Case Report
Late onset venous thoracic outlet syndrome following clavicle non-union fracture: A case report
Vascular 2015, Vol. 23(2) 183–187 ! The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1708538114538253 vas.sagepub.com
Daniel J Wong1, Tammy M Holm2, George SM Dyer3 and Jonathan D Gates4
Abstract A 59-year-old woman was admitted three times over a six-month period with recurrent upper extremity deep venous thrombosis (UEDVT). It was determined that this patient was suffering from an unusual presentation of Paget-Schro¨etter syndrome secondary to a 20-year-old non-union of a midshaft clavicle fracture. Following thrombolysis the patient underwent resection and plate fixation of the clavicle fracture non-union. Despite the anatomic proximity of the subclavian vessels to the clavicle, vascular complications from fracture are rare. Treatment of midshaft clavicle fractures is often non-operative. Non-union rates are generally less than 10%, and easily treated secondarily without complication. Clavicular pseudo-arthroses from trauma have been implicated in the development of the thoracic outlet syndromes, however, onset 20 years after fracture has never before been reported.
Keywords Paget-Schro¨etter, clavicle fracture, pseudarthrosis, thoracic outlet
Introduction Upper extremity deep vein thrombosis (UEDVT) represents a minority of deep vein thrombosis (DVTs), however, it is important to be aware of given its increasing incidence and serious complications including pulmonary embolism (PE), persistent pain and swelling, and loss of vascular access.1,2 Here we present an unusual case of recurrent UEDVT stemming from a nonunion of a fracture of the midshaft of the clavicle 20 years previous. In this case, the resulting pseudarthrosis from fracture non-union lead to subclavian vein compression with activity and recurrent thrombosis requiring surgical repair.
warfarin for anticoagulation. Against medical advice, she stopped warfarin two months post discharge and was admitted to our hospital two months later with right upper extremity swelling. At that time, she had a chest x-ray that demonstrated non-union of a fracture the right clavicle (Figure 1). She underwent successful thrombolysis (Figure 2) and balloon venoplasty but declined to have the fracture non-union repaired at that time and was discharged on enoxaparin. She again declined repair of the fracture at her follow up visit. Due to financial reasons, the patient stopped her enoxaparin 3 days prior to her most recent presentation. 1
Yale University School of Medicine, New Haven, CT, USA Department of Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA 3 Department of Orthopaedic Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA 4 Department of Surgery, Division of Trauma, Burns, and Critical Care, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA 2
Case report A 59-year-old woman with a history of a recurrent right upper arm DVT and a fracture non-union of the right midshaft clavicle from a fall 20 years earlier presented to our hospital complaining of right arm discoloration and pain. This was her third admission in six months with the same complaint. At first presentation to an outside hospital, she was diagnosed with a right axillary DVT, underwent thrombolysis, and was discharged on
Corresponding author: Jonathan D Gates, Brigham and Women’s Hospital, Division of Trauma, Burns, and Critical Care, 75 Francis Street, Boston, MA 02115, USA. Email: [email protected]
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Figure 1. (a) Chest radiograph of patient white arrow indicates site of non-union. (b) Close up area of non-union of right clavicle.
Figure 2. Pre-thrombolysis venography from second admission. Arrow indicates relation of medial end of non-union fracture to subclavian vein.
The patient’s medical history was significant for peripheral vascular disease, Raynaud’s syndrome, and a stroke 10 years prior with a negative hypercoagulability work up at that time (factor V Leiden, factor II G20210A). The patient remains an active smoker. On presentation her vital signs were within normal limits. Her physical exam was remarkable only for moderate swelling of the right upper extremity and a bluish hue in the distal portion of her 2nd finger on the right hand. Her motor function, sensation, and pulse exam were intact bilaterally. Her basic metabolic panel and complete blood count were normal except for a mild normocytic anemia. Her initial coagulation studies were not reported secondary to sample clotting and a factor Xa level was not drawn.
