Case Report Subclavian Vein Stent Fracture and Venous Motion Alexandros Mallios,1,2 Kevin Taubman,1 Paul Claiborne,1 and John Blebea,1 Tulsa, Oklahoma; and Paris, France
Primary subclavian vein stents are not recommended for venous thoracic outlet syndrome before surgical decompression by first rib resection due to a high risk of fracture because they are compressed between the clavicle and first rib. After rib removal, however, stent insertion has been advocated for venous restenosis, and it is felt that stent fracture is unlikely to occur. We present a case suggesting that repetitive differential vein movement during respiration may be one of the causative factors for stent fractures occurring in this anatomic region.
Spontaneous upper extremity deep vein thrombosis, either due to effort thrombosis (Pagete Schroetter syndrome) or entirely idiopathic, is an uncommon disorder, which is estimated to occur in only 2 of 100,000 people yearly.1 It often happens in young otherwise healthy individuals with an occupational history of repetitive shoulder abduction. This results in mechanical compression of the subclavian vein at the costoclavicular space, inflammation, and eventual thrombosis.2,3 It represents the venous form of thoracic outlet syndrome (vTOS) but comprises only 3% of patients experiencing TOS.4 Thrombolysis and early decompression of the thoracic outlet is the currently recommended therapeutic approach.5e7 Residual venous stenosis, or subsequent stenosis developing after surgical decompression, may be treated with
Presented at the 2013 Annual Meeting of the Midwestern Vascular Surgical Society, Chicago, IL, September 6e8, 2013. 1 Department of Surgery, University of Oklahoma, College of Medicine, Tulsa, OK. 2 Department of Vascular Surgery, Institut Mutualiste Montsouris, Paris, France.
Correspondence to: Alexandros Mallios, MD, Department of Vascular Surgery, Institut Mutualiste Monstsouris, 42 Bd Jourdan, Paris 75014, France; E-mail: [email protected] Ann Vasc Surg 2015; -: 1–4 http://dx.doi.org/10.1016/j.avsg.2015.04.064 Ó 2015 Elsevier Inc. All rights reserved. Manuscript received: February 21, 2015; manuscript accepted: April 5, 2015; published online: ---.
balloon angioplasty with or without stenting.8,9 Stent placement before thoracic outlet decompression by rib resection has been associated with stent fracture and venous thrombosis due to continued musculo-osseous compression.10e12 We herein describe the case of a patient with a prior possibly inadequate, first rib resection for vTOS and subsequent stenting, who nonetheless had stent fracture and venous restenosis. Dynamic radiologic imaging demonstrated significant asymmetrical stent motion during respiration, which may be a responsible cofactor for the stent fracture. This is the first time such a mechanism for subclavian vein stent fracture has been reported.
CASE REPORT A 56-year-old man who had previously been treated for vTOS at another institution presented with recurrent painful right arm swelling. Six years earlier, he had undergone a transaxillary first rib resection after thrombolysis. Because of persistent symptoms, 2 months later, he underwent percutaneous balloon angioplasty (PTA) with an 8-mm cutting balloon followed by 10-mm and 12-mm balloon dilatations that successfully treated the residual vein stenosis. One year later, recurrent symptoms prompted treatment with repeat PTA and placement of a self-expanding stainless steel 12 40-mm stent (Wallstent; Boston Scientific, Natick, MA; Fig. 1). The patient did well for 5 years until presentation to us with recurrent arm swelling. Imaging revealed a large 1
2 Case Report
Annals of Vascular Surgery
Fig. 1. PTA and stenting 1 year after thoracic outlet decompression: (A) venogram shows significant subclavian vein stenosis (black arrow). (B) Expanded balloon during angioplasty expands the area of stenosis. The remnant of the first rib is indicated by the arrowheads.
(C) Wallstent has been inserted and demonstrates full expansion without extrinsic compression. (D) Final venogram indicates good flow and resolution of the initial stenosis.
anterior remnant of the first rib, high-grade restenosis of the subclavian vein with minimal flow and a stent fracture (Fig. 2, Video 1). Dynamic radiologic imaging demonstrated the medial half of the stent to be moving in concert with the movements of the medial part of the subclavian vein during respiration. The lateral half of the stent was located in the relatively immobile distal portion of the subclavian vein beyond the thoracic outlet (Fig. 3, Video 1). The fracture of the stent was localized at the fulcrum of the mobile and immobile parts of the stent, posterior to the head of the clavicle.
