Peet et al1 first used the term thoracic outlet syndrome (TOS) in 1956 to describe the constellation of symptoms caused by compression of the neurovascular bundle at the thoracic outlet. TOS describes a wide spectrum of clinical presentations with a variety of etiologies, all with the common thread of neurovascular compression in the thoracic outlet region. As our understanding of this condition has improved, treatment has evolved but it remains controversial. The mainstay of management is nonsurgical in most patients; however, surgery is indicated for recalcitrant cases and for vascular involvement. Although TOS is a challenging diagnosis, proper evaluation and treatment leads to symptom relief for most patients.
The thoracic outlet is defined as the interval from the supraclavicular fossa to the axilla that passes between the clavicle and the first rib (Figure 1). It contains three important structures that may be subjected to compression: the subclavian artery, the subclavian vein, and the brachial plexus. Compression may occur at three distinct points in the thoracic outlet: the interscalene triangle, the costoclavicular space, and the retropectoralis minor space2 (Figure 2). The interscalene triangle consists of the anterior scalene muscle, the middle scalene muscle, and the first rib, and it contains the subclavian artery and the upper, middle, and lower trunks of the brachial plexus. The costoclavicular space is made up anteriorly by the clavicle, the subclavius muscle, and the costocoracoid ligament, posteriorly by the first rib and the anterior and middle scalene muscles, and laterally by the scapula. This space contains the subclavian vessels and the divisions of the brachial plexus. Finally, the retropectoralis minor space is located inferior to the coracoid process, anterior to the second through fourth ribs, and posterior to the pectoralis minor muscle; this space houses the cords of the brachial plexus and the axillary artery and vein.
Deep cervical fascia invests the neurovascular structures during their course from the first rib to the axilla. After the fascia splits to encompass the subclavius muscle, it comes back together to form the costocoracoid ligament (Figure 3). Caudal to the subclavius muscle, the costocoracoid fascia thins to become the clavipectoral fascia; this structure invests the pectoralis minor muscle and ultimately becomes the suspensory ligament of the axilla.3
Etiology and Pathology
In 1912, Todd4 suggested that the vertebral column grows faster than the upper extremity in youth, thus causing the scapula to descend and leading to a susceptibility for neurovascular compression with any further scapular descent. Whereas our understanding has evolved, this original insight is valuable because it highlights this anatomic region’s vulnerability to compression. Most cases of TOS are now thought to stem from an anatomic predisposition with superimposed neck trauma, either from a single acute incident or from repetitive stress.5 Symptoms may be delayed several weeks or longer after acute trauma, or they may develop insidiously because of chronic stress.6 Epidemiologic data for TOS are not widely reported; Hooper et al2 suggest that this lack of demographic information is due to disagreement in the definition and diagnostic criteria for the disease. Anecdotally, the typical patient with TOS is a young, thin female with a long neck and drooping shoulders.7,8
The anatomic causes of TOS may be organized into soft-tissue and osseous categories. Soft-tissue causes are associated with to up to 70% of cases of TOS, whereas osseous abnormalities encompass the other 30%9 (Table 1).
Variation in scalene origin and insertion may cause compression within the interscalene triangle. The scalenus minimus, an accessory muscle, can be found in 30% to 50% of patients with TOS; it originates from the cervical transverse processes and inserts into the first rib between the subclavian artery and the T1 root.3,6 Symptomatic compression may result from hypertrophy of the scalene musculature or congenital anomalous ligaments or bands. Trauma and later scarring may produce delayed symptoms.10 The costocoracoid ligament is implicated in venous compression in Paget-Schroetter syndrome, a manifestation of TOS that leads to thrombosis.3
Bony findings associated with TOS include cervical ribs, prominent C7 transverse processes, exostoses, tumor in the region, or callus from prior trauma. Although cervical ribs may cause TOS symptoms in the absence of trauma, 80% of patients with TOS and cervical ribs show the development of symptoms only after injury.11 These patients often have a large cervical rib fused to the first rib. When the ribs themselves do not cause compression, their associated bands and ligaments are implicated.5 Similarly, altered biomechanics from acromioclavicular and sternoclavicular injuries are also noted in some patients with TOS.2
Clinical History and Presentation
Diagnosis of TOS is challenging because of the varied clinical presentation and the lack of objective data to support a diagnosis. As a result, the clinical impression from a thorough history and physical examination remains a crucial component in differentiating TOS from other conditions. Patients are frequently young, active, and healthy. Often, they have seen multiple physicians, undergone misdiagnosis, and some have been told that their condition is psychosomatic. Manifestations of TOS include neurogenic TOS, caused by compression of the brachial plexus, and vascular TOS, subclassified as arterial or venous, depending on whether the subclavian artery or vein is involved. Estimates are that >90% of all TOS cases are of neurogenic origin, whereas approximately 3% to 5% are venous and <1% are arterial.12
Neurogenic Thoracic Outlet Syndrome
Neurogenic TOS presents as a constellation of upper extremity weakness, numbness, paresthesias, and pain in a nonradicular distribution. Symptoms are present during daily activities as well as during sleep. Upper extremity heaviness is common with above-the-shoulder activities. In a systematic review by Sanders et al,12 symptom distribution in neurogenic TOS included upper extremity paresthesia (98%), neck pain (88%), trapezius pain (92%), shoulder and/or arm pain (88%), supraclavicular pain (76%), chest pain (72%), occipital headache (76%), and paresthesias in all five fingers (58%), the fourth and fifth fingers only (26%), or the first, second, and third fingers (14%).
