History
A 10-year-old 5.3-kg (11.7-lb) neutered male Chihuahua was referred for evaluation of a mediastinal mass and pleural effusion identified on thoracic radiographs obtained by the referring veterinarian. Clinical signs included a nonproductive cough of 3 days' duration, respiratory difficulty, and restlessness the night prior to hospital admission.
Physical examination findings included obesity (body condition score, 8/9), tachypnea (44 breaths/min; reference range, 18 to 35 breaths/min), and tachycardia (228 beats/min; reference range, 70 to 120 beats/min) with an irregularly irregular cardiac rhythm. The dog's body temperature was within reference range (37.6°C [99.7°F]; reference range, 37.2° to 39.2°C [99.0° to 102.5°F]). Crackles were bilaterally auscultated within the dorsal lung fields with absent lung sounds ventrally. Palpable hepatomegaly was noted. Saturation of hemoglobin with oxygen as measured by use of pulse oximetry revealed low to normal oxygen saturation (96%) on room air. The mean arterial oscillometric blood pressure was 113 mm Hg (reference range, 60 to 100 mm Hg). Hematologic evaluation revealed mild lymphopenia (1,119 lymphocytes/mL; reference range, 1,200 to 6,500 lymphocytes/mL) and mild hyperglycemia (128 mg/dL; reference range, 75 to 125 mg/dL). Prothrombin and partial thromboplastin times were within reference ranges. Results of heartworm antigen testing were negative. Thoracic radiography was performed (Figure 1).
Left lateral (A), right lateral (B), and ventrodorsal (C) radiographic views of the thorax of a 10-year-old 5.3-kg (11.7-lb) neutered male Chihuahua that was evaluated because of a mediastinal mass and pleural effusion identified on thoracic radiographs obtained by the referring veterinarian and clinical signs of a nonproductive cough of 3 days' duration, respiratory difficulty, and restlessness the night prior to hospital admission.
Citation: Journal of the American Veterinary Medical Association 252, 9; 10.2460/javma.252.9.1059
Determine whether additional imaging studies are required, or make your diagnosis from Figure 1—then turn the page →
Diagnostic Imaging Findings and Interpretation
Three-view thoracic radiography reveals an ill-defined soft tissue opacity within the cranial mediastinum with border effacement of the cranial aspect of the cardiac border and mild caudal and leftward deviation of the cardiac silhouette. Moderate, bilateral pleural effusion (worse on the right side), characterized by widened pleural fissures and retraction of the lung lobes from the thoracic margin, is evident (Figure 2).
Same radiographic images as in Figure I. A and B—A large, ill-defined soft tissue opacity within the cranial mediastinum is present (arrowheads). This soft tissue opacity causes border effacement of the cranial aspect of the cardiac silhouette, great vessels, and cranial pulmonary lobar vasculature, and contributes to a mass effect of the cranial mediastinum, with leftward and caudal displacement of the cardiac silhouette. C—Notice the soft tissue opacity mass (arrowheads) and the thin pleural fissure lines (arrows) between all lung lobes consistent with concurrent pleural effusion.
Citation: Journal of the American Veterinary Medical Association 252, 9; 10.2460/javma.252.9.1059
Differential diagnoses for the cranial mediastinal mass effect included a cranial mediastinal mass (ie, neoplasia, hematoma, granuloma, or abscess). Tissues of origin included cardiac base, branchial structure (such as cyst), lymph node, or thymus. Differential diagnoses for the pleural effusion included secondary modified transudate (neoplastic effusion or hemorrhage), chylous effusion, transudate, and exudate.
Radiographic findings prompted focused thoracic ultrasonography (images not shown). In addition to anechoic pleural effusion, a large, hypoechoic, thin-rimmed, 2.8-cm-diameter structure was present just cranial to the heart. Findings on limited thoracic ultrasonography led to reprioritization of the differential diagnoses list. A cystic or cavitary neoplasm (ie, thymoma or hemangiosarcoma), cyst, cystic hematoma, or abscess was prioritized. A vascular anomaly was additionally included in the list of differential diagnoses.
Findings on a 6-lead ECG revealed atrioventricularnodal independent supraventricular tachycardia (ie, focal atrial tachycardia). Echocardiography revealed compensated myxomatous mitral valve degeneration with normal left atrial size and compensated ventricular function. The fluid-filled structure was seen adjacent to, and causing mild compression of, the right atrium. No flow was identified within the structure on color flow Doppler ultrasonographic evaluation. Abdominal radiography and ultrasonography (images not shown) revealed hepatomegaly, distended hepatic veins, mild peritoneal effusion, and cystolithiasis.
