Portosystemic vascular anomalies in dogs and cats (Proceedings)


Portosystemic vascular anomalies in dogs and cats (Proceedings)

Nov 01, 2010

The normal liver receives arterial blood from the hepatic artery and venous blood from the portal vein. Regarding arterial blood flow, the celiac artery branches off of the aorta and the hepatic artery branches off of the celiac artery. The cranial and caudal mesenteric veins as well as the splenic vein drain into the portal vein. Blood from the hepatic artery and portal vein enters the portal triad, flows through the hepatic sinusoids to the central vein and eventually leaves the liver in the hepatic vein. The hepatic vein drains into the caudal vena cava. Portosystemic shunting is the result of portal blood entering systemic circulation without first passing through the liver and hepatic sinusoids.1,2


Portosystemic shunts may be congenital or acquired. Congenital shunts are the result of abnormal communications between the portal and systemic venous circulation including single congenital portosystemic shunts (CPSS), arterioportal fistulas and primary hypoplasia of the portal vein (PHPV). Most animals have a single type of portosystemic shunt but rarely multiple anomalies are present.1,3

Congenital portosystemic shunts can be intra or extrahepatic. In dogs intrahepatic CPSS are usually single but on rare occasions two vessels may be involved. Intrahepatic CPSS originate from the left or right portal branch and terminate in the caudal vena cava directly or via the hepatic vein of dogs.2,4 In cats intrahepatic shunts may arise from smaller branches of the portal vein.2,4 Intrahepatic portosystemic shunts account for approximately 25% - 33% of portosystemic shunts in dogs and cats.1,3

Extrahepatic CPSS may originate from the splenic vein, right gastric vein or both and enter the abdominal or thoracic caudal vena cava via the azygous vein.2,4 Splenocaval shunts are the most common form of extrahepatic CPSS in dogs.2,4 Cats do not have shunts that arise from the right gastric vein but have two additional unique types of shunts.2 One originates prior to the bifurcation of the portal branches and enters the hepatic vein or caudal vena cava.2 The second originates from the cranial mesenteric vein or portal vein and enters the left renal vein or caudal vena cava.2 Single extrahepatic portosystemic shunts account for 66% to 75% of portosystemic shunts in dogs and cats.1,3

Arterioportal fistulas (a.k.a. hepatic arteriovenous malformations) are rare in dogs and cats. These are usually congenital and result from one or, more commonly, multiple communications between hepatic arterial and portal venous circulation.1,3

Primary hypoplasia of the portal vein (a.k.a. portal vein hypoplasia) is uncommon in dogs and extremely rare in cats. Portal hypoplasia can be intrahepatic, extrahepatic or both.2 Primary hypoplasia of the portal vein can occur alone or with CPSS and arterioportal fistulas.2 Dogs and cats with only PHPV present with less severe signs later in life than those with additional shunt types.3 Milder forms of PHPV were previously referred to as microvascular dysplasia.3 Severe forms of PHPV that result in ascites, have previously been referred to as portal vein hypoplasia with portal hypertension, idiopathic noncirrhotic portal hypertension, hepatoportal fibrosis, veno-occlusive disease.3 It is now believed that these are not unrelated disease processes but different manifestations of the same malformation.1,3

Acquired vascular anomalies occur when collateral vessels open secondary to increased intrahepatic pressure (cirrhosis, arterioportal fistulas, severe forms of portal vein hypoplasia) or portal system pressures (thrombosis, compression). They occur most commonly by the left kidney and the root of the mesentery. Acquired portosystemic shunts occur in a small percentage of extrahepatic CPSS that have been banded with the ameroid constrictor.3 Ascites secondary to increased hydrostatic pressures is common.1,3

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