme preemies also more
prone to kernicterus and are
treated at much lower levels.

22. Family HistoryFamily History
 A child whoseA child whose
sibling neededsibling needed
phototherapy isphototherapy is
12 times more12 times more
likely to alsolikely to also
have significanthave significant
jaundice.jaundice.
 Frequently peakFrequently peak
bilirubin levelsbilirubin levels
correlatecorrelate
between siblings.between siblings.
Risk FactorsRisk FactorsHemolysis
 ABO Incompatibility - most
common cause.
 Only 10-20% of infants
with ABO mismatch
develop significant
jaundice.
 Some, develop very
significant jaundice
quickly.
 Coombs positive ABO is
more likely to cause
hemolysis, but many
babies will be
asymptomatic.
Conversely, Coombs
negative ABO mismatch
does occasionally cause
significant hemolysis, but
this is rather rare.
PathologicPathologic
 G6PDG6PD
DeficiencyDeficiency
 HereditaryHereditary
SpherocytosisSpherocytosis
 GlucuronylGlucuronyl
TransferaseTransferase
Deficiency TypeDeficiency Type
1 (Crigler Najar1 (Crigler Najar
Syndrome)Syndrome)
 GT deficiencyGT deficiency
Type 2 (AriasType 2 (Arias
Syndrome)Syndrome)
 PolycythemiaPolycythemia

23. Breast Milk / Breast Feeding JaundiceBreast Milk / Breast Feeding Jaundice
 Occurs early.
 It is due to the lack of
breast milk.
 Often associated with poor
passage of meconium.
 Treatment - stopping
breastfeeding while
supplementing as needed
to avoid extreme weight
loss, dehydration, and
worsening jaundice.
 It is a different, more benignIt is a different, more benign
entity, which tends to occurentity, which tends to occur
late in the first week orlate in the first week or
afterwards.afterwards.
 It is actually due toIt is actually due to
something in the breast milksomething in the breast milk
which tends to prolongwhich tends to prolong
jaundice.jaundice.
 Usually weight gain is good,Usually weight gain is good,
and the baby is otherwiseand the baby is otherwise
well.well.
 Jaundice might persist asJaundice might persist as
late as 3-4 weeks, butlate as 3-4 weeks, but
usually will peak by 2 weeks.usually will peak by 2 weeks.
 Textbook treatment is toTextbook treatment is to
interrupt breastfeedinginterrupt breastfeeding
(usually do not do this).(usually do not do this).

24. Assessing the Risk of Jaundice by NumbersAssessing the Risk of Jaundice by Numbers
Bhutani Curve

25.  Maisels’ and Kring’s study showed that not all earlyMaisels’ and Kring’s study showed that not all early
higher TSB will continue going up.higher TSB will continue going up.
 They divided the rate of rise to be concerned with intoThey divided the rate of rise to be concerned with into
6-24hr6-24hr >0.22/hr>0.22/hr
24-4824-48 >0.15/hr>0.15/hr
48+48+ >0.06/hr>0.06/hr
Assessing the Risk of Jaundice by NumbersAssessing the Risk of Jaundice by Numbers

26. Hemolytic Disease ofHemolytic Disease of
the Newbornthe Newborn

27. IntroductionIntroduction
Hemolytic disease of the newborn:Hemolytic disease of the newborn:
 It is an isoimmunity hemolysis associatedIt is an isoimmunity hemolysis associated
with ABO or Rh incompatibility.with ABO or Rh incompatibility.
 It results from transplacental passage ofIt results from transplacental passage of
maternal antiboddy active against RBCmaternal antiboddy active against RBC
antigens of the infant, leading to an increasedantigens of the infant, leading to an increased
rate of RBC destruction.rate of RBC destruction.
 It is an important cause of anemia andIt is an important cause of anemia and
jaundice in newborn infantjaundice in newborn infant..

28. Etiology and PathogenesisEtiology and Pathogenesis
 ABO hemolyticABO hemolytic
diseasedisease
ABO incompatibilityABO incompatibility
 Type O mothersType O mothers
 Type A or B fetusesType A or B fetuses
 Presence of IgG anti-A orPresence of IgG anti-A or
Anti-B antibodies in type OAnti-B antibodies in type O
mothermother
 Frequently occurring duringFrequently occurring during
the first pregnancy withoutthe first pregnancy without
prior sensitizationprior sensitization
 Rh hemolyticRh hemolytic
diseasedisease
 An Rh-negative motherAn Rh-negative mother
 An Rh-positive fetusAn Rh-positive fetus
 Leakage of fetal RBC intoLeakage of fetal RBC into
maternal circulationmaternal circulation
 Maternal sensitization to DMaternal sensitization to D
antigen on fetal RBCantigen on fetal RBC

