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Congenital PSS occurs in approximately 70% of PSS in dogs and majority of PSS in cats.  It commonly present as a single, or at most double, extrahepatic or intrahepatic anomalous vessel.  Extrahepatic PSS accounts for 63% of single shunts in dog and is more commonly found in miniature and toy-breed dogs.  Intrahepatic shunts are usually left-sided, resulting from persistent foetal [[Foetal Circulation - Anatomy & Physiology|ductus venosus]], and more common in large breed dogs.  Right-sided or central intrahepatic shunts are recognised and these may have a different embryological origin.

Congenital PSS occurs in approximately 70% of PSS in dogs and majority of PSS in cats.  It commonly present as a single, or at most double, extrahepatic or intrahepatic anomalous vessel.  Extrahepatic PSS accounts for 63% of single shunts in dog and is more commonly found in miniature and toy-breed dogs.  Intrahepatic shunts are usually left-sided, resulting from persistent foetal [[Foetal Circulation - Anatomy & Physiology|ductus venosus]], and more common in large breed dogs.  Right-sided or central intrahepatic shunts are recognised and these may have a different embryological origin.

Acquired PSS occurs in approximately 20% of PSS and often consists of multiple shunts.  They arise due to portal hypertension, following an increased resistance to portal blood flow.  This leads to opening of some of the numerous normal, non-functional microvascular communications.  Underlying causes of portal hypertension included acute fulminant hepatitis, [[Hepatic Lipidosis - WikiClinical|hepatic fibrosis]], [[Hepatic Neoplasia - WikiClinical|hepatic neoplasia]], portal vein thrombosis, hepatic arteriovenous fistulae and congenital hypoplasia of the portal vein.

Acquired PSS occurs in approximately 20% of PSS and often consists of multiple shunts.  They arise due to portal hypertension, following an increased resistance to portal blood flow.  This leads to opening of some of the numerous normal, non-functional microvascular communications.  Underlying causes of portal hypertension included acute fulminant hepatitis, [[Hepatic Lipidosis - WikiClinical|hepatic fibrosis]], [[Hepatic Neoplasia - WikiClinical|hepatic neoplasia]], portal vein [[Thrombosis - Pathology|thrombosis]], hepatic arteriovenous fistulae and congenital hypoplasia of the portal vein.

The pathophysiology of PSS relates to the shunting of blood directly from the systemic circulation, resulting in hyperammonaemia and [[Hepatic Encephalopathy]].

The pathophysiology of PSS relates to the shunting of blood directly from the systemic circulation, resulting in hyperammonaemia and [[Hepatic Encephalopathy]].