Neonatal jaundice - 2017

Aug. 1, 2017

More Related Content


Neonatal jaundice - 2017

  1. NEONATAL JAUNDICE Professor Dr. Sayed Ismail Alazhar school of medicine
  2. Objectives • Definition of jaundice • Metabolism of bilirubin • Types of jaundice • Causes of neonatal jaundices • Management of neonatal jaundice
  3. Neonatal hyperbilirubinemia Definition : Jaundice is the yellow color of the skin and sclerae caused by deposits of bilirubin When is visible ? Adult sclera > 2mg / dl Newborn skin > 5 mg / dl
  4. Incidence of neonatal jaundice Term : Occurs in 60% Preterm : 80% of preterm neonates Jaundice is the most common condition that requires medical attention in newborns.
  5. Bilirubin Metabolism
  6. Types of bilirubin Unconjugated bilirubin (Indirect ) Conjugated bilirubin (Direct ) • Bind to albumen • Fat soluble • Can cross blood brain barrier • Toxic in high level to brain • Conjugated with glucoronic acid • Water soluble • Excreted in urine and stool • Not toxic
  7. 1. Increased Bilirubin Load due to a high hemoglobin concentration. • The normal newborn infant • Hemolysis • Cephalhematoma or bruising , Polycythemia 2. Decreased Bilirubin Conjugation in the liver • Decreased uridine glucuronyl transferase Activity • Glucuronyl Transferase Deficiency Type 1 (Crigler Najar Syndrome) 3. Defective Bilirubin Excretion Mechanisms of Neonatal Jaundice
  8. Etiology Of Jaundice
  10. • Appears after 24 hours • Total bilirubin rises by less than 5 mg/dl per day • Maximum intensity by 4th-5th day in term & 7th day in preterm • Serum level less than 15 mg / dl • Clinically not detectable after 14 days Physiological Jaundice • Appears age Appears within 24 hours of age • Increase of bilirubin > 5 mg / dl / day • Serum bilirubin > 15 mg / dl • Jaundice days Jaundice persisting after 14 days • Stool clay / white colored and urine staining yellow staining clothes • Direct bilirubin > 2 mg / dl Pathological jaundice
  11. Physiological Jaundice Characteristics • Appears after 24 hours • Total bilirubin rises by less than 5 mg/dl per day • Maximum intensity by 4th-5th day in term & 7th day in preterm • Serum level less than 15 mg / dl • Clinically not detectable after 14 days
  12. Why does physiological jaundice develop? • Increased bilirubin load • Defective conjugation • Increased entero-hepatic circulation • Incidence – Term in 60% – Preterm 80%
  13. Breast milk jaundice – It is caused by prolonged increased enterohepatic circulation of bilirubin. (β-GD↑) – Bilirubin peaks at 10-15 days of age. – The level of unconjugated bil. is at 10-30 mg/dL – If nursing is interrupted for 24 hours, the bilirubin level falls quickly β glucuronidase present in the breast milk of some mothers) Breast-milk jaundice; is the commonest cause of Prolonged jaundice in term infants
  14. Pathological Jaundice
  15. Pathological jaundice 1. Appears age Appears within 24 hours of age 2. Increase of bilirubin > 5 mg / dl / day 3. Serum bilirubin > 15 mg / dl 4. Jaundice days Jaundice persisting after 14 days 5. Stool clay / white colored and urine staining yellow staining clothes 6. Direct bilirubin > 2 mg / dl
  16. Conjugated Bilirubin Pathological Unconjugated Bilirubin (indirect) Hepatic Post- hepatic Non-hemolyticHemolytic Pathological Jaundice
  17. 1-Unconjugated (Indirect) hyperbilirubinemia 1. Hemolysis • Rh , ABO and other blood group incompatibilities • spherocytosis , elliptocytosis, Alpha thalassemia • Sepsis ,DIC • Hematomas • Polycythemia 2. Non hemolytic • Breast milk jaundice • Crigler-Najjar syndrome, types I and II • Gilbert syndrome Pathological jaundice
  18. – It is an isoimmunity hemolysis associated with – Rh incompatibility or – ABO Hemolytic disease of the newborn
  19. Erythroblastosis Fetalis
  20. Hemolytic disease of the newborn due to ABO incompatibility •Mothers with type O blood may have circulating antibodies of Ig G class to other red cell antigens that can cross the placenta and cause hemolytic disease in a baby with a different blood type, such as blood type A or B. (ABO incompatibility ) •The baby develop jaundice in the 1st day of life
  21. 2-Conjugated hyperbilirubinemia 1. Hepatic • Idiopathic neonatal hepatitis • Infections - TORCH, sepsis • Inborn errors of metabolism • Galactosemia • Tyrosinemia 2. Post hepatic – Biliary atresia, choledochal cyst
  22. Common causes of jaundice • Physiological • Blood group incompatibility • G6PD deficiency • Breast milk jaundice • Cephalhaematoma • Infections
  23. Jaundice accompanying G6PD deficiency: • Patients having G6PD deficiency also have genetic defects in bilirubin conjugation as seen in gilbert's disease. • It is uncommon to have jaundice in G6PD def infant due to severe hemolytic attack. • Those G6PD deficient neonates who develop higher maximal serum total bilirubin values had significantly lower serum conjugated bilirubin fractions.