29.  Production and transplacental passage ofProduction and transplacental passage of
maternal anti-D antibodies into fetal circulationmaternal anti-D antibodies into fetal circulation
 Attachment of maternal antibodies to Rh-Attachment of maternal antibodies to Rh-
positive fetal RBCpositive fetal RBC
 Destruction of antibody-coated fetal RBCDestruction of antibody-coated fetal RBC
Etiology and PathogenesisEtiology and Pathogenesis

30.  Rh hemolytic disease was rare during the firstRh hemolytic disease was rare during the first
pregnancy involving an Rh-positive fetus.pregnancy involving an Rh-positive fetus.
 Once sensitization has occurred, re-exposure toOnce sensitization has occurred, re-exposure to
Rh D RBC in subsequent pregnancies leads to anRh D RBC in subsequent pregnancies leads to an
anamnestic response, with an increase in theanamnestic response, with an increase in the
maternal anti-Rh D antibody titer.maternal anti-Rh D antibody titer.
 The likelihood of an infant being affectedThe likelihood of an infant being affected
increased significantly with each subsequentincreased significantly with each subsequent
pregnancy.pregnancy.
Etiology and PathogenesisEtiology and Pathogenesis

31. Significant hemolysis occurring in the firstSignificant hemolysis occurring in the first
pregnancy indicates prior maternal exposure topregnancy indicates prior maternal exposure to
Rh-positive RBC.Rh-positive RBC.
 Fetal bleeding associated with a previousFetal bleeding associated with a previous
spontaneous or therapeutic abortionspontaneous or therapeutic abortion
 Ectopic pregnancyEctopic pregnancy
 A variety of different prenatal proceduresA variety of different prenatal procedures
 Transfusion of some other blood productTransfusion of some other blood product
containing Rh D RBC in an Rh-negativecontaining Rh D RBC in an Rh-negative
mothermother
Etiology and PathogenesisEtiology and Pathogenesis

32. Clinical ManifestationsClinical Manifestations
 JaundiceJaundice
 AnemiaAnemia
 HydropsHydrops
 Massive enlargement of the liver and spleenMassive enlargement of the liver and spleen
 Bilirubin encephalopathy (Kernicterus)Bilirubin encephalopathy (Kernicterus)

33. Clinical Features Rh ABO
Frequency Unusual Common
Anemia Marked Minimal
Jaundice Marked Minimal to moderate
Hydrops Common Rare
Hepatosplenomegaly Marked Minimal
Kernicterus Common Rare
Clinical ManifestationsClinical Manifestations

34. Laboratory DiagnosisLaboratory Diagnosis
Laboratory Features Rh ABO
blood type of Mother Rh negative O
blood type of Infant Rh positive A or B
Anemia Marked Minimal
Direct Commb’s test Positive Negative
Indirect Commb’s test Positive Usually positive
Hyperbilirubinemia Marked Variable
RBC morphology Nucleated RBC Spherocytes

35. DiagnosisDiagnosis
RequiresRequires
demonstration ofdemonstration of
blood groupblood group
incompatibilityincompatibility
and ofand of
correspondingcorresponding
antibody bound toantibody bound to
the infant’s RBC.the infant’s RBC.
Antenatal DiagnosisAntenatal Diagnosis
History,History,
Expectant parents’Expectant parents’
blood types,blood types,
Maternal titer of IgGMaternal titer of IgG
antibodies to D or Eantibodies to D or E
(>1:32):(>1:32):
 At 12At 12 ～～ 16 wk16 wk
 At 28At 28 ～～ 32 wk32 wk
 At 36 wk.At 36 wk.
Fetal Rh and ABOFetal Rh and ABO
status,status,
Fetal jaundice level .Fetal jaundice level .
 Postnatal diagnosisPostnatal diagnosis
Jaundice at < 24 hr.Jaundice at < 24 hr.
Anemia (HematocritAnemia (Hematocrit
and hemoglobinand hemoglobin
examination).examination).
Rh or ABORh or ABO
Incompatibility.Incompatibility.
Coomb’s test positive.Coomb’s test positive.
Examination for RBCExamination for RBC
antibodies in theantibodies in the
mother’s serum.mother’s serum.

