eMedicine Specialties > Sports Medicine > Spine
Thoracic Outlet Syndrome
Updated: Aug 15, 2008
Introduction
Background
Thoracic outlet syndrome is not the name of a single entity, but rather a collective title for a variety of conditions attributed to compression of these neurovascular structures as they traverse the thoracic outlet.[1,2,3,4 ]The thoracic outlet is bordered by the scalene muscles, first rib, and clavicle. Neurovascular structures pass from the neck and thorax into the axilla through this space. Thoracic outlet syndrome remains one of the most controversial clinical entities in medicine.[5,6,7 ]
For excellent patient education resources, visit eMedicine's Hand, Wrist, Elbow, and Shoulder Center. Also, see eMedicine's patient education articles Shoulder and Neck Pain and Electromyography (EMG).
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Brachial Plexus Injury
Nerve Entrapment Syndromes
Overuse Injury
Shoulder Impingement Syndrome
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Frequency
United States
The wide variability of symptoms and signs in patients with thoracic outlet syndrome and the lack of an objective confirmatory test for the diagnosis makes correctly identifying patients with thoracic outlet syndrome difficult.[8 ]Therefore, determining its exact incidence remains elusive; estimates range from 3-80 cases per 1000 population.[9 ]Thoracic outlet syndrome is more common in women, particularly those with poor muscular development, poor posture, or both.[10 ]
Functional Anatomy
The neurovascular bundle courses through 3 spaces, or triangles, as it exits the neck to reach the axilla and proximal arm. All 3 spaces can be the source of compression of the various components of the neurovascular bundle, including the brachial plexus and the subclavian vessels.[11 ]These spaces are small at rest and become even smaller with certain arm maneuvers, such as abduction and external rotation.[12,13 ]This can aid in the diagnosis of thoracic outlet syndrome and forms the basis for provocative testing, which is discussed later (see Clinical, Physical).
The first space is the interscalene triangle. It is bordered by the anterior scalene muscle, the middle scalene muscle, and the upper border of the first rib. This space contains the trunks of the brachial plexus and subclavian artery. The interscalene triangle is the most common site for neural compression, vascular compression, or both.[9 ]
The second space is the costoclavicular triangle, which is bordered by the clavicle, first rib, and scapula and contains the subclavian artery and vein and the brachial nerves.
The third and final space is beneath the coracoid process just deep to the pectoralis minor tendon; it is referred to as the subcoracoid space.
Sport-Specific Biomechanics
Thoracic outlet syndrome is most often seen in patients who engage in repetitive motions that place the shoulder at the extreme of abduction and external rotation. An example of such activity is swimming, especially with the freestyle stroke, butterfly stroke, and backstroke. When a swimmer reports tightness and pain around the shoulder, neck, and clavicle as his or her hand enters the water, thoracic outlet syndrome should be suspected.
In addition to swimmers, other athletes affected by thoracic outlet syndrome include water polo, baseball, and tennis players and athletes in any other activity that places repetitive stress on the shoulder at the extremes of abduction and external rotation. These individuals may present with neurologic and arterial or venous symptoms. Venous thoracic outlet syndrome most commonly develops in young male athletes in whom the upper extremity musculature is overdeveloped as a result of work or physical conditioning. Baseball players, whose sport requires repetitive throwing motions, are at increased risk for arterial thoracic outlet syndrome in their dominant arm.
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Clinical
History
The initial presentation of thoracic outlet syndrome is dependent on whether the compression is primarily vascular, neurogenic, or a combination of both. It is also dependent on the underlying continuum of histopathologic changes noted with chronic nerve compression, ranging from intermittent to constant debilitating symptoms.[14 ] Three symptomatic patterns emerge; these are vascular, true neurogenic, and disputed or nonspecific-type thoracic outlet syndrome.
Vascular thoracic outlet syndrome is rare and can involve the subclavian artery or vein. Both forms of vascular thoracic outlet syndrome tend to occur in young patients who perform vigorous overhead arm activity such as throwing. With venous obstruction (if secondary to thrombosis, Paget-von Schrötter syndrome), patients may present with upper extremity swelling, venous distention, or diffuse arm or hand pain (including the forearm).[14,15 ]
With arterial obstruction, patients may report color changes of their affected upper extremity, claudication, or diffuse arm or hand pain (including the forearm). Because of arterial collateral blood flow, the iinitial symptoms tend to be mild, with arm ache and fatigue, particularly after overhead activity. Patients typically seek medical evaluation after ischemic events (eg, ulceration, gangrene, absent pulses) occur.[14 ]
Neurogenic thoracic outlet syndrome involves compression of the brachial plexus. Similar to vascular thoracic outlet syndrome, a pure neurogenic presentation is also rare. Patients present with painless atrophy of the intrinsic muscles of the hand, and athletes may report difficulty grasping a racket or ball as a result of intrinsic muscle weakness. They may also report sensory loss or paresthesias. Pain is often reported but is not as dramatic as in the nonspecific-type thoracic outlet syndrome.[9 ]Again, neurogenic thoracic outlet syndrome tends to affect individuals who perform overhead arm activities.
