Physical Medicine and Rehabilitation for Thoracic Outlet Syndrome 

Updated: Sep 17, 2019
Author: Benjamin M Sucher, DO, FAOCPMR, FAAPMR; Chief Editor: Dean H Hommer, MD 

Overview

Practice Essentials

Thoracic outlet syndrome (TOS) involves compression, injury, or irritation to the neurovascular structures at the root of the neck or upper thoracic region, bounded by the anterior and middle scalenes; between the clavicle and first rib (with possible enlargement/hypertrophy of the subclavius); or beneath the pectoralis minor muscle. Some authors define the thoracic outlet as an opening bordered by the first rib laterally, the vertebral column medially, and the claviculomanubrial complex anteriorly. The syndrome of compression at this site could be primarily neurologic, involving the brachial plexus, most often the lower trunk or medial cord; alternatively, it could involve compression of the subclavian artery and/or vein.[1, 2] Thrombosis, embolus, or aneurysm of these vessels is a less likely possibility.[3, 4]

In addition, imaging with diagnostic ultrasonography has been able to identify deformation of the pectoralis minor in TOS that may be related to the pathophysiology, due to excessive tightness or shortening of the muscle that impinges on the neurovascular bundle.[5]

One proposed classification system broke TOS into the following three categories:

  • True neurogenic TOS - The brachial plexus is injured in these cases as documented by electromyography (EMG) and/or nerve conduction studies
  • True vascular TOS - The subclavian artery and/or vein is damaged or thrombosed, as documented by arteriogram or venogram [1, 2]
  • Nonspecific or disputed TOS - Patients have symptoms, but there are no abnormal tests to document the lesion clearly. This category is by far the most common type of TOS seen in the clinical setting

In the subsequent literature, however, TOS has been categorized into five clinically distinct variations, based on specific pathophysiology. These include arterial, venous, traumatic neurovascular, true neurogenic, and disputed. In each type, at least one neurovascular element is compressed as it traverses the thoracic outlet.[3, 4]

A new category is recommended for cases in which no objective neurologic or vascular abnormality can be identified. These cases could be termed postural thoracic outlet syndrome, which may be more appropriate, owing to the dysfunctional body habitus observed almost universally in these cases.[6, 7]

TOS is a controversial topic in the literature; many proponents support the existence of the condition, but some strongly vocal opponents doubt the validity of TOS as a medical entity. Even the name itself has been questioned because the actual site of pathology is technically the thoracic "inlet," not the "outlet." The primary controversy seems to center around the lack of objective criteria for diagnosis and the confusion with multiple types or clinical presentations.

Since TOS involves proximal neurovascular structures (see the image below), symptoms often are confused with various distal compression neuropathies or cervical radiculopathies.

Progressive postural decompensation with neurovasc Progressive postural decompensation with neurovascular compression. A: Normal resting posture. B: Shoulder protraction beginning; the sternomastoid muscles are shortening, drawing the head anteriorly and inferiorly. C: Advanced deformity with adaptive shortening of scalene and pectoralis minor muscles. Also note narrowed costoclavicular space (ribs 1-5 have been relatively elevated). Neurovascular compression is evident at all 3 sites.

In addition, surgical treatment has been known to have devastating complications, which further fuels debate with the opponents of recognition of this entity. Conservative treatment appears to be the most universally accepted approach, with even surgeons recommending a prolonged trial before any operative procedure.

A review of the pathomechanics and dysfunctional body habitus associated with this type of presentation suggests that the term "postural TOS" may be more appropriate, particularly when no neurologic or vascular abnormality is documented (or testing results are inconclusive).[8, 7]

Signs and symptoms of thoracic outlet syndrome

Pain, numbness and/or tingling, and heaviness of the involved upper extremity are common complaints reported by patients with thoracic outlet syndrome (TOS). Often, the symptoms are vague and generalized. The entire extremity may be involved, although a select study of patients with true neurogenic TOS found hypesthesia in the medial forearm or ulnar digits and weakness of the abductor pollicis brevis muscle.[9] Additionally, neck pain and headaches are reported concomitantly. Autonomic phenomena (eg, cold hands, blanching, swelling) also may be reported.

Workup of thoracic outlet syndrome

The most common stress tests in the physical examination diagnosis of thoracic outlet syndrome (TOS) are the Adson maneuvers, where the head is placed in extension and side bending while the patient takes a deep breath and holds it, followed by rotation to stretch or tether the plexus and/or artery by the anterior and middle scalenes.

Radiographs can help to identify cervical ribs, which may be responsible for plexus injury or have associated fibrous bands. Radiographs may also help to identify elevated first ribs, caused by tight, contracted anterior/middle scalene muscles. Displaced clavicle fractures, nonunion, and exuberant callus also can be identified.

