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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)

Management of hiperbilirubic infant   final Management of hiperbilirubic infant final Presentation Transcript

  • MANAGEMENT OF HYPERBILIRUBIC INFANT
    • WHAT IS HYPERBILIRUBIC INFANT?
    • FORMATION OF BILIRUBIN.
    • CAUSES OF NEONATAL JAUNDICE.
    • BURDEN OF THE DISEASE.
    • CLINICAL MANIFESTATIONS
    • WHY PHOTOTHERAPY.? DO’S AND DON’T’S .
    • TREATMETN & NORWEGIAN GUIDLINE.
    • TAKE HOME MESSAGE.
    We Are Going To Learn…
    • When a new born baby suffers from yellow discoloration of skin and sclera (white part) of eyes it is called as neonatal jaundice or hyperbilirubinemia.
    • It is a result of accumulation of conjugated bilirubin .
    • In most infant, hyperbilirubinemia is a normal transitional phenomenon.
    • But in some infants serum bilirubin levels rise excessively.
    • This unconjugated bilirubin is highly neurotoxic and causes death in infant and lifelong neurologic sequela in infants those who survive.
    What is Neonatal Jaundice?
    • Jaundice is observed during the first week in approximately 60% of term infant and 80% of preterm infant .
    • Hyperbilirubinemia can be toxic, with high levels resulting in an encephalopathy known as kernicterus.
    What is Neonatal Jaundice?
    • 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
    What is Bilirubin?
    • In everybody bilirubin is present in blood.
    • From where does this bilirubin comes from?
    degradation Myoglobin Cytochrome catalase Heme catabolism Bilirubin is the end product of all these three resources and is produced in reticulo-endothelial system Bilirubin Physiology 75% from hemoglobin
  • Heme Biliverdin Heme oxygenase ( Oxidation ) Bilirubin Biliverdin reductase ( Reduction ) Bilirubin Physiology Pathway of Heme - Biliverdin - Bilirubin
    • Increased production in neonate due to larger red cell volume, which produces bilirubin as red cells are broken down and shorter RBC life span, so broken down faster.
    • Heme is catabolized within the reticuloendothelial (RE) system by heme oxygenase to form biliverdin .
    • Biliverdin is metabolized to bilirubin in the presence of biliverdin reductase.
    Bilirubin Physiology
    • Increased bilirubin production,
    • Less effective binding and transportation,
    • Less efficient hepatic conjugation,
    • Enhanced absorption of bilirubin via the enterohepatic circulation.
    Metabolism of Bilirubin
  • Metabolism of Bilirubin
    • Neonatal jaundice can occasionally become more pronounced. Blood group incompatibilities (e.g., Rh, ABO) may increase bilirubin production through increased hemolysis . Historically, Rh isoimmunization was an important cause of severe jaundice .
    • Therefore Rh prophylaxis in Rh-negative women, Rh isoimmunization remains common in developing countries.
    Causes of Neonatal Jaundice
    • Out of 4-millions new born at least 60% of the babies get infected.
    • In these babies serum levels are elevated therefore it is must to measure TSB or TCB if jaundice occurs in baby within 1 st 24 hours of birth.
    • Disease occur pertaining to the weight of the baby .i.e
    • birth weight > OR =2500gms.
    • High chances of disease occurs after 37 complete weeks of gestation.
    Burden of Disease
    • 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 Manifestation
      • Determination of direct and indicrect bilirubin fractions
      • Determination of hemoglobin
      • Reticulocyte count
      • Blood type
      • Coombs’ test
      • Examination of the peripheral blood smear
    Diagnosis
    • Direct-reacting hyperbilirubinemia
      • Hepatitis
      • Cholestasis
      • Inborn errors of
      • metabolism
      • Sepsis
    Classifications - I
    • Direct and Indirect- reacting Hyperbilirubinemia
      • Hepatitis,
      • Sepsis,
      • Liver damage
      • complicated by
      • Hemolysis.
    • Indirect-reacting hyperbilirubinemia
      • Hemolysis:
      • Reticulocytosis,
      • Evidences of red
      • blood cell
      • Destruction,
      • A positive Coomb’s
      • test, Blood group
      • incompatibility,
      • Positive results of
      • specific
      • Examination.
    • Physiologic Jaundice:
      • Clinical jaundice appears at
      • 2-3 days.
      • Total bilirubin rises < 5 mg/dl
      • (86 umol/L) per day.
      • Peak bilirubin occurs at 3-5
      • days of age.
      • Peak bilirubin concentration in
    Classifications – II…cont.
    • Pathologic Jaundice:
      • Clinical jaundice appears in 24
      • hours of age.
