Clinical approach to icterus in the cat (Proceedings)

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Clinical approach to icterus in the cat (Proceedings)

May 01, 2011

Icterus is a term used to describe the clinical appearance of hyperbilirubinemia. While reference values may vary, in most instances a serum bilrubin > 1 mg/dl is considered abnormal but clinically detectable icterus usually does not occur until the bilirubin is > 3 mg/dl.

Bilirubin metabolism

Bilirubin is formed from the breakdown of hemoglobin (primary source), myoglobin and other proteins containing porphyrin. The cells of the mononuclear phagocytic system in the spleen, liver and bone marrow phagocytize damaged red blood cells. The red blood cells are broken down and hemoglobin released. Hemoglobin is broken down into heme and globin. Globin is converted to amino acids. Heme is broken down into iron and protoporphyrin. Protoporphyrin is converted to biliverdin and then bilirubin. Bilirubin is released from the phagocytic cells, attached to a transport protein and transferred into the hepatocytes of the liver through a saturable membrane transport system. Once in the hepatocyte, bilirubin binds to the protein ligandin, which prevents efflux back into the bloodstream. This bilirubin is then conjugated and most of it excreted into the bile canaliculi with much less moving into the bloodstream. Some of the bilirubin in the bloodstream remains unbound and passes into the urine but some is protein bound in circulation (biliprotein, delta bilirubin). This is why both conjugated and unconjugated bilirubin can be found in circulation. The conjugated bilirubin in the bile is excreted into the small intestine where bacteria convert it to urobilinogen. Almost all urobilinogen is excreted into the feces as stercobilin with only a small amount reabsorbed that either is taken up by the liver or excreted in the kidneys.

Pathophysiology

Hyperbilirubinemia can result from excessive bilirubin production (pre hepatic), impaired hepatic uptake/conjugation (hepatic) or decreased excretion (post hepatic). Excess bilirubin production is most commonly due to hemolysis but may also occur with extensive internal bleeding and breakdown of damaged red blood cells. With extravascular hemolysis bilirubin production occurs as described above but with intravascular hemolysis hemoglobin is free in circulation then complexes with haptoglobin and is removed by hepatocytes where hemoglobin breakdown occurs.

Hepatocellular dysfunction from decreased functional mass, poor perfusion or defects in uptake or conjugation can also cause hyperbilirubinemia and icterus. This occurs with inflammatory, infiltrative and necrotic diseases of the liver.

Decreased bilirubin excretion results from impaired bile flow outside of the liver. Inflammatory, infectious, neoplastic and obstructive diseases that affect the cystic duct, gall bladder, common bile duct, or duodenum can affect bile flow.