Changes

Portosystemic shunts may be '''congenital''' or '''acquired''' in disease the cause portal hypertension.  In the developing embryo, the cardinal veins form the systemic abdominal veins (the caudal vena cava, azygos, renal and gonadal veins) whereas the vitelline veins form the hepatic sinusoids, the portal vein and its tributaries, of which the largest are the left gastric, splenic, cranial and caudal mesenteric and gastroduodenal veins.  The ductus venosus, a component of the foetal circulation that directs blood directly from the ubilical vein to the vena cava, is also part of the vitelline system.  If a functional connection (ductus venosus or otherwise) remains between the vitelline and cardinal systems after birth, a PSS develops.  However, in the normal animal, there are numerous non-functional connection between the two systems that may open if the pressure in the portal vein rises, leading to the formation of multiple extrahepatic acquired shunts.   

Portosystemic shunts may be '''congenital''' or '''acquired''' in disease the cause portal hypertension.  In the developing embryo, the cardinal veins form the systemic abdominal veins (the caudal vena cava, azygos, renal and gonadal veins) whereas the vitelline veins form the hepatic sinusoids, the portal vein and its tributaries, of which the largest are the left gastric, splenic, cranial and caudal mesenteric and gastroduodenal veins.  The ductus venosus, a component of the foetal circulation that directs blood directly from the ubilical vein to the vena cava, is also part of the vitelline system.  If a functional connection (ductus venosus or otherwise) remains between the vitelline and cardinal systems after birth, a PSS develops.  However, in the normal animal, there are numerous non-functional connection between the two systems that may open if the pressure in the portal vein rises, leading to the formation of multiple extrahepatic acquired shunts.   

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.

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 often 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 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:

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:

*'''Pre-hepatic'''

*Pre-hepatic

**'''Right-sided congestive heart failure''', including '''cardiac tamponade'''.

**'''Right-sided congestive heart failure''', including '''cardiac tamponade'''.

*'''Hepatic'''

*Hepatic

**'''Acute fulminant hepatitis''', '''chronic hepatic failure with fibrosis''' or '''[[Hepatic neoplasia|neoplasia]]'''

**'''Acute fulminant hepatitis''', '''chronic hepatic failure with fibrosis''' or '''[[Hepatic neoplasia|neoplasia]]'''

*'''Post-hepatic'''

*Post-hepatic

**'''[[Thrombosis|Thrombosis of the portal vein]]''', '''hepatic arteriovenous fistulae''' and '''congenital hypoplasia of the portal vein.'''

**'''[[Thrombosis|Thrombosis of the portal vein]]''', '''hepatic arteriovenous fistulae''' and '''congenital hypoplasia of the portal vein.'''