Contributors: Kyle Braund, Phil Nicholls, Penny Watson
Species: Feline | Classification: Diseases
- Cause: malformation, toxicity, neoplasia, endocrinopathy, metabolic (lipidosis), auto-immune (lymphocytic cholangitis), infection.
- Signs: non-specific - lethargy, anorexia, vomiting. Signs of hepatic encephalopathy.
- Diagnosis: biochemistry, hepatic function tests, ultrasonography, hepatic biopsy.
- Treatment: elimination of cause, supportive.
- Prognosis: depends on severity and treatment of inciting factor.
- See also Liver: acute disease Liver: acute disease.
Print off the owner factsheet Liver problems in your cat Liver problems in your cat to give to your client.
- Insidious onset when reserve functional capacity is lost (>60%).
- Anorexia Anorexia, depression.
- Vomiting, diarrhea.
- Abdominal distension (ascites).
- End-stage liver failure.
- <5 yrs - lymphocytic cholangitis and feline infectious peritonitis.
- >6 yrs - hyperthyroidism.
- >10 yrs - neoplasia.
- Middle aged - hepatic lipidosis.
- Long-term therapy can be expensive.
- Expenses incurred in establishing a diagnosis.
- Anesthesia - as many commonly used drugs are metabolized in liver.
Warn owner of increased risk of anesthesia.
- Idiopathic chronic hepatitis.
- Drugs - cats have a relative sensitivity to many drugs due to low levels of glucuronyl transferase delaying metabolism, eg acetaminophen, griseofulvin, megestrol acetate, ketoconazole.
- Infectious, eg FeLV Feline leukemia virus, FIP Feline sarcoma virus; bacterial, fungal and parasitic.
- Portosystemic shunt (congenital) Congenital portosystemic shunt (CPSS).
- Neoplasia, lymphoma Lymphoma or metastatic.
- Cumulative 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 massive 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 Hypoglycemia.
- Decreased production of albumin → hypoalbuminemia.
- Failure to detoxify ammonia and other mercaptans from intestine → hepatic encephalopathy Hepatic encephalopathy.
- Vomiting Vomiting.
- Neurological signs.
- Decreased appetite.
- Behavioral changes.
- Abdominal distension (ascites).
- Unkempt hair coat.
Signs of hepatic encephalopathy
- May occur with portosystemic shunt Congenital portosystemic shunt (CPSS), acute or end-stage liver disease.
- Behavior changes - dementia, dullness, aggression.
- Neurological abnormalities - circling, ataxia, head pressing, aimless pacing, seizures.
- Ptyalism .
- ALT Blood biochemistry: gamma glutamyl transferase, AST, ALP Blood biochemistry: alkaline phosphatase, GGT Blood biochemistry: gamma glutamyl transferase - abnormalities indicate liver disease or injury (not a measure of liver function).
May be reactive elevations, eg hyperthyroidism Hyperthyroidism.
- Increased ALP Blood biochemistry: alkaline phosphatase, is a sensitive indicator of cholestasis and a specific indicator of hepatobiliary disease in cats as there is no steroid-induced isoenzyme in this species.
- Bilirubin Blood biochemistry: total bilirubin, not sensitive guide but an increase >3 g/dl suggests liver disease.
- Serum bile acids (SBA Blood biochemistry: bile acid - supercedes BSP clearance test) for hepatobiliary function and portosystemic shunts.
- Ammonia Blood biochemistry: ammonia for hepatobiliary function and portosystemic shunts.
- To check for hemolytic disease.
Exclude systemic causes of enzyme elevation, eg hyperthyroidism, before undertaking invasive diagnostic procedures.
- Fine needle aspiration (FNA Fine-needle aspirate).
- Percutaneous blind or ultrasound guided needle biopsy.
- Laparoscopy-guided biopsy.
- Laparotomy Laparotomy: midline (evaluate clotting function before biopsy).
- Doppler ultrasound - ascites , portosystemic shunt.
- Evaluate parenchyma and biliary system.
- Multifocal radiolucencies - neoplasia or infection/abscessation.
- Identify focal lesions.
- Guide needle biopsy.
If there is no dilation of the extrahepatic biliary tract, and no hemolytic disease in the presence of jaundice, hepatocellular disease is likely → take liver biopsy.
- Diffuse echogenicity - hepatic lipidosis.
Gross Autopsy Findings
- Systematic examination of other organ systems helps interpretation of chronic disease.
- If history consistent, consider samples for toxicology (liver, kidney, fat, urine etc - consult lab).
