Anatomy of the patent ductus venosus in the cat

The biplanar mesenteric vein portovenograms of 10 cats with left divisional intrahepatic portosystemic shunts consistent with a patent ductus venosus (PDV) were reviewed. A corrosion cast of the hepatic portal vasculature was made post mortem from one individual that died post operatively following surgical attenuation of the shunting vessel. On the basis of the combined surgical, post mortem and imaging data, these left divisional shunts were found to have consistent anatomy, each having a straight vessel which drained into a venous ampulla before draining into the caudal vena cava at the level of the diaphragm. The left phrenic vein and left hepatic vein both entered the ampulla independently of the shunting vessel. The anatomical similarity between these findings in the cat and the PDV in the dog suggest that it is appropriate to describe this particular portosystemic shunt as a PDV.     

Cellophane banding of congenital intrahepatic portosystemic shunts in two Irish wolfhounds

Two three-month-old, male Irish wolfhound siblings were diagnosed with breed-typical left divisional congenital intrahepatic portosystemic shunts consistent with patent ductus venosus. The shunts were amenable to surgical dissection at a posthepatic location. Both dogs had cellophane banding for shunt attenuation. One dog was euthanased after developing post-ligation neurological dysfunction, which was refractory to treatment. The other dog survived and demonstrated shunt attenuation. Successful surgical management using cellophane banding of a patent ductus venosus has not been previously described in a large-breed dog.     

The angiographic anatomy of the portal venous system in the neonatal dog

The angiographic anatomy of the portal venous system in 50 dead, neonatal Labrador/Retriever type puppies is described. Angiography was performed by the injection of radioopaque contrast media through a catheter placed within the umbilical vein. In 49 pups the ductus venosus was a straight vessel arising from the left main portal vein and terminating in an ampulla into which the left hepatic and left phrenic veins entered prior to the ampulla entering the caudal vena cava. The diameter of the ductus venosus was significantly narrower (P<0.001) in pups born alive (n=10) when compared to stillborn individuals (n=39). No discreet narrowing of the ductus venosus indicating a sphincter was found, with closure appearing to be uniform along the vessel's length. A well-developed, patent portal venous system was present in the majority of individuals. One pup showed variation from the others studied having a vascular connection between the portal sinus and the vena cava within the liver. This may represent a normal variant of the ductus venosus, or may be an anatomical abnormality leading to the development of an intrahepatic portosystemic shunt. If this was an intrahepatic shunt, no concurrent ductus venosus was present.     

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.     

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.     

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.     

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.     

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.     

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.     

New perspectives on the development of extrahepatic portosystemic shunts

In this essay we use clinical evidence and knowledge of anatomy to examine the relationship between blood flow and formation of congenital extrahepatic portosystemic shunts in dogs and cats. First we report on the clinical findings in a series of 50 dogs and 10 cats and then systematically review peer‐reviewed data on the detailed anatomy of shunts in dogs and cats. In dogs four types of shunt: spleno‐caval, left gastro‐phrenic, left gastro‐azygos and those involving the right gastric vein account for 94% of extrahepatic shunts. Cats also exhibit four types of shunt: spleno‐caval, left gastrophrenic, left gastro‐caval and left gastro‐azygos, and the first three of these account for 92% shunts in this species. Our findings lead us to propose that preferential blood flow influences the subsequent formation of one of a number of defined and consistent congenital extrahepatic portosystemic shunts in dogs and cats.     

Use of portocaval venografts with ameroid constrictor placement and hepatic lobectomy for treatment of intralobular intrahepatic portocaval shunts in four dogs

Liver lobectomy for complete attenuation of intrahepatic portosystemic shunts appears to be a safe and effective surgical treatment. When the intrahepatic shunt vessel can be definitively palpated within a liver lobe or its presence confirmed portographically, liver lobectomy represents a technically simple and effective method of complete shunt attenuation. To maintain portal pressure at an acceptable value after lobectomy, an extrahepatic portocaval shunt vessel can be created by use of an external jugular vein graft. A second shunt vessel can be created if portal pressure remains increased after placement of 1 shunt. Gradual and safe attenuation of the shunt vessel is achieved by placement of an ameroid constrictor on the extrahepatic graft at the time of the initial surgery.     

Surgical management of left-divisional intrahepatic portosystemic shunts: outcome after partial ligation of, or ameroid ring constrictor placement on, the left hepatic vein in twenty-eight dogs (1995-2005)

OBJECTIVES: To evaluate outcome in dogs with left divisional intrahepatic portosystemic shunts (PSS) treated by partial ligation (PL) or ameroid ring constrictor (ARC) placement on the left hepatic vein. DESIGN: Retrospective study. ANIMALS: Dogs (n=28) with left divisional intrahepatic PSS. METHODS: Retrieved data from medical records of dogs with left divisional intrahepatic PSS that had PL (n=17) or ARC (n=11) were signalment, history, clinical signs, preoperative blood work, portal pressure measurements, ARC size, complications and postoperative technetium scintigraphy. Outcome assessed by owner interview 6 months-10 years after surgery was classified as excellent, good or poor. Differences were tested by exact chi2 test. RESULTS: Major complications occurred in 3 dogs: coagulopathy (1 PL dog died), ascites (1 PL dog survived) and seizures (1 ARC dog died). Eight PL dogs had technetium portal scintigraphy; 1 dog was negative and 7 dogs positive for persistent shunting. Seven ARC dogs had scintigraphy; 4 dogs were negative and 3 positive for persistent shunting. In PL dogs, long-term clinical outcome was excellent (92%) or good (8%) whereas, in ARC dogs it was excellent (20%), good (50%) or poor (30%). This outcome difference between treatment groups was significant (P=.0012). CONCLUSION: Dogs treated by PL had significantly better long-term outcome compared with ARC treated dogs. CLINICAL RELEVANCE: Based on these data, ARC placement on the left hepatic vein in dogs with left-divisional intrahepatic PSS cannot be recommended.     

Congenital portosystemic shunts in Maltese and Australian Cattle Dogs

SUMMARY Congenital portosystemic shunts were definitively diagnosed in 62 dogs over a period of 15 years. Maltese and Australian Cattle Dogs were significantly over-represented, accounting for 14 and 13 cases, respectively. Maltese invariably had a single extrahepatic shunt derived from the left gastric or gastrosplenic vein, whereas Cattle Dogs usually had large intrahepatic shunts involving the right liver lobes. The clinical syndromes resulting from anomalous portosystemic communications were indistinguishable in the 2 breeds. Fasting blood ammonia concentration was elevated in 20 of 22 dogs tested, providing a minimally invasive and effective means of diagnosis. Complete or partial shunt attenuation was performed successfully in all 9 Maltese and in 2 of 6 Cattle Dogs in which it was attempted.     

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

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

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.     

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.     

Congenital feline portosystemic shunts

Five young cats with portosystemic communications, 2 with single intrahepatic and 3 with single extrahepatic portosystemic communications, were managed surgically. One cat with a ductus venosus was treated successfully by surgery. Ptyalism and behavioral changes were similar in all 5 cats. Biochemical abnormalities included low BUN values, increased blood ammonia values, and increased sulfobromophthalein retention. None of the cats had portal hypertension at the time of surgery. Seemingly, single portosystemic shunts should be considered a surgical disease in the cat.     

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 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.