Contributors: Phil Nicholls, Penny Watson, Mark W Jackson

 Species: Feline   |   Classification: Diseases

Introduction Pathogenesis Diagnosis Treatment Outcomes Further Reading


  • Cause: overwhelming toxic or metabolic (eg lipidosis) insult, neoplasia or infection; acute on chronic liver disease.
  • Signs: non-specific; anorexia, vomiting, depression +/- polydipsia/polyuria; signs of hepatic encephalopathy.
  • Diagnosis: biochemistry, ultrasonography, hepatic biopsy.
  • Treatment: underlying cause if recognized; otherwise supportive and symptomatic.
  • Prognosis: depends on etiology, severity and treatment of inciting factor.
  • See also Liver: chronic disease Liver: chronic disease.

Acute Presentation

  • Collapse/coma.
  • Seizures.




  • Viral: FeLV Feline leukemia virus disease, FIP Feline infectious peritoniti , (usually chronic presentation).
  • Bacterial: extension of neutrophilic cholangitis* (previously suppurative cholangiohepatitis) Liver: cholangitis, or hematogenous.
  • Mycotic: eg, histoplasmosis Histoplasma capsulatum, if associated with pulmonary disease.
  • Protozoal, ie toxoplasma Toxoplasmosis.
  • Parasitic: liver flukes (not in UK).
  • * Based on WSAVA recommendations the classification of feline liver disease has been clarified and is now:
    • Neutrophilic cholangitis (acute and chronic).
    • Lymphocytic cholangitis (acute and chronic).
    • Chronic cholangitis (fluke infestation in endemic areas).

Immune mediated

  • Lymphocytic cholangitis (acute and chronic, previously cholangiohepatitis).


Cats have a relative sensitivity to many drugs due to low levels of glucuronyl transferase delaying metabolism.



  • Unvaccinated animals.


  • Overwhelming hepatic insult   →   functional reserve capacity exceeded   →   failure to perform diverse metabolic functions   →   clinical signs.
  • Hepatic functional reserve large   →   75% damage before exhausted   →   periacinar zonal necrosis, infiltration of inflammatory cells due to toxins, living agents and metabolic disease will cause extensive damage.
  • Decreased production of clotting factors   →  bleeding tendency.
  • Hepatic cellular damage   →   cellular release of bilirubin   →  icterus.
  • Inflammation of biliary system   →   partial obstruction to biliary flow   →  icterus.
  • Inadequate bile delivery to intestine   →   impairment of fat digestion   →  diarrhea.
  • Failure to maintain euglycemia   →  hypoglycemia.
  • Decreased production of albumin   →  hypoalbuminemia.
  • Failure to detoxify ammonia and other mercaptans from intestine   →  hepatic encephalopathy Hepatic encephalopathy.


  • Dependent on etiology, within days of ingestion of toxin, infection.


Presenting Problems

  • Lethargy.
  • Anorexia.  
  • Icterus.
  • Vomiting Vomiting.
  • Diarrhea.
  • Coma.
  • Polydipsia/polyuria.

Client History

  • Diarrhea Diarrhea: dietary.
  • Polydipsia/polyuria.
  • Icterus.
  • Altered mentation.
  • Excessive salivation.
  • Behavioral changes.
  • Seizures Seizures.
  • Coma.
  • Bleeding tendency.

Clinical Signs

  • Icterus.
  • Abdominal pain.
  • Depression.
  • Neurological dysfunction related to cerebrum.
  • Petechial hemorrhages.

Diagnostic Investigation



  • Blood culture to identify bacteremia.
  • Gall bladder aspirate and culture (surgical or by ultrasound guided percutaneous aspirate).
  • Check for possible coagulopathy.

2-D Ultrasonography

  • Abdominal examination to identify pancreatic/gall bladder disease.
  • Evaluation of hepatic parenchyma/identification of diffuse or focal lesions.



  • Liver usually normal size or enlarged in acute hepatic failure.

Gross Autopsy Findings

  • Liver occasionally looks normal in acute disease - histology essential.
  • Examine firstin situto rule out portosystemic shunts Congenital portosystemic shunt (CPSS). Remove brain and fix whole if neurological signs accompany.
  • Bacteriological sample where indicated - swab through incised seared surface.

Histopathology Findings

  • Consider fresh samples for toxicology, (liver, kidney, fat, stomach contents, urine - consult lab).
  • Consider frozen sections for fatty liver.

Differential Diagnosis

Primary liver diseases

Secondary liver diseases

Causes of jaundice


Initial Symptomatic Treatment

  • Cage rest and nutritional support to optimize conditions for hepatic regeneration and prevent scarring.
  • Intravenous fluids Fluid therapy: overview, to maintain fluid and electrolyte balance.
  • Intravenous diazepam Diazepam, if seizures, avoid repeated use.
  • Antibiotics, if indicated, to counter primary and secondary infections and reduce gut ammonia production (ampicillin Ampicillin, neomycin Neomycin).
  • Sucralfate Sucralfate (500mg SID), if gastrointestinal bleeding.

Standard Treatment

  • Dextrose added to intravenous fluids if hypoglycemia.
  • If encephalopathy, may use enemas to remove substrates for bacterial metabolism and lactulose Lactulose, to minimize ammonia Blood biochemistry: ammonia, and mercaptan production.
  • Discontinue any suspect drugs.
  • Feed high quality protein diet.
    Cottage cheese alone is inadequate as a protein source in cats. It is deficient in arginine which is essential in the urea cycle and therefore very important in liver disease.
  • Protein reduction only indicated if there is encephalopathy.
    Protein restriction can seriously impair liver's ability to regenerate and indiscriminate restriction may reduce or prevent recovery since cats have a high protein requirement.


Subsequent Management



  • Serum biochemistry every 2-3 weeks.
  • If persistent abnormalities, follow-up liver biopsy.



  • Depends on severity and elimination of underlying insult.
  • Poor if coagulopathy and/or hepatic encephalopathy present.
  • Less severe forms may result in complete regeneration.
  • Persistent inflammation may result in chronic hepatitis Liver: chronic disease.

Expected Response to Treatment

  • Resolution of vomiting, depression, anorexia, etc. within days of treatment initiation.
  • Serum biochemistry returns to normal within 3 weeks.

Reasons for Treatment Failure

  • Failure to identify and treat underlying disease/inciting factor.
  • Failure to maintain rest may lead to fibrosis of liver and permanent damage.

Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Center S A, Warner K, Corbett J et al (2000) Proteins invoked by vitamin K absence and clotting times in clinically ill cats. JVIM 14 (3), 292-297 PubMed.
  • Center S A (1999) Chronic liver disease - current concepts of disease mechanisms. JSAP 40 (3), 106-114 PubMed.

Other sources of information

  • Marks S L (2008) Feline hepatic disorders: update on diagnosis and management. Proceedings of the 51st BSAVA Congress, pp 201-205.
  • Rothuzien J, Bunch S E, Cullen J M, Charles J A, Desmet V J, Twedt D C, van den Ingh T, van Winkle T, Washabua J (eds) (2006) WSAVA Liver Standardization Group. Standards for Clinical and Histological Diagnosis of Canine and Feline Liver diseases. Saunders/Elsevier, Edinburgh.
  • Michel R (1995) Nutritional management of liver disease. Veterinary Clinics North America (SA) 25, 485.

Other Sources of Information