She was admitted and therapeutically anticoagulated with a heparin drip. She underwent right axillary and subclavian vein thrombolysis followed by balloon venoplasty (Figure 3). Since this was her third admission for UEDVT, the patient consented to an operative repair of the fracture non-union of the right clavicle prior to discharge. Upon initial dissection a 5 cm, fibrous mass was found in the non-union area lateral and posterior to the subclavian vein. Initially it was believed that the callus was causing direct compression of the subclavian vein. However, after dissection it became clear to the surgical team that motion around the non-union site was allowing excessive movement of the medial portion with of clavicle. This mobile medial portion of the clavicle was in turn compressing the subclavian vein when the patient moved. The fibrous mass was excised and the clavicle reduced and fixed with plate and screws (Figure 4). The patient did well post-operatively. Her neurovascular exam remained intact and she was discharged home on enoxaparin with a plan to initiate warfarin for 3–6 months. On initial post-operative follow up the patient remained adherent to anticoagulation and had no further symptoms of venous thrombosis.
Discussion While less common than lower extremity DVT, UEDVT is an important disorder given the increasing incidence and complications including post-thrombotic syndrome, loss of vascular access, and PE which can be present is anywhere between 5% and 35% of cases.1,3,4 The etiology of UEDVT is divided into primary causes, which are idiopathic or anatomic, and secondary causes related to inciting factors such as indwelling catheters or other hypercoagulable states.
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Figure 3. (a) Pre-thrombolysis and venoplasty venography of axillary and subclavian. (b) Venography following lysis and venoplasty.
Figure 4. Post-fixation chest x-ray.
Compression of the subclavian vein as it enters the chest at the costoclavicular junction leading to venous thrombosis is known as Paget-Schro¨etter syndrome or effort thrombosis.5 This disorder, also called venous thoracic outlet syndrome (VTOS) represents about 3% of all thoracic outlet syndromes (TOS), and is distinct in both anatomy and symptomatology from the arterial and neurologic TOSs.6,7 In contrast to the subclavian artery and brachial plexus, the subclavian vein passes anterior to the anterior scalene muscle as it enters chest. The vein is subject to compression by hypertrophied anterior scalene or subclavius muscles, anatomic abnormalities such as cervical ribs, or
demanding activity such as strenuous exercise (weight lifting, rowing) or hyperabduction and external rotation of the arm (baseball pitching).1,2,8,9 The most common symptoms associated with UEDVT include arm and hand edema as well as discomfort and heaviness. On examination, distended veins, cyanosis, and palpable superficial veins can be present. Similar to lower extremity DVT, anti-coagulation is the first line treatment in preventing more serious complications such as PE. However, in patients with Paget-Schro¨etter syndrome, anti-coagulation alone is insufficient, and there are relatively high rates of subsequent PE (6–15%) and even higher rates of persistent symptoms (50%).6,10 Thrombolysis and surgical decompression of the anatomic defect are the mainstays of treatment. Although there has been debate over the timing of surgical decompression following thrombolysis with some arguing for delaying surgery to allow for venous endothelium recovery, recent studies comparing immediate with delayed surgical decompression have demonstrated excellent results for immediate repair with very low rates of complications (1%).6,11 Clavicle fractures are a common orthopedic injury with midshaft fractures representing 60–80% of clavicle fractures; the vast majority (97% in a recent series) resolve with non-operative treatment.12 Although rare, acute vascular complications from clavicle fracture, especially midshaft and medial fractures, have been reported including arterial transection, arterial pseudoaneursym, and hematoma formation from venous laceration.13–15 The late development of venous, arterial, and neurologic TOS from fractures of the clavicle have occasionally been noted in the literature before.16–21 Venous TOS from traumatic clavicular non-union is exceedingly rare in the literature