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==Description==

==Description==

'''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]].

'''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 stomach, intestines, [[Pancreas - Anatomy & Physiology|pancreas]] and [[Spleen - Anatomy & Physiology|spleen]]) directly into '''systemic venous system''', bypassing the [[Liver - Anatomy & Physiology|liver]].

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 they 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 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.

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.

**'''[[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.'''

The pathophysiology of PSS relates to the shunting of portal blood directly from the systemic circulation, resulting in hyperammonaemia and [[Hepatic Encephalopathy|hepatic encepalopathy]].  Animals with PSS also have reduced function of the hepatic component of the monocyte phagcoyte system (chiefly the Kupffer cells) and they often develop bacteraemia.  Gram negative bacteria deriving from the GI tract are involved most commonly.

The pathophysiology of PSS relates to the shunting of portal blood directly from the systemic circulation, resulting in hyperammonaemia and [[Hepatic Encephalopathy|hepatic encephalopathy]].  Animals with PSS also have reduced function of the hepatic component of the monocyte phagocyte system (chiefly the Kupffer cells) and they often develop bacteraemia.  Gram negative bacteria deriving from the GI tract are involved most commonly.

==Signalment==

==Signalment==

==Diagnosis==

==Diagnosis==

===Clinical Signs===

===Clinical Signs===

All portosystemic shunts are likely to cause [[Hepatic Encephalopathy|hepatic encephalopathy]](HE) and PSS is the major cause of this disease. HE mainly causes waxing and waning neurological signs, including central blindness, seizures, depression and bizarre behaviour.  Cats often show hypersalivation/ptyalism.

All portosystemic shunts are likely to cause [[Hepatic Encephalopathy|hepatic encephalopathy]](HE) and PSS is the major cause of this disease. HE mainly causes waxing and waning neurological signs, including central blindness, seizures, depression and bizarre behaviour.  Cats often show hypersalivation/ptyalism.

In additon, animals with congenital PSS may show the following signs:

In additon, animals with congenital PSS may show the following signs:

====Radiography====

====Radiography====

A definitive diagnosis relies on visualisation of the shunting blood vessel but radiography may reveal changes that are supportive of a diagnosis of PSS:

A definitive diagnosis relies on visualisation of the shunting blood vessel but radiography may reveal changes that are supportive of a diagnosis of PSS:

*'''Renomegaly''' is thought to occur as the kidneys attempt to remove and metabolise ammonia

*'''Renomegaly''' is thought to occur as the kidneys attempt to remove and metabolise ammonia.

*'''Microhepatica''' probably occurs because the liver is deprived of growth factors from the pancreas and other abdominal organs which are usually carried to it in the portal blood, for example the somatomedins (insulin-like growth factors, IGFs).

*'''Microhepatica''' probably occurs because the liver is deprived of growth factors from the pancreas and other abdominal organs which are usually carried to it in the portal blood, for example the somatomedins (insulin-like growth factors, IGFs).

*'''Urate uroliths''' are '''radiolucent''' and will not be detected by radiographs.

*'''Urate uroliths''' are '''radiolucent''' and will not be detected by radiographs.

==Treatment==

==Treatment==

In animals with acquired PSS, the underlying cause should be treated and HE should be managed as described [[Hepatic Encephalopathy|here]]. Acquired shunts should never be ligated as they occur as a compensatory response to portal hypertension and ligation would increase portal pressure.

In animals with acquired PSS, the underlying cause should be treated and HE should be managed as described [[Hepatic Encephalopathy|here]]. '''Acquired shunts should never be ligated''' as they occur as a compensatory response to portal hypertension and ligation would increase portal pressure.

Animals affected by congenital PSS may be managed either medically or surgically but a recent study has shown that those undergoing surgical ligation of the shunting vessel have a longer median survival time.  Medical management is often employed in those animals that show few clinical signs on presentations, are older or which have a shunt that is not amenable to ligation.   

Animals affected by congenital PSS may be managed either medically or surgically but a recent study has shown that those undergoing surgical ligation of the shunting vessel have a longer median survival time.  Medical management is often employed in those animals that show few clinical signs on presentations, are older or which have a shunt that is not amenable to ligation.   

A suitable regime would incorporate the following features:

A suitable regime would incorporate the following features:

*A '''diet''' with '''protein of high quality''' and with both soluble and insoluble fibre.  Severe protein restriction is only necessary in animals showing signs of HE and it is otherwise detrimental because animals with PSS are often hypoalbuminaemic.  A protein of high quality is selected so that excess amino acids are not available to colonic bacteria and suitable sources include cottage cheese in dogs or white fish in cats.  Soluble fibre acts in a similar manner to lactulose (below) whereas insoluble fibre decreases intestinal transit time and helps to prevent constipation.

*A '''diet''' with '''protein of high quality''' and with both soluble and insoluble fibre.  Severe protein restriction is only necessary in animals showing signs of HE and it is otherwise detrimental because animals with PSS are often hypoalbuminaemic.  A protein of high quality is selected so that excess amino acids are not available to colonic bacteria and suitable sources include cottage cheese in dogs or white fish in cats.  Soluble fibre acts in a similar manner to lactulose (below) whereas insoluble fibre decreases intestinal transit time and helps to prevent constipation.

*'''Lactulose''', a synthetic disaccharide that causes acidification of the colonic environment when it is fermented by bacteria. This environment promotes the conversion of ammonia to ammonium and the latter ions are not easily absorbed due to their electrical charge.  The trapped ammonia is therefore excreted in faeces. Lactulose is also a cathartic laxative that reduces the amount of time available for colonic bacteria to act on surplus amino acids.

*'''[[Lactulose]]''', a synthetic disaccharide that causes acidification of the colonic environment when it is fermented by bacteria. This environment promotes the conversion of ammonia to ammonium and the latter ions are not easily absorbed due to their electrical charge.  The trapped ammonia is therefore excreted in faeces. Lactulose is also a cathartic laxative that reduces the amount of time available for colonic bacteria to act on surplus amino acids.

*Administration of '''oral antibiotics''' to reduce the numbers of colonic bacteria.  Neomycin, ampicillin or metronidazole are commonly used for this purpose.

*Administration of '''oral antibiotics''' to reduce the numbers of colonic bacteria.  Neomycin, ampicillin or metronidazole are commonly used for this purpose.