A magnetic resonance imaging (MRI) scan of the cervical spine and supraclavicular/brachial plexus area is useful to identify other causes, or a computed tomography (CT) scan of the brachial plexus area and apical lung may be indicated.

MRI and CT scans can identify cervical root injury from degenerative spurs, disc herniation, or other causes.

Other imaging studies that can be used in the assessment of TOS include the following

  • Diagnostic ultrasonographic imaging
  • Doppler and noninvasive blood flow studies
  • Angiography/CT angiography/venography
  • Autonomic assessment (thermography)

EMG and nerve conduction studies, also known as electrodiagnostic studies, are necessary to identify true neurogenic TOS and to rule out other sites of compression neuropathy.

Management

Modalities with deep heat (eg, therapeutic ultrasound), electric stimulation, superficial heat (eg, Hydrocollator packs), stretching exercises, postural correction exercises, and strength and endurance exercises are all useful or necessary components of thoracic outlet syndrome (TOS) treatment.

Mobilization and manipulation procedures (often performed by an osteopathic physician) usually are indicated and necessary to release tight, contracted/restricted vertebral segments and soft tissue (myofascial) regions, especially the anterior/middle scalenes and pectoralis minor muscle entrapment sites.

Generally, surgery is used as a last resort after a prolonged trial (ie, months) of conservative treatment. First rib resection has been advocated by many surgeons to treat TOS. Many also use scalenectomy, in combination with rib removal or as a second procedure, if the initial surgery is ineffective.[10] Resection of accessory ribs and fibrous bands should be performed, especially if observed to be tethering the plexus.

In cases where clavicular fracture is responsible for plexus compression, removal of hyperabundant callus may be necessary.

Pathophysiology

Many authors have discovered accessory cervical ribs associated with TOS[11] ; however, they have noted tough fibrous bands coming off the accessory ribs that are believed to be more responsible for the pathology. There have even been reports of bony fusion of variant cervical ribs, resulting in bifid ribs with attached fibrous bands.[12] The bands cause tethering of the brachial plexus, which results in traction and, therefore, symptoms. Other authors report compression or irritation of the neurovascular bundle more distally under the pectoralis minor muscle or from anterior displacement of the humeral head.

Additionally, clavicle fractures can result in plexopathy from expanding hematomas or pseudoaneurysms that compress the plexus, with variable latent periods following the fracture. Delayed onset of symptoms may suggest exuberant callus from the healing fracture site. Nonunion of the fracture site also can result in direct compression by the lateral fragment, which is pulled inferiorly.

Trapezius weakness due to spinal accessory nerve injury (following cervical lymph node biopsy) also has been implicated as a cause of TOS. This results in "droopy shoulder" with secondary compression of the neurovascular bundle, which is particularly aggravated with arm elevation (abduction).[13]

Epidemiology

Frequency

United States

The inability to make a definitive and accurate diagnosis makes determination of the exact prevalence of this condition impossible. The prevalence of nonspecific thoracic outlet syndrome (TOS) has been reported as high as 23% of soft-tissue injuries of the cervical spine. TOS is overlooked or misdiagnosed commonly, especially upon presentation to the emergency department. The true or classical neurogenic or vascular TOS incidence is considered rare, with only 1 case per million population estimated for the neurogenic type. Some believe that TOS is the most common cause of acute arterial occlusion in the upper limbs of adults younger than 40 years. It is more common with occupations or activities that involve prolonged posturing of the neck, such as secretaries, cashiers, machine operators, surgeons, truck drivers, and overhead work or lifting. There is no increased incidence in athletes.

Mortality/Morbidity

No known mortality is associated directly with thoracic outlet syndrome (TOS). Morbidity often encompasses debilitating functional loss of the involved upper extremity, loss of livelihood or occupation, especially if the work involves overhead activity (eg, hairdressing, carpentry, painting). True neurogenic TOS causes neurologic deficit. Depending on the amount of nerve injury, there usually is weakness of the hand and sensory deficits in the lower trunk distribution. Devastating complications, usually to the brachial plexus, have been reported from surgical treatment for TOS.

Sex

Females are diagnosed more commonly with thoracic outlet syndrome than males, with some reports of a 9:1 female-to-male ratio. The shape of the chest wall is believed to predispose women by encouraging closure of the thoracic outlet. Large, pendulous breasts have been particularly implicated, with these adding to the anterior forces on the chest, leading to drooped shoulder posturing and further closing the outlet.[13]

Age

Age of onset of thoracic outlet syndrome is from the second to the eighth decade, with a peak occurring in the fourth decade. In the younger age group, there appears to be a greater likelihood of anatomic or structural abnormality, such as cervical rib variants and fibrous bands.

