Use of recombinant tissue-plasminogen activator in a dog with chylothorax secondary to catheter-associated thrombosis of the cranial vena cava

A 4-year-old, castrated male Maltese developed cranial vena caval thrombosis and chylothorax following central venous catheterization for treatment of postoperative sepsis. Vena caval thrombolysis was attempted using recombinant human tissue-plasminogen activator (t-PA). Thrombolytic therapy led to an acute reduction in the size of the caval thrombus and was followed by prompt resolution of the chylothorax. Hemorrhage at the entry sites of a jugular catheter and esophagostomy tube placed at the time of treatment was a dose-limiting complication of t-PA therapy in this dog.     

Lymphangiographic evaluation of experimentally induced chylothorax after ligation of the cranial vena cava in dogs

Ligation of the cranial vena cava (CrVC) distal to the entrance of the azygous vein resulted in chylothorax in 7 of 10 dogs. Of the remaining 3 dogs, 1 developed a serosanguineous effusion that did not become chylous, and 2 dogs did not develop pleural effusion. In 2 of the 7 dogs developing chylothorax, the pleural effusion became serosanguineous within 2.5 weeks after CrVC ligation. Mesenteric lymphangiography was performed 2 to 6 weeks after ligation of the CrVC. Lymphangiectasia was seen in 4 dogs with chylothorax, but was not seen in the 3 dogs with serosanguineous effusions or the 2 dogs that did not develop effusions. One dog with chylothorax died prior to repeat lymphangiography. Less dye entered the thoracic duct, and alternate lymphaticovenous communications to the caudal vena cava were evident in the dogs without chylothorax. Ligation of the thoracic duct at the lymphaticovenous junction was performed in 3 dogs. These dogs did not develop pleural effusion. Lymphangiography was performed immediately after ligation and indicated filling of abdominal lymphatics but not of the thoracic duct. Lymphangiographic findings 6 weeks after ligation also indicated filling of intestinal lymphatics. Results of the present study indicated that ligation of the CrVC causes chylothorax, and that thoracic lymphangiectasia is a consistent finding in animals with experimental chylothorax. Obstruction of the thoracic duct did not induce lymphangiectasia or chylothorax. Impedence of thoracic duct flow into the CrVC may be a cause of clinical chylothorax in the dog.     

Chylothorax associated with thrombosis of the cranial vena cava

This study reviewed confirmed cases of concurrent chylothorax and cranial vena caval (CrVC) thrombosis in dogs and cats, and determined predisposing factors for the development of chylothorax associated with CrVC thrombosis. The extent and location of the thrombus, the treatment regime, and the outcome are described. In all 4 cases, implantation of a jugular device was a predisposing factor to thrombosis of the CrVC, and there was extensive thrombosis of the CrVC extending from at least 1 jugular vein to just cranial to the heart. Chylothorax resolved in 3 of the 4 cases after medical and/or surgical intervention. The development of chylothorax concurrently with thrombosis of the CrVC in dogs and cats is likely dependent on the extent and location of the thrombus. Veterinary patients with indwelling jugular devices that develop acute respiratory signs should be assessed for chylothorax associated with thrombosis of the CrVC.     

Use of a jugular vein autograft for reconstruction of the cranial vena cava in a dog with invasive thymoma and cranial vena cava syndrome

A spayed female dog was evaluated because of edema of the ventral cervical region, lethargy, cough, and reduced exercise tolerance. Invasive thymoma and cranial vena cava syndrome were diagnosed by use of ultrasound-guided fine-needle biopsy and contrast-enhanced helical computed tomography. Resection of the cranial vena cava and an autogenous jugular vein graft were used for restoration of normal venous return to the right atrium and alleviation of the cranial vena cava syndrome.     

Cranial vena cava syndrome secondary to cryptococcal mediastinal granuloma in a cat

The successful management of cranial vena cava syndrome with suspected secondary chylothorax due to mediastinal cryptococcal granuloma in a 4-year-old male domestic shorthair cat is described. Treatment included long-term antifungal medication, short-term corticosteroids, intermittent thoracocentesis, rutin, octreotide, and enalapril.     

Cranial vena cava aneurysm in a dog

A 1.5-year-old mixed breed dog was presented for evaluation of arrhythmia and a cranial mediastinal density was noted on thoracic radiographs. The density was determined to be a cranial vena cava aneurysm based on ultrasonographic and angiographic testing. No treatment was initiated and the dog remains asymptomatic for the cranial vena cava aneurysm at 6 years of age. Although rare, cranial vena cava aneurysm should be a differential diagnosis for dogs with cranial mediastinal abnormalities on thoracic radiographs.     

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.     

