115: Thoracic Outlet Syndrome

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Thoracic Outlet Syndrome

Karl-August Lindgren, MD, PhD


Cervical rib syndrome

Costoclavicular syndrome

Scalenus anticus syndrome

ICD-9 Code

353.0  Thoracic outlet syndrome

ICD-10 Code

G54.0  Thoracic outlet syndrome


Thoracic outlet syndrome is a symptom complex caused by compression or irritation of the neurovascular structures as they leave the thoracic cage through its narrow outlet. The thoracic outlet contains many structures in a confined space. The base of the thoracic outlet is formed by the first rib and the fascia of Sibson, which is attached to the transverse process of the seventh cervical vertebra, the pleura, and the first rib. The outlet is bounded superiorly by the subclavius muscle and the clavicle, anteriorly by the anterior scalene muscle, and posteriorly by the middle scalene muscle. The brachial plexus and the subclavian artery pass over the first rib between the anterior and middle scalene muscles (Fig. 115.1).

FIGURE 115.1 Anatomy of the thoracic outlet area. (Reprinted from the Christine M. Kleinert Institute for Hand and Microsurgery, Inc.)

Neurovascular compression occurs most frequently at three levels:

 in the superior thoracic outlet, bordered posteriorly by the spine, anteriorly by the manubrium, and laterally by the first rib;

 in the costoscalene hiatus, bordered anteriorly by the anterior scalene muscle, posteriorly by the middle scalene muscle, and caudally by the first rib; and

 in the costoclavicular passage, bordered laterally by the clavicle, posteriorly by the scapula, and medially by the first rib.

The clinical symptoms of thoracic outlet syndrome are divided into categories according to the structures under pressure. True neurologic thoracic outlet syndrome is often caused by the distal C8-T1 roots or proximal fibers of the lower trunk of the plexus being stretched over a taut congenital band extending from the tip of a rudimentary cervical rib to the first rib. The most common form of thoracic outlet syndrome is the disputed neurologic thoracic outlet syndrome. The term disputed has been chosen because so many of the basic tenets of this syndrome are in dispute. Symptoms caused by pure venous compression (venous thoracic outlet syndrome) occur in 1.5% of patients and are manifested as axillary-subclavian vein thrombosis, usually in young patients engaged in vigorous physical activity that emphasizes upper limb and shoulder motion (such as cricket, tennis, and baseball). Arterial thoracic outlet syndrome is very rare and may be suspected if the patient presents with claudication of the arm, coldness, and ischemia of a finger or a hand. Individuals who have congenital bone or fibromuscular variations at these spaces and experience trauma are at risk for development of thoracic outlet syndrome. Anatomic variations and anomalies probably play a secondary role in the etiology. Congenital bands and ligaments are observed in a large majority of patients with thoracic outlet syndrome, and nine different types have been recognized [1]. In a human cadaver study, only 10% had a bilaterally normal anatomy. Anatomic anomalies of the thoracic-cervical-axillary region were found in 60% of human fetuses [2]. It is suggested that anatomic abnormalities confer a predisposition to symptoms of thoracic outlet syndrome after stress or injury [3]. Variation in the course of the brachial plexus that may predispose to symptoms of thoracic outlet syndrome has also been presented. Cervical ribs are regarded as predisposing factors, and a prevalence of cervical ribs was found to be 2.21% in a London population [4]. However, cervical ribs are present since birth. In 80% of patients with cervical ribs, symptoms did not develop until after a neck injury. Post-traumatic thoracic outlet syndrome has been presented in several articles [57].

According to Roos [1], anomalies are always the reason behind symptoms of thoracic outlet syndrome. However, only a few other surgeons have observed such anomalies. In the case of the first rib, the costovertebral and costotransverse joints allow a fair amount of rotation to take place along the long axis of the rib. Moreover, this rib has attached to it the anterior and middle scalene muscles, which act either by raising the thorax or by flexing and rotating the cervical part of the spine. In consequence, this first rib bears more stresses and strains than any of the other ribs, and these are greatest at the costotransverse joint [8]. Osteoarthritic changes are found more frequently in the costotransverse joint of the first rib. The lack of a superior supporting ligament may explain why this joint of the first rib is relatively weaker than those of the other ribs [8].

The elevation of the ribs during inspiration increases the anteroposterior diameter of the upper thorax. The range of this motion is reduced in older people. A disturbance of the function of the upper thoracic aperture will predispose to thoracic outlet syndrome symptoms. A dysfunction of the first rib at the costotransverse joint causes a restricted movement of the first rib [9]. In patients with thoracic outlet syndrome, the C8 and T1 nerve roots are most commonly affected. These roots constitute the part of the brachial plexus closest to the costotransverse joint. The stellate ganglion is located in the immediate vicinity of the first costotransverse joint and has numerous connections to the C8 and T1 roots. Minimal trauma associated with static, repetitive work, especially in young women, can cause abnormal stress on the upper aperture, and the poorly stabilized first rib can subluxate at the costotransverse joint. A subluxation at the first costotransverse joint could irritate the nerve roots C8 and T1 emerging in front of this joint. This irritation could explain the predominantly subjective pain and sensory loss in the ulnar distribution. The weakness of the hand and the various symptoms resembling complex regional pain syndrome may be explained by the irritation of the stellate ganglion.


