Hepatic encephalopathy in Cats (Felis) | Vetlexicon
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Hepatic encephalopathy

ISSN 2398-2950

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  • Cause: underlying disorders eg congenital portosystemic shunts (PSS) Congenital portosystemic shunt (CPSS), urea cycle enzyme deficiencies or acquired PSS secondary to other hepatic disease.
  • Signs: alteration in behavior, eg head pressing, disorientation, seizures, ataxia, depression and collapse +/- gastrointestinal signs, weight loss.
  • Episodes may be related to feeding.
  • Hypersalivation  Ptyalism in a kitten with a portosystemic shunt is a common manifestation in cats.
  • Diagnosis: signs and biochemical assays.
  • Treatment: reduction in ammonia and mercapten production; antibiotics and reduced protein diet.
  • Emergency if in hepatic coma.
  • Prognosis: acute crisis can often be managed; long term prognosis depends on cause of liver dysfunction.

Presenting signs

  • History: abnormal behavior, often episodic in nature.
  • Clinical signs:
    • Disorientation.
    • Head pressing.
    • Seizures.
    • Ataxia.
    • Compulsive behavior (circling, aimless wandering, vocalizing).

Acute presentation

  • Hepatic coma.

Age predisposition

  • Congenital portosystemic shunts: usually < 1 year (may present later).
  • Urea cycle enzyme deficiencies: young (6 months to 3 years).
  • Chronic hepatic disease: usually older individuals.

Cost considerations

  • Medical management of acquired shunts.

Special risks

General anesthesia

  • Reduced metabolism and increased activity of anesthetic drugs particularly phenothiazines, barbiturates and benzodiazepines.
  • Hypoxia due to seizure activity and compromise of the airway will lead to cytotoxic brain edema and possibly raised intracranial pressure, therefore oxygen supply should be monitored carefully.
  • Monitoring portal venous pressure to avoid portal hypertension due to the ligating process will reduce complications.



Congenital portosystemic shunts

  • Venous malformations connecting the portal and systemic circulations permitting portal blood to circumvent the liver.
  • May be intra- or extrahepatic Congenital portosystemic shunt (CPSS):
    • Portocaval shunts.
    • Portoazygous shunts.
    • Persistent ductus venosus (less common).
  • Blood is diverted away from the liver thus preventing toxins from being metabolized.

Acquired portosystemic shunts

  • Secondary to chronic hepatic disease: end-stage hepatic fibrosis leads to increased resistance to intrahepatic blood flow causing collateral circulation pathways to develop which bypass the liver.
    Acquired shunts are very rare in cats.