 

Presentation

History

Pain, numbness and/or tingling, and heaviness of the involved upper extremity are common complaints reported by a patient with thoracic outlet syndrome (TOS). Often, the symptoms are vague and generalized. The entire extremity may be involved; additionally, neck pain and headaches are reported concomitantly. A retrospective study by Kim et al of 13 patients with true neurogenic TOS reported a more specific pattern of findings, determining that hypesthesia in the medial forearm or ulnar digits was among the condition’s most common neurologic symptoms.[9]

Symptoms may begin insidiously after repetitive or stressful activity, such as prolonged computer keyboard use or mechanical and overhead work. Trauma, such as an automobile accident with occurrence of a whiplash injury, also has been associated with onset of TOS with a frequency of up to 23%. Sports activities, especially throwing and swimming, have been implicated as well; symptoms may be similar to those of a clavicular fracture, with a delayed onset from hours to weeks.

Autonomic phenomena (eg, cold hands, blanching, swelling) also may be reported. The proximity of the stellate ganglion to the first rib articulation, which is often dysfunctional or restricted in TOS, has been postulated as a cause.

According to the Society for Vascular Surgery, neurogenic TOS can be diagnosed when three of the following four criteria exist[14] :

  • Pathologic signs and symptoms (pain and/or tenderness) at the thoracic outlet
  • Signs and symptoms of nerve compression (distal neurologic changes, frequently more severe when the arms are overhead or dangling)
  • Absence of other pathology that might cause the symptoms
  • A positive response to a correctly executed scalene muscle test injection

Physical

A careful neurologic and musculoskeletal examination is essential to diagnose thoracic outlet syndrome (TOS) adequately. Often, the most important aspect of the physical examination is to diagnose or rule out other problems of the neck and arm.[15, 16]  Typically, there are no objective findings such as loss of a reflex or strength, but specific weakness of the abductor pollicis brevis has been noted in cases of true neurogenic TOS.[9]

The mainstay of the physical examination diagnosis of TOS involves the so-called stress tests (or provocative maneuvers) (see the images below). The sensitivity and specificity of these tests have been low in the studies on TOS completed to date. Different techniques for performing and interpreting these tests are discussed in the literature and vary even more in the bedside clinical situation.

Scalene focal (left) and regional (right) stress t Scalene focal (left) and regional (right) stress tests for thoracic outlet syndrome. Both tests can be easily combined to enhance the stress effect (may be helpful in mild cases).
Pectoral focal (left) and regional (right) stress Pectoral focal (left) and regional (right) stress tests for thoracic outlet syndrome.

The most common tests are the Adson maneuvers, where the head is placed in extension and side bending while the patient takes a deep breath and holds it, followed by rotation to stretch or tether the plexus and/or artery by the anterior and middle scalenes. The maneuver is held for 15-30 seconds while the clinician observes for onset of symptoms and obliteration of the pulse. Symptoms have been reported to the side of bending and, more commonly, to the side away from bending. If the symptoms are reported on the side of bending, then this finding overlaps with the Spurling sign, commonly used to assist in the diagnosis of cervical radiculopathy. Some examiners ask the patient to pull the head forward while maintaining the test position, causing the anterior scalene to contract against the plexus to enhance the stress effect.

Hyperabduction of the involved arm also can be used to stress the outlet; however, this maneuver often causes symptoms and loss of pulse even in normal individuals and may be misleading. The area of compression with this maneuver is considered more distal and frequently located at the anterior humeral head and plexus, with tethering under the pectoralis minor muscle.

Costoclavicular bracing (military maneuver) closes the space between the clavicle and first rib and may reproduce symptoms.

Focal stress tests involve applying pressure directly to the anterior scalene or upper segment of the pectoralis minor. These tests are considered positive if symptoms are reproduced within 15-30 seconds. In addition, some authors have noted a positive Tinel sign (percussing over the plexus) as diagnostic for TOS.

The elevated arm stress test has been noted to be highly sensitive for TOS. The upper extremity is held in the "stick-'em-up" position with the arms abducted and elbows flexed (both at 90°) for 3 minutes, while the patient simultaneously and vigorously flexes and extends the fingers (grasp and release). This test is considered positive if the patient cannot complete the full 3 minutes. Unfortunately, this test is challenging even for individuals without neurovascular symptoms to complete; thus, it may have limited practical usefulness in most clinical situations. In one study, over 80% of patients with carpal tunnel syndrome presenting to an electrodiagnostic medicine laboratory had a positive elevated arm stress test results.

