Ultrasonographic findings associated with congenital hepatic arteriovenous fistula in three dogs

Three dogs were determined to have hepatic arteriovenous fistulas. This condition is similar to a portosystemic shunt; however, cure necessitates hepatic lobectomy instead of a venous ligature. Because of this, it is useful to differentiate these 2 conditions before surgery. Ultrasonography was found to be simple, sensitive, and specific in diagnosing hepatic arteriovenous fistulas and differentiating them from portosystemic shunts.     

Ultrasonographic diagnosis of unusual portal vascular abnormalities in two cats

Two cases of ascites secondary to portal vascular abnormalities associated with portal hypertension are described. In the first case a five-month-old cat was presented with recurrent ascites and investigations showed that the underlying cause was a hepatic arteriovenous fistula. Ultrasonography showed direct communication of the coeliac artery and right branch of the portal vein. There was also hepatofugal flow in the main portal vein consistent with portal hypertension. The ultrasonographic features were similar to those seen in dogs with hepatic arteriovenous fistulae. In the second case, ascites, portal hypertension and an intraluminal mass in the main portal vein was diagnosed in a 16-year-old cat that had been presented with hyperthyroidism and hepatomegaly. Acquired portosystemic collaterals involving the left renal vein were present. Additional diagnostic investigations were not permitted. Ultrasonography was useful in both cases to document portal hypertension and the underlying cause.     

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.     

Hepatic lesions associated with intrahepatic arterioportal fistulae in dogs

Seven cases of hepatic arterioportal fistulae in young dogs (mean age 6 months) are described. All cases were presumed to be congenital in origin. The onset of clinical signs, which frequently included gastrointestinal and neurological disturbances, was usually sudden. All dogs had clinical evidence of portal hypertension in the form of ascites, and all developed multiple extrahepatic portacaval venous shunts consequential to portal hypertension. The neurological disturbances were likely the result of portacaval shunting. The arterial and venous vessels involved in the fistulae had markedly altered wall structure. Hepatic regions adjacent to the fistulae frequently evidenced marked bile duct proliferation. Hepatic parenchymal atrophy, relative collapse of distributing portal veins, dilatation of hepatic arterial branches and proliferation of hepatic arterioles were seen throughout the liver; these changes closely resembled those present with portacaval shunting in the absence of hepatic arterioportal fistulae. The importance of recognizing that hepatic arterioportal fistulae and multiple extrahepatic portacaval shunts usually coexist and separately influence the morphological appearance of the liver is stressed.     

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.     

Evaluation of three peripheral arteriovenous fistulas for hemodialysis access in dogs

OBJECTIVE: To design and create 3 types of arteriovenous fistulas (AVF) in normal dogs, to monitor the dogs for secondary cardiovascular complications, and to verify adequacy of these fistulas for hemodialysis vascular access. STUDY DESIGN: Experimental study. ANIMALS: ur normal adult dogs. METHODS: Cadaveric dissections were performed, and surgical protocols were generated for carotid-jugular (CJ), brachial-cephalic (BC), and distal caudal femoral-lateral saphenous anastomosis (DCFLS) AVF. Each surgical procedure was then performed in 2 live dogs. Echocardiography was performed at days 0, 1, 3, 7, 14, 28, and 56 to evaluate the dogs for evidence of volume overload secondary to AVF formation. Estimation of luminal diameter and confirmation of fistula patency were performed using percutaneous color Doppler ultrasound. At day 56, hemodialysis was performed using each fistula as a vascular access. RESULTS: No significant changes occurred in the echocardiographic variables over time. All fistulas were patent at day 56 with mean luminal diameters of 4.5 mm (CJ), 4 mm (BC), and 1.5 mm (DCFLS). The BC fistula was superior for ease of needle placement and stabilization and provided adequate blood flow for clinical hemodialysis. CONCLUSIONS: Based on this short-term study, arteriovenous fistulas appear to be a safe and effective means for hemodialysis access in dogs. CLINICAL RELEVANCE: The arteriovenous fistulas described provide an alternative to the central venous catheters currently used for chronic hemodialysis access in dogs.     

