Surgical Management of Multiple Congenital Intrahepatic Shunts in Two Dogs

Objective —To present details of an unusual type of portosystemic shunt and its surgical management in two dogs.
Animals —Two young dogs that had a tentative diagnosis of a portosystemic shunt on the basis of clinical signs and serum biochemical abnormalities. Abdominal ultrasonography and contrast portography demonstrated multiple intrahepatic shunts. In both cases, the multiple shunts arose from a single branch of the portal vein.
Outcome—It was possible to locate and attenuate flow through the shunts via a transportal venotomy under conditions of hepatic vascular occlusion. Clinical and biochemical abnormalities resolved after surgery in both dogs. Postoperative sonography revealed complete obliteration of the shunt plexus in one of the dogs.     

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.     

Effect of breed on anatomy of portosystemic shunts resulting from congenital diseases in dogs and cats: a review of 242 cases

OBJECTIVE: To evaluate the effect of species and breed on the anatomy of portosystemic vascular anomalies in dogs and cats. DESIGN: Retrospective study of 233 dogs and nine cats presenting to the University Veterinary Centre, Sydney. METHODS: Case records were evaluated for breed, sex, age, anatomical and histological diagnosis. Cases were included when a portosystemic vascular anomaly resulted from a congenital or developmental abnormality of the liver or portal venous system. RESULTS: Disease conditions included single congenital portosystemic shunt with patent portal vasculature (214 dogs, nine cats), portal vein aplasia (nine dogs), multiple acquired shunts resulting from portal vein hypoplasia (seven dogs), biliary atresia (one dog) and microvascular dysplasia (one dog). One Maltese had a single, congenital shunt and multiple acquired shunts resulting from hepatic cirrhosis. Breeds that were significantly over-represented included the Maltese, Silky Terrier, Australian Cattle Dog, Bichon Frise, Shih Tzu, Miniature Schnauzer, Border Collie, Jack Russell Terrier, Irish Wolfhound and Himalayan cat. Bichon Frise with shunts were significantly more likely to be female than male (12:2, P < 0.001). Two hundred and fourteen dogs (91.4%), and all cats, had shunts that were amenable to attenuation. Inoperable shunts occurred in 19 dogs (8.2%). Fifty six of 61 (92%) operable shunts in large breed dogs were intrahepatic, versus 10/153 (7%) in small breeds (P < 0.0001). Breeds that were not predisposed to portosystemic shunts were significantly more likely to have unusual or inoperable shunts than dogs from predisposed breeds (29% versus 7.6%, P < 0.0001). No significant relationship between breed and shunt type could be determined in cats. CONCLUSION: Breed has a significant influence on shunt anatomy in dogs. Animals presenting with signs of portosystemic shunting may suffer from a wide range of operable or inoperable conditions. Veterinarians should be aware that unusual or inoperable shunts are much more likely to occur in breeds that are not predisposed to congenital portosystemic shunts.     

COMPARISON OF TRANSCOLONIC 123I-IODOAMPHETAMINE AND PORTAL VEIN INJECTION OF 99mTc-MACROAGGREGATED ALBUMIN SHUNT FRACTION CALCU-LATIONS IN EXPERIMENTAL DOGS WITH ACQUIRED POR-TOSYSTEMIC SHUNTS

Shunt fraction was determined using transcolonic ¹²³I-iodoamphetamine (IMP) and portal vein injection of ^99mTc-macroaggregated albumin (MAA) in a group of eight dogs with chronic cirrhosis and acquired portosystemic shunts subsequent to total common bile duct ligation. Hepatic parenchymal damage was confirmed by alterations in liver function tests and liver histology. Seven of the eight dogs developed portal hypertension and had angiographic evidence of hepatofugal portal blood flow with multiple peripheral portosystemic anastomoses. Shunt fractions determined in the seven dogs with shunts varied from 39 to 100 using IMP and 45 to 93 using MAA. The remaining dog had normal portal pressure, a normal portal angiogram, and normal IMP and MAA scintigraphic studies. There was an excellent correlation between the two methods of shunt fraction calculation (R²= 0.98) and the line of regression was not significantly different from unity (IMP = 1.09 × MAA - 0.03).     

