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.     

Clinical findings and diagnosis of thrombosis of the caudal vena cava in cattle

This paper describes the causes, clinical findings and diagnosis of caudal vena caval thrombosis in cattle. Occlusion of the vein is caused by a 'white' thrombus, and typical clinical signs include chronic weight loss, poor general condition and intermittent fever. Most affected cattle have respiratory signs; in some, pulmonary haemorrhage, ascites and sudden death occur. Haematological analyses, endoscopy of the respiratory tract and ultrasonographic examination of the pleura, liver and abdomen should be carried out in cattle suspected of having thrombosis of the caudal vena cava. The most important diagnostic finding is dilatation of the caudal vena cava seen via ultrasonography. Normally, the caudal vena cava appears triangular in cross section but in cattle with thrombosis it is oval or circular. The prognosis is poor and there is no treatment.     

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.     

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.     

Congenital obstruction of the caudal vena cava in a dog

A 16-week-old female Rottweiler was examined because of labored breathing and abdominal distention. Ascites, hepatomegaly, and pleural effusion were detected during physical and radiographic examinations. Selective angiography revealed a stenotic lesion at the junction of the caudal vena cava and the right atrium. A fibrous diaphragm with a pin-hole orifice was observed at surgery. Clinical signs of disease resolved after successful removal of the membranous obstruction.     

Segmental aplasia of the caudal vena cava in a dog

Ultrasonography, angiography, magnetic resonance imaging, and exploratory laparotomy of a 2-year-old wheaten terrier with lethargy, exercise intolerance, and ascites revealed segmental aplasia of the caudal vena cava with azygos continuation, complicated by thrombus formation. Surgeries were performed on the blind-ended vessel to remove thrombi, enhancing shunting of blood through the azygos vein.     

Chronic peritoneal effusion secondary to partial caudal vena cava obstruction following traumatic pneumothorax in a dog.

A three-year old, female Boxer Dog was treated initially with thoracocentesis for a right-sided pneumothorax. The dog was re-evaluated after three weeks because of an enlargement of the abdomen. A positive venogram revealed a ventral displacement of the caudal vena cava between the diaphragm and the heart, with a severe reduction of the diameter of the vein. An exploratory thoracotomy showed a displaced accessory lung lobe with an adhesion to the parietal pleura. Inflation of this lung lobe created a dynamic obstruction of the caudal vena cava, which resulted in ascites. Surgery offered successful treatment.     

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.     

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.     

Origin of the infrarenal part of the caudal vena cava in the pig

The vascular topography in the lumbar region of pig embryos and young fetuses was three-dimensionally reconstructed to study some controversial aspects of the origin and development of the infrarenal part of the caudal vena cava. Contrary to general belief, it was found that the supracardinal veins, which form the azygos veins in the thorax, do not take part in the construction of the caudal vena cava in the lumbar region. These veins do appear in the abdomen, but they are only involved in the formation of the lumbar and ascending lumbar veins. The infrarenal part of the caudal vena cava arises from the lumbar part of the right caudal cardinal vein. Whilst this venous pattern is established, the lumbar part of the left caudal cardinal vein disappears and its former location is occupied by large lymphatic connections between the cysterna chyli and the retroperitoneal mesenteric lymphatic sac. On the basis of these findings, a number of hypotheses on the development of anatomical variations of the caudal vena cava should be reconsidered.     

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.     

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.     

Phaeochromocytoma treated by en bloc resection including the suprarenal caudal vena cava in a dog

A 10-year-old, neutered male Cairn terrier was examined after experiencing intermittent vomiting of several months' duration and sudden onset of acute depression. Abdominal ultrasound examination revealed an adrenal mass invading the suprarenal part of the caudal vena cava. The vascular invasion could not be corrected so en bloc ligation/excision of the adrenal neoplasm and the suprarenal part of the vena cava was performed. Microscopic examination identified an adrenal phaeochromocytoma. The dog recovered well and had no significant vascular or renal dysfunction at follow-up 20 months after surgery. To the authors' knowledge, this is the first report of a dog surviving long term after resection of the suprarenal caudal vena cava.     

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.     

Acquired caudal vena cava occlusion and high protein ascites in a dog

High protein ascites developed following acquired obstruction of the vena cava in a dog. The cause of the obstruction was fibrosis associated with migration of a foreign body to the area. Diagnosis was made by venography and biochemical and cytological assessment of the ascitic fluid. The dog responded to surgical resection of the fibrous tissue and removal of the foreign body, a needle.