Stenting Through a Portacath for Totally Occluded Superior Vena Cava in a Case of Non-Hodgkin’s Lymphoma<br />

Superior vena cava syndrome (SVCS) is a distressing manifestation of benign or malignant disease obstructing return of blood flow through the superior vena cava (SVC).1 Patients with this syndrome can be extremely uncomfortable or may develop life-threatening complications such as laryngeal or cerebral edema. Percutaneous delivery of metallic stents into the vena cava has been used with success to relieve obstruction to blood flow quickly and completely.2–4 We describe a patient with totally occluded SVC secondary to portacath implantation for non-Hodkin’s lymphoma in whom a wallstent was successfully percutaneously deployed. Case Report. A 73-year-old woman was diagnosed with non-Hodgkin’s lymphoma in March 2000 for progressive abdominal distension. She was given 6 courses of chemotherapy (cyclophosphamide, adriamycin, vincristine and prednisolone) through the right subclavian vein by placing a portacath in the right infraclavicular region. The portacath was left in situ. The patient did not receive radiation therapy. Her abdominal computed tomography (CT) scans showed complete resolution of the mass with some residual scarring. The patient presented to our hospital with symptoms of shortness of breath, chest pressure and facial puffiness. Two months prior to admission, she began to notice bilateral periorbital edema, facial edema and orthopnea. Two weeks prior to admission, her symptoms progressed to include bilateral arm swelling. On presentation, the patient was in moderate respiratory distress and was unable to breath comfortably while lying flat on her back. Her physical examination was remarkable for facial plethora and marked symmetric edema of her head, neck and arms. A provisional diagnosis of SVCS was made. The patient was taken to the cardiac catheterization laboratory, where venous access was obtained via the right femoral vein and the right internal jugular vein. The mean pressure in the cephalad SVC was 32 mmHg. The right atrial pressure was 10 mmHg. Total occlusion of the SVC was demonstrated by simultaneous venography cephalad to the obstruction and right atrial angiography caudal to the obstruction (Figure 1). The occlusion measured about 5 cm in length. The portacath was explanted from the subcutaneous pocket under local anesthesia and the venous sheath was cannulated with a single puncture needle. A 0.032´´ double-length Terumo guidewire (Terumo Corporation, Somerset, New Jersey) was passed through the lumen of the sheath inside the right atrium and to the inferior vena cava. To provide access across the obstruction from below, the Terumo wire was snared with a simple angioplasty guidewire, which was bent to hook the Terumo guidewire (Figure 2). A 6 French (Fr) right guiding catheter was used to support the angioplasty guidewire. After hooking the Terumo wire inside the guiding catheter, it was snared out via the right femoral venous access and withdrawn out of the right femoral vein. The Judkins right coronary catheter was then positioned via the right femoral vein across the SVC obstruction and simultaneously the portacath sheath was pulled into the right subclavian vein. The Terumo wire was exchanged with a 0.018 Platinum angioplasty guidewire and placed inside the right subclavian vein. A 4-cm long, 6-mm diameter balloon catheter (Symmetry) was then positioned across the SVC obstruction over the angioplasty guidewire. The obstruction was dilated at 10 atmospheres (atm) for 2 minutes with restoration of antegrade SVC flow. A narrow residual lumen with thrombus was evident soon after balloon deflation. The 6 mm balloon was exchanged with a 12-mm diameter, 6-cm long XXL balloon over the guidewire across the area of residual stenosis and dilated with 12 atm. The SVC lumen showed thrombus and residual stenosis after balloon dilatation. A 64-mm long, 14-mm compressed diameter, self-expanding Easy wall stent (Boston Scientific/Scimed, Inc., Maple Grove, Minnesota) was delivered to the SVC, covering the whole length of the obstruction with the proximal portion lying in the right atrium. A light “waist” remained in the middle portion of the stent (Figure 3). After stent deployment, an excellent lumen (about the same size as the native SVC) was evident (Figure 4). Brisk flow was present in the SVC, including the stented areas. Filling defects were no longer visible. The SVC pressure fell dramatically and was equal to the right atrial pressure (12 mmHg). There were no adverse effects in the catheterization laboratory. The patient experienced prompt, dramatic relief of symptoms. Her breathing was better by that evening and resolution of her facial and upper extremity swelling was evident by the following morning. The patient continued to do well and was discharged after 2 days on anticoagulation therapy. At 1-month follow-up, she was symptom free with no evidence of congestion. Discussion. Superior vena cava obstruction occurs in approximately 3–20% of patients with underlying malignancies.5,6 Although benign causes are rare, iatrogenic etiologies such as obstruction by indwelling central venous catheters are encountered due to their increasing use in recent years. In either case, the end result is often distressing symptoms that compromise quality of life, and SVC obstruction can be fatal if untreated. Rapid relief of symptoms and long-term patency of the SVC have been achieved with percutaneously placed intravascular stents.7 In this case, the SVC obstruction was secondary to a portacath that was placed inside the subclavian vein for chemotherapy. The portacath sheath was seen inside the right atrium on venogram (there was probably distal migration). The vast majority of reported cases have used the Gianturco stent.8,9 Other stent designs used include the self-expanding Wallstent10,11 and the Palmaz stent,12 which is deployed and expanded over a balloon-tipped catheter. Stents in the venous system are quickly and completely covered with neointima while stent wires are encased by the tunica intima and layers of fibrous connective tissue.13,14 Stent migration is very rare; however, migration may occur if the stent is incompletely expanded in the vein or if it is not accurately placed. It is recommended to leave both ends flared with a slight “waist” in the center to ensure against stent migration. In our case, we deployed the stent in the SVC with a slight “waist” in the mid portion to prevent stent migration. Failure of stent placement may occur when tumor completely encases the SVC. The SVC in our patient was totally occluded; however, we successfully placed the stent through the patent sheath of the portacath. Patients often respond to stent placement with immediate improvement in facial congestion and resolution of peripheral edema within 1–7 days. Our patient had dramatic improvement, with resolution of facial congestion and upper extremity edema within 24 hours. She was totally asymptomatic prior to discharge. Anticoagulation may carry a higher risk of bleeding in patients with SVC syndrome because of the higher number of patients with malignancies and metastatic disease. We preferred to put our patient on warfarin due to evidence of thrombus on venography with the intention to continue anticoagulation for at least 6 months. Conclusion. SVC stenting is a well-accepted therapy for SVC obstruction. The incidence of SVC obstruction is increasing with venous cannula. We report a unique case of SVC obstruction stenting through a portacath.

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