Contributors: Nick Bexfield

 Species: Canine   |   Classification: Diseases

Introduction Pathogenesis Diagnosis Treatment Outcomes Further Reading


  • Includes: chronic active hepatitis, copper associated hepatitis, drug induced hepatitis, lobular dissecting hepatitis, idiopathic hepatitis.
  • Cause: malformation, toxicity, neoplasia, endocrinopathy, infection.
  • Signs: may present as acute hepatitis, or may be non-specific: lethargy, anorexia, vomiting. Signs of hepatic encephalopathy.
  • Diagnosis: biochemistry, hepatic function tests, ultrasonography, ultimately hepatic biopsy.
  • Treatment: elimination of cause if known, supportive and symptomatic measures.
  • Prognosis: depends on underlying cause.

Presenting Signs

  • Signs may be insidious or may be acute in onset when reserve functional capacity is exceeded (>70%).

Acute Presentation

  • End-stage liver failure.

Age Predisposition

  • Any age, although mean age is 5-7 years. Usually <2 years of age in dogs with idiopathic hepatic fibrosis Liver: idiopathic fibrosis.

Breed Predisposition

Cost Considerations

  • Long-term therapy can be expensive.
  • Expenses incurred in establishing a diagnosis.

Special Risks

  • Anesthesia as many commonly used drugs are metabolized in liver.
    Warn owner of increased risk of anesthesia.




  • Cumulative hepatic insult → functional reserve capacity exceeded (>70% damage) → failure to perform diverse metabolic functions → clinical signs.
  • Increased resistance to blood flow through liver due to hepatocytes swelling → development of portal hypertension →ascites. Ascites may also develop due to hypoalbuminemia Hypoproteinemia.
  • Acquired shunting vessels may develop due to sustained portal hypertension.
  • Failure to detoxify ammonia from intestine due to reduced hepatic mass and presence of acquired shunting vessels → hepatic encephalopathy Hepatic encephalopathy.
  • Portal hypertension → gastrointestinal wall congestion and edema → gastrointestinal ulceration → hematemesis and melena.
  • Inadequate bile delivery to intestine → impairment of fat digestion → diarrhea.
  • Decreased production of clotting factors →bleeding tendency.
  • Inflammation of biliary system → partial obstruction to biliary flow →icterus.
  • Decreased production of urea in the urea cycle → reduced blood urea.
  • Decreased production of albumin →hypoalbuminemia.
  • Chronic liver disease may result in fibrosis. If the injury is severe and/or ongoing, the liver will respond by laying down fibrous tissue. This represents a final common pathway to a variety of insults to the liver.
  • When bridging fibrosis causes permanent distortion of the liver associated with regenerative nodules, it is termed cirrhosis Liver: cirrhosis.


  • >12 weeks of active illness.


Client History

  • Anorexia.
  • Depression.
  • Vomiting.
  • Diarrhea.
  • Polydipsia/polyuria.
  • Jaundice.
  • Abdominal enlargement.
  • Signs of hepatic encephalopathy Hepatic encephalopathy.

Clinical Signs

  • Lethargy.
  • Decreased appetite.
  • Vomiting.
  • Diarrhea.
  • Polydipsia/polyuria.
  • Unkempt hair/coat.
  • Jaundice.
  • Small liver on palpation.
  • Poor bodily condition.
  • Ascites.

Signs of hepatic encephalopathy

  • Behavioral changes - dementia, dullness, aggression, disorientation.
  • Neurological abnormalities - circling, ataxia, head pressing, aimless pacing, seizures.
  • Ptyalism (excessive salivation).
  • Coma.

Diagnostic Investigation



  • Non-regenerative anemia Anemia: non-regenerative.
  • Presence of target cells.
  • Also to check for hemolytic disease as a cause of the jaundice.


Exclude systemic causes of enzyme elevation before undertaking invasive diagnostic procedures.

2-D Ultrasonography
  • See Ultrasonography: liver Ultrasonography: liver.
  • Doppler ultrasound - portosystemic shunt.
  • Evaluate parenchyma and biliary system Liver normal vessels - ultrasound.
  • 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 → do liver biopsy
  • Diffuse echogenicity - hepatic lipidosis, hepatic cirrhosis.

  • See Radiology: liver Radiology: liver.
  • Small (microhepatica) - portosystemic shunt, hepatic cirrhosis Liver: cirrhosis , hepatic fibrosis.
  • Liver size can be normal Radiography: abdomen.
  • Hepatomegaly.
  • Focal masses.
  • Multifocal radiolucencies - infection or abscessation.
  • Contrast study: surgically expose and inject iodine contrast media into portal vein to identify portosystemic shunt.

Gross Autopsy Findings

  • Swollen, pale, nodular liver.
  • Shrunken liver late in disease process.
  • Variable-sized regenerative nodules.
  • Focal/multifocal masses.

Histopathology Findings

  • 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.