The area of intrastent stenosis was easily crossed with a hydrophilic guidewire. Advancing the wire into the superior vena cava (SVC) was challenging because the proximal end of the stent extended to the opposite wall of the SVC. Once this was accomplished through the use of an angled guiding catheter, a 10-mm balloonexpandable stainless steel covered stent (iCAST; Atrium, Hudson, NH) was implanted. A covered stent was used in case balloon expansion caused vein rupture and bleeding from laceration by the fractured segments of the original stent. The addition of another stent appeared
Vol.
-,
No.
-, -
2015
Fig. 2. Five years after insertion, there is fracture of the stent in its midportion (arrows). The stent fracture appears to overlie on the large first rib remnant (outlined with dots), posterior to the head of the clavicle. The arrowheads indicate the previously placed surgical clips. to increase the stiffness of this portion of the vein, decreased the associated vertical motion, and prevented midstent angulated motion (Video 2). Recovery of the patient was uneventful, and he was discharged on the first postoperative day.
DISCUSSION Current recommendations for the treatment of vTOS include thrombolysis followed by early surgical decompression comprising first rib resection and scalenectomy. If open surgical repair or patch angioplasty of the area of stenosis is not performed, intraoperative venography with treatment of any significant residual stenosis by balloon angioplasty with or without stent placement is recommended.1,5e9,13,14 Such angioplasty and/or stenting before surgical decompression, however, is not recommended because the causative muscular and bony compression has not been relieved and early rethrombosis can be expected.10 Urschel et al.10 reported a series of 22 patients with vTOS treated with thrombolysis, angioplasty, and stenting without surgical decompression. All patients had reocclusion of the vein within a 6-week period. Meier et al.11 reported a similar albeit smaller experience in which stented patients without rib resection all developed fracture of the stent. Such clinical experiences have clearly demonstrated that the tight and dynamic compression at the thoracic outlet between the clavicle and the first
Case Report 3
Fig. 3. The stent fracture (blue arrow) can be seen exactly at the junction of the medial-mobile and lateralimmobile, portion of the stent. The black arrows indicate the position of the medial part of the stent during inspiration (lower) and expiration (higher), respectively. The red and green lines represent the centerline of the stent during inspiration (lower) positions and expiration (higher), respectively. Note the stable position of the lateral half of the stent, whereas the medial half shows substantial downward movement with inspiration.
rib overcomes the mechanical integrity of stents placed within this location. What has not previously been appreciated is the significant movement of the subclavian vein in the same area. The fulcrum of such motion is at the thoracic outlet where the mobile intrathoracic portion of the proximal subclavian vein transitions to the extrathoracic region as it crosses the first rib. One can postulate that not just the surrounding tissues but also the venous branches that join both the proximal axillary and distal subclavian veins serve to tether this lateral portion of the vein and limit its movement. In the superficial femoral artery, the effect of vessel motion on stent integrity has been extensively studied and been found to be a significant causative factor in stent fractures.15 A similar process may also take place at the thoracic outlet and may contribute to subclavian vein stent fracture in addition to the more direct mechanical compression of the bones and muscle structures in the area. Giving credence to such a hypothesis, Kapoor et al.16 reported on several hemodialysis patients who had been stented in the proximal subclavian and/or brachiocephalic vein for catheter-induced stenosis. These patients had stent fractures more proximal than the costoclavicular junction. The authors suggested that pulsations of the central arteries, during the reduced
4 Case Report
anteroposterior distance of the chest wall during expiration, caused a compression of the respective veins by the aortic arch on the left side and brachiocephalic arterial trunk on the right. Finally, we also experienced the case of a patient where a stent fracture has occurred as a result of chronic compression between the innominate artery and the sternum.17 Dynamic imaging in our patient clearly demonstrated vertical stent motion during respiration with the fulcrum located exactly at the zone of the fracture of the stent, posteriorly to the head of the clavicle. One can assume that the forces governing this observed stent and/or vein mobility, in addition to persisting compression from a large first rib anterior remnant, caused a repetitive strain over the years on the stent skeleton that may have lead to the observed fracture. Based on video imaging, it appears that the lateral part of the subclavian vein remains stable during inspiration, whereas the proximal medial segment follows the motion of the mediastinum and moves downward, leading to an area of repeated flexion in the midportion of the stent. Radiologic images indicate most likely an inadequate resection of the first rib and of course we cannot exclude scarring of muscle and ligament in the surrounding area as a contributing factor. Nonetheless, our observation for differential flexion of the subclavian vein in this region is reported for the first time. The clinical significance of this finding in patients who have not received a stent in this location is unknown but one could further hypothesize that it could also contribute to the pathophysiology of venous injury and the later development of spontaneous thrombosis. The underlying mechanism of vTOS may be more complicated and multifactorial than simple mechanical compression at the costoclavicular junction. SUPPLEMENTARY DATA Supplementary data related to this article can be found at http://dx.doi.org/10.1016/j.avsg.2015. 04.064.
