Ann Thorac Surg 1997;64:531-533
© 1997 The Society of Thoracic Surgeons
Case Reports
Homograft as a Conduit for Superior Vena Cava Syndrome
Sunil K. Ohri, FRCS,
David R. Lawrence, FRCS,
Edward R. Townsend, FRCS
Thoracic Surgical Unit, Harefield Hospital, Harefield, Middlesex, United Kingdom
Accepted for publication February 18, 1997.
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Abstract
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This report outlines the management of a 30-year-old man with severe multiresistant mycobacterium tuberculosis of his right lung. Despite medical therapy he had open tuberculosis with positive sputum smears. A right pneumonectomy was undertaken, but due to distorted hilar anatomy, the superior vena cava was resected. Postoperatively, superior vena cava syndrome developed and failure of venous drainage was demonstrated by bilateral arm venography and computed tomographic scanning. The superior vena cava syndrome was successfully relieved using an aortic homograft as a superior vena cava replacement instead of a spiral vein graft or a prosthetic conduit.
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Introduction
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Obstruction of the superior vena cava (SVC) is a recognized clinical syndrome that most commonly occurs in patients with mediastinal extension of pulmonary malignancies. The majority of such patients are palliated by radiotherapy/chemotherapy and only a small proportion receive surgical treatment. Benign and iatrogenic etiologies are less well recognized causes of SVC obstruction. We describe the case of a 30-year-old man in whom acute SVC syndrome developed after a difficult pneumonectomy for open tuberculosis (TB). The favored conduits for SVC replacement are discussed and our choice of homograft material explained for this particular case.
A 30-year-old man was referred for surgical control of multidrug-resistant Mycobacterium tuberculosis. Initial chest roentgenogram had found complete collapse of the right lung (Fig 1
). He admitted having been treated for TB with rifinah and streptomycin, but had discontinued treatment for personal reasons. A diagnosis of autopneumonectomy secondary to TB was made. His sputum was smear positive for TB, and rifampicin, isoniazid, pyrazinamide, and ethambutol therapy was commenced. Subsequently, he admitted to have been treated in Africa in 1992 for 90 days, and again in 1993 and 1994 using many different combinations of anti-TB agents. Drug sensitivities in the United Kingdom found his TB to be resistant to rifampicin, rifabutin, streptomycin, isoniazid, pyrazinamide, ethambutol (low resistance), clarithromycin, clofazimine, and cycloserine. On this basis, his TB chemotherapy was rationalized to amikacin, ofloxacin, and ethambutol. A left pleural effusion was found to contain multidrug-resistant TB organisms. He tested negative for the human immunodeficiency virus but was hepatitis B surface antigen positive. To achieve anatomobiological eradication of the disease a right pneumonectomy was planned [1].
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Fig 1. . Posteroanterior chest roentgenogram showing almost complete collapse of the right lung with mediastinal shift toward the right side. A loculated effusion is present on the left side.
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At thoracotomy, a small rigid and chronically collapsed right lung was found fused to the chest wall and diaphragm. An extrapleural dissection was undertaken, the inferior pulmonary vein and azygos veins were ligated. The right main bronchus was stapled off. The rest of the lung hilum was dissected out, but many fibrous adhesions were present around the pulmonary artery at the hilum. The hilum was stapled to avoid further risk of dissection and damage to the right pulmonary artery. The lung was removed but a large quantity of blood flowed from structures within the mediastinum; this was controlled by oversewing the area. Postoperatively it was noted that the patient had swollen neck veins and over the next 24 hours he became cerebrally irritated. A clinical diagnosis of SVC syndrome was made. He underwent contrast enhanced computed tomographic scanning that revealed the absence of SVC with the development of venous collaterals around the posterior chest wall (Fig 2). Bilateral arm venography confirmed the diagnosis with the presence of brachial veins on both sides but larger veins, including the SVC, could not be opacified (Fig 3). It was now apparent that the SVC had been resected during the pneumonectomy. He was returned to the operating room to replace his SVC with a homograft (homovital). An aortic homograft was chosen because it was of appropriate length and diameter (19 mm). The homograft was prepared by ligating the coronary arteries and removing the aortic valve, creating a simple conduit. A median sternotomy was performed and the brachiocephalic vein identified; subsequently the SVC's remnant was dissected from the pericardium. End-to-side anastomosis was performed with the brachiocephalic vein and homograft. Fogarty catheters were then employed to remove thrombus found on preoperative venography (see Fig 3). Finally the lower end of the homograft was anastomosed to the remnant of the SVC.
