Difference between revisions of "Portosystemic Shunt"
| Line 27: | Line 27: | ||
*Usually young animals; 2 years of ages but sometimes up to 10 years or older | *Usually young animals; 2 years of ages but sometimes up to 10 years or older | ||
*Failure to thrive | *Failure to thrive | ||
| − | * | + | *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 |
*Ptyalism in cats | *Ptyalism in cats | ||
| − | *Dysuria, stranguria, haematuria | + | *Dysuria, stranguria, haematuria associated with urate stone formation |
**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 stones. | ||
| + | *Intermittent vomiting or diarrhoea | ||
| Line 44: | Line 45: | ||
====Other Tests==== | ====Other Tests==== | ||
| − | *Increased bile acids | + | *Increased postprandial ± preprandial bile acids |
*Increased ammonia levels | *Increased ammonia levels | ||
| − | |||
===Diagnostic Imaging=== | ===Diagnostic Imaging=== | ||
| − | + | A definitive diagnosis relies on visualisation of the shunting blood vessel either with ultrasonography or contrast portography or at surgery. | |
| − | |||
==Treatment== | ==Treatment== | ||
| − | *Surgical ligation of anomolous vessels | + | *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. | **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== | ==Prognosis== | ||
Revision as of 16:00, 7 August 2009
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This article is still under construction. |
Signalment
- Relatively common in dog
- 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 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.
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
- Usually young animals; 2 years of ages but sometimes up to 10 years or older
- Failure to thrive
- 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
- Ptyalism in cats
- Dysuria, stranguria, haematuria associated with urate stone formation
- An increase in ammonium concentration in the blood decreases the ability of enzymes to convert uric acid to allantoin, therby results in urate stones.
- 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.