Annals of Vascular Surgery
REFERENCES 1. Joffe HV, Goldhaber SZ. Upper-extremity deep vein thrombosis. Circulation 2002;106:1874e80. 2. Blom JW, Doggen CJ, Osanto S, et al. Old and new risk factors for upper extremity deep venous thrombosis. J Thromb Haemost 2005;3:2471e8. 3. Illig KA. Management of central vein stenoses and occlusions: the critical importance of the costoclavicular junction. Semin Vasc Surg 2011;24:113e8. 4. Sanders RJ, Hammond SL, Rao NM. Diagnosis of thoracic outlet syndrome. J Vasc Surg 2007;46:601e4. 5. Druy EM, Trout HH, Giordano JM, et al. Lytic therapy in the treatment of axillary and subclavian vein thrombosis. J Vasc Surg 1985;2:821e7. 6. Lee MC, Grassi CJ, Belkin M, et al. Early operative intervention after thrombolytic therapy for primary subclavian vein thrombosis. J Vasc Surg 1998;27:1101e7. 7. Angle N, Gelabert HA, Farooq MM, et al. Safety and efficacy of early surgical decompression of the thoracic outlet for Paget-Schroetter syndrome. Ann Vasc Surg 2001;15: 37e42. 8. Kreienberg PB, Chang BB, Darling RC, et al. Long-term results in patients treated with thrombolysis, thoracic inlet decompression, and subclavian vein stenting for PagetSchroetter syndrome. J Vasc Surg 2001;33:S100e5. 9. Schneider DB, Dimuzio PJ, Martin ND, et al. Combination treatment of venous thoracic outlet syndrome: open surgical decompression and intraoperative angioplasty. J Vasc Surg 2004;40:599e603. 10. Urschel HC Jr, Patel AN. Paget-Schroetter syndrome therapy: failure of intravenous stents. Ann Thorac Surg 2003;75:1693e6. 11. Meier GH, Pollak JS, Rosenblatt M, et al. Initial experience with venous stents in exertional axillary-subclavian vein thrombosis. J Vasc Surg 1996;24:974e81. 12. Bjarnason H, Hunter DW, Crain MR, et al. Collapse of a Palmaz stent in the subclavian vein. AJR Am J Roentgenol 1993;160:1123e4. 13. Illig KA, Doyle AJ. A comprehensive review of PagetSchroetter syndrome. J Vasc Surg 2010;51:1538e47. 14. Stone DH, Scali ST, Bjerk AA, et al. Aggressive treatment of idiopathic axillo-subclavian vein thrombosis provides excellent long-term function. J Vasc Surg 2010;52: 127e31. 15. Nikanorov A, Smouse HB, Osman K, et al. Fracture of selfexpanding nitinol stents stressed in vitro under simulated intravascular conditions. J Vasc Surg 2008;48:435e40. 16. Kapoor B, Lockhart M, Sharma D, et al. Brachiocephalic vein stent fracture: case series and literature review. Semin Dial 2010;23:110e3. 17. Mallios A, Costanzo A, Boura B, et al. Long-term preservation of native arteriovenous dialysis fistulas. Ann Vasc Surg 2014;28:749e55.