The disputed or nonspecific-type thoracic outlet syndrome refers to a large group of patients with unexplained pain in the arm, scapular region, and cervical region. Typically, their symptoms begin after a traumatic event (eg, motor vehicle accident). Much debate surrounds this diagnosis, with certain providers believing the disorder is underdiagnosed.[6 ]and others believing it is overdiagnosed.[7 ]
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Physical
The examination should begin with an assessment of the patient’s posture. A slumped posture of the shoulders and upper back and a “poked-forward” position of the head and neck are comfortable but potentially damaging for the scapular and neck muscles and are thought to contribute to the susceptibility for thoracic outlet syndrome.[14 ]
The symmetry of both arms should be evaluated. Cervical active range-of-motion assessment and the Spurling test (ie, patient’s head is placed in extension and lateral flexion, with axial compression applied by the examiner to the patient’s head in an effort to recreate radicular pain) should be performed. Active and passive range of motion of both shoulders should be examined. A careful neurovascular examination of both upper extremities is needed, taking care to remember that the muscles and nerves supplied by the lower brachial plexus are most commonly affected.
Vascular thoracic outlet syndrome has different examination signs depending on whether the venous or arterial vessels are affected. With venous compression, patients often present with edema and cyanosis of the upper extremity. They may also have distended veins in the shoulder or chest. With arterial compression, patients often present with pallor, a weak or absent pulse, and coolness of the upper extremity. Decreased blood pressure greater than 20 mm Hg in the affected arm compared with the contralateral arm is sometimes noted and is a reliable indicator of arterial involvement.[9 ]Rarely, small infarcts are noted in the hands and fingers, which are due to embolization.
The classic finding in a person with neurogenic thoracic outlet syndrome is the Gilliatt-Sumner hand. This physical examination finding includes atrophy of the abductor pollicis brevis with lesser involvement of the interossei and hypothenar muscles.[9 ]Patients may also have decreased sensation that follows the ulnar nerve distribution because the lower trunks of the brachial plexus are usually more involved than the upper trunks.
Patients with disputed or nonspecific-type thoracic outlet syndrome tend to have diffuse upper extremity pain with guarding. Examination tends to be difficult and findings nonfocal. Weakness and decreased sensation tend to be unreliable signs that are difficult to quantify.
Because of the variability of the structures involved in thoracic outlet syndrome, many provocative maneuvers have been described to aid in diagnosis. They include the Adson maneuver, Wright test, and Roos stress test.[10,14 ] Note, however, that these tests have high rates of false-positive and false-negative results.[14 ]
The Adson maneuver is performed by positioning the tested shoulder in slight abduction and extension. Then, the patient extends his or her neck and turns the head toward this affected shoulder. The patient inhales while the examiner simultaneously palpates the ipsilateral radial pulse. If the pulse diminishes or the patient has paresthesias, the test result is considered positive as long as this maneuver does not cause symptoms on the asymptomatic contralateral side.
The Wright test is performed by progressively hyperabducting and externally rotating the patient’s affected arm while assessing the ipsilateral radial pulse. Again, the test result is considered positive if the pulse diminishes or paresthesias develop.[10 ]
The Roos stress test is performed with the patient positioning both of his or her shoulders in abduction and external rotation of 90° with elbow flexion at 90°. The patient then opens and closes his or her hands for several minutes. Reproduction of symptoms or a sensation of heaviness or fatigue is considered a positive test result.[10 ]
Causes
Causes of thoracic outlet syndrome can be divided into bony and soft-tissue factors. Bony factors include abnormalities such as anomalous cervical ribs, hypoplastic first thoracic ribs, and exostoses of the first rib or clavicle.[16,17 ]The rate of anomalous cervical ribs is considered to be 0.17-0.74% in the general population, and the rate of rudimentary first ribs is 0.29-0.76%.[14 ]
Soft-tissue factors include congenital anomalies such as anomalous fibrous muscular bands near the brachial plexus and hypertrophic muscles in athletes and weight lifters.[17,18 ]Space-occupying lesions (eg, tumors, cysts) and inflammatory processes also occur in the soft tissues and can cause thoracic outlet syndrome.
