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.     

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.     

Canine leishmaniasis with nephrotic syndrome and aortic and caudal vena cava thromboembolism

Objective – To describe a case of leishmaniasis associated with nephrotic syndrome and aortic and caudal vena cava thrombosis in a dog. Case Summary – A 3‐year‐old male Boxer was referred to the Faculty of Veterinary Medicine, Lisbon, with vomiting, polyuria, polydipsia, lethargy, anorexia, and weight loss. On admission, the dog was thin, quiet, and dehydrated. Initial laboratory abnormalities were compatible with a diagnosis of leishmaniasis (confirmed by serology and bone marrow aspirate), and nephrotic syndrome. Three days later, the animal developed lumbar pain, paraparesis, and absent femoral pulses. Coagulation tests showed a marked reduction in antithrombin (AT) and a mild increase in serum fibrinogen concentration. A diagnosis of thromboembolism was made. In spite of treatment aimed at controlling the primary condition and decreasing further thrombus formation, necrosis developed in the distal right pelvic limb and the nail beds of the left pelvic limb. Against medical advice, medication was stopped and, 15 days later, the dog returned to the hospital, showing extensive necrosis of both pelvic limb extremities. Euthanasia was performed at the owner's request. Necropsy showed a thrombus localized at the distal aorta and extending into the right iliac artery, and an additional thrombus extending from both femoral veins onto the caudal vena cava. New or Unique Information Provided – Thromboembolic disease is rare in dogs with leishmaniasis with nephrotic syndrome. This case suggests that a marked decrease in AT and a mild increase in serum fibrinogen may elicit a hypercoagulable state in these patients.     

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.     

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.     

ULTRASONOGRAPHIC LOCALIZATION OF A CAUDAL VENA CAVA THROMBUS IN A DOG WITH LEISHMANIASIS

A dog with visceral leishmaniasis developed rear limb edema, and distension of the caudal epigastric veins. Glomerular disease with nephrotic syndrome and hypercoagulable state was diagnosed. Sonographically there was massive thrombosis of the caudal vena cava.     

Ultrasonographic identification of vascular invasion by adrenal tumors in dogs

Adrenalectomy is the treatment of choice for adrenal tumors that are producing adverse clinical signs. Surgical planning prior to adrenalectomy is aided by identifying tumors with invasion into adjacent vessels or the presence of a tumor thrombus extending into the caudal vena cava. In this paper, we evaluated the sensitivity and specificity of ultrasound in determining if vascular invasion or tumor thrombus is present. Thirty-four dogs with 36 adrenal tumors were reviewed retrospectively. Overall, 36% of tumors had vascular invasion. Abdominal ultrasound was 100% sensitive and 96% specific in identifying the presence of a tumor thrombus in the caudal vena cava. The sensitivity and specificity was 76% and 96%, respectively, when all forms of vascular invasion were evaluated and included patients with vascular wall invasion without concurrent thrombus. Abdominal ultrasound is a good screening tool for identifying vascular invasion or tumor thrombus associated with adrenal tumors in dogs.     

Diagnosis by ultrasonography of congestion of the caudal vena cava secondary to thrombosis in 12 cows

This paper describes the clinical, ultrasonographic, radiographic and postmortem findings in 12 cows with thrombosis of the caudal vena cava. The principal clinical signs were chronic bronchopneumonia and fever in 11 cows; one cow had epistaxis and one cow bled from the mouth; eight cows had anaemia and leucocytosis, and the clotting time for the glutaraldehyde test was markedly decreased in all the cows; in nine of the cows the activity of gamma-glutamyltransferase was high, suggesting chronic hepatic congestion. The most important ultrasonographic finding was congestion of the caudal vena cava attributable to thrombosis of the vein. In all the cows the caudal vena cava was round to oval on cross-section, rather than the normal triangular shape. The hepatic, splenic and portal veins were dilated in five, three and one cow, respectively. The results of radiography and endoscopy supported a diagnosis of bronchopneumonia, but there were radiographic changes in the diaphragmatic lung lobes that supported a diagnosis of vena caval disease in only four cows. Postmortem there was a thrombosis of the caudal vena cava in all the cows, and the thrombi were located in the thoracic, subphrenic and abdominal part of the caudal vena cava at the level of the liver in four, one and seven cows, respectively. In three cows, the thrombus was situated where a hepatic abscess had broken into the caudal vena cava, and in one cow it was at the site of a diaphragmatic abscess. In another cow, there was a fistula between the major bronchus of the right diaphragmatic lung lobe and the caudal vena cava where the thrombus was situated. Three cows had liver abscesses that had not broken into the caudal vena cava. There was severe bronchopneumonia in 11 of the cows, some of which also had multiple pulmonary abscesses.     

Ureteral obstruction and hydronephrosis in a cat associated with retroperitoneal infarction

A 9-month-old cat was presented for routine vaccination before rehoming. Physical examination revealed a palpable mass in the cranial abdomen. The right kidney was severely enlarged (6cmx4cm) on plain abdominal radiographs, and failed to opacify normally during intravenous urography. Ultrasonography demonstrated a hydronephrotic right kidney. During exploratory coeliotomy, a retroperitoneal mass was identified, adherent to the caudal edge of the right kidney, enveloping the ureter and blocking urine outflow. The ureter caudal to the mass was of normal size. Right ureteronephrectomy was performed; the mass was subsequently freed from adhesions to the caudal vena cava and sublumbar muscles and excised. Histopathological examination revealed the mass to be composed of both normal and necrotic adipose tissue and fibrous tissue surrounding the ureter and a thrombosed, recanalised vessel. This appearance was consistent with an area of infarction and fibrosis with obstruction of the ureter. The cat was clinically well 3 months postoperatively.     

