Ascites associated with intrahepatic arteriovenous fistula in a cat.

A 1 1/2-year-old male domestic short-haired cat with ascites was found to have an intrahepatic fistula between the hepatic artery and portal vein. The diagnosis was made by means of angiography. The ascites was attributed to portal hypertension caused by the fistula.     

CT features of extrahepatic arterioportal fistula in two cats

Two cats presented with large volume ascites and the cause was suspected to be portal hypertension. On contrast CT they both showed enhancement of the main portal vein during the arterial phase and an anomalous connection between the celiac artery and extrahepatic portal vasculature, prompting a diagnosis of extrahepatic arterioportal fistula. An extrahepatic arterioportal fistula is a connection between any artery and the portal vein outside the liver and, to our knowledge, this is the first report in cats.     

Circulatory disorders of the liver in dogs and cats

Summary

This paper presents a review of the literature on hepatic circulation and circulatory disorders of the liver in the dog and cat, and also includes a number of our own not previously published data. Circulatory disorders of the liver are frequently observed in dogs and cats. These disorders can be divided into congenital portosystemic shunts, disorders associated with outflow disturbances, and disorders associated with portal hypertension. Outflow disturbances result in passive congestion of the liver and in both species are mainly due to cardiac failure. Portal hypertension with resultant portosystemic collateral circulation and ascites mainly results from chronic liver disease, particularly cirrhosis. The main vascular disorder resulting in portal hypertension and ascites in the dog is primary hypoplasia of the portal vein.     

Ascites due to pre-sinusoidal portal hypertension in dogs: a retrospective analysis of 17 cases

Accumulation of a pure transudate abdominal effusion in the absence of significant hypoalbuminaemia is uncommon in dogs and is due to pre-sinusoidal portal hypertension. Reported causes of pre-sinusoidal portal hypertension vary, but suggest a reasonable prognosis. A retrospective analysis of 17 dogs that presented to our institution with ascites due to pre-sinusoidal portal hypertension identified idiopathic hepatic fibrosis or canine chronic hepatitis as the underlying cause in the majority of cases. Twelve (70.5%) dogs were 4 years of age or younger at time of presentation. Total serum protein was higher in dogs with chronic hepatitis than it was in dogs without inflammatory disease. The prognosis was generally poor and no histological, imaging or biochemical parameters were useful as prognostic indicators. Dogs died or were euthanased due to severe clinical signs associated with the portal hypertension and/or perceived poor prognosis.     

Partial Hepatectomy with Temporary Hepatic Vascular Occlusion in Dogs with Hepatic Arteriovenous Fistulas

A technique for temporary hepatic vascular occlusion during partial hepatectomy for hepatic arteriovenous (AV) fistulas in the dog is presented in seven dogs, and three additional cases of hepatic AV fistulas are reviewed. Hematologic, serum biochemical, radiologic, and nuclear scintigraphic parameters before and after surgery are discussed; abnormalities included anemia, hypoproteinemia, leukocytosis, increased liver function tests, retrograde filling of the portal vein during celiac angiography, and increased arteriovenous ratios during nuclear scintigraphy. Hemodynamic and pathologic findings are presented, and portal hypertension and secondary multiple portosystemic shunts are described. Clinical improvement was observed in four dogs with follow-up periods ranging from 5 months to 3 years.     

Congenital hepatic arteriovenous fistula with intrahepatic portosystemic shunt and aortic stenosis in a dog

Examination of a 2-month-old male golden retriever presented to the hospital revealed malnutrition, ascites, cardiac murmur and hyperammonemia. Identification of subaortic stenosis and hepatic arteriovenous fistula was made through ultrasonography and angiocardiography. In addition, intrasurgical mesenteric portography showed an intrahepatic portosystemic shunt. The dog did not show portal hypertension and secondary multiple extrahepatic portosystemic shunts. Surgical correction was attempted after medical treatment. The hepatic artery branch which was connected to the hepatic arteriovenous fistula was separated, and completely ligated using silk ligature. However, the separation of the intrahepatic shunt blood vessel was unsuccessful and the dog died 15 hr postoperatively.     

Ascites and portal hypertension in three young dogs with non-fibrosing liver disease

Three young dogs were evaluated because of the sudden development of ascites. In each case ascites was referable to non-fibrosing hepatic disease associated with portal hypertension. Obstruction to portal flow was pre-sinusoidal in two cases and post sinusoidal in the other. In all cases ascites developed in the absence of severe hypoalbuminaemia. The ratio of the protein content of ascitic fluid in relation to the protein content of plasma proved useful in differentiating between pre- and post sinusoidal portal hypertension. All three animals died or were euthanased because of the sequelae of portal hypertension.     

