Identification of the shunt
A standard ventral midline celiotomy is performed from the xiphoid to pubis to explore the portal system. The portal vein
and caudal vena cava are located by retracting the duodenum medially. The portal vein is identified ventral to the caudal
vena cava at the most dorsal aspect of the mesoduodenum. The caudal vena cava is examine for identification of any abnormal
blood vessels. Normally, from the renal and phrenicoabdominal veins to the hile of the liver there should be no blood vessels
entering the caudal vena cava ventrally. Any blood vessel in this area should be suspect as an extrahepatic shunting blood
vessel. Turbulence in this portion of the vena cava is another important clue for locating a possible shunt. If nothing abnormal
is noticed the left omental bursa is entered and all tributaries from the portal vein are identified. Most often, shunting
vessels come from the gastrosplenic vein in dogs and left gastric vein in cats. If no shunting vessel can be located, investigation
for an intrahepatic shunt is started. Inspection of the hepatic veins cranial to the liver and inspection of liver lobes for
dilation are the first steps in identification of an intrahepatic shunt.
Ligation of the shunt
Complete occlusion of the shunt at the time of surgery is associated with a better prognosis. However, complete occlusion
may not be possible at the time of surgery because the liver parenchyma cannot accommodate the augmentation in blood flow.
It then results in portal hypertension. Occlusion of a PSS has been performed traditionally with a suture placed around the
shunt and tight while the portal pressure was measured. This technique resulted in acute or chronic portal hypertension in
15 to 20 % of the cases. Acute portal hypertension resulted in death in most of the cases. Chronic portal hypertension induced
ascites and the opening of acquired shunts.
To palliate to these problems and achieve complete occlusion of the PSS gradual occlusion has been performed with ameroid
constrictor or cellophane band. Both of these devices induce a slow and complete occlusion of the PSS over 4 to 8 weeks. The
liver parenchyma can then accommodate the augmentation in blood flow without inducing portal hypertension.
Postoperatively, patients are examined for signs of portal hypertension: sepsis, abdominal pain, bloody diarrhea, and ascites.
If signs of portal hypertension occur, the patient is taken back to surgery and the suture released. Failure to remove the
ligature will result in septic shock and death. Hypothermia during surgery and postoperatively should be corrected aggressively.
Dextrose (2.5%) intravenously is maintained. Thrombosis of the portal vein has been reported as complication of a partial
ligation of intrahepatic PSS. Postoperative seizures have been reported as a complication of ligation of PSS and they carry
a poor prognosis. Seizures may occur immediately or up to 3 days postoperatively.
Surgical mortality associated with treatment of PSS can be as high as 20 %. The intraoperative and immediate postoperative
periods are most critical. Hypothermia and hypoglycemia should be anticipated and treated promptly. With the devices for gradual
occlusion the incidence of complications seems significantly reduced.
Post-operatively the animals should be maintained on a low protein diet, amoxicillin or neomycin, and lactulose. Bile acids
should be monitored at one, three and six months after surgery. Lactulose should be interrupted one month after surgery. The
antibiotics should then be removed from the treatment. Three months after surgery the diet can be progressively return to
normal. If the animal is showing signs of hepatic encephalopathy then the low protein diet is re-instituted.