Careful observation for asymmetry of the upper chest wall may reveal clavicular irregularity consistent with prior fracture. A nontender hard mass over the middle third of the clavicle often is noted. Deformity from displaced fracture (with or without nonunion) or exuberant callus could be responsible for direct compression of the plexus. Pressure on the clavicle can reproduce or aggravate symptoms, especially when nonunion is present; motion can be detected between the fragments.

Causes

Thoracic outlet syndrome (TOS) most likely has multiple causes. The primary cause is believed to be mechanical or postural. Stress, depression, overuse, and habit all can lead to the forward head, droopy shoulder, and collapsed chest posture that allows the thoracic outlet to narrow and compress the neurovascular structures (see the image below).[13] Accessory ribs or fibrous bands also may be present, predisposing the site to narrowing and compression. Large breasts have been implicated as a contributing cause by pulling the chest wall forward (anterior and inferior); this theory has been supported by relief of discomfort following reduction mammoplasty. TOS has also been associated with breast implants, which may increase tension under the chest wall muscles and irritate the neurovascular tissue.

Progressive postural decompensation with neurovasc Progressive postural decompensation with neurovascular compression. A: Normal resting posture. B: Shoulder protraction beginning; the sternomastoid muscles are shortening, drawing the head anteriorly and inferiorly. C: Advanced deformity with adaptive shortening of scalene and pectoralis minor muscles. Also note narrowed costoclavicular space (ribs 1-5 have been relatively elevated). Neurovascular compression is evident at all 3 sites.

Trauma can lead to decompensation or shifting of structures in the shoulder and chest wall, leading to symptom onset. Additionally, trauma with fracture of the clavicle can result directly in compression of the plexus from bone fragments, exuberant callus, hematoma, or pseudoaneurysm. Following median sternotomy, brachial plexus injury can occur from displacement of the ribs, which usually involves the C8 fibers, distinguished from the typical pattern that primarily involves T1.

Primary vascular lesions, such as thrombus or aneurysm, may be present as well as secondary problems such as emboli. Tumors, such as upper lobe lung lesions (Pancoast tumor), are also possible causes.

Many other problems may predispose an individual to TOS, some of which are classic perpetuators of myofascial pain syndrome, including the following:

  • Sleep disorder

  • Hormonal imbalance (estrogen, thyroid)

  • Inflammatory disorder (rheumatoid arthritis)

  • Fibromyalgia

  • Nutritional insufficiency (B vitamins, folate, vitamin C)

  • Anemia

  • Infection

  • Masses, tumors, axillary lymph nodes

  • Mechanical disorders (short leg, hyperlordosis, hypolordosis)

  • Psychologic (stress, depression)

  • Nerve entrapment/impingement (other sites)

 

DDx

Diagnostic Considerations

These include the following:

  • Cervical myelopathy

  • Cervical radiculopathy

  • Double crush syndrome (thoracic outlet syndrome and compression at another distal or proximal site)

  • Paget-von Schroetter syndrome, effort syndrome (spontaneous venous thrombosis, primary deep venous thrombosis of the upper extremity)

  • Pancoast (apical lung) tumor

  • Shoulder tendonitis, bursitis, impingement[15]

  • Shoulder (glenohumeral) instability

  • Raynaud syndrome

  • Ulnar neuropathy (cubital tunnel syndrome, Guyon canal syndrome)

Differential Diagnoses

 

Workup

Laboratory Studies

Laboratory studies are used to rule out other systemic problems.

Imaging Studies

In cases of nonspecific thoracic outlet syndrome (TOS), all studies have normal findings; however, testing to evaluate for other treatable problems or to establish true neurogenic or true vascular TOS usually is indicated.

Radiographs

Radiographs of the chest (with apical lordotic views) and cervical spine should be obtained.

Rule out significant cervical spine degenerative changes that may be causing neck/shoulder pain or impingement of the spinal nerve roots; also eliminate the possibility of upper lobe lung masses.

Radiographs can also help to identify cervical ribs, which may be responsible for plexus injury or have associated fibrous bands.

Radiographs may help to identify elevated first ribs, caused by tight, contracted anterior/middle scalene muscles. Displaced clavicle fractures, nonunion, and exuberant callus also can be identified.

Magnetic resonance imaging (MRI) and computed tomography (CT) scanning

An MRI of the cervical spine and supraclavicular/brachial plexus area is useful to identify other causes, or a CT scan of the brachial plexus area and apical lung may be indicated.