Cranial vena caval thrombosis secondary to invasive mediastinal lymphosarcoma in a cat

A 12-year-old female cat was diagnosed with a cranial vena caval thrombosis in association with a mediastinal lymphosarcoma. The cause of the cranial vena caval thrombosis was thought to be invasion of the venous wall by neoplastic lymphoid cells. Clinical signs of cranial vena caval thrombosis, such as swelling and oedema of the submandibular area, the ventral part of the neck and the forelimbs, were related to a space-occupying mediastinal lymphosarcoma, which also induced respiratory distress and cyanosis. Non-selective angiocardiography demonstrated the occlusion of the cranial vena cava and abnormal venous collateral vessels feeding the heart which are accepted as the venographic hallmark of clinically overt cranial vena caval syndrome. At postmortem examination, an intracaval thrombus, 5 cm in length, was seen extending from the costocervical vein to the sulcus terminalis of the right atrium.     

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.     

Combined chylothorax, chylopericardium, and cranial vena cava syndrome in a dog with thymoma

A dog was examined because of anorexia and development of submandibular, sternal, and forelimb edema. Physical examination revealed engorged jugular veins and engorged blood vessels of the conjunctivae and nictitating membranes. Thoracic radiography revealed pleural and pericardial effusions, later identified as chyle. Contrast angiography revealed an intravascular mass, later identified as thymoma, in the cranial vena cava.     

Persistent left cranial vena cava draining into the left atrium associated with pulmonary stenosis in a French bulldog

A 5-month-old female French bulldog was evaluated for the presence of a heart murmur. Through clinical and echocardiographic evaluations, a severe Type A pulmonary stenosis was diagnosed. Angiography during right ventricular catheterization for valvuloplasty revealed drainage from a persistent left cranial vena cava (PLCVC) into the left atrium; this was confirmed later by contrast echocardiography. This report is the first to describe this anatomical variant of a PLCVC in a dog.     

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.     

Primary cranial mediastinal hemangiosarcoma in a young dog

Primary cranial mediastinal hemangiosarcomas are uncommon tumors. A 30-kg, 2-year-old, intact female German shepherd was presented for evaluation of cachexia and respiratory distress of a few days’ duration. Lateral radiographic projection of the thorax revealed significant pleural effusion. Computed tomography revealed a cranial mediastinal mass effect adjacent to the heart. On surgical exploration, a pedunculated mass attached to the esophagus, trachea, brachiocephalic trunk, left subclavian artery and cranial vena cava without attachment to the right atrium and auricular appendage was removed and debrided by use of blunt dissection and dry gauzes, respectively. Histopathology results described the cranial mediastinal mass as hemangiosarcoma. At 8 months and 5 days post-operatively, the patient died. Primary cranial mediastinal hemangiosarcomas, although a seemingly rare cause of thoracic pathology in young dogs, should be considered in the differential diagnosis for pleural effusion and soft tissue mass effect in the cranial mediastinum. This is the first case report in a dog to describe primary cranial mediastinal hemangiosarcoma.     

Hyponatremia and hyperkalemia associated with idiopathic or experimentally induced chylothorax in four dogs

Two dogs with idiopathic chylothorax and 2 dogs with experimentally induced (ie, ligation of the cranial vena cava) chylothorax were treated by intermittent thoracic drainage. Of these 4 dogs, 3 that did not have evidence of renal failure had normal or near-normal serum sodium and potassium concentrations before thoracic drainage began, and all 3 developed repeatedly marked hyponatremia and hyperkalemia during thoracic drainage. Another dog became weak and depressed, ostensibly because of hyperkalemia. Serum sodium and potassium concentrations in 1 dog with spontaneous chylothorax returned to normal after chylothorax resolved and thoracic drainage was stopped. The other 3 dogs died or were euthanatized, and the effect of stopping thoracic drainage could not be evaluated. In 3 dogs in which it was measured, normal-to-high plasma cortisol concentration was observed before and after adrenocorticotropin administration, and 2 dogs also had hyperaldosteronemia. Hyponatremia was hypothesized to be caused by sodium loss via thoracic drainage whereas hyperkalemia may have been multifactorial in origin, but probably was attributable, at least, in part to decreased renal potassium clearance.     

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.     

Thrombosis of the cranial vena cava in a cow with bronchopneumonia and traumatic reticuloperitonitis

This paper reports the clinical findings, surgical and medical management, and necropsy of a 6-year-old cow with thrombosis of the cranial vena cava and thrombo-embolic pneumonia following traumatic reticuloperitonitis. The clinical diagnosis was confirmed by necropsy.     

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.     

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.     

Spontaneous resolution of iatrogenic chylothorax in a cat

Chylothorax is an uncommon condition of dogs and cats defined by the accumulation of chylous effusion within the pleural space. Chylothorax has been experimentally created in dogs and cats by ligation of the cranial vena cava and has been reported to occur spontaneously in dogs with naturally occurring obstruction of the cranial vena cava. In the cat of this report, iatrogenic chylothorax was caused by surgical ligation and transection of the left brachiocephalic vein during a tracheal resection and anastomosis procedure. The chylous effusion resolved with medical management 9 weeks after surgery.     

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.