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Thoracic Outlet Obstruction

Author: Mark K Eskandari, MD, Associate Professor, Departments of Radiology and Division of Vascular Surgery, Feinberg School of Medicine, Northwestern University; Attending Surgeon, Division of Vascular Surgery, Northwestern Memorial Hospital; Consulting Staff, Division of Vascular Surgery, Northwestern Medical Faculty Foundation; Consulting Staff, Department of Surgery, Jesse Brown Veterans Affairs Medical Center; Consulting Staff, Department of Surgery, Evanston Northwestern Healthcare
Coauthor(s): Nicholas D Garcia, MD, Chief of Surgery, Exeter Health Resources; Director, Board of Directors, Core Physician Services; Medical Director, Vascular Lab, Exeter Hospital; Mark D Morasch, MD, Associate Professor of Surgery, Division of Vascular Surgery, Northwestern University, The Feinberg School of Medicine
Contributor Information and Disclosures

Updated: Nov 2, 2009

Introduction

History of the Procedure

Thoracic outlet syndrome (TOS) has been an important clinical entity for more than a century. In 1821, Sir Astley Cooper first described axillary–subclavian artery symptoms due to compression from a cervical rib. In 1875, James Paget described the clinical symptoms resulting from subclavian vein thrombosis (eg, arm swelling, pain). In 1884, von Schroetter correctly attributed these upper extremity venous symptoms to thrombosis or compression of the subclavian vein at the thoracic outlet. Consequently, venous thrombosis at the thoracic outlet is known as venous TOS or Paget-Schroetter syndrome.

Problem

Thoracic outlet syndrome (TOS) has distinct clinical pictures (ie, neurogenic, arterial, venous) caused by compression of the neurovascular structures at the thoracic outlet. The classification is based on which structure is primarily involved.

Frequency

Neurogenic thoracic outlet syndrome (TOS) is the most common presentation, occurring in approximately 95% of patients. Arterial TOS is the next most common presentation and occurs in about 2-3% of patients who are affected. Venous TOS is the least common, representing only 1-2% of patients with TOS.

Approximately 70% of patients with neurogenic TOS are females aged 20-50 years. Venous TOS occurs with a male-to-female ratio of 2:1.

Etiology

The potential for either neurologic or vascular compression exists at the thoracic outlet. When compression occurs, one of the thoracic outlet syndromes (TOSs) may develop. Neurogenic and arterial TOS result from compression that occurs in the scalene triangle (see Image 1), and venous TOS results from compression in the costoclavicular space (see Image 2).¹

Pathophysiology

Neurogenic thoracic outlet syndrome (TOS) most commonly is associated with a history of neck trauma. Swollen and scarred muscles or aberrant scalene anatomy can irritate cords of the brachial plexus locally and lead to the neurologic symptoms.

Arterial TOS often is associated with cervical ribs or a rudimentary first rib. This aberrant anatomy leads to repeated intermittent arterial compression coinciding with arm movement. This repetitive localized trauma leads to intimal lesions, focal arterial stenosis, poststenotic dilatation, aneurysmal change, and subsequent thromboembolic complications. The second portion of the subclavian artery, which has a retroscalene position, often is the site of positional compression and stricture.

Venous TOS usually results from compression of the subclavian vein by the subclavius muscle and costoclavicular ligament.² When local structures are placed in abnormal or unaccustomed positions by extremes of activity or injury, vein compression and subsequent vein thrombosis can result. Venous TOS tends to occur in the more active dominant extremity. Arterial and venous TOS usually are associated with certain predisposing anatomic abnormalities, while neurogenic TOS is more likely to result following traumatic injury.

Presentation

Neurogenic thoracic outlet syndrome (TOS) is a clinical diagnosis that only is made when objective findings are supported by subjective symptoms and physical findings. Other diagnoses that should be considered include tendonitis, fibromyalgia, cervical disc herniation, spinal stenosis, carpal tunnel syndrome, repetitive motion syndrome, and epicondylitis.

A history of a motor vehicle collision (MVC) or other neck trauma is usually elicited, and patients may report a variety of symptoms, such as neck, shoulder, and arm pain. Symptoms of compression from all cords of the brachial plexus are the most common neurologic pattern noted with TOS.

Previous authors have written that ulnar nerve involvement is the typical pattern of symptoms related to neurogenic TOS, but this is not the case. Paresthesias and weakness in an arm, occipital headaches, and paraspinal muscle pain are common. The paraspinal muscle pain and occipital headaches are secondary to referred nerve pain. As expected, specific symptoms coincide with the area of the brachial plexus that is compressed. On physical examination, symptoms usually can be reproduced with pressure on the scalenes and with abduction/external rotation (AER) of the arms. Coldness and color changes in the hand usually are secondary to sympathetic nerve involvement rather than arterial involvement.

