Liver: chronic disease in Cats (Felis) | Vetlexicon
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Liver: chronic disease

ISSN 2398-2950


Introduction

  • Cause: malformation, toxicity, neoplasia, endocrinopathy, metabolic (lipidosis), auto-immune (lymphocytic cholangitis), infection.
  • Signs: non-specific - lethargy, anorexia, vomiting. Signs of hepatic encephalopathy.
  • Diagnosis: biochemistry, hepatic function tests, ultrasonography, hepatic biopsy.
  • Treatment: elimination of cause, supportive.
  • Prognosis: depends on severity and treatment of inciting factor.
  • See also Liver: acute disease Liver: acute disease.
    Print off the owner factsheet Liver problems in your cat  Liver problems in your cat  to give to your client.

Presenting signs

  • Insidious onset when reserve functional capacity is lost (>60%).
  • Anorexia Anorexia, depression.
  • Vomiting, diarrhea.
  • Abdominal distension (ascites).

Acute presentation

  • End-stage liver failure.

Age predisposition

  • <5 yrs - lymphocytic cholangitis and feline infectious peritonitis.
  • >6 yrs - hyperthyroidism.
  • >10 yrs - neoplasia.
  • Middle aged - hepatic lipidosis.

Cost considerations

  • Long-term therapy can be expensive.
  • Expenses incurred in establishing a diagnosis.

Special risks

  • Anesthesia - as many commonly used drugs are metabolized in liver.
    Warn owner of increased risk of anesthesia.

Pathogenesis

Etiology

  • Idiopathic chronic hepatitis.
  • Drugs - cats have a relative sensitivity to many drugs due to low levels of glucuronyl transferase delaying metabolism, eg acetaminophen, griseofulvin, megestrol acetate, ketoconazole.
  • Infectious, eg FeLV Feline leukemia virus, FIP Feline sarcoma virus; bacterial, fungal and parasitic.
  • Portosystemic shunt (congenital) Congenital portosystemic shunt (CPSS).
  • Neoplasia, lymphoma Lymphoma or metastatic.
  • Endocrinopathies.

Pathophysiology

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

Diagnosis

Presenting problems

  • Lethargy.
  • Anorexia.
  • Vomiting Vomiting.
  • Diarrhea.
  • Polydipsia/polyuria.
  • Icterus.
  • Neurological signs.

Client history

  • Lethargy.
  • Decreased appetite.
  • Behavioral changes.
  • Nausea.
  • Vomiting.
  • Diarrhea.
  • Polydipsia/polyuria.
  • Abdominal distension (ascites).

Clinical signs

  • Unkempt hair coat.
  • Ascites Ascites 01: whole cat  Ascites 02: whole cat  Ascites 03: whole cat .
  • Icterus.

Signs of hepatic encephalopathy

  • May occur with portosystemic shunt Congenital portosystemic shunt (CPSS), acute or end-stage liver disease.
  • Behavior changes - dementia, dullness, aggression.
  • Neurological abnormalities - circling, ataxia, head pressing, aimless pacing, seizures.
  • Ptyalism Ptyalism in a kitten with a portosystemic shunt .
  • Coma.

Diagnostic investigation

Biochemistry

Hematology

  • To check for hemolytic disease.

Histopathology

Exclude systemic causes of enzyme elevation, eg hyperthyroidism, before undertaking invasive diagnostic procedures.

  • Fine needle aspiration (FNA Fine-needle aspirate).
  • Percutaneous blind or ultrasound guided needle biopsy.
  • Laparoscopy-guided biopsy.
  • Laparotomy Laparotomy: midline (evaluate clotting function before biopsy).

2-D Ultrasonography

  • Doppler ultrasound Liver: normal - ultrasound - ascites   Abdomen: ascites - DV ultrasound , portosystemic shunt.
  • Evaluate parenchyma and biliary system.
  • Multifocal radiolucencies - neoplasia or infection/abscessation.
  • Identify focal lesions.
  • Guide needle biopsy.
    If there is no dilation of the extrahepatic biliary tract, and no hemolytic disease in the presence of jaundice, hepatocellular disease is likely   →   take liver biopsy.
  • Diffuse echogenicity - hepatic lipidosis.

