Thoracic outlet syndrome

Thoracic outlet syndrome (TOS) consists of a group of distinct pathologies arising as a result of compression of structures at the thoracic outlet. The structures at risk are, from anterior to posterior, the subclavian vein, subclavian artery and brachial plexus. Compression or impingement causes venous (VTOS), arterial (ATOS) or neurogenic (NTOS) TOS. NTOS is the most common presentation, caused by compression of the brachial plexus at the scalene triangle or pectoralis minor space. Other compression syndromes at the carpal and cubital tunnels should be excluded. Management is usually conservative, employing physiotherapy and postural exercises, but pain or muscle wasting may be indications for surgery. VTOS is caused by compression of the subclavian vein at the costoclavicular junction, resulting in venous thrombosis, the Paget-Schroetter syndrome, often as a result of exercise in fit young muscular people or musicians. Positional swelling of the upper limb without thrombosis is termed McCleery's syndrome. In the presence of thrombosis, clot lysis, first rib excision and venoplasty may be indicated. ATOS occurs due to compression of the subclavian artery at the scalene triangle, often in association with an anomalous bony structure, such as cervical rib, causing post-stenotic aneurysmal dilation of the artery, thrombosis and embolization. Acute upper limb ischaemia necessitates urgent cervical rib excision and arterial reconstruction.     

Upper extremity arterial injury in athletes

Between 1983 and 1986, 23 athletes were evaluated for arm and hand complaints. Eleven players had symptoms of thoracic outlet compression. Severe arm fatigue (eight patients) and finger ischemia (three patients) were the presenting symptoms. In the remaining 12 athletes, symptoms of hand ischemia were predominant. Noninvasive testing with Doppler ultrasonography and duplex scanning (positional testing and finger systolic pressure recording) and cold immersion were used to aid in diagnosis. In the 11 athletes with thoracic outlet compression, arteriography confirmed the finding with compression of the subclavian artery in five, the axillary artery in one, both subclavian and axillary arteries in two, posterior humeral circumflex artery in one, and subclavian aneurysm in two. Compression of the suprascapular artery was identified in four, the subscapular artery in two, and the posterior humeral circumflex artery in one. Thrombosis of a first baseman's ulnar artery and occlusion of the palmar arch in a frisbee player were documented by arteriography. Decompression of the thoracic outlet consisted of anterior scalenectomy in five, pectoralis minor muscle division in one, and resection of both muscles in two. Removal of cervical rib with interposed vein graft was performed in the two players with arterial aneurysm. Hand ischemia in the remaining athletes was treated conservatively with Dextran-heparin infusion for acute ischemia. Repeat noninvasive study of all players demonstrated absence of compression in their playing position, and all have resumed their playing careers. Hand ischemia in athletes can be evaluated noninvasively and treated conservatively. Resection of hypertrophied muscles to decompress the thoracic outlet together with release of branch artery compression in selected athletes promotes perfusion to arm and shoulder muscles and helps to avoid the catastrophic complication of repetitive trauma leading to sudden arterial thrombosis.     

Vascular thoracic outlet syndrome

Abstract The surgical treatment of 30 cases of vascular thoracic outlet syndrome (TOS) in 25 patients is presented. Patients included 17 women and 8 men with average age of 26.1 years. The causes of compression were cervical rib (n = 16), soft tissue anomalies (n = 12), and scar tissue after clavicle fracture (n = 2). Ten subclavian artery aneurysms containing intraluminal thrombus as well as one subclavian artery occlusion were found. All such cases had multiple distal arterial embolization. Presenting features of cases with arterial TOS included: hand ischemia (n = 11), transient ischemic attack (TIA) (n = 1), and claudication or vasomotor phenomena during the arm hyperabduction (n = 11). Two patients with venous TOS developed hand edema during arm hyperabduction, and five other patients had axillary-subclavian venous thrombosis. In all cases decompressive procedures using a combined supraclavicular and infraclavicular approach were performed. Decompression was achieved by cervical rib excision (n = 12), combined cervical and first rib excision (n = 4), and first rib excision (n = 14). In all cases division of all soft tissue elements was also accomplished. Associated vascular procedures included resection and replacement of 10 subclavian artery aneurysms, one subclavian-axillary and one axillary-brachial bypass, as well as nine brachial embolectomies. All five cases with axillary-subclavian vein thrombosis before decompression were treated with anticoagulant therapy. The mean follow-up period was 3 years and 2 months (range 1 to 6 years). Two pleural entry injuries and two transient brachial plexus injuries were noted. All reconstructed arteries were patent during the follow-up period. Complete resolution of symptoms with a return to full activity was noticed in all cases with arterial TOS and in two cases with venous TOS without axillary-subclavian vein thrombosis. In cases with axillary-subclavian vein thrombosis relief of symptoms was mild, and there were limitations on daily activity. Vascular TOS is seen less frequently than the neurogenic form; however, in most cases it requires surgical treatment. We prefer a combined supraclavicular and infraclavicular approach because it offers complete exposure of the subclavian artery, cervical and first ribs, and all soft tissue anomalies. Electronic Publication     

