Cranial Vena Cava Syndrome in Guinea Pigs with Chronic Jugular Vein Catheters.

Guinea pigs are a premier small animal model for infectious disease research, and chronic indwelling venous access ports may be used to facilitate various procedures. Here we report catheter-related lesions in 5 uninfected Dunkin-Hartley guinea pigs with chronic jugular vein catheters used for imaging studies. Three guinea pigs were found dead with no premonitory signs. At necropsy, there was severe bilateral pulmonary atelectasis due to 20 to 29 mL of pleural effusion resulting from catheter-related thrombosis and cranial vena cava syndrome. In addition, one of these 3 guinea pigs had a polymicrobial catheter infection with abscessation. A 4th clinically normal guinea pig was euthanized at the end of the study, having spontaneously lost its catheter 7 mo prior, and had 17 mL of pleural effusion. The 5th guinea pig was euthanized following pooling of contrast material around the distal catheter in the cranial vena cava on CT. By histology, affected animals had recent and remote thrombosis or fibrosis (or both) of the cranial vena cava and right atrial wall, with osseous and cartilaginous metaplasia. Cranial vena cava syndrome should be considered as a differential for dyspnea or death in chronically catheterized laboratory animals.

Use of rivaroxaban for treatment of cranial vena cava syndrome secondary to transvenous pacemaker lead thrombosis in a dog.

A six-year-old Brussels griffon was presented for cervical swelling three months after implantation of a transvenous pacemaker. Transthoracic echocardiography demonstrated a thrombus associated with the pacemaker lead, partially obstructing right atrial inflow. The laboratory findings were consistent with protein-losing nephropathy. Initial medical therapy consisted of rivaroxaban (0.68 mg/kg orally every 24 hours), clopidogrel (2.5 mg/kg orally every 24 hours), and enalapril (0.5 mg/kg orally every 12 hours). Resolution of cervical and thoracic edema was noted within two weeks of initiating therapy. Recheck echocardiography two months and one year later revealed decreasing thrombus size despite worsening proteinuria. To the authors' knowledge, this is the first documented use of rivaroxaban for successful medical treatment of cranial vena cava syndrome caused by intracardiac pacemaker lead thrombosis in a hypercoagulable patient.

Acquired collateral venous pathways in a dog with cranial vena cava obstruction.

An 8-year-old neutered female Yorkshire terrier with mediastinal neoplasm and subsequent cranial vena cava invasion developed multiple venous collaterals from the brachiocephalic venous trunks to the caudal vena cava. Collateral venous pathways have been described in dogs with obstruction or increased blood flow resistance of the caudal vena cava but cranial vena cava collaterals have not been reported until now in veterinary patients. In this report, the CTA characteristics of such peculiar vascular routes are described and compared to similar findings reported in human medical literature. The recognition of such ancillary CT finding could help radiologists to reach a more accurate diagnosis of superior 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.

Syndrome de la veine cave crâniale secondaire à un granulome médiastinal àCryptococcuschez un chat. La gestion réussie d'un syndrome de veine cave crâniale accompagnée d'un chylothorax secondaire suspecté causé par un granulome médiastinal à Cryptococcus chez un chat commun mâle âgé de 4 ans est décrite. Le traitement a inclus une médication antifongique à long terme, des corticostéroïdes à court terme, une thoracentèse intermittente, de la rutine, de l'octréotide et de l'énalapril.(Traduit par Isabelle Vallières).

Cranial vena caval syndrome secondary to central venous obstruction associated with a pacemaker lead in a dog.

This report describes the case of an 11-year-old castrated male Shih Tzu who developed chylothorax three years following implantation of a transvenous pacemaker. Imaging demonstrated one definitive obstruction in the cranial vena cava and 3 additional suspected filling abnormalities within both external jugular veins, brachiocephalic veins and cranial vena cava. A thrombus was visualized in the cranial vena cava via transesophageal echocardiography. Thoracic duct ligation and cisterna chyli ablation were performed, with a resultant change in the nature of the fluid from chylous to a modified transudate. Repeat angiography and computed tomography three months later demonstrated a stenosis within the cranial vena cava. Balloon angioplasty was attempted, however it was unsuccessful in decreasing pleural effusion. Palliative thoracocentesis was continued until the patient developed a lung lobe torsion, at which time euthanasia was elected. Necropsy confirmed cranial vena caval syndrome secondary to transvenous pacemaker implantation induced fibrous proliferation within the vessel lumen.

Cranial vena caval thrombosis associated with endocardial pacing leads in three dogs.

Three dogs were examined several years following implantation of transvenous, single-lead, endocardial, right-ventricular permanent pacing systems for signs consistent with cranial vena caval syndrome. Angiograms performed in all dogs revealed filling defects within the cranial vena cava and, in some instances, intracardiac filling defects. Medical therapy was instituted in two dogs, with one surviving several weeks. One dog underwent surgery to address intra-cardiac thrombosis but did not survive the immediate postoperative period. Postmortem examinations were performed in two dogs and confirmed cranial vena caval and intracardiac thrombosis. Cranial vena caval thrombosis associated with transvenous pacing leads appears to carry significant morbidity and mortality.

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.

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.

Canine and feline caval syndrome.

The caval syndrome is a serious complication of chronic heartworm (Dirofilaria immitis) disease in dogs and cats. The syndrome is characterized by acute anorexia, respiratory distress, weakness, right-sided cardiac murmur, anemia, hemoglobinuria, hepatic and renal dysfunction, signs of forward and backward heart failure, and, possibly, disseminated intravascular coagulation (DIC). Retrograde migration of adult heartworms from the pulmonary arteries to the right ventricle, right atrium, and venae cavae causes disruption of the tricuspid apparatus. Valvular insufficiency, with concurrent pulmonary hypertension, reduces cardiac output thus resulting in forward and backward heart failure. Additionally, red blood cells are traumatized and hemolyzed as they flow through the mass of worms. Therapy consists of supportive care and the removal of the heartworm mass from the right ventricular inflow tract. Caval syndrome in dogs and cats is associated with high mortality rates and generally has a guarded to poor prognosis.

