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Chest and Abdominal Conditions

Arterial Thoracic Outlet Syndrome

Daniels, Brian MD1; Michaud, Leslie MD2; Sease, Franklin Jr MD1,3; Cassas, Kyle J. MD, FACSM3; Gray, Bruce H. DO4

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Current Sports Medicine Reports: March/April 2014 - Volume 13 - Issue 2 - p 75-80
doi: 10.1249/JSR.0000000000000034
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Thoracic outlet syndrome is a long-described controversial clinical entity involving compression of neurovascular structures in four related syndromes: arterial compression, venous compression, neurogenic compression, and a poorly defined pain syndrome (35). Galen and Vesalius described a patient presenting in the second century AD with compression of neural and vascular elements (6). Traditionally various names have been used to describe thoracic outlet syndrome, including scalenus anticus, costoclavicular, hyperabduction, cervical rib, or first rib syndromes (1,40). Peet et al. (25) was the first to use the term “thoracic outlet syndrome” in 1956. Literature that is more recent uses the term thoracic outlet syndrome but specifies the neurovascular structure involved.

The brachial plexus is the most commonly involved structure; however this will focus on arterial thoracic outlet syndrome (ATOS) involving the subclavian or axillary arteries. ATOS makes up 1% of thoracic outlet syndrome cases (34). It is the least common type of thoracic outlet syndrome but perhaps the most concerning secondary to ischemic complications. The purpose of this article is to describe the clinical picture and anatomic predisposing factors of ATOS and outline its evaluation and management.


The thoracic outlet is a space through which the nerve and vessels that supply the upper extremity pass. It is composed of three compartments, the most proximal being the scalene triangle, followed by the costoclavicular space, and finally the subcoracoid space. Figure 1 demonstrates sites of potential compression.

Potential sites of subclavian/axillary artery compression within the thoracic outlet include the scalene triangle (A), the costoclavicular space (B), and the subcoracoid space(C). Other sites of compression outside the thoracic outlet include the humeral head (D) and the quadrilateral space (E).

The scalene triangle is bordered by the first rib at its base and the anterior and middle scalene muscles from their origin on the cervical spine vertebrae to their insertion on the first rib. It is here that the brachial plexus passes and is joined later by the subclavian artery. Table 1 lists many of the causes for ATOS in this area, with cervical ribs being the most common. However, acquired causes also are important when discussing athletes (9). Overhead athletes, including weightlifters (1,32), baseball players (38), and aquatic athletes (1,22), are subject especially to compression here due to muscle hypertrophy or repetitive motion.

Table 1
Table 1:
Abnormalities associated with ATOS [adapted from (5,8,27,32, 42)].

After passing over the first rib, the neurovasculatures all pass beneath the clavicle and the subclavian muscle in an area called the costoclavicular space. This space is compromised with shoulder abduction as the clavicle moves posteriorly, but it can be compromised also from callus due to a prior fracture (39).

Finally the neurovascular bundle passes through the subcoracoid space, which is defined as the area underneath the pectoralis minor from its origin on the second, third, and fourth ribs to its insertion on the coracoid. This area is implicated more in overhead throwing athletes, such as baseball players. Wright (45) first documented this hyperabduction syndrome in 1945. It has been described also as pectoralis minor syndrome (36), although hyperabduction syndrome helps describe the etiology. However transient occlusion of the second part of the axillary artery has been observed and demonstrated angiographically and ultrasonographically in healthy individuals (30,31). In some cases, ATOS has been caused by axillary artery injury due to anterior dislocation of the humeral head (28) or compression of the humeral head due to repetitive trauma (9), although the humeral head is not in the thoracic outlet.

The subclavian artery gives off several branches before it courses through the scalene triangle including the vertebral artery. As it passes by the first rib and crosses under the clavicle, it becomes the first part of the axillary artery. As it courses underneath the pectoralis minor muscle, it becomes the second part of the axillary artery. As it travels by the humeral head, the artery is called the third part of the axillary artery before it becomes the brachial artery.