  24. • Crigler-Najjar syndrome type I - rare • Complete absence of UDPGT and is characterized by severe hyperbilirubinemia with the ongoing risk of kernicterus at any point during an individual's lifespan. • Currently, liver transplantation is the only definitive therapy • Patients with Crigler-Najjar syndrome type II partial absence of UDPGT similar to type I but dramatically respond to therapy with phenobarbital, which is how the diagnosis is made Glucuronyl transferase
  25. Risk factors for jaundice • J - jaundice within first 24 hrs of life or premature • A - a sibling who was jaundiced as neonate • U - unrecognized hemolysis (ABO) • N nursing – non-optimal sucking/nursing • D - deficiency of G6PD , DRUGS , Ceftriaxone, • I - infection • C – Cephalhematoma /bruising • E - East Asian/North Indian
  26. Differential Diagnosis of jaundice ↑production ↓conjugation Impaired excretion Biliary obstruction ↑ Unconjugate ↑ Unconjugate ↑ Conjugated ↑ Conjugated Physiological Hemolysis Hematoma Polycythemia Sepsis Gilbert’s Crigler-Najarr Hypothyroidism Prematurity Rotor’s Dubin Johnson Hepatitis Metabolic Biliary Atresia Hepatitis
  27. Approach to jaundiced baby 1. Determine birth weight, gestation and postnatal age 2. Assess clinical condition (well or ill) ,degree of jaundice 3. Decide whether jaundice is physiological or pathological 4. Look for evidence of kernicterus in deeply jaundiced NB
  28. Clinical assessment of jaundice Area of body Bilirubin levels/dlmg • Face 6 • Upper trunk 9 • Lower trunk & thighs 12 • Arms and lower legs 15 • Palms & soles > 15
  29. High bilirubin level kernicterus (Bilirubin Encephalopathy)
  30. Major Clinical Features of Acute Bilirubin Encephalopathy • Lethargy • poor sucking • poor or absent Moro's, • Retrocollis-opisthotonos Convulsions Retrocollis (backward arching of the neck) Opisthotonus (backward arching of the back
  31. This infant presented at age 30 days with a serum bilirubin level of 30 mg/dL (513 μmol/L) secondary to the Crigler-Najjar syndrome type I. He demonstrates retrocollis and opisthotonos, signs of the intermediate to advanced stage of acute bilirubin encephalopathy.
  32. Major clinical features of chronic bilirubin encephalopathy • Athetosis • Upward gaze • Sensorineural hearing loss • Intellectual deficits, mild MR
  33. Laboratory tests • Total & direct bilirubin* • Blood group and Rh for mother and baby* • Hematocrit, retic count and peripheral smear* • G6PD assay • Coomb’s test • Sepsis screen • Liver and thyroid function • TORCH titers • Liver scan when conjugated hyperbilirubinemia • Ultrasonography of the liver and bile ducts in cholestatsis (must in all)*
  34. Measurement of bilirubin by jaundice meter
  35. Laboratory Diagnosis Laboratory Features Of Hemolytic Disease 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
  36. Reticulocyte count (>7 mg/dL) can indicate the presence of an ongoing hemolytic process in neonates Direct hyperbilirubinemia in the neonate is defined as a direct fraction more than 2 mg/dL • or more than 20%of the total bilirubin concentration is always pathologic.
