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Endovascular Treatment of Superior Vena Cava Syndrome without Removing a Central Venous Catheter
~
-
lnterventional Radiologist at Work
Endovascular Treatment of Superior Vena Cava Syndrome without Removing a Central Venous Catheter1 -
Joseph Perno, MD, PhD Samuel G. Putnam Ill, MD Gary 5. Cohen, MD David Ball, DO
Index terms: Catheters and catheterization, central venous access * Central venous access Venae cavae, syndrome
JVIR 1999; 10:917-918 Abbreviations: SVC cava
=
superior vena
TREATMENT of superior vena cava (SVC) syndrome has been revolutionized by the advent of intravascular stents and thrombolysis (1-4). Causes of SVC syndrome include malignancy, fibrosing mediastinitis, radiation therapy, granulomatous disease, and venous occlusion secondary to indwelling central venous catheters (5). Malignant disease is by far the most common cause, accounting for 85%-90% of reported SVC syndrome cases (1).Signs and symptoms of SVC syndrome include (i) edema and cyanosis of the head, neck, and upper extremities; (ii) engorgement of the veins with lack of venous pulsations that normally originate in the right atrium of the heart; and (iii) circumferential enlargement of neck without pitting edema. We describe a unique technique (which, to our knowledge, has not been described in the medical literature) in the treatment of SVC syndrome in a patient with a left upper extremity venous P.A.S. Port (SimsDeltec, St. Paul, MN) in place. Not wishing to remove the P.A.S. Port, the tip of the catheter was deflected superiorly to allow placement of a stent in the SVC.
I CASE REPORT From the Department of Diagnostic Imaging, Temple University Hospital, 3401 N. Broad St., Philadelphia, PA 19140. Received July 27, 1998; revision requested September 4; revision received and accepted November 30. Address correspondence to J.P. O SCVIR. 1999
A 44-year-old woman with a medical history notable for rightsided squamous cell lung cancer treated with chemotherapy and radiation therapy presented with a complaint of facial and bilateral upper extremity edema. Physical examination demonstrated bilateral jugular venous distention and bilat-
eral facial and upper extremity edema without carotid bruits. A chest radiograph demonstrated mediastinal widening, right paratracheal adenopathy, and an elevated right hemidiaphragm with atelectasis of the lung base. Also of note, there was a left upper extremity P.A.S. Port venous access device with the catheter tip overlying the SVC. This device was inserted 3 months previously and was functioning well. No computed tomographic examination of the chest was performed. With ultrasound guidance, the right basilic vein was punctured and a 4-F gtraight multihole catheter (Cook, Bloomington, IN) was advanced to the right subclavian vein by means of sutandard over-thewire technique. A central venogram (Fig 1)demonstrated high-grade narrowing of the SVC, which appeared secondary to external compression. The diagnostic catheter was then exchanged over a 0.035inch Bentson guide wire (Cook) for an 8-F vascular sheath. A 6.5-F Levin-1 catheter (Cook) was then used to advance the Bentson wire through the left brachiocephalic vein into the left subclavian vein, and a second venogram was obtained, which demonstrated patency of the left brachiocephalic and subclavian veins, with reflux down the hemiazygos vein (Fig 2). At this point, we proceeded with treatment of the symptomatic SVC narrowing. The tip of the P.A.S. Port catheter was in the SVC; therefore, it had to be moved before stent placement to avoid trapping the catheter against the vessel wall. We elected not to remove this de-
918
Endovascular Treatment of Superior Vena Cava Syndrome
July-August 1999 JVIR
1.
2.
Figures 1,2. (1) Central venogram demonstrating high-grade stenosis of the SVC and mediastinal widening with right paratracheal adenopathy. (2) Left brachiocephalic venogram demonstrating patency of the left brachiocephalic and subclavian veins. Left internal jugular vein inflow is noted (arrow). Contrast material flows through the left superior intercostal vein (arrowhead) to the accessory hemiazygos vein.