Hepatic arteriovenous fistulae and portal vein hypoplasia in a Labrador retriever

An 18-month-old male Labrador retriever was referred for investigation of chronic intermittent diarrhoea and vomiting of two months duration. A diagnosis of hepatic arteriovenous fistulae was made. These are extremely rare hepatic vascular anomalies which confer arterial pressure to the portal vein. Liver atrophy, portal vein hypoplasia, portal hypertension and multiple acquired portosystemic collateral vessels are the main complications. Surgical excision is a challenge as resection of large lesions may be associated with significant blood loss. In this dog, persistence of portal vein hypoplasia and extensive collateral pathways following surgery led to a reserved prognosis.     

ULTRASONOGRAPHIC DIAGNOSIS OF PORTAL VEIN THROMBOSIS IN FOUR DOGS

Ante mortem diagnosis of portal vein thrombosis was determined ultrasonographically in four dogs. In each dog the thrombus was visible in two-dimensional, grey-scale images of the portal vein obtained through a right intercostal window. Duplex-Doppler measurements and color-Doppler images provided information about the effects of thrombosis on portal blood flow. Reduced portal blood flow compatible with portal hypertension was detected in three dogs. A hypercoagulable state was probably involved in the pathogenesis of portal vein thrombosis in two dogs, one with pancreatitis and gastrointestinal blood loss and another with protein-losing nephropathy and probable immune-mediated anemia. The third dog had chronic ehrlichiosis; thrombosis was probably secondary to vasculitis. The remaining dog had thrombosis secondary to invasion of the portal vein by a recurrent duodenal neoplasm. This dog was euthanized because the tumor was considered inoperable. The dog with pancreatitis developed acute portal hypertension due to obstruction of the portal vein by the thrombus and was euthanized. The dogs with protein-losing nephropathy and ehrlichiosis were treated medically and recovered. Although portal vein thrombosis is uncommon, this complication should be considered in dogs with a variety of abdominal or systemic disorders. Ultrasonography is a practical method for diagnosis of portal vein thrombosis and detection of the underlying cause.     

INDIRECT AND DIRECT DETERMINATION OF THE PORTAL VEIN PRESSURE IN NORMAL AND ABNORMAL DOGS AND NORMAL CATS1

Portal hypertension resulting in ascites and portosystemic shunts leading to hepatoencephalopathy are major clinical manifestations of hepatic circulatory disease. Diffuse liver disease impairing sinusoidal blood flow can induce portal hypertension, portosystemic shunts, or both. The liver may also be involved secondarily in posthepatic hypertension and become the site of ascitic fluid formation. Portosystemic shunts may or may not be associated with portal hypertension. Selective catheterization of the hepatic and portal veins permits one to record pressures and to outline gross and subgross vascular anomalies by injecting contrast medium. Sequential pressure recordings in the caudal vena cava, in a free and wedged hepatic vein position, in the splenic pulp, and directly in the portal vein are the bases for the differentiation of prehepatic, liver-induced, and posthepatic portal hypertension. In addition to localizing the disease process along the postcaval-portal vein axis, pressure measurements are a reliable basis for the prognosis and selection of the most appropriate therapy. In dogs with portacaval shunts, wedge hepatic vein pressure recordings assist in the detection of hepatic sinusoidal anomalies that limit blood flow and preclude surgical ablation of the shunts. The various technics and their suitability for direct and indirect portal vein pressure recording are described and evaluated. Normal portal vein pressure values in 11 dogs and two cats, using different technics, are provided. The clinical usefulness of the various technics of pressure recording and angiography was illustrated in ten dogs with ascites, hepatoencephalopathy, or both.     

Idiopathic hepatic veno-occlusive disease causing Budd-Chiari-like syndrome in a cat

Budd-Chiari-like syndrome (BCLS) is a rare clinical entity characterised by portal hypertension and ascites. This report describes a case of BCLS in a cat due to obstruction at the level of the hepatic veins. The diagnosis was based on the clinical findings and a histopathological assessment of the liver demonstrating perivenular fibrosis around the central and sublobular veins. Although these lesions are similar to those observed in man with BCLS, the aetiology in this case remains unknown.     

