Evaluation of a percutaneously controlled hydraulic occluder in a rat model of gradual venous occlusion

OBJECTIVE: To evaluate the efficacy of a percutaneously controlled hydraulic occluder (HO) in a rat model of gradual venous occlusion. STUDY DESIGN: Experimental study. ANIMALS: Ten male Sprague-Dawley rats. METHODS: HOs and perivascular transit time ultrasound flow probes were applied to the caudal vena cava (CVC). Occluders in group I rats (n=6) were gradually attenuated over 8 weeks, whereas occluders in group II rats (n=4) were not attenuated. Vena caval blood flow measurements were performed weekly in all rats for 8 weeks. After euthanasia, the CVC was evaluated grossly and by histopathology. RESULTS: Premature occlusion of the vena cava occurred during the 1st week in 3 rats (1 in group I, 2 in group II) because of kinking of the vena cava between the HO and the flow probe. For the remaining rats, mean blood flow in group I decreased significantly from 40.71 mL/min/kg at baseline to 4.68 mL/min/kg at 8 weeks (P=.0094, power=0.91). Group II rats maintained vena caval blood flow at all times during the study. Complete occlusion of the vena cava was confirmed at necropsy in all group I rats. CONCLUSIONS: Gradual occlusion of the CVC of rats was achieved with HOs over 8 weeks. This model is limited by the size of the experimental animals and comparatively large implants. CLINICAL RELEVANCE: HOs may provide a method for gradual occlusion of congenital portosystemic shunts.     

Cranial vena caval syndrome secondary to transvenous pacemaker implantation in two dogs

Superior vena caval syndrome is a rare, but reported complication of transvenous pacemaker implantation in humans. This syndrome can occur secondary to fibrotic and/or thrombotic obstruction of venous blood flow into the right atrium. The therapeutic approach depends on the suspicion of the presence of an active thrombus and may include antithrombotics, angioplasty and/or surgical venoplasty. We describe two dogs that developed severe pleural effusion secondary to stricture formation in the cranial vena cava 4 years after dual chamber transvenous pacemaker implantation. The stenosis was most likely due to fibrosis secondary to the transvenous pacemaker leads. Balloon angioplasty of the lesion resulted in resolution of the pleural effusion in both patients. Balloon angioplasty appears to be a viable therapeutic approach in dogs with cranial vena caval syndrome caused by focal stenotic lesions.     

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 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.     

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.     

Transvenous pacemaker placement in a dog with atrioventricular block and persistent left cranial vena cava

The case reported herein describes the placement of a permanent transvenous pacemaker in an older dog with a previously undiagnosed persistent left cranial vena cava (PLCVC) and recent onset symptomatic third-degree atrioventricular (AV) block. On presentation the dog was found to have atrial flutter and third-degree AV block and echocardiography demonstrated evidence of chronic valvular disease and pulmonary arterial hypertension. The persistent left cranial vena cava was discovered via angiography when difficulties were encountered with pacemaker placement. Successful right ventricular pacing necessitated passage of the lead through the coronary sinus. The attendant complications in pacemaker placement in the presence of a PLCVC are well-described in man but, to the authors' knowledge, have not been described in companion animals.     

Caudal vena cava kinking in dogs with ascites

A 9-year-old dog with spontaneous ascites was found to have hepatic vein distension and a tortuous vena cava on abdominal ultrasound. In right lateral recumbency, the caudal vena cava crossed the diaphragm and became kinked before entering into the right atrium. Following this observation, we performed an experimental study in a normal dog to determine whether kinking of the caudal vena cava could be the result and not the cause of ascites. Ascites was induced using warm saline injected through a needle inserted into the abdominal cavity. Venograms were collected from different body positions, under four conditions: before and after a total of one, two and 3 liters of saline had been injected. Caudal vena cava kinking was observed in the experimental dog after 2 liters of fluid had been injected. Vena cava obstruction may cause ascites, but we found that sometimes caudal vena cava kinking can be the result and not the cause of the peritoneal effusion.     

En block resection of a large hepatocellular carcinoma involving the caudal vena cava in a dog

A 13-year-old neutered female Shih Tzu was referred for investigation of a cranial abdominal mass. Investigations including conventional radiography, abdominal ultrasonography and computed tomography confirmed the mass in the caudate lobe of the liver. As a collateral vein originating from the caudal vena cava (CVC) communicated with the azygos vein, the CVC was ligated and transected cranial to the right renal vein and cranial to the mass under temporary occlusion of the thoracic descending aorta and posthepatic CVC. The mass combined with the CVC was excised. The mass was confirmed as hepatocellular carcinoma (HCC). This report describes the first case with successful en bloc resection of a large HCC involving the CVC in a dog.     