Hepatic Organelle Pathology in Dogs with Congenital Portosystemic Shunts

Diversion of portal blood in congenital portosystemic shunts (CPSS) results in liver atrophy and passage of toxins into the systemic circulation causing hepatic encephalopathy. In some dogs, there is indirect evidence for hepatic insufficiency, but histologic findings are equivocal. This study determined whether hepatocyte integrity in PSS is comprised at a subcellular level using analytical subcellular fractionation of liver biopsies. Six dogs with CPSS had hypoproteinemia (6/6), increased serum alkaline phosphatase (6/6) and alanine aminotransferase (4/6) activity, hypocholesterolemia (6/6), and decreased blood urea (2/6). Liver biopsy specimens had increased activities (mU/mg protein) of alkaline phosphatase (17.9 +/- 10.1; controls 5.1 +/- 5.3: P less than 0.01), but not of other plasma membrane enzymes. There were increased activities of endoplasmic reticular (neutral alpha-glucosidase: 1.67 +/- 0.7; controls 0.86 +/- 0.2: P less than 0.01) and lysosomal enzymes (N-acetyl-beta-glucosaminidase: 12.6 +/- 2.3; controls 6.24 +/- 2.7: P less than 0.01; alpha-mannosidase: 0.85 +/- 0.5; controls 0.39 +/- 0.3: P less than 0.05). Subcellular fractionation on reorientating sucrose density gradients showed a high-density peak of alkaline phosphatase suggestive of a specific increase in the biliary canalicular component of enzyme activity. Neutral alpha-glucosidase was shifted to denser fractions, indicative of an increase in the proportion of rough-to-smooth endoplasmic reticulum and consistent with enhanced synthesis of membranous enzymes. There was also evidence for increased fragility of intracellular organelles, particularly lysosomes. In contrast, histology showed either no abnormalities or minor degenerative changes compatible with hepatic underperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hepatic Abscesses Associated With Diabetes Mellitus in Two Dogs

Two diabetic dogs were presented for anorexia, persistent fever, and poor control of hyperglycemia. Both had neutrophilia with left shift, hypoalbuminemia, and increased serum alkaline phosphatase (SAP) activity. Radiography indicated intrahepatic gas densities in 1 dog and a hepatic mass in the other. Abdominal sonography demonstrated multiple well-demarcated hypoechoic hepatic lesions consistent with abscesses. Both dogs were successfully treated by surgical resection of the abscessed liver lobes inconjunction with antibiotics and supportive therapy. Good control of hyperglycemia was achieved in both dogs after recovery. Intracellular and extracellular Gram-negative rod-shaped bacteria were abundant in the abscesses from both dogs. These cases suggest an association between diabetes mellitus and hepatic abscessation.     

Dual-phase CT Angiography of the Normal Canine Portal and Hepatic Vasculature

A dual-phase computed tomography (CT) angiographic technique was developed to image the hepatic and portal vascular systems using a nonselective peripheral injection of contrast medium. The arterial phase of the dual-phase scan imaged the hepatic arteries and veins, and the portal phase imaged the portal vein as well as its tributaries and branches. There were three steps involved in acquiring the dual-phase scan: a survey helical scan for orientation, a dynamic scan for timing, and finally the dual-phase helical scan. Five normal dogs were imaged using a helical scan technique. The timing of the arterial and portal phases of the scan was calculated using time vs. attenuation graphs generated from a dynamic scan. The median time of appearance of contrast medium in the cranial abdominal aorta was 8.6 s and the median time of appearance of contrast medium in the hepatic artery occurred 0.4 s later. The median time of peak enhancement in the cranial abdominal aorta was 12.0 s. The median time of appearance of contrast medium in the portal vein was 14.6 s and median time of peak enhancement was 33.0 s. The dual-phase scans provided excellent vascular opacification. The hepatic arteries, hepatic veins, cranial and caudal mesenteric veins, splenic vein, gastroduodenal vein, and portal vein branches were all consistently well defined. Dual-phase CT angiography is a minimally invasive technique which provides an excellent three-dimensional representation of portal and hepatic vascular anatomy.     