MRI and CT scans can identify cervical root injury from degenerative spurs, disc herniation, or other causes. Some authors have reported that MRI can identify distortion or displacement of the plexus in the thoracic outlet or supraclavicular space, usually from fibrous bands but also from clavicular abnormality (callus, fracture displacement). In addition, MRI has been reported to demonstrate differences in the costoclavicular measurements during provocative stress maneuvers, in patients with thoracic outlet compression.[17]

In the aforementioned study by Kim et al evaluating the characteristics of true neurogenic TOS, the most common radiologic finding was CT angiography–determined focal stenosis of the subclavian artery.[9]

Diagnostic ultrasonographic imaging

Ultrasonography has been used to measure the pectoral bowing ratio (PBR) in TOS patients. The PBR objectively measures deformation of the pectoralis minor muscle during arm abduction and is considered abnormal if greater than 10%. This ratio reflects the amount of indentation by the neurovascular bundle as it is tethered under the shortened muscle as the arm abducts above 90°. Repeat imaging following successful myofascial release treatment can demonstrate that the PBR reverts to a normal value of less than 10%.[5, 7]

Doppler and noninvasive blood flow studies

Doppler and plethysmography studies can identify interruption of blood flow to the involved extremity. A near-complete cut-off of flow during the stress maneuver with reproduction of the primary symptoms should be noted.

Hyperabduction is somewhat controversial, since most normal individuals lose flow with the position and also may develop symptoms.

Angiography/venography

Angiography and venography can identify blockage of the vessels from thrombi or emboli, which result in vascular symptoms.

Angiography can detect aneurysms that may be compressing the plexus and causing neurologic symptoms. This finding documents true vascular TOS.

Autonomic assessment (thermography)

Autonomic assessment has demonstrated thermal/temperature asymmetry consistent with nerve irritation or some interference with blood flow.

Following successful treatment, thermal symmetry usually is restored and should correlate well with reduction or elimination of symptoms. This technique remains controversial, and, although the sensitivity has been considered high, the specificity is low and has not been well established.

Other Tests

EMG and nerve conduction studies, also known as electrodiagnostic studies, are necessary to identify true neurogenic thoracic outlet syndrome (TOS) and to rule out other sites of compression neuropathy. With true neurogenic TOS, reported abnormalities include the following:

  • Low-amplitude ulnar sensory response. This finding may be variable, since the fifth digit is believed to be supplied primarily by C8 nerve fibers, whereas the T1 fibers are more deflected, stretched, or angulated by a cervical band (or rib) and thereby more likely to sustain injury in TOS.

  • Low-amplitude median motor response. The thenar muscles are supplied more from the T1 root, whereas the hypothenar muscles receive primarily C8 innervation.

  • Normal median sensory response.

  • Neurogenic motor units within the C7-T1 or lower trunk distribution on needle EMG.

  • Abnormal medial antebrachial cutaneous response (low-amplitude or unobtainable). Some authors believe that this finding can aid in the early diagnosis of neurogenic TOS. This test primarily assesses the T1 fibers. In the aforementioned study by Kim et al, 100% of the patients, all of whom had true neurogenic TOS, demonstrated reduced action potential amplitude in the medial antebrachial cutaneous sensory nerve, as measured via nerve conduction study.[9]

  • Abnormal C7-T1 root stimulation (prolonged latency).

  • Abnormal F-wave study (prolonged latency, with either full F-wave or axillary Floop)

  • Absent or attenuated N13 response in ulnar-derived somatosensory evoked potentials

The degree of nerve injury determines the abnormalities described above. In severe injuries with massive axon loss all of the above findings are seen. In cases where part of the lower plexus is spared, the findings are less dramatic. In these cases, the needle EMG is more likely to show abnormalities.

Procedures

In most patients with nonspecific thoracic outlet syndrome (TOS), there are no indicated procedures. An anterior scalene block can be performed to anesthetize the anterior scalene muscle and to relieve pressure from the brachial plexus. Thus, this type of block is diagnostic but also may be therapeutic.

The anterior scalene block is a potentially dangerous procedure because the plexus can be injured directly in the process; however, its reliability, accuracy, and safety may be improved with the use of electrophysiologic guidance to verify needle tip placement.

Jordan and Machleder believe that a negative response to this block excludes a surgical treatment option, while a positive response predicts which patients should benefit from surgical decompression.[18]

In a study of patients being tested for neurogenic TOS, Torriani et al concluded that diagnostic injection of anesthetic into the anterior scalene muscle can be safely performed with ultrasonographic guidance.[19] The investigators administered injections to 26 patients with suspected neurogenic TOS, reporting technical success (ie, anterior scalene muscle identification, intramuscular needle placement, and intramuscular medication delivery) in all procedures, with no major complications occurring. They concluded that this was a well-tolerated diagnostic test.

Histologic Findings

Biopsy results have not been reported systematically, and the procedure is not indicated unless some other condition is being considered.