      • Total bilirubin rises by higher
      • than 5 mg/dl (86 umol/L) per
      • day.
      • Peak concentration of total
      • bilirubin is more than 12
      • mg/dL in the term infant and
      • 15 mg/ dL in the preterm
      • infant.
    • Physiologic Jaundice:
      • Peak bilirubin concentration in
      • Full-term infant <12mg/dl
      • (205.2 umol/L).
      • Peak bilirubin concentration in
      • Premature infant <15mg/dl
      • (257umol/L).
      • Clinical jaundice is resolved
      • by 2 weeks in the term infant
      • by 3-4 weeks in the Preterm
      • infant.
    Classifications - II
    • Pathologic Jaundice:
      • Clinical jaundice is not
      • resolved in 2 weeks in the term
      • infant and in 4 weeks in the
      • Preterm infant.
      • Clinical jaundice appears again
      • after it has been resolved.
      • Direct bilirubin concentration
      • is more than 1.5 mg/dL
      • (26umol/L).
        • Infective
        • Jaundice:
        • Neonatal hepatitis
        • (TORCH infection),
          • Neonatal sepsis.
    Causes of Pathologic Jaundice Jaundice Associated Without Infection: Hemolytic disease of The newborn (ABO incompatibility, Rh incompatibility, BiliaryAtresia). Jaundice associated With breast- feeding. Breast Milk Jaundice: Caused by prolonged increased enterohepatic circulation of bilirubin. ( β- GD↑) The hyperbilirubinemia peaks at 10-15 days of age. The level of unconjugated hyperbilirubinemia is at 10-30 mg/dL (172-516 umol/L). If nursing is interrupted for 72 hours, the bilirubin level falls quickly.
      • 1. Genetic Disease:
      • Congenital deficiencies of the enzymes:
          • glucose-6-phosphate dehydrogenase (G-6-PD)
        • 2. Thalassemia
        • 3. Cystic fibrosis
      • 4. Drug: Vitamin k
      • Novobiocin
    Causes of Pathologic Jaundice
    • Gestational Age
    • Race
    • Family history of jaundice requiring phototherapy
    • Hemolysis (ABO or other)
    • Severe bruising
    • Breastfeeding
    Time Course of Jaundice Risk Factors for Neonatal 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.
    • 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.
    • Family History
    • A child whose sibling needed phototherapy is 12 times more likely to also have significant jaundice.
    • Frequently peak bilirubin levels correlate between siblings.
    Risk Factors
    • Pathologic
    • G6PD Deficiency
    • Hereditary Spherocytosis
    • Glucuronyl Transferase Deficiency Type 1 (Crigler Najar Syndrome)
    • GT deficiency Type 2 (Arias Syndrome)
    • Polycythemia
    • Hemolysis
    • 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.
  • Breast 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 benign entity, which tends to occur late in the first week or afterwards.
    • It is actually due to something in the breast milk which tends to prolong jaundice.
    • Usually weight gain is good, and the baby is otherwise well.
    • Jaundice might persist as late as 3-4 weeks, but usually will peak by 2 weeks.
    • Textbook treatment is to interrupt breastfeeding (usually do not do this).
  • Assessing the Risk of Jaundice by Numbers Bhutani Curve
    • Maisels’ and Kring’s study showed that not all early higher TSB will continue going up.
    • They divided the rate of rise to be concerned with into
    • 6-24hr >0.22/hr
    • 24-48 >0.15/hr
    • 48+ >0.06/hr
    Assessing the Risk of Jaundice by Numbers
  • Hemolytic Disease of the Newborn
  • Introduction
    • Hemolytic disease of the newborn:
      • It is an isoimmunity hemolysis associated with ABO or Rh incompatibility.
      • It results from transplacental passage of maternal antiboddy active against RBC antigens of the infant, leading to an increased rate of RBC destruction.
      • It is an important cause of anemia and jaundice in newborn infant .
  • Etiology and Pathogenesis
    • ABO hemolytic disease
      • ABO incompatibility
        • Type O mothers
        • Type A or B fetuses
        • Presence of IgG anti-A or Anti-B antibodies in type O mother
        • Frequently occurring during the first pregnancy without prior sensitization
    • Rh hemolytic disease
        • An Rh-negative mother
        • An Rh-positive fetus
        • Leakage of fetal RBC into maternal circulation
        • Maternal sensitization to D antigen on fetal RBC
        • Production and transplacental passage of maternal anti-D antibodies into fetal circulation
        • Attachment of maternal antibodies to Rh-positive fetal RBC
        • Destruction of antibody-coated fetal RBC
    Etiology and Pathogenesis
      • Rh hemolytic disease was rare during the first pregnancy involving an Rh-positive fetus.
