Endovascular Treatment of Chronic Superior Vena Cava Syndrome Associated with Hemodialysis Access

Abstract

Superior vena cava (SVC) syndrome was first described in 1757 by William Hunter as a complication of a syphilitic aneurysm. With the advent of antibiotics, 74% to 93% of reported cases are now secondary to a malignant process. Benign causes include goiter, mediastinal fibrosis, pericardial constriction, Behçet's disease, polyarteritis nodosa, and thrombosis secondary to catheter placement, most notably pacing wires. This case report describes a patient who was diagnosed with chronic SVC syndrome after multiple hemodialysis access procedures were performed over a short span of time. The patient is a fifty-five-year-old man with hypertension and end-stage renal disease, etiology unknown, who presented with left upper limb swelling one week after placement of an arteriovenous (AV) graft in his left forearm. One month prior he had had an AV fistula created in the left distal forearm. Owing to difficulty in accessing the fistula, a Shiley catheter was placed in the left internal jugular vein for temporary dialysis. The AV graft was placed later that week. He presented the following week with progressive left upper limb edema associated with limitation of hand movement and pain/numbness of the fingers. The pain was relieved with upper limb elevation. An outpatient fistulogram showed a patent AV graft and AV fistula, a small amount of thrombosis around the Shiley catheter tip, and occlusion of the SVC. Collaterals were noted involving the right innominate vein, SVC, and the left innominate vein. A catheter and guidewire were then passed through the venous limb of the AV graft into the SVC. Urokinase was delivered as a bolus and then as a continuous infusion into the left innom inate vein and SVC to dissolve any clots that might be in the SVC or around the Shiley catheter. A computed tomography scan of the chest failed to reveal any pathology around the SVC. Systemic heparin therapy was also started. Twenty-four hours later the patient underwent repeat venography, which demon strated some clot lysis and a patent but severely narrowed SVC. Three self-expanding Wallstents were then placed. The stents were dilated to 14 mm. Completion venography revealed adequate patency of the SVC. After the procedure the patient did well with prompt resolution of his left upper limb swelling and pain. The Shiley catheter was removed during this hospitalization and his dialysis was initiated via the AV graft. Endovascular treatment of chronic SVC syndrome manifesting after hemodialysis access procedures is a viable option that is associated with excellent short-term patency.