Thoracic outlet syndrome

Thoracic Outlet Syndromes (TOS) consists of a group of distinct pathologies arising from compression or impingement of structures at the thoracic outlet. The structures at risk are, from anterior to posterior, subclavian vein (venous — VTOS), subclavian artery (arterial — ATOS) and brachial plexus (neurogenic — NTOS). NTOS is the most common presentation, usually caused by compression of the brachial plexus at the scalene triangle or pectoralis minor space. Neurogenic compression syndromes at the carpal and cubital tunnels should be excluded. Management of NTOS is usually conservative, employing physiotherapy and postural exercises, but pain or muscle wasting may be indications for surgery. VTOS is caused by compression of the subclavian vein at the costoclavicular junction, resulting in venous thrombosis (Paget—Schroetter syndrome) often as a result of exercise in fit young muscular people or musicians. Positional swelling of the upper limb without thrombosis is termed McCleery's syndrome. In acute thrombosis, clot lysis, first rib excision and venoplasty may be indicated. ATOS occurs due to compression of the subclavian artery at the scalene triangle, often in association with an anomalous bony structure, such as cervical rib, causing post-stenotic aneurysmal dilation of the artery, thrombosis and distal embolization. Acute upper limb ischaemia necessitates urgent cervical rib excision and arterial reconstruction.     

An osteopathic approach to conservative management of thoracic outlet syndromes

Thoracic outlet syndromes (TOS) are a group of disorders in which there is compression of the brachial plexus or the subclavian artery or vein or both as they pass through the thoracic outlet. Most patients have neurologic symptoms of the arm and hand. These syndromes are generally named according to the site of compression or the compressing structures. There are many factors that predispose patients to the development of TOS. The differential diagnosis includes many diseases that can add to or imitate TOS symptoms. Diagnosis is based mainly on the findings of the history and physical examination. Most patients respond well to a conservative care regimen, which should be tailored to the individual patient's needs. In most instances, surgery should be reserved as a treatment of last resort.     

Subclavian vein obstruction without thrombosis

BACKGROUND: Unilateral arm swelling caused by subclavian vein obstruction without thrombosis is an uncommon form of venous thoracic outlet syndrome (TOS). In 87 patients with venous TOS, only 21 patients had no thrombosis. We describe the diagnosis and treatment of these patients. MATERIAL AND METHODS: Twenty-one patients with arm swelling, cyanosis, and venograms demonstrating partial subclavian vein obstruction were treated with transaxillary first rib resection and venolysis. RESULTS: Eighteen (86%) of 21 patients had good-to-excellent improvement of symptoms. There were two failures (9%). CONCLUSIONS: Unilateral arm swelling without thrombosis, when not caused by lymphatic obstruction, may be due to subclavian vein compression at the costoclavicular ligament because of compression either by that ligament or the subclavius tendon most often because of congenital close proximity of the vein to the ligament. Arm symptoms of neurogenic TOS, pain, and paresthesia often accompany venous TOS while neck pain and headache, other common symptoms of neurogenic TOS, are infrequent. Diagnosis was made by dynamic venography. First rib resection, which included the anterior portion of rib and cartilage plus division of the costoclavicular ligament and subclavius tendon, proved to be effective treatment.     