Figures 3,4. (3) Postdeployment venogram demonstrating patent SVC. (4) Repositioning of P.A.S. Port catheter tip within SVC stent.
vice, because it had been functioning well and we did not want to subject the patient to a second invasive procedure. The diagnostic catheter was exchanged for a 15-mm Amplatz Goose Neck snare and guiding catheter (Microvena, Great Bear Lake, MN). The tip of the P.A.S. Port catheter was snared and withdrawn into the right brachiocephalic vein. The snare was exchanged for a 0.035-inch Amplatz Super Stiff
guide wire (Medi-tech/Boston Scientific, Watertown, MA), which was advanced easily through the SVC narrowing. A Palmaz stent (model 3907; Johnson & Johnson, Princeton, NJ) was removed from its packaged balloon and crimped onto a 12 x 40-mm Ultrathin angioplasty balloon (Medi-techBoston Scientific). A 12-mm balloon was selected after measuring the SVC above the stenosis. The stent was deployed in the SVC, spanning the stenosis. A
postdeployment venogram demonstrated a widely patent SVC (Fig 3).The P.A.S. Port catheter was gently readvanced into the SVC using the partially inflated Ultrathin balloon. A final radiograph demonstrated the catheter tip within the stent (Fig 4). After stent placement in the SVC, the patient continued receiving intravenous heparin therapy throughout her hospital stay, maintaining the partial thromboplastin time at approximately 60-80 seconds. Before discharge, approximately 2 weeks after admission, warfarin therapy was started and the heparin therapy was discontinued. There was no clinical evidence for recurrence of SVC syndrome during the patient's hospital stay. The patient died approximately 6 months after treatment. The above procedure introduces a technique involving manipulation of a preexisting catheter in a patient who subsequently developed SVC syndrome. By deflecting the P.A.S. Port catheter tip, the patient was s ~ a r e dtime. discomfort. additional risks of a second procedure, and expense. References 1. Shah R, Sabanathan S, Lowe RA, Mearns A. Stenting in malignant obstruction of superior vena cava. J Thorac Cardiovasc Surg 1996; 112: 335-340. 2. Fontaine AB, Nijiar A. Treatment of iatrogenic superior vena cava syndrome with a vascular stent. JVIR 1996; 7:607-609. 3. Irving JD, Dondelinger RF, Reidy JF, et al. Gianturco self-expanding stents: clinical experience in the vena cava and large veins. Cardiovasc Intervent Radio1 1992; 15:328-333. 4. Solomon N, Wholey MH, Jarmolowski CR. Intravascular stents in the management of superior vena cava syndrome. Cathet Cardiovasc Diagn 1991; 23:245-252. 5. Pithie A, Soutar JS, Pennington CR. Catheter tip position in central vein thrombosis. JPEN 1988; 12:613-614.
-
lnterventional Radiologist at Work
Endovascular Treatment of Superior Vena Cava Syndrome without Removing a Central Venous Catheter1 -
Joseph Perno, MD, PhD Samuel G. Putnam Ill, MD Gary 5. Cohen, MD David Ball, DO
Index terms: Catheters and catheterization, central venous access * Central venous access Venae cavae, syndrome
JVIR 1999; 10:917-918 Abbreviations: SVC cava
=
superior vena
TREATMENT of superior vena cava (SVC) syndrome has been revolutionized by the advent of intravascular stents and thrombolysis (1-4). Causes of SVC syndrome include malignancy, fibrosing mediastinitis, radiation therapy, granulomatous disease, and venous occlusion secondary to indwelling central venous catheters (5). Malignant disease is by far the most common cause, accounting for 85%-90% of reported SVC syndrome cases (1).Signs and symptoms of SVC syndrome include (i) edema and cyanosis of the head, neck, and upper extremities; (ii) engorgement of the veins with lack of venous pulsations that normally originate in the right atrium of the heart; and (iii) circumferential enlargement of neck without pitting edema. We describe a unique technique (which, to our knowledge, has not been described in the medical literature) in the treatment of SVC syndrome in a patient with a left upper extremity venous P.A.S. Port (SimsDeltec, St. Paul, MN) in place. Not wishing to remove the P.A.S. Port, the tip of the catheter was deflected superiorly to allow placement of a stent in the SVC.
