Difference between revisions of "Portosystemic Shunt"
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==Signalment== | ==Signalment== | ||
| − | *Relatively common in dog | + | *Relatively common in dog, especially small breed dogs |
| + | *Purebred dogs are more at risk | ||
*Occasionally seen in cats, horses, cows and pigs | *Occasionally seen in cats, horses, cows and pigs | ||
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'''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 | + | 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. | ||
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==Diagnosis== | ==Diagnosis== | ||
===Clinical Signs=== | ===Clinical Signs=== | ||
| − | * | + | *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]] | + | *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 |
| + | **Bizarre behaviour | ||
| + | **Head pressing | ||
| + | **Seizures | ||
| + | **Intermittent blindness. | ||
*Ptyalism in cats | *Ptyalism in cats | ||
| − | *Dysuria, stranguria, haematuria | + | *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 | + | **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 | ||
Revision as of 16:10, 7 August 2009
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This article is still under construction. |
Signalment
- Relatively common in dog, especially small breed dogs
- Purebred dogs are more at risk
- Occasionally seen in cats, horses, cows and pigs
Description
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 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.
The pathophysiology of PSS relates to the shunting of blood directly from the systemic circulation, resulting in hyperammonaemia and Hepatic Encephalopathy.
Diagnosis
Clinical Signs
- Young animals, usually under 1 years of ages, but can sometimes be up to 10 years or older
- Failure to thrive, small body stature or weight loss
- 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
- Bizarre behaviour
- Head pressing
- Seizures
- Intermittent blindness.
- Ptyalism in cats
- 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 urolithiasis.
- Intermittent vomiting or diarrhoea
Laboratory Tests
Haematology
- Microcytosis
Biochemistry
- Decreased blood urea nitrogen (BUN)
- Hypoalbuminaemia
- Hypocholesterolaemia
- Hypoglycaemia
Other Tests
- Increased postprandial ± preprandial bile acids
- Increased ammonia levels
Diagnostic Imaging
A definitive diagnosis relies on visualisation of the shunting blood vessel either with ultrasonography or contrast portography or at surgery.
Treatment
- Surgical ligation of the anomolous vessels
- Beware of possible portal hypertension post ligation. For this reason, a partial ligation is performed initally, followed by a complete ligatio a few months later.
- Medical treatment of Hepatic Encephalopathy
Prognosis
References
- Ettinger, S.J. and Feldman, E. C. (2000) Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2 (Fifth Edition) W.B. Saunders Company.
- Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier.