Jaundice in cats

© Foster, D (2007) Post-graduate Foundation in Veterinary Science Seminar: Feline Medicine and Surgery, Adelaide, Australia

Bilirubin is the major biliary pigment and is derived from the breakdown of haemoglobin. Consequently, jaundice may result from increased breakdown of red blood cells (prehepatic jaundice), dysfunction of hepatic biliary metabolism (hepatic jaundice) or reduced excretion of bile from the liver into the gastrointestinal tract (post-hepatic jaundice). Prehepatic jaundice is easily diagnosed by documenting marked anaemia coincident with hyperbilirubinemia. Obviously, prehepatic jaundice requires investigation as to the cause of the anaemia. 

Bilirubin is formed in cells of the mononuclear phagocytic system and is unconjugated. It is released into the circulation and bound to albumin, limiting its glomerular filtration. The liver removes bilirubin from the plasma and is stored within hepatocytes until conjugated with glucuronic acid and is released back into circulation. The kidney has a high threshold for conjugated bilirubin in cats (9 times that of dogs) and hence bilirubinuria always occurs with hyperbilirubinemia in this species. Conjugated bilirubin is then excreted into the bile by an energy-dependant saturable process - a number of diseases can interfere with this process directly, including septicaemia and pancreatitis. Once in the intestinal tract, bilirubin is deconjugated and excreted into the faeces. Assays differentiating conjugated from unconjugated bilirubin are inaccurate and many hepatopathies result in elevations in both, therefore differentiation is of little clinical use.

Liver enzyme analysis

Classically, liver enzymes are grouped into leakage enzymes (ALT, AST) and induced enzymes (ALP, GGT). ALT (alanine aminotransferase) is not liver specific but its half-life is short in the cat, meaning it is quite a sensitive, but not specific, indicator of liver dysfunction. Small elevations are considered significant in cats. ALP and GGT are closely associated with bile canaliculi and enzyme elevations are caused by biliary stasis. Again, these enzymes are not specific to the liver, but their half life is short in cats and hence even small elevations in ALP in cats should not be ignored. Cats do not have a steroid induced iso-enzyme of ALP.

Bile acids

Bile acids are organic ions synthesised in the liver from cholesterol. They are excreted into the bile and are useful for increasing the miscibility of fat and enhance absorption into the blood stream. Their lipophilic nature renders them cytotoxic - and retention in the liver leads to hepatocellular damage. They undergo an extremely efficient enterohepatic circulation. They therefore provide useful information on liver function as opposed to damage or disease. Pre- and post-prandial samples (1-2 hrs apart) are the most useful way of assessing function. Generally speaking, if jaundice is due to pre- or post-hepatic causes, bile acids will be elevated, so determining bile acid concentrations is usually pointless as it can be assumed they will be elevated. Pre- and post-prandial samples should be less than 30 units /L. One-off samples are only useful in ruling out abnormalities - a normal serum bile acid concentration does not exclude liver dysfunction.

Ammonia

Blood ammonia levels are usually only measured when there is a suspicion of hepatic encephalopathy. As ammonia is labile, it needs to be measured within 30 minutes by a reliable in-house method. It is often impractical to measure ammonia concentration in practise. Ammonia tolerance tests are not recommended in cats. As cats require a pre-formed source of arginine (they cannot make arginine from ornithine or citrulline), normal cats can sometimes be 'swamped' by an ammonia challenge and become hyperammonaemic. This is particularly important in anorexic cats that may be protein malnourished.

Coagulation studies

Coagulation tests should always be considered as a part of the diagnostic workup and management of the jaundiced cat as the liver plays an integral role in coagulation homeostasis by provision of coagulation and fibrinolytic proteins / proteases. Before performing aspiration, percutaneous Tru-cut biopsy and especially before major surgery, clotting profiles should be assessed. In Australia, commercial laboratories offer PT, APTT and thrombin studies. These lack relative sensitivity and specificity in cats but are a reasonable evaluation of coagulation. A new assay - PIVKA (modified PT) measures the interference in clot formation due to the build up of non-functional vitamin K-dependant factors in the blood stream. many cats with hepatic disease have elevated PIVKA without obvious clinical bleeding problems. PIVKA may become available in this country and is potentially useful as a test to identify cats at risk of haemorrhage. If there is reasonable doubt, it is safe to supplement with Vit K1 and is recommended in any cat with hepatic related jaundice, particularly those with EHBDO (Extra-hepatic biliary duct obstruction).

Idiosyncrasies of Hepatic metabolism in the cat

Hepatic disease causing jaundice

Extrahepatic disease causing jaundice