Primary subclavian vein stents are not recommended for venous thoracic outlet syndrome before surgical decompression by first rib resection due to a high risk of fracture because they are compressed between the clavicle and first rib. After rib removal, however, stent insertion has been advocated for venous restenosis, and it is felt that stent fracture is unlikely to occur. We present a case suggesting that repetitive differential vein movement during respiration may be one of the causative factors for stent fractures occurring in this anatomic region.
Spontaneous upper extremity deep vein thrombosis, either due to effort thrombosis (Pagete Schroetter syndrome) or entirely idiopathic, is an uncommon disorder, which is estimated to occur in only 2 of 100,000 people yearly.1 It often happens in young otherwise healthy individuals with an occupational history of repetitive shoulder abduction. This results in mechanical compression of the subclavian vein at the costoclavicular space, inflammation, and eventual thrombosis.2,3 It represents the venous form of thoracic outlet syndrome (vTOS) but comprises only 3% of patients experiencing TOS.4 Thrombolysis and early decompression of the thoracic outlet is the currently recommended therapeutic approach.5e7 Residual venous stenosis, or subsequent stenosis developing after surgical decompression, may be treated with
Presented at the 2013 Annual Meeting of the Midwestern Vascular Surgical Society, Chicago, IL, September 6e8, 2013. 1 Department of Surgery, University of Oklahoma, College of Medicine, Tulsa, OK. 2 Department of Vascular Surgery, Institut Mutualiste Montsouris, Paris, France.
Correspondence to: Alexandros Mallios, MD, Department of Vascular Surgery, Institut Mutualiste Monstsouris, 42 Bd Jourdan, Paris 75014, France; E-mail: [email protected] Ann Vasc Surg 2015; -: 1–4 http://dx.doi.org/10.1016/j.avsg.2015.04.064 Ó 2015 Elsevier Inc. All rights reserved. Manuscript received: February 21, 2015; manuscript accepted: April 5, 2015; published online: ---.
balloon angioplasty with or without stenting.8,9 Stent placement before thoracic outlet decompression by rib resection has been associated with stent fracture and venous thrombosis due to continued musculo-osseous compression.10e12 We herein describe the case of a patient with a prior possibly inadequate, first rib resection for vTOS and subsequent stenting, who nonetheless had stent fracture and venous restenosis. Dynamic radiologic imaging demonstrated significant asymmetrical stent motion during respiration, which may be a responsible cofactor for the stent fracture. This is the first time such a mechanism for subclavian vein stent fracture has been reported.
CASE REPORT A 56-year-old man who had previously been treated for vTOS at another institution presented with recurrent painful right arm swelling. Six years earlier, he had undergone a transaxillary first rib resection after thrombolysis. Because of persistent symptoms, 2 months later, he underwent percutaneous balloon angioplasty (PTA) with an 8-mm cutting balloon followed by 10-mm and 12-mm balloon dilatations that successfully treated the residual vein stenosis. One year later, recurrent symptoms prompted treatment with repeat PTA and placement of a self-expanding stainless steel 12 40-mm stent (Wallstent; Boston Scientific, Natick, MA; Fig. 1). The patient did well for 5 years until presentation to us with recurrent arm swelling. Imaging revealed a large 1
2 Case Report
Annals of Vascular Surgery
Fig. 1. PTA and stenting 1 year after thoracic outlet decompression: (A) venogram shows significant subclavian vein stenosis (black arrow). (B) Expanded balloon during angioplasty expands the area of stenosis. The remnant of the first rib is indicated by the arrowheads.
(C) Wallstent has been inserted and demonstrates full expansion without extrinsic compression. (D) Final venogram indicates good flow and resolution of the initial stenosis.
anterior remnant of the first rib, high-grade restenosis of the subclavian vein with minimal flow and a stent fracture (Fig. 2, Video 1). Dynamic radiologic imaging demonstrated the medial half of the stent to be moving in concert with the movements of the medial part of the subclavian vein during respiration. The lateral half of the stent was located in the relatively immobile distal portion of the subclavian vein beyond the thoracic outlet (Fig. 3, Video 1). The fracture of the stent was localized at the fulcrum of the mobile and immobile parts of the stent, posterior to the head of the clavicle.