36. TreatmentTreatment

37. TreatmentTreatment
Main GoalsMain Goals
To prevent intrauterineTo prevent intrauterine
or extrauterine deathor extrauterine death
of fetal or infant formof fetal or infant form
severe anemia andsevere anemia and
Hypoxic -Hypoxic -
To avoid neurotoxicityTo avoid neurotoxicity
fromfrom
hyperbilirubinemiahyperbilirubinemia
Treatment of Unborn InfantTreatment of Unborn Infant
Utero transfusionUtero transfusion
 IndicationIndication
– HydropsHydrops
– Anemia (Hematocrit<30%)Anemia (Hematocrit<30%)
 MethodMethod
– Packed RBC matching with thePacked RBC matching with the
mother’s serummother’s serum
– Umbilical vein transfusionUmbilical vein transfusion

38.  Delivery in AdvanceDelivery in Advance
Indication:Indication:
Pulmonary maturityPulmonary maturity
Fetal distress –Fetal distress –
Maternal titer of RhMaternal titer of Rh
antibodies > 1:32,antibodies > 1:32,
3535 ～～ 37 w.k of gestation37 w.k of gestation
 Treatment of LivebornTreatment of Liveborn
InfantInfant
– Immediate resuscitationImmediate resuscitation
and supportive therapy:and supportive therapy:
 Temperature stabilizationTemperature stabilization
 Correction of acidosis: 1-Correction of acidosis: 1-
2mEq/kg of sodium2mEq/kg of sodium
bicarbonatebicarbonate
 A small transfusionA small transfusion
compatible packed RBCcompatible packed RBC
 Volume expansion forVolume expansion for
hypotensionhypotension
 Provision of assistedProvision of assisted
ventilation for respiratoryventilation for respiratory
failurefailure
TreatmentTreatment

39. Phototherapy:Phototherapy:
 Blue spectrum of 427-475Blue spectrum of 427-475
nm (or White or Green)nm (or White or Green)
 Irradiance:10-12μW/cm2Irradiance:10-12μW/cm2
 Protection of eyes andProtection of eyes and
genital.genital.
 Indication:Indication:
Bilirubin≥10mg/dl atBilirubin≥10mg/dl at ＜＜ 12 hr12 hr
Bilirubin≥12-14mg/dl atBilirubin≥12-14mg/dl at ＜＜ 1818
hrhr
Bilirubin≥15mg/dl at ≥24 hrBilirubin≥15mg/dl at ≥24 hr
Side effect of Phototherapy:Side effect of Phototherapy:
 DiarrheaDiarrhea
 DehydrationDehydration
 Riboflavin destructionRiboflavin destruction
 HypocalcemiaHypocalcemia
 Bronze-baby syndromeBronze-baby syndrome
TreatmentTreatment

40. Exchange TransfusionExchange Transfusion
Indication:Indication:
– HemoglobinHemoglobin ＜＜ 120g/L120g/L
– Hydrops, hepatosplenomegalyHydrops, hepatosplenomegaly
and heart failureand heart failure
– Bilirubin in the 1stBilirubin in the 1st 12 of12 of
life>0.75mg/dl/hrlife>0.75mg/dl/hr
– Bilirubin concentration>20mg/dlBilirubin concentration>20mg/dl
– Factors supporting earlyFactors supporting early
exchange transfusion:exchange transfusion:
Previous kernicterus in a sibling,Previous kernicterus in a sibling,
reticulocyte counts greater thanreticulocyte counts greater than
15%, asphyxia of neonate and15%, asphyxia of neonate and
premature infantpremature infant
TreatmentTreatment
 Blood volume ofBlood volume of
exchange transfusionexchange transfusion
– Double-volume exchangeDouble-volume exchange
transfusion :150-180ml/kgtransfusion :150-180ml/kg
 Blood choose of RhBlood choose of Rh
incompatibilityincompatibility
– Rh in accordance with motherRh in accordance with mother
– ABO in accordance with neonateABO in accordance with neonate
 Blood choose of ABOBlood choose of ABO
incompatibilityincompatibility
– Plasm of AB typePlasm of AB type
– RBC of O typeRBC of O type

41. Drug Treatment:Drug Treatment:
 Intravenous immuneIntravenous immune globulin (IVIG)globulin (IVIG)
 Human albuminHuman albumin
 Glucocorticoids: DexamethasoneGlucocorticoids: Dexamethasone
 InducerInducer of liver enzyme: Luminalof liver enzyme: Luminal
TreatmentTreatment

