Michael D. Dake, MD • Gerald Zemel, MD • Bart L. Dolmatch, MD • Barry T. Katzen, MD

The Cause of Superior Vena Cava Syndrome: Diagnosis with Percutaneous Atherectomy 1 The cause of superior vena cava syndrome (SVCS) in two patients was identified by means of eridovascular biopsy of the superior vena cava (SVC) performed with a percutaneous atherectomy catheter. In both cases, the extracted tissues were neoplastic, therefore obviating additional invasive procedures. After a specific diagnosis was established, external-beam radiation therapy was used to treat the SVCS. The atherectomy catheter was used in conjunction with other percutaneous techniques, including balloon angioplasty and endovascular stenting of the SVC. Index terms: Atherectomy • Venae cavae, grafts and prostheses, 946.456 • Venae cavae, stenosis or obstruction, 946.33 Radiology 1990; 174:957-959

1 From the Miami Vascular Institute, Baptist Hospital of Miami, 8900 N Kendall Dr, Miami, FL 33176 (M.D.D., G.Z., B.T.K.), and the Department of Radiology, Washington Hospital Center, Washington, DC (B.L.D.) Received October 26, 1989; revision requested November 21; revision received and accepted December 4. Address reprint requests to B.T.K. RSNA, 1990

vena cava syndrome (SVCS) is caused by a variety of benign and malignant disease processes that obstruct the superior vena cava (SVC) (1-5). Occasionally, in an individual patient, the exact cause of the SVCS is unclear. We describe the percutaneous use of an atherectomy catheter to obtain tissue and define the cause of the obstruction in two patients with SVCS. In both cases, after a diagnosis of malignancy was established, the SVC was treated with balloon angioplasty, and in one case, an expandable wire stent was placed percutaneously, as previously described (6-11). C UPERIOR

CASE REPORTS Case 1.—A 73-year-old woman noted the gradual onset of a right-sided neck and facial swelling during a 2-week period. She had a 40-pack-year smoking history, and 2 years earlier, an adenocarcinoma of the right lung that extended to the SVC had been resected. After right-sided thoracotomy, she did not receive adjuvant radiation therapy or chemotherapy. During the 2 years since surgery, she has been followed up clinically and has been asymptomatic. During this period, multiple follow-up chest radiographs and three computed tomographic (CT) scans of the chest were obtained. All showed only postoperative changes without evidence of recurrent tumor. After she was convinced that the rightsided facial and neck puffiness were not transient, she sought medical attention. Findings from a chest radiograph were unchanged from a previous examination, and a CT scan of the chest was remarkable only for postsurgical changes in the right side of the mediastinum. There was no evidence of a mediastinal mass or SVC obstruction. During this evaluation, the patient had no complaints other than the swelling. A superior vena cavogram demonstrated a high-grade narrowing of the SVC. The stenosis was adjacent to a 1.5-cm calcified lymph node and multiple surgical clips that overlay the right side of the mediastinum. No intraluminal filling defects suggestive of a clot were evident.

After the superior vena cavogram was obtained, it was unclear whether the SVCS was due to postsurgical scarring and cicatrix, fibrosis associated with the calcified lymph node, and/or recurrent tumor. Without a diagnosis there was a reluctance to recommend surgical or radiation therapy. At this point, the patient was transferred to our hospital for possible percutaneous therapy. With the approval of the hospital's human research committee and the patient's consent, placement of a Gianturco expandable wire stent was planned. After cannulation of a right antecubital vein and the right femoral vein, a superior vena cavogram was obtained. It was without change from the outside study and demonstrated an irregular narrowing of the SVC just below the junction with the left brachiocephalic vein (Fig la). A pressure gradient of 105 mm Hg was measured across the stricture. A long straight 10-F angiographic sheath with a dilator was then introduced over a wire through the right femoral venotomy site. The tip of the sheath was positioned in the proximal left brachiocephalic vein in a manner that bridged the SVC stenosis. Through the sheath, a 9-F atherectomy catheter (Simpson Peripheral Atherocath; Devices for Vascular Intervention, Redwood City, Calif) was introduced. The atherectomy catheter was advanced within the sheath to the level of the stenosis. Use of "roadmapping" techniques allowed the exact site of the lesion to be identified. The 10F sheath was withdrawn into the inferior vena cava. The cutting window of the cylindrical atherectomy housing was positioned across the stenosis (Fig lb). The positioning balloon was inflated to 30 psi (206,841 Pa), and the cutting blade was slowly advanced through the metal housing. A total of five passes were made along the right lateral aspect of the narrowed SVC. The catheter was then removed through the sheath, and the material that was retrieved from the distal housing was given to a pathologist in attendance. Some of the cuttings were examined after frozen sectioning, and others were reserved for permanent sections.

