Adult Chest Surgery

Chapter 123. Thoracic Outlet Syndromes 

Thoracic outlet syndrome (TOS) is a condition that arises from the compression of one or more of the neurovascular structures that traverse the superior aperture of the chest. The name was previously designated according to the etiology of the compression, that is, scalenus anticus, costoclavicular, hyperabduction, cervical rib, or first rib syndrome. Most compressive factors operate against the first rib and produce a variety of symptoms, depending on which neurovascular structures are compressed. These factors, along with common etiologies and symptoms, are illustrated in Fig. 123-1. My introduction (H.U.) to TOS came in 1947 at Princeton University, where, as a member of the undefeated freshman football team, my neck was knocked severely to the right, paralyzing my arm for several days. After the season, I was sent by train to Johns Hopkins Hospital to be evaluated by Dr. George Bennett, the eminent orthopedic surgeon who had recently operated on Joe DiMaggio's knee. He made the diagnosis of a cervical rib syndrome on the right and offered me an operation or a brace. Recognizing early that surgery was for others, I tried the brace. A piece of stainless steel covered only with leather was fashioned on my shoulder pad. It extended up past my right ear to prevent my neck from being driven to the right. I used this for the next year. However, in those days, no one wore a face mask, and I was often chagrined to find a piece of nose or face or teeth on the ground after a substantial block from the single-wing formation. For this reason, the NCAA ultimately outlawed the brace. Subsequently, the foam rubber "doughnut" was developed to prevent the neck from being forced to extremes in any direction. It is commonly used today. Conservative treatment, then as now, is usually effective. With no surgery, I contributed significantly to our undefeated team, which produced "Coach of the Year" Charles W. Caldwell, Jr., and the last Heisman Trophy winner in the Ivy League, Richard W. Kazmaier, Jr.

Figure 123-1.


The relation of muscle, ligament, and bone abnormalities in the thoracic outlet that may compress neurovascular structures against the first rib.

Since my diagnosis in 1947, many changes in the recognition and management of these multiple conditions have evolved. This chapter elucidates the improvements in the diagnosis and management of thoracic outlet neurovascular compression that have transpired over the past 50 years. Recognizing that such procedures as breast implantation and median sternotomy may produce TOS has been revealing. Prompt thrombolysis followed by surgical venous decompression for the Paget-Schroetter syndrome (i.e., effort thrombosis of the axillary-subclavian vein) has improved results in this condition significantly as compared with the conservative anticoagulation approach. Complete first rib extirpation at the initial operation reduces the incidence of recurrent neurologic symptoms or the need for reoperation. Well over 20,000 patients have been evaluated for TOS in my experience; 4914 underwent neurovascular decompression operations, whereas 1721 had reoperations for recurrent symptoms (primarily from other centers). The evaluation of these patients provides the basis for my recommendation for conservative management and the indications for surgical intervention.

The incidence of any type of compression—arterial, venous, or nerve—presenting to the physician varies with the type of referral practice and specialty the particular physician may have. For example, the orthopedist is prone to see a high number of cervical ribs, the neurologist will see nerve compression patients, and a vascular surgeon will see more aneurysms and arterial/venous occlusions. The thoracic surgeon lies somewhere in between. In addition, the kinds of diagnostic techniques that are available may determine which center a patient is attracted to for management of a particular pathology.


Peet and colleagues coined the term thoracic outlet syndrome to designate compression of the neurovascular bundle at the thoracic outlet.1 Until 1927, the cervical rib was commonly thought to be the cause of symptoms of this syndrome.2 Galen and Vesalius were the first to describe the presence of a cervical rib. Hunauld, who published an article in 1742, is credited by Keen3 as the first observer to describe the importance of a cervical rib in causing symptoms. In 1818, Cooper medically treated symptoms of a cervical rib with some success. In 1861, Coote4 performed the first operation of cervical rib removal. In 1916, Halsted5 stimulated interest in dilation of the subclavian artery distal to the cervical ribs. Law6 in 1920 reported the role of adventitious ligaments in producing cervical rib syndrome. In 1927, Adson and Coffey7 suggested a role for scalenus anticus muscle in producing cervical rib syndrome. This was further developed by Naffziger and Grant8 and by Ochsner and colleagues9 in 1935, who popularized resection of the scalenus anticus muscle. In 1943, Falconer and Weddell10incriminated the costoclavicular membrane in the production of neurovascular compression. Wright11 in 1945 described the hyperabduction syndrome with compression in the costoclavicular area by the tendon of the pectoralis minor. Rosati and Lord12 in 1961 added claviculectomy to anterior exploration, scalenectomy, cervical rib resection when present, and resection of the pectoralis minor and subclavius muscle, as well as the costoclavicular membrane.