CONTRAST‐ENHANCED PORTAL MAGNETIC RESONANCE ANGIOGRAPHY IN DOGS WITH SUSPECTED CONGENITAL PORTAL VASCULAR ANOMALIES

Contrast‐enhanced multiphase magnetic resonance angiography (CE‐MRA) was used in 17 dogs with a suspected congenital portal vascular anomaly. Portal vascular anomalies were identified in 16 of the 17 dogs. Eleven had a single intrahepatic portocaval shunt (two central divisional, three right divisional, and six left divisional), one dog had a double intrahepatic portocaval shunt, one dog had a hepatic arteriovenous malformation, one dog had a complex intrahepatic porto‐caval shunt. Two dogs had an extrahepatic portosystemic shunt and no shunt was identified in one dog. Total imaging time was <10 min and image quality was good to excellent in all dogs. Portal CE‐MRA is a feasible, fast and non invasive technique to diagnose portal vascular anomalies in dogs, with a large field‐of‐view and good anatomic depiction of the abnormal vessels. Based on these results, CE‐MRA is an efficient imaging technique for the diagnosis of portal vascular anomalies in dogs.     

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.     

Immunohistochemical detection of arteriolar hyperplasia in canine liver biopsy samples using the claudin-5 antibody

Claudins are key tight junctional proteins between adjacent epithelial, mesothelial or endothelial cells, which are responsible for the permeability of the paracellular space. This paper describes that the endothelial cells of normal hepatic arterioles, portal venules and portal lymphatics as well as the endothelium of sinusoids from dogs show strong membranous claudin-5 cross-reactivity. In 25 liver biopsy samples taken from dogs with portal vein hypoperfusion, an increased number of arterioles was detected in the portal areas (PAs) by the use of humanised anti-claudin-5 antibody. The increased number of hyperplastic hepatic arterioles per PA was 5-6, 8-12 and 15-20 in the case of small, medium-sized and large PAs, respectively. It is suggested that the claudin-5 marker can improve the detection of hepatic arteriolar proliferation in the PAs of liver samples.     

Dynamic computed tomographic quantitation of hepatic perfusion in dogs with and without portal vascular anomalies

OBJECTIVE: To compare hepatic, pancreatic, and gastric perfusion on dynamic computed tomography (CT) scans of clinically normal dogs with those of dogs with portal vascular anomalies. SAMPLE POPULATION: Dynamic computed tomography (CT) scans of 10 clinically normal dogs and 21 dogs with portal vascular anomalies. PROCEDURES: Retrospective analysis of dynamic CT scans. Hepatic arterial perfusion, hepatic portal perfusion, total hepatic perfusion, hepatic perfusion index, gastric perfusion, and pancreatic perfusion were calculated from time attenuation curves. RESULTS: Mean +/- hepatic arterial perfusion was significantly higher in affected dogs (0.57 +/- 0.27 mL/min x mL(-1)) than in clinically normal dogs (0.23 +/- 0.11 mL/min x mL(-1)), and hepatic portal perfusion was significantly lower in affected dogs (0.52 +/- 0.47 mL/min x mL(-1)) than in clinically normal dogs (1.08 +/- 0.45 mL/min x mL(-1)). This was reflected in the hepatic perfusion index, which was significantly higher in affected dogs (0.59 +/- 0.34), compared with clinically normal dogs (0.19 +/- 0.07). Gastric perfusion was significantly higher in dogs with portal vascular anomalies (0.72 +/- 0.44 mL/min x mL(-1)) than in clinically normal dogs (0.41 +/- 0.21 mL/min x mL(-1)), but total hepatic perfusion and pancreatic perfusion were not significantly different. Among subgroups, dogs with congenital intrahepatic portosystemic shunts and dogs with arterioportal fistulae had higher hepatic arterial perfusion than did clinically normal dogs. Dogs with congenital intrahepatic portosystemic shunts also had an increase in gastric perfusion and hepatic perfusion index. CONCLUSIONS AND CLINICAL RELEVANCE: Hepatic perfusion variables measured on CT scans revealed differences in hemodynamics between clinically normal dogs and those with portal vascular anomalies.     