with only a handful of cases reported.22–24 The development of TOS in these cases is attributed to hypertrophic callus formation at the site of fracture causing direct compression of neuro-vascular structures or from pseudarthrosis formation leading to compression from the mobile clavicle.22 The chronic or intermittent with activity compression of the vein leads to inflammation, fibrosis, venous injury, and thrombosis resulting in UEDVT. Interestingly patients with multiple trauma who undergo conservative treatment of clavicular fracture may be at greater risk for development of TOS because of the limitations of the traditional figure-of-8 strategy when a patient is lying supine.25 Our patient did suffer multiple trauma along with her original clavicular fracture but the exact details of how long she spent supine during her initial treatment are unknown. Our case is of particular interest because of the extremely late presentation, 20 years after the original
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trauma. In our review of the literature, venous complications presented within weeks to at most two years in all but one case where the patient presented 17 years after clavicular trauma and did not undergo surgery.22 A congenital clavicular pseudarthrosis causing VTOS in the fourth decade of life has been reported although most congenital pseudo-arthoses become evident during childhood.26 Additionally our case is unusual, because despite the large callus found at time of operation, the culprit for the venous compression was the mobile medial end of the clavicle that caused intermittent compression of the subclavian vein with activity. It is remarkable that the patient would have the onset of true effort thrombosis after 20 years of non-union suggesting a change in activity that was unreported, or perhaps an age related altering of anatomy that led to more frequent or severe compression of the vein. It is also possible that the patient had been undergoing subclinical thrombosis and recanalization for years with progressive accumulation of venous defects leading to her ultimate presentation.6
Conclusion Non-union of fractures of the clavicle resulting in TOS is rare but not unheard of. It is important to consider venous TOS syndrome or Paget-Schro¨etter syndrome in a patient with recurrent UEDVT and a history of clavicular fracture, because treatment with thrombolysis and anticoagulation is insufficient and delaying in definitive treatment may lead to serious complications. Treatment for venous TOS includes thrombolysis and venoplasty, followed by surgery to fix the primary anatomic defect which can be accomplished safely without delay. Finally while most venous complications following clavicular fracture occur within weeks to months, this case demonstrates that the onset of symptoms can follow decades after the initial trauma. Conflict of interest The authors declare no conflict of interest.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. Joffe H and Goldhaber S. Upper-extremity deep vein thrombosis. Circulation 2002; 106: 1874–1880. 2. Spieza L and Simioni P. Upper extremity deep vein thrombosis. Intern Emerg Med 2010; 5: 103–109. 3. Prandoni PPP, Bernardi E, Cogo A, et al. Upper-extremity deep vein thrombosis. Risk factors, diagnosis, and complications. Arch Intern Med 1997; 157: 57–62.
4. Mai C and Hunt D. Upper-extermity deep venous thrombosis: a review. Am J Med 2011; 124: 402–407. 5. Hughes ESR. Venous obstruction in upper extremity. Br J Surg 1948; 36: 155–163. 6. Illig K and Doyle A. A comprehensive review of Page-Schroetter syndrome. J Vasc Surg 2010; 51: 1538–1547. 7. Sanders RJ, Hammond SL and Rao NM. Diagnosis of thoraic outlet syndrome. J Vasc Surg 2007; 46: 601–604. 8. DiFelice G, Paletta GJ, Phillips B, et al. Effort thrombosis in the elite throwing athlete. Am J Sports Med 2002; 30: 708. 9. Daskalkis E and Bouhoutsos J. Subclavian and axillary vein compression of musculoskeletal origin. Br J Surg 1980; 67: 573–576. 10. He´ron E, Lonzinguez O, Emmerich J, et al. Long-term sequelae of spontaneous axillary-subclavian venous thrombosis. Ann Intern Med 1999; 31: 510–513. 11. Molina J, Hunter D and Dietz C. Paget-Schroetter syndrome treated with thrombolytics and immediate surgery. J Vasc Surg 2007; 45: 328–334. 12. Faldini C, Nanni M, Leonetti D, et al. Nonoperative treatment of closed displaced midshaft clavicle fractures. J Orthopaed Traumatol 2010; 11: 229–236. 