- Remove brain and fix whole if likely hepatic encephalopathy.
- Swollen, pale, nodular liver.
- Shrunken liver late in disease process.
- Variable-sized regenerative nodules.
- Focal/multifocal masses.
- Frozen sections best demonstrate lipidosis, but formalin fixation acceptable.
- Varies with cause, eg:
- Moderate to severe inflammation associated with 'piece-meal' necrosis of hepatocytes; begins in portal triad and extends into parenchyma.
- Small islands of hepatocytes surrounded by inflammatory cells (lymphocytes, plasma cells, sometimes neutrophils) → bridging necrosis → active cirrhosis.
- Special stains for copper accumulation (Rubeanic acid, Rhodamine).
- Fibrosis and parenchymal nodules that disrupt normal hepatic architecture.
- Presence of specific neoplastic cells, especially metastatic.
Primary liver diseases
- Cholangiohepatitis and lymphocytic cholangitis Liver: cholangitis.
- Neoplasia, eg lymphosarcoma Lymphoma, bile duct carcinoma, systemic mastocytosis.
- Portosystemic shunts Congenital portosystemic shunt (CPSS).
- Toxic hepatopathy (see Liver: acute disease Liver: acute disease).
Secondary liver diseases
- Feline infectious peritonitis (FIP) Feline infectious peritonitis.
- Toxoplasmosis Toxoplasmosis.
- Hyperthyroidism Hyperthyroidism.
- Neoplasia - metastatic.
- Hepatic lipidosis Liver: lipidosis - idiopathic, secondary to obesity Obesity, endocrine disorders.
Causes of jaundice
- Jaundice .
- Causes of hemolytic anemia: Hemobartonella felis Mycoplasma haemofelis, 'Candidatus Mycoplasma haemominutum' and 'Candidatus Mycoplasma turicensis' , auto-immune 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 or inflammation Pancreatitis, bile stones.
Causes of ascites
- Primary hepatic disease.
- FIP Feline infectious peritonitis.
- Bacterial peritonitis Peritonitis.
- Glomerulonephritis (nephrotic syndrome) Glomerulonephritis.
- Congestive heart failure Heart: congestive heart failure.
- Chylous ascites.
- Other fluids (hemorrhage, bladder Bladder: trauma rupture, or biliary rupture).
- Antibiotics Therapeutics: antimicrobial drug Therapeutics: gastrointestinal system to prevent secondary infections and to reduce gut ammonia production.
- H2 receptor blockers, eg ranitidine Ranitidine or cimetidine Cimetidine.
- Sucralfate Sucralfateif gastrointestinal bleeding.
- Spironolactone Spironolactone if ascites; if refractory, try furosemide Furosemide.
- Lactulose Lactulose and antibiotics for hepatic encephalopathy.
- Feed high quality protein diet Dietetic diet: for liver insufficiency.
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 restriction 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 and zinc Zinc supplementation may be required.
- Cage rest.
- Ursodeoxycholic acid Ursodeoxycholic acid to displace toxic bile acids, stimulate bile flow and modulate immune response.
- Repeat hepatic function tests and hepatic biopsy.
- Depends on underlying cause and degree of hepatic damage.
Expected Response to Treatment
- Clinical improvement.
- Resolution of hepatic pathology.
Reasons for Treatment Failure
- Development of hepatic cirrhosis Liver: cirrhosis.
- Recent references from PubMed and VetMedResource.
- Godfrey D R & Rest J R (2000) Suspected necrolytic migratory erythema associated with chronic hepatopathy in a cat. JSAP 41 (7), 324-328 PubMed.
- Center S A (1999) Chronic liver disease - current concepts of disease mechanisms. JSAP 40 (3), 106-114 PubMed.
Other sources of information
- Johnson S E (2000) Chronic hepatic disorders. In:Textbook of Veterinary Internal Medicine.5th edn. Ettinger S J & Feldman E C (eds). W B Saunders, Philadelphia. pp 1298-1325.
- Laflamme D P (2000) Nutritional management of liver disease. In:Kirk's Current Veterinary therapy XIII.Bonagura J D (ed). W B Saunders, Philadelphia. pp 693-697.
- Center S A (1996) Feline hepatic disease - Current therapeutic concepts. Proceedings of BSAVA Waltham Symposium on liver disease. pp 56-63.
- Watson T (1996) Nutritional management of canine liver disease. Proceedings of BSAVA Waltham Symposium on liver disease.pp 42-46.
- Michel R (1995) Nutritional management of liver disease. Vet Clin North Am Small Anim Pract 25, 485.