Читать книгу Canine and Feline Epilepsy - Luisa De Risio - Страница 84

Hepatic encephalopathy (HE) is a biochemical disorder of the brain secondary to various hepatic disorders such as congenital and acquired portosystemic shunt, micro-vascular dysplasia, congenital urea-cycle enzyme deficiencies, and acute or chronic severe parenchymal liver damage associated with cirrhosis, neoplasia, chronic active hepatitis, liver steatosis (lipidosis) in cats or toxicosis (Hardy, 1990). HE is more common in dogs than in cats.

Congenital portosystemic shunts represent the most common cause of HE. They generally occur as single vessels that provide direct vascular communication between the portal venous supply and the systemic venous circulation (caudal vena cava or azygous vein), bypassing the liver, and are not associated with portal hypertension. Approximately 25% to 33% of congenital portosystemic shunts are intrahepatic and the remainder are extrahepatic in dogs and cats (Berent and Tobias, 2009). The majority of intrahepatic portosystemic shunts occur in large or giant breed dogs, whereas most extrahepatic portosystemic shunts are seen in small and toy breed dogs (Berent and Tobias, 2009). In animals with congenital portosystemic shunts, the liver has been deprived of growth factors from birth and is therefore abnormally small with a hypofunctional parenchymal mass.

Acquired portosystemic shunts are usually multiple, extrahepatic and occur in animals with chronic portal hypertension secondary to hepatic arteriovenous malformations, noncirrhotic portal hypertension, or chronic hepatitis and cirrhosis (Berent and Tobias, 2009). Portosystemic shunts (congenital or acquired) occur far more commonly in dogs than in cats.

Hepatic microvascular dysplasia is a microscopic malformation of the hepatic micro-vasculature resulting in shunting of portal blood into the systemic circulation. Micro-vascular dysplasia can occur as an isolated disease or in association with macroscopic portosystemic shunts and can occur with or without concurrent portal hypertension. Hepatic microvascular dysplasia has been reported most commonly in the cairn terrier and Yorkshire terrier (Christiansen et al., 1995).

Urea-cycle enzyme deficiencies are rare congenital errors of metabolism in which one of the enzymes involved in ammonia metabolism fails.

Parenchymal hepatic diseases severely decrease the capacity of the liver to remove toxic products of intestinal metabolism and synthesize factors necessary for normal cerebral function.

The pathophysiology of HE is complex, multifactorial and incompletely understood (Box 4.2). The reader is referred to the cited references for a more detailed description of HE pathophysiology.