The most common presentation for ATOS is arterial embolization (5). The embolization is most often distal to the area of compression, but retrograde thrombosis has been documented (12,18). This is thought to be the end product of chronic changes to the intimal wall of the subclavian/axillary artery (5). Ischemic events are often the result of a number of changes to the endothelium of the artery from repetitive compression and turbulent blood flow causing partial or complete thrombosis, aneurysmal degeneration, stenosis with poststenotic dilation, and poststenotic aneurysm (20).



Patients with ATOS may complain initially of a dull ache, numbness, or discomfort in the affected extremity, which becomes worse with activity and improves with rest (10,39). Traditionally, the term “claudication” was used to describe ischemic symptoms in this area. As claudication refers to the act of ambulation, the authors recommend that this term be exchanged with exertional pain. As the problem progresses, the patient may complain of cyanosis or pallor and coolness of the affected upper extremity. They also may complain of early fatigability or a “dead arm” sensation (24,28,32,38,41). Only rarely will a patient with ATOS complain of weakness or sensory deficit (28). However, if there is a deficit, it may help localize the neurovascular compromise.

Extensive collateral arterializations of the upper extremities may result in mild initial presentation. This raises concern that patients may delay seeking medical attention until ischemic events have occurred. More serious presenting symptoms can include cerebrovascular accident and acute hand and/or digital ischemia or gangrene (24). These are often late sequelae of arterial injury after thrombosis formation.

Physical examination

The physical examination is important when considering the diagnosis of ATOS. The differential diagnosis is broad and listed in Table 2. The presence of physical clues such as a marked blood pressure discrepancy between the symptomatic and asymptomatic side, loss of distal pulse with mild limb elevation, or evidence of digital ischemia in an embolic pattern should strongly support the diagnosis. The absence of these clues however does not eliminate the diagnosis.

Table 2
Table 2:
Differential diagnosis of ATOS [adapted from (3,16)].

There are no pathognomonic signs to diagnose ATOS. Therefore a complete evaluation of the musculoskeletal, nervous, and vascular systems should be made. Visual inspection should investigate for asymmetry of musculature, atrophy, abnormal posture, scapular dyskinesia, and skin or nail color changes with or without vascular engorgement. Palpation should note specific areas of tenderness as well as the presence of a cervical rib. Neck and shoulder examination should evaluate range of motion both actively and passively and include strength and provocative maneuvers. Evaluation for distal sites of nerve compression as well as reflex testing should be performed also (32). If multiple sites are involved, less pressure is needed at any individual site. This is called “multiple crush syndrome” (40,44).

The vascular physical examination starts out by obtaining the blood pressure in both arms while the patient is sitting. It is important for the physician to perform these measurements, since these measurements have some subjectivity. The greater the arterial lumen is compromised by compression, stenosis, or occlusion, the greater the difference in systolic pressures will be between the two arms. Most patients do not have a fixed arterial compression, and consequently, the blood pressure readings are not significantly different. However if the blood pressure readings differ by 20 mm Hg, this is considered significant (4,16). These readings also can be done with the arm in an abducted position as well. This provocative maneuver must be interpreted carefully since asymptomatic baseball players as well as asymptomatic nonathletes may demonstrate fall in blood pressure with the arm in the throwing position (13,15,31). Palpating the radial artery while abducting the arm can provide additional clues to the presence of arterial compromise. Typically “normal” patients will lose their radial pulse when the arm is abducted beyond 90°. A patient with ATOS may lose this pulse much earlier as the arm is elevated and the shoulder abducted. We have found that auscultating the supraclavicular space at the time of arm abduction can improve the sensitivity of this maneuver. A systolic bruit results from narrowing of the artery with abduction and will be heard prior to a change in the radial pulse intensity.