Diagnostic imaging and pacemaker implantation in a domestic goat with persistent left cranial vena cava

Difficulty was encountered with the insertion of a right atrial pacing lead via the left jugular vein during lead and pacemaker implantation in a clinically normal goat as part of an ongoing rapid atrial pacing – induced atrial fibrillation research project. Fluoroscopic visualization of an abnormal lead advancement path prompted angiographic assessment which revealed a persistent left cranial vena cava (PLCVC) and prominent coronary sinus communicating with the right atrium. Angiography facilitated successful advancement and securing of the pacing lead into the right side of the interatrial septum. Cardiac magnetic resonance imaging/magnetic resonance angiography (MRI/MRA) allowed further characterization of this rare venous anomaly. Even though PLCVC has been reported once in a goat, to the authors' knowledge this is the first report to include MRI/MRA characterization of PLCVC and prominent coronary sinus with successful cardiac pacemaker implantation using the PLCVC.     

RADIOGRAPHIC EVALUATION OF CAUDAL VENA CAVA SIZE IN DOGS

Dilation of the caudal vena cava (CVC) on lateral thoracic radiographs is often interpreted as suggestive of right-sided congestive heart failure. To quantitate the clinical utility of evaluating CVC size as an indicator of right-sided heart disease, we compared the ratio of the diameter of the CVC as measured on a left lateral thoracic radiograph to the descending aorta (Ao), length of the thoracic vertebra above the tracheal bifurcation (VL), and width of the right fourth rib (R4) in 35 dogs with right heart disease and 35 control dogs. Each CVC ratio (CVC/Ao, CVC/VL, CVC/R4) was statistically larger in dogs with right heart disease. Response operating characteristic curves and likelihood ratios were used to determine ratios helpful in identifying dogs with right heart disease. A CVC/Ao > 1.50, CVC/VL > 1.30, or CVC/R4 > 3.50 are strongly suggestive of a right-sided heart abnormality in a patent.     

Automobile-induced obstruction of the intrathoracic caudal vena cava in a dog

A two-year-old labrador retriever was examined after a year's history of persistent ascites and exercise intolerance that began shortly after the dog was struck by an automobile. Contrast venography showed tortuosity of the intrathoracic caudal vena cava with partial obstruction caused by kinking of the vessel. Surgical resection of a fibrous connective band that was found to be tethering the intrathoracic vena cava ventrally, creating a partial obstruction, was performed. A hypothesis of the aetiology of this phenomenon is presented.     

Tricuspid valve stenosis caused by fibrous adhesions to an endocardial pacemaker lead in a dog

Acquired tricuspid valve stenosis (TVS) is a rare complication of endocardial lead placement in humans that has not been described in the veterinary literature. We describe a 6.5-year-old Border terrier that was presented with right-sided congestive heart failure 5.5 years after placement of a transvenous pacemaker. Severe TVS was confirmed by cardiac ultrasonography and appeared to be secondary to excessive endocardial pacemaker lead within the right atrium. Repositioning of the lead proved impossible and subsequent postmortem examination demonstrated fusion of the tricuspid valve (TV) leaflets around the endocardial lead with associated narrowing of the tricuspid valve orifice. In addition, the loop of the endocardial lead was anchored by thick fibrous tissue to the right atrial wall. This case report suggests that if sufficient endocardial lead is left inside the heart, in dogs undergoing transvenous pacemaker therapy, the redundant lead can become adherent to the tricuspid valve apparatus and cause valvular stenosis.     

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.     

Pathophysiology of the gastric dilation-torsion complex in the dog*

The gastric dilation-torsion complex in the dog involves a series of related pathophysiological changes which may culminate in death if therapy is not promptly initiated. This complex probably starts with gastric dilation which may or may not lead to gastric torsion. Gastric dilation interferes with blood flow through the caudal vena cava as well as the portal vein. Venous return to the heart is decreased, cardiac output decreases, and arterial hypotension ensues. With the onset of this hypotension, the animal is subjected to impairment of tissue perfusion, cellular catabolism, and decreased renal function. In addition, endotoxic shock and disseminated intravascular coagulation may occur. These two processes will likely lead to death of the animal.     