Diagnosis of thoracic outlet syndrome

Thoracic outlet syndrome (TOS) is a nonspecific label. When employing it, one should define the type of TOS as arterial TOS, venous TOS, or neurogenic TOS. Each type has different symptoms and physical findings by which the three types can easily be identified. Neurogenic TOS (NTOS) is by far the most common, comprising well over 90% of all TOS patients. Arterial TOS is the least common accounting for no more than 1%. Many patients are erroneously diagnosed as "vascular" TOS, a nonspecific misnomer, whereas they really have NTOS. The Adson Test of noting a radial pulse deficit in provocative positions has been shown to be of no clinical value and should not be relied upon to make the diagnosis of any of the three types. The test is normal in most patients with NTOS and at the same time can be positive in many control volunteers. Arterial TOS is caused by emboli arising from subclavian artery stenosis or aneurysms. Symptoms are those of arterial ischemia and x-rays almost always disclose a cervical rib or anomalous first rib. Venous TOS presents with arm swelling, cyanosis, and pain due to subclavian vein obstruction, with or without thrombosis. Neurogenic TOS is due to brachial plexus compression usually from scarred scalene muscles secondary to neck trauma, whiplash injuries being the most common. Symptoms include extremity paresthesia, pain, and weakness as well as neck pain and occipital headache. Physical exam is most important and includes several provocative maneuvers including neck rotation and head tilting, which elicit symptoms in the contralateral extremity; the upper limb tension test, which is comparable to straight leg raising; and abducting the arms to 90 degrees in external rotation, which usually brings on symptoms within 60 seconds.     

Role of anterior scalene muscle hypertrophy in thoracic outlet syndrome

A case of hypertrophic anterior scalene muscle surgically treated is reported. The patient suffered from upper limb intermittent claudication at any sustained upper extremity activity such as lifting a weight or opening and closing the hand with the arm abducted. Doppler and angiographic study showed significant compression of subclavian artery with hyperabduction and Adson manoeuver. Simple anterior scalenotomy was followed by prompt recovery of symptoms. The results of scalenotomy and other surgical approaches to thoracic outlet syndrome are reviewed in the literature. The most common anomalies of anterior scalene muscle in the TOS are also described. Doppler and arteriographic study in different functional positions are necessary in the evaluation of subclavian artery compression by osseous or muscular structures. In the reported case scalenotomy was at least as effective as 1st rib resection.     

Etiology and pathology

Until the 1920s, TOS was believed to be a vascular condition caused by compression of the subclavian artery by a congenital anomaly, either a cervical rib or tight anterior scalen muscle. Today it is regarded primarily as a neurologic condition caused by neck trauma injuring and scarring the scalene muscles.     

Das Thoracic-outlet-Syndrom

Congenital and acquired bone and/or fibromuscular anomalies, positional characteristics, and trauma play roles in the etiology of thoracic outlet syndrome (TOS). For clinical examination, the elevated arm stress test is most important. Visualization of the subclavian artery and vein by digital subtraction angiography with different arm positions in the upright patient is mandatory. About 75% of operated TOS patients show embolic occlusions of the digital arteries. Neurologic evaluation includes measuring the proximal ulnar and median nerve conduction times. Reduction in proximal nerve conduction times, morphologic lesions of the subclavian artery, extreme venous compression, disabling pain during the night, and abuse of analgesics are absolute indications of transaxillary exarticulation of the first rib. The results of primary operation are favorable: 85% completely pain-free, 12% markedly improved, and 3% unchanged or worse.     

Cerebral embolic stroke and arm ischemia in a teenager with arterial thoracic outlet syndrome: a case report

A rare presentation of arterial thoracic outlet syndrome (TOS) is described in a young woman. Arterial TOS caused by a cervical rib produced acute upper extremity ischemia due to subclavian artery aneurysm formation. Clinical presentation also included left hemiparesis caused by right subclavian artery thrombosis and retrograde embolization of thrombus via the common carotid artery to the right middle cerebral artery distribution. Surgical repair of the subclavian artery was performed, but permanent neurologic deficit remained. Acute thrombosis of the right subclavian artery can produce cerebrovascular complication. The assessment of such risk in patients with arterial TOS is warranted and the arterial lesion corrected surgically.     

