Felis ISSN 2398-2950
Liver: acute disease
Contributor(s): Mark W Jackson, Philip K Nicholls, Penny Watson
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
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
This article is available in full to registered subscribers
Sign up now to purchase a 30 day trial, or
Login
Treatment
This article is available in full to registered subscribers
Sign up now to purchase a 30 day trial, or
Login
Outcomes
This article is available in full to registered subscribers
Sign up now to purchase a 30 day trial, or
Login
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.