  37. Liver function tests: • Aspartate aminotransferase (ASAT or SGOT) and alanine aminotransferase (ALAT or SGPT) levels are elevated in hepatocellular disease. • Alkaline phosphatase and γ -glutamyltransferase (GGT) levels are often elevated in cholestatic disease. • A γ -GT/ALAT ratio of more than 1 is strongly suggestive of biliary obstruction. However, it does not distinguish between intrahepatic and extrahepatic cholestasis (do ultrasoud) Reducing substance in urine: is a useful screening test for galactosemia, provided the infant has received sufficient quantities of milk.
  38. Other Tests • Hearing tests (Brainstem auditory-evoked potentials) should be obtained in aftermath of severe neonatal jaundice to exclude sensorineural hearing loss. • MRI in kernicterus
  39. bilateral basal ganglia hyperintensity
  40. Management 1. Phototherapy 2. intravenous immune globulin (IVIG) 3. Exchange transfusion 4. Drugs
  41. Baby under triple unit intense phototherapy Baby under conventional phototherapy Baby under triple unit intense phototherapy
  42. Principle of phototherapy Native bilirubin ( water Insoluble) 450-460nm of light `Photo isomers of bilirubin (water Soluble) Urine
  43. 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 μmol X0.055 = mg/dl
  44. In the left panel, the solid line refers to the current recommendation of the American Academy of Pediatrics (AAP) for low-risk infants, the line consisting of long dashes (- - - - -) for infants at intermediate risk, and the line with short dashes (-----) for infants at high risk. In the right panel, the dotted line (......) represents the AAP suggested intervention level for exchange transfusion in infants considered at low risk, the line consisting of dash-dot-dash (-.-.-.-.) for intermediate risk, and the line consisting of dash-dot-dot-dash (-..-..-..-) for infants at high risk. ( AAP,2004)
  45. Phototherapy Technique • Perform hand wash • Place baby naked in cradle or incubator • Fix eye shades • Keep baby at least 45 cm from lights • Start phototherapy • Frequent extra breast feeding every 2 hourly • Turn baby after each feed • Temperature record 2 to 4 hourly • Weight record- daily • Monitor urine frequency • Monitor bilirubin level
  46. A common mistake while managing hyperbilirubinemia is the false believes in the efficacy of the ordinary florescent lamps (not Day-light), and D5% orally.
  47. Side effects of phototherapy • Increased insensible water loss • Loose stools • Skin rash • Bronze baby syndrome • Hyperthermia • May result in hypocalcemia
  48. Intravenous immune globulin • IVIG in infants with Rh or ABO isoimmunization can significantly reduce the need for exchange transfusions. • Now IVIG has replaced exchange transfusion as the second-line treatment in infants with isoimmune jaundice. • 1 gm/kg/dose IV
  49. Exchange transfusion • Exchange transfusion is indicated for avoiding bilirubin neurotoxicity when other therapeutic modalities have failed or are not sufficient. • the procedure may be indicated in infants with erythroblastosis who present with severe anemia, hydrops, or both, even in the absence of high serum bilirubin
  50. Phenobarbital (Luminal) • Hyperbilirubinemia: 3-8 mg/kg/d PO/IV initially; may increase up to 12 mg/kg/d Not to exceed IV administration rate of 1 mg/kg/min or 30 mg/min for infants
  51. Prolonged indirect jaundice Causes • Breast milk jaundice • Hypothyroidism • Pyloric stenosis • Ongoing hemolysis • Crigler Najjar syndrome
  52. Conjugated hyperbilirubinemia Suspect • High colored urine • White or clay colored stool Caution • Always refer to hospital for investigations so that biliary atresia or metabolic disorders can be diagnosed and managed early
  53. Remember that: • Jaundice is the most frequent cause of admission after early discharge from nursery. • It is not physiological if: appear in first 24 hrs, increases by > 0.5 mg/dL/hr , evidence of hemolysis, abnormal examination, direct bilirubin is > 20% of total, or persists > 3 weeks. • Jaundice present in the first 24 hrs of life must be investigated and treated as an emergency.