Specific provocative maneuvers for ATOS have been described. Adson and Coffey (2) originally described his test in 1927 “by having the patient elevate the chin and extend the neck or rotate the head to the affected side while taking a deep inspiration: this produces paresthesia over the distribution of the brachial plexus and, frequently, obliteration of the pulse at the wrist on the affected side.” This test, along with others, have demonstrated high false-positive rates (26,34,43). Provocative tests had a mean sensitivity value of 72% and a mean specificity value of 53% in one study of patients suspected of having thoracic outlet syndrome, although there is no mention from which type of thoracic outlet syndrome the patients were suffering (14).


Considering the diagnosis of ATOS is uncertain based on history and physical examination alone, the diagnosis often is missed initially (17). Once the suspicion for ATOS is made, however, the initial office evaluation should include cervical spine and chest radiographs to rule out the presence of bony abnormalities, such as an elongated spinous process of C7, cervical rib, anomalous rib, or other bony abnormality such as enlarged callus formation from a previously fractured clavicle (8,19,32).

Advanced imaging is indicated when there is suspicion of embolization, a bruit with the arm in neutral position, suspicion of an aneurysm, or a blood pressure difference of 20 mm Hg compared with the contralateral arm (4). Advanced imaging techniques include conventional arteriography, computed tomography (CT), magnetic resonance imaging, and ultrasonography.

Conventional arteriography is the oldest and most established imaging technique. It may demonstrate the presence of an abnormality; however it cannot determine what anatomic structure is causing the problem. As an initial imaging technique, it has been replaced largely with other modalities as discussed below (8).

Spiral CT scans are performed with the affected arm at the patient’s side and again with the arms hyperabducted and externally rotated in an attempt to reproduce the vascular compression (8,29). Intravenous contrast is injected into the contralateral vein to obtain the desired angiograph. The greatest benefit of CT angiography is the superior analysis of the vasculature in relation to bony structures. Limitations include patient position (supine), use of ionizing radiation, and the limited visualization of the brachial plexus, if there is concern for neurogenic involvement (8). This modality would be most beneficial after a positive finding on conventional radiography demonstrating a bony abnormality.

Magnetic resonance imaging (MRI) has the advantages of being able to delineate all of the anatomic components of the thoracic outlet. It is performed also with the affected arm at the patient’s side and again with the arm hyperabducted and externally rotated, although one study demonstrated that all the abnormalities were elicited with the arms hyperabducted only (7). Fibrous bands, muscle hypertrophy, and abnormal muscles can all be seen on MRI. Magnetic resonance angiography also can be employed to complement abnormalities seen on MRI. Limitations again include patient position (8), but open MRI eliminates that problem (37). The biggest limitation of open MRI, however, is the strength of the magnet. There is currently no strong evidence for the use of MRI in the diagnosis of ATOS (11), but that may be due to study design and the low incidence of the problem. Two case reports have demonstrated failure of MRI to detect arterial thrombosis, however, and both were confirmed with conventional arteriography, although in both instances, the arteriography was performed at least 10 d after the MRI was performed (10,23). Despite all of this contradictory data and with the added benefit of being a nonionizing technique, MRI may be the next step after radiography.

Ultrasonography has the advantage of assessing blood flow while examining the patient and reproducing symptoms. Another advantage is the ability to perform the examination dynamically and with the patient upright, as there is a reported 32% false-negative rate in conventional angiography associated with the supine position (7). In addition, this test can be performed often in the office. The main disadvantage to ultrasonography is its inability to demonstrate the exact location of the stenosis or compression relative to other structures (8).


Treatment varies depending on the structure involved. Surgery, however, is indicated immediately for acute arterial insufficiency (33). What is well known is that the consequences of ATOS tend to be more severe than those seen with neurogenic or venous etiologies. While there are studies that look at the conservative treatment of thoracic outlet syndrome in general (14), there are no studies that look at the conservative management of ATOS specifically. There are cases where the presenting complaint was pain, but an abnormality was noted with the arterial flow that responded well to conservative therapy that includes rest and rehabilitation (38). Criado et al. (5), on the other hand, suggest arterial imaging in patients presenting with any thoracic outlet syndrome and has bony abnormalities on radiographs, as arterial damage is an evolving process and may not necessarily have a benign course. Delayed diagnosis has been reported to lead to thrombosis of an aneurysm and extensive embolization and even retrograde embolic stroke (9,12,18).