Symptom patterns can further classify neurogenic TOS as secondary to upper or lower plexus compression. In most patients, lower and combined plexus pathology is seen (85% to 90%).9 Lower plexus involvement represents compression of C8 and T1, and manifests as symptoms in the area of the ulnar forearm and hand and possibly the axillary and anterior shoulder region. Upper plexus compression involves the C5-C7 nerve roots, and presents as pain in the supraclavicular region that may radiate into the ipsilateral head, face, upper chest, periscapular region, or radial nerve distribution to the dorsal index finger and thumb.2 Neurogenic TOS must be differentiated from other compression syndromes, such as carpal tunnel syndrome and cervical nerve root compression. Such a distinction may be made by the wide anatomic distribution and the nonradicular nature of symptoms in TOS.
Vascular Thoracic Outlet Syndrome
Vascular TOS consists of both venous and arterial clinical subtypes. Venous TOS is characterized by significant swelling of the upper extremity; it is commonly associated with deep pain in the upper extremity, chest, and shoulder, along with a feeling of heaviness that is worse after activity. The patient may have cyanotic discoloration of the extremity. The subclavian vein is commonly compressed at the costoclavicular junction where it passes anterior to the anterior scalene; however, it may be compressed at other areas depending on the underlying etiology.13 A well-known subtype of venous TOS is Paget-Schroetter syndrome, described as thrombosis of the subclavian vein caused by repetitive injury in relatively young and healthy persons.
Arterial TOS is a rarer condition, but it has potentially devastating consequences. It presents as nonradicular pain, numbness, coolness, and pallor that worsens in cold temperatures. It is caused by intermittent or prolonged arterial compression of the subclavian artery, typically by a cervical rib. Compression over time leads to intimal damage, eventual aneurysm formation, thrombosis, embolic events, and even potentially limb-threatening ischemia. Often, arterial TOS coexists with neurogenic TOS. Signs that point to arterial TOS include unilateral Raynaud-type symptoms of episodic pallor, erythema, and cyanosis with a distribution of symptoms to the distal circulation of the hands or fingers in the absence of any other cause, such as collagen vascular disease or other vascular disorders. Chronic pain, coldness, and paresthesias may also be present with long-standing microembolic disease. Early fatigue may occur with exercise.8,14
The clinical presentation of TOS varies widely, ranging from mild positional discomfort to severe limb- or life-threatening symptoms. In addition, patients may present with unilateral or bilateral signs or symptoms that are related to compression of a combination of neurologic and vascular components. Isolated vascular TOS is more easily diagnosed but is rare. Thus, the examiner must distinguish which symptoms are related to brachial plexus compression, which symptoms are vascular in nature, and which symptoms have no relationship with thoracic outlet pathology. The clinical history can help narrow the differential diagnosis, which includes cervical spine pathology, intrinsic shoulder dysfunction, and other peripheral compression neuropathies. Nonradicular and anatomically widespread symptoms that are influenced by arm, neck, and shoulder position warrant a suspicion for TOS.2 Cervical spine problems are more often characterized by constant neck and shoulder pain that presents in a radicular distribution, with the pain aggravated by the position of the neck. Intrinsic shoulder pathology causes shoulder pain that may radiate into the upper arm, but numbness is not a commonly associated finding. Shoulder position and direct palpation on joint structures aggravate symptoms. More distal compression neuropathies, such as carpal and cubital tunnel syndromes, have symptoms isolated to predictable nerve distributions and are aggravated more by the position of the wrist and elbow than by the position of the shoulder or neck.6
Physical examination should include an evaluation of the cervical spine, shoulder, and upper extremity. Attention should be directed toward evaluating the position of the head, neck, and shoulder, looking for the presence of thoracic kyphosis. The patient’s overall posture should be assessed. Comparing the upper extremity with the contralateral arm yields information regarding skin color, temperature, hair distribution, muscle atrophy, and nail changes. The Gilliatt-Sumner hand, a characteristic finding of neurogenic TOS, is described as atrophy of the abductor pollicis brevis and, to a lesser degree, the hypothenar musculature and the interossei.7,15 A blood pressure difference of 20 mm Hg between the upper extremities is a significant but rare finding of vascular TOS.6 The upper extremity and chest wall may be congested and edematous with prominent superficial veins in venous TOS; in arterial TOS, the upper extremity may appear pale. Distal skin changes, ulcerations, and signs of microembolic events are rare findings.14 Palpation of the supraclavicular region may reveal tenderness, masses, or other abnormalities. Quality and location of pain with movements of the neck, shoulder, and upper limb should be recorded.
