Journal of Vascular Surgery
Volume 38, Issue 2 , Pages 215-223, August 2003

Open surgical and endovascular treatment of superior vena cava syndrome caused by nonmalignant disease

Presented at the Fifty-sixth Annual Meeting of The Society for Vascular Surgery, Boston, Mass, Jun 9-12, 2002.

  • Manju Kalra, MBBS

      Affiliations

    • Division of Vascular Surgery, Mayo ClinicRochester, MinnUSA,
  • ,
  • Peter Gloviczki, MD

      Affiliations

    • Division of Vascular Surgery, Mayo ClinicRochester, MinnUSA,
    • Corresponding Author InformationReprint requests: Peter Gloviczki, MD, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA
  • ,
  • James C Andrews, MD

      Affiliations

    • Department of Surgery and Radiology, Mayo ClinicRochester, MinnUSA,
  • ,
  • Kenneth J Cherry Jr, MD

      Affiliations

    • Division of Vascular Surgery, Mayo ClinicRochester, MinnUSA,
  • ,
  • Thomas C Bower, MD

      Affiliations

    • Division of Vascular Surgery, Mayo ClinicRochester, MinnUSA,
  • ,
  • Jean M Panneton, MD

      Affiliations

    • Division of Vascular Surgery, Mayo ClinicRochester, MinnUSA,
  • ,
  • Haraldur Bjarnason, MD

      Affiliations

    • Department of Surgery and Radiology, Mayo ClinicRochester, MinnUSA,
  • ,
  • Audra A Noel, MD

      Affiliations

    • Division of Vascular Surgery, Mayo ClinicRochester, MinnUSA,
  • ,
  • Cathy Schleck, BS

      Affiliations

    • Section of Biostatistics, Mayo Clinic, Rochester, Minn, USA
  • ,
  • William S Harmsen, MS

      Affiliations

    • Section of Biostatistics, Mayo Clinic, Rochester, Minn, USA
  • ,
  • Linda G Canton, RN, BSN

      Affiliations

    • Division of Vascular Surgery, Mayo ClinicRochester, MinnUSA,
  • ,
  • Peter C Pairolero, MD

      Affiliations

    • Division of Vascular Surgery, Mayo ClinicRochester, MinnUSA,

Received 14 June 2002; accepted 11 February 2003.

Article Outline

Abstract 

Objectives

The purpose of this study was to evaluate the role of endovascular and open surgical reconstructions in patients with superior vena cava (SVC) syndrome caused by nonmalignant disease.

Methods

Clinical data from 32 consecutive patients who underwent endovascular or open surgical reconstruction of central veins because of symptomatic benign SVC syndrome between November 1983 and June 2001 were retrospectively reviewed.

Results

The study included 17 male and 15 female patients (mean age, 38 years; range, 5-69 years). Presenting symptoms were head fullness (n = 26), dyspnea or orthopnea (n = 23), headache (n = 17), or dizziness (n = 11); physical signs were head swelling (n = 31), chest wall collateral vessels (n = 29), facial cyanosis (n = 18), or arm swelling (n = 17). Etiologic factors included mediastinal fibrosis (n = 19), indwelling catheter (n = 8), idiopathic thrombosis (n = 4), or post-surgery (n = 1). Two patients were heterozygous for factor V Leiden; 1 patient had antithrombin III deficiency. Twenty-nine patients underwent surgical reconstruction with 31 bypass grafts: spiral saphenous vein (n = 20), superficial femoral vein (n = 4), human allograft (n = 1), or expanded polytetrafluoroethylene (ePTFE, n = 6). Eleven patients underwent percutaneous transluminal angioplasty or stenting; 3 primary and 8 secondary endovascular procedures were performed to treat graft stenosis (n = 7) or occlusion (n = 1). There were no early deaths. Five early graft failures in 3 ePTFE grafts and 2 bifurcated vein grafts (thrombosis, n = 4; stenosis, n = 1) were successfully treated with open surgical revision. Over a mean follow-up of 5.6 years (range, 0.4-16.6 years) in surgical patients, 17 additional secondary interventions were performed in 8 patients, 14 endovascular and 3 surgical. Primary, assisted primary, and secondary patency rates of surgical bypass grafts were 63%, 79%, and 85%, respectively, at 1 year, and 53%, 68%, and 80%, respectively, at 5 years. Graft patency was significantly higher in vein grafts compared with ePTFE grafts (P = .02). Mean follow-up after percutaneous transluminal angioplasty or stenting was 3.1 years (range, 1 day–11.7 years). Twelve secondary endovascular interventions were performed in 6 patients (primary group, 3 of 3; secondary group, 3 of 9 grafts in 8 patients) to maintain patency in 11 of 12 reconstructions. Mean follow-up in the entire patient cohort was 5.3 years (range, 0.4-16.6 years). In 79% of patients symptoms had resolved or were significantly improved at last follow-up.

Conclusions

Surgical treatment of benign SVC syndrome is effective over the long term, with secondary endovascular interventions to maintain graft patency. Straight spiral saphenous vein graft remains the conduit of choice for surgical reconstruction, with results superior to those with bifurcated vein and ePTFE. Endovascular treatment is effective over the short term, with frequent need for repeat interventions. It does not adversely affect future open surgical reconstruction and may prove to be a reasonable primary intervention in selected patients. Patients who are not suitable for or who fail endovascular intervention merit open surgical reconstruction.

