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.     

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.     

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.     

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.     

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.     

ANATOMY OF EXTRAHEPATIC PORTOSYSTEMIC SHUNTS IN DOGS AS DETERMINED BY COMPUTED TOMOGRAPHY ANGIOGRAPHY

Congenital extrahepatic portosystemic shunts are anomalous vessels joining portal and systemic venous circulation. These shunts are often diagnosed sonographically, but computed tomography (CT) angiography produces high‐resolution images that give a more comprehensive overview of the abnormal portal anatomy. CT angiography was performed on 25 dogs subsequently proven to have an extrahepatic portosystemic shunt. The anatomy of each shunt and portal tributary vessels was assessed. Three‐dimensional images of each shunt type were created to aid understanding of shunt morphology. Maximal diameter of the extrahepatic portosystemic shunt and portal vein cranial and caudal to shunt origin was measured. Six general shunt types were identified: splenocaval, splenoazygos, splenophrenic, right gastric‐caval, right gastric‐caval with a caudal shunt loop, and right gastric‐azygos with a caudal shunt loop. Slight variations of tributary vessels were seen within some shunt classes, but were likely clinically insignificant. Two shunt types had large anastomosing loops whose identification would be important if surgical correction were attempted. A portal vein could not be identified cranial to the shunt origin in two dogs. In conclusion, CT angiography provides an excellent overview of extrahepatic portosystemic shunt anatomy, including small tributary vessels and loops. With minor variations, most canine extrahepatic portosystemic shunts will likely be one of six general morphologies.     

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.     

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.     

Per Rectal Portal Scintigraphy Using 99mTechnetium Pertechnetate to Diagnose Portosystemic Shunts in Dogs and Cats

Per rectal portal scintigraphy using 99mTechnetium pertechnetate (99mTcO4-) was used to diagnose portosystemic shunts (PSS) before surgical confirmation in seven dogs and two cats. Shunt fractions, representing the percent of portal blood that bypasses the liver, were determined by computer analysis of the scintigraphic images. Animals with portosystemic shunts had a mean preoperative shunt fraction of 84.02% (n = 9). The mean postoperative shunt fraction in four animals was 58.22%. The mean shunt fraction in ten control dogs was 5.00%. Per rectal portal scintigraphy is an innovative, easily performed, inexpensive method to diagnose congenital portosystemic shunts in dogs and cats.     

Cellophane banding for the gradual attenuation of single extrahepatic portosystemic shunts in eleven dogs

Objective To evaluate the efficacy and short term effects of a cellophane banding technique for progressive attenuation of canine single extrahepatic portosystemic shunts.
Design A prospective trial of 11 dogs with single congenital extrahepatic shunts.
Procedure Rectal ammonia tolerance testing and routine biochemical tests were performed preoperatively on all dogs. In seven dogs, preoperative abdominal Doppler ultrasonography was also performed. Exploratory laparotomy revealed a single extrahepatic portocaval shunt in each animal, which was attenuated using a cellophane band with an internal diameter of 2 to 3 mm. The abdomen was closed routinely. Follow-up biochemical analysis and abdominal Doppler ultrasonography or splenoportography were performed postoperatively.
Results The shunt was not amenable to total ligation in 11 dogs, based upon reported criteria. All dogs recovered uneventfully from surgery without evidence of portal hypertension, and showed clinical improvement thereafter. Shunt occlusion was deemed to have occurred in 10 dogs based on resolution of biochemical and/or sonographic abnormalities. One dog continued to have sonographic evidence of portosystemic shunting when evaluated 3 weeks after surgery, despite normal ammonia tolerance, but was lost to subsequent follow-up. Two dogs, in which 3 mm cellophane bands were placed, experienced delayed shunt occlusion.
Conclusion Cellophane banding is simple to perform, and causes progressive attenuation of single extrahepatic shunts in dogs. Further work is needed to determine the maximum diameter of a cellophane band which will produce total attenuation, and the long-term safety and reliability of the treatment.     

USE OF MAGNETIC RESONANCE ANGIOGRAPHY FOR DIAGNOSIS OF PORTOSYSTEMIC SHUNTS IN DOGS

A prospective study was conducted to determine the sensitivity and specificity of diagnosis of portosystemic shunts (PSS) and the accuracy of anatomically locating single congenital PSS in dogs using magnetic resonance angiography (MRA). MRA was performed on 10 normal dogs and 23 dogs with PSS. Sensitivity and specificity of MRA to diagnose any shunt among all dogs were 80% and 100%, respectively. Among dogs identified with PSS, sensitivity and specificity of MRA for diagnosis of multiple extrahepatic shunts were 63% and 97%, respectively, and for diagnosis of single congenital shunts were 79% and 100%, respectively. Using MRA, radiologists correctly identified shunts as extrahepatic or intrahepatic in 83% of patients and correctly identified the origin and insertion of the shunts in 57% and 97% of patients, respectively. Use of MRA is specific for diagnosis of PSS and is a sensitive indicator of anatomic location of single congenital portosystemic shunts.     

