Caudal vena caval thrombosis following treatment of deep digital sepsis

A diagnosis of caudal vena caval thrombosis was made by ultrasonography of a Holstein cow presented for lethargy and poor milk production. Medical treatment was unsuccessful and the cow was euthanized. The diagnosis was confirmed at necropsy and Fusobacterium necrophorum was isolated from the thrombus. This paper discusses potential novel sources of caval thrombosis in this case.     

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.     

Caudal vena cava thrombosis-like syndrome in a horse

A 9-year-old Quarter horse was presented for chronic refractory pneumonia. On necropsy, an hepatic abscess, caudal vena cava thrombosis, pulmonary thromboembolism, and embolic pneumonia were identified. Similar lesions have been reported in cattle as caudal vena cava thrombosis syndrome, however this syndrome has not previously been reported in horses.     

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.     

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.     

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.     

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.     

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.     

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.     

Caudal vena cava obstruction and ascites in a cat treated by balloon dilation and endovascular stent placement

OBJECTIVE: To present details of an unusual case of caudal vena caval obstruction and its management in a cat. STUDY DESIGN: Clinical case report. STUDY POPULATION: A 15 month old male castrated domestic shorthaired cat. RESULTS: The diagnostic evaluation included the use of digital subtraction angiography and ultrasonography to locate the caudal vena caval obstruction. Treatment initially involved puncture and balloon dilation of the obstructed area of the cava. After reobstruction, the stenotic area was redilated and stented. The cat was euthanatized 4 weeks later because of vomiting, anorexia, and abnormal behavior, presumed to be associated with liver disease. CONCLUSION AND CLINICAL RELEVANCE: Interventional radiography provided a minimally invasive way to manage this unusual vascular anomaly.     

Passive liver congestion associated with caudal vena caval compression due to oesophageal leiomyoma

A large caudodorsal mediastinal mass was identified in a dog which had been presented for vomiting and anorexia. A few weeks later, the dog developed ascites and hindlimb oedema. Radiography showed that the caudodorsal mediastinal mass was compressing the caudal vena cava, probably inducing passive congestion of the liver. At postmortem examination, the mass was diagnosed as a large oesophageal leiomyoma. To the authors' knowledge, an oesophageal tumour leading to compression of the caudal vena cava associated with passive congestion of the liver has not been described previously in dogs. Secondary signs relating to the oesophageal mass appeared to be more prominent than the digestive signs. Causes of passive congestion of the liver and the differential diagnoses for a caudodorsal mediastinal mass are discussed.     

Extensive caudal vena cava thrombosis secondary to unilateral renal tubular cell carcinoma in a dog

A nine-year-old German shorthaired pointer cross was admitted because of partial anorexia, exercise intolerance and haematuria. On clinical examination, subcutaneous oedema, purpura and ascites were detected along with a palpable mass in the right craniodorsal abdomen. Laboratory findings included regenerative anaemia, leucocytosis, thrombocytopenia, azotaemia, increased blood serum alkaline phosphatase and proteinuria. Radiographic and ultrasonographic examinations revealed a large neoplasm involving the right kidney. Computed tomography further showed that the neoplastic tissue had spread into the lymph nodes, the wall of the caudal vena cava, the liver and lungs. The right renal vein, caudal vena cava and iliac veins appeared enlarged and secondarily thrombosed. A diagnosis was made of renal tubular cell carcinoma with secondary venous thrombosis. Gross postmortem examination confirmed the imaging findings, while light and electron microscopic examination revealed that the neoplasm was a solid carcinoma originating from the proximal convoluted renal tubules.     

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.