Contrast‐enhanced ultrasonography is a feasible technique for quantifying hepatic microvascular perfusion in dogs with extrahepatic congenital portosystemic shunts

Extrahepatic‐congenital portosystemic shunt is a vascular anomaly that connects the portal vein to the systemic circulation and leads to a change in hepatic microvascular perfusion. However, an assessment of hepatic microvascular perfusion is limited by conventional diagnostic modalities. The aim of this prospective, exploratory study was to assess hepatic microvascular perfusion in dogs with extrahepatic‐congenital portosystemic shunt using contrast‐enhanced ultrasonography (CEUS) using perfluorobutane (Sonazoid^®). A total of 17 dogs were included, eight healthy dogs and nine with extrahepatic‐congenital portosystemic shunt. The time‐to‐peak (TTP), rising time (RT), and rising rate (RR) in the hepatic artery, portal vein, and hepatic parenchyma, as well as the portal vein‐to‐hepatic parenchyma transit time (ΔHP‐PV) measured from time‐intensity curve on CEUS were compared between healthy and extrahepatic‐congenital portosystemic shunt dogs. The RT of the hepatic artery in extrahepatic‐congenital portosystemic shunt dogs was significantly earlier than in healthy dogs (P = 0.0153). The TTP and RT of the hepatic parenchyma were significantly earlier in extrahepatic‐congenital portosystemic shunt dogs than in healthy dogs (P = 0.0018 and P = 0.0024, respectively). ΔHP–PV was significantly shorter in extrahepatic‐congenital portosystemic shunt dogs than in healthy dogs (P = 0.0018). CEUS effectively revealed changes in hepatic microvascular perfusion including hepatic artery, portal vein, and hepatic parenchyma simultaneously in extrahepatic‐congenital portosystemic shunt dogs. Rapid hepatic artery and hepatic parenchyma enhancements may reflect a compensatory increase in hepatic artery blood flow (arterialization) caused by a decrease in portal vein blood flow and may be used as an additional diagnostic test to distinguish extrahepatic‐congenital portosystemic shunt dogs from healthy dogs.     

Anomalous portosystemic anastomoses associated with chronic hepatic insufficiency in six young dogs.

Chronic hepatic insufficiency due to anomalies of the portal venous system was diagnosed in 6 young dogs. The disorder was characterized by a variety of abnormal central nervous system signs or ascites, or both. Laboratory findings were characteristic of chronic, generalized hepatic dysfunction. The diagnosis was established by angiographic studies of the portal venous system. Of the 6 dogs, 3 died, 1 was euthanatized, and 2 are still alive and require medical management for ascites.     

克伦特罗对绵羊肝脏血流量和氮代谢的影响

在4头门静脉、肝静脉、肠系膜静脉和股动脉上安装血管导管的绵羊中研究了克伦特罗（CL,0.8 mg/kgBW,肠系膜静脉给药,每天2次,连续5 d）对其肝脏生长代谢的影响。结果表明:CL对肝脏血流量影响较小。而在CL作用下绵羊血浆中尿素氮水平明显下降,肝静脉和门静脉血液尿素氮流量分别减少16.86％（P<0.01）和15.51％（P<0.05）。肝静脉多肽流量在CL处理期也较对照期下降38.71％（P<0.01）,门静脉处多肽水平处理期则与对照期相当。克伦特罗还增加绵羊肝脏IGF-I的合成和分泌,门静脉和肝静脉中的增加幅度分别为38.84％（P<0.01）和33.18％（P<0.01）。提示CL可通过增强对绵羊肝脏氮的储留及肝脏IGF-I的合成和分泌从而促进机体的生长代谢。     

Splanchnic Surface Oximetry during Experimental Portal Hypertension and Surgical Manipulation of Portosystemic Shunts in Dogs

Surface oxygen tension (PSO2) was measured in dogs during experimental manipulation of the portal vein and hepatic artery, and during surgery to correct portosystemic shunting. There was no alteration in PSO2 of liver, pancreas, duodenum, or jejunum during partial (50%) or complete reduction of hepatic artery flow. After 100% reduction in portal vein blood flow, PSO2 was lower in jejunum, duodenum, and liver. With 50% reduction in portal flow, PSO2 was significantly decreased only in jejunum. In six dogs with single extrahepatic shunts, there was a significant correlation between portal pressure and jejunal PSO2. It was concluded that measurement of visceral organ PSO2 represents an accurate noninvasive means of obtaining objective data on the effect of reduction in hepatic blood flow on perfusion of other select splanchnic organs.     