 

Treatment

Rehabilitation Program

Physical Therapy

Modalities with deep heat (eg, therapeutic ultrasound), electric stimulation, superficial heat (eg, Hydrocollator packs), stretching exercises, postural correction exercises, and strength and endurance exercises are all useful or necessary components of thoracic outlet syndrome treatment. Ultrasound is the preferred modality, as it is capable of heating deep muscular and soft-tissue structures, which is essential to increase elasticity and facilitate effective stretching and/or manipulation, especially for the scalenes (see the first image below) and pectoralis minor muscles (see the second image below). Ideally, ultrasound should be performed immediately before the stretching or manual treatment, since the deep tissues cool (from 41-42°C back to 37°C) within 20-30 minutes.

Stretching technique for the pectoralis minor musc Stretching technique for the pectoralis minor muscle. Left: The patient has taken the slack out of the muscle. Center: He then rotates the body away from the side being stretched, increasing traction. Right: Maximum rotation and stretch effect are achieved slowly. Image courtesy of The Journal of the American Osteopathic Association
Sagittal plane posture of patient with thoracic ou Sagittal plane posture of patient with thoracic outlet syndrome before (left) and after (right) treatment. Notice the release of the pelvis that occurred with the reduction in hyperlordosis, which allowed the shoulder girdle to drop back and open the thoracic outlet. Image courtesy of The Journal of the American Osteopathic Association

Mobilization and manipulation procedures (often performed by an osteopathic physician) usually are indicated and necessary to release tight, contracted/restricted vertebral segments and soft tissue (myofascial) regions, especially the anterior/middle scalenes (see the first image below) and pectoralis minor muscle (see the second image below) entrapment sites. Ultrasonography has been used to identify the pectoralis minor and guide the manipulating hand as an aid for more precise targeting and effective manual release of the muscle.[5]

Myofascial release technique for the scalene muscl Myofascial release technique for the scalene muscles. Left: Side-lying approach. Right/top: Supine approach with pillow under thorax. Right/bottom: Supine approach with head extended off the table and supported by the operator's knees. Image courtesy of The Journal of the American Osteopathic Association
Stretching technique for the scalene (anterior and Stretching technique for the scalene (anterior and middle) muscles. Left: The arm on the side to be stretched is secured down (hooked under the seat) to allow more control and effective stretch. Center: The opposite hand wraps partially around the head for good control to assist with the stretch. Right: After proceeding as far as tolerated, the patient leans the whole trunk away from the side being stretched, creating additional traction (downward) on the muscle by the arm that is secured. Image courtesy of The Journal of the American Osteopathic Association

Spray and stretch with a vapo-coolant spray is an effective adjunct to the other modalities mentioned here. Note that the research-based scientific evidence for these modalities is limited.

Occupational Therapy

Work simplification and back protection techniques often are helpful. These educational tools are available from the occupational therapist, as well as from the physical therapist.

Medical Issues/Complications

Essentially, there are no randomized, controlled trials demonstrating that specific treatment modalities are more effective than placebo. In general, research into thoracic outlet syndrome (TOS) and its treatment can be difficult for the following several reasons:

  • If the etiology of the problem cannot be agreed upon, then focusing treatment becomes difficult.

  • The proposed areas of pathophysiology and diffuse nature of symptoms are not easily amenable to surgery or other treatment modalities.

  • Many patients with TOS have coexistent chronic pain syndrome with disability and depression.

Treatment of the chronic pain and disability can be a much more complex problem and involves employment of multiple disciplines with consideration for a biopsychosocial model of treatment. Patients with nonspecific TOS and suggestion of chronic pain syndrome with disability may do best with chronic pain treatment and treatment of psychological issues.

Additional issues of concern include the following:

  • More advanced/severe TOS can result in functional loss of the upper extremity.

  • Concomitant cervical degenerative joint/disc disease limits the neck range of motion (ROM) that is necessary to stretch associated soft tissue restriction and limit conservative treatment options (eg, physical therapy).

  • Shoulder arthritis/bursitis/tendonitis can interfere with stretching of the pectoral muscles and limit the effectiveness of conservative therapy approaches.

  • Manual treatment to the pectoral/chest wall muscles must be sensitive to overlying breast tissue and implants (prostheses) in female patients.

  • Manual treatment must consider the proximity of the involved muscles to the brachial plexus. Vigorous stretching or manipulation of these structures may not be tolerated well and can aggravate symptoms. The phrenic nerve and accessory phrenic nerve overlie the anterior scalene muscle and also must be considered.

  • Scalene nerve block has been used as a treatment and as a diagnostic test; however, this procedure is dangerous due to the close proximity of the brachial plexus to the scalenes (see Procedures for more details).