MYELOPATHY SECONDARY TO AORTOCAVAL FISTULA IN A CAT

A 15-month-old neutered male cat was presented for progressive paraparesis of 3 months' duration and suspected cardiomegaly. Neuroanatomical localization was a T3-L3 myelopathy. On abdominal ultrasound, an anomalous vessel with turbulent blood flow was identified arising from the caudal vena cava. Myelography showed a bilateral ventrolateral extradural spinal cord compression from T12 to L4. Nonselective angiography and contrast-enhanced computed tomography clearly indicated a vascular complex and vena caval aneurysm with an engorged internal vertebral venous plexus. Surgical occlusion of the anomalous vessels was unsuccessful.     

Central Venous Pressure Measurements in the Caudal Vena Cava of Sedated Cats

The caudla vena cava (CVA) was evaluated as an laternative site for the measurement of central venous pressure (CPV) in six healthy, sedated (ketamine 10 mg/km, midazolam 0.1 mg/kg, and atropine 0.04 mg/kg IM) cats. The CVC was cathererized via medial saphenous puncture, and estimates of CPV from this site compared to those obtained via a jugular catheter. Simulataneous CPV values were recorded electronically (mmgh), via calibrated pressure transducer positioned at the level of the manubrium in cats in lateral recumbency. Five readings, performed at 1 minute intervals, were collected from the jugular and CVC catheters at rest (baseline) and following a rapid fluid bolus. Twenty-four hours later, cats were resedated, baseline measurements repeated, and CVPs recorded following a rapid, 25% whole-blood volume bleed. CVP measurements from the jugular and CVC were statistically compared using repeated measures ANOVA (p<0.05). There were no significant differences between the two sites in the baseline and bleed trials. Significant defferences between jugular and CVC CVPs were noted at 1 and 2 minutes following the fluid bolus. It was concluded that CVC is an alternative site for measurement of CPV in sedated cats.     

Radiographic evaluation of caudal vena cava size as a useful parameter for the diagnosis of heart disease in dairy cattle

To quantify the radiographic parameters of the caudal vena cava (CVC) in healthy cattle and demonstrate their clinical usefulness, the present study compared the ratios of the diameter of the thoracic CVC to the diameter of the aorta (Ao) and length of the thoracic vertebrae (VL), which are all positioned in the same intercostal space, in 81 healthy control cattle (43 growing, 38 adult) and 10 cattle with heart disease. The average diameter of the CVC (CVCave) was correlated with the size of the Ao and VL in the control cows. Although the diameter and pulsation index of the CVC differed significantly between the growing and adult cows, the ratios of CVC/Ao and CVC/VL were fixed values for both the growing and mature cattle. However, in the cattle with heart disease, the pulsation index of the CVC was significantly lower or there was absence of pulsation due to a dilated CVC, and the ratio of CVCave/Ao and CVCave/VL were significantly higher than those in the healthy cattle.     

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.     

Blastomycosis granuloma involving the cranial vena cava associated with chylothorax and cranial vena caval syndrome in a dog

A four-year-old, sexually intact, male dachshund was diagnosed with pulmonary blastomycosis. Itraconazole was administered for 60 days, and the dog was considered to be disease-free at three- and 12-month reevaluations. Two years following discontinuation of itraconazole, the dog developed a granuloma of the cranial vena cava resulting in chylothorax and cranial vena caval obstruction. To the authors' knowledge, this is the first case of a blastomycotic granuloma involving the vena cava reported in the dog. Blastomycosis should be considered as a differential diagnosis for both chylothorax and cranial vena caval syndrome in the dog.     

Central venous access to the cranial vena cava via the omobrachial vein in the dog

Background– The omobrachial vein is a superficial vein that crosses the brachial region of the dog. It terminates in the cranial vena cava, offering a novel site for central venous catheterization into the cranial thorax. Case Summary– The omobrachial vein served as a point of access to the cranial vena cava for treatment and monitoring of a critical canine patient in this report. The omobrachial vein was catheterized using the modified‐Seldinger technique due to contamination of or lack of availability of commonly used central venous catheter insertion sites. Conclusion– Access to the cranial vena cava via the omobrachial vein was easily achieved, and the catheter was maintained without complication for 10 days. Although the site was successfully used in the patient in this report, omobrachial vein anatomy is not consistent in all dogs.