A portosystemic shunt (PSS), also known as a liver shunt,
is a bypass of the liver by the body’s circulatory system.
It can be either a congenital (present at birth) or acquired
condition.

Congenital PSS is a hereditary condition in dogs and cats,
its frequency varying depending on the breed. The shunts
found mainly in small dog breeds such as Miniature Schnauzers
and Yorkshire Terriers, and in cats such as Persians,
Himalayans, and mix breeds are usually extrahepatic
(outside the liver), while the shunts found in large
dog breeds such as Irish Wolfhounds and Labrador Retrievers
tend to be intrahepatic.

Acquired PSS is uncommon and is found in dogs and cats
with liver disease such as cirrhosis causing portal
hypertension, which is high blood pressure in the portal vein.

Congenital PSS is caused by the failure of the fetal
circulatory system of the liver to change. Normally,
the blood from the placenta bypasses the liver and
goes into circulation via the ductus venosus, a blood
vessel found in the fetus. A failure of the ductus venosus
to close causes an intrahepatic shunt, while extrahepatic
shunts are usually a developmental abnormality of the
vitelline veins, which connect the portal vein to the
caudal vena cava. Thus in the juvenile and adult animal
with PSS, blood from the intestines only partly goes
through the liver, and the rest mixes into general
circulation. Toxins such as ammonia are not cleared
by the liver. Most commonly, extrahepatic shunts are
found connecting the portal vein or left gastric vein
to the caudal vena cava.

Congenital shunts are usually solitary. Acquired shunts
are usually multiple, and are caused by portal hypertension
in dogs with liver disease. This is most commonly seen
in older dogs with cirrhosis, but may also be seen in
younger dogs with liver fibrosis caused by lobular dissecting
hepatitis

Symptoms and diagnosis

Symptoms of congenital PSS usually appear by six months of
age and include failure to gain weight, vomiting, and signs
of hepatic encephalopathy (a condition where toxins normally
removed by the liver accumulate in the blood and impair the
function of brain cells) such as seizures, depression,
tremors, drooling, and head pressing. Urate bladder stones
may form because of increased amounts of uric acid in circulation
and excreted by the kidneys. Initial diagnosis of PSS is through
laboratory bloodwork showing either elevated serum bile acids
after eating or elevation of fasting blood ammonia levels, which
has been shown to have a higher sensitivity and specificity
than the bile acids test.

Treatment

Surgical treatment is best, when it can be performed. Pressure
within the portal vein is measured as the shunt is closed, and
it must be kept below 20 cm H2O or else portal hypertension will
ensue. Complete closure of extrahepatic shunts results in a very
low recurrence rate, while incomplete closure results in a recurrence
rate of about 50 percent. However, not all dogs with extrahepatic
shunts tolerate complete closure (16 to 68 percent).Intrahepatic shunts
are much more difficult to surgically correct than extrahepatic shunts
due to their hidden nature, large vessel size, and greater tendency
toward portal hypertension when completely closed.

When surgery is not an option, PSS is treated as are other forms of
liver failure. Dietary protein restriction is helpful to lessen signs
of hepatic encephalopathy, and antibiotics such as neomycin or
metronidazole and other medicines such as lactulose can reduce
ammonia production and absorption in the intestines.

The prognosis is guarded for any form of PSS.

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Dr Andrew Jones, DVM