Surgical Intervention

First rib resection has been advocated by many surgeons to treat thoracic outlet syndrome. Many also use scalenectomy, in combination with rib removal or as a second procedure, if the initial surgery is ineffective.[10] Resection of accessory ribs and fibrous bands should be performed, especially if observed to be tethering the plexus.

In cases where clavicular fracture is responsible for plexus compression, removal of hyperabundant callus may be necessary. Occasionally, resection of associated musculature is required, including the subclavius and infraclavicular soft tissue. Reduction of clavicular nonunion fragments and internal fixation (with pins) may be indicated.

Complications from surgical treatment have been devastating, especially brachial plexopathy (eg, injury to the long thoracic nerve with scapular winging). Generally, surgery is used as a last resort after a prolonged trial (ie, months) of conservative treatment.

Some authors have advocated breast reduction in extreme cases, where very large breasts obviously are adding uncontrollable weight loads to the anterior chest wall.

Consultations

See the list below:

  • Physical medicine and rehabilitation specialists (physiatrists) are generally familiar with thoracic outlet syndrome (TOS) and conservative treatment options. They usually are best positioned to implement and direct the therapy program, and they also have been trained extensively in electrodiagnosis, which may provide the best objective evidence for the disorder in its true neurogenic form. Neurologists are also capable diagnosticians for TOS.

  • The image below depicts an algorithm for the treatment of nonprogressive thoracic outlet syndrome (TOS).

    Algorithm for the treatment of nonprogressive thor Algorithm for the treatment of nonprogressive thoracic outlet syndrome (TOS). Anti-inflammatory medication, muscle relaxants, and activity modifications all are used as indicated and tolerated in all cases. Values for very severe TOS are greater than those for severe TOS, and the patient probably should be referred for surgical evaluation.
  • Some internists or cardiologists who specialize in peripheral cardiovascular disorders may be able to help with the diagnostic workup, especially when vascular or autonomic symptoms predominate. They also may be familiar with the use of medications to help control symptoms (eg, vasodilators, calcium-channel blockers). Rheumatologists can assist in ruling out connective tissue disorders or autoimmune diseases that might be associated with TOS or might be complicating the clinical picture.

  • Thoracic and cardiovascular surgeons are the most likely surgical specialists to treat TOS; however, not all of these surgeons have an active interest or willingness to deal with the disorder. Occasionally, neurosurgeons can offer operative treatment for TOS patients.

  • Plastic surgeons (or some general surgeons) may be used for reduction mammoplasty, when indicated.

  • Anesthesiologists may be needed to perform diagnostic and therapeutic blocks.

  • Orthopedists may be required to diagnose and treat concomitant shoulder joint pathology and other related disorders, such as complications from clavicular fractures.

Other Treatment

See the list below:

  • Osteopathic manipulation has been shown to be highly effective in treating thoracic outlet syndrome, especially in combination with vigorous stretching exercise. The most useful procedures involve a vigorous myofascial release to the scalenes and pectoral muscles (especially pectoralis minor). These techniques are applied most easily immediately following modality treatment with ultrasound, which heats the deep muscular structures and renders them more elastic and responsive to manipulation and stretching.

  • All other areas of restriction or dysfunction also should be addressed and treated with manipulation, since even pelvic/sacral abnormality can influence the thoracic outlet. This abnormality is most obvious with unleveling, or a sacral tilt that shifts the thorax and places skeletal and muscular strain on the shoulder girdle region. Some orthoses, such as a heel lift, may be a useful adjunct in such cases.

  • Injection of trigger points in associated muscular structures may be indicated and necessary. An injection of deep muscular structures, such as a scalene block, however, is dangerous (close proximity to brachial plexus) and should be avoided or performed by an anesthesiologist. Even so, a study by Torriani et al of diagnostic injections indicated that anesthetic can be safely injected into the anterior scalene muscle with ultrasonographic guidance (see Procedures).[19]

 

Medication

Medication Summary

Muscle relaxants (eg, Flexeril, Soma, Robaxin, Parafon forte) are options to help decrease muscle tightness and restriction, thereby facilitating conservative treatment with exercise and manipulation. Tizanidine (Zanaflex) is being used for muscle tension cephalgia and may hold promise for thoracic outlet syndrome (TOS).

Anti-inflammatory medication can decrease irritability and pain and enhance conservative treatment results. Long-acting preparations often are most effective and are tolerated better (eg, Relafen, Daypro, Celebrex). Voltaren or Arthrotec and Celebrex are relatively long-acting alternatives that are less irritating to the GI tract than Naproxen or Clinoril.

