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.     

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.     

Ultrasonographic findings in a cow with ascites due to thrombosis of the caudal vena cava.

This case report describes a three-year-old Swiss Braunvieh cow with ascites due to thrombosis of the caudal vena cava. Ultrasonography verified the ascites and revealed dilatation of the abdominal portion of the caudal vena cava (4.8 cm). It was presumed that the caudal vena cava was occluded by a thrombus or by perivenous compression cranial to the dilatation. Post mortem findings included: a massive accumulation of fluid in the abdominal cavity; a 15 cm long thrombus in the subphrenic region of the caudal vena cava; multiple pulmonary abscesses; severe thrombosis of the pulmonary vasculature; hepatic congestion; oedematous abomasal folds; and severe thrombophlebitis of the left jugular vein and both udder veins, due to poor intravenous injection technique. Ascites caused by thrombosis of the caudal vena cava is rare because collateral routes of venous return, including the udder veins, are usually established. It was therefore concluded that the ascites was attributable to bilateral thrombosis of the udder veins.     

Cardiac musculature of the cranial and caudal venae cavae and the pulmonary vein in the fowl.

The cardiac musculature of cranial and caudal venae cavae and pulmonary vein was examined to clarify its distribution pattern in the fowl using both light and electron microscopies. The musculature was distributed from the heart to the root of subclavian vein in the cranial vena cava, to the cranial margin of the liver in the caudal vena cava, and to the left and right distal pulmonary veins in the pulmonary vein, respectively. Judging from the morphology and distribution pattern in the venous wall, the cardiac musculature in the fowl is thought to share the same phylogenic origin with that in mammals. The ultrastructure of cardiac myocytes including transitional cells in the cranial vena cava and the pulmonary vein resembled that of atrial myocytes. While, the typical specialized myocytes such as Purkinje fiber were found in the caudal vena cava of the fowl.     

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.     

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.     

COMPUTED TOMOGRAPHIC CHARACTERISTICS OF COLLATERAL VENOUS PATHWAYS IN DOGS WITH CAUDAL VENA CAVA OBSTRUCTION

Collateral venous pathways develop in dogs with obstruction or increased blood flow resistance at any level of the caudal vena cava in order to maintain venous drainage to the right atrium. The purpose of this retrospective study was to describe the sites, causes of obstruction, and configurations of venous collateral pathways for a group of dogs with caudal vena cava obstruction. Computed tomography databases from two veterinary hospitals were searched for dogs with a diagnosis of caudal vena cava obstruction and multidetector row computed tomographic angiographic (CTA) scans that included the entire caudal vena cava. Images for each included dog were retrieved and collateral venous pathways were characterized using image postprocessing and a classification system previously reported for humans. A total of nine dogs met inclusion criteria and four major collateral venous pathways were identified: deep (n = 2), portal (n = 2), intermediate (n = 7), and superficial (n = 5). More than one collateral venous pathway was present in 5 dogs. An alternative pathway consisting of renal subcapsular collateral veins, arising mainly from the caudal pole of both kidneys, was found in three dogs. In conclusion, findings indicated that collateral venous pathway patterns similar to those described in humans are also present in dogs with caudal vena cava obstruction. These collateral pathways need to be distinguished from other vascular anomalies in dogs. Postprocessing of multidetector‐row CTA images allowed delineation of the course of these complicated venous pathways and may be a helpful adjunct for treatment planning in future cases.     