Trauma or mechanical stress to the neck, shoulders, or upper extremities can lead to thoracic outlet syndrome. In fact, a combination of neck trauma and anatomic predisposition (ie, cervical rib) is considered the main etiology of thoracic outlet syndrome. Posttraumatic conditions such as hematoma, myositis ossificans, and scar formation can be important variables, as can a droopy shoulder secondary to trapezius muscle weakness.[19 ]Thoracic outlet syndrome can be secondary to malunion of a clavicle fracture.[20 ]
Interestingly, multiple points of compression may be present as the peripheral nerves descend from the thoracic outlet to the hand (simultaneous thoracic outlet syndrome and ulnar nerve compression at the elbow or carpal tunnel syndrome in the wrist). This has been referred to as double-[21 ]or multiple-crush syndrome.[22 ]
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Differential Diagnoses
| Acromioclavicular Joint Injury | Elbow and Forearm Overuse Injuries |
| Brachial Plexus Injury | Shoulder Impingement Syndrome |
| Cervical Disc Injuries | Thoracic Disc Injuries |
| Cervical Discogenic Pain Syndrome | Thoracic Discogenic Pain Syndrome |
| Cervical Radiculopathy | |
| Clavicular Injuries |
Other Problems to Be Considered
Acute coronary syndrome
Carpal tunnel syndrome
Cervical cord tumor
Dead arm syndrome (ie, multidirectional shoulder instability)
Epicondylitis (see eMedicine topics lateral epicondylitis and medial epicondylitis)
Fibromyalgia
Hypothyroidism
Multiple Sclerosis
Pectoralis minor compression
Reflex sympathetic dystrophy (complex regional pain syndrome)
Syringomyelia
Superior pulmonary sulcus tumors and Pancoast syndrome[23 ]
Tendinitis
Vasculitis
Workup
In thoracic outlet syndrome with vascular compromise or nerve compression, with resultant atrophy of the intrinsic hand muscles, the diagnosis is not controversial and specific tests can confirm the diagnosis. However, no infallible clinical tests, laboratory tests, radiographic tests, or electrical studies establish the diagnosis of thoracic outlet syndrome syndrome in patients with disputed or nonspecific-type thoracic outlet syndrome.[24 ]Many tests are available to refine the differential diagnosis and confirm or exclude other potential conditions (see Differentials and Other Problems to Be Considered).
Laboratory Studies
To exclude systemic disease and inflammation, a few simple blood tests may refine the differential diagnosis for thoracic outlet syndrome, including a blood glucose level, complete blood cell (CBC) count, erythrocyte sedimentation rate (ESR), basic metabolic panel, thyrotropin level, and rheumatologic workup, if indicated.
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Imaging Studies
Radiography
Cervical spine and upper thoracic spine radiographs may demonstrate bony abnormalities. Chest, shoulder, and clavicle radiographs may also identify bony abnormalities.
Computed tomography (CT) scanning and magnetic resonance imaging (MRI)
CT scanning and MRI are more useful for identifying other conditions that might cause similar symptoms, rather than for establishing the diagnosis of thoracic outlet syndrome.[25 ]
Magnetic resonance angiography (MRA)MRA can be useful for the diagnosis of arterial vascular thoracic outlet syndrome.
Venography and duplex scanning
Venography and duplex scanning (ie, ultrasonography combined with Doppler velocity waveforms) are used to assist in the diagnosis of subclavian vein compression (thrombosis). These tests can be performed dynamically with positions that recreate the tension placed on the thoracic outlet during certain motions such as abduction and external rotation.
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Other Tests
Electrodiagnostic studies can be helpful for classic cases of neurogenic thoracic outlet syndrome and therefore can be useful when the results are positive. However, many symptoms are intermittent in neurogenic thoracic outlet syndrome; therefore, negative test results do not rule out this diagnosis. Electrodiagnostic testing can also be helpful in diagnosing other neuromuscular disorders.
Nerve conduction velocity has been used for the diagnosis of thoracic outlet syndrome as defined by a reduction to less than 85 m/s of either the ulnar or median nerves across the thoracic outlet and was found to corroborate the clinical diagnosis. A nerve conduction velocity of less than 60 m/s was considered an indication for surgery.[22 ]However, as with many aspects of thoracic outlet syndrome, this remains controversial and has not been universally accepted.
Somatosensory evoked potentials are equally controversial, with some studies favoring their use[26 ]and others not.[27 ]
Electromyography may be helpful in confirming the presence or absence of a specific alternative diagnosis.
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Treatment
Acute Phase
Surgery in cases of thoracic outlet syndrome is indicated for acute vascular insufficiency and progressive neurologic dysfunction. For subclavian venous thrombosis, treatment addresses 3 problems: the clot, the extrinsic compression, and the intrinsic damage to the vein.[28,29 ] Thrombolysis with urokinase is the most commonly recommended treatment, with continued anticoagulation for several months. The timing of surgical decompression is debated, but surgical decompression is needed for long-term improvement.[22,30,31 ] Patients with acute ischemia of the upper extremity require prompt diagnosis and surgical treatment.[32 ]
All other patients should receive nonoperative treatment that includes relative rest, nonsteroidal anti-inflammatory medications (NSAIDs), cervicoscapular strengthening exercises, and modalities such as ultrasound, transcutaneous nerve stimulation, and biofeedback. Conservative care has been shown to be successful in most patients.[33 ] In those patients in whom pain is refractory to conservative care, surgery should be considered.
