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Thoracic Outlet Syndrome Imaging

Practice Essentials

Thoracic outlet syndromes (TOSs) are caused by compression of the neurovascular structures passing through the thoracic outlet (see the images below). Various examination techniques can be used to distinguish among the etiologies of the types of thoracic outlet syndrome. Ultrasonography is readily available and relatively inexpensive, and it can be performed in both arterial and venous thoracic outlet syndrome. The American College of Radiology Appropriateness Criteria recommendations suggest that CT and MR angiography or venography are both appropriate in establishing the diagnosis of TOS.
 CT and MRI are typically performed as 2-step procedures (neutral position and arm abduction) to reproduce the vascular compression seen on provocative maneuvers. CT angiography or venography provides superior analysis of the vasculature in relation to the bony structures, whereas MR angiography or venography is more efficient in the depiction of accessory muscles, muscle hypertrophy, and fibrous bands
. Angiography and venography remain the criterion standards for the radiologic diagnosis of these conditions, and they have the added benefit of enabling potential endovascular treatment.

The findings of the Allen maneuver, the hyperabduction maneuver, are considered positive when the radial pulse disappears during extreme abduction of the arm. This finding, however, is also present in individuals who do not have thoracic outlet syndrome and in individuals with asymptomatic cervical ribs; therefore, this finding is not diagnostic.

A positive Adson finding occurs when the radial pulse is reduced or disappears or when the blood pressure changes with the patient (1) in a sitting position, (2) holding a deep inspiration, (3) fully extending the neck, or (4) turning the head toward the ipsilateral and contralateral sides. Some investigators believe that the cause of these findings is compression by the anterior scalene muscle. A supraclavicular bruit may be audible with this maneuver, and it is believed to result from an associated subclavian stenosis.

The costoclavicular maneuver is performed when the patient assumes an exaggerated military posture and positions his or her shoulders back and downward; this positioning induces compression between the clavicle and the first rib.

An angiogram in a 35-year-old woman with right arm

An angiogram in a 35-year-old woman with right arm ischemia that demonstrates right subclavian artery occlusion from the medial margin of the first rib to the axillary artery at the level of the humeral head. The patient was successfully treated with right first rib resection.

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This venogram shows occlusion of the right subclav

This venogram shows occlusion of the right subclavian vein extending to the first rib, with multiple collateral vessels.

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These syndromes can be classified into 3 subgroups, based on the neurologic or vascular structures involved. The specific clinical presentations, demographics, treatments, and outcomes vary among the subgroups. The 3 subgroups are as follows:

Neurologic thoracic outlet syndrome (nTOS) is responsible for approximately 95% of cases of thoracic outlet syndrome. This type is secondary to compression of the brachial plexus caused by various soft tissue and bony abnormalities at the point where the nerves pass between the anterior and middle scalene muscles.
 

Venous thoracic outlet syndrome (vTOS) results from subclavian vein compression, often between the first rib, costoclavicular ligament, and subclavius tendon within the costoclavicular space. It is seen in approximately 3% of cases.
 Repetitive arm movements traumatize the vein, causing posttraumatic inflammation, focal intimal fibrosis, stenosis, blood flow stasis, and eventual thrombosis leading to acute symptoms of upper extremity deep venous thrombosis. This is referred to as effort thrombosis or Paget-Schroetter syndrome and is often observed in young individuals and competitive athletes who engage in physical activities requiring repetitive arm and shoulder movements. Other terms for this condition include spontaneous thrombosis and traumatic thrombosis.

Arterial thoracic outlet syndrome (aTOS) is the least common form of thoracic outlet syndrome and is caused by subclavian artery (SCA) compression. It is seen in approximately 1-2% of cases.
This type is associated with the most serious complications, including limb ischemia (which may result in the loss of the affected upper extremity) (see the images below).

A 45-year-old woman with symptoms of progressive r

A 45-year-old woman with symptoms of progressive right arm ischemia. Occlusion of the right subclavian artery near the junction between the clavicle and first rib is shown.

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An angiogram obtained in a 45-year-old woman with

An angiogram obtained in a 45-year-old woman with progressive symptoms of right arm ischemia after 16 hours of thrombolysis that demonstrates a tight residual stenosis in the right subclavian artery. The patient presented emergently 2 days later with repeat occlusion of the right subclavian artery in the same location and was treated with surgical bypass (same patient as in the previous image).

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Rarely, compression of a combination of structures may be responsible for the symptoms.  A subset of patients with mixed neurovascular syndrome has been reported. These patients present with nTOS with co-existing arterial involvement. These patients demonstrate better outcomes than those with nTOS only after surgical intervention, with 100% showing improvement or resolution of neurogenic symptoms postoperatively in one study.
 

This article is limited to the vascular causes of thoracic outlet syndrome. Unlike arterial and venous TOS, nTOS diagnosis is largely clinical and subjective in nature, with no definitive imaging or diagnostic studies available to confirm its presence.
 

Despite considerable investigation into identifying a clinical maneuver for the accurate diagnosis of vascular thoracic outlet syndrome, no clinical test has been shown to have a consistently high degree of accuracy. The same positive findings are occasionally found in individuals without vascular thoracic outlet syndrome; therefore, the clinicians should consider a positive result at clinical examination in context with the clinical history and the results of other diagnostic tests.

Intervention

Prognosis and treatment differ for the 2 types of venous thoracic outlet syndrome.

Patients with primary venous thrombosis more commonly present with acute symptoms, including arm swelling and pain, which often limit their activity. Anticoagulant therapy reduces the extension of thrombus, as well as the associated (minute) risk of pulmonary embolism; however, multiple authors have demonstrated minimal long-term benefits of anticoagulation.

