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, Standard Poodles 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……..