Portosystemic Shunt

Blood circulation is so arranged in most animals, including us, that blood from the intestines, which is rich in the products of digestion, is conveyed via the portal circulation to the liver. There the blood is processed, the nutrients used to provide substances essential for growth and replacement of cells in the body. Waste products, the most important of which is probably ammonia are converted into less harmful substances. In the case of ammonia this is urea which is subsequently excreted via the kidneys.

When a portosystemic shunt (PSS) is present blood in the portal vein effectively bypasses the liver, i.e it is shunted straight into the caudal vena cava, a major vein returning blood to the heart.

How does this affect my dog?

Liver cells are deprived of the necessary nutrients and therefore the liver fails to grow and ceases to function correctly. This, in turn, affects the whole body so that the growing dog fails to thrive and appears poor and stunted. In addition the circulating ammonia and other toxic products can affect the brain causing a condition called hepatic encephalopathy which can result in a variety of signs including convulsions.

How is portosystemic shunt caused?  Is it an infection?

No. The condition is a non-inflammatory (non infectious) condition and produces signs which are similar to liver failure due to cirrhosis, often seen in older dogs.

What causes it then?

Two forms of portosystemic shunt are recognised:

(a)  Congenital shunt.  This is the most common form. It occurs in young dogs and is due to a fault in development in the embryo before birth. This results in blood vessels being present which allow the blood to bypass the liver. These vessels may be either within the liver, or on the outside, when they are known as extra hepatic shunts.

(b)  Acquired shunts usually occur in older dogs and are the result of something causing increased pressure in the portal circulation. These usually take the form of multiple small blood vessels rather than a single shunt.

Acquired portosystemic shunts usually occur secondary to chronic end stage liver disease and are very much more difficult to treat.

"Acquired portosystemic shunts usually occur secondary to chronic end stage liver disease and are very much more difficult to treat."

Is the condition hereditary?

The genetic basis of congenital portosystemic shunt is not presently understood. However affected lines have been recognised in Yorkshire Terriers, Maltese, Old English Sheepdogs, Irish Wolfhounds, Cairn Terriers, Poodles and Beagles.

Small breed dogs usually have extra hepatic shunts while larger breeds have the more difficult to control intra hepatic type of blood vessel anomaly.

If the condition is present from birth are symptoms easy to recognise in the puppy?

Clinical signs usually do not become apparent immediately although in some cases a puppy only a few weeks old will be smaller and less active than the rest of the litter. Clinical signs are usually apparent in the first six months of life, although some dogs with congenital PSS are not diagnosed until later in life, sometimes as late as seven or eight years of age. However these are exceptions.

What are the symptoms?

Signs are broadly due to the inability of the liver to process the products of digestion, not only nutrients but also ammonia which has been absorbed from the intestines. Since this cannot be converted to urea by the liver it remains in high concentration in the circulating blood. This can affect the brain, resulting in hepatic encephalopathy resulting in a variety of signs which include vomiting, loss of appetite, mental disturbances and convulsions. These signs often wax and wane, often improving when the dog is given broad spectrum antibiotics and fluids. Many owners note that these signs are worse if the dog receives high protein meals. Urinary symptoms may also be noted. A high level of ammonia can result in the formation of bladder stones (urinary calculi) which can result in straining to pass urine which may be blood stained (haematuria). Increased thirst may also noted.

How is the condition diagnosed?

Today blood tests measuring serum bile acids can be diagnostic. Blood samples are taken before (fasting samples) and approximately two hours after a meal (post-prandial sample). The fasting (pre-prandial) sample may be normal but if the post-prandial sample is consistently high (typically exceeding 100 mmols/L), PSS may be suspected.  Some breeds may have abnormally high levels of bile acids and not have a PSS.

Other tests including radiography, ultrasound scans and other sophisticated tests may be necessary.

Tests to measure pre and post-prandial ammonia may also be necessary.

If my puppy is not growing, how early can these tests be carried out?

It is possible to carry out blood tests on puppies as young as 6-8 weeks. If bile acid values are not abnormally elevated in the post-prandial sample, it is unlikely the pup is suffering from liver shunt.

What is the treatment?

If, following exhaustive tests, it appears the shunt is extra hepatic, surgery can be very successful in curing the signs. However this is a complicated operation and there are many attendant risks which we will be happy to discuss with you.

If surgery is not possible or is not totally successful, clinical management using antibiotics and other drugs together with a low protein diet will relieve symptoms, sometimes for months or even years but should not be considered curative. Treatment is similar to that which is used for dogs which have end stage liver disease.