The role of the first rib in causing symptoms of neurovascular compression was recognized by Bramwell13 in 1903. Murphy14 is credited with the first resection of the first rib. Brickner15 and Milch16 in 1925 and later Telford and Stopford17 suggested that the first rib was the culprit. Clagett18 in 1962 emphasized the importance of the first rib and popularized the posterior thoracoplasty approach for first rib resection to relieve neurovascular compression. Falconer and Li in 196219 emphasized the anterior approach for first rib resection to relieve costoclavicular compression. Roos20 in 1966 introduced the transaxillary route for first rib extirpation, and our modification of his technique is presented in this chapter.


In the late 1950s and early 1960s, the operation of choice in our practice was the supraclavicular scalenotomy. This procedure involved a partial scalenectomy with neurolysis of the brachial plexus (when indicated) combined with resection of a cervical rib (if present). Early results in 336 patients were extremely good (310 of 336). However, the longer-term follow-up was not as satisfactory. Five-year improvement was present in 150 of 336 patients. However, at 20 years, only 31 of 336 patients were still improved. (We are unable to tell whether this represents 10% or 20% of the total series because 20 patients were lost to follow-up.) For this, and other reasons set forth in the presentation by Dr. O. T. Clagett in 1962,18 the posterior approach for resection of the first rib, the so-called common denominator for thoracic outlet compression forces, was adopted. Subsequently, the initial operation usually was performed through the transaxillary approach because no muscle division was required, and morbidity for the patient was reduced. The supraclavicular or infraclavicular approach, or a "combined approach," was used for arterial lesions. The posterior approach is now reserved for reoperation in patients with recurrent TOS for removal of rib remnants, regenerated fibrocartilage with neurolysis of C7, C8, and T1 nerve roots, and brachial plexus.


The most common symptoms of nerve compression are pain and paresthesias. About 95% of patients exhibit these symptoms; fewer than 10% exhibit motor weakness. Pain and paresthesias are segmental in 75% of cases, and 90% involve the ulnar nerve distribution.21 TOS can occur in older patients (oldest age 87 years). When nerve compression symptoms occur in patients older than age 60, other causes should be suspected, most frequently degenerative or traumatic cervical spine pathology or cardiac or pulmonary etiologies.

There may be multiple points of compression of the peripheral nerves between the cervical spine and hand in addition to the thoracic outlet. In the instance of multiple compression sites, less pressure is required at each site to produce symptoms. Thus a patient may have concomitant TOS, ulnar nerve compression at the elbow, and carpal tunnel syndrome. This phenomenon has been designated the multiple crush syndrome.22


The pain experienced by individuals with TOS is frequently insidious in onset and commonly involves the neck, shoulder, arm, and hand. Some patients experience atypical pain, involving the anterior chest wall and parascapular area. This symptom is termed pseudoangina because it simulates angina pectoris.

A group of patients with chest pain simulating angina pectoris but with normal coronary angiograms was evaluated in 1973. When either medical or surgical therapy for TOS relieved the symptoms of pseudoangina (in 330 patients), the diagnosis was deemed to have been confirmed.23

It is important to remember that there are at least two types of pain pathways in the arm—the commonly acknowledged (C5-T1) somatic, "more superficial" pain, and the afferent sympathetic nerve fibers that transmit "deeper" painful stimuli from the heart, esophagus, chest wall, and arm.

The cell bodies of the two types of afferent neurons are situated in the dorsal root ganglia of the corresponding spinal segments. They synapse in the dorsal gray matter of the spinal cord, and the axons of the second-order neurons ascend in the spinal cord up to the brain. Compression of the "superficial" C8-T1 cutaneous afferent fibers elicits stimuli that are transmitted to the brain and recognized as integumentary pain or paresthesias in the ulnar nerve distribution. In contrast, compression of the predominantly "deeper" sensory fibers elicits impulses that are appreciated by the brain as deep pain originating in the arm or the chest wall, even if the source of the impulses is cardiac (referred pain).

The pseudoangina experienced in thoracic outlet compression shares with angina pectoris the same dermatomal distribution. The heart, arm, and chest wall have afferent fibers converging on T2-T5 spinal cord segments, and their cell bodies are located in the corresponding dorsal root ganglia. Referred pain to the chest wall is a component of both pseudoangina and angina pectoris. Because somatic pain is more common than visceral pain, the brain has "learned" from past experience that activity arising in a given pathway is caused by a pain stimulus in a particular somatic area.


