The term thoracic outlet syndrome (TOS) describes a condition arising from compression of the subclavian artery, the subclavian vein, and the brachial plexus between the scalene muscles and the first rib (Fig. 142-1). There exists a wide spectrum of patient symptoms, which include vascular and/or neurologic signs. Neurogenic TOS accounts for most cases, whereas venous (2%–3%) and arterial TOS (1%) are relatively rare. Objective vascular studies such as venograms and arteriograms may identify signs of vascular compromise to aid in the diagnosis of arterial or venous TOS, but neurologic findings are more varied, and there is no single specific test to diagnose neurogenic TOS.
Anatomy relevant to thoracic outlet obstruction.
The neurologic signs and symptoms of neurogenic TOS can range from mild paresthesias and numbness to intrinsic hand muscle atrophy. There is little controversy in this latter group of patients regarding diagnosis or treatment. However, the diagnosis of TOS is controversial in patients with the neurologic-type complaints of paresthesias, numbness, and pain but with no positive objective test to identify the cause. This chapter focuses on the management and surgical therapy of neurogenic TOS.
Many surgeons are highly skeptical of the merits of surgical intervention for patients with TOS because of the high incidence of major complications and the variable reports of successful outcome. Exceptions to this rule include uncommon cases involving vascular compromise and even rarer cases involving severe neurologic muscle atrophy in the hand.1 Patients with intrinsic hand muscle atrophy that localizes to the level of the brachial plexus with no distal sites of nerve compression are likely to have a cervical rib or anomalous ligamentous band(s) that compresses the lower trunk of the brachial plexus. Compression of the artery may lead to poststenotic dilatation and subsequent thrombosis and embolization. Patients with symptomatic arterial TOS may present with signs and symptoms of microembolization in the digits on the affected side. Venous compression, which usually occurs at the junction of the clavicle and first rib, leads to occlusion and thrombosis. Patients characteristically become symptomatic with evidence of venous congestion after a precipitating physical activity (Paget–Schroetter syndrome).
The clinical syndrome (TOS) derives from three anatomic areas in which compression of the neurovascular structures may occur: the scalene triangle, the costoclavicular space, and the subcoracoid space (Fig. 142-2). The scalene triangle is the region bordered by the anterior scalene muscle, the middle scalene muscle, and the first rib. The brachial plexus and subclavian artery pass over the first rib between the scalene muscles, and the subclavian vein also passes over the first rib but external to the scalene triangle. The costoclavicular space is bordered by the clavicle and the first rib, with the costoclavicular ligament located anteriorly and the edge of the middle scalene muscle ...