Abbreviations: SVC = superior vena cava, SVCS = superior vena cava syndrome.

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Both frozen and permanent sections showed adenocarcinoma. After use of the atherectomy catheter, a repeated cavogram was without significant change. The pressure gradient across the narrowing did not decrease. Subsequently, the SVC stenosis was dilated with an angioplasty balloon with an outside diameter of 12 mm. The pressure gradient was reduced to 5 mm Hg following dilation. Through the 10-F sheath, a modified Gianturco expandable wire stent was placed across the SVC stenosis. The stent, consisting of two stent bodies (2.5 and 3.0 cm in length and 3.0 cm in diameter), was placed without difficulty. A subsequent cavogram demonstrated an SVC diameter of 10 mm at the previous stenosis. Rapid flow through the SVC was observed fluoroscopically. The pressure gradient across the stent was 12 mm Hg. After stent placement, the patient was treated with oral anticoagulants. During the next 48 hours, the patient's neck and facial edema completely resolved. Three days after the procedure, she was discharged to receive outpatient externalbeam radiation therapy. Five months after the procedure, she was asymptomatic following her course of radiation treatment. She has not been receiving anticoagulants. A recent chest radiograph was without change when compared with a radiograph taken at the time of hospital discharge. Case 2.—An 81-year-old woman noticed a right upper-extremity swelling that progressed during a 3-week period. Her medical history included a right mastectomy 31 years earlier for breast carcinoma. Adjuvant radiation therapy was started at that time. Sixteen years later, she underwent a left mastectomy, without adjuvant therapy, for a second primary breast carcinoma. Five years before this admission, a right upper lobectomy was performed for squamous cell carcinoma. There was no evidence of persistent tumor following a thoracotomy, and she received no adjuvant therapy. During the 5-year period following the thoracotomy, follow-up chest radiographs demonstrated no sign of recurrent tumor. On initial presentation to a physician, 2 weeks before admission, the possibility of right-upper-extremity cellulitis was considered, and antibiotics were prescribed without effect. The swelling progressed to involve the left upper extremity. A repeat chest radiograph showed a large right-sided paratracheal mass that was not present on radiographs obtained 5 months earlier. A CT scan of the chest obtained without intravenous administration of contrast material demonstrated a large right-sided paratracheal mass with mediastinal infiltration in the region of the SVC. Percutaneous needle aspiration of the mass was requested. Review of the radiographs indicated that a transpulmonary approach would be necessary. Therefore, to avoid possible pneumothorax in a patient with limited pulmonary reserve, an 958 • Radiology

E TE E II a.

b.