A careful history and physical examination are essential for diagnosis. The multiple physical signs of thoracic outlet compression, as well as the classic diagnostic tests, have been reviewed.22,24

Briefly, the objective test for thoracic outlet peripheral nerve compression in our clinic is the nerve conduction velocity (NCV) test.23,25,26 Reduction in NCV below 85 m/s of either the ulnar or median nerves across the thoracic outlet corroborates the clinical diagnosis. More than 8000 NCV studies have been performed annually at Baylor University Medical Center for many years. Approximately 2000 patients per year demonstrate TOS.27,28

The electromyogram should be normal and rules out other neuromuscular disorders. With conduction velocities above 60 m/s, the patient is usually improved with appropriate conservative physical therapy.


The principles of conservative management have been outlined by Novak and MacKinnon, as well as by Caldwell and Crane.26,29 Initially, most patients are treated conservatively with physical therapy, except those with vascular problems. The primary goals of physical therapy are to "open up" the space between the clavicle and first rib, improve posture, strengthen the shoulder girdle, and loosen the neck muscles. This is accomplished by pectoralis stretching, strengthening the muscles between shoulder blades, assumption of good posture, and active neck exercises, including chin tuck, flexion, rotation, lateral bending, and circumduction. It is imperative to rule out other causes of TOS-like symptoms, such as cardiac or pulmonary disease.

Indications for Surgery

Failure of appropriate conservative therapy together with significantly reduced NCVs below 60 seconds (normal 85 m/s) and the elimination of other possible etiologies for the patient's symptoms are the usual indications for surgery.


Initial therapy involves complete first rib resection, anterior scalenectomy, resection of the costoclavicular ligament, and neurolysis of C7, C8, and T1 nerve roots and the brachial plexus through a transaxillary approach (described below).30 The first rib with the compressive elements also may be removed through the supraclavicular approach31 (see Chap. 122). The supraclavicular approach has the disadvantage of working through and retracting the brachial plexus as well as producing a visible scar in women (the preponderant gender with TOS). The posterior thoracoplasty approach for first rib resection may be used for initial therapy, but it is better reserved for reoperation and neurolysis of the brachial plexus (not described).32,33 Cervical ribs may be removed through any of the approaches described. Dorsal sympathectomy also may be performed with neurovascular decompression through any of the preceding incisions for sympathetic maintained pain syndrome (SMPS), reflex sympathetic dystrophy, causalgia, and Raynaud's phenomenon and disease33 (see Chap. 121).

Upper Plexus versus Lower Plexus Management

Most patients with neurologic TOS requiring operation have been managed successfully with transaxillary resection of the first rib. However, for upper plexus (median nerve) compression, Roos20 and Stoney34 felt that transaxillary rib resection alone was not enough and that it should be combined with the supraclavicular approach to achieve best results.

Upper plexus compression was described initially by Swank and Simeone31 with symptoms secondary to C5, C6, and C7 nerve root compression. Sensory changes were primarily in the first three fingers and muscle weakness or pain in the anterior part of the chest, triceps, deltoids, and parascapular muscle areas, as well as down the outer arm to the extensor muscles of the forearm. In contrast, lower plexus irritation involves C8 and T1 nerve root compression. It includes sensory changes in the fourth and fifth fingers with muscle weakness or pain from the rhomboid and scapular muscles to the posterior axilla and down the ulnar distribution to the forearm, involving the elbow, flexors of the wrist, and intrinsic muscles of the hand. Roos,20 Urschel,35 and Wood and Ellison36 expanded the upper plexus symptoms to involve pain in the neck, face, mandible, and ear with occipital headaches. Wood and Ellison also noted dizziness, vertigo, and blurred vision in some patients with upper plexus lesions.

In addition to clinical symptoms and signs, median nerve conduction slowing indicated upper plexus compression, whereas ulnar nerve conduction slowing suggested lower plexus compression.

There are several reasons for using transaxillary first rib resection alone to relieve upper plexus symptoms. Anatomic observations show that the median nerve, usually incriminated in upper plexus compression of C5, C6, and C7 nerve roots, also receives significant fibers from C8 and T1 nerve roots. In addition, most muscles and ligaments that compress the upper plexus attach to the first rib. Thus, removing the first rib with release of all the muscles and ligaments involved in the compression theoretically should relieve upper plexus compression.