The area of intrastent stenosis was easily crossed with a hydrophilic guidewire. Advancing the wire into the superior vena cava (SVC) was challenging because the proximal end of the stent extended to the opposite wall of the SVC. Once this was accomplished through the use of an angled guiding catheter, a 10-mm balloonexpandable stainless steel covered stent (iCAST; Atrium, Hudson, NH) was implanted. A covered stent was used in case balloon expansion caused vein rupture and bleeding from laceration by the fractured segments of the original stent. The addition of another stent appeared
Vol.
-,
No.
-, -
2015
Fig. 2. Five years after insertion, there is fracture of the stent in its midportion (arrows). The stent fracture appears to overlie on the large first rib remnant (outlined with dots), posterior to the head of the clavicle. The arrowheads indicate the previously placed surgical clips. to increase the stiffness of this portion of the vein, decreased the associated vertical motion, and prevented midstent angulated motion (Video 2). Recovery of the patient was uneventful, and he was discharged on the first postoperative day.
DISCUSSION Current recommendations for the treatment of vTOS include thrombolysis followed by early surgical decompression comprising first rib resection and scalenectomy. If open surgical repair or patch angioplasty of the area of stenosis is not performed, intraoperative venography with treatment of any significant residual stenosis by balloon angioplasty with or without stent placement is recommended.1,5e9,13,14 Such angioplasty and/or stenting before surgical decompression, however, is not recommended because the causative muscular and bony compression has not been relieved and early rethrombosis can be expected.10 Urschel et al.10 reported a series of 22 patients with vTOS treated with thrombolysis, angioplasty, and stenting without surgical decompression. All patients had reocclusion of the vein within a 6-week period. Meier et al.11 reported a similar albeit smaller experience in which stented patients without rib resection all developed fracture of the stent. Such clinical experiences have clearly demonstrated that the tight and dynamic compression at the thoracic outlet between the clavicle and the first
Case Report 3
Fig. 3. The stent fracture (blue arrow) can be seen exactly at the junction of the medial-mobile and lateralimmobile, portion of the stent. The black arrows indicate the position of the medial part of the stent during inspiration (lower) and expiration (higher), respectively. The red and green lines represent the centerline of the stent during inspiration (lower) positions and expiration (higher), respectively. Note the stable position of the lateral half of the stent, whereas the medial half shows substantial downward movement with inspiration.
rib overcomes the mechanical integrity of stents placed within this location. What has not previously been appreciated is the significant movement of the subclavian vein in the same area. The fulcrum of such motion is at the thoracic outlet where the mobile intrathoracic portion of the proximal subclavian vein transitions to the extrathoracic region as it crosses the first rib. One can postulate that not just the surrounding tissues but also the venous branches that join both the proximal axillary and distal subclavian veins serve to tether this lateral portion of the vein and limit its movement. In the superficial femoral artery, the effect of vessel motion on stent integrity has been extensively studied and been found to be a significant causative factor in stent fractures.15 A similar process may also take place at the thoracic outlet and may contribute to subclavian vein stent fracture in addition to the more direct mechanical compression of the bones and muscle structures in the area. Giving credence to such a hypothesis, Kapoor et al.16 reported on several hemodialysis patients who had been stented in the proximal subclavian and/or brachiocephalic vein for catheter-induced stenosis. These patients had stent fractures more proximal than the costoclavicular junction. The authors suggested that pulsations of the central arteries, during the reduced
4 Case Report
anteroposterior distance of the chest wall during expiration, caused a compression of the respective veins by the aortic arch on the left side and brachiocephalic arterial trunk on the right. Finally, we also experienced the case of a patient where a stent fracture has occurred as a result of chronic compression between the innominate artery and the sternum.17 Dynamic imaging in our patient clearly demonstrated vertical stent motion during respiration with the fulcrum located exactly at the zone of the fracture of the stent, posteriorly to the head of the clavicle. One can assume that the forces governing this observed stent and/or vein mobility, in addition to persisting compression from a large first rib anterior remnant, caused a repetitive strain over the years on the stent skeleton that may have lead to the observed fracture. Based on video imaging, it appears that the lateral part of the subclavian vein remains stable during inspiration, whereas the proximal medial segment follows the motion of the mediastinum and moves downward, leading to an area of repeated flexion in the midportion of the stent. Radiologic images indicate most likely an inadequate resection of the first rib and of course we cannot exclude scarring of muscle and ligament in the surrounding area as a contributing factor. Nonetheless, our observation for differential flexion of the subclavian vein in this region is reported for the first time. The clinical significance of this finding in patients who have not received a stent in this location is unknown but one could further hypothesize that it could also contribute to the pathophysiology of venous injury and the later development of spontaneous thrombosis. The underlying mechanism of vTOS may be more complicated and multifactorial than simple mechanical compression at the costoclavicular junction. SUPPLEMENTARY DATA Supplementary data related to this article can be found at http://dx.doi.org/10.1016/j.avsg.2015. 04.064.
