Vascular Surgery

22 SAJS VOL. 53 NO. 1 MARCH 2015 Thoracic outlet syndrome (TOS) is controversial in terms of definition, anatomy, aetiology and treatment. The definition of TOS is generally accepted as ‘upper extremity symptoms due to compression of the neurovascular bundle in the area of the neck just above the first rib’.[1] The thoracic outlet, also known as the cervicothoracobrachial junction, consists of three important compartments through which vital structures such as nerves and blood vessels run. These compartments are the interscalene space, the costoclavicular space and the retropectoralis minor space. Neurogenic TOS, resulting from nerve compression, is the most common pathology, accounting for >95% of TOS cases. [1] The majority of cases result from anatomical distortion at the interscalene triangle.[2] For various reasons, the described anatomical spaces transform and evolve into ‘entrapment spaces’. The aetiology of this is largely unclear, but it is thought that changes may be congenital or acquired, and that these alterations involve either the bony structures or the soft tissues.[1,2] The observation of anatomical anomalies, especially of the brachial plexus, initiated this study. The aetiology of neurogenic TOS is multifactorial, with bony tissue abnormalities and soft-tissue abnormalities described as definite contributors to the syndrome. These abnormalities contribute to the syndrome by altering the space within which the brachial plexus trunks run. Brachial plexus anomalies, however, have not classically been described in direct association with TOS. Recent interest in brachial plexus anomalies suggests them as a cause for various pathologies, including TOS.[3] We hypothesised that brachial plexus anomalies, alone or in conjunction with additional pathology, are almost always associated with neurogenic TOS. The objective of this study was to attempt to clearly define anatomical anomalies causing TOS.