Firstly there can be a lot of variation of clinical signs depending on the severity of the condition, which could depend on how much blood flow is diverted past the Liver. Some of the clinical signs of portosystemic shunts that might be recognised in a puppy or young adult that have been reported could include:
· Failure for a puppy to grow
· Poor weight gain
· Depression, Listlessness, apathy.
· Weakness
· Seizures
· Salivation, drooling
· Vomiting
· Poor appetite
· Balance problems
· Bladder stones
· Blindness

Portosystemic Shunts
Portosystemic shunts are abnormal vascular connections between the hepatic portal vein [the blood vessel that connects the gastrointestinal tract with the liver] and systemic circulation. Such anomalies cause blood in the gastrointestinal tract to be diverted past the liver, there by limiting the liver's vital functions in metabolism and detoxification of compounds and the body's defences against intestinally derived pathogens. This effectively exposes the body to toxic by products of digestion [toxins and bacteria] and mimics the effects of liver failure.

Portosystemic shunts can be present at birth [i.e. congenital] or acquired as the result of another disease process later on. Congenital shunts are more common, representing approx. 75% of all canine cases, and generally result from anatomic abnormalities of the portal vasculature or fetal vessels. One or occasionally two vessels are involved, and the shunts are classified according to their location as either outside of [extrahepatic] or within [intrahepatic] the liver.

Congenital Shunts
Congenital shunts occur more commonly in pure-bred dogs than in mixed breeds; miniature Schnauzers, Yorkshire Terriers, and Irish Wolfhounds appear to be at increased risk. The prevalence of portosystemic shunts in certain breeds suggests an inherited predisposition. This has only been proven in Irish Wolfhounds, where a number of previously unknown genes appear to be involved.

Extrahepatic shunts are most common, accounting for 61% to 94% of congenital shunts, and are typically seen in small breeds of dogs, such as the Miniature Schnauzer and Yorkshire Terrier. Intrahepatic shunts represent between 6% and 40% of congenital shunts and are more common in large and giant breeds such as Irish Wolfhounds and Golden Retrievers. The majority of intrahepatic shunts are as a result of the embryonic connection between the umbilical vein and the caudal vena cava remaining open; in most dogs this connection closes 3 days after birth but, for unknown reasons, remains open in dogs with intrahepatic congenital shunts.

Hepatic microvascular dysplasia is an unusual form of intrahepatic portosystemic shunting in which no gross vascular abnormality can be identified. This rare condition is associated with somewhat milder clinical signs and appears to be the consequence of a developmental abnormality; it has a higher prevalence in Cairn Terriers, suggesting a hereditary basis.

ACQUIRED SHUNTS
Acquired shunts arise secondary to diffuse liver disease where excessive and sustained pressure at some point within the portal vein causes embryonic, non-functional vascular communications to open. These are generally seen in older dogs with cirrhosis, hepatitis or neoplasia of the liver. In contrast to congenital portosystemic shunts, a number of vessels are usually affected.

What are the signs of Portosystemic shunts?
The clinical signs exhibited by the dogs reflects the failure of the liver to eliminate various toxic matter, drugs and bacteria absorbed from the gastrointestinal tract. Problems increase dramatically after eating. A large percentage may show an intolerance to anaesthetics or tranquillisers, and may show increased recovery times following their use. Other clinical signs arise from the liver being deprived of portal blood flow, which is essential for the normal development of the liver; as a result the liver is underdeveloped and its metabolic, storage and excretory functions are further impaired…

Signalment & History.
Dogs with congenital portosystemic shunts are typically pure bred dogs of less than one year old. Generally the lower the fraction of shunting, the milder and later in onset the clinical signs. Nevertheless the affected are often in poor body condition and of small body stature, especially when compared to their litter mates. Owners may complain that the animal fails to grow and that skin and coat condition are poor.

Gastrointestinal Signs.
Vomiting and Diarrhoea are present in about two thirds of cases. Evidence of lower urinary tract disease is present in approximately one-half of cases and is usually due to ammonium urate crystals, which are formed because of excessive excretion of ammonia and uric acid in urine. Some dogs, particularly those that develop signs later in life, have polydipsia and polyuria ascites, although the latter is generally seen only in dogs with acquired shunts.
Management.
Surgery is possible in some cases but can carry a very high risk factor, and a high cost. Dietery manipulations for its control are designed to limit neurotoxin production, which occurs principally in the large intestine. The major toxins are all derived from nitrogenous materials [protein and urea] and are synthesised by bacteria found within the large intestine. The production of these toxins is reduced by limiting the amount of protein fed and ensuring that the dietary protein is high quality and highly digestible. These steps reduce the amount of protein that reaches the large intestine; further reductions can be attained by feeding smaller meals more frquently to maximise the digestive capacity of the small intestine. Specific diets are commercially produced tp provide a balanced protein-calorie intake including dietary fibre which assists in limiting toxin production. Lactulose, a soluble fibre, is often used as a supplement and can readily be purchased. Supplementation with zinc salts also improves the detoxification of ammonia and the control of hepatic encephalopathy. Antibiotics are used in most cases to reduce the bacteria within the large intestine that are responsible for the production of neurotoxins. Oral administered neomycin is commonly used for this purpose and is often used in combination with lactulose in both short and long term medical management of portosystemic shunts……..

[This material used with kind permission of Jay Bianco,
Author & Creator of the "Maltese only" web site. Copyright 1999]