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Neonatal jaundice

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introduction, physiology, pathology, causes, clinical features, predisposing factors of neonatal jaundice.

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NEONATAL JAUNDICE
Physiological jaundice occurs in nearly two- thirds of newborns, with excellent out come. However, serum bilirubin levels can exceed physiological limits, leads to brain damage. The normal term newborn produces about 6- 10mg/kg/day of bilirubin. In adults 3 to 4 mg/kg/day of bilirubin is produced. INTRODUCTION:
Where does bilirubin come from? 34mg bilirubin being produced from 1gm of Hb3
Higher erythrocyte mass. Shorter RBC lifespan. Increased turnover of nonhaemoglobin heme proteins. Increased Bilirubin Production Defective uptake. Defective conjugation. Reduced Hepatic Metabolism High levels of intestinal beta- glucuronidase. Paucity of intestinal bacteria. Dec. gut motility. Increased Enteroheptic Circulation PHYSIOLOGICALMECHANISMSOF NEONATAL JAUNDICE
CLINICALASSESSMENTOF JAUNDICE In newborns, the jaundice is detected by blanching the skin with fingers, revealing the yellow staining of skin and subcutaneous tissues. Jaundice is seen first in the face at serum bilirubin levels of 5 to 6 mg/dl & then progresses in a cephalo-caudal manner to the trunk and extremities It is difficult to detect jaundice in eyes of a newborn as unlike adults, neonates keep their eyes shut because of physiological photophobia.
Kramer described the approximate serum bilirubin level with the level of skin discoloration. Once palms and soles are distinctly yellow stained, serum bilirubin exceeds 15 mg/dl. After phototherapy is started, skin gets bleached and it becomes difficult to assess jaundice clinically.
This device measures the intensity of yellow staining of skin and subcutaneous tissues. The value is displayed as either transcutaneous bilirubin index or a bilirubin levels. It is a good screening method. TRANSCUTANEOUS BILIRUBINOMETRY:
PHYSIOLOGICALJAUNDICE It appears on second or third day of life, rises at a rate less than 5 mg/dl/day Peaks at 4 or 5 days of age; spontaneously disappears by day 10-14 days of life. It is always indirect reacting hyperbilirubinemia & serum bilirubin levels do not exceed 15 mg/dl. Term infants with physiological jaundice do not require any treatment and outcome is excellent.
PATHOLOGICALJAUNDICE Jaundice appears on day 1 of age. Persists beyond 2 weeks. Rise in serum bilirubin level is more than 0.5 mg/dl/hour. Conjugated serum bilirubin is >2 mg/dl or >20% of total bilirubin. Associated with signs of illness ++ Suspect if.
CAUSESOF JAUNDICE Jaundice appearing within 24hrs of age Hemolytic diseases of newborn. Intrauterine infections. G-6PD deficiency. Hereditary spherocytosis. Crigler-Najjar syndrome. Alpha-thalassemia. Jaundice appearing b/w 24 & 72hrs of age Physiological. Septicemia. Polycythemia. Concealed hemorrhages Jaundice appearing after 72hrs Septicemia. Idiopathic jaundice. Hypothyroidism. Metabolic disorders.
BREASTMILK JAUNDICE: Breastmilk jaundice is a misnomer since no factor in breastmilk has consistently been shown to be causative of jaundice in neonates and this terminology should be better avoided. o Diagnosis: It is suspected in breastfed neonates whose physiological jaundice fails to decline after first week of birth And persists beyond two weeks of birth.
o MANAGEMENT OF BREASTMILK JAUNDICE: Phototherapy is indicated, if serum bilirubin exceeds 20 mg/dl. Exchange transfusions, if serum bilirubin reaches 25-30 mg/dl. Temporary interruption of breastfeeding may be followed by fall in serum bilirubin values. However, in majority of cases the jaundice can be managed without need of stopping breastfeeding.