Figure 1. (a) Superior vena cavogram shows irregular narrowing of SVC below brachioce-

phalic vein bifurcation. (b) Nine-French atherectomy device across the SVC stenosis through a 10-F sheath.

a.

b. Figure 2. (a) Superior vena cavogram obtained via a right femoral approach demonstrates

complete SVC and left brachiocephalic vein occlusion with multiple large venous collateral vessels present. A right subclavian venous stenosis is also identified. (b) A prototype 9-F over-the-wire atherectomy catheter is demonstrated across the SVC and left brachiocephalic vein occlusions. The inflated balloon and cutting chamber are located at the site of SVC occlusion. endovascular SVC biopsy with a 9-F atherectomy catheter (Simpson Peripheral Atherocath) was planned after consultation with the referring physician. A superior vena cavogram demonstrated a 70% right brachiocephalic vein narrowing with occlusion of the left brachiocephalic vein and SVC over a 4-cm segment (Fig 2a). A prominent azygos vein was evident, and large mediastinal venous collateral vessels were present. In view of the total venous occlusion, a urokinase infusion was begun via a right femoral venous approach. A coaxial sys-

tem was employed with an open-ended wire that was embedded in the upper SVC occlusion and a 5-F multipurpose catheter in the lower portion of the occlusion. A split urokinase dose regimen was begun by infusing 50,000 U / h through each port. Twenty-two hours after the start of thrombolytic therapy, a contrast injection through the open-ended wire and catheter demonstrated no evidence of thrombolysis. The urokinase infusion was then terminated. From the right femoral approach, catheter and guide wire recanalization techniques were then used to March 1990 • Part 2

place a guide wire across the SVC-left brachiocephalic vein occlusion and into the patent left subclavian vein. A prototype over-the-wire 9-F atherectomy catheter (Devices for Vascular Intervention) was introduced through a 9-F standard angiographic sheath over a 0.018-inch guide wire and placed across the SVC occlusion (Fig 2b). Three passes with the cutting blade were made across the lateral aspect of the SVC. Frozen and permanent sections of the atherectorny specimen showed squamous cell carcinoma. A repeat superior vena cavogram showed a patent SVC with a very narrow lumen. Subsequently, the residual SVC stenosis was dilated with an angioplasty balloon with an outside diameter of 10 mm. A final superior vena cavogram showed mild persistent luminal narrowing; however, antegrade blood flow was present across the SVC. There was no measurable pressure gradient. The placement of an endovascular stent was considered; however, the manufacturer could no longer supply such a stent. The patient then underwent systemic anticoagulation with heparin, and a course of external-beam radiation therapy was begun. During the next 24 hours, the bilateral upper-extremity edema resolved completely. However, radiation therapy was discontinued 4 days later when the patient's condition deteriorated. She became hypotensive and was treated for respiratory failure. A CT scan showed no mediastinal hemorrhage or other new thoracic abnormality. Upper-extremity edema recurred 7 days following angioplasty. Radiation therapy has not been restarted.

DISCUSSION SVCS may cause swelling of the upper extremities, face, and neck; cerebral edema; and/ or upper-airway obstruction (1,2). Although the vast majority of SVCSs are due to a malignant tumor (ie, most often a lung carcinoma extending into the mediastinum), a variety of nonmalignant and benign iatrogenic causes are well known (2-5). In some patients, the exact cause of SVCS is unknown at the time symptoms appear. Nonspe-

Volume 174 • Number 3 • Part 2

cific measures, including elevation of a swollen extremity, corticosteroids, and balloon angioplasty may be helpful; however, without a tissue diagnosis, specific therapy, such as surgery or radiation therapy, is usually not encouraged. If a diagnosis of malignanCy is established, appropriate treatment can be directed at the tumor. Therapy for SVCS due to malignancy is often gratifying, with relief of symptoms and long-term survival reported after prompt institution of treatment (12,13). If surgery is not warranted or if the difficulty and/or risk of a percutaneous needle biopsy is high, tissue may be obtained through an endovascular approach. Previous reports of percutaneous transluminal vascular biopsy techniques have included the use of endoscopic biopsy forceps (14-17), an endomyocardial bioptome (18), bronchoscopic brushes (19,20), and transcatheter suction (21) to diagnose masses that invade the SVC, inferior vena cava, and renal vein. An atherectomy catheter can be used as a biopsy device in conjunction with previously described percutaneous methods of treating SVCS, such as balloon angioplasty and endovascular stenting (6-11). • References 1.