Cushing's disease complicated with thrombosis in a dog

Thrombosis is a potential complication of hyperadrenocorticism (HAC) in dogs. An 8-year-old male Beagle diagnosed with pituitary-dependent HAC had complicated with thrombosis in the caudal vena cava and abdominal aorta, which was treated by hypophysectomy and antithrombotic therapy. After hypophysectomy, hypercortisolemia disappeared and the general condition was also significantly improved. Ultrasonography after hypophysectomy revealed that the thrombus remained in the abdominal aorta, but the thrombus in the caudal vena cava had disappeared. However 692 days after the hypophysectomy, the dog had an acute onset of dyspnea and died. Postmortem examination revealed the presence of thrombi in the abdominal aorta and the pulmonary artery. Observations from this case show that HAC dogs must be attention to thrombosis.     

Surgical treatment of right-sided renal lymphoma with invasion of the caudal vena cava

An eight-year-old, male castrated basset hound presenting with a three-month history of lethargy was examined. Diagnostic tests including radiography and ultrasonography showed a right-sided renal mass. A 99mTc diethylenetriamine penta-acetic acid scan demonstrated that this kidney was non-functional. At surgery, invasion of the caudal vena cava was found, and the renal segment of the vena cava and the right kidney were resected. The left renal vein was anastomosed to the more proximal vena cava using a polytetrafluoroethylene graft, and the dog recovered well. Two days postsurgery, the dog suffered an acute episode of aspiration pneumonia and was euthanased. The renal mass was diagnosed as lymphoma on histopathology.     

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.     

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.     

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.     

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.     

Cor triatriatum dexter of unusual morphology in a miniature schnauzer

A five-year-nine-month-old, male entire, miniature schnauzer presented for further investigation of pleural effusion. Echocardiography revealed a perforated membrane dividing the right atrium into two chambers: the true right atrium (a small, lower-pressure, cranioventral chamber communicating with the tricuspid valve and right ventricle) and the accessory right atrium (a larger, higher-pressure, caudodorsal chamber), consistent with a cor triatriatum dexter. This was confirmed using computed tomography angiography. Imaging studies revealed that both the cranial and caudal vena cava entered the higher-pressure accessory right atrium and the coronary sinus entered both the accessory and true right atrial chambers. This differed from the more usual canine cor triatriatum dexter presentation with the cranial vena cava entering the lower-pressure cranial chamber and the caudal vena cava entering the higher-pressure caudal chamber. Balloon membranostomy was successful in reducing the pressure gradient between the two right atrial chambers with subsequent resolution of the clinical signs. The patient continues to do well after three-years of follow-up.     

USE OF TRANSSPLENIC INJECTION OF AGITATED SALINE AND HEPARINIZED BLOOD FOR THE ULTRASONOGRAPHIC DIAGNOSIS OF MACROSCOPIC PORTOSYSTEMIC SHUNTS IN DOGS

We describe the use of ultrasonography‐guided percutaneous splenic injection of agitated saline and heparinized blood for the diagnosis of portosystemic shunts (PSS) in 34 dogs. Agitated saline mixed with 1 ml of heparinized autologous blood was injected into the spleen of 34 sedated dogs under sonographic guidance. The transducer was then sequentially repositioned to visualize the portal vein, the caudal vena cava, and the right atrium through different acoustic windows. It was possible to differentiate between intrahepatic and extrahepatic shunts depending on the entry point of the microbubbles into the caudal vena cava. Portoazygos shunts and portocaval shunts could be differentiated based on the presence of microbubbles in the caudal vena cava and/or the right atrium. In one dog, collateral circulation due to portal hypertension was identified. In dogs with a single extrahepatic shunt, the microbubbles helped identify the shunting vessel. The technique was also used postoperatively to assess the efficacy of shunt closure. All abnormal vessels were confirmed by exploratory laparotomy or with ultrasonographic identification of the shunting vessel. Ultrasound‐guided transsplenic injection of agitated saline with heparinized blood should be considered as a valuable technique for the diagnosis of PSS; it is easy to perform, safe, and the results are easily reproducible.     

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.     

Transportal Approach for Attenuating Intrahepatic Portosystemic Shunts in Dogs

A novel surgical approach, using portal venotomy during total hepatic vascular occlusion, was used to locate and attenuate congenital intrahepatic portosystemic shunts in nine dogs. Shunt location was consistent with a persistent ductus venosus in only two dogs. In the remaining seven dogs the shunts were window-like orifices arising from either the left (two dogs) or right portal vein branch (five dogs) and communicating with the ipsilateral hepatic vein or caudal vena cava. The transportal approach using total hepatic vascular occlusion consistently provided good access to the portosystemic shunts, including those with window-like communications. A 7 to 16 minute period of total vascular occlusion was well-tolerated hemodynamically, with few intraoperative complications. Intrahepatic shunts were successfully attenuated in eight dogs, while one dog with portal atresia was euthanatized. The postoperative course was complicated by high protein pulmonary edema (one dog), an encapsulated biliary pseudocyst (one dog) and uncontrollable hemorrhage caused by an uncharacterized coagulopathy (one dog). Three dogs required a second operation to further attenuate their shunts. The clinical condition of all seven surviving dogs was improved after surgery.