True neurologic thoracic outlet syndrome is manifested with a long history of sensory symptoms, mainly along the medial forearm, associated with hand weakness and wasting, particularly of the thenar muscles (Fig. 115.2). In the upper plexus type presented by Roos [1], pain is felt over the brachial plexus radiating from the ear, through the anterior cervical region, over the clavicle into the upper part of the chest, posteriorly into the rhomboid and scapular areas, across the trapezius, and down the outer arm into the radial aspect of the forearm in a C5-C6 distribution. In the lower plexus type, pain is felt in the supraclavicular and infraclavicular fossae, radiating into the upper part of the back and from the axilla down the inner arm along the ulnar nerve distribution.

FIGURE 115.2 The hands of a patient with true neurologic thoracic outlet syndrome. Wasting of the muscles is clearly shown in the left hand.

In contrast, disputed neurologic thoracic outlet syndrome possesses none of these characteristics. The most common symptoms are pain and paresthesias in an ulnar distribution and numbness, tingling, weakness, or dysfunction of the hand. The list of symptoms attributed to disputed neurologic thoracic outlet syndrome is long. These patients are often told by their physicians that their symptoms are exaggerated or that their complaints are not real. Coldness, easy fatigability, ischemia of a finger or a hand, and pallor on elevation are considered to be symptoms of arterial origin. Swelling, discoloration, and a heavy feeling in the hand are considered to be symptoms of venous origin. Swelling, hyperesthesia, discoloration, and a feeling of alternate cold and warm could also be signs of complex regional pain syndrome. Traction on the stellate ganglion has also been considered a possible cause of pain in these patients [8]. In general, in the absence of peripheral emboli, most “vascular symptoms” or “Raynaud phenomena” probably result from irritation of the sympathetic nerves rather than from compression of the subclavian artery in the thoracic outlet. A common feature of the symptoms is their intermittence and provocation by use of the arm above shoulder level. Aggravation of the symptoms often occurs after rather than during exercise.

Physical Examination

The diagnosis of thoracic outlet syndrome is a clinical one based on a detailed history and physical examination. This takes time and effort. Years of inappropriate diagnosis and ineffective therapy take a heavy toll on these patients. In the physical examination, the individual as a whole must be taken into consideration. One must remember that many of these patients have some psychological complaints. A thorough clinical examination including a logical explanation for the symptoms will often relieve the psychic burden.

The physical examination starts with an inspection of the neck, shoulders, and upper extremities. Color, muscle atrophy, edema, temperature, and nails are examined. This examination requires the patient to be examined with the shirt off. The cervical spine is then examined to exclude symptoms of cervical origin caused by a cervical disc or spondylarthrotic intervertebral foramen. A typical pain radiculation in C5 to C8 distribution indicates that a nerve root irritation is present. A local distribution of pain with neck extension indicates a facet joint problem.

A neurologic examination is performed to include sensory testing, muscle strength testing (C5-C8), and reflexes. Tinel sign is tested to exclude carpal tunnel syndrome. Palpation of the median, ulnar, and radial nerves from the axilla to the hand may reveal tenderness. This tenderness will vanish if a successful therapy is administered [10].

Almost all clinical tests used in the examination of the patient with thoracic outlet syndrome aim to provoke the symptoms felt by the patient, presuming that the compressing structure may be provoked to irritate the neurovascular bundle in the area of the thoracic outlet during the test. These maneuvers are unreliable in general [11]. A clinical test in extensive use is the Adson test [12]. With the patient sitting, hands resting on the thighs, both radial pulses are simultaneously palpated. During forced inspiration, hyperextension of the neck, and turning of the head to the affected side, the radial pulse is palpated for obliteration, and auscultation is done for supraclavicular bruit. The test has changed during the years. In 1927, when Adson described his test, the vascular changes were considered to be pathognomonic of thoracic outlet syndrome. Later, neurologic changes occurred more frequently than vascular ones, and these can be detected better when the head is rotated to the contralateral rather than the ipsilateral side, as initially described.

Radial pulse obliteration or subclavian bruit is found in 69% of normal patients [13]. All studies clearly indicate that pulse obliteration with the arm and head in various positions is a normal finding and has no relation to thoracic outlet syndrome.

In the hyperabduction test, symptoms are reproduced by hyperabduction of the arm. However, more than 80% of normal individuals experience obliteration of the radial pulse during this test [14]. In the exaggerated military maneuver, also called Eden test, symptoms are reproduced by pulling back the acromioclavicular joint in an exaggerated military “attention” position. The neurovascular structures could be compressed between the first rib and the clavicle, without any anatomic predisposing factors. This maneuver is also referred to as the costoclavicular test. Arterial compression is found in 60% of asymptomatic individuals by this test.

In the abduction–external rotation test, also called Roos test or elevated arm stress test (EAST), the hands are in the “stick up” position and are then repeatedly opened and closed for 3 minutes. Roos [1

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