IMAGING DIAGNOSIS—PORTAL VEIN APLASIA AND INTERRUPTION OF THE CAUDAL VENA CAVA IN THREE DOGS

Severe portal vascular anomalies have been reported previously accompanying azygos continuation of the caudal vena cava, polysplenia, and situs anomalies in dogs and people. Three dogs with portal vascular anomalies were identified by means of CT angiography as having portal vein aplasia with portal insertion into the caudal vena cava, azygos continuation of the caudal vena cava, and interruption of the pre‐hepatic caudal vena cava. This information confirms that complex embryological defects may occur in patients presenting for congenital portosystemic shunt, and that CT angiography is a non‐invasive method of completely evaluating these potentially non‐surgical portal vascular anomalies.     

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.     

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.     

HELICAL COMPUTED TOMOGRAPHIC PORTOGRAPHY IN TEN NORMAL DOGS AND TEN DOGS WITH A PORTOSYSTEMIC SHUNT

Contrast enhanced helical computed tomography (CT) of the liver and portal system is routinely performed in human patients. The purpose of this project is to develop a practical protocol for helical CT portography in the dog. Ten clinically normal dogs were initially evaluated to develop a protocol. Using this protocol, ten dogs with confirmed portosystemic shunts (PSS) were then evaluated. Each patient was anesthetized, and a test dose of sodium iothalamate (400 mg I/ml) at 0.55 ml/kg was injected. Serial images were acquired at the level of T12-13 or T13-L1. The time to maximum enhancement of the portal vein was determined. This time period was used as the period between the second injection (2.2 ml/kg) and the start of the helical examination of the cranial abdomen. Delay times for normal dogs ranged from 34.5 s-66.0 s (median: 43.5 s) or 1.41 s/kg-4.12 s/kg (median: 2.09 s/kg). For patients with a PSS, the delay times were 16.5-70.5 s (median: 34.5 s) or 1.47-19.17 s/kg (median: 3.39 s/kg). The aorta, caudal vena cava, portal vein, shunt vessels, and their respective branches were well visualized on the CT images. Clinical case results were surgically confirmed. The surgeons reported that the information gained from the CT portography resulted in a subjective decrease in surgical time and degree of dissection necessary compared with similar surgeries performed without angiographic information. We believe that helical CT portography in the dog will be a useful adjunct in the diagnosis of PSS. The use of helical CT portography may allow clinicians to give clients a more accurate prognosis prior to surgery and will allow patients with lesions that are not surgically correctable to avoid a costly and invasive procedure.     

INTRAHEPATIC VENOUS COLLATERALS PREVENTING SUCCESSFUL STENT-SUPPORTED COIL EMBOLIZATION OF INTRAHEPATIC SHUNTS IN DOGS

The purpose of the following study was to evaluate stent-supported coil embolization of the hepatic vein in combination with antithrombotic treatment as a method for treatment of intrahepatic shunts, and to describe the complications associated with this procedure. Seven dogs with an intrahepatic shunt were included in a prospective clinical trial. A stepwise procedure was performed. First intervention: transjugular retrograde portography and stent implantation into caudal vena cava; second intervention: hepatic vein embolization combined with an antithrombotic treatment; third intervention in dogs with residual shunting: hepatic vein embolization without antithrombotic treatment. A right shunt was found in one dog and a left shunt in six dogs. Primary intrahepatic venous collaterals were found in one dog and hepatic vein embolization was not performed. Stent implantation into the caudal vena cava was performed in the other six dogs. There was no stent migration or thrombosis. Following the first coil intervention two dogs died due to vessel laceration while removing an oversized or migrated coil. On follow-up the shunt was completely closed in one dog. Secondary intrahepatic venous collaterals developed after the first or second coil intervention in two and one dog, respectively. In conclusion, stent-supported coil embolization of the hepatic vein in combination with an antithrombotic treatment was of limited success because primary or secondary intrahepatic venous collaterals tend to occur.     

