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.     

MULTIDETECTOR ROW COMPUTED TOMOGRAPHY AND ULTRASOUND CHARACTERISTICS OF CAUDAL VENA CAVA DUPLICATION IN DOGS

Caudal vena cava duplication has been rarely reported in small animals. The purpose of this retrospective study was to describe characteristics of duplicated caudal vena cava in a large group of dogs. Computed tomography (CT) and ultrasound databases from two hospitals were searched for canine reports having the diagnosis “double caudal vena cava.” One observer reviewed CT images for 71 dogs and two observers reviewed ultrasound images for 21 dogs. In all CT cases, the duplication comprised two vessels that were bilaterally symmetrical and approximately the same calibre (similar to Type I complete duplication in humans). In all ultrasound cases, the duplicated caudal vena cava appeared as a distinct vessel running on the left side of the abdominal segment of the descending aorta and extending from the left common iliac vein to the left renal vein. The prevalence of caudal vena cava duplication was 0.46% for canine ultrasound studies and 2.08% for canine CT studies performed at these hospitals. Median body weight for affected dogs was significantly lower than that of unaffected dogs (P < 0.0001). Breeds with increased risk for duplicated caudal vena cava were Yorkshire Terrier (odds ratio [OR] = 6.41), Poodle (OR = 7.46), West Highland White Terrier (OR = 6.33), and Maltese (OR = 3.87). Presence of a duplicated caudal vena cava was significantly associated with presence of extrahepatic portosystemic shunt(s) (P < 0.004). While uncommon in dogs, caudal vena cava duplication should be differentiated from other vascular anomalies when planning surgeries and for avoiding misdiagnoses.     

Ultrasonographic measurement of caudal vena cava to aorta ratios for determination of volume depletion in normal beagle dogs

A noninvasive method for quantifying hydration status would be helpful for clinical management and for research applications in dogs. This prospective, experimental, pilot study aimed to assess the feasibility of ultrasonographic measurement of the caudal vena cava to aorta ratio as a method for quantifying volume depletion in dogs. In 12 normal beagle dogs, furosemide was administered intravenously at a dose of 1 mg/kg, every 2 h, for 8 h, to induce consecutive volume depletion. Every 30 min after administration, ultrasonographic images of the caudal vena cava and aorta, and physical and biological parameters related to dehydration were acquired. On transverse and longitudinal planes of caudal vena cava and aorta images, the height and area of the caudal vena cava and aorta were measured to calculate the caudal vena cava/aorta ratios. All images were acquired by approaching from the right intercostal space with the dogs in left lateral recumbency. A negative correlation was present between the percentage of weight loss in dogs and all four investigated caudal vena cava/aorta ratios (transverse plane width of the caudal vena cava [TW]/aorta; transverse plane height of caudal vena cava [TH]/aorta; longitudinal plane area of the caudal vena cava [TA]/aorta; and longitudinal plane maximal height of the caudal vena cava [L]/aorta). Significant differences (P < 0.001) were seen between dogs with and without clinical signs of dehydration for all caudal vena cava/aorta ratios. Findings indicated that ultrasonographic caudal vena cava/aorta ratios are feasible methods for quantifying volume depletion and for use as an adjunct to standard subjective methods for estimating hydration status in dogs.     

MULTIDETECTOR‐ROW COMPUTED TOMOGRAPHIC CHARACTERISTICS OF PRESUMED PREURETERAL VENA CAVA IN CATS

Preureteral vena cava (circumcaval ureter, retrocaval ureter) occurs in a third of the feline population and has been associated with ureteral strictures in humans. The aim of this retrospective cross‐sectional study was to describe the contrast‐enhanced multidetector row computed tomographic (MDCT) characteristics of presumed preureteral vena cava in a group of cats. Medical records from two institutions located in different continents were searched from 2010–2013 for cases with complete contrast‐enhanced MDCT examinations of the abdomen (i.e. included the entire course of the ureters and prerenal and renal segments of the caudal vena cava) and a diagnosis of preureteral caudal vena cava. For cases meeting inclusion criteria, CT scan data were retrieved and characteristics of the preureteral caudal vena cava were recorded. Presence of concomitant renal or ureteral diseases was also recorded. A total of 272 cats had contrast‐enhanced abdominal CT scans during the study period and of these, 68 cats (22.43 ± 4.96%) had a diagnosis of presumed preureteral vena cava. In all affected cats, a “reverse‐J ureter” was observed, i.e. a ureter running medially at the level of L4–5, passing dorsally to the caudal vena cava and then exiting ventrally between the caudal vena cava and aorta returning to its normal position. Having a preureteral vena cava resulted in an increased risk for concurrent urinary signs (OR = 3.00; CI: 95%; 1.28–6.99; P = 0.01). Findings supported the use of contrast‐enhanced MDCT for characterizing morphology of preureteral vena cava and its relation with ureters in cats.     

