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Approach to a child with jaundice
 

Approach to a child with jaundice

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Neonatal Jaundice

Neonatal Jaundice
Pediatrics
Phototherapy

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    Approach to a child with jaundice Approach to a child with jaundice Presentation Transcript

    • APPROACH TO A CHILD WITH JAUNDICE APPROACH TO A CHILD WITH JAUNDICE S.BALASANKAR S.BALASANKAR 2009 MBBS 2009 MBBS
    • JAUNDICE Jaundice is the visible manifestation of increased level of bilirubin in the body.  It is not a disease rather a symptom of diseases. In adults sclera appears jaundiced when serum bilirubin exceeds 2 mg/dl. However it is difficult to see sclera in newborn due to difficulty in opening eye. But in new born it is very easy to see
    • BURDEN Important problem in the 1st week of life. Almost all neonates (60% Term and 80% Preterm) will have bilirubin > 5 mg/dl in the 1st week of life and become visibly jaundiced, vast majority being benign Some of the term babies (8 to 9%) have levels exceeding 15 mg/dl in 1st 7 days of life. High bilirubin level is toxic to the developing CNS.(KERNICTERUS; Bilirubin≥25mg/dl)
    • BILIRUBIN End product of hemoglobin metabolism that is excreted in bile. In neonates -75% : from catabolism of circulating RBCs -25% :*from ineffective erythropoiesis (bone marrow) *from turnover of heme proteins &
    • Hyperbilirubinemia -Direct( Conjugated) -Indirect( Un-conjugated) Conjugated Hyperbilirubinemia is present, * >20% of total bilirubin is conjugated * >2mg/dl is conjugated If neither criteria is met, hyperbilirubinemia is classified as Un-conjugated.
    • NEONATAL JAUNDICE
    • Jaundice after 1 week: a) Prolonged direct Jaundice › Neonatal hepatitis (common) › Extra-hepatic biliary atresia › Breast milk jaundice › Metabolic disorders › Intra-hepatic biliary atresia › Amino acid toxicity › Inspissated bile syndrome (uncommon)
    • b) Prolonged Indirect Jaundice > Criggler Najjar Syndrome > Breast milk jaundice > Hypothyroidism > Pyloric stenosis > Ongoing hemolysis, malaria
    • CLINICAL CLASSIFICATION: PHYSIOLOGICAL JAUNDICE PATHOLOGICAL JAUNDICE
    • PHYSIOLOGICAL JAUNDICE: • In new born babies bilirubin metabolism is immature which results in the occurrence of hyperbilirubinemia in the first few days of life. Also there is increased bilirubin load on the hepatic cell due to physiological polycythemia.
    • Immaturity could be at various steps of bilirubin metabolism like:  Defective uptake from plasma into liver cell( deficiency of LIGANDIN)  Defective conjugation( UDP-glucoronosyl transferase: <1% of adult activity during the first 10 days of life)  Decreased excretion  Increased entero-hepatic circulation
    • Increased Bilirubin production: Larger circulating red blood cell volume Shortened RBC lifespan (70-90 days vs 120 days in adult) Substantial production from other sources
    • Characteristics:  First appears between hours of age  Maximum intensity seen on 4-5th day in term and 7th day in preterm neonates  Does not exceed 15 mg/dl  Clinically undetectable after 14 days.  No treatment is required but baby should be observed closely for signs of worsening jaundice.
    • PATHOLOGICAL JAUNDICE Presence of any of the following signs denotes that the jaundice is pathological.  Clinical jaundice detected before 24 hours of age  Rise in serum total bilirubin by more than 5 mg/dl/ day (>5mg/dl on first day , 10 mg/dl on second day and 12- 13 mg/dl thereafter in term babies)
    •  Serum bilirubin more than 15 mg/dl  Clinical jaundice persisting beyond 14 days of life  Clay/white colored stool and/or dark urine staining the nappy yellow  Direct bilirubin >2 mg/dl at any time. Treatment is required in the form of phototherapy or exchange blood transfusion. One should investigate to find the cause of pathological jaundice.
    • It can be Overproduction Hyperbilirubinemia Under-secretion Hyperbilirubinemia
    • Overproduction Hyperbilirubinemia: Blood group incompatibilities Maternal-fetal or feto-fetal transfusions Non Immune Hemolytic anemias Structurally Abnormal Red cells Extra-vascular Hemolysis