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Fig 2. . Thoracic computed tomographic scan after right pneumonectomy with intravenous contrast into both arms. Multiple small collaterals vessels are present on the posterior chest wall. The jugular veins are evident on both sides. The subclavian artery and the superior vena cava could not be opacified with contrast medium, but axillary veins were still patent.
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Fig 3. . Bilateral arm venography. (A) The right brachial vein is patent but the axillary vein and subclavian veins do not opacify with contrast medium and there is some evidence of venous thrombosis. (B) A similar finding is illustrated on the left side.
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Postoperatively, he improved with an increase in urine output and a gradual reduction in facial swelling and the size of his neck veins. Postoperative sputum cultures were negative. Perioperative heparinization was converted to warfarin and continued for 6 weeks to allow his subclavian and axillary veins to recannalize and reduce the risk of new thrombus formation. Histologic examination of the resected specimen confirmed that the lung had been totally destroyed with caseous necrosis. Bilateral arm vein venography undertaken 2 weeks postoperatively found a patent SVC conduit (Fig 4), and after 6 months follow-up he remains well.
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Fig 4. . Bilateral arm vein venography 2 weeks postoperatively. The homograft superior vena caval conduit is seen draining the right and left subclavian and brachiocephalic veins. Evidence of mural thrombosis in the right axillary and subclavian veins exists despite thrombectomy at the operation.
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Comment
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Superior vena cava replacement is indicated for the resolution of symptoms in malignant and benign diseases of the superior mediastinum that may invade/compress the SVC. The majority of patients who present with SVC obstruction will have underlying malignant disease. The poor outcome in malignant SVC obstruction is found largely in pulmonary malignancies, which by definition are at least T4 tumors and often with N2 disease; not surprisingly these patients have a poor prognosis [2]. However an increasing number of patients are now presenting who have benign iatrogenic SVC obstruction secondary to SVC line insertion, hyperalimentation, and transvenous pacemaker electrodes [3]. These patients require SVC replacement with a durable patency conduit. Biological and nonbiological materials have been reported for SVC replacement [2, 4–6]. Success as regards long-term patency has been found for spiral vein graft and polytetrafluoroethylene conduits [2, 6]. Autogenous vein has the advantages of any biological material with a low thrombogenic potential, although this may be enhanced by a long-spiral suture line. The disadvantages of this technique, which make the polytetrafluoroethylene graft attractive, are the time required to construct the spiral vein graft and the polytetrafluoroethylene conduit's immediate availability in a variety of sizes. Furthermore, the polytetrafluoroethylene graft, by virtue of its physical strength, is less likely to undergo compression; this may be relevant in the context of progressive benign disorders such as mediastinal fibrosis or in malignant disease when postoperative radiotherapy is planned. The homograft possesses all the advantages of both prosthetic material and autogenous vein. In the context of this infected case, a major consideration was avoiding prosthetic material because mediastinitis is an associated risk with using this material [2]. The homograft's other main advantage over prosthetic material is that postoperative antiplatelet or anticoagulation may be avoided if clinically contraindicated. In our case we elected to anticoagulate the patient to reduce the risk of venous thrombosis. Homograft material (either aortic or pulmonary) appears to fulfill the rigorous requirements for an SVC conduit, but clearly other cases need to be undertaken before its long-term efficacy can be proven.
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Footnotes
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Address reprint requests to Mr Ohri, Thoracic Surgical Unit, Harefield Hospital, Harefield, Middlesex UB9 6JH, United Kingdom (e-mail: drl{at}romesh.demon.co.uk).
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References
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- Rizzi A, Rocco G, Robustellini M, et al. Results of surgical management of tuberculosis: experience in 206 patients undergoing operation. Ann Thorac Surg 1995;59:896–900.[Abstract/Free Full Text]
- Dartevelle PG, Chapelier AR, Pastorino U, et al. Long-term follow-up after prosthetic replacement of the superior vena cava combined with resection of mediastinal-pulmonary malignant tumours. J Thorac Cardiovasc Surg 1991;102:259–65.[Abstract]
- Parish JM, Marschke RF Jr, Dines DE, et al. Etiologic considerations in superior vena cava syndrome. Mayo Clin Proc 1981;56:407–13.[Medline]
- Larsson S, Lepore V. Technical options in reconstruction of large mediastinal veins. Surgery 1992;111:311–7.[Medline]
- Campo CD, Love J, Bowes F. Prosthetic replacement of the superior vena cava with a custom-made pericardial graft: an experimental study. Can J Surg 1992;35:305–9.[Medline]
- Doty DB. Bypass of superior vena cava. J Thorac Cardiovasc Surg 1982;83:326–38.[Abstract]
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Abstract
Introduction