Über das Thoracic-outlet-Syndrom

Regarding the etiology of thoracic outlet syndrome (TOS), congenital bone and/or fibromuscular anomalies, positional characteristics and trauma play a role. Signs and symptoms are extremely variable, depending on whether the compression of the plexus, of the artery or of the vein is predominant. In the clinical examination the AEST test is of utmost importance. The visualization of the subclavian artery and vein by DAS in different positions is mandatory. Less than 5% of the patients show a subclavian artery aneurysm, but 76% have obstructions of digital arteries. Every patient, must undergo a neurological examination including the measuring of the proximal ulnar and median nerve conduction times. Anatomical lesions of the subclavian artery, reduction of the proximal nerve conduction times and high-degree venous compression as well as disabling pain during the night with abuse of analgesics are absolute indications for the decompression of the neurovascular bundle. This is achieved by the transaxillary exarticulation of the first rib together with a cervical rib and fibromuscular bands if present. The results of the primary operation are favourable: completely painfree 85%, markedly improved 12%, unchanged or worse 3%. The results of operations for persisting and recurrent TOS are disappointing: completely painfree 48%, markedly improved 31%, but 21% unchanged or worse.     

First rib resection in thoracic outlet syndrome

Most patients with thoracic outlet syndrome (TOS) present with exercise-induced upper extremity paresthesia. Neurogenic TOS is the most common type where the brachial nerve plexus is compressed against a tight thoracic outlet. Vascular compromise although rare can result from thoracic outlet pressure against the subclavian artery or more commonly the subclavian vein. This article reviews the pathophysiology of TOS and describes several effective surgical interventions. Complete first rib resection with surgical decompression is an essential part of the treatment for TOS. First rib resection via supraclavicular or a preferred transaxillary route should be considered when conservative modalities provide no symptom improvement.     

Arterial injuries in the thoracic outlet syndrome

Purpose: This article reviews experience with arterial injury caused by thoracic outlet syndrome. Special emphasis is placed on the influence of athletic or work activities on the axillary-subclavian artery system and the mechanism by which the humeral head compresses the axillary artery and the circumflex humeral arterial branches.Methods: Retrospective review identified 34 patients (age range 13 to 67 years) treated for upper extremity symptoms or ischemic complications of thoracic outlet syndrome from 1983 to 1993. Evaluation included assessment of occupational and recreational activities plus duplex ultrasonography and contrast arteriography with positional maneuvers.Results: Twenty-two patients (27 arms) had subclavian artery injury, which was most commonly caused by compression by a bony abnormality (cervical rib, 16; anomalous first rib, two; cervical rib and anomalous first rib, two). Fourteen of the 27 arms had distal embolization. All 27 had surgical decompression of the subclavian artery; 15 required concomitant arterial reconstruction. Twelve additional patients (nine athletes) had axillary artery involvement, all from arterial compression by the head of the humerus during abduction maneuvers; all had concomitant compression of the posterior circumflex humeral artery. Axillary arterial injury included thrombosis (one), aneurysm (two), and symptomatic extrinsic compression only (nine). Five patients with axillary artery involvement were treated without a surgical procedure; of the remainder, three underwent decompression procedures only, and four had direct arterial repair. In both groups all subclavian and axillary artery reconstructions were patent at last follow-up examination (mean 31 months).Conclusion: Most patients with thoracic outlet syndrome who have arterial involvement have a bony anomaly causing subclavian artery compression. This study demonstrates that humeral head compression of the axillary artery and its circumflex branches is a surprisingly common pathologic mechanism. Awareness of this condition affords a better therapeutic approach to arterial injuries caused by thoracic outlet syndrome. (J VASC SURG 1995;21:57-70.)     

Subclavian arterial injury associated with blunt trauma.