Portal hypertension in a dog due to circumscribed fibrosis of the wall of the extrahepatic portal vein

A two-and-a-half-year-old German shepherd dog with ascites and a high concentration of blood ammonia was investigated. Sonographically, its liver was normal but the portal vein was dilated and the flow of blood within it was slow. A liver biopsy showed that the liver was normal, and did not reveal any possible cause of portal hypertension or ascites. Postmortem, the cranial part of the portal vein was dilated with a cross-striped internal surface, but the caudal part looked normal; there was a stenotic ring between the normal and dilated parts. Histology of the dilated segment revealed marked hypertrophy of both the internal circular and the external longitudinal smooth muscle layers. At the site of the stenosis, the longitudinal muscular layer was replaced by connective tissue. Circumscribed fibrosis in the wall of the portal vein was responsible for the stenosis and the subsequent prehepatic portal hypertension. The cross-striped pattern in the dilated part of the vein was the result of hypertrophy of the inner circular smooth muscle layer.     

Pericardial ectopic liver in a cat

An aged domestic short-haired cat was presented for examination because of a six week history of weight loss, diarrhoea, and increased appetite. Clinical examination revealed the cat to be emaciated, icteric and the liver was enlarged. Laboratory tests confirmed the presence of hepatic disease and radiographic examination showed hepatomegaly and ascites together with an enlarged globular heart. Ultrasonography showed a heart of normal size surrounded by tissue and/or fluid within the pericardial sac. Following euthanasia, necropsy revealed the presence of ectopic hepatic tissue within the pericardial sac. Both normally positioned liver and the intrapericardial hepatic tissue showed chronic active pericholangitis and nodular hyperplasia. There was no evidence of a diaphragmatic peritoneal-pericardial hernia, but the intrapericardial mass was connected to the liver by a thin cord of tissue ventral to the caudal vena cava.     

ULTRASONOGRAPHIC DIAGNOSIS OF PORTOSYSTEMIC SHUNTING IN DOGS AND CATS

The value of ultrasonography was evaluated in 85 dogs and 17 cats presented with a clinically suspected portosystemic shunt (PSS). A PSS was confirmed in 50 dogs and nine cats (single congenital extrahepatic in 42, single congenital intrahepatic in 11, and multiple acquired in six). Six dogs and one cat had hepatic microvascular dysplasia, and 29 dogs and seven cats had a normal portal system. Ultrasonography was 92% sensitive, 98% specific, and had positive and negative predictive values of 98% and 89%, respectively, in identifying PSS, with an overall accuracy of 95%. When a PSS was identified with ultrasonography, extrahepatic, intrahepatic, and multiple acquired PSS could be correctly differentiated in 53/54 patients (98%). The combination of a small liver, large kidneys, and uroliths had positive and negative predictive values of 100% and 51% for the presence of a congenital PSS in dogs. The portal vein/aorta (PV/Ao) and portal vein/caudal vena cava (PV/ CVC) ratios were smaller in animals with extrahepatic PSSs compared with animals with microvascular dysplasia, intrahepatic PSSs and those without portal venous anomalies (P<0.001). All dogs and cats with a PV/Ao ratio of < or = 0.65 had an extrahepatic PSS or idiopathic noncirrhotic portal hypertension. Dogs and cats with PV/Ao and PV/CVC ratios of > or = 0.8 and > or = 0.75, respectively, did not have an extrahepatic PSS. Reduced or reversed portal flow was seen in four of four patients with multiple acquired PSSs secondary to portal hypertension. The presence of turbulence in the caudal vena cava of dogs had positive and negative predictive values of 91% and 84%, respectively, for the presence of any PSS terminating into that vein.     

DOPPLER ULTRASONOGRAPHIC DIAGNOSIS AND ANATOMY OF CONGENITAL INTRAHEPATIC ARTERIOPORTAL FISTULA IN A PUPPY

A dilated, tortuous blood vessel was identified sonographically in the right medial liver lobe in a puppy with severe ascites. This vessel was thought to represent the dilated right medial portal vein branch. Using pulsed wave Doppler ultrasonography, retrograde, abnormally pulsatile flow was detected in both the dilated right medial portal vein branch and the main portal vein. The right medial liver lobe was surgically resected then fixed in formalin. Silicon rubber was injected and outlined the connection between the portal vein and hepatic artery.     