Radiography

  • Liver size is often normal.
  • Hepatomegaly.
  • Small (microhepatica   Liver: microhepatica - radiograph lateral  ) - portosystemic shunt.
  • Focal masses.
  • Choleliths.
  • Contrast study - to identify portosystemic shunt Liver: portosystemic shunt (acquired 02) - portovenography  .

Confirmation of diagnosis

Discriminatory diagnostic features

  • Biochemistry.

Definitive diagnostic features

  • Liver biopsy.
    Wedge biopsies preferable to needle biopsies as they provide more tissue and therefore more likely to represent the pathological process.

Gross autopsy findings

  • Systematic examination of other organ systems helps interpretation of chronic disease.
  • If history consistent, consider samples for toxicology (liver, kidney, fat, urine etc - consult lab).
  • Remove brain and fix whole if likely hepatic encephalopathy.
  • Swollen, pale, nodular liver.
  • Shrunken liver late in disease process.
  • Variable-sized regenerative nodules.
  • Focal/multifocal masses.

Histopathology findings

  • Frozen sections best demonstrate lipidosis, but formalin fixation acceptable.
  • Varies with cause, eg:
    • Moderate to severe inflammation associated with 'piece-meal' necrosis of hepatocytes; begins in portal triad and extends into parenchyma.
    • Small islands of hepatocytes surrounded by inflammatory cells (lymphocytes, plasma cells, sometimes neutrophils)   →   bridging necrosis   →   active cirrhosis.
    • Special stains for copper accumulation (Rubeanic acid, Rhodamine).
    • Fibrosis and parenchymal nodules that disrupt normal hepatic architecture.
    • Presence of specific neoplastic cells, especially metastatic.

Differential diagnosis

Primary liver diseases

Secondary liver diseases

Causes of jaundice

Causes of ascites

Treatment

Standard treatment

  • Antibiotics Therapeutics: antimicrobial drug  Therapeutics: gastrointestinal system to prevent secondary infections and to reduce gut ammonia production.
  • H2 receptor blockers, eg ranitidine Ranitidine or cimetidine Cimetidine.
  • Sucralfate Sucralfateif gastrointestinal bleeding.
  • Spironolactone Spironolactone if ascites; if refractory, try furosemide Furosemide.
  • Lactulose Lactulose and antibiotics for hepatic encephalopathy.
  • Feed high quality protein diet Dietetic diet: for liver insufficiency.
    Cottage cheese alone is inadequate as a protein source in cats. It is deficient in arginine which is essential in the urea cycle and therefore very important in liver disease.
  • Protein restriction only indicated if there is encephalopathy.
    Protein restriction can seriously impair liver's ability to regenerate and indiscriminate restriction may reduce or prevent recovery since cats have a high protein requirement.
  • Vitamin and zinc Zinc supplementation may be required.
  • Cage rest.
  • Ursodeoxycholic acid Ursodeoxycholic acid to displace toxic bile acids, stimulate bile flow and modulate immune response.

Subsequent management

Treatment

  • Repeat hepatic function tests and hepatic biopsy.

Prevention

Outcomes

Prognosis

  • Depends on underlying cause and degree of hepatic damage.

Expected response to treatment

  • Clinical improvement.
  • Resolution of hepatic pathology.

Reasons for treatment failure

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Godfrey D R & Rest J R (2000) Suspected necrolytic migratory erythema associated with chronic hepatopathy in a cat. JSAP 41 (7), 324-328 PubMed.
  • Center S A (1999) Chronic liver disease - current concepts of disease mechanisms. JSAP 40 (3), 106-114 PubMed.

Other sources of information

  • Johnson S E (2000) Chronic hepatic disorders. In:Textbook of Veterinary Internal Medicine.5th edn. Ettinger S J & Feldman E C (eds). W B Saunders, Philadelphia. pp 1298-1325.
  • Laflamme D P (2000) Nutritional management of liver disease. In:Kirk's Current Veterinary therapy XIII.Bonagura J D (ed). W B Saunders, Philadelphia. pp 693-697.
  • Center S A (1996) Feline hepatic disease - Current therapeutic concepts. Proceedings of BSAVA Waltham Symposium on liver disease. pp 56-63.
  • Watson T (1996) Nutritional management of canine liver disease. Proceedings of BSAVA Waltham Symposium on liver disease.pp 42-46.
  • Michel R (1995) Nutritional management of liver disease. Vet Clin North Am Small Anim Pract 25, 485.