Some internists or rheumatologists may recommend vasodilators and calcium-channel blockers, if significant vascular and vasoconstrictive involvement exists. These agents are not primary drugs of choice for TOS but should be considered ancillary or secondary options to be considered and integrated into treatment as clinically indicated.

Muscle relaxants

Class Summary

Used to relax and loosen the tight musculature involved in TOS, facilitate stretching and manipulation treatments, relieve pain, and assist with sleep.

Cyclobenzaprine (Flexeril)

Muscle relaxer of moderate duration, centrally acting, related to TCAs chemically. This drug often produces a "hangover" effect, which can be minimized by taking the nighttime dose 2-3 h before going to sleep.

Carisoprodol (Soma)

Short-acting medication with significant potential for addiction, that works at the spinal cord level.

Methocarbamol (Robaxin)

Short-acting muscle relaxer that probably works through CNS mechanisms.

Chlorzoxazone (Flexaphen, Paraflex, Parafon Forte)

Short-acting muscle relaxer, working via central pathways (spinal cord and subcortical).

Nonsteroidal anti-inflammatory drugs

Class Summary

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Nabumetone (Relafen)

Nonacidic NSAID rapidly metabolized after absorption to a major active metabolite that inhibits cyclo-oxygenase enzyme, which in turn inhibits pain and inflammation.

Oxaprozin (Daypro)

For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which is responsible for prostaglandin synthesis.

Celecoxib (Celebrex)

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.

Naproxen (Anaprox, Naprelan, Naprosyn)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.

Sulindac (Clinoril)

Decreases activity of cyclo-oxygenase and in turn inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators.

Diclofenac (Voltaren, Cataflam)

Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclo-oxygenase which in turn decreases formation of prostaglandin precursors.

Diclofenac and misoprostol (Arthrotec)

Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclo-oxygenase which in turn decreases formation of prostaglandin precursors.

Misoprostol is prostaglandin analog that protects lining of GI tract by replacing depleted prostaglandin E1 in prostaglandin-inhibiting therapies.

 

Follow-up

Further Outpatient Care

See the list below:

  • Outpatient care for thoracic outlet syndrome includes physical therapy, manipulation, and occupational therapy. See the Treatment section.

Further Inpatient Care

See the list below:

  • No inpatient care is indicated for thoracic outlet syndrome, unless the patient is treated surgically.

Deterrence

See the list below:

  • In some cases, thoracic outlet syndrome (TOS) may be preventable. Proper flexibility and strength, along with good posture, are very important for individuals who are at risk for developing this condition. One should avoid stressful positions and limit the amount of time completing repetitive or overhead activities. A workstation evaluation may be very beneficial to identify potential causes of TOS. If repetitive or overhead activities are required at work, one should take frequent rest breaks, change positions whenever possible, and ensure a proper workstation setup. Avoidance of working with outstretched arms and heavy lifting or carrying also can help to avoid developing TOS symptoms.

Complications

Complications that may develop in individuals with thoracic outlet syndrome include the following:

  • Chronic pain

  • Disability and loss of functional ability with the upper extremity

  • Depression

  • Neurologic deficit

  • Thrombosis

  • Ischemia

  • Pseudoaneurysm

Prognosis

Prognosis is generally good for most cases of thoracic outlet syndrome (TOS), unless it is severe and requires surgery. Some patients may develop chronic pain and disability that can be complicated by legal and psychological issues. Recognition and prompt treatment of such psychological and disability issues can limit the complications.

Most patients obtain relief of paresthesias and numbness with a return of strength or activity tolerance; however, recurrence is common, especially with resumption of the activity that led to symptom onset. Posture correction and strengthening usually is necessary to maintain improvement.

In a study by Likes et al of patients with TOS, 100 out of 271 patients (37%) who were initially managed with TOS-specific physical therapy improved with this treatment alone.[20]

In a study of competitive athletes with TOS, however, only mild to modest symptom improvement was seen in those with neurogenic TOS who were initially treated with TOS-specific physical therapy. Consequently, 67% of the neurogenic TOS patients went on to be treated with supraclavicular first rib resection and brachial plexus neurolysis. Nonetheless, of the 81% of the group with neurogenic TOS who were able to return to full competitive athletics, 32% did so after management only with physical therapy.[21]

Patient Education

See the list below:

  • Educating patients about the causes or perpetuating factors involved in thoracic outlet syndrome is essential. Offer training to minimize the likelihood of recurrence.

  • Proper use of keyboards and adjustment of workstation ergonomics are useful. Specific techniques for exercise and motivation are necessary. Appropriate management of stress and depression also are helpful.

  • For excellent patient education resources, see eMedicineHealth's patient education article Shoulder and Neck Pain.