 

Benign disease is a rare cause of superior vena cava (SVC) syndrome, accounting for only 22% of cases.1, 2 About half of affected patients (11%) have mediastinal fibrosis.3, 4, 5 However, the exponential increase in use of indwelling central venous catheters and cardiac pacemakers over the last two decades has resulted in more patients with SVC obstruction of benign etiology. In this group of relatively young patients with normal life expectancy, a durable method of treatment is desirable. Traditional management is open surgery, with bypass grafting from the innominate vein or jugular vein to the SVC or right atrial appendage.6, 7, 8, 9, 10, 11, 12, 13, 14, 15

Endovascular therapy with balloon angioplasty (percutaneous transluminal angioplasty [PTA]), and in recent years with stenting of the SVC, has been performed with increasing frequency.16, 17, 18, 19, 20, 21 This is accepted as the mainstay of treatment to relieve SVC obstruction due to malignant disease, keeping in mind the short life expectancy of these patients. The role of endovascular therapy in SVC syndrome of nonmalignant etiology is undecided, because long-term durability of this method of treatment remains to be assessed. The literature reports 90% to 100% initial success rates, with good short-term secondary patency rates of up to 85% at 1 year in small series of patients.17, 19, 22, 23, 24

We evaluated the role of endovascular and surgical reconstruction in contemporary management of SVC syndrome caused by nonmalignant disease. We assessed long-term clinical results of surgical treatment, and feasibility of and short-term outcome after endovascular interventions performed to treat benign SVC syndrome at our institution.

Back to Article Outline

Patients and methods 

Clinical data for 32 consecutive patients with SVC syndrome caused by nonmalignant disease treated at the Mayo Clinic over 18 years from November 1, 1983, to June 30, 2001, were retrospectively analyzed. Data collected included details of preoperative clinical status, noninvasive and invasive evaluation, operative and endovascular procedures, post-procedure surveillance, early and late adjunctive procedures, and clinical outcome during follow-up.

On the basis of venographic pattern of SVC obstruction, patients were classified into four groups with the classification of Stanford and Doty.25 All surgical patients with bypass grafts underwent imaging before discharge from the hospital, and all patients had at least one return visit at 3 to 6 months after surgery or endovascular treatment. Patients with no return visit within the last 6 months were contacted by telephone to determine follow-up clinical status. Post-treatment clinical outcome was evaluated in all patients and graded according to the classification scheme proposed by the Subcommittee on Reporting Standards in Venous disease26: +3, complete relief of symptoms, +2, mild symptoms of chronic venous disease, +1, clinical improvement, or 0, no clinical change.

Statistical analysis 

Statistical analysis was performed in the surgical group of 29 patients. In 2 patients who underwent two bypass procedures sequentially, only the first graft was included in the analysis. The Kaplan-Meier method was used to estimate graft survival with respect to patency for three end points: survival free of assisted primary patency, secondary patency, and any intervention to treat occlusion.27 The date of operation was the starting point of the analysis. For each analysis, grafts were classified as patent or occluded, only on the basis of objective evidence on radiologic imaging studies, ie, computed tomography (CT), magnetic resonance imaging (MRI), or venography. For the end point of loss of primary patency, a graft requiring assistance to maintain patency (assisted primary) was counted as an event on the date of assistance. For the end point of intervention to treat occlusion, assistance to maintain patency was also counted as an event. The 95% confidence interval was calculated at 1-year, 3-year, and 5-year survival estimates. Univariate assessment of risk factors for each of the three survival end points was performed with a log-rank test.28 P < .05 was considered statistically significant.

Survival analyses were also performed to account for all 31 grafts in the 29 patients, with Cox proportional hazards models, adjusting for correlated data between 2 grafts in the 2 patients with multiple grafts. These results were similar to those of the original analysis of 29 grafts (1 graft per patient) and led to the same conclusions. Hence the simpler analysis of 29 grafts is reported. Descriptive data, however, include all 31 grafts for completeness. Statistical analysis was not performed on data for the 3 patients who underwent primary endovascular interventions (PTA with or without stenting of the SVC), because of the small number.

Results 

Patients 

Seventeen male patients and 15 female patients (median age, 38 years; range, 5-69 years) with SVC syndrome of nonmalignant cause who underwent surgical or endovascular intervention were included in the study. All patients had persistent signs and symptoms of SVC obstruction despite medical management and physical measures to decrease venous congestion of the head and neck. Median duration of symptoms was 14 months (mean, 20 months; range, 3-72 months). The most common symptoms of SVC syndrome were head and neck fullness, and dyspnea on exertion or orthopnea (Table I). The most frequently encountered signs included head and neck swelling and chest wall collateral vessels. One 5-year-old boy had signs of SVC obstruction and severe protein-losing enteropathy secondary to compromised drainage of the thoracic duct as a result of high central venous pressure. At birth, he had undergone excision of a mediastinal tumor (benign teratoma) along with a segment of SVC and right atrium.

