Canis ISSN: 2398-2942

Liver: toxic hepatitis

Contributor(s): Nick Bexfield, Kyle Braund

Introduction

  • Same as: acute hepatic disease Liver: acute disease.
  • Cause: ingestion of plant toxins, chemicals, therapeutic agents, insect envenomation.
  • Signs: non-specific; those of acute hepatitis including anorexia, lethargy, vomiting, diarrhea, jaundice.
  • Diagnosis: recognition of acute hepatic failure, history of exposure to toxin.
  • Treatment: supportive and elimination of toxin if recognized.
  • Prognosis: depends on toxin and severity of hepatic insult.

Pathogenesis

Etiology

Drugs

Chemicals

  • Arsenic Arsenic toxicity.
  • Carbon tetrachloride.
  • Chlorinated hydrocarbons.
  • Heavy metals.
  • Phosphorus.
  • Phenols.

Plant toxins

  • Mushrooms (Amanita phalloides;A. vernaMushroom poisoning.
  • Aflatoxins/mycotoxins Mycotoxicoses.
  • Blue-green algae; cyanobacteria.
  • Cycad palm seeds (Cycadaceaespp) Cycad palms.
  • Chinaberry tree (Melia azedarach).

Envenomation

Endotoxins and enterotoxins

Pathophysiology

  • 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 Hypoglycemia.
  • Decreased production of albumin →hypoalbuminemia Hypoproteinemia.
  • 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.

Timecourse

  • Within hours of ingestion of toxin.
  • Less than or equal to 2 weeks duration with no previous evidence of hepatobiliary disease.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • MacPhail C M, Lappin M R, Meyer D J et al (1998) Hepatocellular toxicosis associated with administration of carprofen in 21 dogs. JAVMA 212 (12), 1895-1901 PubMed.
  • Bunch S E (1993) Hepatotoxicity associated with pharmacologic agents in dogs and cats. Vet Clin North Am Small Anim Pract 23 (3), 659-670 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.
  • Ortega L, Landa Garcia J I, Torres Garcia A et al (1985) Acetaminophen-induced fulminant hepatic failure in dogs. Hepatology (4), 673-676 PubMed.
  • Vogel G, Tuchweber B, Trost W & Mengs U (1984) Protection by silibinin against Amanita phalloides intoxication in beagles. Toxicol Appl Pharamacol 73 (3), 355-362 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. 6th end. Eds: S J Ettinger & E C Feldman. Philadephia: W B Sunders. pp 1464-1477.
  • Center S A (1996)Acute hepatic injury: hepatic necrosis and fulminant hepatic failure.In:Strombeck's Small Animal Gastroenterology. Eds: W G Guilford. Philadelphia: W B Saunders. pp 654-705.


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