A Syndrome Resembling Idiopathic Noncirrhotic Portal Hypertension in 4 Young Doberman Pinschers

We describe 4 young male Doberman Pinschers (3 littermates and 1 unrelated dog) with a syndrome resembling idiopathic or noncirrhotic portal hypertension of humans. Each dog was evaluated for a hepatopathy resulting in portal hypertension, development of portosystemic collateral vessels, and hepatic encephalopathy. These dogs differ from previous reports of young dogs with hepatic insufficiency associated with portal hypertension and acquired portal systemic shunting by their lack of intrahepatic arteriovenous fistulae, portal vein atresia, or intrahepatic fibrosis. Clinicopathologic features included erythrocyte microcytosis, normal to mildly increased liver enzyme activities, increased concentrations of serum bile acids, reduced plasma indocyanine green clearance, and normal total bilirubin concentration. Abdominal ultrasonography disclosed a small liver and portosystemic collateral vessels. Radiographic imaging studies confirmed hepatofugal portal circulation and discounted hepatic arteriovenous fistulae. Histopathologic features in liver tissue from each dog were similar and consistent in all sections examined. Common findings included increased cross-sectional views of hepatic arterioles; hepatic lobular atrophy; scanty increase in connective tissue around some large portal triads; and absence of inflammation, disturbed lobular architecture, bile duct proliferation, or intrahepatic cholestasis.     

Ultrasonographic findings in dogs with hyperammonemia: 90 cases (2000-2002)

OBJECTIVE: To determine ultrasonographic abnormalities in dogs with hyperammonemia. DESIGN: Retrospective study. ANIMALS: 90 client-owned dogs with hyperammonemia. PROCEDURE: Ultrasonography of the abdominal vessels and organs was performed in a systematic way. Dogs in which the ultrasonographic diagnosis was a congenital portosystemic shunt were included only if they underwent laparotomy or necropsy. Dogs in which the abdominal vasculature appeared normal and dogs in which the ultrasonographic diagnosis was acquired portosystemic shunts and portal hypertension were included only if liver biopsy specimens were submitted for histologic examination. RESULTS: Ultrasonography excluded portosystemic shunting in 11 dogs. Acquired portosystemic shunts were found in 17 dogs, of which 3 had arterioportal fistulae and 14 had other hepatic abnormalities. Congenital portosystemic shunts were found in 61 dogs, of which 19 had intrahepatic shunts and 42 had extrahepatic shunts. Intrahepatic shunts originated from the left portal branch in 14 dogs and the right portal branch in 5. Extrahepatic shunts originated from the splenic vein, the right gastric vein, or both and entered the caudal vena cava or the thorax. Ultrasonography revealed splenic-caval shunts in 24 dogs, right gastric-caval shunts in 9 dogs, splenic-azygos shunts in 8 dogs, and a right gastric-azygos shunt in 1 dog. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that ultrasonography is a reliable diagnostic method to noninvasively characterize the underlying disease in dogs with hyperammonemia. A dilated left testicular or ovarian vein was a reliable indicator of acquired portosystemic shunts.     

Obstructed portal venous flow and portal vein thrombus in a dog

A young adult Doberman Pinscher had clinical signs and laboratory data consistent with the copper-associated hepatopathy commonly found in Doberman Pinschers. Hepatic biopsy and hepatic copper analysis did not support this diagnosis. Furthermore, changes seen in the hepatic biopsy specimen did not explain the acquired portosystemic shunting or the portal hypertension that the dog had. A mesentery venoportagram revealed markedly delayed filling of one portal vein, and necropsy revealed a small thrombus partially occluding that hepatic vein. It was not determined whether obstructed portal venous flow caused the portal vein thrombus or vice versa; however, it was theorized that the portal vein thrombus, once formed, contributed to further portal hypertension and/or delayed portal vein filling.     

Diagnostic imaging features of hepatic myelolipoma incarcerated in a peritoneopericardial diaphragmatic hernia in a cat

A 1-year-old male Persian cat was presented for castration. Liver incarcerated in a peritoneopericardial diaphragmatic hernia (PPDH) was diagnosed through pre-anesthetic tests. Multiple homogeneous hyperechoic nodules in the hepatic parenchyma were identified using ultrasound. The nodules showed decreased attenuation compared with normal hepatic parenchyma, and the herniated hepatic parenchyma showed increased arterial and decreased portal enhancement on computed tomography. From the histopathology, we diagnosed hydropic degeneration with portal fibrosis and myelolipoma. This report presents diagnostic imaging features of hepatic myelolipoma incarcerated in a PPDH in a cat. When perfusion of the hepatic parenchyma is altered, surgical treatment should be considered.