42.  Intramuscular injection of 300ug of human anti-Intramuscular injection of 300ug of human anti-
D globulin to an Rh-negative mother:D globulin to an Rh-negative mother:
 Within 72 hr of delivery of an ectopic pregnancyWithin 72 hr of delivery of an ectopic pregnancy
 Abdominal trauma in pregnancyAbdominal trauma in pregnancy
 AmniocentesisAmniocentesis
 Chorionic villus biopsyChorionic villus biopsy
 AbortionAbortion
PreventionPrevention

43. PhototherapyPhototherapy

44.  Since 1960,Since 1960, PhototherapyPhototherapy has been the mainstay of treatinghas been the mainstay of treating
hyperbilirubinemia.hyperbilirubinemia.
 It causes structural isomerization, formingIt causes structural isomerization, forming lumirubinlumirubin, which, which
is then excreted in the bile and urine.is then excreted in the bile and urine.
 Since photoisomers are water soluble, they should not be ableSince photoisomers are water soluble, they should not be able
to cross the blood-brain barrier, so starting phototherapyto cross the blood-brain barrier, so starting phototherapy
should decrease the risk of kernicterus by turning 20-25% ofshould decrease the risk of kernicterus by turning 20-25% of
bilirubin into a form unable to cross, even before the level hasbilirubin into a form unable to cross, even before the level has
lowered significantly.lowered significantly.
PhototherapyPhototherapy … cont.… cont.

45. Phototherapy …cont.Phototherapy …cont.
 Initially, in photo oxidationInitially, in photo oxidation bilirubinbilirubin is bleached throughis bleached through
the action of light, the process is slow.the action of light, the process is slow.
 The photoisomers ofThe photoisomers of bilirubinbilirubin are excreted inare excreted in
bile and, to some extent, in urine.bile and, to some extent, in urine.
 Phototherapy may reduce the risk of bilirubin-inducedPhototherapy may reduce the risk of bilirubin-induced
neurotoxicity as soon as the lights are turned on. At anyneurotoxicity as soon as the lights are turned on. At any
given total serum bilirubin concentration, the presence ofgiven total serum bilirubin concentration, the presence of
20-25% of photoisomers means that only 75-80% of the20-25% of photoisomers means that only 75-80% of the
total bilirubin may be present in a form that can enter thetotal bilirubin may be present in a form that can enter the
brain.brain.

46.  Bilirubin absorbs light best atBilirubin absorbs light best at
450 nm, but longer wavelenths450 nm, but longer wavelenths
penetrate skin better.penetrate skin better.
 Make sure skin is as exposed asMake sure skin is as exposed as
possible and that light is not toopossible and that light is not too
far from baby.far from baby.
 Fiberoptic light (bili blanket) isFiberoptic light (bili blanket) is
much less efficacious on its own.much less efficacious on its own.
PhototherapyPhototherapy

47. Copyright ©2004 American Academy of PediatricsCopyright ©2004 American Academy of Pediatrics
Subcommittee on Hyperbilirubinemia, Pediatrics 2004;114:297-316Subcommittee on Hyperbilirubinemia, Pediatrics 2004;114:297-316
Guidelines for phototherapy in hospitalized infants
of 35 or more weeks' gestation

48.  The distance between the infant and the light source should not beThe distance between the infant and the light source should not be
greater than 50 cm (20 inch) and can be less (down to 10 cm)greater than 50 cm (20 inch) and can be less (down to 10 cm)
provided the infant's temperature is monitored .provided the infant's temperature is monitored .
 Efficiency of phototherapy depends on the amount of bilirubin that isEfficiency of phototherapy depends on the amount of bilirubin that is
irradiated. Irradiating a large skin surface area is more efficient thanirradiated. Irradiating a large skin surface area is more efficient than
irradiating a small area, and the efficiency of phototherapy increasesirradiating a small area, and the efficiency of phototherapy increases
with serum bilirubin concentration.with serum bilirubin concentration.
 The nature and character of the light source may affect energyThe nature and character of the light source may affect energy
delivery. Irradiation levels using quartz halide spotlights are maximaldelivery. Irradiation levels using quartz halide spotlights are maximal
at the center of the circle of light and decrease sharply towards theat the center of the circle of light and decrease sharply towards the
perimeter of the circle. Large infants and infants who can moveperimeter of the circle. Large infants and infants who can move
away from the circle's center may receive less efficientaway from the circle's center may receive less efficient
phototherapy.phototherapy.
Do’s and Don’ts of PhototherapyDo’s and Don’ts of Phototherapy