13. Cooney D and Kloss B. Case report: delayed subclavian vein injury secondary to clavicular malunion. J Emerg Med 2012; 43: 648–650. 14. Gryska P. Major vascular injuries - principles of management in selected cases of arterial and venous injury. N Engl J Med 1962; 266: 381–385. 15. Renger R, de Brujin A, Aarts H, et al. Endovascular treatment of a pseudoaneurysm of the subclavian artery. J Trauma 2003; 55: 969–971. 16. Wilkins R and Johnston R. Ununited fractures of the clavicle. J Bone Joint Surg Am 1983; 65: 773–778. 17. Kochar T, Jayadev C, Smith J, et al. Delayed presentation of subclavian venous thrombosis following undisplaced clavicle fracture. World J Emerg Surg 2008; 25. 18. Claes T, Deeber P, Bellemans J, et al. Deep venous thrombosis of the axillary and subclavian vein after osteosynthesis of a midshaft clavicular fracture - a case report. Am J Sports Med 2010; 38: 1255–1258. 19. Dash U and Handler D. A case of compression of the subclavian vessel by a fractured clavicle treated by excision of the frist rib. JBJS (A) 1960; 42: 798–801. 20. Wright S. Subclavian vein thrombosis following clavicular fracture. Emer Med J 2009; 26: 840. 21. Fujita K, Matsuda K, Sakai Y, et al. Late thoracic outlet syndrome secondary to malunion of the fractured clavicle: case report and review of the literature. J Trauma 2001; 50: 332–335. 22. Parry D, Waterworth A and Scott D. Post-traumatic clavicular pseudo-arthrosis - an unusual case of venous thoracic outlet syndrome. Eur J Vasc Endovasc Surg 2000; 20. 23. Charrette EJP, Iyengar KS, Lynn RB, et al. Symptomatic non-thrombotic subclavian vein obstruction: surgical relief in six patients. Vasc Surg 1973; 7: 220–231. 24. Lee HH, Wang SJ and Wu SS. Clavicular nonunion associated with thoracic outlet syndrome treated with
Downloaded from vas.sagepub.com at WEST VIRGINIA UNIV HEALTH on July 4, 2015
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Knowles pin fixation, autogenous bone marrow graft, and autologous fibrin clots. J Trauma 2009; 66: E20–23. 25. Ishimaru D, Ho, Sumi H, et al. Late thoracic outlet syndrome after clavicle fractures in patients with multiple trauma: a pitfall of conservative treatment. Open J Orthoped 2012; 2: 90–93.
26. Lozano P, Doaz M, Riera R, et al. Venous thoracic outlet syndrome secondary to congenital pseudoarthrosis of the clavicle. Presentation in the fourth decade of life. Eur J Vasc Endovasc Surg 2003; 25: 592–593.
Downloaded from vas.sagepub.com at WEST VIRGINIA UNIV HEALTH on July 4, 2015
Late onset venous thoracic outlet syndrome following clavicle non-union fracture: A case report
Vascular 2015, Vol. 23(2) 183–187 ! The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1708538114538253 vas.sagepub.com
Daniel J Wong1, Tammy M Holm2, George SM Dyer3 and Jonathan D Gates4
Abstract A 59-year-old woman was admitted three times over a six-month period with recurrent upper extremity deep venous thrombosis (UEDVT). It was determined that this patient was suffering from an unusual presentation of Paget-Schro¨etter syndrome secondary to a 20-year-old non-union of a midshaft clavicle fracture. Following thrombolysis the patient underwent resection and plate fixation of the clavicle fracture non-union. Despite the anatomic proximity of the subclavian vessels to the clavicle, vascular complications from fracture are rare. Treatment of midshaft clavicle fractures is often non-operative. Non-union rates are generally less than 10%, and easily treated secondarily without complication. Clavicular pseudo-arthroses from trauma have been implicated in the development of the thoracic outlet syndromes, however, onset 20 years after fracture has never before been reported.
Keywords Paget-Schro¨etter, clavicle fracture, pseudarthrosis, thoracic outlet
Introduction Upper extremity deep vein thrombosis (UEDVT) represents a minority of deep vein thrombosis (DVTs), however, it is important to be aware of given its increasing incidence and serious complications including pulmonary embolism (PE), persistent pain and swelling, and loss of vascular access.1,2 Here we present an unusual case of recurrent UEDVT stemming from a nonunion of a fracture of the midshaft of the clavicle 20 years previous. In this case, the resulting pseudarthrosis from fracture non-union lead to subclavian vein compression with activity and recurrent thrombosis requiring surgical repair.
