Thoracic Outlet Syndrome in Emergency Medicine

Updated: Aug 25, 2020
  • Author: Andrew K Chang, MD, MS; Chief Editor: Erik D Schraga, MD  more...
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Thoracic outlet syndrome (TOS) is a broad term that refers to compression of the neurovascular structures in the area just above the first rib and behind the clavicle that results in upper extremity symptoms. It represents a constellation of symptoms. The cause, diagnosis, and treatment are controversial. The brachial plexus (95%), subclavian vein (4%), and subclavian artery (1%) are affected such that TOS is usually classified into neurogenic, venous, and arterial forms. [1] Most presentations to the emergency department (ED) are nonemergent and require only symptomatic treatment and referral.



The brachial plexus trunks and subclavian vessels are subject to compression or irritation as they course through three narrow passageways from the base of the neck toward the axilla and the proximal arm. The most important of these passageways is the interscalene triangle, which is also the most proximal. This triangle is bordered by the anterior scalene muscle anteriorly, the middle scalene muscle posteriorly, and the medial surface of the first rib inferiorly. This area may be small at rest and may become even smaller with certain provocative maneuvers. Anomalous structures, such as fibrous bands, cervical ribs, and anomalous muscles, may constrict this triangle further. Repetitive trauma to the plexus elements, particularly the lower trunk and C8-T1 spinal nerves, is thought to play an important role in the pathogenesis of thoracic outlet syndrome (TOS).

The second passageway is the costoclavicular triangle, which is bordered anteriorly by the middle third of the clavicle, posteromedially by the first rib, and posterolaterally by the upper border of the scapula.

The last passageway is the subcoracoid space beneath the coracoid process just deep to the pectoralis minor tendon.



Common etiologies for each anatomic form of thoracic outlet syndrome (TOS) include the following:

  • Neurogenic TOS: Etiology is most often a hyperextension neck injury, such as whiplash after a motor vehicle accident or a fall. [2] Other causes include repetitive injury most often form sitting at a keyboard for long hours.

  • Venous TOS: Etiology is obstruction of the subclavian vein, either thrombotic or nonthrombotic. [2] The cause is a combination of predisposing and precipitating factors. The predisposition is congenital anatomic narrowing at the point where the subclavian and jugular veins join to form the innominate vein. The precipitating factor that leads to thrombosis is excessive activity of the arm such as throwing a baseball, swimming, weight lifting, or working with the arms elevated. Coagulopathies can also be a precipitating cause.

  • Arterial TOS: Etiology is subclavian artery stenosis or aneurysm with thrombus formation and distal emboli usually due to a cervical rib or anomalous first rib. [2] The aneurysm and stenosis are usually asymptomatic until embolization occurs.



United States data

Because no objective confirmatory test is available for thoracic outlet syndrome (TOS), there is much disagreement with regards to its true incidence. Reported figures range from 3-80 cases per 1000 people. [3, 4]

Sex- and age-related demographics

Overall, the entity is approximately three times more common in women than in men. However, the sex ratio varies depending on the type of TOS (eg, neurologic, venous, arterial), as follows:

  • Neurologic - Female-to-male ratio approximately 3.5:1

  • Venous - More common in males than in females

  • Arterial - No gender predilection

The onset of symptoms usually occurs in persons aged 20-50 years. Although infrequent, TOS has been reported in adolescents. [5]



Neurologic thoracic outlet syndrome (TOS) is generally neither progressive nor likely to resolve spontaneously.

Arterial or venous TOS usually has a good outcome with adequate treatment.


Neurologic complications include chronic pain.

Arterial complications include thrombosis, thromboembolism, acute ischemia, and poststenotic aneurysm formation.

Venous thrombosis may develop.