To better assess the optimal management of upper plexus TOS, we reviewed 2210 primary operations for TOS in 1988 patients, 222 of whom had bilateral transaxillary resections, during a period of 30 years.35 Two-hundred and fifty operations were for symptoms, signs, and NCVs showing median nerve or upper plexus compression only; 452 were for compression of both the median and ulnar nerves or the combination of upper and lower plexus by symptoms, signs, and NCVs. One-thousand five-hundred and eight operations were carried out for symptoms, signs, and NCVs demonstrating predominantly ulnar nerve or lower plexus compression.

This study of 2210 consecutive operations showed that transaxillary first rib resection with anterior scalenectomy relieves symptoms of the upper plexus (96%) and combined upper and lower plexus (95%) as well as it did for the lower plexus (95%).35 Wood and Ellison36 and Sanders37 independently corroborated these findings. Patients are seen at 3 weeks and 3 months. Yearly contacts are made by telephone.


Arterial Compression

The diagnosis is suspected by history, physical examination, and Doppler studies and confirmed with arteriography.21 Therapy for arterial compression depends on its degree of involvement.

1.     An asymptomatic patient with cervical or first rib arterial compression producing poststenotic dilatation of the axillary subclavian artery should undergo rib resection, preferably through the transaxillary approach, removing the ribs, both first and cervical, without resecting the artery. The dilatation usually returns to normal after removal of compression.

2.     Compression from the first or cervical rib producing aneurysm with or without thrombus should be treated with rib resection and aneurysm excision with graft through the supraclavicular and infraclavicular combined approach.

3.     Thrombosis of the axillary subclavian artery or distal emboli secondary to TOS compression should be treated with first rib resection, thrombectomy, embolectomy, arterial repair or replacement, and dorsal sympathectomy.

One-hundred and fifty-one patients with axillary-subclavian artery aneurysm and 62 patients with occlusion were treated successfully. Dorsal sympathectomy was performed when indicated. The bypass grafts38 were successful, with the exception of three that occluded and required reoperation and one that could not prevent amputation because of the time that had elapsed before the patient presented for therapy. No cerebrovascular accidents occurred.

Venous Compression

Effort thrombosis of the axillary subclavian vein, or Paget-Schroetter syndrome, is usually secondary to unusual repetitive use of the arm in addition to the presence of one or more compressive elements in the thoracic outlet (see Chap. 125). Historically, Sir James Paget39 in London in 1875 and Von Schroetter40 in Vienna in 1884 independently described this syndrome of thrombosis of the axillary-subclavian vein that bears their names. The word effort was added to thrombosis because of the frequent association with exertion, which produced either direct or indirect compression of the vein. The thrombosis is caused by either trauma or unusual occupations that require repetitive muscular activity. Typical occupations include professional athletes, linotype operators, painters, and beauticians. Cold and traumatic factors, such as carrying skis over the shoulder, tend to increase the proclivity for thrombosis. Elements of increased thrombogenicity also increase the incidence of this problem and exacerbate its symptoms on a long-term basis.41,42

The diagnosis is suspected by a careful history and physical examination with Doppler studies and is confirmed by a venogram.

Intermittent or partial obstruction should be treated by first rib removal through the transaxillary approach with resection of the costoclavicular ligament medially, first rib inferiorly, and the scalenus anticus muscle laterally. The clavicle is left in place. The vein is decompressed, and all the bands and adhesions are removed.

For many years, complete thrombosis Paget-Schroetter syndrome was treated by elevation of the arm and use of anticoagulants, with subsequent return to work. If symptoms recurred, the patient was considered for a first rib resection, with or without thrombectomy, as well as resection of the scalenus anticus muscle and removal of any other compressive element in the thoracic outlet, such as the costoclavicular ligament, cervical rib, or abnormal bands.21 Thirty-six patients were treated by this approach; only 10 ended with a good to excellent result.

Availability of thrombolytic agents combined with prompt surgical decompression of the neurovascular compressive elements in the thoracic outlet reduced morbidity and the necessity for thrombectomy with substantially improved clinical results, including the ability to return to work.42,43 This technique involves hospitalizing the patient, and through an antecubital indwelling catheter, a venogram is performed and thrombolytic therapy initiated. After lysis of the clot, prompt first rib resection with removal of compressive elements is performed.