warfarin for anticoagulation. Against medical advice, she stopped warfarin two months post discharge and was admitted to our hospital two months later with right upper extremity swelling. At that time, she had a chest x-ray that demonstrated non-union of a fracture the right clavicle (Figure 1). She underwent successful thrombolysis (Figure 2) and balloon venoplasty but declined to have the fracture non-union repaired at that time and was discharged on enoxaparin. She again declined repair of the fracture at her follow up visit. Due to financial reasons, the patient stopped her enoxaparin 3 days prior to her most recent presentation. 1
Yale University School of Medicine, New Haven, CT, USA Department of Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA 3 Department of Orthopaedic Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA 4 Department of Surgery, Division of Trauma, Burns, and Critical Care, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA 2
Case report A 59-year-old woman with a history of a recurrent right upper arm DVT and a fracture non-union of the right midshaft clavicle from a fall 20 years earlier presented to our hospital complaining of right arm discoloration and pain. This was her third admission in six months with the same complaint. At first presentation to an outside hospital, she was diagnosed with a right axillary DVT, underwent thrombolysis, and was discharged on
Corresponding author: Jonathan D Gates, Brigham and Women’s Hospital, Division of Trauma, Burns, and Critical Care, 75 Francis Street, Boston, MA 02115, USA. Email: [email protected]
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Figure 1. (a) Chest radiograph of patient white arrow indicates site of non-union. (b) Close up area of non-union of right clavicle.
Figure 2. Pre-thrombolysis venography from second admission. Arrow indicates relation of medial end of non-union fracture to subclavian vein.
The patient’s medical history was significant for peripheral vascular disease, Raynaud’s syndrome, and a stroke 10 years prior with a negative hypercoagulability work up at that time (factor V Leiden, factor II G20210A). The patient remains an active smoker. On presentation her vital signs were within normal limits. Her physical exam was remarkable only for moderate swelling of the right upper extremity and a bluish hue in the distal portion of her 2nd finger on the right hand. Her motor function, sensation, and pulse exam were intact bilaterally. Her basic metabolic panel and complete blood count were normal except for a mild normocytic anemia. Her initial coagulation studies were not reported secondary to sample clotting and a factor Xa level was not drawn.
She was admitted and therapeutically anticoagulated with a heparin drip. She underwent right axillary and subclavian vein thrombolysis followed by balloon venoplasty (Figure 3). Since this was her third admission for UEDVT, the patient consented to an operative repair of the fracture non-union of the right clavicle prior to discharge. Upon initial dissection a 5 cm, fibrous mass was found in the non-union area lateral and posterior to the subclavian vein. Initially it was believed that the callus was causing direct compression of the subclavian vein. However, after dissection it became clear to the surgical team that motion around the non-union site was allowing excessive movement of the medial portion with of clavicle. This mobile medial portion of the clavicle was in turn compressing the subclavian vein when the patient moved. The fibrous mass was excised and the clavicle reduced and fixed with plate and screws (Figure 4). The patient did well post-operatively. Her neurovascular exam remained intact and she was discharged home on enoxaparin with a plan to initiate warfarin for 3–6 months. On initial post-operative follow up the patient remained adherent to anticoagulation and had no further symptoms of venous thrombosis.
Discussion While less common than lower extremity DVT, UEDVT is an important disorder given the increasing incidence and complications including post-thrombotic syndrome, loss of vascular access, and PE which can be present is anywhere between 5% and 35% of cases.1,3,4 The etiology of UEDVT is divided into primary causes, which are idiopathic or anatomic, and secondary causes related to inciting factors such as indwelling catheters or other hypercoagulable states.
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Figure 3. (a) Pre-thrombolysis and venoplasty venography of axillary and subclavian. (b) Venography following lysis and venoplasty.
Figure 4. Post-fixation chest x-ray.
