CTA and Venography
Computed tomography (CT) is a valuable modality because it can be performed rapidly and effectively to depict the relationship of vascular structures to surrounding bone and muscle.47 In addition, CTA and venography provide high-quality representations of the vasculature, and 3-D reconstruction reliably identifies areas of neurovascular compression in patients with TOS.47,48 Furthermore, CT may be performed in a dynamic fashion, with the upper extremity in various positions to reproduce dynamic compression of the neurovascular structures (Figure 3A). Comparison of the images with the upper extremities in the anatomical position and elevated allows the physician to evaluate narrowing of the compartments and dynamic compression of neurovascular structures.8 CT is particularly valuable in arterial and venous TOS. In arterial TOS, the cross-sectional area or diameter of the artery can be measured to calculate the degree of stenosis.8,47 In venous TOS, dynamic narrowing of the vein can be visualized and may be associated with venous thrombosis or collateral circulation (Figure 3B). Although a variety of maneuvers is possible during CTA, the size of the CT tunnel as well as mandatory supine positioning of the patient may limit the series. Drawbacks of CT for diagnosing TOS include difficulties in analyzing the brachial plexus because of limited contrast resolution. In addition, the risks of CT (ionizing radiation, administration of iodinated contrast medium) must be considered before image acquisition.
MRI
MRI is a noninvasive and nonionizing technique that offers good resolution of the anatomical components of the thoracic outlet8 and that, because of its superior soft-tissue contrast, is the modality of choice for imaging brachial plexus nerve compression in TOS (Figure 4). Neurologic compression is identified with MRI when the fat surrounding the brachial plexus disappears.8 MRI reliably identifies the source of compression, which may include bony structures, muscle hypertrophy (scalenus, scalenus minimus, subclavius, pectoralis minor), and fibrous bands.49 Because of their craniocaudal direction, the sagittal plane is often most useful in demonstrating neurovascular compression.42 Analyzing the caliber of the vessel along its course may evaluate vascular compression, and magnetic resonance (MR) angiography and venography (Figures 5A, 5B) can often complement the findings.50 Specifically, in arterial TOS, poststenotic aneurysmal dilatation may be seen, whereas thrombosis and collateral circulation can be visualized in cases of venous TOS.50 Limitations of MRI in the diagnosis of TOS historically were similar to those of CT, and included supine positioning as well as restricted upper extremity maneuvers because of the size of the tunnel and the presence of surface coils.42 However, newer higher channel surface coils and wider bores allow for imaging in a wider range of motion, including arm hyperabduction (Figures 5C, 5D), which is often necessary to elicit pathology.
Management
Generally, therapeutic options for TOS are aimed at relieving the source of neurovascular compression. It is important that treatment be directed only toward symptomatic patients, as many patients have anatomy consistent with TOS and remain asymptomatic.5 Treatment of TOS is predominately conservative and involves a combination of patient education, activity modification, medication, and rehabilitation to promote appropriate body mechanics and posture.18
Physical Therapy
Physical therapy should be aimed at decreasing pressure on the neurovascular structures of the thoracic outlet by relaxing the scalene muscles, strengthening the shoulder muscles, and working on postural exercises to help the patient sit and stand straighter.51 The scalene muscles are the primary targets for TOS rehabilitation, but focus should also be given to the upper trapezius, levator scapulae, sternocleidomastoid, pectoral, and suboccipital muscles.18 Physical therapy is often combined with hydrotherapy, massage, nonsteroidal anti-inflammatory drugs, and muscle relaxants for maximal symptomatic relief. Some patients have found relief with selective anesthetic or botulinum toxin A injections in the scalene muscles.18 A minimum of 4 to 6 weeks (often 4-6 months) of physical therapy and conservative treatment should be attempted before consideration of any invasive intervention.13,18
Anticoagulation
In venous TOS with evidence of thrombus but no obstructive clot, conservative management is typically sufficient. In rare cases, however, intimal damage secondary to vascular compression in arterial and venous TOS leads to thrombus formation, impairing upper extremity perfusion and producing symptoms. Treatment guidelines for venous TOS involve catheter-directed thrombolysis within 2 weeks of symptom onset.15 Thrombolysis replaced the prior recommendation of systemic anticoagulation combined with extremity rest and elevation because anticoagulation and rest alone result in up to 75% morbidity,52,53 whereas thrombolysis reestablishes vessel patency in nearly all patients.54 After thrombolysis, patients should receive intravenous heparin, and conversion to oral anticoagulation should occur as soon as manageable. In patients with arterial TOS, the goal of treatment is revascularization to prevent or decrease ischemia. In mild arterial ischemia, catheter-directed thrombolysis can be attempted. However, the threshold for surgical thromboembolectomy must remain low, as acute upper extremity ischemia may result in compartment syndrome and permanent loss of function.13 Fixed arterial lesions, whether occlusive or aneurysmal, are an absolute indication for thromboembolectomy with possible thoracic outlet decompression.13