      • Once sensitization has occurred, re-exposure to Rh D RBC in subsequent pregnancies leads to an anamnestic response, with an increase in the maternal anti-Rh D antibody titer.
      • The likelihood of an infant being affected increased significantly with each subsequent pregnancy.
    Etiology and Pathogenesis
      • Significant hemolysis occurring in the first pregnancy indicates prior maternal exposure to Rh-positive RBC.
        • Fetal bleeding associated with a previous spontaneous or therapeutic abortion
        • Ectopic pregnancy
        • A variety of different prenatal procedures
        • Transfusion of some other blood product containing Rh D RBC in an Rh-negative mother
    Etiology and Pathogenesis
  • Clinical Manifestations
    • Jaundice
    • Anemia
    • Hydrops
    • Massive enlargement of the liver and spleen
    • Bilirubin encephalopathy (Kernicterus)
  • Clinical Manifestations Clinical Features Rh ABO Frequency Unusual Common Anemia Marked Minimal Jaundice Marked Minimal to moderate Hydrops Common Rare Hepatosplenomegaly Marked Minimal Kernicterus Common Rare
  • Laboratory 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
  • Diagnosis
    • Requires
    • demonstration of
    • blood group
    • incompatibility
    • and of
    • corresponding
    • antibody bound to
    • the infant’s RBC.
    • Antenatal Diagnosis
    • History,
    • Expectant parents’
    • blood types,
    • Maternal titer of IgG
    • antibodies to D or E
    • (>1:32):
    • At 12 ~ 16 wk
    • At 28 ~ 32 wk
    • At 36 wk.
    • Fetal Rh and ABO
    • status,
    • Fetal jaundice level .
    • Postnatal diagnosis
    • Jaundice at < 24 hr.
    • Anemia (Hematocrit
    • and hemoglobin
    • examination).
    • Rh or ABO
    • Incompatibility.
    • Coomb’s test positive.
    • Examination for RBC
    • antibodies in the
    • mother’s serum.
  • Treatment
  • Treatment
    • Main Goals
    • To prevent intrauterine
    • or extrauterine death
    • of fetal or infant form
    • severe anemia and
    • Hypoxic -
    • To avoid neurotoxicity
    • from
    • hyperbilirubinemia
    • Treatment of Unborn Infant
    • Utero transfusion
        • Indication
          • Hydrops
          • Anemia (Hematocrit<30%)
        • Method
          • Packed RBC matching with the mother’s serum
          • Umbilical vein transfusion
      • Delivery in Advance
      • Indication:
      • Pulmonary maturity
      • Fetal distress –
      • Maternal titer of Rh
      • antibodies > 1:32,
      • 35 ~ 37 w.k of gestation
    Treatment
    • Treatment of Liveborn Infant
      • Immediate resuscitation and supportive therapy:
        • Temperature stabilization
        • Correction of acidosis: 1-2mEq/kg of sodium bicarbonate
        • A small transfusion compatible packed RBC
        • Volume expansion for hypotension
        • Provision of assisted ventilation for respiratory failure
      • Phototherapy:
        • Blue spectrum of 427-475 nm (or White or Green)
        • Irradiance:10-12μW/cm2
        • Protection of eyes and genital.
        • Indication:
          • Bilirubin≥10mg/dl at < 12 hr
          • Bilirubin≥12-14mg/dl at < 18 hr
          • Bilirubin≥15mg/dl at ≥24 hr
    Treatment
        • Side effect of Phototherapy:
          • Diarrhea
          • Dehydration
          • Riboflavin destruction
          • Hypocalcemia
          • Bronze-baby syndrome
      • Exchange Transfusion
        • Indication:
          • Hemoglobin < 120g/L
          • Hydrops, hepatosplenomegaly and heart failure
          • Bilirubin in the 1st 12 of life>0.75mg/dl/hr
          • Bilirubin concentration>20mg/dl
          • Factors supporting early exchange transfusion:
          • Previous kernicterus in a sibling, reticulocyte counts greater than 15%, asphyxia of neonate and premature infant
    Treatment
        • Blood volume of exchange transfusion
          • Double-volume exchange transfusion :150-180ml/kg
        • Blood choose of Rh incompatibility
          • Rh in accordance with mother
          • ABO in accordance with neonate
        • Blood choose of ABO incompatibility
          • Plasm of AB type
          • RBC of O type
      • Drug Treatment:
        • Intravenous immune globulin (IVIG)
        • Human albumin
        • Glucocorticoids: Dexamethasone
        • Inducer of liver enzyme: Luminal
    Treatment
    • Intramuscular injection of 300ug of human anti-D globulin to an Rh-negative mother:
      • Within 72 hr of delivery of an ectopic pregnancy
      • Abdominal trauma in pregnancy
      • Amniocentesis
      • Chorionic villus biopsy
      • Abortion
    Prevention
  • Phototherapy
    • Since 1960, Phototherapy has been the mainstay of treating hyperbilirubinemia.
