Changes

==Signalment==

==Signalment==

*Relatively common in dog

*Relatively common in dog, especially small breed dogs

*Occasionally seen in cats, horses, cows and pigs

*Occasionally seen in cats, horses, cows and pigs

'''Portsystemic shunts (PSS)''' are anomalous vessels vascular connections between the portal and systemic venous systems.  This allows for some portal blood draining from the stomach, intestines, pancreas and spleen to bypass the liver and drains directly into the systemic circulation.  PSS may be congenital or acquired secondary to portal hypertension.

'''Portsystemic shunts (PSS)''' are anomalous vessels vascular connections between the portal and systemic venous systems.  This allows for some portal blood draining from the stomach, intestines, pancreas and spleen to bypass the liver and drains directly into the systemic circulation.  PSS may be congenital or acquired secondary to portal hypertension.

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 anomolous vessel.  Extrahepatic PSS accounts for 63% of single shunts in dog and is most commonly found in small breed dogs.  Intrahepatic shunts are usually left-sided and result from persistent foetal ductus venosus and is 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 anomolous 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 and result from persistent foetal ductus venosus and is 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 as a result of portal hypertension following 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 fibrosis, 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 as a result of portal hypertension following 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 fibrosis, hepatic neoplasia, portal vein thrombosis, hepatic arteriovenous fistulae and congenital hypoplasia of the portal vein.

==Diagnosis==

==Diagnosis==

===Clinical Signs===

===Clinical Signs===

*Usually young animals; 2 years of ages but sometimes up to 10 years or older

*Young animals, usually under 1 years of ages, but can sometimes be up to 10 years or older

*Failure to thrive

*Failure to thrive, small body stature or weight loss

*Waxing and waning neurological signs due to [[Hepatic Encephalopathy]]: bizarre behaviour, head pressing, seizures, intermittent blindness.  These are usually most severe an hour or two post prandial but this may not be obvious in all cases

*Waxing and waning neurological signs due to [[Hepatic Encephalopathy]].  These are usually most severe an hour or two post prandial but this may not be obvious in all cases

*Ptyalism in cats

*Ptyalism in cats

*Dysuria, stranguria, haematuria associated with urate stone formation

*Dysuria, stranguria, haematuria, pollakiuria and urethral obstruction

**An increase in ammonium concentration in the blood decreases the ability of enzymes to convert uric acid to allantoin, therby results in urate stones.

**An increase in ammonium concentration in the blood decreases the ability of enzymes to convert uric acid to allantoin, therby results in urate urolithiasis.

*Intermittent vomiting or diarrhoea

*Intermittent vomiting or diarrhoea