Thoracic Outlet Syndrome
Thoracic Outlet Syndrome
Summary
Thoracic outlet syndrome (TOS) refers to a group of conditions that produce varying neurologic or vascular symptoms depending on the etiology. Etiologies include compression of neurologic or vascular structures at various anatomical sites in the upper extremity with neurologic involvement being far more common. The diagnosis of thoracic outlet syndrome is largely clinical, with clinical history and physical exam findings being the most sensitive and specific. The majority of cases can be treated successfully with nonoperative management. Surgery, which aims to decompress sites of anatomic compression, may be helpful in patients with symptoms refractory to nonoperative treatment.
General overview
Two separates entities:
- Neurogenic thoracic outlet syndrome (nTOS)
- Vascular thoracic outlet syndrome (vTOS).
Caused by anatomical sites of compression of nervous structures/brachial plexus (nTOS) or shoulder girdle vessels (vTOS)
Incidence is 1 to 2% of general population:
nTOS is more common (19:1).
More common in women than men (3.5:1):
Theoretical risk factors are long neck and drooping shoulders.
Clinical symptoms include upper extremity pain, paresthesias, numbness, weakness, fatigability, heaviness, swelling, discoloration, and Raynaud phenomenon:
Pain and paresthesias most common.
Treatment:
Operative versus nonoperative management depending on cause.
Anatomy
Nervous tissue:
Brachial plexus:
Five roots: C5, C6, C7, C8, T1
Three trunks: Superior, middle, and inferior
Six divisions: Anterior and posterior divisions of three trunks
Three cords: Posterior, lateral, and medial
Five branches: Median, axillary, radial, musculocutaneous, and ulnar nerves
Lower trunk (C8–T1) > upper trunk (C5–C7) involvement in nTOS.
Vasculature:
Subclavian vein:
Runs anterior to interscalene triangle proximally
Becomes axillary vein after crossing first rib
Joins artery and brachial plexus in costoclavicular and retropectoralis minor space.
Subclavian artery:
Branches off brachiocephalic trunk
Becomes axillary artery after crossing first rib.
Axillary artery (▶Fig. 21.1):
Divided into three parts:
First: Lateral border of first rib to superior border of pectoralis minor
muscle
Second: Lies deep to the pectoralis minor muscle
Third: Extends from inferior border of the pectoralis minor muscle to the inferior border of the teres major muscle.
Fig. 21.1 Anatomy of the thoracic outlet.
 |
Sites of compression from proximal to distal (▶Fig. 21.2):
Interscalene triangle:
Anterior scalene muscle: Anterior border
Middle scalene muscle: Posterior border
First rib: Inferior border.
Costoclavicular space:
Clavicle: Anterior border
First rib: Posteromedial border
Costoclavicular ligament/scapula: Posterolateral border.
Retropectoralis minor space:
Pectoralis minor: Anterior border
Ribs 2 to 4: Posterior border
Coracoid: Superior border.
Anatomical anomalies causing TOS:
Congenital:
Soft tissue:
Variation in scalene muscle origin or insertion
Presence of scalenus minimus
Fibromuscular bands constricting inlet spaces.
Fig. 21.2 Common sites of neurologic or vascular compression are shown. From proximal to distal, these include the interscalene triangle, the costoclavicular space, and the retropectoralis space.
 |
Presence of cervical ribs
Prominent C7 vertebrae transverse processes
First rib anomalies
Vertebral anomalies.
Vascular:
Atypical vessel course and branching.
Acquired:
Osseous:
Osteochondroma of first rib/clavicle
Malunion after fracture of first rib/clavicle
Hyperostosis
Posterior sternoclavicular dislocation.
Occupational:
Repetitive overhead activity produces cumulative effects of micro
trauma.
Hypertrophy:
Hypertrophic scalene muscles.
Neurogenic thoracic outlet syndrome (nTOS)
Definition:
Compression of brachial plexus and/or distal branches
Lower trunk most commonly involved (C8–T1)
Primarily a clinical diagnosis.
Clinical presentation:
Age of onset typically between third and fifth decade of life
Wide variability in sensory or motor symptoms:
Pain, paresthesias, dysesthesia, numbness, muscle weakness, fatigability, clumsiness, and heaviness
Upper trunk (C5–C7):
Motor: Fatigue and weakness in deltoid, biceps, and triceps
Sensory: Pain in lateral neck radiating to ear and face; follows dermatomal distributions.
Lower trunk (C8–T1):
Motor: Fatigue and weakness in intrinsic part of hand:
Can lead to hand dysfunction.
Sensory: Paresthesias or dysesthesias of medial forearm, and ring
and small fingers.
Most common complaint is pain from nerve compression
Pain at rest or with activity:
Symptoms typically more pronounced with overhead activity and cervical rotation.
Evaluation:
Physical examination:
Neurovascular upper extremity examination:
Sensation, strength, reflexes, perfusion, and pulses.
Specialized tests:
Adson’s test:
Affected side: With hand on radial pulse, hyperextend shoulder/
arm and have patient turn head ipsilaterally
Decrease in pulse amplitude + reproducibility of symptoms = positive
Best sensitivity of all tests along with Roos’ test
Hoffman’s test has lowest sensitivity of all tests.
Roos’ test (Elevated Arm Stress Test = “EAST”):
With both arms at 90 degrees of abduction and external rotation, hands are slowly opened and closed for 3 minutes
Reproducibility of symptoms = positive.
Wright’s test:
Affected side: Abduct and externally rotate arm as patient inhales
deeply
Tests retropectoralis minor space
Best specificity of all tests.