Contrast-enhanced CT of the thorax was recommended to further evaluate the structure cranial to the cardiac base. The patient was scanned in sternal recumbency before and after the administration of a nonionic iodinated contrast agenta with a 16-slice CT scannerb in the transverse plane as follows: 150 mA, 100 kVp, 500-millisecond exposure time, 1-mm slice thickness, and 18-cm collection diameter, with an FC07 (sharp soft tissue) convolution kernel. Arterial, venous, and 3-minute delayed image datasets were acquired. Sagittal and dorsal reconstructions were also available.
A large, 3-cm-wide × 3-cm-high × 4-cm-long, ovoid, heterogeneously enhancing soft tissue dense structure is present within the right cranial aspect of the cranial mediastinum (Figure 3). The structure is contiguous with the cranial vena cava, with persistent pooling of the contrast agent within the gravity-dependent aspect of the lesion. Moderate, nonenhancing, gravity-dependent fluid is present within the pleural space of the hemithoraces bilaterally. Patchy renal cortical enhancement is seen on all contrast-enhanced sequences. The azygous vein and caudal vena cava are enlarged, and hepatomegaly is present. There is narrowing of the trachea and right mainstem bronchus.
Contrast-enhanced CT transverse (A; window level [WL], 72 Hounsfield units [HU] and window width [WW], 498 HU), midline sagittal (B; WL, 184 HU and WW, 778 HU), and dorsal (C; WL, 32 HU and WW, 364 HU) thoracic images of the dog in Figure 1. A and B—Notice the large, ovoid, heterogeneously contrast-enhancing soft tissue dense structure that was causing the mass effect of the cranial mediastinum. Notice the pooling of the contrast agent within the gravity-dependent aspect of the lesion (asterisk). The lesion was contiguous with the cranial vena cava (CrVC) cranially and right atrium (RA) caudally. There is severe distention of the azygous vein (Az) and its tributaries and the caudal vena cava (CaVC); hepatomegaly is evident (panel B). The venous distention includes the hepatic veins (not shown). C—There is moderate, nonenhancing, gravity-dependent fluid within the pleural space bilaterally (arrows). Concurrent leftward and caudal displacement of the heart are noted. Notice the brachiocephalic trunk at the level of the first ribs draining into the cranial vena cava. Numerous incidental cholecystoliths are seen within the gallbladder (GB). Ao = Aorta. LA = Left atrium. LV = Left ventricle. MPA = Main pulmonary artery. RV = Right ventricle.
Citation: Journal of the American Veterinary Medical Association 252, 9; 10.2460/javma.252.9.1059
On the basis of CT findings, primary consideration for the large structure within the cranial mediastinum was given to congenital or traumatic diverticular cranial vena cava aneurysm with secondary impaired venous return causing congestive hepatopathy, bicavitary effusion, and azygous, caudal caval, and hepatic venous congestion. The patchy renal cortical enhancement was likely caused by compromised renal blood flow (as with incomplete delivery of the contrast agent to the kidneys resulting from pooling of the contrast agent within the cranial vena cava) or ischemia with equal consideration given to artifact or abnormalities of arterial and venous phase timing. Mild tracheal and right mainstem bronchus chondromalacia were also considered likely and may have contributed to the dog's clinical signs.
Treatment and Outcome
Thoracocentesis yielded 125 mL of fluid. Findings on fluid analysis and cytologic evaluation of the pleural fluid were consistent with a modified transudate with a lymphocytic cell population secondary to inflammation or lymphatic hemorrhage, and no neoplastic cells were seen. The dog's arrhythmia was treated with diltiazem (0.05 mg/kg [0.023 mg/lb], IV, once; and then 1.4 mg/kg [0.64 mg/lb], PO, q 8 h). Because of a lack of response, digoxin (0.002 mg/kg [0.00091 mg/lb], PO, q 12 h) was added and effectively reduced the heart rate. After discussing the benefits and risks of surgical and conservative management of the aneurysm, the owners elected conservative care. Clopidogrel was administered prophylactically (1 mg/kg [0.45 mg/lb], PO, q 24 h) for prevention of thromboembolic disease. Nine months following hospital discharge, the owner and referring veterinarian reported no further clinical signs and the patient was doing well on continual treatment with diltiazem, digoxin, and clopidogrel.