Surgical treatments for ATOS depend on the abnormal structure involved. ATOS can be associated with subclavian artery thrombosis with or without distal embolization. When thrombus is present, catheter-directed thrombolysis is the preferred initial treatment. Once the thrombus is removed, then surgical decompression of the thoracic outlet should follow.

The surgical procedure usually consists of removal of the first rib and cervical rib, if present, as advocated by Roos (32). Accessory muscle slips or fibrous bands also should be transected, freeing the artery of any extrinsic compression. If the compression lies in the subcoracoid space, resection of the pectoralis minor muscle has been supported (21). Another study presented compression due to the humeral head. All patients were either advanced athletes or manual laborers. They also underwent surgical resection and repair of the compressed area (9). Arteriograms showing stenosis of the subclavian artery by a cervical rib as well as compression of the axillary artery by humeral head are seen in Figure 2.

(A) An arteriogram of the aortic arch showing a stenosis of the right subclavian artery at the first rib. (B) An arteriogram showing subluxation of the humeral head (large arrow) and compression of the axillary artery (small arrow). The artery appeared arteriographically normal with the arm in the neutral position.

The integrity of the artery dictates if repair or resection is necessary. If the artery is only compressed and no distal embolization or aneurysmal degeneration is noted, then removal of the compression is all that is necessary, as dilatation usually returns to normal (40). However if the artery is compromised or embolectomy cannot be achieved, then bypass is performed usually (10,18,21). Aneurysmal arteries are replaced rather than repaired.

The transaxillary approach can be used for uncomplicated thoracic outlet syndrome, but if bypass is necessary, then either a supra- or infraclavicular approach is preferred by the authors. The subclavian artery should not be treated with balloon angioplasty or a stent prior to surgical decompression and then only for residual arterial disease not addressed with the open procedure.

Our opinion is that anticoagulation is usually not necessary after surgical decompression of the thoracic outlet; however hypercoagulability studies should be performed in all patients who present with embolization (4) as patients presenting with ATOS have had abnormalities (18). In those patients with normal coagulation studies, only those patients with residual distal ischemia need be anticoagulated and then only until the ischemia resolves. Long-term antiplatelet therapy may not be necessary unless the patient required a secondary procedure using endovascular techniques.

Noninvasive studies including blood pressure in neutral and abducted position and duplex ultrasound of the subclavian artery should be performed after surgical recovery. Physical therapy and rehabilitation should commence once the surgeon deems it appropriate. Patients with arterial reconstruction should be followed closely for the first year then yearly thereafter.

For athletes affected by this condition, return to play must be a discussion between the athlete, the sports physician, and the vascular surgeon. Currently there are no guidelines regarding a timeline of return to participation.


ATOS is a rare, but potentially dangerous entity, resulting in significant morbidity if not treated promptly. Considering that athletes, particularly overhead athletes, place repetitive stress on the vasculature of the upper extremity, it is important for sports physicians to be aware of the temporal course of this disorder and to monitor for symptoms. Practitioners should have a high index of suspicion for an abnormality if a patient presents complaining of cyanosis, a cool limb, exertional pain, or early fatigability. A thorough physical examination should be performed and imaging obtained. If ATOS is diagnosed, referral to a vascular surgeon is recommended.

The authors declare no conflicts of interest and do not have any financial disclosures.