Gradual Occlusion of Extrahepatic Portosystemic Shunts in Dogs and Cats Using the Ameroid Constrictor

Gradual occlusion of the splenic vein, using a specialized device (ameroid constrictor), was evaluated experimentally in three normal beagle dogs. Splenoportograms were used to verify that total occlusion of the splenic vein had occurred in all dogs within 4 to 5 weeks after application of the device. The ameroid constrictor (AC) was also evaluated as a method of gradual vascular occlusion in 12 dogs and two cats with single, extrahepatic, portosystemic shunts (PSS). Serum bile acid (SBA) concentrations were measured and portal scintigraphy (PS) was performed on all 14 animals preoperatively and 10, 20, 30, and 60 days postoperatively. Two dogs (14%) died from portal hypertension in the early postoperative period. One dog and one cat developed multiple acquired PSS, confirmed by mesenteric portography 90 days after the operation. Portal scintigraphy confirmed total occlusion of the primary shunt in the other 10 animals. Shunt fractions (SF), as measured by PS on postoperative days 30 and 60, declined significantly from preoperative values. Significant decreases were noted between preoperative and postoperative values for preprandial SBA on postoperative day 60 and for postprandial SBA on postoperative day 30. SBA concentrations did not correlate with SF. Based on this study, gradual vascular occlusion using the AC is recommended as a method for treatment of single, extrahepatic, PSS.     

Congenital Interruption of the Portal Vein and Caudal Vena Cava in Dogs: Six Case Reports and a Review of the Literature

Objective —To describe six dogs with congenital abnormalities involving the portal vein, caudal vena cava, or both.
Animals —Six client-owned dogs with congenital interruption of the portal vein or the caudal vena cava, or both.
Methods —Portal vein and caudal vena cava anatomy was evaluated by contrast radiography and visualization at surgery. Vascular casts or plastinated specimens were obtained in three animals.
Results —Portal blood shunted into the caudal vena cava in four dogs and the left hepatic vein in one. Two of these five dogs also had interruption of the caudal vena cava with continuation as azygous vein, as did an additional dog, in which the portal vein was normally formed. Portal vein interruption was present in 5 of 74 (6.8%) dogs with congenital portosystemic shunts evaluated at the Veterinary Teaching Hospital during the study period.
Conclusions —Serious malformations of the abdominal veins were present in more than 1 in 20 dogs with single congenital portosystemic shunts.
Clinical Relevance —Veterinarians involved in diagnosis and surgery for portosystemic shunts should be aware of these potential malformations, and portal vein continuity should be evaluated in all dogs before attempting shunt attenuation.     

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.     

A new dissection technique for approach to right-sided intrahepatic portosystemic shunts: anatomic study and use in three dogs

OBJECTIVE : To determine the feasibility of indirect suture passage around the right portal vein for attenuation of right-sided intrahepatic portosystemic shunts (IHPSS). STUDY DESIGN : Anatomic study of cadavers and prospective evaluation of clinical cases. ANIMALS : Nine canine cadavers (median weight, 20.5 kg) and 6 client-owned dogs suspected of having right-sided IHPSS. METHODS : Silicone casts of the caudal vena cava and pre- and intrahepatic portal veins were made in fresh canine cadavers. A suture was passed dorsal to the portal vein above and below its bifurcation and pulled laterally so that it surrounded the right portal vein. The number and size of portal and caudal vena cava branches that interfered with the suture passage were recorded. Intra- and postoperative complications were evaluated in 3 dogs with right-sided IHPSS and 3 dogs suspected of having right-sided IHPSS that had right portal vein dissection and occlusion using this technique. RESULTS : Suture passage and placement around the right portal vein were easily accomplished in all 9 specimens. A 1 mm branch from the dorsal surface of the right portal vein was included in the encircling ligature in 4 specimens. The dissection technique was used successfully in 3 dogs with right-sided IHPSS and 2 other clinical cases. The portal branch to the papillary process of the caudate lobe interfered with suture placement in 1 dog with a central IHPSS. CONCLUSIONS : Indirect suture passage for ligation of the right portal vein can be successfully performed in normal dogs and dogs with congenital portosystemic shunts. CLINICAL RELEVANCE : Hemorrhage, vascular trauma, and surgery time may be reduced using this technique for attenuation of right-sided IHPSS.     

