Previous Page
ASSESSMENT VASCULAR/SHOULDER INJURIES
VASCULAR THORACIC OUTLET SYNDROME (SUBCLAVIAN ARTERY) A common site of upper-limb arterial compromise is the subclavian artery (8), with compression at the scalene triangle or the costoclavicular space, commonly termed vascular thoracic outlet syndrome (vTOS). The scalene triangle is bordered by the anterior scalene, the middle scalene and the first rib, and the costoclavicular space exists between the first rib and the clavicle (Figs. 1 & 2). Mechanisms and structures responsible for compression of the subclavian artery have been postulated and include cervical ribs, anomalous first ribs, clavicular fractures and fibrous bands within the soft tissue of the anterior scalene muscle (9–12). The reported incidence of vTOS varies considerably, from 4% to over 20% of patients presenting with thoracic outlet type symptoms (13–15). The clinical
HYPERABDUCTION SYNDROME (AXILLARY ARTERY) Anatomically, the axillary artery is divided into three segments. The first portion arises from underneath the clavicle, the second portion dips underneath pectoralis minor, and the third portion lies anterior and inferior to the humeral head (Figs. 3 & 4). The latter two portions are thought to be compressed through movement of the upper limb into abduction, external rotation and horizontal extension – hence the term ‘hyperabduction syndrome’. Case studies reporting axillary artery thrombosis or aneurysm formation most commonly describe overhead-throwing athletes, such as baseball pitchers and handball, tennis and volleyball players (5,7,17–20). However, blood-flow limitations can also occur in non-athletes who perform repetitive overhead motions (8,10). Due to the abundant collateral circulation of the upper limb, symptoms (early- onset fatigue, coolness, paraesthesia, anaesthesia, pain) of arterial flow limitations due to thrombosis or aneurysm formation may present only with extreme physical exertion or not at all, until dislodged emboli travel distally and occlude smaller peripheral arteries, resulting in hand and digit
Figure 1: Costoclavicular space
presentation is variable, depending on the extent of compression of neural or vascular structures. In general, however, patients complain of some or all of the following symptoms, which present often intermittently, in a non- dermatomal pattern throughout the upper limb: pain, fatigue, paraesthesia, anaesthesia, weakness and coolness.
Figure 2: Scalene triangle with subclavian artery Confusingly, the term vTOS is
also used inconsistently to describe compression of the axillary artery. However, for the purposes of this article, we use vTOS to mean compression of the subclavian artery; we refer to compression of the axillary artery as hyperabduction syndrome, as originally described by Wright (16).
Figure 3: Axillary artery
ischaemia (10). The true prevalence of axillary artery pathology, ie. localised vessel damage resulting in thrombosis or aneurysm, is unknown. The proposed mechanism for
compressive trauma of the second portion of the axillary artery is a tight or hypertrophied pectoralis minor muscle (21,22) combined with hyperabduction. For the third portion, it is proposed that, through shoulder abduction, external rotation and horizontal extension, the artery is compressed by the humeral head, possibly as a result of excessive translation at the glenohumeral joint (5,10,20,22–24). Repeated compression from the humeral head is thought to be the cause of damage to the vessel wall, leading to thrombosis, aneurysm formation and endothelial dysfunction.
Figure 4: Pectoralis minor sitting over axillary artery
In addition to these proposed mechanisms, an anatomical anomaly, termed the ‘arch of Langer’, has also been suggested as a cause of axillary artery compression (25). The arch of Langer is a muscular or fibrous slip that originates from latissimus dorsi, with variable insertions into the pectoralis major muscle, the coracobrachialis muscle, the coracoid process, the intertubercular sulcus of the humerus, and the pectoralis minor muscle. The fibres traverse across the axilla and have the potential to compress the underlying neurovascular bundle. In lean individuals, this anatomical anomaly can be detected with the arm in the hyperabducted position and with palpation over the lateral border of latissimus dorsi. A palpable
23