Computed tomographic and magnetic resonance imaging features of canine segmental caudal vena cava aplasia

O bjective : To describe the computed tomographic and magnetic resonance imaging features of segmental caudal vena cava aplasia and associated vascular anomalies in dogs.
M ethods : A retrospective study was performed reviewing computed tomographic and magnetic resonance imaging archives of eight institutions for dogs with segmental caudal vena cava aplasia. Inclusion criteria included a computed tomographic or magnetic resonance imaging study and supportive diagnostic and follow-up information. Abdominal vessels were reviewed for size, shape, location and course (including tributaries and branches) and classified as normal, abnormal or shunt vessels.
R esults : Ten dogs with segmental caudal vena cava aplasia were identified. In all dogs, postrenal caval blood was shunted to either a right or a left azygos vein, with seven different angiographic patterns. Affected dogs were predominantly female (70 per cent) and young (mean 2·6 years). Additional portocaval and porto-azygos shunt vessels were identified in two cases each. Computed tomographic angiography and magnetic resonance angiography depicted details of abdominal vessels including thrombus formation in one dog.
C linical S ignificance : Segmental caudal vena cava aplasia is a vascular congenital anomaly in the dog that can be associated with thrombosis and portosystemic shunts. Computed tomographic angiography and magnetic resonance angiography are excellent tools to demonstrate the complex vascular anatomy and to guide treatment planning for portosystemic shunts and thrombolytic therapy.     

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 evaluation of partially attenuated congenital extrahepatic portosystemic shunts in 14 dogs

Doppler ultrasonography was used to evaluate the portal vein in 14 dogs before, immediately after and four weeks after a partial ligation of a congenital extrahepatic portocaval shunt. By four weeks after the operation, the hepatofugal or zero flow in the portal vein segment cranial to the shunt origin had become a hepatopetal flow in 13 of the dogs, which became clinically healthy. The other dog continued to have a hepatofugal flow in the portal vein cranial to the origin of the shunt and continued to show clinical signs of hepatic encephalopathy. The shunt remained functional in six of the dogs, and three of them developed portosystemic collaterals in addition. In the other eight dogs the patent shunt was non-functional, because a hepatopetal flow was detected in the shunt adjacent to the portal vein. This flow was the result of the splenic vein entering the shunt, and the splenic blood dividing; some flowed via the shunt towards the portal vein, preventing the portal blood from shunting, and the rest flowed via the attenuated shunt segment to the caudal vena cava. Shunting of the splenic venous blood was clinically insignificant.     

Evaluation of a portocaval venograft and ameroid ring for the occlusion of intrahepatic portocaval shunts in dogs

OBJECTIVE:To evaluate the use of a portocaval venograft and ameroid constrictor in the surgical management of intrahepatic portosystemic shunts (PSS). STUDY DESIGN: Prospective, clinical study. Animal Population: Ten client-owned 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 greater than 8 mm Hg, a single extrahepatic portocaval shunt was created using a jugular vein. An ameroid ring was placed around the venograft and the intrahepatic PSS was attenuated. Transcolonic pertechnetate scintigraphy was performed before surgery, 5 days after surgery, and 8 to 10 weeks after surgery. Dogs with continued portosystemic shunting were evaluated further by laparotomy or portography. Clinical outcome and complications were recorded. RESULTS: Mean (+/- SD) portal pressure increased from 6 +/- 3 to 19 +/- 6 mm Hg with PSS occlusion; in all 10 dogs, the increase in portal pressure was greater than 8 mm Hg. There were no intraoperative complications, and, after creation of the portocaval shunt, the intrahepatic PSS could be completely ligated in 8 of 10 dogs. The final portal pressure was 9 +/- 4 mm Hg. Postoperative complications included coagulopathy and death (1 dog), ascites (3 dogs), and incisional discharge (3 dogs). Five of 8 dogs had continued portosystemic shunting at 8 to 10 weeks after surgery. Multiple extrahepatic PSS were demonstrated in 4 of these dogs. Clinical outcome was excellent in all 9 surviving dogs. CONCLUSIONS AND CLINICAL SIGNIFICANCE: The surgical technique resulted in a high incidence of multiple extrahepatic PSS. Short-term clinical results were promising, but long-term outcome must be evaluated further.     