Predisposing factors



  • Portal blood bypassing liver (congenital shunts) and/or hepatic dysfunction   →   toxins accumulating in the blood   →   neurological deficits.
  • Toxins implicated include:
    • Ammonia.
    • GABA/benzodiazepine.
    • Glutamate.
    • Methionine.
    • Reduced branched chain amino acids.
    • Increased short chain fatty acids.
    • Increased aromatic amino acids.
    • Manganese.
    • TNF-alpha.
    • Reactive oxygen species/reactive nitrogen species.
  • There are several theories as to the pathogenesis of hepatic encephalopathy and origin is probably multifactorial.
  • Excess [blood ammonia ] produced by action of gut bacteria on dietary protein is probably important but still controversial since the degree of correlation between hepatic encephalopathy severity and blood ammonia concentration is variable. Ammonium ions are detoxified predominantly in the liver via the urea cycle, with resultant production of glutamine. In liver failure, hepatic ammonia detoxification is ineffective, leading to hyperammonemia. The brain lacks a urea cycle and relies on production of glutamine for detoxification of ammonia, wnhich is a direct neurotoxin acting via chloride channel inhibition. 
  • Hepatic dysfunction   →   changes in the circulating amino acid composition - decrease in the concentration of branch chain amino acids and increase in the concentration of aromatic amino acids.
  • Branch chain amino acids are required for the production of excitatory neurotransmitters, levels of which decrease.
  • Aromatic amino acids are metabolized to produce 'false' neurotransmitters, which increase in concentration, thus causing the neurological signs.
  • Manganese is excreted via the hepatobiliary route and its concentration increases in liver disease. Patients with chronic liver disease and hepatic encephalopathy have increased brain manganese concentration, although whether this is causative or coincidental is unknown. Manganese-induced neurotoxicity causes astrocyte dysfunction, neuronal loss and gliosis.
  • Increases in brain glutamate (an excitatory neurotransmitter).
  • Increased cerebral concentration of an endogenous benzodiazepine-like substance. The GABAergic theory suggests hepatic encephalopathy is due to increased circulating levels of GABA derived from the gastrointestinal tract, although the theory has been modified to include the involvement of endogenous benzodiazepines, which are also increased in hepatic encephalopathy patients.
  • Circulating levels of tumor necrosis factor-a (THF-a), a proinflammatory cytokine are increased in liver failure patients and appear to correlate with HE severity. In liver failure, TNF-a production increases whilst TNF-a clearance may be reduced. Pathological derangements of the brain in HE may be induced in part by TNF-a excess. The TNF-a hypothesis links a nmber of the other hypotheses together. TNF-a increases CNS endothelial ammonia diffusion, enhances glutamate receptor-mediated neurotoxicity and is associated with significantly increased levels of GABA. Additionally, THF-a increases peripheral type benzodiazepine receptors and excess manganese potentiates in vitro production of TNF-a.


Presenting problems

  • Behavioral changes.
  • Ptyalism.
  • Poor body condition.

Client history

  • Ptyalism.
  • Abnormal behavior, often episodic.
  • Episodes may be related to feeding.
  • Affected individuals may be in poor body condition.

Clinical signs

  • Hypersialism Ptyalism in a kitten with a portosystemic shunt .
  • Disorientation.
  • Head pressing.
  • Seizures.
  • Ataxia.
  • Collapse.
  • Signs often episodic.
  • Blindness.
  • Hepatic coma.

Diagnostic investigation



Coagulation tests


  • Ammonium urate crystalluria.
  • Low concentration common.


  • Small liver outlines on plain radiographs Liver: microhepatica - radiograph lateral in about 50% of congenital portosystemic shunts.
  • Renomegaly.

Contrast radiography

  • Contrast venography Liver: portosystemic shunt (acquired 02) - portovenography may reveal presence and position of a portosystemic shunt Liver: portosystemic shunt (acquired 02) - portovenography .

2-D Ultrasonography

  • Identification of shunts.
  • May reveal radiolucent renal calculi in bladder.
  • Altered hepatic echogenicity in acquired portosystemic shunts.
  • Color-flow Doppler assists in shunt localization.


  • Administration of per rectum Technetium 99 produces increased fraction in heart before hepatic uptake in animals with portosystemic shunts.


  • Scintography/radioisotope studies: for demonstration of hepatic shunting Scintigraphy: hepatic for PSS.
  • Contrast-enhanced magnetic resonance angiography.
  • Time-of-flight magnetic resonance angiography.

Confirmation of diagnosis

Discriminatory diagnostic features

  • Clinical signs.
  • Biochemistry.

Definitive diagnostic features

  • Radiography (contrast venography).
  • Ultrasonography.
  • Scintigraphy.
  • MRI of abdomen.

Gross autopsy findings

  • Portosystemic shunt.
  • Small liver.
  • End-stage hepatic fibrosis.


Initial symptomatic treatment

  • Fluid therapy Fluid therapy: overview in hepatic coma.
    Avoid fluid overload.
  • If necessary administer mannitol Mannitol (0.5-1 g/kg IV over 30 mins) if cerebral edema suspected.
  • Starve and give parenteral +/- colonic antibiotics and lactulose enemas (<20 ml/kg made of three parts lactulose diluted in seven parts warm water, q4-6 h) to reduce ammonia production and absorption.
  • Decrease colonic toxin production and absorption by the use of enemas (20% lactulose TID).
  • Intravenous branch chain amino acids in hepatic coma have been used experimentally.

