notes on neonatal jaundice

NEONATAL JAUNDICE

 Characterized by elevated levels of bilirubin in the blood
 It may be physiological or pathological
Bilirubin metabolism
Red blood cells lysed release Hbg. Heme
Physiological Jaundice molecules converted to bilirubin.
 Occurs between days 3-5, clinically benign Unconjugated bilirubin bound to serum
 Occurs in 50% of neonates in the first week of life albumin and transferred to liver where
 Results from increased bilirubin production due it is conjugated to glucuronate by
glucuronyl transferase. Conj. Bilirubin is
to degradation of HbF (fetal haemoglobin) excreted into bile. A fraction of bilirubin
 Relative deficiency in glucuronyl transferase in is reabsorbed into blood via portal
immature liver circulation.
Pathological
 Jaundice in the first day of life is always pathological
 Can be direct or indirect
 Indirect (unconjugated bilirubin) causes
o Increased RBC lysis (↑ production Hbg)
 Blood group incompatibility
 Infection (sepsis, TORCH, UTI)
 Sequestered blood (cephalohaematoma, bruising)
 RBC enzyme defect
 RBC structural abnormality
o Decreased hepatic uptake and conjugation of bilirubin
 Immature glucuronyl transferase
 Gilbert syndrome
 Pyloric stenosis
 Hypothyroidism
 Infants of diabetic mother
 Breastmilk jaundice
o Increased enterohepatic reabsorption
 Breast feeding jaundice
 Due to dehydration from inadequate milk supply
 Bowel obstruction
 Direct (conjugated)
o Hepatocellular diseases
 Hepatitis
 TPN
 Metabolic
 Alpha-1 antitrypsin
 CF
o Biliary tree abnormalities
 Extrahepatic biliary atresia

Clinical features
 Physiological
o Asymptomatic except for transient icterus