The vascular examination documents the presence and quality of the radial pulse with the arm in different positions. Several provocative tests in this context are shown in Figure 4. The Wright test was originally described as a decrease in the radial pulse with the arm in hyperabduction and external rotation, with the head turned in the opposite direction. With this maneuver, the radial pulse dampens or obliterates in up to 7% of the normal population.6 The Adson test describes bringing the arm into extension, turning the head toward the affected side, and taking a deep breath. Gergoudis et al16 challenged the clinical utility of this test by showing that 66 of 130 normal persons (51%) had a diminished pulse with the Adson maneuver. The Roos test, or the elevated arm stress test, represents a more reliable diagnostic examination for TOS. In this maneuver, the patient places both arms in the 90° abducted position with the elbows flexed to 90°. The hands are then opened and closed for a 3-minute period. Normal persons may have minor discomfort due to muscular fatigue, but patients with TOS have more dramatic symptoms that replicate their usual discomfort such that they may not be able to complete the test.8,9
Provocative testing for TOS has been criticized for leading to a high number of false positives. Warrens et al17 showed that 58% of random volunteers had at least one positive test result with provocative maneuvers; however, performing multiple tests in conjunction and considering their results together may increase their specificity. In a series by Gillard et al,18 the specificity for the Adson test and for the Roos test was 76% and 30%, respectively; however, when both tests were positive, specificity increased to 82%. Braun et al19 used pulse oximetry to attempt to provide a more objective measure in this context, showing that provocative exercise led to a statistically significant decrease in pulse oximetry readings, an increase in the heart rate, and the reproduction of symptoms.
Chest and cervical spine radiographs can identify cervical ribs, prominent C7 transverse processes, and low-lying shoulder girdles, all of which may contribute to thoracic outlet compression20 (Figure 5). Three-dimensional imaging, such as CT and MRI, has not been well studied, but it may be effective in the setting of an identifiable congenital anomaly, a space-occupying lesion (eg, a pancoast tumor), metastatic disease, or malunited fractures of ribs or the clavicle. Although some authors have proposed that ultrasonography is limited in the diagnosis of TOS because the area of interest is obscured,6 Longley et al21 reported 92% specificity and 95% sensitivity using ultrasonographic methods in the diagnosis of venous TOS.
Angiography may be used in conjunction with MRI or CT, but this technology’s role in diagnosis remains unclear. Aralasmak et al22 showed that magnetic resonance angiography can dynamically evaluate the neurovascular bundle in patients with known TOS; however, the authors could not distinguish between physiologic and pathologic compression, nor could they correlate imaging findings with clinical symptoms. Conventional arteriography is rarely useful in TOS and is only indicated in the circumstances of embolic disease, a bruit with the arm in a neutral position, suspicion of an aneurysm, or differing blood pressure measurements between the upper extremities. Other cases of arterial TOS are likely more positional and are better diagnosed on physical examination than with angiography. Conversely, venography is indicated in the workup of suspected venous TOS, demonstrating compression of the subclavian vein as well as collateralization from nearby circulation. When an acute thrombosis is detected, early catheter-directed thrombolysis and surgical decompression may be indicated to decrease the risk of a recurring thrombosis. It is important to note that patients who experience arterial or venous thrombosis should undergo coagulation studies because a TOS thrombosis can represent a two-hit phenomenon of mechanical thoracic outlet compression in conjunction with underlying hypercoaguability.6
Historically, neurophysiologic studies were considered normal in cases of TOS unless the pathology was found late and permanent nerve damage had already occurred.6 However, Tsao et al23 suggest that nerve fibers derived from T1, and to a lesser degree from C8, may show changes in neurogenic TOS. These changes manifest as abnormal nerve conduction velocity studies of the medial antebrachial cutaneous nerve and the median motor nerve to the abductor pollicis brevis. Electromyography may show fibrillations in T1 and C8 distributions; however, they are not shown as consistently as nerve conduction velocity changes.
