Superior vena cava syndrome (SVCS) is the clinical manifestation of obstructed blood flow through the superior vena cava (SVC) secondary to extrinsic compression, tumor invasion, or thrombosis. The SVC is the main venous conduit of blood return from the head, upper extremities, and upper torso. It begins at the confluence of the right and left innominate veins and continues in the middle mediastinum 6–8 cm to drain into the right atrium. During its course the SVC is surrounded by rigid structures including the trachea, right bronchus, sternum, aorta, and pulmonary artery. Due to the physiologic requirements of high volume and low pressure flow it is a large diameter vessel with a thin wall making it susceptible to extrinsic compression by tumor against its rigid surroundings. SVC obstruction results in increased collateral blood flow through the azygos, internal mammary, lateral thoracic, paraspinous, and esophageal veins.

Over 90% of cases of SVCS result from a neoplastic process. Approximately 65–80% of cases are due to lung cancer with small cell cancer being the most common histology, 10–15% of cases are due to lymphoma, and the remainder are caused by thymomas, germ cell tumors, and metastatic disease. Benign causes include mediastinal fibrosis, histoplasmosis, and iatrogenic thrombosis of the SVC secondary to central venous catheters and cardiac pacemakers.

SVCS is a relatively easy clinical diagnosis to make. The presenting symptoms in decreasing order of frequency include dyspnea (63%), facial swelling or head fullness (50%), cough (24%), arm swelling (18%), chest pain (15%), and dysphagia (9%).