Outcomes of cellophane banding for congenital portosystemic shunts in 106 dogs and 5 cats

OBJECTIVE : To report outcomes after cellophane banding of single congenital portosystemic shunts in dogs and cats. STUDY DESIGN : Retrospective study of sequential cases. ANIMALS : One hundred and six dogs and five cats. METHODS : Medical records were reviewed for breed, sex, age at surgery, shunt anatomy, results of pre- and postoperative biochemical analysis, development of postligation neurologic dysfunction, portal hypertension or other serious complications, and the owners' perception of their animal's response to surgery. RESULTS : Ninety-five dogs and all 5 cats had extrahepatic shunts. Eleven dogs had intrahepatic shunts. Six dogs (5.5%) died as a result of surgery from portal hypertension (2 dogs), postligation neurologic dysfunction (2), splenic hemorrhage (1) and suspected narcotic overdose (1). Serious complications were more common in dogs with intrahepatic shunts than those with extrahepatic shunts (P=.002). Postligation neurologic dysfunction necessitated treatment in 10 dogs and 1 cat; 8 dogs and the cat survived. Clinical signs attributed to portosystemic shunting resolved or were substantially attenuated in all survivors. Postoperative serum bile acid concentrations or results of ammonia tolerance testing were available for 88 animals; 74 (84%) were normal and 14 (16%) were abnormal. Multiple acquired shunts were documented in two animals. CONCLUSIONS : Cellophane banding is a safe and effective alternative to other methods of attenuation. CLINICAL RELEVANCE : Slow occlusion of portosystemic shunts using a variety of methods is being evaluated world wide. Cellophane banding is a relatively simple procedure with comparable safety and efficacy to previously reported techniques.     

USE OF TRANSSPLENIC INJECTION OF AGITATED SALINE AND HEPARINIZED BLOOD FOR THE ULTRASONOGRAPHIC DIAGNOSIS OF MACROSCOPIC PORTOSYSTEMIC SHUNTS IN DOGS

We describe the use of ultrasonography‐guided percutaneous splenic injection of agitated saline and heparinized blood for the diagnosis of portosystemic shunts (PSS) in 34 dogs. Agitated saline mixed with 1 ml of heparinized autologous blood was injected into the spleen of 34 sedated dogs under sonographic guidance. The transducer was then sequentially repositioned to visualize the portal vein, the caudal vena cava, and the right atrium through different acoustic windows. It was possible to differentiate between intrahepatic and extrahepatic shunts depending on the entry point of the microbubbles into the caudal vena cava. Portoazygos shunts and portocaval shunts could be differentiated based on the presence of microbubbles in the caudal vena cava and/or the right atrium. In one dog, collateral circulation due to portal hypertension was identified. In dogs with a single extrahepatic shunt, the microbubbles helped identify the shunting vessel. The technique was also used postoperatively to assess the efficacy of shunt closure. All abnormal vessels were confirmed by exploratory laparotomy or with ultrasonographic identification of the shunting vessel. Ultrasound‐guided transsplenic injection of agitated saline with heparinized blood should be considered as a valuable technique for the diagnosis of PSS; it is easy to perform, safe, and the results are easily reproducible.     

Neurological dysfunction in three dogs and one cat following attenuation of intrahepatic portosystemic shunts

Neurological dysfunction is an uncommon complication following extrahepatic portosystemic shunt ligation. Three dogs and one cat are described that developed neurological signs within 21 to 42 hours of attenuation of intrahepatic portosystemic shunts. None of these cases had biochemical evidence of hepatic encephalopathy postoperatively. Two dogs died during management of status epilepticus following aspiration of food. One dog died six months postoperatively. The cat had persistent neurological dysfunction at discharge, but was alive and had recovered most of its neurological function at the time of writing, 37 months after surgery. This report demonstrates the potential for animals with intrahepatic portosystemic shunts to develop postoperative neurological signs and highlights the difficulty of managing such cases. Two dogs had both intrahepatic and extrahepatic portosystemic shunts. Large intestinal malrotation (partial situs inversus) may have been linked to the development of a portosystemic shunt in the remaining dog.     

TRANSVENOUS COIL EMBOLIZATION OF PORTOSYSTEMIC SHUNT IN DOGS

This paper describes transvenous coil embolization of portosystemic shunt in 10 dogs. Clinical signs resolved in 4 dogs with extrahepatic shunt, and in 3 dogs with intrahepatic shunt. Two dogs of less than 3 kg died because of migration of coils to the level of the main pulmonary artery. One dog was euthanized when acute portal hypertension developed following transvenous coil embolization. Transvenous coil embolization seems to be a less invasive alternative to surgical ligation in dogs with a single intrahepatic portosystemic shunt.     

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.     

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.     

USE OF TRANSCOLONIC 123I-IODOAMPHETAMINE TO DIAGNOSE SPONTANEOUS PORTOSYSTEMIC SHUNTS IN 18 DOGS

Transcolonic ¹²³I-Iodoamphetamine is rapidly absorbed across the colonic mucosa and binds to amine receptors in the liver and lungs. During the first ten minutes following colonic administration, a simple ratio of lung counts to lung counts plus liver counts provides an accurate estimate of the fraction of portal blood that bypasses hepatic sinusoids in dogs with portosystemic shunts. Studies were performed on 24 dogs with suspect portosystemic shunt. Shunt fraction values for 18 dogs with surgically confirmed portosystemic shunt were obviously higher than published values for normal dogs, and also significantly higher than values for the other six dogs, later confirmed to lack shunts. Postoperative studies were repeated on ten dogs with single shunt vessels 1–2 days after shunt closure. Total shunt ligation resulted in normal postoperative shunt fraction, whereas partial shunt ligation resulted in persistant elevation of shunt fraction. Transcolonic iodoamphetamine scintigraphy is noninvasive, easy to perform, and provides an accurate method to diagnose dogs with portosystemic shunt.     

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.     

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).