Congenital Intrahepatic Arteriovenous Fistulae in a Young Beagle Dog

Abstract

Congenital intrahepatic arteriovenous fistulae, a rare hepatic vascular anomaly, in an 8-mo-old female beagle dog was investigated. The animal showed anorexia, repeated vomiting, hemorrhagic diarrhea, and jaundice for approximately 2 wk. There was mild to severe increase of serum alkaline phosphatase, glutamic-oxalacetic transaminase, glutamic pyruvic transaminase, total cholesterol, total bilirubin, and γ-glutamyl transpeptidase. Macroscopically, the main abdominal organs showed hemorrhagic edema together with bloody ascites. Other characteristic findings were severe hepatic atrophy (right medial, quadrate, left medial, and lateral lobes) with multiple vascular cysts and compensatory hypertrophy of the other lobes. The cystic vessels seemed to extend from the proper hepatic arteries and their branches but were indistinguishable from the portal vein. Histopathologically, the atrophied hepatic lobes were characterized by wide, fibrous septa containing severe hyperplasia and anastomosis of the arteriolae and venulae and proliferation of bile ducts.

Congenital Intrahepatic Vascular Anomaly in a Clinically Normal Laboratory Beagle

“…Vascular changes, in addition to the presence of multiple intermingling, dilated, and abnormal vessels-including elastolysis, splitting and reduplication of the internal elastic lamina, intimal hyperplasia, mucinous degeneration of the subintima and media, and smooth muscle hyperplasia-have been reported by numerous authors, including Moore and Whiting (1986), Easley and Carpenter (1975), Schaeffer et al (2001), and Yoshizawa et al (1997). All authors also report fibrosis, parenchymal atrophy, and biliary hyperplasia.…”

“…Vascular hamartomas and congenital intrahepatic arteriovenous fistulae are rare in dogs (Schermerhorn et al 1997), and there has been only one previously reported case in a laboratory beagle (Yoshizawa et al, 1997). They arise from focal failure of differentiation of the common embryologic anlage into capillary, arterial, or venous structures and represent communications between the hepatic arteries and portal venous radicals, which leads to a retrograde flow of blood within the portal vein (Moore and Whiting 1986).…”

“…With time there is extracellular fibrosis and connective tissue substitution of muscle and elastic fibers (Hosgood 1989). All other reported cases of intrahepatic arteriovenous fistula in dogs have presented with acute onset neurological and gastrointestinal signs, ascites, and secondary (acquired) portocaval shunts from two to eighteen months of age (Easley and Carpenter 1975;Koide et al 2004;McGavin and Henry 1972;Moore and Whiting 1986;Schaeffer et al 2001;Schermerhorn et al 1997;Yoshizawa et al 1997). Although no clinical or biochemical abnormalities were apparent in this case, we hypothesize that as the lesion was limited to one liver lobe (the right median), which accounts for less than 25% of the normal liver, and considering the marked hypertrophy of the left and caudate lobes, the animal was able to compensate.…”

“…Vascular hamartomas and congenital intrahepatic arteriovenous fistulae are rare in dogs (Schermerhorn et al 1997), and there has been only one previously reported case in a laboratory beagle (Yoshizawa et al 1997). They have not been reported before in a clinically normal animal.…”

Congenital Hepatic Arteriovenous Fistula with Intrahepatic Portosystemic Shunt and Aortic Stenosis in a Dog

“…66(3): 299-302, 2004 Hepatic arteriovenous fistula is a condition characterized by a communication between the portal or the hepatic vein and hepatic artery. All previous case reports of dogs regarding this condition showed vascular abnormality with communication between the portal and hepatic artery [1,3,6,7,9,13]. Dogs with hepatic arteriovenous fistula usually exhibit ascites and secondary multiple portosystemic shunt (PSS) due to portal hypertension [8,12].…”