Compression of the subclavian vein as it enters the chest at the costoclavicular junction leading to venous thrombosis is known as Paget-Schro¨etter syndrome or effort thrombosis.5 This disorder, also called venous thoracic outlet syndrome (VTOS) represents about 3% of all thoracic outlet syndromes (TOS), and is distinct in both anatomy and symptomatology from the arterial and neurologic TOSs.6,7 In contrast to the subclavian artery and brachial plexus, the subclavian vein passes anterior to the anterior scalene muscle as it enters chest. The vein is subject to compression by hypertrophied anterior scalene or subclavius muscles, anatomic abnormalities such as cervical ribs, or
demanding activity such as strenuous exercise (weight lifting, rowing) or hyperabduction and external rotation of the arm (baseball pitching).1,2,8,9 The most common symptoms associated with UEDVT include arm and hand edema as well as discomfort and heaviness. On examination, distended veins, cyanosis, and palpable superficial veins can be present. Similar to lower extremity DVT, anti-coagulation is the first line treatment in preventing more serious complications such as PE. However, in patients with Paget-Schro¨etter syndrome, anti-coagulation alone is insufficient, and there are relatively high rates of subsequent PE (6–15%) and even higher rates of persistent symptoms (50%).6,10 Thrombolysis and surgical decompression of the anatomic defect are the mainstays of treatment. Although there has been debate over the timing of surgical decompression following thrombolysis with some arguing for delaying surgery to allow for venous endothelium recovery, recent studies comparing immediate with delayed surgical decompression have demonstrated excellent results for immediate repair with very low rates of complications (1%).6,11 Clavicle fractures are a common orthopedic injury with midshaft fractures representing 60–80% of clavicle fractures; the vast majority (97% in a recent series) resolve with non-operative treatment.12 Although rare, acute vascular complications from clavicle fracture, especially midshaft and medial fractures, have been reported including arterial transection, arterial pseudoaneursym, and hematoma formation from venous laceration.13–15 The late development of venous, arterial, and neurologic TOS from fractures of the clavicle have occasionally been noted in the literature before.16–21 Venous TOS from traumatic clavicular non-union is exceedingly rare in the literature with only a handful of cases reported.22–24 The development of TOS in these cases is attributed to hypertrophic callus formation at the site of fracture causing direct compression of neuro-vascular structures or from pseudarthrosis formation leading to compression from the mobile clavicle.22 The chronic or intermittent with activity compression of the vein leads to inflammation, fibrosis, venous injury, and thrombosis resulting in UEDVT. Interestingly patients with multiple trauma who undergo conservative treatment of clavicular fracture may be at greater risk for development of TOS because of the limitations of the traditional figure-of-8 strategy when a patient is lying supine.25 Our patient did suffer multiple trauma along with her original clavicular fracture but the exact details of how long she spent supine during her initial treatment are unknown. Our case is of particular interest because of the extremely late presentation, 20 years after the original
Downloaded from vas.sagepub.com at WEST VIRGINIA UNIV HEALTH on July 4, 2015
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trauma. In our review of the literature, venous complications presented within weeks to at most two years in all but one case where the patient presented 17 years after clavicular trauma and did not undergo surgery.22 A congenital clavicular pseudarthrosis causing VTOS in the fourth decade of life has been reported although most congenital pseudo-arthoses become evident during childhood.26 Additionally our case is unusual, because despite the large callus found at time of operation, the culprit for the venous compression was the mobile medial end of the clavicle that caused intermittent compression of the subclavian vein with activity. It is remarkable that the patient would have the onset of true effort thrombosis after 20 years of non-union suggesting a change in activity that was unreported, or perhaps an age related altering of anatomy that led to more frequent or severe compression of the vein. It is also possible that the patient had been undergoing subclinical thrombosis and recanalization for years with progressive accumulation of venous defects leading to her ultimate presentation.6
Conclusion Non-union of fractures of the clavicle resulting in TOS is rare but not unheard of. It is important to consider venous TOS syndrome or Paget-Schro¨etter syndrome in a patient with recurrent UEDVT and a history of clavicular fracture, because treatment with thrombolysis and anticoagulation is insufficient and delaying in definitive treatment may lead to serious complications. Treatment for venous TOS includes thrombolysis and venoplasty, followed by surgery to fix the primary anatomic defect which can be accomplished safely without delay. Finally while most venous complications following clavicular fracture occur within weeks to months, this case demonstrates that the onset of symptoms can follow decades after the initial trauma. Conflict of interest The authors declare no conflict of interest.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. Joffe H and Goldhaber S. Upper-extremity deep vein thrombosis. Circulation 2002; 106: 1874–1880. 2. Spieza L and Simioni P. Upper extremity deep vein thrombosis. Intern Emerg Med 2010; 5: 103–109. 3. Prandoni PPP, Bernardi E, Cogo A, et al. Upper-extremity deep vein thrombosis. Risk factors, diagnosis, and complications. Arch Intern Med 1997; 157: 57–62.