Severe Unconjugated hyperbilirubinemia can result in neuronal damage. Acute bilirubin encephalopathy refers to clinical manifestations of bilirubin toxicity. The term Kernicterus is reserved for chronic & permanent sequelae of bilirubin toxicity. This condition is characterized by - Yellow staining of basal ganglia & brain stem nuclei. - Involves diffuse neuronal damage. BILIRUBINENCEPHALOPATHY
Risk of bilirubin toxicity depend on : Serum bilirubin levels, Gestational age, Underlying cause of jaundice, Other co- morbid conditions Factors predisposi ng to bilirubin toxicity include : Acidosis, Birth asphyxia, Pyogenic meningitis, Intracranial hemorrhage, Drugs displacing bilirubin from albumin. PREDISPOSINGFACTORS:
What is the highest bilirubin value that is safe? In term neonates with hemolytic disease, kernicterus rarely occurs with bilirubin levels lower than 20 mg/dl. In case of non-hemolytic jaundice, serum bilirubin levels up to 25 mg/dl are generally safe. However in premature babies, brain damage may occur at lower bilirubin levels, so called LOW BILIRUBIN KERNICTRUS.
Early phase(1-2 days): Poor sucking, Hypotonia, lethargy., High pitched cry, Loss of Moro reflex Intermediate phase(3-7 days): Hypertonia. Opisthotonus, Retrocollis, bulging of anterior fontanel, Fever, seizures Advanced phase(>1 week): Pronounced opisthotonus, Apnea, seizures, coma, death. Chronic phase(1st year): Hypotonia, brisk tendon reflexes. After 1st year: Choreoathetosis, tremors, dental dysplasia, mental retardation CLINICALFEATURES:
Review maternal & perinatal history: Age of onset of jaundice, Color of urine and feces, Maternal illness during pregnancy, Delay in meconium passage, Difficulty in breast feeding Physical examination: Excessive weight loss, Signs of dehydration, Pallor hemolysis, TORCH infections, Prematurity, Sepsis, Hepatosplenomegaly, Laboratory tests: Total serum bilirubin, Blood group & Rh of mother & baby, Direct coombs test, Hematocrit, Sepsis screen, Thyroid profile, TORCH titres WORKUPFORPATHOLOGICALJAUNDICE
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Neonatal jaundice

  • 2. Physiological jaundice occurs in nearly two- thirds of newborns, with excellent out come. However, serum bilirubin levels can exceed physiological limits, leads to brain damage. The normal term newborn produces about 6- 10mg/kg/day of bilirubin. In adults 3 to 4 mg/kg/day of bilirubin is produced. INTRODUCTION:
  • 3. Where does bilirubin come from? 34mg bilirubin being produced from 1gm of Hb3
  • 4. Higher erythrocyte mass. Shorter RBC lifespan. Increased turnover of nonhaemoglobin heme proteins. Increased Bilirubin Production Defective uptake. Defective conjugation. Reduced Hepatic Metabolism High levels of intestinal beta- glucuronidase. Paucity of intestinal bacteria. Dec. gut motility. Increased Enteroheptic Circulation PHYSIOLOGICALMECHANISMSOF NEONATAL JAUNDICE
  • 5. CLINICALASSESSMENTOF JAUNDICE In newborns, the jaundice is detected by blanching the skin with fingers, revealing the yellow staining of skin and subcutaneous tissues. Jaundice is seen first in the face at serum bilirubin levels of 5 to 6 mg/dl & then progresses in a cephalo-caudal manner to the trunk and extremities It is difficult to detect jaundice in eyes of a newborn as unlike adults, neonates keep their eyes shut because of physiological photophobia.
  • 6. Kramer described the approximate serum bilirubin level with the level of skin discoloration. Once palms and soles are distinctly yellow stained, serum bilirubin exceeds 15 mg/dl. After phototherapy is started, skin gets bleached and it becomes difficult to assess jaundice clinically.
  • 7. This device measures the intensity of yellow staining of skin and subcutaneous tissues. The value is displayed as either transcutaneous bilirubin index or a bilirubin levels. It is a good screening method. TRANSCUTANEOUS BILIRUBINOMETRY:
  • 8. PHYSIOLOGICALJAUNDICE It appears on second or third day of life, rises at a rate less than 5 mg/dl/day Peaks at 4 or 5 days of age; spontaneously disappears by day 10-14 days of life. It is always indirect reacting hyperbilirubinemia & serum bilirubin levels do not exceed 15 mg/dl. Term infants with physiological jaundice do not require any treatment and outcome is excellent.
