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Management of hiperbilirubic infant final

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  • Bilirubin Physiology: Ligandins responsible for transport from plasma membrane to endoplasmic reticulum.
    Bilirubin conjugated in presence of UDPGT (uridine diphosphate glucuronyl transferase) to mono and diglucoronides, which are then excreted into bile canaliculi.
  • Enterohepatic Circulation: Meconium contains 100-200mg of conjugated bilirubin at birth.
    Conjugated bilirubin is unstable and easily hydrolyzed to unconjugated bilirubin.
    This process occurs non-enzymatically in the duodenum and jejunum and also occurs in the presence of beta-glucuronidase, an enteric mucosal enzyme, which is found in high concentration in newborn infants and in human milk.
    Conjugation: Since conjugated bilirubin crosses the placenta very little, conjugation is not active in the fetus with levels of UDPGT about 1% of adult levels at 30 - 40 weeks gestation
    After birth, the levels of UDPGT rise rapidly but do not reach adult levels until 4-6 weeks of age.
    Ligandins, which are necessary for intracellular transport of bilirubin, are also low at birth and reach adult levels by 3-5 days.
    CONJUGATED VS UNCONJUNCATED HYPERBILI: Conjugated hyperbilirubinemia is always pathologic
    When the total bili is quite high, the conjugated fraction can rise to as high as 20% of the total, although it usually stays under 1.0.
    Always check a total and direct, so that you can be sure you are excluding conjugated hyperbilirubinemia, which has totally different etiologies and treatments.
    Bilirubin conjugation is biologically critical because it transforms a water-insoluble bilirubin molecule into a water-soluble molecule. Water-solubility allows conjugated bilirubin to be excreted into bile. UDPGT activity is low at birth but increases to adult values by age 4-8 weeks. In addition, certain drugs (phenobarbital, dexamethasone, clofibrate) can be administered to increase UDPGT activity.
  • Configurational isomerization is a very rapid process that changes some of the predominant 4Z,15Z bilirubin isomers to water-soluble isomers in which one or both of the intramolecular bonds are opened (E,Z; Z,E; or E,E). In human infants, the 4Z,15E isomer predominates, and, at equilibrium conditions, the isomer constitutes about 20-25% of circulating bilirubin after a few hours of phototherapy. This proportion is not significantly influenced by the intensity of light. Data have shown that formation of photoisomers is significant after as little as 15 minutes of phototherapy.
    Structural isomerization consists of intramolecular cyclization, resulting in the formation of lumirubin. This process is enhanced by increasing the intensity of light. During phototherapy, lumirubin may constitute 2-6% of the total serum bilirubin concentration.
  • Advantage of Fibreoptic lights:
    Low risk of overheating the infant
    No need for eye shields
    Ability to deliver phototherapy with the infant in a bassinet next to the mother's bed
    Simple deployment for home phototherapy
    The possibility of irradiating a large surface area when combined with conventional overhead phototherapy units (double/triple phototherapy)
  • Transcript

    • 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