Hepatic encephalopathy

From Dog

Hepatic encephalopathy (HE) is a clinical syndrome characterised by neurological depression as a result of liver disease.

The neurological abnormalities associated with this condition are attributed to elevated levels of circulating ammonia, mercaptans, aromatic amino acids, gamma amino butyric acid and short-chain fatty acids. These circulating chemicals are normal metabolized by the liver and elevated levels result in their crossing the blood-brain barrier and inciting central nervous dysfunction.

In dogs, hepatic encephalopathy is associated with:

Affected dogs develop clinical symptoms of depression, mental dullness, central or amaurotic blindness, polyuria, polydipsia, anorexia, vomiting and occasionally seizures[9].

Temporary resolution of clinical signs may be associated with antimicrobial therapy, due to reduced colonic bacteria. Affected dogs may also have prolonged recovery from sedation or anaesthesia.

Hepatic encephalopathy is not a diagnosis per se, rather a clinical state due to an underlying disease. Elevated levels of circulating ammonia are confirmatory of this condition, but a full investigation of cause is required to establish a correct diagnosis.

The use of ultrasonography is indicated to detect portosystemic shunt or portal hypertension[10].

Specific treatment for hepatic encephalopathy is achieved by decreasing the formation of gut-derived encephalotoxins[11] via temporary food withholding and use of colonic irrigation with antimicrobials. Use of intravenous fluids is recommended to correct any metabolic derangements.

Feeding a high quality low-protein diet appears to be an essential component of this strategy. Protein is broken down by enteric bacteria into ammonia, which is a potent encephalotoxin that readily crosses the blood-brain barrier. Reduction of protein in the gastrointestinal tract limits subsequent bacterial degradation and thus reduces the potential for hyperammonemia[12]. Soy-based appear to offer a better response compared to meat-based diets and decreases the risk for hepatic encephalopathy as well as better support of liver function[13].

Other recommended treatments include oral administration of lactulose to acidify the gastrointestinal tract and antimicrobial therapy to reduce enteric bacterial load[14].


  1. Gow AG et al (2012) Dogs with congenital porto-systemic shunting (cPSS) and hepatic encephalopathy have higher serum concentrations of C-reactive protein than asymptomatic dogs with cPSS. Metab Brain Dis 27(2):227-229
  2. Mertens M et al (2010) Diagnosis of congenital portosystemic shunt in miniature schnauzers 7 years of age or older (1997-2006). J Am Anim Hosp Assoc 46(4):235-240
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  10. Duque J et al (2011) Imaging diagnosis-transcranial color-coded duplex sonography in a dog with hepatic encephalopathy. Vet Radiol Ultrasound 52(1):111-113
  11. Johnson SE (1987) Portal hypertension. Part II. Clinical assessment and treatment. Compend Contin Educ Pract Vet 9:917–928
  12. Bunch SE (1994) Specific and symptomatic medical management of diseases of the liver. In: Ettinger SJ Feldman EC, , editors. Textbook of Veterinary Internal Medicine. Philadelphia: WB Saunders
  13. Proot S et al (2009) Soy protein isolate versus meat-based low-protein diet for dogs with congenital portosystemic shunts. J Vet Intern Med 23(4):794-800
  14. Fredholm D (2009) Multiple acquired extrahepatic portosystemic shunts secondary to veno-occlusive disease in a young German shepherd. Can Vet J 50(7):763-766