Portosystemic Shunt

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
• Neurological signs due to Hepatic Encephalopathy: bizarre behaviour, head pressing, seizures, intermittent blindness
• Ptyalism in cats
• Dysuria, stranguria, haematuria due to 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.

Laboratory Tests

Haematology

• Microcytosis

Biochemistry

• Decreased blood urea nitrogen (BUN)
• Hypoalbuminaemia
• Hypocholesterolaemia
• Hypoglycaemia

Other Tests

• Increased bile acids
• Increased ammonia levels

Treatment

• Surgical ligation of 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.

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.