P. 70

An Urban Experience
L. Findji1
1Fitzpatrick Referrals, Oncology and Soft Tissue surgery, Guildford, United Kingdom
Portosystemic shunts for dummies
Portosystemic shunts are abnormal vessels allowing communication between the splanchnic and systemic circulations. They are either congenital or acquired, single or multiple, extrahepatic or intrahepatic.
Clinical signs associated with HE can be broadly separated in neurological, gastrointestinal and urinary. Neurological signs include depression, listlessness, ataxia, pacing, circling, head pressing, cortical blindness, seizures and coma. They have been classically described as correlated with meals, but it has been shown to only be the case in 25% to 50% of patients. Gastrointestinal signs occur in about 30% of canine cases and include anorexia, vomiting and gastrointestinal bleeding. In
cats, ptyalism is a very common clinical sign, present in 75% of cases. Urinary signs include dysuria, stranguria, pollakiuria and haematuria and are associated with ammonium urate crystalluria.
Clinical pathology changes most commonly encountered in animals with PSS include mild to moderate microcytic normochromic nonregenerative anaemia, elevated alkaline phosphatase (ALP) and alanine aminotransferase (ALT) activities, hypoalbuminaemia, decreased
blood urea nitrogen (BUN), hypocholesterolaemia
and hypoglycaemia. Coagulation times are almost consistently prolonged in affected dogs, these abnormalities are infrequently clinically signi cant. Urinalysis abnormalities include hyposthenuria, ammonium biurate crystalluria and signs of secondary urinary tract infection. The most common laboratory tests used for diagnosis of liver dysfunction include bile acids stimultation test (BAST) and plasma ammonia levels.
Survey radiographs are of limited value in the diagnostic of PSS. Portovenography, either jejunal or transplenic, can be performed pre- and/or intra-operatively and is very sensitive and speci c for PSS detection. Ultrasound is still widely used for assessment of PSS, with 74%
to 95% sensitivity and 67% to 100% speci city. Scintigraphy is quite sensitive for detection of PSS, but cannot discriminate between EHPSS and IHPSS, nor can it give any information of the number of shunts. Computed tomographic angiography has become
the gold-standard for characterisation of PSS2, as it is
non-invasive, more accurate than portographies3 and ultrasound4, and allows precise characterisation of the shunt morphology5.
Medical treatment
A medical treatment can be used to decrease the clinical signs and optimise patients prior to surgical correction of operable CPSS, or for long-term management of multiple acquired or inoperable CPSS.
It aims at decreasing the clinical signs associated with HE by reducing the amount of neurotoxic by-products of protein metabolism. It is therefore based on the administration of a low-protein diet, antibiotics to decrease the number of ammonia-producing bacteria in the digestive tract, lactulose to decrease the production and absorption of ammonia, gastroprotectants and antacids to prevent or treat gastrointestinal ulcers
and bleeding. Seizure control is sought through administration of phenobarbital, potassium bromide, gabapentin, or propofol. Levetiracetam is another anticonvulsant commonly used to prevent or control seizures in PSS patients6, which the author routinely prescribes to patients for a few days before surgery at 10-20mg/kg TID.
Surgical treatment Identi cation of the shunt
Most PSS are found to terminate on the caudal vena cava at the level of the epiploic foramen, which should therefore be inspected  rst. Any blood vessel found
to enter the caudal vena cava between the renal and phrenico-abdominal veins and the liver should be considered as potentially being a PSS. Blood  ow turbulences are often visible in the caudal vena cava
or shunt vessel, which further supports the shunt identi cation. If no abnormal vessel is found through the epiploic foramen, the omental bursa must be opened
by tearing the super cial leaf of the greater omentum. This allows inspection of the tributaries of the portal
vein. Most often, shunting vessels originate from the gastrosplenic vein in dogs and left gastric vein in cats. Portoazygos shunts are found as abnormal vessels penetrating the diaphragmatic crura or aortic hiatus. Occasionally, shunts cross through the diaphragm at
the oesophageal hiatus. If no abnormal vessel is found, the presence of an IHPSS should be evaluated. This is done by identifying the left hepatic veins cranial to the liver for the left lobe, or branches of the portal vein caudal to the liver for the right and centre lobes. Temporary occlusion of any of these veins communicating with the shunt results in immediate signs of portal hypertension. Acute or gradual occlusion of this vessel is then carried

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