I CASE REPORT From the Department of Diagnostic Imaging, Temple University Hospital, 3401 N. Broad St., Philadelphia, PA 19140. Received July 27, 1998; revision requested September 4; revision received and accepted November 30. Address correspondence to J.P. O SCVIR. 1999
A 44-year-old woman with a medical history notable for rightsided squamous cell lung cancer treated with chemotherapy and radiation therapy presented with a complaint of facial and bilateral upper extremity edema. Physical examination demonstrated bilateral jugular venous distention and bilat-
eral facial and upper extremity edema without carotid bruits. A chest radiograph demonstrated mediastinal widening, right paratracheal adenopathy, and an elevated right hemidiaphragm with atelectasis of the lung base. Also of note, there was a left upper extremity P.A.S. Port venous access device with the catheter tip overlying the SVC. This device was inserted 3 months previously and was functioning well. No computed tomographic examination of the chest was performed. With ultrasound guidance, the right basilic vein was punctured and a 4-F gtraight multihole catheter (Cook, Bloomington, IN) was advanced to the right subclavian vein by means of sutandard over-thewire technique. A central venogram (Fig 1)demonstrated high-grade narrowing of the SVC, which appeared secondary to external compression. The diagnostic catheter was then exchanged over a 0.035inch Bentson guide wire (Cook) for an 8-F vascular sheath. A 6.5-F Levin-1 catheter (Cook) was then used to advance the Bentson wire through the left brachiocephalic vein into the left subclavian vein, and a second venogram was obtained, which demonstrated patency of the left brachiocephalic and subclavian veins, with reflux down the hemiazygos vein (Fig 2). At this point, we proceeded with treatment of the symptomatic SVC narrowing. The tip of the P.A.S. Port catheter was in the SVC; therefore, it had to be moved before stent placement to avoid trapping the catheter against the vessel wall. We elected not to remove this de-
918
Endovascular Treatment of Superior Vena Cava Syndrome
July-August 1999 JVIR
1.
2.
Figures 1,2. (1) Central venogram demonstrating high-grade stenosis of the SVC and mediastinal widening with right paratracheal adenopathy. (2) Left brachiocephalic venogram demonstrating patency of the left brachiocephalic and subclavian veins. Left internal jugular vein inflow is noted (arrow). Contrast material flows through the left superior intercostal vein (arrowhead) to the accessory hemiazygos vein.
Figures 3,4. (3) Postdeployment venogram demonstrating patent SVC. (4) Repositioning of P.A.S. Port catheter tip within SVC stent.
vice, because it had been functioning well and we did not want to subject the patient to a second invasive procedure. The diagnostic catheter was exchanged for a 15-mm Amplatz Goose Neck snare and guiding catheter (Microvena, Great Bear Lake, MN). The tip of the P.A.S. Port catheter was snared and withdrawn into the right brachiocephalic vein. The snare was exchanged for a 0.035-inch Amplatz Super Stiff
guide wire (Medi-tech/Boston Scientific, Watertown, MA), which was advanced easily through the SVC narrowing. A Palmaz stent (model 3907; Johnson & Johnson, Princeton, NJ) was removed from its packaged balloon and crimped onto a 12 x 40-mm Ultrathin angioplasty balloon (Medi-techBoston Scientific). A 12-mm balloon was selected after measuring the SVC above the stenosis. The stent was deployed in the SVC, spanning the stenosis. A
postdeployment venogram demonstrated a widely patent SVC (Fig 3).The P.A.S. Port catheter was gently readvanced into the SVC using the partially inflated Ultrathin balloon. A final radiograph demonstrated the catheter tip within the stent (Fig 4). After stent placement in the SVC, the patient continued receiving intravenous heparin therapy throughout her hospital stay, maintaining the partial thromboplastin time at approximately 60-80 seconds. Before discharge, approximately 2 weeks after admission, warfarin therapy was started and the heparin therapy was discontinued. There was no clinical evidence for recurrence of SVC syndrome during the patient's hospital stay. The patient died approximately 6 months after treatment. The above procedure introduces a technique involving manipulation of a preexisting catheter in a patient who subsequently developed SVC syndrome. By deflecting the P.A.S. Port catheter tip, the patient was s ~ a r e dtime. discomfort. additional risks of a second procedure, and expense. References 1. Shah R, Sabanathan S, Lowe RA, Mearns A. Stenting in malignant obstruction of superior vena cava. J Thorac Cardiovasc Surg 1996; 112: 335-340. 2. Fontaine AB, Nijiar A. Treatment of iatrogenic superior vena cava syndrome with a vascular stent. JVIR 1996; 7:607-609. 3. Irving JD, Dondelinger RF, Reidy JF, et al. Gianturco self-expanding stents: clinical experience in the vena cava and large veins. Cardiovasc Intervent Radio1 1992; 15:328-333. 4. Solomon N, Wholey MH, Jarmolowski CR. Intravascular stents in the management of superior vena cava syndrome. Cathet Cardiovasc Diagn 1991; 23:245-252. 5. Pithie A, Soutar JS, Pennington CR. Catheter tip position in central vein thrombosis. JPEN 1988; 12:613-614.