  • 9. PATHOLOGICALJAUNDICE Jaundice appears on day 1 of age. Persists beyond 2 weeks. Rise in serum bilirubin level is more than 0.5 mg/dl/hour. Conjugated serum bilirubin is >2 mg/dl or >20% of total bilirubin. Associated with signs of illness ++ Suspect if.
  • 10. CAUSESOF JAUNDICE Jaundice appearing within 24hrs of age Hemolytic diseases of newborn. Intrauterine infections. G-6PD deficiency. Hereditary spherocytosis. Crigler-Najjar syndrome. Alpha-thalassemia. Jaundice appearing b/w 24 & 72hrs of age Physiological. Septicemia. Polycythemia. Concealed hemorrhages Jaundice appearing after 72hrs Septicemia. Idiopathic jaundice. Hypothyroidism. Metabolic disorders.
  • 11. BREASTMILK JAUNDICE: Breastmilk jaundice is a misnomer since no factor in breastmilk has consistently been shown to be causative of jaundice in neonates and this terminology should be better avoided. o Diagnosis: It is suspected in breastfed neonates whose physiological jaundice fails to decline after first week of birth And persists beyond two weeks of birth.
  • 12. o MANAGEMENT OF BREASTMILK JAUNDICE: Phototherapy is indicated, if serum bilirubin exceeds 20 mg/dl. Exchange transfusions, if serum bilirubin reaches 25-30 mg/dl. Temporary interruption of breastfeeding may be followed by fall in serum bilirubin values. However, in majority of cases the jaundice can be managed without need of stopping breastfeeding.
  • 13. Severe Unconjugated hyperbilirubinemia can result in neuronal damage. Acute bilirubin encephalopathy refers to clinical manifestations of bilirubin toxicity. The term Kernicterus is reserved for chronic & permanent sequelae of bilirubin toxicity. This condition is characterized by - Yellow staining of basal ganglia & brain stem nuclei. - Involves diffuse neuronal damage. BILIRUBINENCEPHALOPATHY
  • 14. Risk of bilirubin toxicity depend on : Serum bilirubin levels, Gestational age, Underlying cause of jaundice, Other co- morbid conditions Factors predisposi ng to bilirubin toxicity include : Acidosis, Birth asphyxia, Pyogenic meningitis, Intracranial hemorrhage, Drugs displacing bilirubin from albumin. PREDISPOSINGFACTORS:
  • 15. What is the highest bilirubin value that is safe? In term neonates with hemolytic disease, kernicterus rarely occurs with bilirubin levels lower than 20 mg/dl. In case of non-hemolytic jaundice, serum bilirubin levels up to 25 mg/dl are generally safe. However in premature babies, brain damage may occur at lower bilirubin levels, so called LOW BILIRUBIN KERNICTRUS.
  • 16. Early phase(1-2 days): Poor sucking, Hypotonia, lethargy., High pitched cry, Loss of Moro reflex Intermediate phase(3-7 days): Hypertonia. Opisthotonus, Retrocollis, bulging of anterior fontanel, Fever, seizures Advanced phase(>1 week): Pronounced opisthotonus, Apnea, seizures, coma, death. Chronic phase(1st year): Hypotonia, brisk tendon reflexes. After 1st year: Choreoathetosis, tremors, dental dysplasia, mental retardation CLINICALFEATURES:
  • 17. Review maternal & perinatal history: Age of onset of jaundice, Color of urine and feces, Maternal illness during pregnancy, Delay in meconium passage, Difficulty in breast feeding Physical examination: Excessive weight loss, Signs of dehydration, Pallor hemolysis, TORCH infections, Prematurity, Sepsis, Hepatosplenomegaly, Laboratory tests: Total serum bilirubin, Blood group & Rh of mother & baby, Direct coombs test, Hematocrit, Sepsis screen, Thyroid profile, TORCH titres WORKUPFORPATHOLOGICALJAUNDICE