Blunt subclavian artery trauma is an uncommon but challenging surgical problem. The purpose of this study was to retrospectively review the management of blunt subclavian artery injuries treated by the Trauma and Vascular Surgery Services at the East Tennessee State University-affiliated hospitals between 1992 and 1998. Six patients with seven blunt subclavian artery injuries were identified. Physical signs indicating blunt subclavian artery injury were pain or contusion around the shoulder joint; fractures of the clavicle, scapula, or ribs; periclavicular hematomas; and ipsilateral pulse or neurologic deficits. Seven subclavian artery injuries were treated-two arterial transections, two pseudoaneurysms, and three intimal dissections. Associated injuries included four clavicle fractures, one humerus fracture, one combined rib and scapular fractures, and two pneumothoraxes. Vascular surgical treatment included three primary arterial repairs, two saphenous vein interposition grafts, and one polytetrafluoroethylene (PTFE) graft. One patient was treated nonoperatively with anticoagulation. No deaths occurred. Morbidity occurred in two patients with chronic upper extremity neuropathy producing prolonged disability from pain and weakness; one patient had reflex sympathetic dystrophy, and the other had a brachial plexus injury. In conclusion, blunt subclavian artery trauma can be successfully managed with early use of arteriography and prompt surgical correction by a variety of vascular techniques. Vascular morbidity is usually low, but long-term disability because of chronic neuropathy may result from associated brachial plexus nerve injury despite a successful arterial repair.     

Combined endovascular and open surgical approach for the management of subclavian artery occlusion due to thoracic outlet syndrome

A 32-year-old male with arterial thoracic outlet syndrome (TOS) underwent endovascular treatment for the chronic total occlusive lesion from the subclavian to the brachial artery after resection of the first rib and cervical rib. A combined endovascular and surgical treatment represents an attractive alternative to the traditional surgical approach for the treatment of complicated arterial TOS.     

Distal arterial reconstruction using Esmarch's bandage technique to salvage upper extremity function in thoracic outlet syndrome caused by cervical ribs: A report of two cases

We present herein the cases of two patients with thoracic outlet syndrome (TOS) who required arterial reconstruction due to gangrene of the fingers and/or hand. In both patients, the cervical ribs had produced intimal injury of the subclavian arteries, and the successive distal arterial embolism brought about severe ischemia of the affected upper extremity. To treat the TOS, the cervical ribs were resected through a supraclavicular incision. In the first patient, arterial reconstruction was performed from the subclavian artery to the radial collateral artery, a branch of the deep brachial artery, which resulted in minimizing amputation of the gangrenous hand. In the second patient, resection and direct anastomosis of the injured subclavian artery were performed, and bypass surgery from a brachial artery to an interosseous artery was carried out, preserving finger function. Reversed saphenous vein grafts were utilized and Esmarch's bandage technique was applied as a substitute for a vascular clamp in both patients. Following these case reports, we discuss the technique of performing distal bypass in the upper extremities and comment on the usefulness of Esmarch's bandage technique for preserving upper extremity function.     

Surgical treatment of the thoracic outlet compression syndrome

Narrowing of the thoracic outlet may give rises to symptoms in the arm from compression of the nerves, the subclavian artery, and the subclavian vein. Anatomic studies show that nerve compression may affect fibers from T-1, C-8, and not infrequently C-7, providing an explanation for the diffuse nature of the nerve symptoms in the arm. Relief from this compression at the thoracic outlet is readily accomplished by transaxillary resection of the first rib together with any associated cervical rib, fibrous cervical rib analogues, or other fibrous bands encroaching on the neurovascular structures. A study of 40 patients with the syndrome who were treated in this way and followed up after an interval of three to ten years shows that those with nerve and vein symptoms can expect a good result but the results of treatment in those with arterial symptoms is less satisfactory.     

Vascular Complications of Cervical Rib

Vascular symptoms are fairly common in cases of cervical rib, while vascular complication consisting in poststenotic aneurysm of the subclavian artery, possibly combined with thrombosis, is rare. Suspected arterial complications associated with cervical rib should prompt arteriography visualizing the whole subclavian artery. The presence of a poststenotic aneurysm is a clear indication for operation. At the operation the arterial compression should be relieved completely; the need for arterioplasty will depend on the size of the aneurysm and its content, if any, of thrombotic masses. Six cases of poststenotic aneurysm of the subclavian artery associated with cervical rib are reported.