Rehabilitation Program
Physical Therapy
Physical therapy that addresses postural abnormalities and muscle imbalance relieves symptoms in most patients with thoracic outlet syndrome by relieving pressure on the thoracic outlet. This is based on 3 potential effects of abnormal static or repetitive postures and positions.
First, increased pressure directly around nerves at various entrapment points or increased tension on nerves creates chronic nerve compression. Second, certain postures maintain muscles in abnormally shortened positions, resulting in a new length. When these adapted muscles are stretched, pain occurs. Third, abnormal posture results in some muscles being stretched and others being shortened to new lengths, resulting in both being placed at a mechanical disadvantage and leading to muscle imbalance.[14 ] This is the basis for physical therapy.
Although, many conservative protocols for physical therapy are described, few outcome studies have been published. The few studies available demonstrate positive outcomes for most patients.[34,35,36 ]
Patient treatment includes several components that address the brachial plexus nerve compression and muscle imbalance in the cervicoscapular region. Key points emphasized in treatment begin with education. Postural correction focuses on positions of most risk and least risk for compression, with integration into the patient's activities of daily living at work, home, and sleep. For example, patients should avoid overhead arm positions while sleeping. Postural and position correction can be aided by wrist splints, elbow pads, soft neck rolls for nighttime use, and lumbar supports for sitting. In addition, the impact of body habitus and general physical conditioning should be evaluated and discussed (ie, obesity, breast hypertrophy).
Physiotherapy focuses on pain control and range of motion with specific stretching exercises. Stretching should begin with short, tight muscles (ie, upper trapezius, levator scapulae, scalenes, sternocleidomastoid, pectoralis major, pectoralis minor, suboccipitalis) and should not be aggressive. Once pain control and cervical motion are regained, strengthening exercises of the lower scapular stabilizers are begun, as is an aerobic conditioning program.[36,37 ]The importance of patient compliance should not be overlooked.
Surgical Intervention
Little argument exists for the surgical treatment of a patient with severe compression or compromise of the subclavian vein or artery.[8,12,13,29 ]However, less severe cases are more controversial. Likewise, patients with atrophy of the intrinsic muscles of the hand secondary to thoracic outlet syndrome with no distal sites of compression need surgical intervention.[14 ]
Because of the high prevalence of surgical complications and variable reports of success, many surgeons offer surgery to patients with disputed or nonspecific-type thoracic outlet syndrome only as a last resort after prolonged conservative management and a detailed discussion regarding the risks and complications of surgery. Potential complications from surgery can include pneumothorax, injury to the subclavian artery or vein, injury to the brachial plexus and long thoracic nerve, apical hematoma, intercostobrachial nerve injury, and injury to the thoracic duct.[38 ]
The surgical approach used varies and may be specialty dependent, with the transaxillary approach preferred by many thoracic and vascular surgeons and the anterior supraclavicular approach favored by most neurosurgeons.[9 ]Both approaches allow for first rib removal and part or total scalene muscle removal.
Success rates for surgery vary dramatically in the literature. One review of 47 patients with thoracic outlet syndrome revealed 75% lower plexus and 50% upper plexus compressions remained asymptomatic at 4.6 years.[39 ]Morbidity in this study involved 17% of patients and was most frequently the result of incisional pain. However, not all studies have been so impressive. One retrospective analysis of patients with nonspecific neurogenic thoracic outlet syndrome demonstrated work disability at 1 year after surgery in 60% of patients. At 4.8 years of follow-up, 72.5% patients were limited in activities.[40 ]
This has led many surgeons to agree with Wood et al, who empathically stated in 1988 that some errors always occur in diagnosis, and, therefore, surgery should be advised "on a basis of exclusion and with great reservation."[24 ]This is especially true for disputed or nonspecific-type thoracic outlet syndrome.[9 ]
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Consultations
Consultation with a sports medicine specialist and surgeon is recommended.
Recovery Phase
Rehabilitation Program
Physical Therapy
Postoperative physical therapy is essential for strengthening and range of motion.
Maintenance Phase
Rehabilitation Program
Physical Therapy
Continued regular stretching of the muscles around the cervical girdle (eg, scalene, pectoralis major and minor, trapezius, levator scapulae, and sternocleidomastoid muscles) is essential.
Recommended exercises for thoracic outlet syndrome include neck stretching, abdominal breathing, and postural exercises. Ineffective therapies include shoulder shrugs (useful for prevention), weight lifting, and neck traction. Exercises should be performed at home at least twice a day.
Medical Issues/Complications
- Patients may require continued postoperative anticoagulation with warfarin.
- To help prevent recurrence of thoracic outlet syndrome, the patient should avoid sleeping with his or her arms in an overhead position.
Medication
Acute findings of ischemia or thrombosis require immediate evaluation and anticoagulation.
Anticoagulants
Anticoagulants are used to treat acute arterial or venous occlusion.
