Contributors: Nick Bexfield, Kyle Braund, James Simpson

 Species: Canine   |   Classification: Diseases

Introduction Pathogenesis Diagnosis Treatment Outcomes Further Reading


  • Cause: overwhelming toxic insult, infectious or metabolic disease.
  • Signs: non-specific; anorexia, vomiting, depression +/- polydipsia/polyuria, jaundice, ascites, bleeding, encephalopathy.
  • Diagnosis: biochemistry, hepatic function tests, ultrasonography, hepatic biopsy.
  • Treatment: underlying cause if recognized; otherwise supportive and symptomatic.
  • Prognosis: depends on severity and treatment of inciting factor.
  • See also Liver: chronic disease Liver: chronic disease - overview.

Presenting Signs

  • Anorexia
  • Depression.
  • Vomiting.
  • Diarrhea.
  • Polyuria/polydipsia.
  • Icterus.
  • Abdominal pain.
  • Behavioral changes.
  • Seizures.
  • Coma.
  • Bleeding tendency.

Acute Presentation

  • Collapse/coma.
  • Dehydrated.
  • Seizures.

Cost Considerations

  • Intensive and supportive care can be prolonged and expensive.








  • Diffuse tumor infiltrate, eg lymphoma Lymphoma.


  • Unvaccinated animals.


  • Overwhelming hepatic insult → functional reserve capacity exceeded → failure to perform diverse metabolic functions → clinical signs.
  • Hepatic functional reserve large → 70% damage before capacity exhausted → peri-acinar zonal necrosis, infiltration of inflammatory cells due to toxins, living agents and metabolic disease will cause massive damage.
  • Local and systemic release of cytokines and other pro-inflammatory mediators → pyrexia, anorexia, depression.
  • Decreased production of clotting factors → bleeding tendency.
  • 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 Blood biochemistry: glucose.
  • Decreased production of albumin →hypoalbuminemia Blood biochemistry: albumin.
  • Failure to detoxify ammonia and other mercaptans from intestine →hepatic encephalopathy Hepatic encephalopathy.
  • Increased resistance to blood flow through liver due to hepatocytes swelling → development of portal hypertension →ascites.
  • Portal hypertension → gastrointestinal wall congestion and edema → gastrointestinal ulceration →hematemesis and melena.


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


Presenting Problems

Client History

  • Anorexia.
  • Depression.
  • Vomiting.
  • Diarrhea.
  • Polydipsia/polyuria.
  • Behavioral changes.
  • Abdominal enlargement.
  • Jaundice.
  • Seizures.
  • Coma.
  • Bleeding tendency.

Clinical Signs

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

Diagnostic Investigation

Biochemistry2-D Ultrasonography
  • Abdominal examination Ultrasonography: liver to identify pancreatic disease, gall bladder disease Liver: gall bladder sediment 01- ultrasound.
  • Evaluation of hepatic parenchyma Liver normal vessels - ultrasound , identification of diffuse or focal lesions.
  • Liver normal to enlarged size.
  • Liver biopsy to determine etiology if initial tests non-diagnostic - may perform at laparotomy or by ultrasound guided percutaneous biopsy Biopsy: hepatic.
    Check for possible coagulopathy prior to biopsy.
  • Fine needle aspiration of limited use in diagnosis of acute liver disease except in lymphoma.
  • Microbiology:
    • Blood culture Blood: culture to identify bacteremia.
    • Culture of bile can be very useful in cases of acute bacterial cholangiohepatitis.
  • Serology:
  • Urinalysis:
    • Dark field examination to identify Leptospira spp.
      This test has a relatively low sensitivity and specificity for the detection of leptospirosis.
    • Bilirubin may be present Blood biochemistry: direct bilirubin.
    • Ammonium urate crystals may be visible, especially in animals with portosystemic shunts.

Histopathology Findings

  • Predominant change is moderate/severe hepatic necrosis (centrilobular to massive) - might be prudent to stain for Helicobater spp in cases of hepatobiliary disease.
  • Varies with cause, eg mild multifocal to extensive hepato-cellular necrosis, ballooning degeneration, and apoptosis. Bridging necrosis with lobular collapse seen in liver of dogs with carprofen-induced acute hepatic illness.

Differential Diagnosis


Initial Symptomatic Treatment

  • Cage rest to optimize conditions for hepatic regeneration and prevent scarring.
  • Intravenous fluids Fluid therapy to maintain fluid balance.
  • Intravenous diazepam Diazepam or other anticonvulsants (with care) if seizuring.