Hepatic Fibrosis in Dogs

Hepatic fibrosis is commonly diagnosed in dogs, often as a sequela to chronic hepatitis (CH). The development of fibrosis is a crucial event in the progression of hepatic disease that is of prognostic value. The pathophysiology of hepatic fibrosis in human patients and rodent models has been studied extensively. Although less is known about this process in dogs, evidence suggests that fibrogenic mechanisms are similar between species and that activation of hepatic stellate cells is a key step. Diagnosis and staging of hepatic fibrosis in dogs requires histopathological examination of a liver biopsy specimen. However, performing a liver biopsy is invasive and assessment of fibrotic stage is complicated by the absence of a universally accepted staging scheme in veterinary medicine. Serum biomarkers that can discriminate among different fibrosis stages are used in human patients, but such markers must be more completely evaluated in dogs before clinical use. When successful treatment of its underlying cause is feasible, reversal of hepatic fibrosis has been shown to be possible in rodent models and human patients. Reversal of fibrosis has not been well documented in dogs, but successful treatment of CH is possible. In human medicine, better understanding of the pathomechanisms of hepatic fibrosis is leading to the development of novel treatment strategies. In time, these may be applied to dogs. This article comparatively reviews the pathogenesis of hepatic fibrosis, its diagnosis, and its treatment in dogs.     

Detection of portal and systemic bacteremia in dogs with severe induced hepatic disease and multiple portosystemic shunts

OBJECTIVE: To determine existence of portal and systemic bacteremia in dogs with induced severe hepatic disease, compared with clinically normal dogs, before and after vena caval banding. ANIMALS: 6 control dogs and 10 dogs with induced severe hepatic disease and multiple portosystemic shunts (PSS). PROCEDURE: Dogs of the diseased group were given dimethylnitrosamine (2 mg/kg of body weight, PO) twice weekly until multiple PSS developed. Surgery was performed on dogs of both groups, and blood for baseline aerobic and anaerobic bacterial culture was collected from catheters placed in the portal and hepatic veins and caudal vena cava. All dogs underwent vena caval banding, and blood for aerobic and anaerobic bacterial culture was collected from the portal and hepatic venous catheters at 120, 240, and 360 minutes after banding. RESULTS: Compared with control dogs (16% gram-positive and 84% gram-negative bacteria), diseased dogs had significantly higher percentage of gram-positive bacteria (42% of positive culture results, P < or = 0.01) and significantly lower percentage of gram-negative bacteria (58% of positive culture results, P < or = 0.01) isolated. Pseudomonas aeruginosa was isolated most frequently from dogs of both groups; more than 1 organism was isolated from 5 dogs of each group. Antimicrobial susceptibility included that to aminoglycosides (particularly amikacin), fluorinated quinolones, and imipenem. CONCLUSION: Portal and systemic, predominantly gram-negative, bacteremia is present in catheterized, clinically normal dogs and dogs with dimethylnitrosamine-induced hepatic disease and multiple PSS.     

Arteriovenous Fistulas as an Aid in Blood Collection from Canine Blood Donors

To facilitate blood collection from blood donor dogs, arteriovenous fistulas were established between the common carotid arteries and external jugular veins in five adult dogs. Twelve to 16 mm, side-to-side anastomoses were created using simple interrupted 6–0 polypropylene sutures. Starting 1 month after the surgical procedure, 500 ml of blood was collected from each dog as required. Electrocardiography, thoracic radiography, and cardiac output and rate were used to monitor cardiac changes. Blood flow characteristics, and proliferative and dystrophic cellular changes occurring in the vessels were documented in one dog.
The mean blood collection times were 2 minutes and 45 seconds from the fistula site and 9.0 minutes from the opposite jugular vein. Ventricular hypertrophy and myocardial changes were observed on electrocardiogram in two dogs, and radiographic evidence of pulmonary hypertension was noted in three dogs. Reversed blood flow was documented in the common carotid artery and external jugular vein distal to the arteriovenous fistula. Four dogs were still in use as blood donors 1 to 1 1/2 years after establishment of the fistulas. Clinical signs of congestive heart failure were not observed.