Neonatal jaundice is caused by all EXCEPT
(c) Anemia (41-IAP. Text book of pediatrics 5th edition; 603-8-Nelson 19th/ed)In neonates, jaundice tends to develop because of two factors - the breakdown of fetal hemoglobin as it is replaced with adult hemoglobin and the relatively immature hepatic metabolic pathways which are unable to conjugate and so excrete bilirubin as quickly as an adult. This causes an accumulation of bilirubin in the blood (hyperbilirubinemia), leading to the symptoms of jaundice.If the neonatal jaundice does not clear up with simple phototherapy, other causes such as biliary atresia, PFIC, bile duct paucity, Alagille syndrome, alpha 1-antitrypsin deficiency, and other pediatric liver diseases should be considered.Non ConjugatedHemolyticIntrinsic causes of hemolysis* Membrane conditions* Spherocytosis* Hereditary elliptocytosis* Systemic conditions* Sepsis* Arteriovenous malformation* Enzyme conditions* Glucose-6-phosphate dehydrogenase deficiency (also called G6PD deficiency)* Pyruvate kinase deficiency* Globin synthesis defect* sickle cell disease* Alpha-thalassemia, e.g. HbH diseaseExtrinsic causes of hemolysis* Alloimmunity (The neonatal or cord blood gives a positive direct Coombs test and the maternal blood gives a positive indirect Coombs test)* Hemolytic disease of the newborn (ABO)* Rh disease* Hemolytic disease of the newborn (anti-Kell)* Hemolytic disease of the newborn (anti-Rhc)* Other blood type mismatches causing hemolytic disease of the newbornNon-hemolytic causes* Breast milk feeding* Cephalohematoma* Polycythemia* Sepsis* Hypothyroidism* Gilbert's syndrome* Crigler-Najjar syndromeConjugatedHepatic causes* Infections* Sepsis* Hepatitis B* TORCH infections* Metabolic* Galactosemia* Alpha-1 -antitrypsin deficiency* Cystic fibrosis* Dubin-Johnson Syndrome* Rotor syndrome* Drugs* Total parenteral nutrition* IdiopathicPost-hepatic* Biliary atresia or bile duct obstruction* Alagille syndromeNEONATAL JAUNDICE / HYPERBILIRUBINEMIA* Approximately 60% of-term and 80% of preterm babies develop jaundice during the first week of life, usually multifocal* In majority early neonatal jaundice is due to rise in unconjugated (indirect) bilirubin*** Yellow colour usually results from the accumulation of unconjugated, non polar, lipid soluble bilirubin in the skin* Most common cause of neonatal hyper bilirubinemia is physiological jaundice* Conjugated hyperbilirubinemia is always pathological and expert help should be sought early to identy biliary atresia* The neonatal production rate of bilirubin is 6-8 mg 1kg /24 hour (In contrast to 3-4 mg/kg/24hr in adults)Unconjugated hyper bilirubinemia may be caused or increased by any factor1. Increases the load of bilirubin to be metabolized by the liver (Hemolytic anemias, polycythemia, bruising or internal hemorrhage, shortened red blood cell life as a result of immaturity or transfusion of cells, increased enterohepatic circulation, infections)2. Damages or reduces the activity of the transferase enzyme or other related enzymes (Genetic deficiency, hypoxia, infection, thyroid deficiency.3. Competes for or blocks the transferase enzyme(Drugs- oxytocin, phenolic detergents and other substances requiring glucuronic acid conjugation)4. Leads to an absence or decreased amounts of the enzyme or to reduction of bilirubin uptake by liver cells ('Genetic defects and prematurity)* Early and frequent feeding decreases, whereas breast feeding and dehydration increases serum levels of bilirubin* Delay in passage of meconium which contains lmg bilirubin/ dL may contribute to jaundice by enterohepatic reciruculation after deconjugation by intestinal glucuronidase cell* The toxic effects of elevated serum concentration of unconjugated bilirubin are increased by factors that reduce the retension of bilirubin in the circulation (Hypoproteinemia, displacement of bilirubin from its binding sites on albumin by competitive binding of drugs such as sulfisoxazole and moxalactam, acidosis and inceased free fatty acids concentration secondary to hypoglycemia, starvation or hypothermia)* Neurotoxic effects are adversely influenced by - Asphyxia, prematurity, hyperosmolality and infections* Bilirubin toxicity or kernicterus can cause permanent sequalae characterized by Tetrad of* Choreo athetoid cerebral palsy* High frequency central hearing loss* Vertical gaze palsy* Dental enamel hypoplasia
Increased RBC destruction
Hyperbilirubinemia
Anemia
Breast feeding
New Born Infants