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.

• Drugs: anticonvulsants, azathioprine Azathioprine, ketoconazole Ketoconazole, methoxyflurane Methoxyflurane, sulfonamides Trimethoprim, tetracycline Tetracycline .
• Chemicals: carbon tetrachloride, heavy metals, selenium, tannic acid.
• Biological substances: aflatoxin, blue-green algae.

Metabolic

• Acute pancreatitis Pancreatitis, acute hemolytic anemia Anemia: immune-mediated hemolytic, hepatic lipidosis Liver: lipidosis, trauma Trauma: overview, heat stroke Hyperthermia.

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

Treatment

Outcomes