SIMULTANEOUS CONGENITAL AND ACQUIRED EXTRAHEPATIC PORTOSYSTEMIC SHUNTS IN TWO DOGS

Two dogs with simultaneous congenital and acquired portosystemic shunts are reported. The first dog was an eight-month-old, male Golden Retriever with a history of peritoneal effusion, polyuria/polydipsia, and stunted growth. The dog had a microcytic, hypochromic anemia, a mildly elevated AST, and a moderate to severely elevated preprandial and postprandial serum bile acids. Transcolonic portal scintigraphy confirmed the presence of a portosystemic shunt. An intraoperative mesenteric portogram was performed. Two conjoined congenital extrahepatic portosystemic shunts and multiple acquired extrahepatic portosystemic shunts were identified. The second dog was a five-month-old, mixed breed with two week history of peritoneal effusion. Abdominal ultrasound and transcolonic scintigraphy were used to diagnose a portosystemic shunt. A single extrahepatic portosystemic shunt, portal hypertension, and multiple acquired collateral shunts were identified at surgery. The histologic alterations observed in these dogs were consistent with a portosystemic shunt. In these dogs, the presence of congenital and acquired portosystemic shunts and histopathologic findings are considered to represent a combination of congenital portosystemic shunts and noncirrhotic portal hypertension or portal vein hypoplasia.     

USE OF QUANTITATIVE HEPATIC SCINTIGRAPHY TO EVALUATE SPONTANEOUS PORTOSYSTEMIC SHUNTS IN 12 DOGS

Quantitative hepatic scintigraphy is a valid means for estimating total liver blood flow and relative portal hepatic perfusion. The Hepatic perfusion index (HPI) was determined for a group of 12 dogs with portosystemic shunts prior to and two days after corrective surgery. HPI values for the dogs prior to operation were significantly elevated (p<0.001) as compared with those for a group of normal dogs, indicating reduced effective portal hepatic perfusion in dogs with shunts. Dogs showing a favorable clinical response after surgery had a significant decrease (p<0.02) in HPI values after operation. One dog showing a poor clinical response after operation had an increase in HPI score after operation. Quantitative hepatic scintigraphy is a valuable diagnostic test for screening presumptive cases of portosystemic shunts and monitoring the response to surgical intervention.     

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.     

ULTRASONOGRAPHIC DIAGNOSIS OF CONGENITAL PORTOSYSTEMIC SHUNTS IN DOGS: RESULTS OF A PROSPECTIVE STUDY

The aims of this study were to determine if accurate diagnosis of congenital portosystemic shunt was possible using two dimensional, grey-scale ultrasonography, duplex-Doppler, and color-flow Doppler ultrasonography in combination, and to determine if dogs with congenital portosystemic shunts have increased or variable mean portal blood flow velocity. Eighty-two dogs with clinical and/or clinicopathologic signs compatible with portosystemic shunting were examined prospectively. Diagnosis of congenital portosystemic shunt was subsequently confirmed in 38 of these dogs using operative mesenteric portography: 14(37%) dogs had an intrahepatic shunt and 24(63%) had an extrahepatic shunt. Ultrasonography had a sensitivity of 95%, specificity of 98%, and accuracy of 94%. Ultrasonographic signs in dogs with congenital portosystemic shunts included small liver, reduced visibility of intrahepatic portal vessels, and anomalous blood vessel draining into the caudal vena cava. Correct determination of intra - versus extrahepatic shunt was made ultrasonographically in 35/38 (92%) dogs. Increased and/or variable portal blood flow velocity was present in 21/30 (70%) dogs with congenital portosystemic shunts. In one dog with an intrahepatic shunt the ultrasonographic diagnosis was based partly on finding increased mean portal blood flow velocity because the shunting vessel was not visible. Detection of the shunting vessel and placement of duplex-Doppler sample volumes were facilitated by use of color-flow Doppler. Two-dimensional, grey-scale ultrasonography alone is sufficient to detect most intrahepatic and extrahepatic shunts; sensitivity is increased by additional use of duplex-Doppler and color-flow Doppler. Increased and/or variable portal blood flow velocity occurs in the majority of dogs with congenital portosystemic shunts.     