This technique has been carried out in 440 patients with Paget-Schroetter syndrome. Thrombectomy was necessary in only 4 extremities. Long-term results indicated that 405 extremities had good results; that is, the patient returned to work without symptoms. Twenty-four patients had fair results, that is, with intermittent swelling but still able to work, and 11 patients were regarded as having poor results, that is, chronic swelling. Seven occurrences of poor results were observed in the 35 patients seen initially at more than 3 months after the thrombotic episode. No patient had phlegmasia cerulea dolens (i.e., severe deep vein thrombosis of the upper extremity). There were no deaths. These results were in great contrast to 35 patients treated with anticoagulants only, with only 10 having good results, 16 fair results, and 9 poor results.42

Delay in initiating thrombolytic therapy or the prolonged use of Coumadin or heparin is contraindicated. There were no obvious complications of thrombolytic therapy.

With a prolonged interval between venous occlusion and diagnosis (>3 months), the same management produced less favorable results. Attempts to open the occluded vein mechanically with the laser or bypass grafts have been uniformly unsatisfactory.

Percutaneous venous balloon dilation with stent placement has been performed in multiple cases. Its use demonstrates the lack of understanding of the underlying anatomic pathology (the external constriction of the vein in the thoracic outlet by a medical insertion of the costoclavicular ligament and hypertrophy of the scalenus anticus muscle). The balloon dilation is only temporary, and the stent is then constricted. Since the venous flow and pressure are far less than the arterial flow, the stent clots, occludes, and subsequently is very difficult to manage.

Claviculectomy is used occasionally for decompression, particularly if a fracture of the clavicle has occurred secondary to trauma.44

Sympathetic Compression

Compression of the sympathetic nerves in the thoracic outlet may occur alone or in combination with peripheral nerve and blood vessels. The sympathetics are intimately attached to the artery as well as the bone. They may be compressed or "irritated" in primary or recurrent TOS situations.

As a cause of atypical chest pain—or pseudoangina—cardiac pain is simulated. Many arterial compressions result in more severe symptoms because of the additive or synergistic sympathetic stimulation. Trauma frequently is associated with the SMPS or reflex sympathetic dystrophy.

For uncomplicated, nontraumatic TOS symptoms, first rib resection alone with neurovascular decompression relieves the sympathetic symptoms without requiring dorsal sympathectomy.

However, if trauma is significant in the etiology, or if causalgia or SMPS is present, concomitant dorsal sympathectomy is routinely required to ameliorate the symptoms. Also, where surgery is required for recurrent TOS symptoms, the relief of accompanying causalgia usually requires dorsal sympathectomy. Initially, dorsal sympathectomies were performed at an interval after traumatic or recurrent TOS operations. However, because of the high necessity index and the inconvenience of a second operation, dorsal sympathectomy is now combined routinely with the initial TOS operative procedure for either trauma or reoperated recurrence patients.45,46

Major indications for dorsal sympathectomy include hyperhidrosis, Raynaud's phenomenon, Raynaud's disease, causalgia, SMPS or reflex sympathetic dystrophy, and vascular insufficiency of the upper extremity. Except for hyperhidrosis, most indications for sympathectomy require the usual diagnostic techniques, including cervical sympathetic block, to assess the relief of symptoms with temporary sympathetic blockade. When Raynaud's phenomenon of a minor to moderate degree is associated with TOS, the simple removal of the first rib along with a cervical rib (if present) and stripping of the axillary-subclavian artery (neurectomy) generally relieves most symptoms after the initial operation.47 It is rarely necessary to perform a sympathectomy unless the Raynaud's phenomenon is very severe, in which case a dorsal sympathectomy is carried out with first rib resection. The only contraindication to dorsal sympathectomy is venous obstruction, that is, Paget-Schroetter syndrome.


Historically, the anterior cervical approach to the cervical sympathetic chain has been used.48 The stellate ganglion lies on the transverse process of C6, and this approach is used by neurosurgeons and vascular surgeons. For hypertension, Urschel and Razzuk49 popularized the posterior approach with a longitudinal paraspinal incision with the patient in the prone position. Small pieces of the second ribs are removed, and the sympathetic chain is identified in the usual position. This approach has the advantage of allowing bilateral procedures at the same time without changing the patient's surgical position. The most common current approach is the transaxillary, transthoracic approach, which is performed through the second interspace with a transverse subhairline incision.50 This is more painful than the other approaches, but with video-assisted thoracoscopy, it can be performed with minimal discomfort.46

The approach used most frequently for TOS is the transaxillary approach for first rib resection and a dorsal sympathectomy.45,51 This has the advantage of minimal pain and combines two procedures with low morbidity. Video assistance is also used frequently with this approach (see Chap. 124).