1. Abdollahi K, Wood VE. Thoracic outlet syndrome. In: DeLee J, Drez D, Miller MD, editors. DeLee and Drez’s Orthopaedic Sports Medicine: Principles and Practice. 3rd ed. Philadelphia: WB Saunders; 2010. p. 1128–37.
2. Adson AW, Coffey JR. Cervical rib: a method of anterior approach for relief of symptoms by division of the scalenus anticus. Ann. Surg. 1927; 85: 839–57.
3. Bayford T. Thoracic outlet syndrome: an overview of diagnosis and treatment. SportEX Med. 2009; 44: 13–7.
    4. Brantigan CO, Roos DB. Diagnosing thoracic outlet syndrome. Hand Clin. 2004; 20: 27–36.
    5. Criado E, Berguer R, Greenfield L. The spectrum of arterial compression at the thoracic outlet. J. Vasc. Surg. 2010; 52: 406–11.
    6. Davidović LB, Lotina SI, Vojnović BR, et al. Treatment of the thoracic outlet vascular syndrome. Srp. Arh. Celok. Lek. 1998; 126: 23–30.
    7. Demondion X, Bacqueville E, Paul C, et al. Thoracic outlet: assessment with MR imaging in asymptomatic and symptomatic populations. Radiology 2003; 227: 461–8.
    8. Demondion X, Herbinet P, Van Sint Jan S, et al. Imaging assessment in thoracic outlet syndrome. Radiographics 2006; 26: 1735–50.
    9. Durham JR, Yao JST, Pearce WH, Nuber GM, McCarthy WJ. Arterial injuries in the thoracic outlet syndrome. J. Vasc. Surg. 1995; 21: 57–70.
    10. Edwards NM, Casey R, Johnson R. Extensive arterial embolus in the arm of a college runner with thoracic outlet syndrome: a case report. Clin. J. Sport Med. 2009; 19: 331–2.
    11. Estilaei SK, Byl NN. An evidence-based review of magnetic resonance angiography for diagnosing arterial thoracic outlet syndrome. J. Hand Ther. 2006; 19: 410–20.
    12. Fields WS, Lemak NA, Ben-Menachem Y. Thoracic outlet syndrome: review and reference to stroke in a major league pitcher. Am. J. Roentgenol. 1986; 146: 809–14.
    13. Gergoudis R, Barnes RW. Thoracic outlet arterial compression: prevalence in normal persons. Angiology 1980; 31: 538–41.
    14. Gillard J, Pérez-Cousin M, Hachulla É, et al. Diagnosing thoracic outlet syndrome: contribution of provocative tests, ultrasonography, electrophysiology, and helical computed tomography in 48 patients. Joint Bone Spine 2001; 68: 416–24.
    15. Harris J, Huang W, Tyrer P, Burnett A, May J. Clinical and photoplethysmographic assessment of thoracic outlet arterial compression. J. Vasc. Tech. 1989; 13: 20–3.
    16. Huang JH, Zager EL. Thoracic outlet syndrome. Neurosurgery 2004; 55: 897–903.
    17. Ioannou CV, Kafetzakis A, Kounnos C, et al. A delayed diagnosis that altered the professional orientation of an athlete with upper limb chronic arterial embolization. Med. Sci. Monit. 2012; 18: CS1–3.
    18. Lee TS, Hines GL. Cerebral embolic stroke and arm ischemia in a teenager with arterial thoracic outlet syndrome: a case report. Vasc. Endovascular Surg. 2007; 41: 254–7.
    19. Mandal AKJ, Jordaan J, Missouris CG. Fractured clavicle and vascular complications. Emerg. Med. J. 2004; 21: 648–9.
    20. Marine L, Valdes F, Mertens R, et al. Arterial thoracic outlet syndrome: a 32‐year experience. Ann. Vasc. Surg. 2013; 27(8): 1007–13.
    21. McCarthy WJ, Yao JST, Schafer MF. Upper extremity arterial injury in athletes. J. Vasc. Surg. 1989; 9: 317–27.
    22. McMaster WC. Swimming injuries. An overview. Sports Med. 1996; 22: 332–6.
