Ann Thorac Surg 2001;71:1351-1353
© 2001 The Society of Thoracic Surgeons
Case report
Surgical repair of superior vena cava syndrome
Moisés C. Calderon, MDa,
Victor M. Lozano, MDa,
Arturo Jaquez, MDa,
Cesar Villaseñor, MDa
a Department of Cardiothoracic Surgery, Hospital Angeles de las Lomas, Mexico City, Mexico
Accepted for publication September 19, 2000.
Address reprint requests to Dr Calderon, Paseo de la Soledad 69, La Herradura, Edo Mex, 53920, Mexico
e-mail: moisesc{at}infosel.net.mx
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Abstract
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We present the case of a 53-year-old woman with a history of breast cancer, chemotherapy, and a long-term central venous access catheter, who presented with acute, severe superior vena cava syndrome. Angiography showed fibrous obstruction of the superior vena cava with thrombosis of the innominate, both axillary subclavian and internal jugular veins. Surgical repair consisted of thrombectomy of all the involved vessels and patch repair of superior vena cava and innominate vein. The patient had an uneventful recovery and remains asymptomatic 12 months after the procedure.
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Introduction
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Superior vena cava (SVC) thrombosis is frequently the result of neoplastic, traumatic, or infectious processes in the mediastinum. Thrombosis secondary to an indwelling catheter is usually a slow process, allowing for organization and fibrotic replacement of the clot. These patients usually present with progressive arm, neck, and head swelling, which facilitates the clinical diagnosis and early, nonaggressive treatment [1].
We were asked to see a 53-year-old woman with a history of breast cancer and recent chemotherapy, without evidence of residual disease who presented with sudden and extremely painful neck, head, and bilateral arm swelling. She had a long-term port central venous access catheter placed through the left subclavian vein. Thoracic computed tomographic scan ruled out malignant mediastinal disease. Venography showed bilateral deep vein thrombosis of both arms, extending to the innominate and both internal jugular veins, and suggesting a long-standing fibrotic process at the SVC. (Fig 1). During the diagnostic process (4 hours), the patient rapidly became disoriented and developed respiratory insufficiency. She was immediately taken to the operating room. Femoral venous access was achieved under local anesthesia and general endotracheal anesthesia was started. The anterior mediastinum was exposed by a median sternotomy. The pericardium was opened, exposing the superior cavo-atrial junction. Without using cardiopulmonary bypass, a cross clamp was placed in the right atrium 2 cm distal to the superior cavo-atrial junction to avoid any pulmonary embolic event. The SVC was found to be collapsed and fibrotic, and the innominate vein completely thrombosed. A longitudinal incision was made over the anterior aspect of the SVC and extended the full length of the innominate vein. The tip of the central venous indwelling catheter was found at the level of the cavo-atrial junction. The catheter was removed.
Successful thrombectomy of both internal jugular, subclavian, and axillary veins was achieved. The SVC and innominate veins were repaired with a polytetrafluoroethylene baffled patch (Fig 2). The patient had an uneventful recovery and was discharged on the seventh postoperative day. She has been maintained on oral anticoagulation and remains fully asymptomatic 12 months after the operation.
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Comment
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Superior vena cava obstruction can be caused by a large number of benign and malignant processes. Benign pathology such as mediastinal granulomatous diseases, idiopathic mediastinal fibrosis, and compression by aortic aneurysms are more common and are responsible for less than 25% of adult patients. The increasing use of subclavian vessels for permanent vascular access and pacemaker lead implantation has increased the frequency of subclavian vein thrombosis; however, this rarely causes SVC syndrome. When malignancy is responsible for the disease, there are multiple treatment alternatives, such as chemotherapy, radiotherapy, percutaneous transluminal angioplasty with stenting, and even bypass; however, most benign etiologies respond adequately to medical management, and in acute cases, to thrombolysis [2]. Acute and rapidly progressive cases like the one presented above are infrequent and striking. They can rapidly develop cerebral edema and intracranial thrombosis, which can lead to coma and death. We presume, in this patient, that SVC fibrosis resulted from continuous inflammatory injury to the vessel from chemotherapy due to improper placement of the indwelling catheter; this later caused acute and multiple retrograde thrombosis. It is also possible that during long-term follow-up the repair can develop thrombosis and the patient can remain asymptomatic because of the development of extensive collateral vessels. In the previously described patient, we planned a control cavogram one year after the procedure; however, the patient refused, so we did a venous vascular Doppler of the innominate vein and superior vena cava, and demonstrated patency and flow in both vessels (Figs 3 and 4). Immediate surgical intervention with thrombectomy and patch repair was an effective and lifesaving procedure, with a good long-term result.
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Fig 3. Venous Doppler of innominate vein demonstrating patency and flow, 12 months after the procedure.
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Fig 4. Venous Doppler of superior vena cava demonstrating patency and flow, 12 months after the procedure.
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References
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Rösch J., Uchida B.T., Hall L.D., et al. Gianturco-Rösch expandable Z stents in the treatment of superior vena cava syndrome. Cardiovasc Intervent Radiol 1992;15:319-327.[Medline]
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Doty B.P. Bypass of superior vena cava: six years experience with spiral vein graft for obstruction of superior vena cava due to benign or malignant disease. J Thorac Cardiovasc Surg 1982;83:326-338.[Abstract]
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Abstract
Introduction