    • It causes structural isomerization, forming lumirubin , which is then excreted in the bile and urine.
    • Since photoisomers are water soluble, they should not be able to cross the blood-brain barrier, so starting phototherapy should decrease the risk of kernicterus by turning 20-25% of bilirubin into a form unable to cross, even before the level has lowered significantly.
    Phototherapy … cont.
  • Phototherapy …cont.
    • Initially, in photo oxidation bilirubin is bleached through the action of light, the process is slow.
    • The photoisomers of bilirubin are excreted in bile and, to some extent, in urine.
    • Phototherapy may reduce the risk of bilirubin-induced neurotoxicity as soon as the lights are turned on. At any given total serum bilirubin concentration, the presence of 20-25% of photoisomers means that only 75-80% of the total bilirubin may be present in a form that can enter the brain.
    • Bilirubin absorbs light best at 450 nm, but longer wavelenths penetrate skin better.
    • Make sure skin is as exposed as possible and that light is not too far from baby.
    • Fiberoptic light (bili blanket) is much less efficacious on its own.
    Phototherapy
  • Copyright ©2004 American Academy of Pediatrics Subcommittee on Hyperbilirubinemia, Pediatrics 2004;114:297-316 Guidelines for phototherapy in hospitalized infants of 35 or more weeks' gestation
    • The 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) provided the infant's temperature is monitored .
    • Efficiency of phototherapy depends on the amount of bilirubin that is irradiated. Irradiating a large skin surface area is more efficient than irradiating a small area, and the efficiency of phototherapy increases with serum bilirubin concentration.
    • The nature and character of the light source may affect energy delivery. Irradiation levels using quartz halide spotlights are maximal at the center of the circle of light and decrease sharply towards the perimeter of the circle. Large infants and infants who can move away from the circle's center may receive less efficient phototherapy.
    Do’s and Don’ts of Phototherapy
    • Narrow spectrum blue fluorescent tube.
    • White fluorescent tubes
    • White quartz lamp.
    • Quartz lamps with single or double banks of 3-4 bulbs attached.
    • Fibreoptic light.
    Lamps Beneficial for Phototherapy
  • Exchange Transfusion
    • Double volume exchange transfusion was a common procedure prior to advent of Rhogam and phototherapy.
    • Now fortunately a rare occurrence
    • Used for bilirubin >25 in a term infant and not decreasing despite phototherapy
  • Neonatal jaundice guidance as suggested by AAP(American Academy of Pediatrics)
    • Promote and support breast-feeding.
    • Establish nursery protocols.
    • Measure TSB or TCB if jaundice occurs in 1 st 24 hours after birth.
    • Visual estimation of jaundice can lead to errors particularly in darkly pigmented infant.
    • Interpret bilirubin levels according to the infant age in hours.
    • Infant <38 weeks if breastfed are at higher risk.
    • Perform risk assessment prior to discharge.
    • Give parents written and oral information.
    • Provide appropriate follow-up bond at the at the time of discharge and risk assessment.
    • Treat new born with, when indicated with phototherapy or exchange transfusion.
  • MANAGING JAUNDICE Take Home Message
    • Consider the risk factors, particularly prematurity and hemolysis.
    • Follow up is key!
    • Consider how well baby is feeding, parents’ ability to return, reliability, etc
    • The higher the number of risk factors, the lower the level at which to intervene
    • Sometimes, you will be surprised. We can’t always prevent hyperbilirubinemia , but we should always prevent kernicterus .
    • Infant should be naked with eyes covered to reduce risk of retina damage.
    • The distance between infant and fluorescent light should be 50cm (20”inches).
    • Hang white curtains around the phototherapy unit and bassinet.
    • If spotlight is used infant should be placed at the centre of spotlight.
    Take Home Message
    • Temp. and homeostasis of infant should be maintained by feeding the infant orally.
    • Monitoring the levels of bilirubin value every hour till they drop down from 7500 micromol/lit (30mg/dL) to 85micromol/lit/h (5mg/dL/h}
    • Phototherapy is discontinued when serum bilirubin falls 25-50micromol/lit (1.5-3mg/dL)
    • Follow up test should be taken within 6-12hrs.
    • AAP had suggested lVlg (intravenous immune globulin) dose ranges from 500-1000mg/Kg.
    Take Home Message
  •  
  •  
  •