Biometrical Studies on the Cornea in Some Domestic Animals

The ringed seal ( Phoca hispida ), as well as other seals, exhibit some unique anatomical properties when compared to their terrestrial counterparts. In the ringed seal, the most conspicuous adaptation is the aortic bulb, a large dilatation of the ascending aorta, which is comparable to that found in other seal species and marine mammals. Coronary arteries are similar to those of terrestrial mammals. The branches of the ascending aorta (brachiocephalic trunk, left common carotid artery and left subclavian artery) are similar to those of higher primates and man. The pulmonary trunk originates from the right ventricle near the ventral midline of the thorax. The peculiarities of the venous system are three pulmonary veins, a pericardial venous plexus, a caval sphincter, a hepatic sinus with paired caudal vena cavae and a large extradural venous system. Generally, three pulmonary veins (right, left, middle) empty into the left atrium. The right and left pulmonary veins drain the cranial and middle lung lobes of their respective lung, while the middle pulmonary vein drains both caudal lung lobes and the accessory lobe. The pericardial venous plexus lies on the pericardial pleura on the auricular (ventral) surface the heart. The azygous vein is formed from the union of right and left azygous veins near the 5th thoracic vertebra. The caval sphincter surrounds the caudal vena cava as it passes through the diaphragm. Caudal to the diaphragm, the vena cava is dilated excessively (the hepatic sinus) and near the kidneys it is biphid. Cardiovascular physiological studies have shown some of these anatomical variations, especially of the venous system and the ascending aorta, to be modifications for diving.     

Extensive venous thrombosis and hind-limb edema associated with adrenocortical carcinoma in a dog.

A 10-year-old, spayed female, mixed-breed dog was referred for evaluation of bilateral hindlimb edema and weakness. Abdominal ultrasonography showed increased echogenicity of the lumen of the caudal vena cava from the level of the urinary bladder to the level of the cranial pole of the right kidney. Bilateral saphenous venograms displayed numerous filling defects in the caudal vena cava, right external iliac vein, right femoral vein, and the right common iliac vein. Extensive venous thrombosis was diagnosed, and the animal was euthanized. Necropsy confirmed the presence of venous thrombosis and revealed a right adrenocortical carcinoma that had invaded the caudal vena cava.     

Vascular anatomy of the equine small colon

The vasculature of 22 small colons from dead adult ponies was perfused with latex or barium sulphate solution. The vascular anatomy was studied by use of dissection and alkali digestion of the latex specimens and microangiography of the barium sulphate-perfused specimens. The small colon is supplied by the caudal mesenteric artery. The left colic artery arises from the caudal mesenteric artery, which then becomes the cranial rectal artery. Branches from the left colic and cranial rectal arteries form anastomosing arcades that become narrower distally along the length of the small colon. From these arcades arise terminal arteries, which enter the small colon wall and give rise to a subserosal, an intermuscular, and a large submucosal plexus, with frequent anastomoses between them. The venous drainage closely parallels the arterial supply, except near to its origin from the portal vein, when the left colic vein and caudal mesenteric vein are separate from the corresponding arteries.     

The Great Vessels and Tributaries of the Heart of the Ringed Seal (Phoca hispida)

The ringed seal (Phoca hispida), as well as other seals, exhibit some unique anatomical properties when compared to their terrestrial counterparts. In the ringed seal, the most conspicuous adaptation is the aortic bulb, a large dilatation of the ascending aorta, which is comparable to that found in other seal species and marine mammals. Coronary arteries are similar to those of terrestrial mammals. The branches of the ascending aorta (brachiocephalic trunk, left common carotid artery and left subclavian artery) are similar to those of higher primates and man. The pulmonary trunk originates from the right ventricle near the ventral midline of the thorax. The peculiarities of the venous system are three pulmonary veins, a pericardial venous plexus, a caval sphincter, a hepatic sinus with paired caudal vena cavae and a large extradural venous system. Generally, three pulmonary veins (right, left, middle) empty into the left atrium. The right and left pulmonary veins drain the cranial and middle lung lobes of their respective lung, while the middle pulmonary vein drains both caudal lung lobes and the accessory lobe. The pericardial venous plexus lies on the pericardial pleura on the auricular (ventral) surface the heart. The azygous vein is formed from the union of right and left azygous veins near the 5th thoracic vertebra. The caval sphincter surrounds the caudal vena cava as it passes through the diaphragm. Caudal to the diaphragm, the vena cava is dilated excessively (the hepatic sinus) and near the kidneys it is biphid. Cardiovascular physiological studies have shown some of these anatomical variations, especially of the venous system and the ascending aorta, to be modifications for diving.     