Experimental evaluation of four methods of progressive venous attenuation in dogs

OBJECTIVE: To determine the most effective and reliable method for progressive attenuation of single extrahepatic portosystemic shunts in dogs. STUDY DESIGN: The effects of the four treatments on femoral vein diameter and histology were compared with controls. ANIMALS: Fourteen healthy adult dogs. METHODS: Twenty-eight canine femoral veins were subjected to sham surgery (4), partial attenuation using silk (5), cellophane banding (6), ameroid constrictor implantation (5), and intravascular thrombogenic coils (8). Changes in vein diameter were evaluated at weekly intervals using venography. After 6 weeks, the dogs were humanely euthanatized, and histopathology was performed on the femoral veins. RESULTS: Only cellophane and ameroid constrictors produced progressive and permanent vein attenuation. Ameroid constrictors produced complete occlusion within 14 days in four of five veins and by 21 days in the fifth vein. Cellophane banding produced slow progressive (but not complete) attenuation in five of six veins. Complete occlusion was demonstrated in four of eight veins after thrombogenic coil implantation; however, recanalization occurred in all but one dog. Perivascular silk did not produce significant progressive attenuation. CONCLUSIONS: Ameroid constrictors produced rapid occlusion of femoral veins. Cellophane banding resulted in slower attenuation. Thrombogenic coils produced attenuation, but this was not sustained in many cases. Silk did not promote ongoing attenuation. CLINICAL RELEVANCE: Both ameroid constrictor implantation and cellophane banding show promise for progressive attenuation of single extrahepatic portosystemic shunts in dogs. Because rapid occlusion was seen with ameroid constrictors, however, cellophane banding maybe a safer technique in animals with increased hepatic vascular resistance. Further evaluation of both treatments in clinical cases is warranted.     

Portal streamlining as a cause of nonuniform hepatic distribution of sodium pertechnetate during per-rectal portal scintigraphy in the dog

The purpose of this study was to evaluate nonuniform patterns of vascular distribution of pertechnetate in the dog during per-rectal portal scintigraphy. Ninety-two studies were reviewed retrospectively to document the patterns of radionuclide distribution. Forty-five studies were classified as normal and 47 were classified as diagnostic for a macrovascular portosystemic shunt. In these dogs, shunt fractions were calculated and compared using a t-test. In dogs with sufficient liver radioactivity for evaluation, the study was classified as having uniform, dorsal, central, or ventral radiopharmaceutical distributions. There were 51 animals (45 normal and six dogs with low-magnitude portosystemic shunts) with sufficient liver activity to assess the radionuclide distribution within the liver. A one-way ANOVA was used to compare shunt fractions between each of the distribution patterns. Two dogs were anesthetized and selective portovenograms were performed. Portovenograms were compared with the scintigraphic images to correlate the vascular distribution of the right, central, and left divisional branches of the portal vein. The shunt fraction in the 45 normal dogs was significantly lower than in the dogs with portosystemic shunts (5.7% +/- 4.8% vs. 78.6% +/- 20.0% (mean +/- SD), P < 0.001). Of the 51 dogs with sufficient liver activity to classify the pattern of distribution, there were 15/51 (31.4%) with uniform radionuclide distribution, 10/51 (19.6%) with focal dorsal distribution, 15/51 (29.4%) with focal ventral distribution, and 10/51 (19.6%) with focal central distribution. There was no significant difference in the shunt fractions between the groups. There were six dogs diagnosed with low-magnitude portosystemic shunt with sufficient liver radioactivity to categorize the vascular distribution of the radionuclide within the liver. Of these six dogs, two had focal dorsal distribution, one had focal central, one had focal ventral and two had uniform distribution. Focal dorsal distribution could result from streamlining of the radionuclide into the right divisional branch of the portal vein. Focal ventral distribution could result from streamlining the radionuclide into the left divisional branch of the portal vein. Focal central distribution could result from streamlining the radionuclide into the central divisional branch of the portal vein.     

Re-evaluation of a portocaval venograft without an ameroid constrictor as a method for controlling portal hypertension after occlusion of intrahepatic portocaval shunts in dogs