Heparin
Potentiates antithrombin III and prevents conversion of fibrinogen to fibrin. Inhibits thrombogenesis.
Dosing
Adult
Loading dose: 80 U/kg IV
Maintenance infusion: 15-25 U/kg/h IV; check aPTT q6h to maintain a range of 40-60 seconds
Pediatric
Loading dose: 50 U/kg/h IV
Maintenance infusion: 15-25 U/kg/h IV
Increase dose by 2-4 U/kg/h IV q6-8h prn according to aPTT results
Interactions
Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, acetylsalicylic acid, dextran, dipyridamole, and hydroxychloroquine may increase toxicity
Contraindications
Documented hypersensitivity; subacute bacterial endocarditis, active bleeding; history of heparin-induced thrombocytopenia
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
In neonates, preservative-free heparin is recommended to prevent possible toxicity (gasping syndrome) caused by benzyl alcohol (a preservative); caution in the presence of severe hypotension and shock; monitor for bleeding with peptic ulcer disease, menstruation, increased capillary permeability, and IM injections
Warfarin (Coumadin)
Interferes with hepatic synthesis of vitamin K–dependent coagulation factors. Tailor dose to maintain an INR in the range of 2-3.
Dosing
Adult
5 mg PO qd for 2-4 d initially; adjust dose to desired PT and/or INR
Pediatric
0.05-0.34 mg/kg/d PO; adjust for desired INR
Interactions
Griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate may decrease the anticoagulant effects.
Oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac may increase the anticoagulant effects
Contraindications
Documented hypersensitivity; severe liver or kidney disease; open wounds; GI ulcers
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Do not switch brands after achieving a therapeutic response; caution in the presence of active tuberculosis or diabetes; patients with protein C or protein S deficiency are at risk of skin necrosis.
Analgesics
The use of analgesics may aid in relieving the discomfort of an acute occlusion of the vascular structures or nervous impingement.
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Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, those with upper GI disease, and those who are taking oral anticoagulants.
Dosing
Adult
325-650 mg PO q4-6h or 1000 mg PO tid/qid; not to exceed 4 g/d
Pediatric
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: Administer as in adults; not to exceed 5 doses in 24 h
Interactions
Rifampin can reduce the analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity.
Contraindications
Documented hypersensitivity; G6PD deficiency
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Hepatotoxicity is possible in patients with chronic alcoholism at various dose levels; severe or recurrent pain or severe or continued fever may indicate serious illness; many OTC products contain acetaminophen, and combined use may result in cumulative doses that exceed the recommended maximum dose.
Ibuprofen (Motrin, Ibuprin)
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Dosing
Adult
200-400 mg PO q4-6h prn; not to exceed 3.2 g/d; may administer 600-800 mg PO tid when used as anti-inflammatory medication
Pediatric
<6 months: Not established
6 months to 12 years: 30-70 mg/kg/d PO divided tid/qid; start at lower end of dosing range and titrate to maximum of 2.4 g/d
>12 years: Administer as in adults
Interactions
Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; coadministration of anticoagulants may increase PT duration (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently.
Contraindications
Documented hypersensitivity to other NSAIDs (high cross-reactivity exists); avoid in patients with recent GI bleeding, peptic ulcer disease, or renal insufficiency and in those at high risk for bleeding
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of anticoagulation abnormalities or during anticoagulant therapy.
Acetaminophen and codeine (Tylenol #3)
Oral analgesic indicated for treatment of moderate pain.
Dosing
Adult
30-60 mg/dose (based on codeine content) PO q4-6h or 1-2 tabs PO q4-6h; not to exceed 12 tab/24h
Pediatric
0.5-1 mg/kg/dose (based on codeine content) PO q4-6h; 10-15 mg/kg/dose (based on acetaminophen content) PO; not to exceed 2.6 g acetaminophen per 24h
Interactions
The toxicity of codeine increases with CNS depressants, TCAs, MAOIs, neuromuscular blockers, CNS depressants, phenothiazines, and narcotic analgesics; rifampin can reduce the analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity.
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients who are dependent on opiates (substitution may result in acute opiate-withdrawal symptoms); caution in the presence of severe renal or hepatic dysfunction; hepatotoxicity is possible in patients with chronic alcoholism at various dose levels; severe or recurrent pain or severe or continued fever may indicate serious illness; many OTC products contain acetaminophen, and combined use with these products may result in cumulative doses that exceed the recommended maximum dose.
Fibrinolytic Agent
Thrombolytics are used to promote fibrinolysis of intraluminal thrombus or embolus in occluded vessels.
Urokinase (Activase)
Direct plasminogen activator that acts on endogenous fibrinolytic system and converts plasminogen to the enzyme plasmin, which, in turn, degrades fibrin clots, fibrinogen, and other plasma proteins. The advantage is that the agent is nonantigenic.