Table I. Signs and symptoms of superior vena cava syndrome of benign origin in 32 patients
No. of patients%
Symptom
Feeling of fullness in head or neck2681
Dyspnea on exertion or orthopnea2372
Headache1753
Dizziness or syncope1134
Visual problems825
Cough722
Nocturnal oxygen requirement39
Proteinlosing enteropathy13
Sign
Head and neck swelling3197
Large chest wall venous collateral vessels2991
Facial cyanosis1856
Arm swelling1753
Pleural effusion26

Mediastinal fibrosis was the cause of SVC obstruction in 19 patients (59%), and central venous thrombosis in 12 patients (38%) (Table II). PTA and stenting of the SVC had been attempted in 9 patients elsewhere, before enrollment in the present study, and was successful in 7 patients, with subsequent reocclusion, and unsuccessful in 2 patients. Two patients had undergone previous failed surgical SVC reconstruction, ie, replacement of the SVC followed postoperatively by tight stenosis resistant to PTA in 1 patient, and pericardial patch angioplasty of the SVC followed by a right innominate vein to right atrium spiral vein graft in the other patient. Risk factors included a history of deep venous thrombosis (DVT) in 8 patients (25%), heterozygosity for factor V Leiden in 2 patients, and antithrombin III deficiency in 1 patient. Seven patients (22%) had hypertension, 3 patients (9%) had diabetes, and 14 patients (44%) were smokers.

Table II. Cause of benign superior vena cava syndrome in 32 patients
No. of patients%
Mediastinal fibrosis1959
Histoplasmosis1031
Nonspecific mediastinal fibrosis (sclerosing medistinitis)619
Nonspecific mediastinal fibrosis (granulomatous disease)26
Post–radiation therapy13
Venous thrombosis1238
Indwelling central venous catheter516
Pacemaker wires26
Ventriculoatrial shunt13
Hypercoagulable state13
Idiopathic39
Surgical excision13
Total32100
Preoperative evaluation 

Preoperative evaluation included bilateral upper extremity venography in all patients. Thirty patients (94%) underwent CT of the chest, and 7 patients (22%) underwent MRI. Duplex ultrasound (US) scanning of the internal jugular veins was performed in 24 patients (75%). On the basis of venographic findings, SVC obstruction was classified as type I (≤90% stenosis of the SVC with antegrade azygos blood flow) in 3 patients (9%), type II (>90% SVC stenosis or occlusion with antegrade azygos blood flow) in 5 patients (16%), type III (>90% SVC stenosis or occlusion with reversal of azygos blood flow) in 13 patients (41%), and type IV (occlusion of SVC and major tributaries including azygos veins) in 11 patients (34%).

Mediastinoscopy and biopsy was performed preoperatively in 9 patients with mediastinal fibrosis; thoracotomy or thoracoscopy and biopsy was performed in 3 patients. In all patients with mediastinal masses a lymph node biopsy specimen was obtained intraoperatively before bypass grafting. One patient with acute on chronic central line–related thrombosis underwent thrombolytic therapy to provide inflow into an internal jugular to right atrial appendage bypass graft.

Svc reconstruction 

Open surgery 

The technique of autologous spiral saphenous vein bypass grafting was as described previously.7, 8, 29 The saphenous vein is harvested and opened longitudinally, and valve leaflets are excised. The opened vein is wrapped around a 32F or 36F polyethylene chest tube, and the edges are stapled or sutured with 7.0 continuous monofilament nonabsorbable suture, interrupting the suture line every three-quarter turn. The length of saphenous vein harvested to create a graft of sufficient length is determined according to the equation proposed by Chiu et al30 in their original experiments, l = RL/r, where r and l are radius and length of saphenous vein, and R and L are radius and length of the spiral vein graft.

Thirty-one bypass grafts were performed in 29 patients. Reconstruction was performed with autologous spiral saphenous vein grafts (SSVG) in 20 patients (65%), ie, 18 straight grafts and 2 bifurcated grafts (Table III). Superficial femoral vein (SFV) was the conduit in 4 patients, and expanded externally supported polytetrafluoroethylene (ePTFE, 10-16 mm diameter) in 6 patients. Human iliocaval vein was used in 1 patient with sclerosing cholangitis and mediastinitis, who underwent concomitant orthotopic liver transplantation. The grafts originated from the internal jugular vein (n = 17) or innominate vein (n = 14) and were anastomosed centrally to the SVC (n = 18) or right atrial appendage (n = 13). All grafts were imaged before patients were discharged. At discharge, 26 of 29 patients were receiving oral anticoagulation therapy with warfarin sodium (target international normalized ratio, 2 to 3).

Table III. Graft material for 31 grafts in 29 patients with surgical reconstruction*
No. of patients%
Autologous vein2477
Spiral saphenous vein2065
Straight graft1755
Bifurcated graft26
Straight graft plus reimplantation opposite innominate vein13
Superficial femoral vein413
Reversed vein graft310
Spiral vein graft13
Iliocaval allograft13
Expanded polytetrafluroethylene619
Total31100

* Two patients received 2 bypass grafts each.

Two patients received 2 grafts sequentially. One patient required straight SSVGs from each innominate vein to the right atrial appendage because of persistent symptoms after placement of the first graft (Fig 1). Both grafts were patent at last follow-up 4 years postoperatively. In the other patient a thrombosed ePTFE graft was replaced with an SSVG graft at 1 year and remains patent after 2 years. Only the first graft in each of these patients was included in the statistical analysis.

  • View full-size image.
  • Fig 1. 

