Neonatal%20jaundice Signs and Symptoms

• Yellowish discoloration of the skin and sclera in infants <28 days old due to the accumulation of serum bilirubin levels of >85 µmol/L (>5 mg/dl)
• Jaundice typically presents on the 2nd-3rd day of life 

Physiologic Jaundice

• More common in breastfed than in bottlefed neonates
• Occurs in neonates <14 days old
• Caused by an abrupt increase in bilirubin load of the liver after birth

Pathologic Jaundice

• Occurs in neonates >14 days old
• Caused by underlying diseases such as ABO incompatibility, sepsis, liver disease, glucose-6-phosphate dehydrogenase deficiency, metabolic disorders

• Heme catabolism produces bilirubin which is circulated through the liver to be conjugated with glucuronic acid
• Most of the water-soluble conjugated bilirubin is excreted through bile, while a portion is deconjugated and reabsorbed through the enterohepatic circulation
• Newborns have naturally higher bilirubin levels than adults
  • Shorter red blood cell (RBC) lifespan
  • Limited bilirubin conjugation of the newborn liver
• Pathologic jaundice can develop when there is abnormally increased bilirubin
  • Unconjugated hyperbilirubinemia: Bilirubin overproduction, impaired hepatic uptake, deficient conjugation
  • Conjugated hyperbilirubinemia: Cholestasis, hepatic disease
• Severe hyperbilirubinemia causes bilirubin to breach the blood-brain barrier, bind to neural structures, and cause potentially disabling and/or fatal kernicterus
• Kernicterus may develop if the following are present:
  • Signs of acute bilirubin encephalopathy
  • Increasing serum bilirubin of >8.5 μmol/L/hr
  • Gestational age >37 weeks with serum bilirubin of >340 μmol/L 

Possible Causes of Jaundice

Unconjugated Hyperbilirubinemia

• Hemolysis resulting from ABO blood group incompatibility, infection, red blood cell (RBC) membrane defects (eg G6PD deficiency), RBC enzyme defects, hemoglobinopathies
• Physiologic jaundice which results from increased bilirubin production brought about by accelerated destruction of RBCs, decreased excretory capacity secondary to low levels of ligandin in hepatocytes, and low activity of the bilirubin-conjugating enzyme uridine diphosphate glucuronyltransferase (UDPGT)
• Breastfeeding which may give rise to decreased bilirubin clearance
• Polycythemia, bruising, internal hemorrhage, mutations of glucuronyltransferase, infant of mother with diabetes 

Conjugated Hyperbilirubinemia

• Neonatal hepatitis, sepsis, urinary tract infection, inborn errors of metabolism
• Infections caused by toxoplasmosis, rubella, cytomegalovirus, herpes simplex virus, and other agents (TORCH)
• Obstructive: Biliary atresia, choledochal cyst

• Danger signs in a newborn infant with jaundice:
  • Changes in brainstem evoked auditory potentials (eg decreased amplitude, prolonged latencies)
  • Changes in muscle tone
  • Seizures
  • Altered cry characteristics

• The above findings require prompt attention to prevent kernicterus

Risk Factors for Severe Hyperbilirubinemia in Infants

• Jaundice observed in the first 24 hour of life
• Total serum bilirubin (TSB) and transcutaneous bilirubinometry (TcB) in high-risk zone
• Blood group incompatibility
• Cephalohematoma or significant bruising
• Sibling who received phototherapy
• Exclusive breastfeeding
• Gestational age 35-36 week
• East Asian race as defined by mother’s description