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.     

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.     

CONTRAST‐ENHANCED MAGNETIC RESONANCE ANGIOGRAPHY FOR DIAGNOSIS OF PORTOSYSTEMIC SHUNTS IN 10 DOGS

Computed tomography angiography, sonography, scintigraphy, and portography can be used to evaluate the portal vasculature to evaluate for a portosystemic shunt (PSS). Time‐of‐flight magnetic resonance angiography (TOF‐MRA) and contrast‐enhanced MRA (CE‐MRA) are other potentially useful techniques. The aim of this study was to evaluate CE‐MRA in 10 dogs suspected of having a PSS. Noncontrast MR images of the abdomen were obtained using a Siemens Symphony MR‐scanner (1.5 T) and a T1‐weighted FLASH‐3D sequence with a very short scan time (about 20 s). After injection of contrast medium, the initial sequence was repeated five times. The sequence with the best contrast medium filling of the portal vasculature was selected subjectively, subtracted from the initial survey image series, and a maximum intensity projection (MIP) of the subtraction data, in multiple views, was created. The cross‐sectional and MIP images were evaluated for abnormal portosystemic vasculature. A single PSS was identified and confirmed at surgery in all dogs. A portocaval shunt was found in five dogs, a portophrenic shunt in three dogs, a portoazygos shunt in one, and a central divisional intrahepatic shunt in one other dog. Based on our results, CE‐MRA is a useful tool for imaging abdominal and portal vasculature and for the diagnosis of a PSS.     

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.     

ACQUIRED PORTAL COLLATERAL CIRCULATION IN THE DOG AND CAT

We describe patterns of acquired portal collateral circulation in dogs and in a cat using multidetector row computed tomography angiography. Large portosystemic shunts included left splenogonadal shunts in patients with portal hypertension. Small portal collaterals were termed varices; these collaterals had several patterns and were related either to portal vein or cranial vena cava obstruction. Varices were systematized on the basis of the venous drainage pathways and their anatomic location, namely left gastric vein varix, esophageal and paraesophageal varices, gastroesophageal and gastrophrenic varices, gallbladder and choledocal varices, omental varices, duodenal varices, colic varices, and abdominal wall varices. As reported in humans and in experimental dog models, esophageal and paraesophageal varices may result from portal hypertension that generates reversal of flow, which diverts venous blood in a cranial direction through the left gastric vein to the venous plexus of the esophagus. Blood enters the central venous system through the cranial vena cava. Obstructions of the cranial vena cava can lead to esophageal and paraesophageal varices formation as well. In this instance, they drain into the azygos vein, the caudal vena cava, or into the portal system, depending on the site of the obstruction. Gallbladder and choledocal varices, omental varices, duodenal varices, phrenico-abdominal varices, colic varices, abdominal wall varices drain into the caudal vena cava and result from portal hypertension. Imaging plays a pivotal role in determining the origin, course, and termination of these vessels, and the underlying causes of these collaterals as well. Knowledge about these collateral vessels is important before interventional procedures, endosurgery or conventional surgery are performed, so as to avoid uncontrollable bleeding if they are inadvertently disrupted.     