Most often used for local fibrinolysis of thrombosed catheters and superficial vessels. When used for local fibrinolysis, urokinase is given as local infusion directly into the area of thrombus and with no bolus given.
The dose should be adjusted to achieve clot lysis or patency of the affected vessel.
Dosing
Adult
Loading dose: 4400 U/kg IV over 10 min, and then increase to 6000 U/kg/h
Maintenance dose: 4400-6000 U/kg/h IV
Pediatric
Administer as in adults
Interactions
Thrombolytic enzymes, alone or in combination with anticoagulants and antiplatelets, may increase the risk of bleeding complications
Contraindications
Documented hypersensitivity; internal bleeding, recent trauma, history of intracranial or intraspinal surgery or trauma, cerebrovascular accident, intracranial neoplasm
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution with IM administration of medications, severe hypertension, or trauma or surgery in previous 10 d; to avoid dislodging a possible deep vein thrombus, do not measure blood pressure in lower extremities; monitor therapy by assessing PT, aPTT, TT, or fibrinogen level approximately 4 h after the initiation of therapy
Follow-up
Return to Play
Return to play following treatment of thoracic outlet syndrome is difficult to generalize and depends on multiple variables, including the type of thoracic outlet syndrome, the presence of contributing factors, the treatment plan, the response to treatment, and the sport played.
Complications
Ischemic changes, including gangrene, are potential complications of arterial thoracic outlet syndrome. Pulmonary embolism is reported in 0-28.5% of patients with subclavian-axillary venous thrombosis. Venous gangrene and upper extremity phlegmasia cerulea dolens account for 2-5% of all cases of phlegmasia. Nerve injury (eg, brachial plexus neurapraxia) is the most serious postoperative complication after thoracic outlet decompression. Bleeding problems from the subclavian vessels and lymph leakage from the thoracic duct occur infrequently.
Prevention
The patient should avoid repetitive motions, stressful lifting, and overhead work. Performing a regular exercise program for improving flexibility and strength is beneficial. Shoulder-elevating movements (eg, shrugs, hand circles) increase range of motion and aid in prevention, but they are not a treatment modality.
Prognosis
Symptoms resolve with conservative therapy in approximately 90% of individuals. Postsurgical success rates over 1 year vary from 43-78%. A good surgical result means improvement, not total cure. Most patients are able to return to their previous lifestyle without difficulty. Job modification is required in individuals who perform repetitive activities, work on assembly lines, perform heavy laboring, or work with their arms elevated.
Education
Inform patients that symptoms recur in 15-20% of patients.[41 ]The initial treatment is conservative in nature and includes a search for other diagnoses (see Differentials and Other Problems to Be Considered). Chronic pain may improve with the continued use of analgesics and a routine exercise and strengthening program.
Miscellaneous
Medicolegal Pitfalls
- Advise patients that surgical decompression may not completely alleviate all symptoms.
- Recurrence is likely, if repetitive and overhead activities are continued.
- All possible causes of symptoms should be excluded before surgical decompression of the thoracic outlet.
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Multimedia
Media file 1: Thoracic outlet syndrome in a 16-year-old volleyball player with a stenotic right subclavian vein (arrow) secondary to fibrosis.
References
Arthur LG, Teich S, Hogan M, Caniano DA, Smead W. Pediatric thoracic outlet syndrome: a disorder with serious vascular complications. J Pediatr Surg. Jun 2008;43(6):1089-94. [Medline].
Sadat U, Weerakkody R, Varty K. Thoracic outlet syndrome: an overview. Br J Hosp Med (Lond). May 2008;69(5):260-3. [Medline].
Kaymak B, Ozçakar L, Inanici F, et al. Forearm bone mineral density measurements in thoracic outlet syndrome. Rheumatol Int. Jul 2008;28(9):891-893. [Medline].
Oates SD, Daley RA. Thoracic outlet syndrome. Hand Clin. Nov 1996;12(4):705-18. [Medline].
Cuetter AC, Bartoszek DM. The thoracic outlet syndrome: controversies, overdiagnosis, overtreatment, and recommendations for management. Muscle Nerve. May 1989;12(5):410-9. [Medline].
Roos DB. Thoracic outlet syndrome is underdiagnosed. Muscle Nerve. Jan 1999;22(1):126-9; discussion 137-8. [Medline].
Wilbourn AJ. Thoracic outlet syndrome is overdiagnosed. Muscle Nerve. Jan 1999;22(1):130-6; discussion 136-7. [Medline].
Urschel HC Jr, Patel AN. Surgery remains the most effective treatment for Paget-Schroetter syndrome: 50 years' experience. Ann Thorac Surg. Jul 2008;86(1):254-60; discussion 260. [Medline].
Huang JH, Zager EL. Thoracic outlet syndrome. Neurosurgery. Oct 2004;55(4):897-902; discussion 902-3. [Medline].