Differential Diagnosis

Primary liver diseasesSecondary liver diseasesCauses of jaundice
  • Causes of hemolytic anemia Anemia: immune mediated hemolytic.
  • Hepatocellular disease (see primary and systemic causes of liver disease).
  • Obstructive: intrahepatic, eg neoplasia, inflammation; extrahepatic, eg pancreatic neoplasia Pancreas pancreatitis or neoplasia - radiograph or inflammation, bile stones.
Causes of ascites
  • Advanced hepatic disease.
  • Hypoalbuminemia.
  • Abdominal neoplasia.
  • Right-sided congestive heart failure Heart: congestive heart failure.
  • Chylous ascites.
  • Bacterial peritonitis Peritonitis.
  • Other fluids (hemorrhage, bladder or biliary rupture).


Initial Symptomatic Treatment

  • Intravenous fluids if acute worsening.
  • Sucralfate Sucralfate and an H2 blocker if gastrointestinal bleeding.
    Cimetidine decreases liver P450 enzymes → alterations in metabolism of many drugs. Use other H2 blocking drugs first, eg ranitidine Ranitidine.
  • Spironolactone Spironolactone if ascites; if refractory, try furosemide Furosemide.
  • Ampicillin Ampicillin and lactulose Lactulose if evidence of hepatic encephalopathy.
  • Ursodeoxycholic acid Ursodeoxycholic acid to stimulate bile flow, displace toxic bile acids, and modulate immune response.
  • Anti-oxidants such as SAMe S-adenosylmethionine , silybin/silymarin (milk thistle) Silybin or vitamin E Vitamin E. SAMe, which increases blood glutathione levels, is widely available as are silybin/silymarin and vitamin E. Research has shown the combination of SAMe and silybin to be complementary in attenuating inflammation in canine hepatocytes.
  • D-penicillamine Penicillamine or 2,2,2-tetramine for copper chelation.
  • Low protein diet Dietetic diet: for liver insufficiency only necessary if evidence of encephalopathy. If no encephalopathy, diet should contain sufficient high quality protein to allow the liver to regenerate. If feeding a prescription diet formulated for dogs with hepatic disease, these should always be supplemented with a source of high quality protein such as cottage cheese.
  • Excessive protein restriction will lead to muscle catabolism and worsening of HE.
  • Steroids are very effective antifibrotics, but should only be used if there is an inflammatory infiltrate. Their use in end-stage fibrosis and cirrhosis is unhelpful and may worsen gastrointestinal ulceration, increase protein catabolism and fluid retention.
  • Few if any dogs have autoimmune hepatitis, so the use of immunosuppressive doses of steroids (2-4 mg/kg SID) is not recommended. A sensible starting dose would be 1 mg/kg SID then gradually reducing the dose and frequency of dosing.
  • Antifibrosing drugs, eg colchicine Colchicine. Recent studies in humans have questioned its effectiveness.
    Studies in dogs are lacking so there is little current evidence to support its use.

Subsequent Management


  • Repeat hepatic function tests and hepatic biopsy.
  • Measure blood albumin Blood biochemistry: albumin to assess the need for dietary supplementation with additional protein.



  • Depends on underlying cause and degree of hepatic damage.
  • Generally poor diagnosis.
  • Prognosis much poorer if ascites present.

Expected Response to Treatment

  • Clinical improvement.
  • Resolution of hepatic pathology.

Reasons for Treatment Failure

  • Development of hepatic cirrhosis.

Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Au A Y, Hasenwinkel J M, Frondoza C G (2013) Hepatoprotective effects of S-adenosylmethionine and silybin on canine hepatocytes in vitro. J Anim Physiol Anim Nutr (Berl) 97 (2), 331-41 PubMed.
  • Mandigers P J, van den Ingh T S, Spee B, Penning L C, Bode P, Rothuizen J (2004) Chronic hepatitis in Doberman pinschers. A review. Vet Q 26 (3), 98-106 PubMed.
  • Watson P J (2004) Chronic hepatitis in dogs: a review of current understanding of the aetiology, progression and treatment. Vet J 167 (3), 228-241 PubMed.
  • Center S A (1999) Chronic liver disease: current concepts of disease mechanisms. JSAP 40 (3), 106-114 PubMed.
  • Sevelius E (1995) Diagnosis and prognosis of chronic hepatitis and cirrhosis in dogs. JSAP 36 (12), 521-528 PubMed.
  • Andersson M, Sevelius E (1991) Breed, sex and age distribution in dogs with chronic liver disease: a demographic study. JSAP 32 (1), 1-5 VetMedResource.

Other sources of information

  • Watson P J (2005) Diseases of the liver. In: BSAVA Manual of Canine and Feline Gastroenterology. 2nd edn. Eds: E J Hall, J W Simpson & D A Williams. BSAVA Publications. pp 240-268.
  • Willard M D (2005) Inflammatory canine hepatic disorders. In:T extbook of Veterinary Internal Medicine. 6th edn. Eds: S J Ettinger & E C Feldman. W B Saunders, Philadelphia. pp 1442-1447.

Other Sources of Information