Hepatic Encephalopathy

Hepatic encephalopathy has been recognized in animals with PSS, end-stage liver disease, and congenital urea cycle enzyme deficiencies. Clinical signs include depression, dementia, stupor, and coma. Muscle tremors, motor abnormalities, and focal and generalized seizures have also been reported. The etiology of hepatic encephalopathy is probably dependent on several factors, including circulating toxins, alterations in amino acid concentrations, and increased cerebral sensitivity to drugs and toxins. Toxins that have been implicated in hepatic encephalopathy include ammonia, mercaptans, short chain fatty acids, indoles, aromatic amino acids, and biogenic amines.

Precipitating factors of hepatic encephalopathy include diuretics, protein overload, hypokalemia, alkalosis, and transfusion of stored red cells, hypoxia, hypovolemia, gastrointestinal hemorrhage, infection, and constipation. Increased cerebral sensitivity to sedative, analgesic, and anesthetic agents may induce coma in animals with PSS, even when normal dosages are used. Protein overload and gastrointestinal hemorrhage provide substrates for bacterial production of ammonia, and constipation can increase retention and absorption of ammonia and other encephalopathic substances. Blood which has been stored for 24 hours contains 170 ug of ammonia/dL, and ammonia concentrations will continue to increase with prolonged storage.

All information on this page is courtesy of the University of Tennessee Veterinary Medicine Website