    A, Venogram 10 months after placement of left innominate vein to right atrial appendage spiral saphenous vein graft in a 46-year-old man with mediastinal fibrosis shows severe stenosis (arrow) at the proximal anastomosis. B, Venogram 6 months after Wallstent (arrow) placement confirms widely patent stent and graft. C, Venogram of right to left internal jugular crossover graft (arrow) performed 16 months later because of persistent right arm and neck swelling. D, Early occlusion of crossover graft at 2 months. E, Venogram 6 months after placement of right innominate vein to right atrial appendage spiral saphenous vein graft shows external compression of the distal graft (arrow). F, Venogram obtained after Wallstent (arrow) placement. Both grafts remain patent 4 years later.

Endovascular treatment 

Endovascular interventions were performed in 11 patients. Three patients with type II SVC lesions due to histoplasmosis were treated primarily with PTA and stenting of the SVC. Palmaz stents (Palmaz 308; Cordis, Johnson & Johnson, Warren, NJ) were used in 2 patients, and a 12 mm Wallstent (Boston Scientific, Medi-Tech, Natick, Mass) was used in 1 patient. Endovascular interventions were also performed to maintain patency of 9 grafts in 8 patients in the open surgical group. These included PTA alone in 4 grafts, and PTA plus stenting in 5 grafts (10-12 mm Wallstents, n = 4; Palmaz 308 stent, n = 1). Patients received oral anticoagulants post-intervention for a minimum of 3 months.

Initial diagnostic venography was performed with simultaneous injection of contrast medium in bilateral superficial arm veins. The interventions were performed with a standard transjugular or transfemoral venous Seldinger technique, insertion of a 7 to 10 mm sheath, and crossing the stenotic lesion in the SVC with a guide wire and 5F catheter. Pressure gradient across the lesion was measured before and after intervention to ensure a satisfactory result. Balloon dilation was performed with 10 to 14 mm balloon catheters, and was followed by deployment of the chosen stent across the lesion in patients with residual stenosis.

Early results 

Mortality and morbidity 

There were no in-hospital or early (30 days) deaths. In 2 patients in whom the SFV was harvested, acute DVT of the popliteal vein developed. A mediastinal hematoma in 1 patient compressed the SSVG and required evacuation. In a fourth patient, with concomitant excision of a large retrosternal goiter, bilateral vocal cord paralysis developed, and prolonged ventilator dependence necessitated tracheostomy.

Patency of reconstruction 

Five early repeat interventions were performed to maintain graft patency. Three ePTFE grafts demonstrated thromboses in the early postoperative period. All underwent thrombectomy, and patch angioplasty of the proximal anastomosis was performed in 1 graft. Both bifurcated SSVG grafts demonstrated early complications. Partial thrombosis of 1 graft was successfully treated with thrombectomy and revision of the side limb anastomosis. Thrombosis of the side limb of the other graft was treated with thrombectomy and reimplantation; however, this graft demonstrated early recurrent thrombosis. All grafts, except one limb of a bifurcated graft, were patent at discharge. Nonsignificant (<50%) stenosis was noted in 5 grafts at postoperative imaging before discharge. Thirty-day primary patency was 84%, assisted primary patency was 87%, and secondary patency was 100%. In the 3 patients who underwent primary PTA and stenting of the SVC, primary patency was 100% at 30 days.

Late results 

Mortality 

Mean clinical follow-up in the surgical group was 5.6 years (range, 0.4-16.6 years). Follow-up after endovascular intervention in 11 patients (3 primary and 8 secondary interventions in bypass grafts) was 3.1 years (range, 1 day–11.7 years). During follow-up 3 patients died of unrelated causes: 1 patient died of bronchogenic carcinoma 9 years after SSVG bypass to treat central line–related thrombosis with complete relief from symptoms; 1 patient died of unknown cause after remaining asymptomatic for more than 8 years after SSVG because of pacemaker wire–related thrombosis; and 1 patient died of long-standing complications related to tuberculous peritonitis 17 months after placement of an ePTFE graft to treat central line–related thrombosis. Four patients were lost to follow-up at 6, 19, 24, and 70 months, respectively, after surgical treatment.

Patency of reconstruction 
Open surgery 

Postoperative graft surveillance with venography was performed at 3 to 6 months, and then at 9 to 12 months in most patients. Thereafter, grafts were imaged noninvasively with CT (n = 33) or MRI (n = 5); venography was reserved for patients with recurrent symptoms or known stenosis. In later years of the study, the second venography was sometimes replaced with CT or MRI. On 68 late postoperative venograms, mild or moderate stenosis was found in 12 grafts, severe stenosis in 11 grafts or limbs, and occlusion in 1 graft. Duplex US scanning was performed in 24 instances; graft patency was indirectly inferred from the flow pattern in the internal jugular vein because the graft in the mediastinum was not directly visualized with this method. In no instance was final patency for statistical analysis based on a duplex US scan. On one occasion graft occlusion was confirmed by ultrasound alone in a patient in whom no further intervention was planned.