    • Blood Group Incompatibilities: Rh negative mother & Rh positive infant ABO incompatibilities Strongly considered if there is jaundice in the first 24 hours of life
    • Non-Immune Hemolytic Anemias: 1. G6PD Deficiency: Deficiency-decreased NADPHdecreased reduced Glutathione – decreased protection of RBCs from oxidants-hemolysis. 2. Excess of Vitamin K given IM
    • Structurally Abnormal RBCs: Spherocytosis Pyknocytes ( irregular borders)
    • Under-secretion Hyperbilirubinemia: Enzymatic Deficiency( Glucoronyl transferase) Hormonal suppression (Breast milk jaundice) Inhibition of conjugation Hepatic cell injury due to Infections Substrate deficiency (hypoglycemia) Mechanical obstruction (biliary atresia)
    • Hormonal Suppression: Pregnandiol present in maternal breast milk suppresses bilirubin conjugation. Breast feeding may be stopped and restarted in a period of 48hours.
    • Thyroxine Deficiency: Thyroxine increases the activity of Glucoronyl transferase which promotes conjugation of bilirubin.
    • Inhibition of Conjugation: Sulfonamides and Vitamin K results in competitive conjugation inhibition of bilirubin. GALACTOSEMIA: Absent or deficient Galactose 1phosphoate uridyl transferase which is needed in glucoronidaton of indirect bilirubin.
    • APPROACH
    • HISTORY Maternal and Perinatal History: Delivery at period of gestation, Postnatal age in hours. Maternal illness during pregnancy which also includes diabetes; drug use. Previous history of malaria. Traumatic delivery, delayed cord clamping, oxytocin use. Birth asphyxia, delayed feeding, delay in meconium passage.
    • Family history of jaundice, liver disease Previous sibling with jaundice for blood group incompatibility. Kernicterus: Lethargy, poor feeding, and hypotonia. Some advanced signs are seizures, retrocollis, paralysis of upward gaze and shrill cry. Breast feeding.
    • ON EXAMINATION: Baby lethargic, poor feeding, temperature instability, with apnea: Sepsis Small for gestation: polycythemia Cataract, rash: TORCH infections Extra vascular bleed: Cephalhematoma Pallor: hemolysis, blood loss
    • Petechiae: sepsis, TORCH infections. Hepatosplenomegaly: Rh-isoimmunization, sepsis, TORCH infections. Dysmorphic features, congenital heart disease (pulmonary stenosis), Intra-hepatic biliary atresia :Alagille syndrome
    • HOW DO YOU LOOK FOR ICTERUS? 1. Dermal staining :progresses from head to toe Examined in good day light skin of forehead, chest, abdomen, thigh, legs, palms, and soles. Blanched with digital pressure and the underlying color of the skin and subcutaneous tissue should be noted.
    • Clinical Jaundice Measure Bilirubin > 12 mg/dl and infant < 24 hr old < 12 mg/dl and infant > 24 hr old Fraction of Bilirubin Follow bilirubin level Indirect Direct
    • Direct bilirubin Evaluate for treatable causes 1.Infections-blood, urine culture, VDRL. 2.Metabolic disorders-urine reducing substances, serum amino acids,T4,TSH. If no abnormality ;screen for Identifiable causes *α-1 antitrypsin deficiency *cystic fibrosis *congenital viral infections If no abnormality; evaluate for anatomical abnormalities *Stool color *USG *Hepato-biliary scintigraphy *Liver biopsy
    • Indirect Hematocrit High(>65%) Polycythemia Low/Normal Reticulocyte count Blood Type Coomb’s test Platelets Evaluate smear
    • Normal Reticulocyte count Look for evidence of, *Infections-blood, urine culture *Enclosed hemorrhage *Congestive cardiac failure *Hypoxia *Hypothyroidism *Drugs/toxins None found Familial Disorders *Criggler Najjar *Gilbert Elevated Reticulocyte Count Consider: 1.Iso-immunization 2.Erythrocyte membrane defect 3.Erythrocyte enzyme defect
    • MANAGEMENT
    • PHYSIOLOGICAL JAUNDICE Explain about benign nature of the disease Encourage to breastfeed frequently & exclusively Ask Mother to bring baby back if baby looks deep yellow or palms & soles have yellow staining.
    • PATHOLOGICAL JAUNDICE Mainly 2 modalities of Treatment: PHOTOTHERAPY EXCHANGE TRANSFUSION
