Changes

| Also known as:

| Also known as:

| '''Portocaval Shunt<br>

| '''Portocaval Shunt<br>

| '''Patent Ductus Venosus'''

'''Patent Ductus Venosus'''

|-}

|-}

==Description==

==Description==

'''Portosystemic shunts (PSS)''' are anomalous vascular connections between the portal and systemic venous systems.  This allows for some portal blood draining from the [[Alimentary - Anatomy & Physiology #Stomach|stomach]], [[Alimentary - Anatomy & Physiology #Small Intestine|intestines]], [[Pancreas - Anatomy & Physiology|pancreas]] and [[Spleen - Anatomy & Physiology|spleen]] to bypass the [[Liver - Anatomy & Physiology|liver]] and drains directly into the systemic circulation.  PSS may be congenital or acquired secondary to portal hypertension.

'''Portosystemic shunts (PSS)''' are anomalous vascular connections between the portal and systemic venous systems.  These vessels shunt blood from the '''hepatic portal vein''' (deriving from the [[Alimentary - Anatomy & Physiology #Stomach|stomach]], [[Alimentary - Anatomy & Physiology #Small Intestine|intestines]], [[Pancreas - Anatomy & Physiology|pancreas]] and [[Spleen - Anatomy & Physiology|spleen]]) directly into '''systemic venous system''', bypassing the [[Liver - Anatomy & Physiology|liver]].

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.

Portosystemic shunts may be '''congenital''' or '''acquired''' in disease the cause portal hypertension.  Congenital shunts represent approximately 70% of the total number diagnosed in dogs and constitute the majority of those diagnosed in cats.  Congenital shunts usually involve a single (or occasionally double) anomalous vessel which may be located outside of the hepatic parenchyma (extrahepatic) or within it (intrahepatic).  Extrahepatic shunts accounts for 63% of single shunts in the dog and they are most commonly found in miniature and toy breeds.  Intrahepatic shunts are usually located within the left lobes of the liver and occur due to persistence of the foetal [[Foetal Circulation - Anatomy & Physiology|ductus venosus]].  This form of shunt is most common in large breed dogs and patent ductus venosus is an inherited condition in Irish wolfhounds.  Intrahepatic shunts running through the central or right liver lobes 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|hepatic fibrosis]], [[Hepatic Neoplasia|hepatic neoplasia]], portal vein [[Thrombosis|thrombosis]], hepatic arteriovenous fistulae and congenital hypoplasia of the portal vein.

Acquired shunts represent approximately 20% of those diagnosed in dogs and they often consist of multiple small vessels.  They arise due to portal hypertension, following an increased resistance to portal blood flow.  The increased pressure in the portal vein and its tributaries causes numerous non-functional microvascular communications with the systemic venous system to open.  The causes of portal hypertension are numerous and they may be divided into pre-hepatic, hepatic and post-hepatic:

**'''Acute fulminant hepatitis''', '''[[Hepatic Lipidosis|hepatic lipidosis]]''' or '''[[Hepatic neoplasia|neoplasia]]'''

**'''[[Thrombosis|Thrombosis of the portal vein]]''', '''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]].