Clinical manifestations and associated disease syndromes in dogs with cranial vena cava thrombosis: 17 cases (1989-1996).

OBJECTIVE: To characterize cranial vena cava thrombosis in dogs with regard to signalment, clinical manifestation, potential inciting causes, treatment, and outcome. DESIGN: Retrospective study. ANIMALS: 17 dogs with a cranial vena cava thrombus. PROCEDURE: Medical and necropsy records were reviewed for signalment, potential causes of thrombus formation, diagnosis, clinicopathologic findings, treatment, and outcome. RESULTS: A signalment predisposition was not found. Ten dogs had cranial vena cava syndrome, and 10 had a pleural effusion. Ten dogs were dyspneic, and 5 had palpable jugular thrombi. Predisposing conditions identified were presumed immune-mediated hematologic disease and corticosteroid administration (6 dogs), sepsis (6), protein-losing nephropathy (2), neoplasia (2), and cardiac disease (1). Central venous catheterization was implicated as a contributing cause. Thrombocytopenia was the most consistent clinicopathologic finding, and ultrasonography was helpful in confirming the diagnosis. Treatment varied, but 15 of the 17 dogs died or were euthanatized within 20 days of clinical manifestation of the thrombus. At necropsy, thrombi were found in other organs, mainly the right atrium, jugular veins, and pulmonary arteries. CLINICAL IMPLICATIONS: Prognosis is poor for dogs with cranial vena cava thrombosis associated with clinical signs. Use of central venous catheters should be avoided in dogs with predisposing diseases such as immune-mediated disease, sepsis, protein-losing nephropathy, neoplasia, and cardiac disease.

Comparison of laboratory data in dogs with heartworm caval syndrome surviving and nonsurviving after surgical treatment.

Laboratory data in 47 dogs with caval syndrome (CS) surviving after surgical HW removal compared with those in 15 dogs with CS which died after the treatment. The number of HWs removed in surviving dogs was significantly greater than in nonsurviving dogs. The Ht value was significantly higher in nonsurviving dogs than in surviving dogs. Plasma enzyme activities ranged widely from normal to extremely high levels, and there were no significant differences in plasma enzyme activities between the surviving and nonsurviving dogs. Serum total protein, and plasma triglyceride, creatinine, glucose, calcium, sodium (Na) and chloride (Cl) levels were much similar between the HW-free and surviving dogs, but significantly different between the HW-free and nonsurviving dogs. Plasma urea nitrogen, uric acid and potassium levels were higher, and plasma Na and Cl levels were lower in nonsurviving dogs than in surviving dogs.

Excision of a locally invasive thymoma causing cranial vena caval syndrome in a dog.

A 9-year-old female Golden Retriever was examined because of inappetance, labored breathing, edema, and distension of the veins of the neck. Thoracic radiography revealed pleural effusion and a cranial mediastinal mass. Biopsy results obtained by use of fine-needle aspiration were consistent with thymoma. At surgery, the tumor was found to have invaded the cranial vena cava. Extra- and intravascular portions were removed without complications, and the dog's clinical signs resolved. To our knowledge, this is the first documented report of an invasive thymoma causing cranial vena caval syndrome that has been successfully treated in a dog. In this instance, the simplest surgical method, namely venotomy and tumor extraction using venous inflow occlusion, was successful, obviating the need for temporary or permanent vascular conduits or grafts. These findings indicate that there is potential for surgical correction of invasive thymoma with cranial vena caval syndrome in some animals, and the prognosis is not always poor.

Systemic oxygen delivery and consumption in dogs with heartworm disease.

To investigate systemic oxygen (O2) transport, we calculated the oxygen delivery index (Do2I), oxygen consumption index (Vo2I) and oxygen extraction ratio (ER) in dogs with heartworm (HW) disease. The Do2I was 770 +/- 331 ml/min/kg in dogs mildly affected with pulmonary HW disease showing respiratory signs, mild anemia and mild cardiac insufficiency (n = 34); 238 +/- 155 ml/min/kg in dogs with ascitic pulmonary HW disease (n = 7); and 577 +/- 320 ml/min/kg in dogs with caval syndrome (CS) which survived (n = 15) or died (n = 7) after surgical HW removal. The Do2I was lower (P < 0.01) in all HW-infected groups, especially in ascites and CS-non-surviving dogs, than in HW-free dogs (n = 11, 1041 +/- 264 ml/min/kg). The Vo2I was higher in some mildly affected dogs (161 +/- 88 ml/min/kg), and lower (P < 0.01) in ascitic dogs (45 +/- 53 ml/min/kg) than in HW-free dogs (123 +/- 44 ml/min/kg). The ER was higher (P < 0.01) in all HW-infected groups than in HW-free dogs. The Do2I correlated significantly with Vo2I (r = 0.84, P < 0.01), and the Vo2I correlated significantly with ER (r = 0.48, P < 0.01). The Do2I correlated significantly with arterial O2 tension (r = 0.33), serum LDH (r = -0.46) and CK (r = -0.46) activities, serum urea nitrogen (UN, r = -0.32) and lactic acid (LA, r = -0.39) concentrations and cardiac index (r = 0.64).(ABSTRACT TRUNCATED AT 250 WORDS)

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.