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THORACIC OUTLET SYNDROME DIAGNOSIS & TREATMENT THORACIC
OUTLET SYNDROME: AN OVERVIEW OF DIAGNOSIS AND TREATMENT
BY TERI BAYFORD, MCSP
Due to the controversy surrounding even the existence of thoracic outlet syndrome (TOS) there has been a relative void of information on how to treat this syndrome. Four structures may be compromised in this syndrome either separately or in combination. These structures are:
1. The subclavian vein (1) - compromise of the subclavian vein is thought to occur in only 2-3% of cases (2,3,4) 2. The subclavian artery - which is thought to be the responsible structure in less than 1% up to 2% of cases, (2,4) 3. The brachial plexus - which is stated as being responsible for between 90- 97% of symptomatic patients (5,6,4) 4. Sympathetic fibres - the sites of compromise of the sympathetic fibres may be the stellate ganglion (lower cervical ganglion) or the sympathetic fibres of the lower trunk of the brachial plexus. Compromise of either the axillary
vein or axillary artery (these being the distal extensions of the subclavian vein and artery respectively) also lie within the TOS umbrella. The controversy surrounding
this syndrome mostly concerns the neurogenic form of TOS. Traditionally the existence of objective electrodiagnostic signs to confirm the subjective symptoms have been demanded in order to confirm a diagnosis. The problem with using an electrodiagnositc test in the diagnosis of the neurological form of thoracic outlet syndrome is that symptoms may exist without permanent morphological change in the neural structure. The conduction velocity investigated
successful conservative treatment of neurogenic TOS is possible if applied within specific guidelines which carefully take into account the pathology underlying the syndrome.
AETIOLOGY Figure 1: Structures involved in TOS
may therefore remain within normal parameters. This may occur because the compromise of the neural structure may be functional and intermittent with only a short segment of the nerve involved (7). MRI investigation may also prove fruitless in objectively confirming dynamic compromise. The scanners themselves may prevent the patient being positioned in a posture that provokes the symptoms for example with 90 degrees upper limb abduction. Vascular presentations may
never be encountered in practice but because of the serious consequences of the vascular syndromes (8), the practitioner must be able to recognise the symptoms and be confident in referring for appropriate investigations to exclude this diagnosis To the sportsman correct timing
is everything and so is the case with the treatment of TOS. Despite the controversy around the existence of this syndrome in the 21st century,
The aetiology of neurogenic TOS is either compression (9) or traction of the brachial plexus or a combination of the two (10). Surrounding structures such as the subclavian artery, subclavian vein, brachial plexus and stellate ganglion may be the source of compromise (Fig.2). Pathognomonic static postures or dynamic activities may be responsible for contributing to the compromise. If one portion of the brachial plexus is compressed this site, by virtue of the compression and the resultant loss of gliding of the neural structure at the compressed site, may lead to a secondary traction injury along the length of the neural structure. If a nerve can not glide the resulting traction can lead to injury (11). In order to understand the aetiology of TOS the anatomy of the area must first be revisited.
ANATOMY
The thoracic outlet (which is a misnomer as anatomically this anatomical boundary is the thoracic inlet (12)) is bordered by the clavicle,
EVERYTHING AND SO IS THE CASE WITH THE TREATMENT OF TOS
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TO THE SPORTSMAN CORRECT TIMING IS
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