Anterior Scalene Blocks
Appropriately placed lidocaine or botulinum toxin injections can relieve muscular contracture or spasm and have been shown to have prognostic benefits. Lum et al24 found that a successful block correlated with a 14% higher rate of good surgical outcomes in patients older than 40 years. Table 2 depicts illustrative points about different diagnostic techniques.
At the authors’ institution, plain radiographs are obtained initially for patients with suspected TOS based on history and physical examination, followed by other diagnostic tests as dictated by their symptoms. Patients with predominantly neurologic signs and symptoms often undergo neurophysiologic testing early in their workup. Vascular manifestations uniformly dictate vascular imaging. Three-dimensional imaging is reserved for surgical planning, for when there is concern for a space-occupying lesion, or for a congenital or acquired deformity.
Treatment strategy depends on the underlying etiology of TOS. Nonsurgical management is indicated first in most patients with neurogenic TOS. Surgery is warranted in arterial or venous TOS and in patients with neurogenic TOS who have persistent symptoms, muscle atrophy, or a progressive deficit. In the appropriate patient population, surgical intervention may reliably improve symptoms and quality of life.26,27
Nonsurgical management is the initial treatment strategy for neurogenic TOS; it has shown good results in some series. Novak et al28 reported that 25 of 42 patients with neurogenic TOS experienced symptomatic relief after at least 6 months of physical therapy. A typical protocol consists of education, activity modification, and physical therapy. Described pain control strategies include anti-inflammatory medications, muscle relaxants, transcutaneous electrical nerve stimulation, and injections. Using ultrasonography-guided botulinum injections, Torriani et al29 reported short-term improvement in 69% of patients with neurogenic TOS. Clarifying goals of treatment is critical for patient outcome. Patient education focuses on relaxation techniques, postural mechanics, and weight and nutritional control. Activity modification includes limiting repetitive, overhead stress and changing employment if necessary. Physical therapy involves stretching, range-of-motion exercises, and tendon and nerve gliding techniques.2 Despite several series reporting positive results, Vanti et al30 reviewed the literature and reported that no definitive benefit of nonsurgical management could be established due to a lack of randomized controlled trials. Nonsurgical management is reported to be less successful in obese patients, in patients who are on workers’ compensation, and in patients with double-crush neurologic pathology involving the carpal or cubital tunnels.28 At the authors’ institution, all patients with suspected neurogenic TOS are coached in lifestyle modification and are referred for a trial of physical therapy that focuses on core strengthening and postural mechanics. If the patients show no improvement in their symptoms after 6 months, they are reevaluated and referred for surgical consideration if appropriate.
For any patient with vascular compression or neurogenic TOS that has failed to respond to nonsurgical management, surgical intervention is warranted. The three main surgical approaches for decompression of the thoracic outlet are transaxillary, supraclavicular, and posterior, although there are many variations and preferences that are surgeon dependent. Table 3 summarizes some of the characteristics of each surgical approach.
First described by Roos36 in 1966, the transaxillary approach is the most commonly performed approach today. Its proponents argue that it provides superior exposure for first rib resection, as well as for removal of cervical ribs and fibrous bands, with a more cosmetic scar.31 Urschel et al,37 in their review of TOS over 50 years, describe the transaxillary approach as their initial surgical approach through which they perform first rib and costoclavicular ligament resection, scalenectomy, and C7, C8, and T1 neurolysis. They argue that while first rib resection can be accomplished via the supraclavicular approach, visualization is inferior and requires retraction of the neurovascular structures.
The supraclavicular approach provides a more favorable exposure of the upper brachial plexus, the neck of the first rib, and the neurovascular structures. This approach is preferred by surgeons who are performing isolated scalenectomies and removal of cervical ribs for neurogenic TOS.8 Scalenectomy in isolation can be considered in patients with upper plexus-type neurogenic TOS, patients with TOS symptoms in the absence of abnormal bony architecture, patients who are excessively muscular or obese, or patients with recurrent TOS following prior first rib resection.9 Although the supraclavicular approach may provide poorer exposure of the first rib compared with the transaxillary approach,8 Terzis et al32 reported good outcomes and fewer complications with the supraclavicular technique for first rib resection. If arterial reconstruction is necessary, the supraclavicular approach is preferred.34
The posterior approach, originally described by Clagett38 in 1962, allows better exposure of the proximal elements of the brachial plexus for neurolysis; however, the approach is more invasive and it can lead to postoperative shoulder morbidity and scapular winging.10,34 Urschel et al37 reserve the posterior approach for removing rib remnants and for performing brachial plexus neurolysis for patients with recurrent TOS.