OBJECTIVE: To evaluate the use of a portocaval venograft without an ameroid constrictor in the surgical management of intrahepatic portosystemic shunts (PSS). STUDY DESIGN: Prospective clinical study. ANIMALS: Seven dogs with intrahepatic PSS. METHODS: Portal pressure was measured after temporary suture occlusion of the intrahepatic PSS. In dogs with an increase in portal pressure > or =8 mm Hg or signs of portal hypertension, a single extrahepatic portocaval shunt was created using a jugular vein. Clinical outcome and complications were recorded. RESULTS: The mean (+/-SD) portal pressure increased from 5.9+/-1.6 to 17.9+/-4.1 mm Hg with PSS occlusion. There were no intraoperative complications and, after creation of the portocaval shunt, the intrahepatic PSS could be completely ligated in all dogs. The final portal pressure was 9.6+/-1.9 mm Hg. Complications developed during postoperative hospitalization in 5 dogs and included incisional discharge (4 dogs), ascites (3), ventricular premature contractions (2), and melena, bloody diarrhea, neurologic signs, coagulopathy, and aspiration pneumonia (each in 1 dog). Six dogs died or were euthanatized with clinical signs related to depression, inappetance, abdominal pain, vomiting, melena, and abdominal distention, with a median survival of 82 days (range, 20-990 days). One dog was clinically normal at 33 months after surgery. CONCLUSIONS: Clinical signs observed in 6 dogs after surgery were consistent with portal hypertension. Use of a portocaval venograft without an ameroid constrictor may reduce the likelihood of hepatic vascular development, thereby increasing the risk of life-threatening portal hypertension should the venograft suddenly occlude. CLINICAL RELEVANCE: Use of a portocaval venograft without an ameroid constrictor to control portal hypertension after ligation of an intrahepatic PSS cannot be recommended.     

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.     

Use of transcolonic portal scintigraphy to evaluate efficacy of cellophane banding of congenital extrahepatic portosystemic shunts in 16 dogs

OBJECTIVE: To evaluate the efficacy of cellophane banding of single congenital extrahepatic portosystemic shunts in dogs using transcolonic portal scintigraphy. To investigate the portal circulation of those dogs with elevated postoperative shunt fractions to determine the cause of the persistent shunting. Further, to evaluate whether presenting signs, clinical pathology findings and liver histopathology are predictive of outcome. DESIGN: Prospective study of 16 dogs presenting with single congenital extrahepatic portosystemic shunts. PROCEDURE: Dogs with single extrahepatic portosystemic shunts attenuated by cellophane banding underwent portal scintigraphy and bile acids tolerance testing pre- and post-operatively. Dogs identified with elevated shunt fractions at 10 weeks post-operatively underwent mesenteric portovenography. Qualitative hepatic histopathology from all dogs was reviewed by a veterinary pathologist and assigned a semi-quantitative score to identify any abnormalities that may predict surgical outcome. RESULTS: At 10 weeks post cellophane banding, 10 of 16 cases (63%) had normal shunt fractions, whilst six dogs (37%) had increased shunt fractions and seven dogs (44%) had increased serum bile acids. Of these dogs, mesenteric portovenography revealed incomplete closure of the shunt in three dogs (18.6%) and multiple acquired shunts in three dogs (18.6%). Liver histopathology findings were similar for all dogs, regardless of outcome. CONCLUSIONS: Cellophane banding is an efficacious method for complete gradual occlusion of single extrahepatic shunts when the shunt vessel is attenuated to < or = 3 mm. Transcolonic portal scintigraphy is a reliable method for assessment of shunt attenuation and, unlike serum bile acids, is not influenced by other causes of liver dysfunction.     

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.     

Congenital portosystemic shunts in toy and miniature poodles

Three male Poodles (two Toy, one Miniature) were presented to their veterinarians for evaluation of urolithiasis and varying degrees of hepatic encephalopathy. All three dogs were diagnosed as having intrahepatic shunts and referred for surgical correction. In each case, shunts arose from the right branch of the portal vein and were amenable to perivascular dissection caudal to where the vessel entered the hepatic parenchyma and to placement of perivascular cellophane bands to achieve shunt attenuation. During the same period, a female Miniature Poodle also presented for treatment of a congenital portosystemic shunt discovered during evaluation for generalised motor seizures. This animal had an extrahepatic portoazygous shunt that was completely ligated. Congenital portosystemic shunts have not previously been identified in Toy and Miniature Poodles at the University Veterinary Centre, Sydney and the anatomical types of shunt seen in this breed have not previously been reported in a consecutive series of cases. The three male dogs are noteworthy for a number of reasons: all had intrahepatic shunts, despite being small breed dogs; all three presented in a similar fashion, and all had shunts of an anatomical type amenable to placement of cellophane bands. One male dog died within 12 hours of surgery, the remaining three dogs survived and their liver function was normal at follow-up between 2 and 3 months after surgery. Use of cellophane bands for successful attenuation of intrahepatic shunts has not been previously reported.