Mean duration of follow-up for graft patency (based on last imaging) was 3.2 years (range, 4 days–10 years). During follow-up 9 grafts required secondary interventions (high-grade stenosis, n = 7; partial thrombosis, n = 1; occlusion, n = 1). Six of 7 high-grade stenoses occurred within the first year (between 3 and 10 months) after operation, and 1 occurred at 37 months. Three of these patients had nonsignificant stenosis at discharge from the hospital. The 7 stenosed vein grafts (6 SSVG, 1 SFV) underwent endovascular interventions (PTA, n = 3; Wallstent, n = 4). In all but 1 patient high-grade stenosis was accompanied by recurrence of symptoms. Thrombolysis and PTA of the internal jugular vein reestablished patency in the partially thrombosed ePTFE graft. The occluded ePTFE graft was replaced with SSVG.

Five grafts eventually occluded during follow-up (ePTFE, n = 3; SSVG, n = 1; SFV, n = 1). Both vein grafts were repeat surgical reconstructions in patients with failed surgical bypass grafts before enrollment in this study, and no further intervention was attempted. One occluded ePTFE graft was replaced with an SSVG, which remains patent at 2 years.

One-year, 3-year, and 5-year cumulative primary patency rates for 29 surgical grafts were 63% (95% confidence interval [CI], 48-85), 53% (95% CI, 36-78), and 53% (95% CI, 32-78); assisted primary patency rates were 79% (95% CI, 64-95), 68% (95% CI, 51-90), and 68% (95% CI, 48-90); and secondary patency rates were 85% (95% CI, 72-100), 80% (95% CI, 64-98), and 80% (95% CI, 61-98) (Fig 2, A). Patency rates were significantly higher for SSVG compared with ePTFE grafts: 1-year and 4-year cumulative primary patency rates were 67% (95% CI, 49-91) and 67% (95% CI, 42-91) versus 50% (95% CI, 23-100) and 17% (95% CI, 17-100), respectively (P = .02). Secondary patency rates were 90% (95% CI, 78-100) and 90% (95% CI, 73-100) versus 67% (95% CI, 38-100) and 50% (95% CI, 16-100), respectively (P = .02) (Fig 2, B).

  • View full-size image.
  • View full-size image.
  • Fig 2. 

    A, Cumulative primary, assisted primary, and secondary graft patency after open surgical bypass in 29 patients. SEM < 10% for all time points. B, Cumulative secondary patency after placement of 23 vein grafts and 6 expanded polytetrafluoroethylene (ePTFE) bypass grafts to treat superior vena cava obstruction. Dotted line represents SEM > 10%.

Endovascular treatment 

Mean duration of follow-up for patency (based on last imaging) was 2 years (range, 1 day–10 years). Venography was performed in 11 patients during follow-up, 5 for surveillance and 6 because of recurrent symptoms. Secondary interventions were performed in all 3 patients treated primarily with PTA and stenting: 1 intervention in 2 patients and 4 interventions in 1 patient (Fig 3). All secondary interventions were performed because of recurrent stenosis associated with recurrent symptoms. One patient chose to undergo SSVG at another institution 19 months after initial stenting rather than repeated endovascular interventions. The fifth intervention in a 38-year-old man was complicated by pericardial tamponade, which responded promptly to pericardial drainage.

  • View full-size image.
  • Fig 3. 

    A, Venogram shows type II superior vena cava obstruction (arrow) due to mediastinal fibrosis in a 38-year-old man. Successful placement of a Palmaz stent resulted in immediate resolution of symptoms. B, Venogram 14 months after stent palcement shows high-grade stenosis of the left innominate vein proximal to the stent. This was successfully treated with balloon angioplasty. C, Venogram 8 months later shows recurrence of stenosis (arrow). D, Venogram after balloon angioplasty to treat stenosis of left innominate vein and stent shows widely patent stent. Patient has undergone two additional balloon angioplasty procedures over 10 months to maintain patency.

In the secondary endovascular intervention group (8 patients), 5 of 9 grafts were patent at last follow-up without further intervention; 1 graft became occluded, and the remaining 3 grafts required further endovascular interventions (1, 2, and 4 interventions, respectively).

Outcome 

Mean duration of follow-up for clinical outcome in all patients was 5.6 years (range, 0.4-16.6 years). At last follow-up or death, symptoms in 79% (95% CI, 60-92) of patients had resolved or were significantly improved (Fig 4). All patients with occluded grafts had recurrent symptoms. Only 1 patient, with the factor V Leiden gene and a patent graft, had no improvement of symptoms.

  • View full-size image.
  • Fig 4. 

    Clinical outcome scores at last follow-up in 32 patients with superior vena cava syndrome due to nonmalignant disease. Twenty-nine patients underwent open surgical treatment; 3 patients underwent primary endovascular treatment.

Risk factor analysis 

Univariate analysis identified only ePTFE graft as a factor associated with poor primary and secondary graft patency (Fig 2, B). Other preoperative factors, ie, gender, age, type and cause of SVC obstruction, previous PTA or stenting, pressure gradient across the lesion, and intraoperative graft blood flow measurements, had no significant effect on outcome relative to graft patency.