The favored surgical approach for TOS at the authors’ institution is similar to that described by Urschel et al;37 it consists of a transaxillary approach for first rib resection, scalenectomy, and neurolysis with vascular reconstruction if necessary. Various other modifications to surgical techniques are described in the literature. Atasoy39 reported that 95% of patients had good outcomes with a combined approach consisting of transaxillary first rib resection, followed by immediate supraclavicular anterior and middle scalenectomy. Vemuri et al40 demonstrated the utility of performing an isolated pectoral minor tenotomy in patients with neurogenic TOS and with symptoms reproducible to the subcoracoid space. Desai et al35 showed the utility of using a paraclavicular approach, essentially adding an infraclavicular incision to the supraclavicular approach, for more complete first rib resections in patients with venous TOS.
Unique to surgery for arterial or venous TOS, vascular reconstruction and management of ischemia or congestion may be required. The timing of surgical intervention is more urgent, particularly in the presence of ischemic changes. Arterial repair strategies include resection and primary repair, saphenous vein graft, arterial autograft, a synthetic prosthesis, or an endovascular stent for mild stenotic disease. Acute, proximal emboli may be treated with embolectomy catheters, local thrombectomy, and anticoagulation, whereas more distal and chronic emboli mandate bypasses if the emboli are causing critical ischemia.14 Venous TOS with subclavian vein thrombus (ie, Paget-Schroetter syndrome) requires a venogram, local thrombolysis, and surgical decompression to prevent recurrent thrombus. Some patients may require late vein reconstruction for chronic venous occlusion.13
Because surgery for TOS involves many complex and intimately related structures, theoretical complications are numerous and may be severe. These complications include pneumothorax, injury to the subclavian vein or artery, brachial plexus, or thoracic duct, and failure to fully decompress the thoracic outlet. Series have shown that a pneumothorax associated with first rib resection is one of the most common complications. Karamustafaoglu et al31 reported an incidence of 25%. Other complications in this series were low and included an incidence of 3% for wound infection and an incidence of <1% for lymphatic or nerve injury. No major vascular injuries occurred. Likewise, in the largest review, Urschel et al37 reported no major arterial injuries. Bleeding requiring a second procedure occurred in only 3 of 5,008 procedures. Long-lasting nerve deficits occurred in only four patients. The major complication seen was recurrent TOS; 1,221 of the 5,008 procedures represented repeat TOS surgeries.
Recurrent Thoracic Outlet Syndrome
Although modern surgical approaches have led to improved outcomes, some patients have persistent or recurrent symptoms following surgery.37 In these patients, initial management consists of nonsurgical care, followed by surgical measures when the diagnosis is again firmly established. Surgical strategies for treating recurrent symptoms generally are dictated by the patient’s symptoms and prior surgical approach and decompression. Likes et al41 showed that recurrent TOS was commonly caused by residual or remnant first ribs following an initial decompression. Complete removal of the first rib led to improvement in all 15 patients in their series.
Future of Thoracic Outlet Syndrome
Future management of TOS will depend on improved diagnostic techniques, including advanced three-dimensional imaging, to better understand the pathologic forces driving this disease. Work by Baumer et al25 shows that high-resolution magnetic resonance neurography can have a high positive predictive value in TOS by allowing visualization of constricting fibrous bands and corresponding increased signal in compressed elements of the brachial plexus. Such technology has the potential to improve our understanding and diagnostic acumen in TOS and allow more targeted treatment. Undoubtedly, however, a high degree of clinical suspicion will remain a crucial component in the evaluation and treatment of TOS.
TOS remains a difficult diagnosis due to its varied manifestations and lack of confirmatory testing. It should be on the differential diagnosis for patients with upper extremity signs and symptoms that are not referable to a more common condition. The mainstay of treatment is nonsurgical management that includes education, activity modification, and physical therapy. For recalcitrant cases, surgical intervention may be considered. Outcomes have been shown to be good with both nonsurgical and surgical care; however, the literature is conflicting regarding the optimal surgical approach, with consideration being given to the underlying etiology and surgeon preference. In cases of vascular TOS, surgery should be considered more promptly because of the underlying potential of limb- or life-threatening complications.
Evidence-based Medicine: Levels of evidence are described in the table of content. In this article, references 1–3, 5–18, 20–37, and 39–41 are level IV studies. References 4 and 38 are level V expert opinion.
References printed in bold type are those published within the past 5 years.
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