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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

Radiographic findings in dogs with naturally-occurring primary hypoadrenocorticism.

Survey radiographs often are obtained in dogs with primary hypoadrenocorticism in adrenal crisis as part of the routine evaluation of a critically ill dog. In this study, standardized methods of cardiac, pulmonary vasculature, and vena cava mensuration were used in 22 dogs with naturally-occurring primary hypoadrenocorticism, and the findings were compared with those in 22 breed-matched, clinically normal dogs. Most (81.8%) untreated dogs with primary hypoadrenocorticism had one or more radiographic abnormalities, including small size of the heart (45.5%), cranial lobar pulmonary artery (36.4%), caudal vena cava (54.5%), or liver (36.4%). Megaesophagus was not found in any of the dogs with hypoadrenocorticism, and therefore, compared to the other common radiographic findings, should be considered a rare finding.     

Aldosterone-, corticosterone- and cortisol-secreting adrenocortical carcinoma in a dog: case report

A 12-year-old, intact female beagle exhibited symptoms of polyuria-polydipsia and hyperorexia for two months. Blood tests showed elevated asparate aminotransferase, alanine aminotransferase, alkaline phosphatase and creatine kinase levels, as well as marked hypokalemia. The results of adrenocorticotropic hormone stimulation test showed elevated cortisol, aldosterone and corticosterone concentrations. Abdominal ultrasonography confirmed a mass in the left adrenal gland. Masses were also seen in the liver and caudal vena cava. Diagnosis was a tumor of the adrenal cortex with metastases. Trilostane administration was initiated. The dog initially showed improved demeanor as a result of regulating hormone secretion. However, after 88 days, the dog weakened rapidly, before dying on the 117th day. Pathological findings confirmed a diagnosis of adrenocortical carcinoma.     

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.     

Pheochromocytoma Presenting as Acute Retroperitoneal Hemorrhage in a Dog

Objective: This report describes the perioperative management of a dog with a right adrenal pheochromocytoma that presented with acute retroperitoneal hemorrhage, cardiac arrhythmia and hypertension. Additionally, a summary of pheochromocytoma and the idiosyncrasies of perioperative management of a pheochromocytoma are provided.
Summary: A 7-year old male, neutered, Dalmation was presented for acute collapse, abdominal pain and tachycardia. Physical examination findings were consistent with hypoperfusion concurrent with multiple cardiac arrhythmias and hypertension. Abdominal ultrasound revealed retroperitoneal effusion and a right adrenal mass intimately associated with the caudal vena cava. Incomplete right adrenalectomy was performed. Histopathology confirmed a pheochromocytoma.
Unique information provided: To the authors' knowledge, this is the first definitive report of acute retroperitoneal hemorrhage as the initial clinical manifestation of histologically confirmed adrenal pheochromocytoma in the dog. ( J. Vet Emerg Crit Care 2001; 11(3): 221–227 )     

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.     

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.     

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.     

IMAGING DIAGNOSIS—PORTAL VEIN APLASIA AND INTERRUPTION OF THE CAUDAL VENA CAVA IN THREE DOGS

Severe portal vascular anomalies have been reported previously accompanying azygos continuation of the caudal vena cava, polysplenia, and situs anomalies in dogs and people. Three dogs with portal vascular anomalies were identified by means of CT angiography as having portal vein aplasia with portal insertion into the caudal vena cava, azygos continuation of the caudal vena cava, and interruption of the pre‐hepatic caudal vena cava. This information confirms that complex embryological defects may occur in patients presenting for congenital portosystemic shunt, and that CT angiography is a non‐invasive method of completely evaluating these potentially non‐surgical portal vascular anomalies.