Back to Article Outline

Discussion 

Endovascular intervention with PTA and stenting is the treatment of choice for patients with SVC syndrome due to malignant disease with symptoms unresponsive to radiation therapy and chemotherapy.17, 31 Surgical intervention has been the mainstay of treatment of benign SVC syndrome since the first SVC bypass graft half a century ago,5 with good long-term results. However, given that SVC syndrome of nonmalignant origin accounts for only a small proportion of cases, the total experience remains small. Doty et al11 reported excellent long-term patency and clinical results of SSVG in 16 patients. We have reported our experience with bypass grafting in 19 patients.10 Success with PTA and stenting in malignant SVC syndrome, and increasing sophistication of endovascular techniques and devices have raised the question of whether endovascular treatment can replace surgery as the primary method of management of benign SVC syndrome as well.22, 23, 32 This question is especially relevant today, with the escalating incidence of iatrogenic thrombosis of the SVC.

Surgical reconstruction of the SVC caused by benign disease has been associated with excellent long-term results.6, 7, 8, 9, 11, 12 Although the first reconstructions were performed with SFV,5 since the description of the technique of spiraling the saphenous vein by Chiu et al30 the SSVG has been the most popular conduit. Doty et al6 first adopted the technique, and in 1982 reported excellent graft patency and freedom from symptoms. Their larger experience reported in 1999, consisting of 16 SSVGs placed to treat benign SVC syndrome, documented 88% long-term graft patency and excellent clinical results at a mean follow-up of 10.9 years.11 The results of the present series confirm these results, with 90% long-term patency in the 23 vein grafts (SSVG, SFV, and allograft iliac vein). SSVG has been our preferred conduit of choice. Straight SSVG is associated with the most rewarding results; concomitant bilateral reconstructions attempted early in our experience resulted in early and late complications. We have since shied from bilateral reconstructions and found that collateralization across the midline is adequate to decompress both sides with a single graft in most patients.

The SFV is a good second choice for graft conduit, and others have performed SVC reconstruction with SFV.5, 13, 33 Concerns about distal thrombosis at the harvest site and chronic venous insufficiency remain; DVT developed in 2 of 4 of our patients at the distal SFV and popliteal vein, with long-term sequelae in one. Similar experience has been reported by others.33 Clagett et al,34 in addition to reporting 7 cases of major venous reconstruction (2 to treat SVC syndrome) with SFV have the largest experience with harvesting SFV for arterial reconstructions. Mid-term follow-up in 61 patients revealed only mild signs of chronic venous insufficiency in fewer than a third of patients, despite evidence of outflow obstruction and mild reflux on noninvasive venous evaluation.35 These results, however, may not be directly applicable to the present group of patients with SVC occlusion, especially that caused by spontaneous or catheter-induced thrombosis. Nonetheless, it is the logical conduit in patients with unavailable or inadequate saphenous vein.

Although graft patency and clinical results were significantly poorer with ePTFE compared with vein in the present series, it remains the best prosthetic material for use in the venous system. Wisselink et al15 reported 100% patency at 1 year for ePTFE bypass grafts placed to treat central vein occlusion in 6 patients receiving hemodialysis. A brachial arteriovenous fistula for dialysis present preoperatively in 5 of these patients may have contributed to the excellent patency by augmenting graft blood flow. We have documented better results with short, large-diameter ePTFE bypass grafts for iliocaval reconstruction in the setting of both benign and malignant disease.8 Dartevelle et al36 and Magnan et al14 reported excellent patency with ePTFE reconstruction of the SVC confined to the mediastinum after resection of malignant tumors. Five of 6 ePTFE grafts in the present series originated in the neck, and the small size of the internal jugular vein precluded use of large-diameter grafts.

All high-grade graft stenoses occurred within the first year postoperatively, and half of these were mild stenosis present on the first postoperative surveillance venogram. Regardless of the treatment method, the discovery of all stenoses was accompanied by recurrence of symptoms except in one patient. Although graft patency cannot be automatically inferred from freedom from symptoms, on the basis of these data, imaging after the first year need be performed only in patients with symptoms or in patients without symptoms but with known nonsignificant stenosis. Similar views have been expressed by Doty et al.11

Open surgery has been the primary method of treatment of symptomatic SVC obstruction of nonmalignant etiology origin at our institution since the mid-1980s, with PTA and stenting used secondarily to maintain patency of vein grafts. Encouraging results with these endovascular interventions over the last decade prompted us to use primarily PTA or stenting in selected patients in the last few years. Initial attempts at treating benign SVC syndrome with endovascular means involved PTA alone, with early recurrent stenosis caused by elastic recoil or compression from surrounding fibrosis.37, 38, 39 In the early 1990s, occasional cases of stent deployment to treat pacemaker wire–induced thrombosis were reported, but repeated interventions were required to maintain patency in the short term.18, 20, 24, 40, 41, 42, 43, 44, 45 Early experience was with Gianturco Z stents, which were subsequently modified by Rosch et al43 to create a multibody design that minimized stent migration. Availability of the more flexible Wallstents and Palmaz stents in larger sizes added to the versatility of endovascular treatment. In 1996 Dondelinger and Trotteur46 presented a series of 20 patients with stents with a secondary patency rate of 80% after mean follow-up of 16 months. Qanaldi et al19 reported 12 patients treated with Wallstents; one symptomatic recurrence occurred at 2 months over mean follow-up of 11 months. All 3 patients in our series treated primarily with PTA and stenting required at least one repeat intervention. Despite excellent early success and prompt relief of symptoms, the need for repeated interventions makes acceptance of this method of treatment difficult in this group of young, otherwise healthy patients. Longer follow-up in a larger number of patients is required to address the suitability of endovascular treatment as a permanent solution for benign SVC syndrome.

