Hepatic encephalopathy is a neurological dysfunction that can occur secondary to hepatic disease or portosystemic shunting. In human medicine, three types of hepatic encephalopathy have been described: type A which develops secondary to acute liver failure, type B develops secondary to portosystemic shunting and type C in which hepatic encephalopathy develops due to liver cirrhosis and portal hypertension. Clinical signs associated with hepatic encephalopathy are variable and range from subtle nonspecific signs, such as apathy, to severe signs such as seizures and coma. Currently, the pathogenesis is not yet fully understood.
Although increased blood ammonia concentrations play a central role in the development of hepatic encephalopathy, many other contributing factors have been described, such as the presence of systemic inflammation, increased blood manganese concentrations, oxidative stress and decreased blood branched-chain to aromatic amino acid concentrations. Besides these, also precipitating factors have been described such as gastro-intestinal bleeding, constipation, dehydration, excessive dietary protein uptake, the presence of electrolyte and acid-base disturbances and the administration of blood products, sedatives and diuretics.
As a wide range of clinical signs are present, treatment intensity might also vary accordingly. In order to optimise the treatment of hepatic encephalopathy, it is not only important to start symptomatic treatment, but also to identify the presence of any precipitating factor and to treat these in addition. After stabilisation of the patient, the underlying cause for hepatic encephalopathy should be determined to be able to treat this as well. Blood ammonia concentrations are commonly used to determine the presence of hepatic encephalopathy. It is, however, important to keep in mind that blood ammonia concentrations can be within normal limits despite the presence of hepatic encephalopathy, and that blood ammonia concentrations are not correlated to the severity of hepatic encephalopathy. Besides, as ammonia is a labile product, accurate measurements are only possible if it is determined immediately after blood sampling, or if the sample is immediately processed and stored frozen. Symptomatic treatment consists of intravenous fluid therapy, enemas, administration of nonabsorbable disaccharides and an adapted diet. Depending on the severity and type of the clinical signs, additional drugs, such as antimicrobial and anticonvulsant drugs, might need to be added. Although a positive response to medical treatment is often seen, blood concentrations of ammonia and branched-chain to aromatic amino acids do not necessarily normalise.
Hepatic encephalopathy can be a life-threatening disease in which not only the underlying disease, but also contributing and precipitating factors need to be identified and treated, if possible, to increase not only the quality of life but also the life expectancy of these animals.
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