Contributors: Phil Nicholls, Penny Watson, Mark W Jackson
Species: Feline | Classification: Diseases
- 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.
- 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).
- Lymphocytic cholangitis (acute and chronic, previously cholangiohepatitis).
Cats have a relative sensitivity to many drugs due to low levels of glucuronyl transferase delaying metabolism.
- Drugs: anticonvulsants, azathioprine Azathioprine, ketoconazole Ketoconazole, methoxyflurane Methoxyflurane, sulfonamides Trimethoprim, tetracycline Tetracycline .
- Chemicals: carbon tetrachloride, heavy metals, selenium, tannic acid.
- Biological substances: aflatoxin, blue-green algae.
- Acute pancreatitis Pancreatitis, acute hemolytic anemia Anemia: immune-mediated hemolytic, hepatic lipidosis Liver: lipidosis, trauma Trauma: overview, heat stroke Hyperthermia.
- 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.
- Vomiting Vomiting.
- Vomiting Vomiting.
- Diarrhea Diarrhea: dietary.
- Altered mentation.
- Excessive salivation.
- Behavioral changes.
- Seizures Seizures.
- Bleeding tendency.
- Abdominal pain.
- Signs of hepatic encephalopathy Hepatic encephalopathy.
- Neurological dysfunction related to cerebrum.
- Petechial hemorrhages.
- Serum enzymes - activity may be first indicator of hepatic disease.
Extent of increased activity does not reflect severity of damage; cannot be used for prognosis.
- Alanine aminotransferase Blood biochemistry: alanine aminotransferase (SGPT, ALT) - intracellular enzyme released when hepatocellular necrosis occurs - ie indicates acute or active hepatocellular damage.
- Alkaline phosphatase Blood biochemistry: alkaline phosphatase, and gamma glutamyl transferase Blood biochemistry: gamma glutamyl transferase - increased production due to intrahepatic or biliary cholestasis.
Sensitive and specific in the cat as no steroid-induced isoenzyme of ALP - as in the dog.
- Ammonia Blood biochemistry: ammonia: produced by intestinal bacteria degraded in liver; increased levels due to hepatic failure or porto-systemic shunt.
Samples should be taken into heparin container and stored on ice until analyzed.
- Bilirubin Blood biochemistry: total bilirubin: elevated bilirubin.
- Bile acids Blood biochemistry: bile acid: increased fasting and 2 hrs post prandial levels; good test of hepatic function.
- Albumin Blood biochemistry: albumin: rarely see significant decrease. Albumin is a negative acute phase protein, non-specific decrease of 10-20% with inflammation.
- Blood culture to identify bacteremia.
- Gall bladder aspirate and culture (surgical or by ultrasound guided percutaneous aspirate).
- Check for possible coagulopathy.
- Abdominal examination to identify pancreatic/gall bladder disease.
- Evaluation of hepatic parenchyma/identification of diffuse or focal lesions.
- Liver biopsy Biopsy: hepatic to determine etiology if initial tests non-diagnostic - may perform at laparotomy Laparotomy: midline, or by ultrasound guided percutaneous biopsy Biopsy: ultrasound-guided.
Check for possible coagulopathy.
- 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.
- Consider fresh samples for toxicology, (liver, kidney, fat, stomach contents, urine - consult lab).
- Consider frozen sections for fatty liver.
Primary liver diseases
- Cholangitis (neutrophilic or lymphocytic) Liver: cholangitis.
- Neoplasia, eg lymphosarcoma, bile duct carcinoma, systemic mastocytosis.
- Portosystemic shunts Congenital portosystemic shunt (CPSS).
- Toxic hepatopathy.
Secondary liver diseases
- Feline infectious peritonitis (FIP Feline infectious peritonitis).
- Toxoplasmosis Toxoplasmosis.
- Neoplasia - metastatic.
- Hepatic lipidosis Liver: lipidosis - idiopathic, endocrine disorders.
- Feline 'triaditis'.
Causes of jaundice
- Causes of hemolytic anemia: Hemobartonella felis Mycoplasma haemofelis, 'Candidatus Mycoplasma haemominutum' and 'Candidatus Mycoplasma turicensis' , autoimmune hemolytic anemia Anemia: immune-mediated hemolytic, FeLV Feline leukemia virus disease.
- Hepatocellular disease, (see primary and systemic causes of liver disease).
- Obstructive: intrahepatic, eg neoplasia, inflammation; extrahepatic, eg pancreatic neoplasia Pancreas: neoplasia, or inflammation, bile stones.
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.
- 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.
- Vitamin K Vitamin K, if coagulopathy.
- Maintain reduced protein, low fat, high carbohydrate diet Dietetic diet: for liver insufficiency.
- Minimize exercise.
- 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.
- 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.