eMedicine Specialties > Sports Medicine > Spine

Thoracic Outlet Syndrome: Treatment & Medication

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
Coauthor(s): Matthew L Silvis, MD, Assistant Professor, Departments of Family and Community Medicine and Orthopedics and Rehabilitation, Pennsylvania State University College of Medicine; Ajay Kalra, MD, Consulting Surgeon, Surgical Specialists; Matt Thornburg, MD, Staff Physician, Department of Family and Community Medicine, University of Missouri Health Care at Columbia; Donald Spadone, MD, Assistant Professor, Department of Surgery, Division of Vascular Surgery, University of Missouri Health Sciences Center
Contributor Information and Disclosures

Updated: Aug 15, 2008

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

Related eMedicine topic:
Intrinsic Hand Deformity

Related Medscape topics:
Resource Center Vascular Surgery
Specialty Site Neurology & Neurosurgery
Specialty Site Surgery

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.

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

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, acetylsalicylic acid, dextran, dipyridamole, and hydroxychloroquine may increase toxicity

Documented hypersensitivity; subacute bacterial endocarditis, active bleeding; history of heparin-induced thrombocytopenia

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.

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

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

Documented hypersensitivity; severe liver or kidney disease; open wounds; GI ulcers

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.

Related eMedicine topics:
Toxicity, Acetaminophen
Toxicity, Narcotics
Toxicity, Nonsteroidal Anti-inflammatory Agents

Related Medscape topics:
Resource Center Adverse Drug Events Reporting
Resource Center Opioids: A Guide to State Opioid Prescribing Policies
Resource Center Pain Management: Advanced Approaches to Chronic Pain Management
Resource Center Pain Management: Pharmacologic Approaches


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.

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

Rifampin can reduce the analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity.

Documented hypersensitivity; G6PD deficiency

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.

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

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.

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

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.

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

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.

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.

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

Thrombolytic enzymes, alone or in combination with anticoagulants and antiplatelets, may increase the risk of bleeding complications

Documented hypersensitivity; internal bleeding, recent trauma, history of intracranial or intraspinal surgery or trauma, cerebrovascular accident, intracranial neoplasm

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

More on Thoracic Outlet Syndrome

Overview: Thoracic Outlet Syndrome
Differential Diagnoses & Workup: Thoracic Outlet Syndrome
Treatment & Medication: Thoracic Outlet Syndrome
Follow-up: Thoracic Outlet Syndrome
Multimedia: Thoracic Outlet Syndrome
References

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Further Reading

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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