Ann Thorac Surg 2009;87:1260-1262. doi:10.1016/j.athoracsur.2008.08.064
© 2009 The Society of Thoracic Surgeons
Case Reports
Acute Superior Vena Cava Occlusion After Stenting of Tracheoesophageal Fistula
Muneera R. Kapadia, MD,
Alberto L. de Hoyos, MD,
Matthew G. Blum, MD*
Division of Thoracic Surgery, Department of Surgery, Northwestern University, Chicago, Illinois
Accepted for publication August 26, 2008.
* Address correspondence to Dr Blum, Northwestern University, Department of Surgery, Division of Thoracic Surgery, Galter 10-105, 201 E Huron St, Chicago, IL 60611 (Email: mblum{at}nmh.org).
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Abstract
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Acute development of superior vena cava syndrome is unusual. This report describes a patient who suddenly presented with a superior vena cava obstruction after esophageal and tracheal stenting for a malignant tracheoesophageal fistula. Stenting of the superior vena cava rapidly alleviated the obstruction and resulted in resolution of symptoms.
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Introduction
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The signs and symptoms of superior vena cava (SVC) syndrome result from obstruction of the SVC. Most causes of SVC syndrome are malignant, either from primary intrathoracic malignancy or metastatic disease, and compression is usually insidious. This report details a patient with acute SVC obstruction after tracheal and esophageal stenting for malignant tracheoesophageal fistula (TEF). Stenting of the SVC rapidly alleviated the obstruction and resulted in resolution of symptoms.
A 60-year-old man presented with stage IIIB lung adenocarcinoma and bulky hilar lymphadenopathy partially obstructing the left main bronchus. He underwent chemoradiation therapy, shortly after which shortness of breath developed. His symptoms resolved after a covered self-expanding metal left mainstem bronchial stent was placed. Two years later he complained of progressive dysphagia, cough, and aspiration when drinking liquids. Computed tomography imaging revealed a TEF with progressive hilar and mediastinal lymphadenopathy and also demonstrated narrowing of the SVC (Fig 1). The azygos vein was patent but narrowed at azygos–caval junction.

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Fig 1. This computed tomography section just above the level of the carina is suggestive of a tracheoesophageal fistula (arrow). The superior vena cava (arrowhead) is narrowed at this level; the azygos vein is patent in this cut but was severely narrowed at its junction with the cava.
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The patient underwent simultaneous flexible esophagoscopy and bronchoscopy. Tumor was growing into the trachea and left main bronchus proximal to the previously placed bronchial stents. Insufflation through the esophagoscope resulted in bubbling in the trachea, confirming the presence of a TEF. To exclude the fistula, the esophagus and trachea were stented with Alimaax (18 x 120 mm) and Aero covered stents (16 x 60 mm), respectively (Alveolus, Charlotte, NC). An additional covered tracheobronchial left bronchial stent (Aero, 10 x 40 mm) was placed to bridge the gap between the new tracheal and old left mainstem stents. At the conclusion of the case, the patient was extubated. However, he required reintubation in the operating room for inadequate respiratory effort and inability to follow verbal commands.
One hour later, he was plethoric above the level of the nipples and his neck was swollen. Neck and facial swelling persisted through the next 12 hours, and despite withdrawal of sedation, his mental status remained depressed. Obstruction of the SVC was confirmed by venogram, and a percutaneous SVC stent was placed (Fig 2). The cervical swelling began resolving within the first hour. The next day he was neurologically appropriate and was extubated. The remainder of the postoperative course was unremarkable, and he was discharged home on a soft diet, with symptomatic exclusion of the fistula even when swallowing liquids.

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Fig 2. A postprocedural chest radiograph shows stents in the trachea (arrow) and left mainstem bronchus, as well as the superior vena cava (arrowhead).
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Comment
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Most malignant TEFs result from esophageal cancer; however, they can be seen secondary to primary lung neoplasms, tracheal carcinomas, laryngeal carcinomas, mediastinal tumors, thyroid tumors, or tumors with extensive mediastinal nodal involvement [1]. TEFs lead to pulmonary sepsis and death secondary to gastrointestinal contamination of the tracheobronchial tree, with median survival between 1 and 6 weeks if untreated [1].
Treatment options include esophageal bypass or exclusion, and esophageal or tracheal stenting, or both. Stenting offers a less invasive alternative, especially in debilitated patients with a limited life expectancy who are unable to tolerate extensive procedures. Stenting adequately palliates symptoms in more than 75% of patients [1]. Covered metal stents placed in parallel in the trachea and esophagus to exclude the fistula yield better results than stenting either the tracheal or esophagus alone [2].
SVC syndrome occurs in approximately 15,000 patients per year in the United States and consists of signs and symptoms resulting from obstruction of the SVC or bilateral brachiocephalic veins [3]. Compression of the SVC results in increased venous pressure in the upper extremities, upper chest, head, and neck. This may cause plethora or cyanosis, cerebral edema leading to headache, confusion, or coma, as well as laryngopharyngeal edema manifesting as cough, dyspnea, or dysphagia [3]. SVC syndrome may result from extrinsic compression, direct invasion, or thrombosis; malignancy, benign tumors, idiopathic fibrosing mediastinitis, sarcoidosis, and indwelling venous catheters are the most common causes [4]. Malignancies most commonly include nonsmall cell lung cancer (50%), small cell lung cancer (22%), lymphoma (12%), and metastatic disease (9%) [3]. The severity of the symptoms usually depends on the rapidity of onset and the degree of SVC compression [3]. Gradual narrowing of the SVC, particularly in association with a patent azygos vein, generally allows for the development of collateral venous drainage, with mild or no symptoms. Sudden SVC occlusion, however, can cause upper body edema, life-threatening neurologic changes, and respiratory failure.
Depending on the underlying cause, SVC syndrome can be treated by a combination of the following therapies: medical management with anticoagulation, diuretics, and elevation of the upper body; radiation or chemotherapy, or both; surgical bypass, and SVC stenting [5]. For patients with SVC syndrome secondary to nonsmall cell lung cancer, radiation therapy and SVC stenting are the mainstays of treatment [6]. Tanigawa and colleagues [7] compared radiation and stenting in a nonrandomized study and found similar rates of symptom resolution for both treatments of 80% and 78%, respectively. Nicholson and colleagues [8] found that stent insertion provided faster relief and greater improvement of symptoms, as well as fewer recurrent symptoms vs radiation therapy. More recently, de Gregorio Ariza and colleagues [5] examined treatment of SVC syndrome with stenting in patients with malignant and benign causes. Clinical success was achieved in 95% of patients within 2 to 3 days. In 78 patients with malignancy, 96% assisted stent patency (4 required thrombolytics and 1 required restenting) was reported.
This article reports the complication of tracheal and esophageal stenting leading to acute SVC syndrome. Two other reports of simultaneous tracheal and SVC stenting in patients with lung cancer causing tracheal compression and SVC syndrome have been published [4, 9]. In those patients, the obstructive symptoms developed slowly over time, and stenting alleviated the symptoms. In our patient, placement of dilating stents in both the esophagus and trachea occupied space in an already crowded mediastinum. The resulting critical compression of the SVC (and possibly the azygos–caval junction) resulted in increased intracranial pressure and depressed mental state. Stenting of the SVC is a well-accepted treatment strategy for SVC syndrome and here resulted in rapid resolution of signs and symptoms.
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References
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