ISSN 2398-2950      

Liver: acute disease

ffelis

Introduction

  • Cause: overwhelming toxic or metabolic (eg lipidosis) insult, neoplasia or infection; acute on chronic liver disease.
  • Signs: non-specific; anorexia, vomiting, depression +/- polydipsia/polyuria; signs of hepatic encephalopathy.
  • Diagnosis: biochemistry, ultrasonography, hepatic biopsy.
  • Treatment: underlying cause if recognized; otherwise supportive and symptomatic.
  • Prognosis: depends on etiology, severity and treatment of inciting factor.
  • See also Liver: chronic disease Liver: chronic disease.

Pathogenesis

Etiology

Infection

  • Viral: FeLV Feline leukemia virus disease, FIP Feline infectious peritoniti , (usually chronic presentation).
  • Bacterial: extension of neutrophilic cholangitis* (previously suppurative cholangiohepatitis) Liver: cholangitis, or hematogenous.
  • Mycotic: eg, histoplasmosis Histoplasma capsulatum, if associated with pulmonary disease.
  • Protozoal, ie toxoplasma Toxoplasmosis.
  • Parasitic: liver flukes (not in UK).
  • * Based on WSAVA recommendations the classification of feline liver disease has been clarified and is now:
    • Neutrophilic cholangitis (acute and chronic).
    • Lymphocytic cholangitis (acute and chronic).
    • Chronic cholangitis (fluke infestation in endemic areas).

Immune mediated

  • Lymphocytic cholangitis (acute and chronic, previously cholangiohepatitis).

Hepatotoxins

Cats have a relative sensitivity to many drugs due to low levels of glucuronyl transferase delaying metabolism.

Metabolic

Specific

  • Unvaccinated animals.

Pathophysiology

  • Overwhelming 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 extensive 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.
  • Decreased production of albumin   →  hypoalbuminemia.
  • Failure to detoxify ammonia and other mercaptans from intestine   →  hepatic encephalopathy Hepatic encephalopathy.

Timecourse

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

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.
  • Center S A, Warner K, Corbett J et al (2000) Proteins invoked by vitamin K absence and clotting times in clinically ill cats. JVIM 14 (3), 292-297 PubMed.
  • Center S A (1999) Chronic liver disease - current concepts of disease mechanisms. JSAP 40 (3), 106-114 PubMed.

Other sources of information

  • Marks S L (2008) Feline hepatic disorders: update on diagnosis and management. Proceedings of the 51st BSAVA Congress, pp 201-205.
  • Rothuzien J, Bunch S E, Cullen J M, Charles J A, Desmet V J, Twedt D C, van den Ingh T, van Winkle T, Washabua J (eds) (2006) WSAVA Liver Standardization Group. Standards for Clinical and Histological Diagnosis of Canine and Feline Liver diseases. Saunders/Elsevier, Edinburgh.
  • Michel R (1995) Nutritional management of liver disease. Veterinary Clinics North America (SA) 25, 485.

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