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.     

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.     

USE OF 99MTCO TRANS-SPLENIC PORTAL SCINTIGRAPHY FOR DIAGNOSIS OF PORTOSYSTEMIC SHUNTS IN 28 DOGS

Ultrasound-guided percutaneous trans-splenic portal scintigraphy (TSPS) using 99mTcO4(-) has been used to image the portal venous system in normal dogs. Compared with per-rectal portal scintigraphy, it provides higher count density, consistent nuclear venograms of the splenic and portal vein, and significantly decreased radiation exposures. This paper describes the use of TSPS for the diagnosis of portosystemic shunts in 28 dogs. TSPS was performed injecting 70 +/- 28 MBq of 99mTcO4(-) (mean +/- SD) into the splenic parenchyma with ultrasound guidance. A dynamic acquisition at a frame rate of four frames/s for 5 min was initiated after placement of the needle and approximately 2s prior to injection. All dogs had diagnoses confirmed via exploratory laparotomy or ultrasonographic identification of the shunting vessel(s). Three studies (10.7%) were nondiagnostic because of intraperitoneal rather than intrasplenic injection of the radionuclide. Three pathways were recognized on the scintigraphic images: (1) portoazygos shunts--the 99mTcO4(-) bolus traveled dorsally, running parallel to the spine and entering the heart craniodorsally; (2) single portocaval or splenocaval shunts--the 99mTcO4(-) bolus ran from the area of the portal vein/splenic vein junction in a linear fashion toward the caudal vena cava entering the heart caudally; (3) internal thoracic shunt-the 99mTcO4 bolus traveled ventrally along the thorax and abdomen entering the cranial aspect of the heart. Single and multiple shunts were easily distinguished. There were no distinguishing features between single intra and extrahepatic portocaval shunts.     

Transvenous retrograde portography for identification and characterization of portosystemic shunts in dogs

Transvenous retrograde portography for identification and characterization of portosystemic shunts in dogs A method for transvenous retrograde portography (TRP) in dogs suspected to have a portosystemic shunt (PSS) and results in 20 dogs are described. For TRP, dogs were anesthetized and positioned in left lateral recumbency A dual-lumen balloon-tipped catheter was inserted into the right jugular vein and advanced into the azygos vein. The balloon was inflated to occlude the azygos vein, and contrast material was injected during fluoroscopic evaluation. The catheter was then positioned in the caudal vena cava just cranial to the diaphragm. The balloon was again inflated to occlude the vena cava, and contrast material was again injected. Once a shunt was identified, selective catheterization was attempted with a guide wire and angled catheter. A PSS was identified in 18 of the 20 dogs. In 10 of the 18, the shunt vessel could be selectively catheterized, allowing measurement of portal pressures while the shunt was occluded with the balloon. In 1 dog, results of TRP were normal, but subsequent exploratory celiotomy revealed a single extrahepatic PSS, which was surgically attenuated. The other dog in which results of TRP were normal did not have a macroscopic PSS. In dogs suspected to have a PSS, TRP may be a useful adjunctive diagnostic test that is less invasive than operative mesenteric vein portography and allows measurement of portal pressures before and after temporary shunt occlusion.     

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.     

家禽肝门静脉系统

以铸型方法观察了家禽肝门静脉的分支。其中，鸡有左、右肝门静脉各１支，左叶有左外叶颅侧支、左外叶尾侧支和左内叶支，右叶有右叶颅侧支及右叶尾侧支；鹅、鸭则有左肝门静脉２支，右肝门静脉１支。左叶有左外叶颅侧支和左外叶尾侧支，右叶有右叶颅侧支和尾侧支。左、右肝门静脉于横部汇集，并向颅侧及尾侧发出许多分支。此外，还强调和讨论了家禽肝门静脉系统在分布上的一些特点     

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.