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:
- Portosystemic shunt
- Liver mass reduction associated with lobectomy
- Congenital diseases - e.g. defects of enzymes of the urea cycle, arginine deficiency or organic acidaemias
- Gastrointestinal hemorrhage - e.g. canine parvovirus
- High dietary protein, purine or methionine content
- Portal hypertension and portal vein aneurysm
- Congenital hepatic fibrosis
- Arterioportal fistula
- Chronic hepatitis
- Encapsulating peritoneal sclerosis
- Caroli disease
- Toxins - e.g. aflatoxicosis due to Aspergillus spp-contaminated feed
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.
Specific treatment for hepatic encephalopathy is achieved by decreasing the formation of gut-derived encephalotoxins 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. 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.
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