Focus the examination on the neurologic and vascular findings. Carefully examine the scalene muscles and supraclavicular fossa for abnormal pulsations, bruits, and pain with palpation. Examine all upper extremity pulses, and perform provocative positioning during the vascular examination. Also seek petechiae and other evidence of embolic events.

The mean age of patients with arterial TOS at presentation is approximately 10 years older than patients with neurogenic symptoms. Occasionally, arterial TOS is recognized during workup for other pathologies. An incidental pulsatile mass or a supraclavicular bruit may be noted during thorough physical examination. Unfortunately, arterial TOS usually remains unrecognized until a thromboembolic complication occurs. Patients who embolize may present with hand claudication, gangrene, and other embolic stigmata.

In 80% of cases of venous TOS, the dominant extremity is involved. The diagnosis is based on the clinical presentation of upper extremity swelling, venous engorgement, and pain. These signs and symptoms, in association with radiologic documentation of venous compression at the thoracic outlet, confirm the diagnosis of Paget-Schroetter syndrome. Sometimes, venous compression cannot be demonstrated, and the diagnosis is made clinically and by the pattern of venous thrombosis.

Pulmonary embolism has been reported in patients with primary venous thrombosis, but this more commonly occurs in patients presenting with secondary venous thrombosis. Secondary venous thrombosis occurs due to processes such as malignancy, polycythemia vera, heart failure, infection, drug abuse, thrombocytosis, estrogens, and most commonly, central venous catheters and indwelling cardiac pacing wires. Upper extremity deep venous thrombosis (DVT) accounts for 1-4% of all DVTs, and primary venous thrombosis accounts for 25% of these cases. Catheter-related DVTs account for most upper extremity DVTs.

Indications

The indication for surgical treatment of neurogenic thoracic outlet syndrome (TOS) is the failure of conservative treatment in a patient with disability so severe that the patient is unable to work or live comfortably. The indication for surgical treatment of venous TOS is controversial but based on symptomatology and venographic evidence of compression at the thoracic outlet. Arterial TOS, however, in most circumstances should be treated surgically with first rib resection and arterial repair.

Relevant Anatomy

The relevant anatomy of thoracic outlet syndrome (TOS) focuses on the scalene triangle and the costoclavicular space. Reports of compression of the neurovascular bundle at the area of the pectoralis minor space exist, but this is very uncommon and shall not be discussed further.

Neurogenic and arterial TOS result from compression that occurs in the scalene triangle, which is defined by the first rib, the anterior scalene muscle, and the middle scalene muscle. The subclavian artery and the branches of the brachial plexus pass through the borders of this triangle (see Image 1).

Venous TOS occurs secondary to compression that occurs in the costoclavicular space. The borders of the costoclavicular space are the first rib, costoclavicular ligament, subclavius muscle, and the anterior scalene. As the subclavian vein passes through this space, it is susceptible to compression by these structures (see Image 2). Other important local structures include the phrenic nerve, the lateral thoracic nerve, and the thoracic duct. The phrenic nerve passes from lateral to medial along the anterior border of the anterior scalene muscle, and the lateral thoracic nerve passes through the body of the middle scalene muscle. The thoracic duct joins cervical lymphatics and drains into the superior aspect of the jugulosubclavian vein confluence behind the left sternocleidomastoid muscle. Be careful to avoid injury to these structures during surgery.

Search for cervical, rudimentary, or broad first ribs. Resect these structures during surgical therapy. Rudimentary ribs usually arise higher in the neck than normal first ribs and typically articulate with the second rib rather than with the sternum. Cervical ribs and rudimentary first ribs occur in less than 0.5% of the population.

Abnormal scalene muscle anatomy also has been identified and may be a cause of some symptoms. For example, these muscles have been noted to interdigitate around the cords of the brachial plexus and, thus, have been implicated in the irritation of the cords of the brachial plexus. In a study of 98 meticulously dissected cadavers, the authors noted a number of abnormalities of the thoracic outlet fibrous bands and cervical ribs, and other abnormalities were found in most of the patients. Only 10% of the dissected cadavers were found to have normal anatomy bilaterally.

Contraindications

No absolute contraindication to the treatment of patients with thoracic outlet syndrome (TOS) exists. An individual patient may have significant comorbidities that outweigh the benefits of surgical repair and thus have a relative contraindication to surgery.

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