William Hunter described the first case of SVC syndrome in 1757, which was caused by a syphilitic aortic aneurysm [1]. In fact, for many years aortic aneurysm was thought to be one of the more common etiologies. As more cases were compiled, however, extrinsic compression from malignancy was shown to be a far more prevalent cause. Current analysis has revealed that approximately 80% of cases are due to extrinsic processes with bronchogenic lung cancer accounting for most [2]. Other common culprits include non-Hodgkins lymphoma and small cell lung cancer [3]. Intrinsic processes, like venous thrombosis, account for the remaining 20% of cases [1]. Patients most often present with dyspnea, cough, head ‘fullness,’ flushing, and upper extremity edema. On physical exam there are sometimes dilated superficial veins on the superior chest wall. The diagnosis can be suggested on chest radiograph by a widened superior mediastinum [1], but a CT and angiography are best for diagnosing the etiology and extent of obstruction, respectively [4,5]. CT criteria require: 1) decreased or absence of opacification of central venous structures inferior to obstruction AND 2) opacification of collateral venous routes. Collateral routes include the azygos system, which is the most common, the vertebral venous system, the internal mammary vein, and the lateral thoracic vein [6]. MR angiography is appropriate for patients with contraindications to iodinated contrast [7]. Treatment is aimed at the underlying cause. In the case of thrombosis, thrombolytic therapy as well as PTA are usually successful if employed within 5 days of symptom onset [8].