Jaundice Overview and Management

Study Notes

Jaundice is characterized by yellowish discoloration of the skin, sclera, and mucous membranes due to hyperbilirubinemia, indicated by total plasma bilirubin levels greater than 2mg/dL (34 µmol/L).
Bilirubin, a greenish-yellow pigment, results from the breakdown of aged erythrocytes by the reticulo-endothelial system.

Bilirubin is excreted in bile, urine, and feces as the end product of heme degradation.
The RES comprises specialized cells, mainly macrophages, responsible for phagocytosis and immune defenses, as well as removal of old or damaged cells and iron recycling.
Different cell types in the RES include:
- Macrophages: Found throughout various tissues.
- Kupffer cells: Liver-specific macrophages.
- Microglia: Brain-specific macrophages.
- Dendritic cells: Important for immune response.

Hyperbilirubinemia: Elevated bilirubin levels above normal (1-2mg/dL) but not always leading to jaundice.
Icterus: Yellowing specifically of the sclera due to hyperbilirubinemia, can be observed before jaundice.
Cholestasis: Impaired bile outflow that leads to increase in bilirubin and other bile contents in the bloodstream.

Pre-hepatic Jaundice: Unconjugated hyperbilirubinemia caused by excess hemolysis; associated conditions include physiological jaundice in newborns, hemolytic diseases, and various red blood cell disorders.
Hepatic Jaundice: Characterized by both conjugated and unconjugated bilirubin in blood, often due to liver cell damage (e.g., viral hepatitis, cirrhosis).
Post-hepatic Jaundice: Resulting from bile flow obstruction in the biliary tract, leading to conjugated bilirubin returning to the bloodstream.

Pre-hepatic causes: Excess hemolysis, hemolytic diseases of newborns, and structural abnormalities in RBCs.
Hepatic causes: Viral hepatitis, alcohol damage, drug-induced liver injury, and inherited syndromes (e.g., Dubin-Johnson).
Post-hepatic causes: Biliary obstruction due to gallstones or tumors.

Adult treatment focuses on underlying causes: anemia treated with iron, hepatitis with antivirals or steroids, and biliary obstruction through surgical intervention.
Infant treatment involves phototherapy, where skin exposure to light transforms bilirubin into water-soluble lumirubin, aiding excretion. Severe cases may require exchange transfusion.

Breastfeeding in neonates helps process bilirubin by promoting stool passage and providing energy for liver function.

Pre-hepatic jaundice results in darker stool and absence of unconjugated bilirubin in urine.
Hepatic jaundice presents with pale clay-colored stools and dark brown urine.
Post-hepatic jaundice features dark brown urine with absent urobilinogen and clay-colored stools.

Kernicterus refers to bilirubin-induced brain damage occurring when bilirubin levels exceed 25mg/dL, leading to lasting neurological impairments.
Unconjugated hyperbilirubinemia can result from genetic disorders, such as Gilbert Syndrome and Crigler-Najjar Syndrome, affecting bilirubin conjugation.

Understand how bilirubin is formed and the functions of the RES.
Be aware of the classification, causes, and treatment of jaundice in both adults and infants.
Emphasize prevention, particularly breastfeeding for newborns.