Thrombosis of the caudal vena cava presenting as an unusual cause of an abdominal mass and thrombocytopenia in a dog

Thrombosis of the caudal vena cava in a dog secondary to metastatic neoplasia is described. The dog had a palpable abdominal mass and persistent thrombocytopenia due to a thrombosed caudal vena cava that was surgically removed. A few days after its removal, the dog died and neoplastic cells of neural crest origin were identified at the edge of the thrombus. Massive thrombosis can be an unusual cause of platelet consumption, leading to thrombocytopenia and disseminated intravascular coagulation. Deep vein thrombosis of the vena cava can occur in dogs and may mimic an abdominal mass. Multiple mechanisms may be involved in the development of venous thrombosis, including endothelial damage by neoplastic cells and the presence of a hypercoagulable state secondary to neoplasia. Extensive collateral circulation may allow removal of diseased vena cava.     

Caudal vena cava obstruction caused by redundant pacemaker lead in a dog

Inferior vena cava obstruction, a rare but serious complication of transvenous pacemaker lead placement in humans, has not been reported in dogs. We describe this complication in a dog that developed ascites 8 months after pacemaker implantation. Radiography disclosed a loop of redundant lead within the caudal vena cava (CVC), and angiography demonstrated obstruction to blood flow. Withdrawal of the loop from the CVC did not restore blood flow. Persistent obstruction was suspected secondary to fibrosis resulting from vascular damage caused by the loop of lead. Angioplasty of the CVC obstruction restored blood flow and resolved the dog's clinical signs.     

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.     

Descriptive anatomic study of the great vessels of the heart in the capuchin monkey Cebus apella (Linnaeus, 1758)

The aim of this study was to describe the anatomy of the great vessels of the heart in capuchin monkey (Cebus apella) and to compare with those of other primates, including humans. The hearts were prepared through fixation in 10% formalin and subsequently dissected using standard techniques and instruments. The arterial and venous systems were perfused with colored latex solution via the femoral vessels. An ascending cylindrical branch with relatively great caliber was identified in the aorta artery, in addition to an aortic arch, from which three great arteries were originated, the brachiocephalic trunk, the left common carotid artery and the left subclavian artery. After a course of variable extension, the pulmonary trunk divided into right and left pulmonary arteries. The caudal vena cava was morphologically similar to that of humans, except for its association with the cardiac lobe of the right lung, whereas the cranial vena cava was formed by the two braquiocephalic veins and received the azygos vein close to right atrium. The pulmonary veins, in number of six, ended at the posterior face of the left atrium, differently from both humans and other primates. In conclusion, the morphology of the great vessels of the heart in Cebus apella was similar to that of humans and other primates, although some differences are evidenced with regards to topography and number of anatomic structures, particularly the relationship of the caudal vena cava with the cardiac lobe of the right lung and the presence of six pulmonary veins in Cebus apella.     

Evaluation of gradual occlusion of the caudal vena cava in clinically normal dogs

OBJECTIVES: To devise a technique for gradual occlusion of the caudal vena cava in dogs and determine effects of complete occlusion of the caudal vena cava. ANIMALS: 8 mixed-breed hounds that weighed between 25 and 30 kg. PROCEDURE: Baseline evaluation of dogs included serum biochemical analyses and determination of glomerular filtration rate (GFR) with dynamic renal scintigraphy and plasma clearance analysis. An occluder was placed around the vena cava in the region cranial to the renal veins. The occluder was attached to a vascular access port. The vena cava was gradually occluded over 2 weeks. The GFR was measured every 2 weeks after surgery, and venograms were performed every 3 weeks after surgery. Blood samples were collected every 48 hours for the first week and then weekly thereafter to measure BUN and creatinine concentrations and activities of alanine transaminase, alkaline phosphatase, and creatinine kinase. Dogs were euthanatized 6 weeks after surgery, and tissues were submitted for histologic examination. The GFR and biochemical data were compared with baseline values. RESULTS: Gradual occlusion of the caudal vena cava was easily and consistently performed with this method, and adverse clinical signs were not detected. Formation of collateral vessels allowed overall GFR to remain constant despite a decrease in function of the left kidney. Measured biochemical values did not deviate from reference ranges. CONCLUSIONS AND CLINICAL RELEVANCE: Gradual occlusion of the caudal vena cava may allow removal of adrenal gland tumors with vascular invasion that would otherwise be difficult or impossible to resect.     

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.     

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.     

Aortic to caudal vena cava ratio measurements using abdominal ultrasound are increased in dogs with confirmed systemic hypertension

Chronically sustained systemic hypertension in dogs can damage the kidneys, eye, brain, heart, and vessels. In human medicine, systemic hypertension has been implicated as the most common risk factor for aorta dilation, which can progress to an aneurysm. Abdominal ultrasound has been commonly used to monitor the size of the abdominal aorta in people with systemic hypertension. In this retrospective cross‐sectional abdominal ultrasound study, evaluation of the size of the abdominal aorta relative to the caudal vena cava was performed in 18 control dogs and 128 dogs with confirmed systemic hypertension. Preexisting conditions contributing to systemic hypertension in these dogs were renal disease, hyperadrenocorticism, diabetes mellitus, adrenal tumors, and previous administration of phenylpropanolamine or palladia. The abdominal aorta and caudal vena cava were assessed from longitudinal images cranial to the trifurcation with measurements made from outer border to outer border of the walls, being careful not to compress the caudal vena cava that would alter its size. Our hypothesis was the ratio of the diameter of the abdominal aorta to caudal vena cava would be higher in dogs with systemic hypertension compared to dogs with normal blood pressure. The mean abdominal aorta‐caudal vena cava ratio was 1.028 in control dogs with a normal blood pressure and 1.515 in dogs with systemic hypertension. In dogs with confirmed systemic hypertension, the abdominal aorta was dilated compared to the caudal vena cava in the caudal abdomen. An increase in the abdominal aorta‐caudal vena cava ratio in a dog should raise suspicion for the presence of systemic hypertension and prompt evaluation of blood pressure.     