Surgical treatment of benign SVC syndrome is effective over the long term, with secondary endovascular interventions to maintain graft patency. Straight SSVG remains the conduit of choice for surgical reconstruction, with results superior to bifurcated vein and ePTFE. Endovascular treatment is effective in the short term, with frequent need for repeat interventions. It does not adversely affect future open surgical reconstruction, and may prove to be a reasonable primary therapeutic intervention in selected patients with suitable anatomy. Patients who are not suitable for or who fail endovascular intervention merit open surgical reconstruction.

Back to Article Outline

References 

  1. Parish JM, Marschke RFJ, Dines DE, Lee RE. Etiologic considerations in superior vena cava syndrome. Mayo Clin Proc. 1981;56:407–413
  2. Nieto AF, Doty DB. Superior vena cava obstruction (clinical syndrome, etiology, and treatment). Curr Prob Cancer. 1986;10:441–484
  3. Chen JC, Bongard F, Klein SR. A contemporary perspective on superior vena cava syndrome. Am J Surg. 1990;160:207–211
  4. Van Putten JW, Schlosser NJ, Vujaskovic Z, Leest AH, Groen HJ. Superior vena cava obstruction caused by radiation induced venous fibrosis. Thorax. 2000;55:245–246
  5. Klassen KP, Andrews NC, Curtis GH. Diagnosis and treatment of superior vena cava obstruction. Arch Surg. 1951;63:311–325
  6. Doty DB. Bypass of superior vena cava (six years’ experience with spiral vein graft for obstruction of superior vena cava due to benign and malignant disease). J Thorac Cardiovasc Surg. 1982;83:326–338
  7. Gloviczki P, Pairolero PC, Cherry KJ, Hallett JW. Reconstruction of the vena cava and of its primary tributaries (a preliminary report). J Vasc Surg. 1990;11:373–381
  8. Gloviczki P, Pairolero PC, Toomey BJ, Bower TC, Rooke TW, Stanson AW, et al.  Reconstruction of large veins for nonmalignant venous occlusive disease. J Vasc Surg. 1992;16:750–761
  9. Doty DB, Doty JR, Jones KW. Bypass of superior vena cava (fifteen years’ experience with spiral vein graft for obstruction of superior vena cava caused by benign disease). J Thorac Cardiovasc Surg. 1990;99:889–895
  10. Alimi YS, Gloviczki P, Vrtiska TJ, Pairolero PC, Canton LG, Bower TC, et al.  Reconstruction of the superior vena cava (benefits of postoperative surveillance and secondary endovascular interventions). J Vasc Surg. 1998;27:287–299
  11. Doty JR, Flores JH, Doty DB. Superior vena cava obstruction (bypass using spiral vein graft). Ann Thorac Surg. 1999;67:1111–1116
  12. Seelig MH, Oldenburg WA, Klingler PJ, Odell JA. Superior vena cava syndrome caused by chronic hemodialysis catheters (autologous reconstruction with a pericardial tube graft). J Vasc Surg. 1998;28:556–560
  13. Marshall WGJ, Kouchoukos NT. Management of recurrent superior vena caval syndrome with an externally supported femoral vein bypass graft. Ann Thorac Surg. 1988;46:239–241
  14. Magnan PE, Thomas P, Giudicelli R, Fuentes P, Branchereau A. Surgical reconstruction of the superior vena cava. Cardiovasc Surg. 1994;2:598–604
  15. Wisselink W, Money SR, Becker MO, Rice KL, Ramee SR, White CJ, et al.  Comparison of operative reconstruction and percutaneous balloon dilatation for central venous obstruction. Am J Surg. 1993;166:200–204
  16. Spittell PC, Vlietstra RE, Hayes DL, Higano ST. Venous obstruction due to permanent transvenous pacemaker electrodes (treatment with percutaneous transluminal balloon venoplasty). Pacing Clin Electrophysiol. 1990;13:271–274
  17. Solomon N, Wholey MH, Jarmolowski CR. Intravascular stents in the management of superior vena cava syndrome. Cathet Cardiovasc Diagn. 1991;23:245–252
  18. Irving JD, Dondelinger RF, Reidy JF, Schild H, Dick R, Adam A, et al.  Gianturco self-expanding stents (clinical experience in the vena cava and large veins). Cardiovasc Intervent Radiol. 1992;15:328–333
  19. Qanadli SD, El Hajjam M, Mignon F, de Kerviler E, Rocha P, Barre O, et al.  Subacute and chronic benign superior vena cava obstructions (endovascular treatment with self-expanding metallic stents). AJR. 1999;173:159–164
  20. Hochrein J, Bashore TM, O’Laughlin MP, Harrison JK. Percutaneous stenting of superior vena cava syndrome (a case report and review of the literature). Am J Med. 1998;104:78–84
  21. Kishi K, Sonomura T, Nishida N, Mitsuzane K, Kobayashi H, Juri M, et al.  Self-expandable metallic stent therapy for inferior vena cava obstruction secondary to malignancy (clinical observations). [in Japanese] Nippon Igaku Hoshasen Gakkai Zasshi. 1994;54:389–398
