Contributors: Nick Bexfield, Penny Watson

 Species: Canine   |   Classification: Diseases

Introduction Pathogenesis Diagnosis Treatment Outcomes Further Reading


  • Includes: chronic hepatitis, copper associated hepatitis, drug induced hepatitis, lobular dissecting hepatitis, granulomatousidiopathic hepatitis, hepatic neoplasia, congenital abnormalities (ductal plate malformations including congenital hepatic fibrosis; portal vein hypoplasia).
  • Cause: chronic hepatitis often idiopathic, some autoimmune, chronic infection, possible toxicity, neoplasia, congential malformation.
  • Signs: may present as acute hepatitis with jaundice, ascites, or may be non-specific: lethargy, anorexia, vomiting, weight loss, signs of hepatic encephalopathy.
  • Diagnosis: biochemistry, hepatic function tests, ultrasonography, definitive diagnosis requires hepatic biopsy.
  • Treatment: elimination of cause if known, supportive and symptomatic measures, antibiotics or steroids or copper chelators as necessary.
  • Prognosis: depends on underlying cause.

Presenting Signs

  • Signs may be insidious and often wax and wane, or may be acute in onset when acute-on-chronic inflammatory flare up or development of portal hypertension resulting in ascites and hepatic encephalopathy, or reserve functional capacity is exceeded (approx >70%).

Acute Presentation

  • Acute-on-chronic inflammatory flare up or portal hypertension or end-stage liver failure.

Age Predisposition

  • Any age.
  • Mean age for chronic hepatitis is 5-7 years. Usually <2 years of age in dogs with idiopathic hepatic fibrosis Liver: idiopathic fibrosis. Older for neoplasia.

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.
  • Risk of hemorrhage during surgery including biopsy as coagulation times may be prolonged particularly in end stage disease.




  • 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 → sinusoidal fibrosis, contraction of myofibroblasts and periportal fibrosis → 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 → diarrhea → gastrointestinal ulceration → hematemesis and melena.
  • Decreased production of clotting factors → bleeding tendency.
  • Inflammation of biliary system and periportal inflammation and fibrosis → 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 results 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 distortion of the liver associated with regenerative nodules, it is termed cirrhosis Liver: cirrhosis.


  • >12 weeks of active illness.


Client History

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), unusual in dogs.
  • Coma.

Diagnostic Investigation



  • Non-regenerative often microcytic anemia Anemia: non-regenerative.
  • Presence of target cells.
  • Also to check gastrointestinal bleeding and 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.
  • 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


  • See 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. Superceded now by CT Computed tomography.

CT Angiography

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:
    • Chronic hepatitis, 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.
    • Congenital ductal plate abnormalities: biliary cysts; abnormal portal triads with multiple small bile ducts and fibrosis.
    • Presence of specific neoplastic cells, especially metastatic.

Differential Diagnosis

Primary liver diseases

Secondary liver diseases

Causes of jaundice

  • Causes of hemolytic anemia Anemia: immune mediated hemolytic.
  • Hepatocellular disease (see primary and systemic causes of liver disease).
  • Biliary disease Biliary system: disease (cholestatic disease): infection, gall bladder mucocele, neoplasia.
  • Biliary tract obstruction: intrahepatic, eg neoplasia, inflammation; extrahepatic, eg chronic pancreatitis, pancreatic neoplasia Pancreas pancreatitis or neoplasia - radiograph or inflammation, gall stones (choleliths).

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 omeprazole Omeprazole or an H2 blocker if gastrointestinal bleeding.
    Cimetidine 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 adding 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 and low copper diet Dietetic diet: for liver insufficiency.
  • Moderately low protein restricted 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 if suspected autoimmune chronic hepatitis. A sensible starting dose would be 1 mg/kg SID then gradually reducing the dose and frequency of dosing.
  • Their use in end-stage fibrosis and cirrhosis is unhelpful and may worsen gastrointestinal ulceration, increase protein catabolism and fluid retention.
  • Cyclosporine Ciclosporin and alternative to steroids in suspected autoimmune chronic hepatitis and less likely to cause side effects in end stage fibrosis.
  • Antifibrosing drugs, eg colchicine Colchicine. Not recommended - no good evidence of efficacy.

Subsequent Management


  • Repeat hepatic function tests and hepatic biopsy.
  • Measure body weight, body condition score and 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 guarded to poor prognosis in chronic hepatitis. Prognosis poorer if ascites present or jaundiced.
  • Prognosis can be good in copper associated chronic hepatitis if effectively chelated.
  • Congenital ductal plate abnormalities and portal vein hypoplasia can have a good prognosis with supportive care.

Expected Response to Treatment

  • Clinical improvement.
  • Resolution of hepatic pathology.

Reasons for Treatment Failure

  • Development of hepatic cirrhosis.
  • End stage liver failure with loss of >70% hepatocyte mass

Further Reading


Refereed papers

  • Recent references from PubMed and PubMed.
  • Webster C R L, Center S A, Cullen J M et al (2019) ACVIM consensus statement on the diagnosis and treatment of chronic hepatitis in dogs. J Vet Intern Med 33 (3), 1173-1200 PubMed.
  • Bexfield N H, Buxton R J, Vicek T J et al (2012) Breed, age and gender distribution of dogs with chronic hepatitis in the United Kingdom. Vet J 193 (1), 124-128 PubMed.
  • Poldervaart R P et al (2009) Primary hepatitis in dogs: a retrospective review (2002 –2006). J Vet Intern Med 23 (1): 72-80 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.
  • 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

  • Lidbury (2023) Chronic Hepatitis. In: Textbook of Veterinary Internal Medicine. 9th edn. Eds: S J Ettinger, E C Feldman & Coté E. W B Saunders, USA.
  • 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, UK. pp 240-268.

Other Sources of Information