38.2.1 What Is the Pertinent Pathophysiology in SVC Syndrome?
The left and right subclavian and internal jugular veins join to form the brachiocephalic (innominate) veins, which in turn join to form the SVC. Venous drainage from the head and upper extremities then finds its final conduit to the heart in this large, but easily compressible, vessel. Extensive collaterals with the SVC include the azygos, the mammary, vertebral, lateral thoracic, paraspinous, and esophageal veins. The largest of these, the azygos vein, is formed from the junction of the right subcostal and the right ascending lumbar veins. It ascends in the posterior mediastinum and then passes anteriorly over the right main stem bronchus to join the SVC as the latter enters into the right atrium. Here, the area is anatomically crowded with lymph nodes, the pulmonary artery, and the tracheobronchial structures hemmed in by the sternum anteriorly. The low-pressure SVC can be obstructed, either indirectly by external compression from vascular structures, tumor, or enlarged lymph nodes or directly by primary or secondary intraluminal thrombus or tumor (Figures 38-1 and 38-2).
This diagram illustrates the venous drainage into the heart. (From Abeloff MD. Clinical Oncology. 3rd ed. Philadelphia, PA: Elsevier Churchill Livingston; 2004: 1048.)
This diagram shows that the low-pressure SVC can be obstructed, either indirectly by external compression of vascular structures, tumor, or enlarged lymph nodes, or directly by primary or secondary intraluminal thrombus or tumor. (From Abeloff MD. Clinical Oncology. 3rd ed. Philadelphia, PA: Elsevier Churchill Livingston; 2004: 1048.)
Obstruction of the SVC will result in upper body venous hypertension, which forces blood to seek an alternate pathway to the heart via the previously described collateral vessels and the inferior vena cava. This upper body venous hypertension results in the classic clinical signs and symptoms of the syndrome. These include facial, neck, and arm swelling, as well as engorgement of the mucous membranes, including those of the upper airway. In some patients, it may result in laryngeal or cerebral edema, predisposing to an increased risk of surgical bleeding.
Most cases of SVC syndrome are due to extrinsic tumor compression from bronchogenic carcinoma or non-Hodgkin lymphoma occurring in the right paratracheal space or right pulmonary hilum.1 From even a cursory glance at the anatomy, it is clear that the disease process may also compromise other major structures in the area, such as the pulmonary arteries, the right heart, and the tracheobronchial tree. With these factors in mind, the practitioner will want to determine the degree to which major structures are involved prior to embarking on induction of general anesthesia (GA).