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.     

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.     

Macroscopic Anatomy of the Great Vessels and Structures Associated with the Heart of the Ringed Seal (Pusa hispida)

The ringed seal [Pusa (Phoca) hispida], as well as other seals, exhibits unique anatomical properties when compared to its terrestrial counterparts. In the ringed seal, the most conspicuous marine adaptation is the aortic bulb. This large dilatation of the ascending aorta is comparable to that found in other seal species and marine 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 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 plexus. Generally, three common pulmonary veins (right, left and caudal) empty into the left atrium. The pericardial venous plexus lies deep to the mediastinal pericardial pleura (pleura pericardica) on the auricular (ventral) surface of the heart. The caval sphincter surrounds the caudal vena cava as it passes through the diaphragm. Caudal to the diaphragm, the vena cava is dilated (the hepatic sinus), and near the cranial extremity of the kidneys, it becomes biphid. The azygos vein is formed from the union of the right and left azygos veins at the level of the 5th thoracic vertebra. Cardiovascular physiological studies show some of these anatomical variations, especially of the venous system and the ascending aorta, to be modifications for diving. This investigation documents the large blood vessels associated with the heart and related structures in the ringed seal.     

A new technique for surgery of the caudal vena cava in dogs using partial venous inflow occlusion

The haemodynamic and metabolic effects of caudal vena cava occlusion were evaluated in six normal anaesthetised dogs. Each animal underwent a single eight minute episode of caudal vena cava occlusion. The procedure was well tolerated by all the dogs. Systolic arterial pressure was reduced by 62 +/- 5 per cent and the heart rate increased by 11 +/- 3 per cent. There was rapid haemodynamic recovery after the release of occlusion, all cardiovascular parameters returning to normal spontaneously within five minutes. Caudal vena cava occlusion is therefore safe for periods of up to eight minutes in normal dogs. This technique allows repair of caudal vena caval lesions without necessitating systemic heparinisation and the use of cavoatrial conduits.     

Kinking of the intrathoracic caudal vena cava in five dogs

Five dogs with kinking of the intrathoracic caudal vena cava (CVC) were studied. One dog had neither clinical nor laboratory abnormalities associated with the kinked CVC, and the cause was unknown. The other four dogs had evidence of post-sinusoidal obstruction of venous flow characterized by high protein ascites (modified transudate). Causes of the kinked CVC were automobile trauma (two dogs), cardiomegaly with ascites, and a large neoplastic lung mass. Surgical removal of the kinked caval segment was successful in the two dogs injured by automobiles. Medical therapy with a diuretic was associated with a decrease in ascites, straightening of the CVC, and improvement in clinical condition of the dog with cardiomegaly and ascites. Surgical removal of the neoplastic lung mass in one dog resulted in straightening of the CVC, but it later died of respiratory failure associated with pulmonary neoplasia.     

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.     

Detection of portal and systemic bacteremia in dogs with severe induced hepatic disease and multiple portosystemic shunts

OBJECTIVE: To determine existence of portal and systemic bacteremia in dogs with induced severe hepatic disease, compared with clinically normal dogs, before and after vena caval banding. ANIMALS: 6 control dogs and 10 dogs with induced severe hepatic disease and multiple portosystemic shunts (PSS). PROCEDURE: Dogs of the diseased group were given dimethylnitrosamine (2 mg/kg of body weight, PO) twice weekly until multiple PSS developed. Surgery was performed on dogs of both groups, and blood for baseline aerobic and anaerobic bacterial culture was collected from catheters placed in the portal and hepatic veins and caudal vena cava. All dogs underwent vena caval banding, and blood for aerobic and anaerobic bacterial culture was collected from the portal and hepatic venous catheters at 120, 240, and 360 minutes after banding. RESULTS: Compared with control dogs (16% gram-positive and 84% gram-negative bacteria), diseased dogs had significantly higher percentage of gram-positive bacteria (42% of positive culture results, P < or = 0.01) and significantly lower percentage of gram-negative bacteria (58% of positive culture results, P < or = 0.01) isolated. Pseudomonas aeruginosa was isolated most frequently from dogs of both groups; more than 1 organism was isolated from 5 dogs of each group. Antimicrobial susceptibility included that to aminoglycosides (particularly amikacin), fluorinated quinolones, and imipenem. CONCLUSION: Portal and systemic, predominantly gram-negative, bacteremia is present in catheterized, clinically normal dogs and dogs with dimethylnitrosamine-induced hepatic disease and multiple PSS.