The initial surgical therapy involves a complete first rib resection, anterior scalenectomy, resection of the costoclavicular ligament, and neurolysis of the C7, C8, and T1 nerve roots and the brachial plexus through a transaxillary approach. The transaxillary, transthoracic approach is performed through the second interspace with a transverse subhairline incision (Fig. 123-2).

Figure 123-2.


A subhairline incision is made for the transaxillary approach to first rib resection.


The first rib is exposed, revealing the scalene muscles and vessels (Fig. 123-3). The anterior scalene is divided, the periosteum is opened, and a triangular-shaped segment of the first rib is excised (Fig. 123-4). The anterior portion of the rib is resected at the cartilage and removed, after which the middle scalene muscle is divided (Fig. 123-5). Next, the posterior section of the rib is resected (Fig. 123-6) with full attention to the T1 and C8 nerve roots to avoid injury. The head and neck of the rib are removed with rongeurs, and the dorsal sympathetic chain is identified and divided through the lower stellate ganglion above the T1 and below the T3 ganglia (Fig. 123-7).

Figure 123-3.


Exposure of the first rib showing the scalene muscles and vessels.


Figure 123-4.


A triangular-shaped wedge is excised from the first rib, and the anterior scalene muscle is divided.


Figure 123-5.


The anterior portion of the rib is resected back to the costocartilage. The middle scalene muscle is divided.


Figure 123-6.


The posterior section of the rib is removed, with attention to the T1 and C8 nerve roots.


Figure 123-7.


The sympathetic chain is identified, and the end of the head and neck of the posterior portion of the first rib is removed using Urschel rongeurs. The nerves are transected from T1 through T3.

Dorsal sympathectomy has been performed in 3214 extremities at our institution; 2974 of these were associated with neurologic TOS, causalgia, and SMPS. Two-hundred and forty operations were associated with arterial complications of TOS. In the neurologic TOS patients, 1721 dorsal sympathectomies were related to recurrent disease and reoperation.

On average, symptoms recur in 3 years (range 6 months to 25 years). In 46 patients, symptoms of sympathetic activity were apparent in fewer than 6 months. This is most likely from "sprouting," or failure to strip the artery of its sympathetic nerves. This complication seems to occur less if the bed of the sympathetic chain is cauterized after dorsal sympathectomy. It also can be explained by high circulating concentrations of catecholamines.

The postsympathetic syndrome was observed in 39 patient extremities. This complication involves excessive postoperative pain (lasting as long as 6 months) in several nerve root distributions of the involved extremity and may be the result of injury to the somatic nerve. Unexpected Horner's syndrome was noted in 27 patients; in 21 patients, the syndrome was only transient and resolved gradually.


Recurrent symptoms, primarily neurogenic, should be documented by objective NCVs. When they are depressed in a symptomatic patient unrelieved by prolonged conservative therapy, he or she should be considered for posterior reoperation. Removal of any rib remnants or regenerated fibrocartilage and neurolysis of the C7, C8, and Tl nerve roots and the brachial plexus are performed.33 Dorsal sympathectomy is added to minimize the causalgia contribution to symptoms. Depo-Medrol and hyaluronic acid are used to minimize recurrent scars.52

We identified two distinct groups of patients who required reoperation: those with pseudorecurrences and those with true recurrences. Pseudorecurrences were observed in 43 patients who were all referred from other surgeons and were never completely relieved of symptoms after the initial operation. They were separated into the following etiologies: mistaken resection of the second rib instead of the first (22 patients), resection of the first rib with a cervical rib left in place (11 patients), resection of a cervical rib with an abnormal first rib remaining (8 patients), and resection of a second rib with a rudimentary first rib left (2 patients).

One-thousand seven-hundred and twenty-one extremities had true recurrences and included patients who were relieved of symptoms after the initial operation but had recurrence of symptoms 4 months to 18 years later. The working and differential diagnoses for recurrence are similar to those for the original operation. Indications for a reoperation are more stringent, in that longer periods of conservative therapy usually are invoked.

In this group, a substantial posterior stump (>1 cm) of the first rib remained in 1560 patients (all referred from outside physicians). Complete resection of the first rib at the initial operation was observed in 161 patients who had recurrent symptoms associated with excessive scar formation on the brachial plexus; 98 were operated initially by us, with a recurrence rate requiring reoperation of 2.0% (4914 primary operations). Even allowing for the fact that some of our patients did not return to us for recurrent TOS, this is much less than most series.