    • PHOTOTHERAPY Mainstay of treatment Under blue-green light(460490nm), insoluble bilirubin is converted into soluble isomers that can be excreted in urine & feces. To be effective, bilirubin must be present in skin; hence nor role for prophylactic phototherapy
    • Term & near term neonates: The American Academy of Pediatrics (AAP) has laid down criteria for managing babies with elevated serum bilirubin based on gestational age and other risk factors( hemolysis , asphyxia, low albumin level, hypothermia)
    • MECHANISMS: CONFIGURATIONAL ISOMERIZATION STRUCTURAL ISOMERIZATION PHOTO OXIDATION
    • Configurational Isomerization Z-isomer converted to E-isomer Reaction is instantaneous but reversible. After exposure of 8-12 hrs, this constitutes about 25% of the TSB which is non-toxic. Excreted slowly from the body; hence not a major mechanism for decrease in TSB.
    • Structural Isomerization Irreversible reaction Bilirubin is converted into Lumirubin. This product forms 2-6% of TSB which is rapidly excreted from body thus is mainly responsible for phototherapy induced decline in TSB.
    • Photo oxidation Minor reaction
    • Administering Phototherapy: Optimum ambient room temperature( 2528celcius) to prevent hypothermia. Remove all clothes of baby except diaper Cover baby’s eyes with an eye patch(to prevent retinal degeneration) ensuring that it does not block the baby’s nostrils. Place the baby under the lights in a cot if weight is more than 2kg or in an incubator if baby is small(<2kg)
    • Keep the distance between the baby & the light 30-45cm. Ensure optimum breastfeeding as intermittent feeding sessions. Monitor temperature of the baby every 24hrs Measure TSB every 12-24hrs. Discontinue, once 2 TSB values 12hr apart fall below current age-specific cut-offs. Monitor for rebound bilirubin rise within 24hrs.
    • Complications of Phototherapy: Loose stools Erythematous macular rash Purpuric rash associated with transient porphyrinemia Over-heating Dehydration Bronze baby syndrome
    • Bronze Baby Syndrome Intense grey-brown discoloration of the skin, serum, and urine, especially in premature infants; when phototherapy was used to reduce hyperbilirubinemia. Preexisting hepatic disease is suspected as a cause of the jaundice and may have prevented the biliary excretion of the photo oxidation products of bilirubin; their retention resulted in the bronze discoloration.
    • EXCHANGE TRANSFUSION Double Volume Exchange Transfusion (DVET) : 160-180ml/kg; is to be performed if TSB levels reach age-specific cut-offs or if the infant shows signs of bilirubin encephalopathy, irrespective of TSB levels. If baby shows signs of cardiac decompensation at birth, partial exchange transfusion with 50ml/kg of packed red cells should be done to quickly restore oxygen carrying capacity of blood. Umbilical venous route.
    • FOLLOWUP Babies with serum bilirubin>20 mg/dl & those who required ET should be kept under follow-up in high-risk clinic for neurodevelopmental outcome. Hearing assessment should be done at 3months of age.
    • PREVENTION Ante-natal screening to detect Rh isoimmunization & prompt administration of Anti D after first obstetric event. Ensure adequate breast feeding. Educate parent about danger signs to ensure immediate checkup. Follow-up high risk babies( large cephalohematoma, family history of jaundice) for 2-3 days of discharge.
    • JAUNDICE IN THE CHILD & ADOLESCENT HISTORY: Age at onset of symptoms. E.g.: Wilson’s disease commonly manifests in preadolescents & adolescents. Past/present use of any drugs H/o of blood transfusion/ dialysis Exposure to viral hepatitis Any h/o of chronic illness; hemoglobinopathies.
    • DDs of Un-conjugated Hyperbilirubinemia: Auto-immune hemolytic anemias Drug induced hemolytic anemias Erythrocyte membrane defects Erythrocyte enzyme defects Hemoglobinopathies Congestive cardiac failure Sepsis Gilbert syndrome.
    • DDs of Conjugated Hyperbilirubinemia: 1.     2.      Obstructive Gall stones Primary sclerosing cholangitis Choledochal cyst Tumors Infections Hepatitis A, B, C, D, E EBV,CMV Varicella zoster HIV Leptospirosis
    • THANK YOU