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Lopez MI, Vincent RJ. Malignant superior vena cava syndrome. In: Kapoor AS, ed. Cancer and the heart. New York: Springer-Verlag, 1986; 206-217. LOchridge SK, Knibbe WP, Doty DB. Obstruction of the superior vena cava. Surgery 1979; 85:14-24. Parish JM, Marschke RF, Dines DE, Lee RE. Etiologic considerations in superior vena cava syndrome. Mayo Clin Proc 1981; 56:407-413. Schraufnagel DE, Hill R, Leech JA, Pare JAP. Superior vena cava obstruction. Am J Med 1981; 70:1169-1174. Mahajan V, Strimlan V, VanOrdstrand HS, Loop FD. Benign superior vena cava syndrome. Chest 1975; 68:32-35. Sherry CS, Diamond NG, Meyers TP, et al. Successful treatment of superior vena cava syndrome by venous angioplasty. AJR 1986; 147:834-835.

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Ali MK, Ewer MS, Balakrishnan PV, et al. Balloon angioplasty for superior vena cava obstruction. Ann Intern Med 1987; 107:856-857. 8. Capek P, Cope C. Percutaneous treatment of superior vena cava syndrome. AJR 1989; 152:183-184. 9. Charnsangavej C, Carrasco CH, Wallace S, et al. Stenosis of the vena cava: preliminary assessment of treatment with expandable metallic stents. Radiology 1986; 161:295-298. 10. Rosch J, Bedell JE, Putnam J, Antonovic R, Uchida B. Gianturco expandable wire stents in the treatment of superior vena cava syndrome recurring after maximum tolerance radiation. Cancer 1987; 60:12431246. 11. Putnam JS, Uchida BT, Antonovic R, Rosch J. Superior vena cava syndrome associated with massive thrombosis: treatment with expandable wire stents. Radiology 1988; 167:727-728. 12. Perez CA, Presant CA, VanAmburg AL. Management of superior vena cava syndrome. Semin Oncol 1978; 5:123-134. 13. Davenport D, Ferree C, Blake D, Raben M. Radiation therapy in the treatment of superior vena caval obstruction. Cancer 1978; 42:2600-2603. 14. Renert WA, Rudin LJ, Casarella WJ. Renal vein thrombosis in carcinoma of the renal pelvis. AJR 1972; 114:735-740. 15. Robins JM, Bookstein JJ. Percutaneous transcaval biopsy technique in the evaluation of inferior vena cava occlusion. Radiology 1972; 105:451-452. 16. Wendth AJ Jr, Garlick WB, Pantoja GE, et al. Transcatheter biopsy of renal carcinoma invading the inferior vena cava. J Urol 1976; 115:331-332. 17. Withers CE, Casola G, Herba MJ, Viloria J. Intravascular tumors: transvenous biopsy. Radiology 1988; 167:713-715. 18. Armstrong P, Hayes DF, Richardson PJ. Transvenous biopsy of carcinoma of the bronchus causing superior vena caval obstruction. Br Med J [Clin Res] 1975; 1:662663. 19. Mills SR, Doppman JL, Head GL, Javadpour N, Brennan MF, Chu EW. Transcatheter brush biopsy of intravenous tumor thrombi. Radiology 1978; 127:667670. 20. Ellis JH, Becker GJ, Jackson VP, Park HM, Holden RW. Transcatheter brush biopsy of a liver mass with CT-proven intracaval extension. Comput Radiol 1985; 9:173176. 21. Coel MN, Chalmers J. Percutaneous catheter transcaval tumor biopsy. Radiology 1975; 116:222.

Radiology • 959

The cause of superior vena cava syndrome: diagnosis with percutaneous atherectomy.

The cause of superior vena cava syndrome (SVCS) in two patients was identified by means of endovascular biopsy of the superior vena cava (SVC) perform...
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