    23. Monica JT, Kwolek CJ, Jupiter JB. Thoracic outlet syndrome with subclavian artery thrombosis undetectable by magnetic resonance angiography. J. Bone Joint Surg. Am. 2007; 89: 1589–93.
    24. Nichols AW. Diagnosis and management of thoracic outlet syndrome. Curr. Sports Med. Rep. 2009; 8: 240–9.
    25. Peet RM, Hendriksen JD, Anderson TP, Martin GM. Thoracic outlet syndrome: evaluation of the therapeutic exercise program. Proc. Mayo Clinic 1956; 31: 281–7.
    26. Plewa MC, Delinger M. The false-positive rate of thoracic outlet syndrome shoulder maneuvers in healthy subjects. Acad. Emerg. Med. 1998; 5: 337–42.
    27. Rayan GM. Thoracic outlet syndrome. J. Shoulder Elbow Surg. 1998; 7: 440–51.
      28. Reeser JC. Diagnosis and management of vascular injuries in the shoulder girdle of the overhead athlete. Curr. Sports Med. Rep. 2007; 6: 322–7.
      29. Remy-Jardin M, Remy J, Masson P, et al. Helical CT angiography of thoracic outlet syndrome: functional anatomy. Am. J. Roentgenol. 2000; 174: 1667–74.
      30. Riddell DH. Thoracic outlet syndrome: thoracic and vascular aspects. Clin. Orthop. 1967; 51: 53–64.
      31. Rohrer MJ, Cardullo PA, Pappas AM, Phillips DA, Wheeler HB. Axillary artery compression and thrombosis in throwing athletes. J. Vasc. Surg. 1990; 11: 761–9.
      32. Roos DB. Congenital anomalies associated with thoracic outlet syndrome. Am. J. Surg. 1976; 132: 771–8.
      33. Safran M. Nerve injuries about the shoulder, part 2. Am. J. Sports Med. 2004; 32: 1063–76.
      34. Sanders RJ, Hammond SL, Rao NM. Diagnosis of thoracic outlet syndrome. J. Vasc. Surg. 2007; 46: 601–4.
      35. Schön N, Netzsch C, Kröger K. Subclavian thrombosis and backpacking. Clin. Res. Cardiol. 2007; 96: 42–4.
      36. Simovitch RW, Bal GK, Basamania CJ. Thoracic outlet syndrome in a competitive baseball player secondary to the anomalous insertion of an atrophic pectoralis minor muscle: a case report. Am. J. Sports Med. 2006; 34: 1016–9.
      37. Smedby O, Rostad H, Klaastad O, et al. Functional imaging of the thoracic outlet syndrome in an open MR scanner. Eur. Radiol. 2000; 10: 597–600.
      38. Strukel RJ, Garrick JG. Thoracic outlet compression in athletes: a report of four cases. Am. J. Sports Med. 1978; 6: 35–9.
      39. Terabayashi N, Ohno T, Nishimoto Y, et al. Nonunion of a first rib fracture causing thoracic outlet syndrome in a basketball player: a case report. J. Shoulder Elbow. Surg. 2010; 19: e20–3.
      40. Urshel HC, Kourlis H. Thoracic outlet syndrome: a 50-year experience at Baylor University Medical Center. Proc. (Bayl. Univ. Med. Cent). 2007; 20: 125–35.
      41. Vanti C, Natalini L, Romeo A, Tosarelli D, Pillastrini P. Conservative treatment of thoracic outlet syndrome: a review of the literature. Eura. Medicophys. 2007; 43: 55–70.
      42. Walden MJ, Adin ME, Visagan R. Cervical ribs: identification on MRI and clinical relevance. Clin. Imaging. 2013; 37: 938–41.
        43. Warrens AN, Heaton JM. Thoracic outlet compression syndrome: the lack of reliability of its clinical assessment. Ann. R. Coll. Surg. Engl. 1987; 69: 203–4.
        44. Wood VE, Biondi J. Double-crush nerve compression in thoracic-outlet syndrome. J. Bone Joint. Surg. Am. 1990; 72: 85–7.
        45. Wright IS. The neurovascular syndrome produced by hyperabduction of the arm. Am. Heart J. 1945; 29: 1–19.
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