Safran MR. Nerve injury about the shoulder in athletes. Part 2: long thoracic nerve, spinal accessory nerve, burners/stingers, thoracic outlet syndrome. Am J Sports Med. Jun 2004;32(4):1063-76. [Medline].
Parziale JR, Akelman E, Weiss AP, Green A. Thoracic outlet syndrome. Am J Orthop. May 2000;29(5):353-60. [Medline].
Rutherford RB, Cronewett JL, Gloviczki P. Vascular Surgery. 5th ed. Philadelphia, Pa: WB Saunders Co; 2000:1184-1219.
Moore WS, ed. Vascular Surgery: A Comprehensive Review. 4th ed. Philadelphia, Pa: WB Saunders Co; 1993:600-3.
Mackinnon SE, Novak CB. Thoracic outlet syndrome. Curr Probl Surg. Nov 2002;39(11):1070-145. [Medline].
Hood DB, Kuehne J, Yellin AE, Weaver FA. Vascular complications of thoracic outlet syndrome. Am Surg. Oct 1997;63(10):913-7. [Medline].
Rayan GM. Lower trunk brachial plexus compression neuropathy due to cervical rib in young athletes. Am J Sports Med. Jan-Feb 1988;16(1):77-9. [Medline].
Roos DB. Congenital anomalies associated with thoracic outlet syndrome. Anatomy, symptoms, diagnosis, and treatment. Am J Surg. Dec 1976;132(6):771-8. [Medline].
Esposito MD, Arrington JA, Blackshear MN, Murtagh FR, Silbiger ML. Thoracic outlet syndrome in a throwing athlete diagnosed with MRI and MRA. J Magn Reson Imaging. May-Jun 1997;7(3):598-9. [Medline].
Al-Shekhlee A, Katirji B. Spinal accessory neuropathy, droopy shoulder, and thoracic outlet syndrome. Muscle Nerve. Sep 2003;28(3):383-5. [Medline].
Fujita K, Matsuda K, Sakai Y, Sakai H, Mizuno K. Late thoracic outlet syndrome secondary to malunion of the fractured clavicle: case report and review of the literature. J Trauma. Feb 2001;50(2):332-5. [Medline].
Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet. Aug 18 1973;2(7825):359-62. [Medline].
Urschel HC Jr, Razzuk MA. Neurovascular compression in the thoracic outlet: changing management over 50 years. Ann Surg. Oct 1998;228(4):609-17. [Medline]. [Full Text].
Arcasoy SM, Jett JR. Superior pulmonary sulcus tumors and Pancoast's syndrome. N Engl J Med. Nov 6 1997;337(19):1370-6. [Medline].
Wood VE, Twito R, Verska JM. Thoracic outlet syndrome. The results of first rib resection in 100 patients. Orthop Clin North Am. Jan 1988;19(1):131-46. [Medline].
Novak CB, Mackinnon SE, Patterson GA. Evaluation of patients with thoracic outlet syndrome. J Hand Surg [Am]. Mar 1993;18(2):292-9. [Medline].
Machleder HI, Moll F, Nuwer M, Jordan S. Somatosensory evoked potentials in the assessment of thoracic outlet compression syndrome. J Vasc Surg. Aug 1987;6(2):177-84. [Medline].
Komanetsky RM, Novak CB, Mackinnon SE, et al. Somatosensory evoked potentials fail to diagnose thoracic outlet syndrome. J Hand Surg [Am]. Jul 1996;21(4):662-6. [Medline].
Sanders RJ, Hammond SL. Venous thoracic outlet syndrome. Hand Clin. Feb 2004;20(1):113-8, viii. [Medline].
Melby SJ, Vedantham S, Narra VR, et al. Comprehensive surgical management of the competitive athlete with effort thrombosis of the subclavian vein (Paget-Schroetter syndrome). J Vasc Surg. Apr 2008;47(4):809-20; discussion 821. [Medline].
Machleder HI. Evaluation of a new treatment strategy for Paget-Schroetter syndrome: spontaneous thrombosis of the axillary-subclavian vein. J Vasc Surg. Feb 1993;17(2):305-15; discussion 316-7. [Medline].
Urschel HC Jr, Razzuk MA. Paget-Schroetter syndrome: what is the best management?. Ann Thorac Surg. Jun 2000;69(6):1663-8; discussion 1668-9. [Medline].
Patton GM. Arterial thoracic outlet syndrome. Hand Clin. Feb 2004;20(1):107-11, viii. [Medline].
Dale WA, Lewis MR. Management of thoracic outlet syndrome. Ann Surg. May 1975;181(5):575-85. [Medline]. [Full Text].
Kenny RA, Traynor GB, Withington D, Keegan DJ. Thoracic outlet syndrome: a useful exercise treatment option. Am J Surg. Feb 1993;165(2):282-4. [Medline].
Lindgren KA. Conservative treatment of thoracic outlet syndrome: a 2-year follow-up. Arch Phys Med Rehabil. Apr 1997;78(4):373-8. [Medline].
