Anatomic Features

The subclavian artery is typically compressed as it courses between the first rib inferiorly, the anterior scalene muscle anteriorly, and the middle scalene muscle and the brachial plexus posteriorly. Arterial TOS occurs much less commonly as a result of compression of the axillary artery by the pectoralis minor muscle anteriorly or by the humeral head posteriorly. The fact is that most cases of arterial TOS are associated with the presence of cervical ribs, anomalous first ribs, or deformities secondary to clavicular or rib fractures or orthopedic surgery.

Complete cervical ribs typically elevate the floor of the thoracic outlet, significantly increasing the compression of the subclavian artery by the anterior scalene muscle (Figure 1). Cervical ribs are found in less than 0.5% of the general population, and are twice as common in women as in men. Their presence is associated with histopathologic changes in the brachial plexus, including fibrosis, vascular hyalinization, mucinous degeneration, and intraneural collagen nodules. Changes are not seen in nerve specimens of patients without cervical ribs. This observation suggests that in cases of arterial compression by a cervical rib, nerve compression is likely also present.

The incidence of cervical ribs reported in large surgical series of neurogenic TOS is between 4% and 5%. In my experience with patients operated on for all types of TOS, the overall incidence of cervical rib or other bony anomaly was 25%, whereas it was 60% among patients with arterial TOS. This difference might reflect practice referral patterns, but may be a result of more stringent surgical criteria for neurogenic TOS.

Clinical Presentation

In young patients with symptoms of acute or chronic upper extremity ischemia, the diagnosis of arterial TOS should be always entertained. The most obvious clinical presentation of TOS is acute upper extremity ischemia with a subclavian artery aneurysm. However, unless frank ischemia occurs, many patients with arterial TOS are asymptomatic. Some have subtle extremity symptoms that do not suggest arterial TOS until imaging studies support such a diagnosis. For this reason, most reports dealing with arterial TOS almost exclusively include cases presenting with arterial embolization.

In my experience with 41 patients operated on for arterial TOS, 12 patients experienced subclavian aneurysms; 24 had severe positional arterial stenosis, with poststenotic dilatation in half of the cases; two had fixed subclavian artery stenoses; two had luminal filling defects; and one had subclavian arterial occlusion. Clinically, 13 patients (32%) presented with acute ischemia, 11 of whom harbored a subclavian aneurysm. Chronic arm symptoms affected 27 patients, of whom 24 had subclavian positional stenosis and/or poststenotic dilatation, one had chronic subclavian occlusion, and two had axillary artery compression. One patient with a subclavian aneurysm had no symptoms.

Some patients complain of chronic symptoms difficult to differentiate from those of neurogenic compression. Arterial and neurogenic compression within the thoracic outlet are not always separate entities. The tight anatomic relationship between the subclavian and axillary arteries with the brachial plexus is such that in many cases both structures, although to different degrees, are pathologically compressed. For this reason, in some patients, arterial compression may be diagnosed and treated as neurogenic TOS. In the absence of acute arterial complications, significant arterial compression of the subclavian or axillary artery can produce symptomatology suggestive of upper extremity claudication, mainly with the use of the arm in elevated positions. Occasionally, patients experience hand and forearm symptoms from minor embolic events that are often misdiagnosed, unless an arterial evaluation is conducted.

The pathologic vascular changes that occur in patients with arterial TOS are progressive and can be classified in stages. Stage 1 patients have severe or complete arterial obstruction seen only with positional changes of the upper extremity, typically with arm abduction and external rotation, with the artery appearing normal in neutral position. Stage 2 patients experience arterial changes in the neutral position in the form of mild poststenotic dilatation, fixed stenosis, or luminal irregularities. Stage 3 patients have true arterial aneurysms or with complete occlusion of the subclavian or axillary arteries (Figures 2 and 3). Although it is unusual, some patients with axillary artery compression have aneurysms at the origin of the circumflex humeral arteries.

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