Annals of Vascular Surgery
REFERENCES 1. Joffe HV, Goldhaber SZ. Upper-extremity deep vein thrombosis. Circulation 2002;106:1874e80. 2. Blom JW, Doggen CJ, Osanto S, et al. Old and new risk factors for upper extremity deep venous thrombosis. J Thromb Haemost 2005;3:2471e8. 3. Illig KA. Management of central vein stenoses and occlusions: the critical importance of the costoclavicular junction. Semin Vasc Surg 2011;24:113e8. 4. Sanders RJ, Hammond SL, Rao NM. Diagnosis of thoracic outlet syndrome. J Vasc Surg 2007;46:601e4. 5. Druy EM, Trout HH, Giordano JM, et al. Lytic therapy in the treatment of axillary and subclavian vein thrombosis. J Vasc Surg 1985;2:821e7. 6. Lee MC, Grassi CJ, Belkin M, et al. Early operative intervention after thrombolytic therapy for primary subclavian vein thrombosis. J Vasc Surg 1998;27:1101e7. 7. Angle N, Gelabert HA, Farooq MM, et al. Safety and efficacy of early surgical decompression of the thoracic outlet for Paget-Schroetter syndrome. Ann Vasc Surg 2001;15: 37e42. 8. Kreienberg PB, Chang BB, Darling RC, et al. Long-term results in patients treated with thrombolysis, thoracic inlet decompression, and subclavian vein stenting for PagetSchroetter syndrome. J Vasc Surg 2001;33:S100e5. 9. Schneider DB, Dimuzio PJ, Martin ND, et al. Combination treatment of venous thoracic outlet syndrome: open surgical decompression and intraoperative angioplasty. J Vasc Surg 2004;40:599e603. 10. Urschel HC Jr, Patel AN. Paget-Schroetter syndrome therapy: failure of intravenous stents. Ann Thorac Surg 2003;75:1693e6. 11. Meier GH, Pollak JS, Rosenblatt M, et al. Initial experience with venous stents in exertional axillary-subclavian vein thrombosis. J Vasc Surg 1996;24:974e81. 12. Bjarnason H, Hunter DW, Crain MR, et al. Collapse of a Palmaz stent in the subclavian vein. AJR Am J Roentgenol 1993;160:1123e4. 13. Illig KA, Doyle AJ. A comprehensive review of PagetSchroetter syndrome. J Vasc Surg 2010;51:1538e47. 14. Stone DH, Scali ST, Bjerk AA, et al. Aggressive treatment of idiopathic axillo-subclavian vein thrombosis provides excellent long-term function. J Vasc Surg 2010;52: 127e31. 15. Nikanorov A, Smouse HB, Osman K, et al. Fracture of selfexpanding nitinol stents stressed in vitro under simulated intravascular conditions. J Vasc Surg 2008;48:435e40. 16. Kapoor B, Lockhart M, Sharma D, et al. Brachiocephalic vein stent fracture: case series and literature review. Semin Dial 2010;23:110e3. 17. Mallios A, Costanzo A, Boura B, et al. Long-term preservation of native arteriovenous dialysis fistulas. Ann Vasc Surg 2014;28:749e55.