Standard treatment

  • Surgical ligation of single, uncomlicated extrahepatic or intrahepatic shunt Congenital portosystemic shunt: attenuation is the most direct treatment.
  • Optimal goal is total ligation; may not be tolerated leading to acquired portosystemic shunt.

Medical management

  • Restricted protein diet Dietetic diet: for liver insufficiency.
    Feed maximal protein level without development of neurological signs since over restriction can seriously affect liver's ability to regenerate.
  • Oral antibiotics eg ampicillin Ampicillin or metronidazole Metronidazole to reduce the population of bacteria in the large intestine.
  • Lactulose Lactulose (0.5 ml/kg TID titrating dose to produce soft but not loose motions).
  • Fluid therapy Fluid therapy: for electrolyte abnormality if in hepatic coma. Ensure animal is not hypoglycemic or hypokalemic and supplement fluids appropriately if these complications develop.
  • Status epilepticus Status epilepticus secondary to hepatic encephalopathy can be controlled with propofol Propofol (1-4 mg/kg IV for induction, given to effect followed by CRI 0.1-0.6 mg/kg/minute).





Congenital portosystemic shunt

  • Good for full recovery if treated in early stages, ie not in hepatic coma with edema.
  • Residual neurological defects including seizures may persist for long periods after recovery from hepatic coma.

Expected response to treatment

  • Improvement in animal's demeanor, weight gain and better coat condition.

Reasons for treatment failure

  • Wrong diagnosis.
  • General anesthetic complications.
  • Portal hypertension.
  • Condition too far advanced at initial presentation.

Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Cabassu J, Seim H B 3rd, MacPhail C M et al (2011) Outcomes of cats undergoing surgical attenuation of congenital extrahepatic portosystemic shunts through cellophane banding: 9 cases (2000-2007). JAVMA 238 (1), 89-93 PubMed.
  • Ruland K, Fischer A, Hartmann K (2010) Sensitivity and specificity of fasting ammonia and serum bile acids in the diagnosis of portosystemic shunts in dogs and cats. Vet Clin Pathol 39 (1), 57-64 PubMed.
  • Lipscomb V J, Lee K C, Lamb C R et al (2009) Association of mesenteric portovenographic findings with outcome in cats receiving surgical treatment for single congenital portosystemic shunts. JAVMA 234 (2), 221-228 PubMed.
  • Lipscomb V J, Jones H J, Brockman D J (2007) Complications and long-term outcomes of the ligation of congenital portosystemic shunts in 49 cats. Vet Rec 160 (14), 465-470 PubMed.
  • d'Anjou M A, Penninck D, Cornejo L et al (2004) Ultrasonographic diagnosis of portosystemic shunting in dogs and cats. Vet Radiol Ultrasound 45 (5), 424-437 PubMed.
  • Watson P J (1997) Decision making in the management of portosystemic shunts. In Practice 19 (3), 106-120 VetMedResource.
  • Maddison J E (1992) Hepatic encephalopathy. Current concepts of the pathogenesis.​ JVIM (6), 341-353 PubMed.

Other sources of information

  • Tobias K M (2003) Portosystemic shunts and other hepatic vascular anomalies .In: Textbook of Small Animal Surgery. 3rd edn, Slatter D (ed), Philadelphia, p 727.
  • Maddison J E (1994) Hepatic encephalopthy in dogs and cats. Veterinary International 6, 37-43.
  • Levy J K, Bunch S E and Komtebedde J (1995) Feline Portosystemic vascular shunts. In: Kirks Current Veterinary Therapy XII W. B. Saunders pp743-749.
  • Taboada J and Dimski D S (1995) Hepatic encephalopathy; clinical signs, pathogenesis and treatment.Veterinary Clinics of North America25, 337-355.