Costoclavicular maneuver:
With both arms at side, retract and depress bilateral shoulders, protrude chest, and hold position
Pulse changes / reproducibility of symptoms = positive.
Imaging:
Cervical spine radiographs:
Identify spondylosis
Identify cervical ribs
Identify clavicular or first rib abnormalities.
Chest radiograph:
Identify apical tumors.
Computed tomography (CT)/Magnetic resonance imaging (MRI):
Better visualize osseous abnormalities if necessary
Confirm space occupying lesions.
Diagnostic studies:
Electromyography test/Nerve conduction study:
Inconclusive most of the time
Difficult to interpret in double crush scenario:
Compression at two different sites (i.e., costoclavicular space +
cubital tunnel).
Typically not sensitive enough until muscle atrophy is present.
Treatment:
Nonoperative:
Physical therapy:
Work on posture:
Activity modification.
Strengthening of shoulder girdle muscles:
Trapezius, serratus anterior, levator scapulae, rhomboids, and erector spinae.
Risks factors for failure of nonoperative therapy:
Obesity, worker’s compensation, and presence of carpal or cubital tunnel syndrome.
nTOS more likely to respond to nonoperative treatment compared with vTOS
Favorable response of 70% with physical therapy/exercise program
Botox injections no better than placebo saline injections.
Operative:
Surgical treatment is performed to address the anatomical structure responsible for compression/symptoms:
Scalenotomy
Scalenectomy
Cervical rib excision
First rib resection
Pectoralis minor tenotomy
Claviculectomy
Supraclavicular neuroplasty.
Supraclavicular or trans-axillary approach
Improvement in functional and outcome scores
Complication rate of 21.6% in recent systematic review
More time off work required and fewer returning to work compared with
nonoperative treatment
No significant difference in improvement, stability, and symptom progression between operative versus nonoperative treatment in a large recent study.
Vascular thoracic outlet syndrome (vTOS)
Definition:
Damage to vascular structures within the thoracic inlet
Caused by primary mechanical compression or thrombosis secondary to repetitive micro trauma
Arterial versus venous:
Arterial: Subclavian artery, axillary artery
First described by Wright in 1945 as due to compression of artery by pectoralis minor with arm in overhead position
Late sequelae can include intimal damage and subsequent thrombosis
Less common than venous vTOS (1:4).
Venous: Subclavian vein, axillary vein:
Paget-Schroetter syndrome:
First described as acute spontaneous venous thrombotic event
Recently discovered to be caused by chronic venous compressive anomaly at the thoracic outlet
Associated with repetitive upper extremity activities
Rare: 2% of all venous thromboses
Affects young, healthy, and athletic individuals (i.e., swimmers,
weightlifters).
Clinical presentation:
Arterial:
Claudication, fatigue, diminished distal upper extremity pulse, cyanosis, ischemia, night pain, and coolness.
Venous:
Dull aching pain, venous engorgement, discoloration/mottling, and palpable axillary cord.
Evaluation:
Physical examination:
Similar to nTOS with emphasis on motor function, sensation, perfusion, and pulses with subsequent changes to these with examination/speciali-zed tests.
Imaging:
Arteriogram/venography:
Gold standard
Includes magnetic resonance angiography, computed tomography angiography, and direct catheter-based arteriography.
Arterial/venous duplex ultrasound:
Cost effective
Easy to obtain.
Cervical spine radiographs:
Evaluate osseous anomalies.
Chest radiographs:
Evaluate space occupying lesions.
Treatment:
vTOS typically requires a more aggressive approach compared with nTOS
High incidence of arterial complications when cervical ribs are present
Current evidence shows improved outcomes with operative treatment compared with nonoperative
Recent systematic review shows 90% of patients treated surgically for vTOS have excellent/good outcomes:
After surgical treatment, 93% of athletes return to full competitive athletics.
Nonoperative:
Venous:
Anticoagulation
Bed rest.
Arterial:
Rarely indicated due to potential complications.
Operative:
Supraclavicular or trans-axillary approach
Venous:
Operative intervention indicated when conservative therapy has failed
Venolysis, anticoagulation, and first rib resection
Postoperative venography:
Useful to confirm clot resolution
Dictates further need for anticoagulation.
Arterial:
Anticoagulation:
Indicated for all patients regardless of surgical intervention required.
Thrombolysis:
Milder cases.
Angioplasty
Thromboembolectomy:
More severe cases
Typically followed by thoracic outlet decompression.
Bypass grafting
Arterial patency in >90% after thoracic outlet decompression and arterial reconstruction at 4.5 years.
Suggested Readings
Köknel Talu G. Thoracic outlet syndrome. Agri 2005;17(2):5–9 Review
Landry GJ, Moneta GL, Taylor LM Jr, Edwards JM, Porter JM. Long-term functional outcome of neurogenic thoracic outlet syndrome in surgically and conservatively treated patients. J Vasc Surg 2001;33(2):312–317, discussion 317–319
Peek J, Vos CG, Ünlü Ç, Schreve MA, van de Mortel RHW, de Vries JPM. Long-term functional outcome of surgical treatment for thoracic outlet syndrome. Diagnostics (Basel) 2018;8(1):E7
Povlsen B, Hansson T, Povlsen SD. Treatment for thoracic outlet syndrome. Cochrane Database Syst Rev 2014; (11):CD007218
Vemuri C, McLaughlin LN, Abuirqeba AA, Thompson RW. Clinical presentation and management of arterial thoracic outlet syndrome. J Vasc Surg 2017;65(5):1429–1439 Rayan GM. Thoracic outlet syndrome. J Shoulder Elbow Surg 1998;7(4):440–451 Review