Novak CB, Collins ED, Mackinnon SE. Outcome following conservative management of thoracic outlet syndrome. J Hand Surg [Am]. Jul 1995;20(4):542-8. [Medline].
Novak CB. Conservative management of thoracic outlet syndrome. Semin Thorac Cardiovasc Surg. Apr 1996;8(2):201-7. [Medline].
Leffert RD. Complications of surgery for thoracic outlet syndrome. Hand Clin. Feb 2004;20(1):91-8. [Medline].
Balci AE, Balci TA, Cakir O, Eren S, Eren MN. Surgical treatment of thoracic outlet syndrome: effect and results of surgery. Ann Thorac Surg. Apr 2003;75(4):1091-6; discussion 1096. [Medline].
Franklin GM, Fulton-Kehoe D, Bradley C, Smith-Weller T. Outcome of surgery for thoracic outlet syndrome in Washington state workers' compensation. Neurology. Mar 28 2000;54(6):1252-7. [Medline].
Atasoy E. Recurrent thoracic outlet syndrome. Hand Clin. Feb 2004;20(1):99-105. [Medline].
Edwards DP, Mulkern E, Raja AN, Barker P. Trans-axillary first rib excision for thoracic outlet syndrome. J R Coll Surg Edinb. Dec 1999;44(6):362-5. [Medline].
Green SM. Tarascon Pocket Pharmacopoeia. Loma Linda, Calif: Tarascon Press; 1999:10-11, 30, 46.
Terao T, Ide K, Taniguchi M, et al. [The management of patients with thoracic outlet syndrome (TOS) and an assistant diagnosis to discriminate between TOS and cervical spondylosis] [Japanese]. No Shinkei Geka. Jul 2008;36(7):615-23. [Medline].
Weber RJ, Lebduskin S. Rehabilitation issues in plexopathies. Phys Med Rehabil. 1988;996-8.
Keywords
thoracic outlet syndrome, aperture syndrome, TOS, nerve compression syndrome, vascular TOS, neurogenic TOS, disputed TOS, vascular thoracic outlet syndrome, neurogenic thoracic outlet syndrome, neurologic TOS, neurologic thoracic outlet syndrome, disputed thoracic outlet syndrome, nonspecific-type TOS, nonspecific TOS, nonspecific thoracic outlet syndrome, effort thrombosis
Paget-von Schrötter variant, Paget-Schroetter syndrome, Paget-von Schroetter syndrome, Paget-Schrötter syndrome, cervical rib syndrome, costoclavicular syndrome, scalenus syndrome, thoracic outlet compression syndrome, scalene triangle, costoclavicular space, pectoralis minor space, shoulder pain, arm pain, hand pain, arterial thoracic outlet syndrome, arterialTOS, venous thoracic outlet syndrome, venous TOS, thrombosis of the axillary-subclavian vein
Contributor Information and Disclosures
Author
Daryl A Rosenbaum, MD, Assistant Professor, Director of Sports Medicine Fellowship, Department of Family and Community Medicine, Wake Forest University School of Medicine; Team Physician, United States Soccer Federation
Daryl A Rosenbaum, MD is a member of the following medical societies: American Academy of Family Physicians, American Medical Society for Sports Medicine, North Carolina Medical Society, and Society of Teachers of Family Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Matthew L Silvis, MD, Assistant Professor, Departments of Family and Community Medicine and Orthopedics and Rehabilitation, Pennsylvania State University College of Medicine
Matthew L Silvis, MD is a member of the following medical societies: American Academy of Family Physicians and American Medical Society for Sports Medicine
Disclosure: Nothing to disclose.
Ajay Kalra, MD, Consulting Surgeon, Surgical Specialists
Ajay Kalra, MD is a member of the following medical societies: Missouri State Medical Association
Disclosure: Nothing to disclose.
Matt Thornburg, MD, Staff Physician, Department of Family and Community Medicine, University of Missouri Health Care at Columbia
Matt Thornburg, MD is a member of the following medical societies: American Academy of Family Physicians and American Medical Association
Disclosure: Nothing to disclose.
Donald Spadone, MD, Assistant Professor, Department of Surgery, Division of Vascular Surgery, University of Missouri Health Sciences Center
Donald Spadone, MD is a member of the following medical societies: American College of Surgeons, American Institute of Ultrasound in Medicine, Association for Academic Surgery, Association for Surgical Education, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.
Medical Editor
Craig C Young, MD, Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Sports Medicine Fellowship Director, Medical College of Wisconsin
Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Managing Editor
Russell D White, MD, Professor of Medicine, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center Lakewood
Disclosure: Nothing to disclose.
CME Editor
Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.
Chief Editor
Sherwin SW Ho, MD, Associate Professor, Department of Surgery, Section of Orthopedic Surgery and Rehabilitation Medicine, University of Chicago
Sherwin SW Ho, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.
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