49.  Narrow spectrum blue fluorescent tube.Narrow spectrum blue fluorescent tube.
 White fluorescent tubesWhite fluorescent tubes
 White quartz lamp.White quartz lamp.
 Quartz lamps with single or double banks of 3-4 bulbsQuartz lamps with single or double banks of 3-4 bulbs
attached.attached.
 Fibreoptic light.Fibreoptic light.
Lamps Beneficial for PhototherapyLamps Beneficial for Phototherapy

50. Exchange TransfusionExchange Transfusion
 Double volume exchange transfusion was a commonDouble volume exchange transfusion was a common
procedure prior to advent of Rhogam and phototherapy.procedure prior to advent of Rhogam and phototherapy.
 Now fortunately a rare occurrenceNow fortunately a rare occurrence
 Used for bilirubin >25 in a term infant and not decreasingUsed for bilirubin >25 in a term infant and not decreasing
despite phototherapydespite phototherapy

51. Neonatal jaundice guidance as suggestedNeonatal jaundice guidance as suggested
by AAP(American Academy of Pediatrics)by AAP(American Academy of Pediatrics)
 Promote and support breast-feeding.Promote and support breast-feeding.
 Establish nursery protocols.Establish nursery protocols.
 Measure TSB or TCB if jaundice occurs in 1Measure TSB or TCB if jaundice occurs in 1stst
2424
hours after birth.hours after birth.
 Visual estimation of jaundice can lead to errorsVisual estimation of jaundice can lead to errors
particularly in darkly pigmented infant.particularly in darkly pigmented infant.
 Interpret bilirubin levels according to the infantInterpret bilirubin levels according to the infant
age in hours.age in hours.

52.  Infant <38 weeks if breastfed are at higher risk.Infant <38 weeks if breastfed are at higher risk.
 Perform risk assessment prior to discharge.Perform risk assessment prior to discharge.
 Give parents written and oral information.Give parents written and oral information.
 Provide appropriate follow-up bond at the at theProvide appropriate follow-up bond at the at the
time of discharge and risk assessment.time of discharge and risk assessment.
 Treat new born with, when indicated withTreat new born with, when indicated with
phototherapy or exchange transfusion.phototherapy or exchange transfusion.

53. MANAGING JAUNDICEMANAGING JAUNDICE
Take Home MessageTake Home Message
 Consider the risk factors, particularly prematurity andConsider the risk factors, particularly prematurity and
hemolysis.hemolysis.
 Follow up is key!Follow up is key!
 Consider how well baby is feeding, parents’ ability toConsider how well baby is feeding, parents’ ability to
return, reliability, etcreturn, reliability, etc
 The higher the number of risk factors, the lower the levelThe higher the number of risk factors, the lower the level
at which to interveneat which to intervene
 Sometimes, you will be surprised. We can’t alwaysSometimes, you will be surprised. We can’t always
preventprevent hyperbilirubinemiahyperbilirubinemia, but we should always prevent, but we should always prevent
kernicteruskernicterus..

54.  Infant should be naked with eyesInfant should be naked with eyes
covered to reduce risk of retinacovered to reduce risk of retina
damage.damage.
 The distance between infant andThe distance between infant and
fluorescent light should be 50cmfluorescent light should be 50cm
(20”inches).(20”inches).
 Hang white curtains around theHang white curtains around the
phototherapy unit and bassinet.phototherapy unit and bassinet.
 If spotlight is used infant should beIf spotlight is used infant should be
placed at the centre of spotlight.placed at the centre of spotlight.
Take Home MessageTake Home Message

55.  Temp. and homeostasis of infant should be maintainedTemp. and homeostasis of infant should be maintained
by feeding the infant orally.by feeding the infant orally.
 Monitoring the levels of bilirubin value every hour tillMonitoring the levels of bilirubin value every hour till
they drop down from 7500 micromol/lit (30mg/dL) tothey drop down from 7500 micromol/lit (30mg/dL) to
85micromol/lit/h (5mg/dL/h}85micromol/lit/h (5mg/dL/h}
 Phototherapy is discontinued when serum bilirubinPhototherapy is discontinued when serum bilirubin
falls 25-50micromol/lit (1.5-3mg/dL)falls 25-50micromol/lit (1.5-3mg/dL)
 Follow up test should be taken within 6-12hrs.Follow up test should be taken within 6-12hrs.
 AAP had suggested lVlg (intravenous immuneAAP had suggested lVlg (intravenous immune
globulin) dose ranges from 500-1000mg/Kg.globulin) dose ranges from 500-1000mg/Kg.
Take Home MessageTake Home Message