4. Mai C and Hunt D. Upper-extermity deep venous thrombosis: a review. Am J Med 2011; 124: 402–407. 5. Hughes ESR. Venous obstruction in upper extremity. Br J Surg 1948; 36: 155–163. 6. Illig K and Doyle A. A comprehensive review of Page-Schroetter syndrome. J Vasc Surg 2010; 51: 1538–1547. 7. Sanders RJ, Hammond SL and Rao NM. Diagnosis of thoraic outlet syndrome. J Vasc Surg 2007; 46: 601–604. 8. DiFelice G, Paletta GJ, Phillips B, et al. Effort thrombosis in the elite throwing athlete. Am J Sports Med 2002; 30: 708. 9. Daskalkis E and Bouhoutsos J. Subclavian and axillary vein compression of musculoskeletal origin. Br J Surg 1980; 67: 573–576. 10. He´ron E, Lonzinguez O, Emmerich J, et al. Long-term sequelae of spontaneous axillary-subclavian venous thrombosis. Ann Intern Med 1999; 31: 510–513. 11. Molina J, Hunter D and Dietz C. Paget-Schroetter syndrome treated with thrombolytics and immediate surgery. J Vasc Surg 2007; 45: 328–334. 12. Faldini C, Nanni M, Leonetti D, et al. Nonoperative treatment of closed displaced midshaft clavicle fractures. J Orthopaed Traumatol 2010; 11: 229–236. 13. Cooney D and Kloss B. Case report: delayed subclavian vein injury secondary to clavicular malunion. J Emerg Med 2012; 43: 648–650. 14. Gryska P. Major vascular injuries - principles of management in selected cases of arterial and venous injury. N Engl J Med 1962; 266: 381–385. 15. Renger R, de Brujin A, Aarts H, et al. Endovascular treatment of a pseudoaneurysm of the subclavian artery. J Trauma 2003; 55: 969–971. 16. Wilkins R and Johnston R. Ununited fractures of the clavicle. J Bone Joint Surg Am 1983; 65: 773–778. 17. Kochar T, Jayadev C, Smith J, et al. Delayed presentation of subclavian venous thrombosis following undisplaced clavicle fracture. World J Emerg Surg 2008; 25. 18. Claes T, Deeber P, Bellemans J, et al. Deep venous thrombosis of the axillary and subclavian vein after osteosynthesis of a midshaft clavicular fracture - a case report. Am J Sports Med 2010; 38: 1255–1258. 19. Dash U and Handler D. A case of compression of the subclavian vessel by a fractured clavicle treated by excision of the frist rib. JBJS (A) 1960; 42: 798–801. 20. Wright S. Subclavian vein thrombosis following clavicular fracture. Emer Med J 2009; 26: 840. 21. Fujita K, Matsuda K, Sakai Y, et al. Late thoracic outlet syndrome secondary to malunion of the fractured clavicle: case report and review of the literature. J Trauma 2001; 50: 332–335. 22. Parry D, Waterworth A and Scott D. Post-traumatic clavicular pseudo-arthrosis - an unusual case of venous thoracic outlet syndrome. Eur J Vasc Endovasc Surg 2000; 20. 23. Charrette EJP, Iyengar KS, Lynn RB, et al. Symptomatic non-thrombotic subclavian vein obstruction: surgical relief in six patients. Vasc Surg 1973; 7: 220–231. 24. Lee HH, Wang SJ and Wu SS. Clavicular nonunion associated with thoracic outlet syndrome treated with
Downloaded from vas.sagepub.com at WEST VIRGINIA UNIV HEALTH on July 4, 2015
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Knowles pin fixation, autogenous bone marrow graft, and autologous fibrin clots. J Trauma 2009; 66: E20–23. 25. Ishimaru D, Ho, Sumi H, et al. Late thoracic outlet syndrome after clavicle fractures in patients with multiple trauma: a pitfall of conservative treatment. Open J Orthoped 2012; 2: 90–93.
26. Lozano P, Doaz M, Riera R, et al. Venous thoracic outlet syndrome secondary to congenital pseudoarthrosis of the clavicle. Presentation in the fourth decade of life. Eur J Vasc Endovasc Surg 2003; 25: 592–593.
Downloaded from vas.sagepub.com at WEST VIRGINIA UNIV HEALTH on July 4, 2015