Standard Treatment

  • Dextrose added to intravenous fluids if hypoglycemic Fluid therapy.
  • Potassium chloride Potassium chloride / gluconate added to intravenous fluids if hypokalemic or anorexic.
  • Antibiotics Therapeutics: antimicrobial drug to counter primary and secondary infections and reduce gut ammonia production.
    Use broad spectrum agents safe for use in liver disease (avoid potentiated sulphonamides and tetracyclines).
  • If encephalopathy, may use enemas to remove substrates for bacterial metabolism, ampicillin Ampicillin or amoxicillin Amoxicillin and lactulose Lactulose to minimize ammonia and other toxin production.
    Check glucose and potassium level if showing signs of hepatic encephalopathy.
  • Discontinue previous medication if possible.
  • If hepatotoxicity is due to phenobarbitone Phenobarbital consider changing to potassium bromide Potassium bromide or gabapentin Gabapentin.
  • Steroids are generally NOT indicated and may actually worsen clinical signs as they increase water retention (ascites) and risk of gastrointestinal ulceration.
  • High quality protein diet if evidence of hepatic encephalopathy Hepatic encephalopathy. Do not limit protein excessively as this will slow hepatic regeneration. Low fat diet if vomiting.
  • Treat ascites with spironolactone Spironolactone + - frusemide Furosemide.
  • Metoclopramide Metoclopramide if vomiting. This is most effectively administered added to the intravenous fluids and given as a 24 hour infusion.
  • Vitamin K Vitamin K if coagulopathy.
  • Fresh frozen plasma or whole blood if actively bleeding.
  • H2 blockers, eg ranitidine Ranitidine or omeprazole Omeprazole and gastrointestinal protectants, eg sucralfate Sucralfate if gastric bleeding.
  • Anti-oxidants such as SAMe or silymarin (milk thistle) especially if toxic cause.
  • Ursodeoxycholic acid Ursodeoxycholic acid to remove toxic bile acids. Do not use in complete biliary obstruction (rare to occur in dogs).


Subsequent Management


  • Minimize exercise.


  • Serum biochemistry weekly.
  • If persistent abnormalities, follow-up liver biopsy Biopsy: hepatic.
    Beware that serum enzyme activity, especially ALT, can continue to be raised for several weeks following an acute hepatic insult as they are also increased in hepatic regeneration.



  • 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 hepatitis.
  • May result in cirrhosis.

Expected Response to Treatment

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

Reasons for Treatment Failure

  • Failure to identify and treat underlying disease/inciting factor.
  • Failure to reverse may lead to fibrosis of liver and permanent damage → cirrhosis Liver: cirrhosis.

Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Watson P J (2004) Chronic hepatitis in dogs: a review of current understanding of the aetiology, progression and treatment. Vet J 167 (3), 228-41 PubMed.
  • Toshach K, Jackson M V V & Dubielzig R R (1997) Hepatocellular necrosis associated with SC injection of an intranasal bordetella bronchiseptica - canine parainfluenza vaccine. JAAHA 33 (2), 126-128 PubMed.
  • Maddison J E (1992) Hepatic encephalopathy. Vet Intern Med 6 (6), 341-353 PubMed.
  • Meyer D J & Williams D A (1992) Diagnosis of hepatic and exocrine pancreatic disorders. Semin Vet Med and Surg 7 (4), 275-284 PubMed.
  • Dayrell-Hart B, Steinberg S A, VanWinkle T J & Farnbach G C (1991) Hepatotoxicity of phenobarbital in dogs: 18 cases. JAVMA 199 (8), 1060-1066 PubMed.

Other sources of information

  • Scherk M A & Center S A (2005)Toxic, Metabolic, Infectious and Neoplastic Liver diseases.In:Textbook of Veterinary Internal Medicine. 5th edn. Eds: S J Ettinger & E C Feldman. Philadelphia: W B Saunders. pp 1464-1477.
  • 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.
  • Center S A (1996)Acute hepatic injury: hepatic necrosis and fulminant hepatic failure. In:Strombeck's Small Animal Gastroentererology. Eds W G Guilford. W B Saunders, Philadelphia. pp 654-705.
  • Watson T (1996)Nutritional management of canine liver disease.Waltham Symposium, Birmingham. pp 42-46.

Other Sources of Information