Comparison of 99mTcO4(-) trans-splenic portal scintigraphy with per-rectal portal scintigraphy for diagnosis of portosystemic shunts in dogs

Objective— To evaluate trans-splenic portal scintigraphy (TSPS) and per-rectal portal scintigraphy (PRPS) for diagnosis of congenital portosystemic shunts (CPSS) in dogs, and compare these results with surgical findings.
Study Design— Prospective, randomized cross over clinical trial.
Animals— Dogs (n=42) with suspected CPSS.
Methods— Dogs had TSPS and PRPS 48 hours apart; quantity of radionuclide administered was recorded. Three independent, blinded reviewers evaluated each scintigraphic study for study quality, shunt presence, number, and location of shunt termination (caudal vena cava, azygos vein). All dogs had exploratory celiotomy. Negative scintigraphic findings were confirmed with intraoperative mesenteric portography. Ameroid constrictors were placed on all extrahepatic CPSS, and hepatic biopsies were obtained.
Results— TSPS was 100% sensitive and specific for diagnosis of CPSS and significantly ( P <.05) more likely than PRPS to detect shunt number and termination. Interpretation was consistent between observers, and TSPS required significantly less radionuclide than PRPS.
Conclusion— TSPS was as sensitive as PRPS for detection of shunting vessels, and consistently yielded studies of higher quality, allowing detection of shunt number and location with consistent interpretation among radiologists.
Clinical Relevance— TSPS provides information about shunt number and location, which allows improved surgical planning. Because it requires significantly less radionuclide, TSPS improves safety, allows for more comprehensive patient care, and earlier surgical intervention.     

Transvenous coil embolisation for the treatment of single congenital portosystemic shunts in six dogs

This article describes the treatment of single congenital portosystemic shunts (CPSs) (intrahepatic and extrahepatic) using an interventional radiology technique involving embolisation of anomalous vessels with percutaneous coils. Briefly, a multipurpose catheter was introduced into the caudal vena cava and then into the portosystemic shunt. An autoexpandable stent was placed in the caudal vena cava, next to the shunt, in order to avoid coil migrations, and a cobra-like vascular catheter was used to pass through the stent and to place the coils in the shunt. This technique was used for treatment of CPS in six dogs. The results indicate that percutaneous embolisation of a CPS using coils, a less invasive technique than the traditional surgical technique, may result in complete closure of the anomalous vessel without development of portal hypertension.     

Portosystemic shunt in an alpaca cria

A 5-month-old alpaca cria was examined for chronic poor growth and repeated episodes of diarrhea. Examination of feces for parasites yielded negative results. Serum bile acid and blood ammonia concentrations were high. Subsequent examination by ultrasonography, percutaneous splenic portography, and colonic scintigraphy did not reveal evidence of a portosystemic vascular anomaly. Exploratory celiotomy with mesenteric vein portography revealed a colonic vein shunt in the caudal portion of the abdomen from the caudal vena cava to the portal vein. The shunt vessel was ligated without incident. Following surgery, the cria began to gain weight and was more alert. Eighteen months after surgery, the cria was doing well, although it had loose feces and was slightly small for its age. Portosystemic shunts are rare in cattle and horses but should be considered in alpacas with chronic poor growth when parasitism has been ruled out.     

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.     

Transportal Approach for Attenuating Intrahepatic Portosystemic Shunts in Dogs

A novel surgical approach, using portal venotomy during total hepatic vascular occlusion, was used to locate and attenuate congenital intrahepatic portosystemic shunts in nine dogs. Shunt location was consistent with a persistent ductus venosus in only two dogs. In the remaining seven dogs the shunts were window-like orifices arising from either the left (two dogs) or right portal vein branch (five dogs) and communicating with the ipsilateral hepatic vein or caudal vena cava. The transportal approach using total hepatic vascular occlusion consistently provided good access to the portosystemic shunts, including those with window-like communications. A 7 to 16 minute period of total vascular occlusion was well-tolerated hemodynamically, with few intraoperative complications. Intrahepatic shunts were successfully attenuated in eight dogs, while one dog with portal atresia was euthanatized. The postoperative course was complicated by high protein pulmonary edema (one dog), an encapsulated biliary pseudocyst (one dog) and uncontrollable hemorrhage caused by an uncharacterized coagulopathy (one dog). Three dogs required a second operation to further attenuate their shunts. The clinical condition of all seven surviving dogs was improved after surgery.     

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.