Dog - Portosystemic Shunt

Introduction

The blood circulation in dogs (and most animals) is arranged so that blood from the intestines, rich in the products of digestion, is taken via the portal vein to the liver where it is further processed. The nutrients are used to provide substances essential for growth and replacement of cells in the body. Waste products, including ammonia are converted into less harmful substances. In the case of ammonia this is converted to urea which is subsequently excreted via the kidneys as urine.

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

How does this affect my dog?

Liver cells are deprived of the necessary nutrients that they'd get from the portal vein and therefore the liver fails to grow and can't function correctly. The growing puppy fails to thrive and appears poor and stunted. The circulating ammonia and other toxic products (which are usually removed by the liver) also affect the brain causing a condition called 'hepatic encephalopathy' which can result in a variety of signs including convulsions.

How is portosystemic shunt caused?

The condition is a non-inflammatory (non infectious) condition that produces signs which are similar to liver failure due to cirrhosis, often seen in older dogs.

Two forms of portosystemic shunt are recognised:

1. Congenital shunt. This is the most common form. It occurs in young dogs and is due to a fault in development before the puppy is born which results in blood vessels being present which allow the blood to bypass the liver. These vessels may be either within the liver, intra-hepatic shunts, or outside the liver, extra hepatic shunts.
2. 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 minute blood vessels (capillaries) rather than a single shunt.

Acquired portosystemic shunts usually occur secondary to (as a result of) 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 a variety of breeds, e.g. Yorkshire Terriers, Old English Sheepdogs, Irish Wolfhounds, Cairn Terriers and Beagles.

Small dogs usually have extra hepatic shunts while larger breeds have the intra hepatic type, which is more difficult to control.

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 into the bloodstream. Ammonia is a byproduct of the 'good bacteria' in the gut. Since this is not converted to urea by the liver it remains in high concentration in the circulating blood and affects the brain, resulting in hepatic encephalopathy. This results in a variety of signs including vomiting, loss of appetite, mental disturbances and convulsions. These signs often wax and wane, and often improve 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 is also noted.

How is the condition diagnosed?

Blood tests for serum bile acids can be diagnostic. Blood samples are taken before the dog has eaten (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 can be suspected.

Other tests including radiographs (x-rays), ultrasound scans, etc 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 a 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. This is a complicated operation and there are many attendant risks. Today intra-hepatic shunts can also be treated surgically with good success but this involves even more complex sugery.

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. Medical treatment is similar to that which is used for dogs which have end stage liver disease and is only palliative, not curative.

If you have any further queries or concerns, please do not hesitate to contact us.