Few other surgeons remove the rib completely at the initial operation for fear of injuring the T1 or C8 nerve roots. Some cover the end of the rib at the transverse process of the vertebra with the scalenus medius muscle.

Results of 1721 operations showed a moderately good early effect after reoperation, with 1531 patients (89%) expressing significant improvement, 130 (7.6%) reporting fair improvement, and only 50 (2.9%) failing to feel better.

Late results (5-year follow-up) in 828 patients who underwent reoperations revealed 621 (75%) with good results and 207 (25%) with fair to poor recovery. Fifty-three patients (3.1%) required a third operation.

The primary technical factors involved in recurrence seem to be complete extirpation of the rib at the first operation. If a rib remnant is left (as is the case with most surgeons outside our group), osteocytes grow out from the end of the bone and produce fibrocartilage and regenerated bone that compress the nerves. Keloid producers, failure to drain hematomas, and early excessive physical therapy after the first operation also may increase fibrosis. Occasionally, other approaches for reoperation have been used.53

Recurrent Arterial Abnormalities

Five patients referred from other physicians (two with false aneurysms, one with a mycotic aneurysm allegedly secondary to trauma at the initial operation, and two with obstructive arterial changes at the thoracic outlet) were reoperated successfully. Vascular reconstructive procedures were performed. In each patient, a saphenous vein bypass graft from the innominate or carotid artery proximally was connected to the brachial artery distally. In the patient with the mycotic aneurysm, the graft was placed first, and the vessels on each side of the aneurysm were ligated. The aneurysm was resected at an interval procedure.


There were no deaths in the series of 4914 primary and 1721 reoperative TOS decompressive procedures. The major complication observed was a rib remnant left by the initial surgeon. From this, fibrocartilage and new bone regenerated, producing a high incidence of recurrence. More retractor help (two arm holders) and increased light improved the technique and facilitated the initial operation. This minimized the time of anesthesia, surgery, retractor use, and arm holding.

The pleura is opened at most operations (with the exception of pleurodesis) to provide drainage of blood and fluids, reducing recurrence.

Bleeding requiring reoperation occurred after only 3 of 5008 operations. Significant infection requiring drainage occurred after nine operations. There were no significant arterial injuries and only one occurrence of postoperative venous bleeding requiring thoracotomy and repair. Venous injuries usually "suck air." Paget-Schroetter syndrome usually is associated with severe inflammation that obliterates the vein and removes its identifying blue color. The axillary structures usually are plastered to the chest wall firmly, making the operation difficult technically.

Significant nerve injuries of the brachial plexus with residual signs occurred in four patients, none of whom could be identified as having had prolonged stretching, inappropriate retraction, or direct surgical injury. Two occurred in diabetic patients and two in older individuals with very prolonged NCVs, suggesting an increased sensitivity to nerve pressure similar to that observed in diabetics.

A review of morbidity from the literature on 881 patients by Dale54 revealed significant bleeding in 11 (1.4%) and nerve injury of the brachial plexus in 13 (1.5%), of the phrenic nerve in 39 (4.9%), of the long thoracic nerve in 3 (0.1%), and of the recurrent laryngeal nerve in 6 (0.2%). In another 168 patients reported54 the phrenic nerve was injured in 6 (4%), the long thoracic and recurrent laryngeal nerves were injured in 1 (0.5%), and Horner's syndrome occurred in 9 (6%). Long-term studies55,56 as well as other complications, have been reported.57


Over 50 years, many changes have resulted in improved recognition and management of TOS. The most remarkable include the use of NCV to obtain a more accurate diagnosis and to follow up with nerve compression patients. Chest pain or pseudoangina can be caused by TOS. Complete rib resection is important at the initial operation to minimize recurrence. Thrombolysis with prompt first rib resection is the optimal treatment for most patients with Paget-Schroetter syndrome. Dorsal sympathectomy is helpful for SMPS, causalgia, and recurrent TOS needing reoperation. Use of techniques of video-assisted thoracic surgery can reduce the morbidity of the transaxillary approach to first rib resection for TOS and are discussed in the next chapter (see Chap. 124).


Mrs. Rachel Montano is to be highly commended for her dedication and commitment to the completion of this chapter.


Dr. Urschel and his group with their large experience have developed the principles of operative treatment of thoracic outlet syndrome. These solid principles–correct diagnosis, application of nonoperative treatment when feasible, and complete resection of the first rib–hold true regardless of the surgical approach or technique chosen.



