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.     

49-month survival following caval venectomy without nephrectomy in a dog with a pheochromocytoma

An 11 yr old spayed female Labrador retriever was diagnosed with a right adrenal tumor. At surgery, adhesions to the right kidney were dissected, allowing the right kidney to be preserved. The tumor showed extensive invasion into the suprarenal vena cava. It was felt that thrombus removal via venotomy could not be performed. Instead, the vena cava was ligated caudal to the liver and cranial to the right renal vein. The neoplastic gland was then excised en bloc together with the portion of the invaded caudal vena cava. Hind limb edema had developed preoperatively and increased transiently in the first days postoperatively. The animal was discharged 6 days postoperatively with no other clinical disorders, and hind limb edema resolved over time. Histopathology identified a pheochromocytoma. The dog died 49 mo later. A neoplastic thrombus of the vena cava may require venotomy to allow thrombus removal. Occasionally, removal of the thrombus by venotomy may prove impossible. In such a situation, en bloc removal of the concerned portion of the vena cava may be performed with a good long-term outcome provided that gradual occlusion of the vena cava by the thrombus has allowed time for collateral circulation to develop.     

Thrombosis of the caudal vena cava presenting as an unusual cause of an abdominal mass and thrombocytopenia in a dog

Thrombosis of the caudal vena cava in a dog secondary to metastatic neoplasia is described. The dog had a palpable abdominal mass and persistent thrombocytopenia due to a thrombosed caudal vena cava that was surgically removed. A few days after its removal, the dog died and neoplastic cells of neural crest origin were identified at the edge of the thrombus. Massive thrombosis can be an unusual cause of platelet consumption, leading to thrombocytopenia and disseminated intravascular coagulation. Deep vein thrombosis of the vena cava can occur in dogs and may mimic an abdominal mass. Multiple mechanisms may be involved in the development of venous thrombosis, including endothelial damage by neoplastic cells and the presence of a hypercoagulable state secondary to neoplasia. Extensive collateral circulation may allow removal of diseased vena cava.     

Extensive venous thrombosis and hind-limb edema associated with adrenocortical carcinoma in a dog.

A 10-year-old, spayed female, mixed-breed dog was referred for evaluation of bilateral hindlimb edema and weakness. Abdominal ultrasonography showed increased echogenicity of the lumen of the caudal vena cava from the level of the urinary bladder to the level of the cranial pole of the right kidney. Bilateral saphenous venograms displayed numerous filling defects in the caudal vena cava, right external iliac vein, right femoral vein, and the right common iliac vein. Extensive venous thrombosis was diagnosed, and the animal was euthanized. Necropsy confirmed the presence of venous thrombosis and revealed a right adrenocortical carcinoma that had invaded the caudal vena cava.     

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.     

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.     

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.     

Nephrotomography and ultrasonography for the localization of hyperfunctioning adrenocortical tumors in dogs

Nephrotomography and ultrasonography were used in 11 dogs with hyperadrenocroticism to assess the value of these techniques for the localization of biochemically diagnosed hyperfunctioning adrenocortical tumors. Both techniques enabled accurate localization of a unilateral adrenal mass in each of the dogs. Cross-sectional diameters of the masses ranged from 1 to 4 cm. In 1 dog, expansion of tumor into the caudal vena cava was revealed by caudal venacavography and ultrasonography. Mineralization in the tumor mass in 2 dogs was easily recognized by nephrotomography, but not by ultrasonography. Paracostal laparotomy confirmed the presence of an adrenocortical tumor in each dog, and expansion of tumor into the caudal vena cava in 1 dog. Cross-sectional diameters of the tumors ranged from 1.2 to 4.5 cm and corresponded well with cross-sectional measurements by nephrotomography and ultrasonography. It was concluded that nephrotomography and ultrasonography have similar diagnostic accuracies for the detection and localization of hyperfunctioning adrenocortical tumors.     

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.     

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.     

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.     

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.     

Budd–Chiari-like syndrome in a dog with a chondrosarcoma of the thoracic wall

Objective: To describe a dog with Budd–Chiari‐like syndrome secondary to caudal vena cava compression from a thoracic wall chondrosarcoma. Case summary: A 9‐year‐old spayed female Shetland Sheepdog cross with a recent history of non‐productive cough developed severe abdominal distension and dyspnea. Marked ascites and enlarged hepatic veins were identified with ultrasonography. At surgery, a right thoracic wall mass was found to be compressing the caudal vena cava. Fluid analysis of the ascites revealed a modified transudate with elevated protein concentration, consistent with Budd–Chiari‐like syndrome. Clinical signs resolved following thoracotomy and complete resection of the mass. New or unique information provided: Obstruction of venous blood flow can result from compression exerted by a space‐occupying thoracic wall mass on the caudal vena cava. Clinical resolution can be achieved with return of adequate venous circulation by removal of the mass and alleviation of the external pressure.     

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.     

Budd-Chiari-like syndrome associated with an adrenal phaeochromocytoma in a dog

A nine-year-old dog was presented with sudden-onset ascites and a history of two previous syncopal episodes. Diagnostic tests pointed to a Budd-Chiari-like syndrome, with obstruction of the caudal vena cava between the liver and heart. The ascites was refractory to treatment and the dog was euthanased. On postmortem examination, a phaeochromocytoma of the left adrenal gland was present, with contiguous invasions into the caudal vena cava, extending cranially as far as the cavoatrial junction. To the authors' knowledge, this is the first reported case of a Budd-Chiari-like syndrome associated with a phaeochromocytoma in a dog.     

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.     

Postcaval Thrombosis and Delayed Shunt Migration After Pleuro-Peritoneal Venous Shunting for Concurrent Chylothorax and Chylous Ascites in a Dog

Simultaneous chylothorax and chylous ascites related to intestinal lymphangiectasia was diagnosed in a 4-year-old spayed female dog. Palliative pleural and peritoneal drainage was accomplished by placement of fenestrated silastic sheeting into surgically created diaphragmatic defects, and implantation of a pleuro-peritoneal venous shunt. The immediate postoperative period was complicated by acute renal failure secondary to postcaval thrombosis originating at the site of placement of the efferent pump catheter and extending to the level of the renal veins. Rapid resolution of this complication was accomplished with systemic anticoagulation. Clinical signs related to fluid accumulation resolved for 10 weeks after which acute decompensation occurred and the dog was euthanatized. Postmortem examination showed that reaccumulation of fluid was associated with migration of the efferent limb of the shunt from the caudal vena cava.     

Intracaval Repair of a Persistent Ductus Venosus in a Dog

A persistent ductus venosus was diagnosed in a 4-month-old Old English sheepdog. Total occlusion of blood flow to the liver was achieved through heparinization, hepatic artery occlusion, and placement of bypass cannulas from the portal vein and caudal vena cava to the right atrium. Intracaval closure of the ductus venosus then was accomplished. Despite postoperative complications of continued hemorrhage and acute renal uremia, the animal recovered. The neurologic abnormalities exhibited before surgery resolved, and the dog became more active and gained weight. The dog died due to undetermined causes three months after surgery. The ductus venosus was found to be closed, and the liver was markedly increased in size at necropsy.     

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.     

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.