The surgical treatment of intrahepatic portosystemic shunts in six cats is described. The preoperative diagnoses were based on the results of abdominal ultrasonography, and mesenteric portography was used during surgery to confirm the diagnosis and establish the morphology of the shunting vessel. In four of the cats the shunt vessel passed through the left division of the liver, compatible with a patent ductus venosus (PDV), in one cat the shunt passed through the central hepatic division and in the other cat it passed through the right hepatic division. During surgery the shunt vessel was manipulated directly either intrahepatically, or post hepatically in the four cats with PDV. In five cats the shunt vessel was partially ligated, and in the other the vessel was completely ligated. The attenuation procedure produced a mean increase in mesenteric venous pressure of 17 cm H2O, with a range from 14 to 20 cm. All the cats recovered from the surgical procedure, but one developed neurological signs shortly after the operation and died from respiratory failure. Four of the cats were clinically normal and required no medication by one month after the operation. One cat required long-term medication to control its continued clinical signs.

Twenty-four cats with clinical and, or, clinicopathological signs compatible with portosystemic shunting were examined prospectively using two-dimensional grey-scale, duplex and colour-flow Doppler ultrasonography. Diagnosis of congenital portosystemic shunt was subsequently confirmed in 14 cats using operative mesenteric portography and surgery. Of the 14 affected cats, nine were purebred; eight were male and six female. The mean age at the time of diagnosis was nine months (range four to 27 months). Ultrasonographic evidence of a small liver was present in seven cats (50 per cent); visibility of intrahepatic portal vessels was reduced in three (21 per cent). An anomalous blood vessel was identified ultrasonographically in each cat; in 10 cats (71 per cent) the vessel was observed to originate from the portal vein and drain into the caudal vena cava. Abnormally variable portal blood flow was present in eight of the 10 cats in which it was measured. At surgery, six shunts were intrahepatic and eight extrahepatic; the ultrasonographic diagnosis of intra- versus extrahepatic shunt was correct in 13 cats (93 per cent). No anomalous blood vessels or abnormalities affecting the portal vein were detected ultrasonographically in any of the 10 cats that did not have congenital portosystemic shunting. Hence, the accuracy of ultrasonography for diagnosis of congenital portosystemic shunting in this series was 100 per cent.

Five cats with a congenital portosystemic shunt (CPSS) were examined using transcolonic portal scintigraphy before and after surgical ligation of the shunting vessel. The mean shunt index before surgery was 52 per cent (range 45 to 61 per cent). Repeat portal scintigraphy, six to eight weeks after surgery, indicated a significant reduction in shunt index (mean 13 per cent, range 5 to 25 per cent) in four cats. In one of these cats a marked reduction in the shunt index, as determined by scintigraphy, preceded normal fasting blood ammonia. In the fifth cat there was no significant change in the shunt index, fasting serum bile acids and blood ammonia six months after surgery, although its clinical signs of hepatic encephalopathy had improved. Portal scintigraphy is useful in the diagnosis of CPSS and enables a quantitative assessment of the effects of surgery and may be a more accurate indicator of the degree of shunting after surgery than blood ammonia and serum bile acids.