Today's Veterinary Practice

TVP_JUL-AUG2018

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CLINICAL INSIGHTS todaysveterinarypractice.com JULY/AUGUST 2018 67 blood flow to the liver. Causes of portal hypertension include chronic liver disease with fibrosis, cirrhosis, some forms of infiltrative neoplasia, congenital hypoplasia of the portal vein, hepatic arteriovenous fistula, portal vein thrombosis, and extraluminal portal vein compression. The most common causes of portal hypertension in dogs are disorders causing right-sided heart failure 15,25–27 and severe diffuse hepatobiliary disease, 28 resulting in cirrhosis. On ultrasonography, acquired extrahepatic PSSs are recognized as multiple small, collateral, tortuous vessels connecting the portal vein or its tributaries to the caudal vena cava and/or renal/gonadal vein, mesenteric and colonic veins, leading to clinical signs of PSS ( FIGURE 11 ). Ascites is commonly found in association with portal hypertension, with reduced main portal vein blood flow to mean velocities of ≤ 10 cm/sec as measured on spectral Doppler ultrasonography. 29 Hepatic Arteriovenous Fistula Hepatic arteriovenous malformations (fistulas) can be congenital or, less commonly, acquired. They connect the hepatic arteries and portal veins. The surge of high-pressure arterial blood into the low-pressure intrahepatic portal system causes development of severe portal hypertension. These animals usually present at a young age with severe ascites. 30,31 Ultrasonographically, severe enlargement of the intrahepatic portal branches and main portal vein is seen ( FIGURE 12 ). Doppler interrogation of these dilated branches shows turbulent pulsatile flow, indicating communication with the arterial system ( FIGURE 12 ). Scanning caudal to the liver, especially in the area of the left renal and gonadal veins, often allows identification of numerous small, tortuous vessels corresponding to acquired PSSs. SUMMARY A working knowledge of the abdominal vascular anatomy is required for localization of small structures and for evaluation of the primary abnormalities of the FIGURE 12. Short-axis view of the left division of the liver in a 6-year-old poodle with multiple hepatic arteriovenous fistulas (A) without color Doppler, (B) with color Doppler, and (C) with power Doppler. Note the tortuous spectrum of vessels on the color and power Doppler images, not seen on the 2-dimensional grayscale image. (D) The pulsed-wave Doppler display from any of the vessels imaged is seen as a continuous flow pattern with an arterial spike and the lack of return to baseline, consistent with arteriovenous fistula. A D C B

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