Intervention is often performed early for rapid symptomatic relief, especially in an otherwise healthy patient who requires full use of the affected arm. Catheter-directed thrombolysis and mechanical thrombectomy have significantly expanded the nonsurgical options for treatment. With surgical thoracic outlet decompression, the success rate has averaged 81%. Other advantages to catheter-directed thrombolysis include the ability to perform diagnostic venograms at the time of thrombolysis in various positions to provoke the symptoms and the ability to perform postthrombolysis venograms to document the extent of residual thrombus.

The disadvantages of thrombolysis include the risk of bleeding, which can be minimized by following prescribed dosing guidelines. Another concern is the fact that the underlying thoracic outlet compression is not addressed; therefore, a surgical procedure may still be needed later. Thrombolysis is most effective if performed within 7-10 days; at least 2 studies have shown a significant decrease in the effectiveness of thrombolysis after 10 days.

The timing of thoracic outlet decompressive surgery after thrombolysis has been a source of considerable debate in the literature. The most common approach involves a waiting period of approximately 3 weeks, during which the patient received oral anticoagulation and the vascular endothelium is allowed to heal. Then, decompressive surgery is performed if a postthrombolysis venogram shows focal extrinsic compression. If extrinsic compression resulting from an anatomic cause is not noted on the follow-up venogram, the need for surgical intervention is less clear.

In a survey by Rutherford and Hurlbert, 86% of vascular surgeons surveyed opted for a conservative approach in this scenario, with anticoagulation therapy administered for 3-6 months, during which the patient is observed for evidence of recurrent thrombosis. If the postthrombolysis venogram reveals an intrinsic stenosis with or without extrinsic compression, percutaneous venoplasty augmented by stent placement becomes an option, although the precise role of venoplasty and stent use remains an area of considerable disagreement.

Most authors do not recommend stent placement without surgical decompression because the stent itself may be compressed or become fragmented by the thoracic outlet narrowing. Dowling et al reported a case of venous thoracic outlet syndrome treated with thrombolysis, angioplasty, and stent placement without immediate first-rib resection. The case was later complicated by stent fracture.
Meier et al reported a series of 6 patients who underwent venous stent placements immediately after thrombolysis for venous thoracic outlet syndrome and 2 patients who underwent delayed stent procedures. Two of the 6 patients who underwent immediate stent placement did not undergo immediate surgical rib resection, and both patients had the complication of stent fracture. Long-term (1-3 yr) patency was achieved in 6 of the 8 patients.

The timing of the intervention continues to be debated. Some authors recommend a phase of venous intimal healing after thrombolysis and before venoplasty or stent placement to reduce further damage to the vessel resulting in recurrent thrombosis. Other authors have proposed the use of venoplasty only after surgical resection of the first rib, when the source of the thoracic outlet compression has been removed. Molina has proposed that thrombolysis be performed first, followed by emergency surgery, for the highest likelihood of avoiding recurrent strictures and chronic symptoms.

Kreienberg et al reported their outcomes that support early surgical and radiologic intervention. Twenty-three patients with venous thoracic outlet syndrome were treated with thrombolysis, followed by immediate (within 24 hr) surgical thoracic inlet decompression (including rib resection and removal of the anterior scalene muscle) and then angioplasty within 24 hours. Stents were placed to treat residual venous stenosis (>50%) in 14 patients. Of the veins treated with only angioplasty, all were patent at a mean follow-up of 4 years. Of those additionally treated with stent placement, 9 were patent at a mean follow-up of 3.5 years. No stent fractures were observed. Occluded stents were associated with longer stenoses and hypercoagulable states. From these findings, Kreienberg et al concluded that early surgical intervention followed by early radiologic intervention is safe and effective and that subclavian venous stent use is effective in short venous stenoses.

If the postthrombolysis venogram demonstrates inadequate thrombolysis or residual obstruction, most vascular surgeons favor discontinuation of thrombolysis and initiation of a conservative treatment approach with anticoagulation, elevation, and support of the arm.

A venogram of a 20-year-old woman with right arm s

A venogram of a 20-year-old woman with right arm swelling that shows occlusion of the right subclavian vein as it passes through the thoracic inlet. A wire was advanced across the occlusion into the superior vena cava.

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A venogram obtained in a 20-year-old woman with ri

A venogram obtained in a 20-year-old woman with right arm swelling after thrombolysis, venoplasty, and stent placement that demonstrates a patent right subclavian vein. Although venous stent placement remains controversial, this patient was doing well at 1-year follow-up (same patient as in the previous image).

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If the patient remains symptomatic with residual stenosis, 80% of vascular surgeons favor surgical intervention with short stenosis (66% favoring jugular vein turndown, 14% favoring claviculectomy) and 48% favor a bypass (either saphenous vein interposition or cephalic vein crossover) with long stenosis. These findings reflect the overall success of surgical intervention.

Secondary venous thrombosis, often associated with central venous catheters, usually occurs with an insidious onset and minimal symptoms if any. Anticoagulation with heparin, followed with the long-term administration of warfarin, is the preferred treatment. In uncomplicated cases, thrombolysis has not had a definite benefit, and it does have significant associated complications.

In patients with a definite contraindication to anticoagulation, McCarthy et al reported success with simple conservative measures such as arm elevation and compressive dressings, and they propose reserving invasive therapies, such as thrombolysis, surgical thrombectomy, and rib resection, for patients with severe symptoms not responsive to anticoagulation. Interventional therapies, such as angioplasty and thrombolysis, are often more difficult to perform in secondary venous thrombosis because these cases are more likely to be chronic.

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