Comments
Cranial vena cava aneurysm is a rare but previously reported cause of cranial mediastinal mass effect in a dog.1 Historically, diagnostic imaging tests deemed valuable in the diagnosis of cranial vena cava aneurysm have included echocardiography, nonselective cephalic angiography with fluoroscopy, and the use of agitated saline (0.9% NaCl) solution in a sonographic contrast-bubble study.1 For the case described herein, we describe for the first time the CT characteristics of a cranial vena cava aneurysm in a dog. Computed tomography was integral in achieving the definitive diagnosis. An aneurysm is a sac-like dilation of a vessel caused by weakening of the wall. Aneurysms are uncommon in veterinary medicine, with venous aneurysms being rarer than arterial.1 Venous aneurysms documented in the veterinary literature include the spinal venous sinus and portal, jugular, linguofacial, and maxillary veins.2–4 A venous aneurysm classification scheme does not exist for veterinary species. In people, superior vena cava aneurysms are classified on the basis of etiology as follows: congenital, acquired, pseudoaneurysms, and arteriovenous.5 In the dog of this report, a congenital aneurysm was suspected on the basis of the lack of traumatic history. Necropsy and histologic evaluation can aid in delineating the different types of aneurysms and may further point to a traumatic or congenital etiology.1
Given the paucity of information on cranial vena cava aneurysms in the veterinary literature, little is known about the ideal treatment approach to venous aneurysms in veterinary species. In people, options include surgical correction and conservative management. Conservative management may be sufficient for fusiform aneurysms. Surgical management should be considered for saccular aneurysms given the potential for thrombosis.6 Surgical and conservative management have more recently been shown to have similar clinical outcomes and survival times in people.1 In veterinary species, a gold standard of treatment for venous aneurysms does not exist.
An interesting feature of the case described in the present report was the lack of blood flow signal within the aneurysm on color flow Doppler interrogation. We attribute this to slow or stagnant venous blood flow rates within the aneurysm, given its large size, thus contributing to a lack of a differential Doppler shift large enough to produce a signal. In hindsight, power Doppler interrogation would likely have been superior in yielding a low-threshold signal because of its greater sensitivity to movement, independence from angle of interrogation, and better ability to separate background noise from true flow in slow-flow states.7 Additional unique features of this case included supraventricular arrhythmia of undetermined etiology and pleural effusion. In the 1 reported dog with a cranial vena cava aneurysm, an arrhythmia classified as ventricular ectopy that did not require treatment was noted.1 In the dog herein, the arrhythmia was supraventricular and required intervention. In both cases, a pathophysiologic link between the arrhythmia and aneurysm was not established. Pleural and peritoneal effusion have not previously been observed with a cranial vena cava aneurysm.1 The authors of the present report propose disruption of venous return to the right atrium, resulting in increased hydrostatic pressure, as the pathophysiology of the modified transudate pleural effusion. Poor venous return could have been caused by the tachyarrhythmia, location of the aneurysm, or pooling of blood within the diverticulum (as suggested by color flow Doppler evaluation), or a combination thereof. However, the role of the arrhythmia in the pathogenesis of the pleural effusion was supported by the fact that further thoracocentesis had not been required since the institution of antiarrhythmic treatment. On the current treatment protocol, no further clinical signs or new sequelae related to the aneurysm had developed in the dog of the present report.
Although rare, cranial vena cava aneurysm should be included as a differential diagnosis for cranial mediastinal mass effect when more common causes have been excluded. Contrast-enhanced CT is superior to radiography at providing a more definitive evaluation of mediastinal anatomy and can aid in determining the underlying cause of mediastinal mass lesions, especially when of vascular origin, as was true for the dog of the present report.
Acknowledgments
The authors declared that there were no financial or other conflicts of interest.
Footnotes
Optiray 320, Liebel Flarsheim Company, Raleigh, NC.
Aquilion 16, Toshiba, Tustin, Calif.
References
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4. Salmeri KR, Bellah JR, Ackerman N, et al. Unilateral congenital aneurysm of the jugular, linguofacial, and maxillary veins in a dog. J Am Vet Med Assoc 1991;198:651–654.
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6. Varma PK, Dharan BS, Ramachandran P, et al. Superior vena caval aneurysm. Interact Cardiovasc Thorac Surg 2003;2:331–333.
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