  22. Yim CD, Sane SS, Bjarnason H. Superior vena cava stenting. Radiol Clin North Am. 2000;38:409–424
  23. Schindler N, Vogelzang RL. Superior vena cava syndrome (experience with endovascular stents and surgical therapy). [review, 36 refs] Surg Clin North Am. 1999;79:683–694
  24. Rosenblum J, Leef J, Messersmith R, Tomiak M, Bech F. Intravascular stents in the management of acute superior vena cava obstruction of benign etiology. J Parenter Enteral Nutr. 1994;18:362–366
  25. Stanford W, Doty DB. The role of venography and surgery in the management of patients with superior vena cava obstruction. Ann Thorac Surg. 1986;41:158–163
  26. Porter JM, Moneta GL. Reporting standards in venous disease (an update [see comments]. International Consensus Committee on Chronic Venous Disease). J Vasc Surg. 1995;21:635–645
  27. Kaplan ER, Meier P. Nonparametric estimation from incomplete observations. J Am Stat Assoc. 1958;53:457–481
  28. Peto R, Peto J. Asymptotically efficient rank invariant procedures [with discussion]. J R Statist Soc. 1972;135:185–207
  29. Gloviczki P, Bower TC, McKusick MA, Pairolero P. Superior vena cava syndrome (endovascular and direct surgical treatment). In:  Gloviczki P,  Yao JST editor. Handbook of venous disorders. London, England: Chapman & Hall; 1996;p. 580–599
  30. Chiu CJ, Terzis J, MacRae ML. Replacement of superior vena cava with the spiral composite vein graft (a versatile technique). Ann Thorac Surg. 1974;17:555–560
  31. Furui S, Sawada S, Kuramoto K, Inoue Y, Irie T, Makita K, et al.  Gianturco stent placement in malignant caval obstruction (analysis of factors for predicting the outcome). Radiology. 1995;195:147–152
  32. Alimi YS, Juhan C. New trends in the surgical and endovascular reconstructions of large veins for nonmalignant chronic venous occlusive disease. Curr Opinion Cardiol. 1998;13:375–383
  33. Gladstone DJ, Pillai R, Paneth M, Lincoln JC. Relief of superior vena caval syndrome with autologous femoral vein used as a bypass graft. J Thorac Cardiovasc Surg. 1985;89:750–752
  34. Wells JK, Hagino RT, Bargmann KM, Jackson MR, Valentine RJ, Kakish HB, et al.  Venous morbidity after superficial femoral-popliteal vein harvest. J Vasc Surg. 1999;29:282–289
  35. Hagino RT, Bengtson TD, Fosdick DA, Valentine RJ, Clagett GP. Venous reconstructions using the superficial femoral-popliteal vein. J Vasc Surg. 1997;26:829–837
  36. Dartevelle PG, Chapelier AR, Pastorino U, Corbi P, Lenot B, Cerrina J, et al.  Long-term follow-up after prosthetic replacement of the superior vena cava combined with resection of mediastinal-pulmonary malignant tumors. J Thorac Cardiovasc Surg. 1991;102:259–265
  37. Sherry CS, Diamond NG, Meyers TP, Martin RL. Successful treatment of superior vena cava syndrome by venous angioplasty. AJR. 1986;147:834–835
  38. Walpole HTJ, Lovett KE, Chuang VP, West R, Clements SD. Superior vena cava syndrome treated by percutaneous transluminal balloon angioplasty. Am Heart J. 1988;115:1303–1304
  39. Grace AA, Sutters M, Schofield PM. Balloon dilatation of pacemaker induced stenosis of the superior vena cava. Br Heart J. 1991;65:225–226
  40. Charnsangavej C, Carrasco CH, Wallace S, Wright KC, Ogawa K, Richli W, et al.  Stenosis of the vena cava (preliminary assessment of treatment with expandable metallic stents). Radiology. 1986;161:295–298
  41. Sunder SK, Ekong EA, Sivalingam K, Kumar A. Superior vena cava thrombosis due to pacing electrodes (successful treatment with combined thrombolysis and angioplasty). Am Heart J. 1992;123:790–792
  42. Dodds GA, Harrison JK, O’Laughlin MP, Wilson JS, Kisslo KB, Bashore TM. Relief of superior vena cava syndrome due to fibrosing mediastinitis using the Palmaz stent. Chest. 1994;106:315–318
  43. Rosch J, Uchida BT, Hall LD, Antonovic R, Petersen BD, Ivancev K, et al.  Gianturco-Rosch expandable Z-stents in the treatment of superior vena cava syndrome. Cardiovasc Intervent Radiol. 1992;15:319–327
  44. Kastner RJ, Fisher WG, Blacky AR, Bacon ME. Pacemaker-induced superior vena cava syndrome with successful treatment by balloon venoplasty. Am J Cardiol. 1996;77:789–790
  45. Lindsay HS, Chennells PM, Perrins EJ. Successful treatment by balloon venoplasty and stent insertion of obstruction of the superior vena cava by an endocardial pacemaker lead. Br Heart J. 1994;71:363–365
  46. Dondelinger RF, Trotteur G. Expandable stents in the venous system. Abstracts of the International Symposium; 1996 Dec 14; Leuven, Belgium

 Competition of interest: none.

PII: S0741-5214(03)00331-8

doi:10.1016/S0741-5214(03)00331-8

Journal of Vascular Surgery
Volume 38, Issue 2 , Pages 215-223, August 2003