1. Peet RM, Henriksen JD, Anderson TP, Martin GM: Thoracic-outlet syndrome: Evaluation of a therapeutic exercise program. Proc Staff Meet Mayo Clin 31:281–7, 1956.[PubMed: 13323047]

2. Borchardt M: Symptomologie und Therapie der Halsripen. Berl Klin Wochenschr 38:1265, 1901. 

3. Keen W: The symptomatology, diagnosis and surgical treatment of cervical ribs. Am J Sci 133:173, 1907. 

4. Coote H: Pressure on the axillary vessels and nerve by an exostosis from a cervical rib; interference with the circulation of the arm; removal of the rib and exostosis; recovery. Med Times Gas 2:108, 1861. 

5. Halsted W: An experimental study of circumscribed dilation of an artery immediately distal to a partially occluding band, and its bearing on the dilation of the subclavian artery observed in certain cases of cervical rib. J Exp Med 24:271, 1916. 

6. Law A: Adventitious ligaments simulating cervical ribs. Ann Surg 72:497, 1920.[PubMed: 17864355]

7. Adson AW, Coffey JR: Cervical rib: A method of anterior approach for relief of symptoms by division of the scalenus anticus. Ann Surg 85:839–57, 1927.[PubMed: 17865683]

8. Naffziger H, Grant W: Neuritis of the brachial plexus-mechanical in origin: The scalenus syndrome. Surg Gynecol Obstet 67:722, 1938. 

9. Ochsner A, Gage M, DeBakey M: Scalenus anticus (Naffziger). Am J Surg 26:699, 1935. 

10. Falconer M, Weddell G: Costoclavicular compression of the subclavian artery and vein: Relation to scalenus syndrome. Lancet 2:539, 1943. 

11. Wright I: The neurovascular syndrome produced by hyperabduction of the arm. Am Heart J 29:1, 1945. 

12. Rosati L, Lord J: Neurovascular compression syndromes of the shoulder girdle. In Modern Surgical Monographs. New York, Grune & Stratton, 1961.

13. Bramwell E: Lesion of the first dorsal nerve root. Rev Neurol Psychiatry 1:236, 1903. 

14. Murphy T: Brachial neuritis caused by pressure of first rib. Aust Med J 15:582, 1910. 

15. Bricker W: Brachial plexus pressure by the normal first rib. Ann Surg 85:858, 1927. 

16. Brickner W, Milch H: First dorsal vertebra simulating cervical rib by maldevelopment or by pressure symptoms. Surg Gynecol Obstet 40:30, 1925. 

17. Telford E, Stopford J: The vascular complications of the cervical rib. Br J Surg 18:559, 1937. 

18. Clagett OT: Research and prosearch. Thorac Cardiovasc Surg 44:153–66, 1962.[PubMed: 13879636]

19. Falconer MA, Li FW: Resection of the first rib in costoclavicular compression of the brachial plexus. Lancet 1:59–63, 1962.[PubMed: 13891419]

20. Roos DB: Transaxillary approach for first rib resection to relieve thoracic outlet syndrome. Ann Surg 163:354–8, 1966.[PubMed: 5907559]

21. Urschel HC Jr: Management of the thoracic-outlet syndrome. N Engl J Med 286:1140–3, 1972.[PubMed: 4336328]

22. MacKinnon S, Dellon A: Surgery of the Peripheral Nerve. New York, Thieme, 1988.

23. Urschel HC Jr, Razzuk MA, Wood RE, et al: Objective diagnosis (ulnar nerve conduction velocity) and current therapy of the thoracic outlet syndrome. Ann Thorac Surg 12:608–20, 1971.[PubMed: 4331517]

24. Urschel HJ, Razzuk M: Thoracic outlet syndrome. In Sabiston DC Jr, Spencer FC (eds): Gibbon's Surgery of the Chest. Philadelphia, Saunders, 1995:536–53.

25. Jebsen RH: Motor conduction velocities in the median and ulnar nerves. Arch Phys Med Rehabil 48:185–94, 1967.[PubMed: 6022543]

26. Caldwell J, Crane C, Krusen E: Nerve conduction studies in the diagnosis of the thoracic outlet syndrome. South Med J 64:210, 1971.[PubMed: 4323565]

27. Greep N, Lemmens H, Roos D: Pain in Shoulder and Arm: An Integrated View. The Hague, Martinus Nijhoff, 1979.

28. Urschel HC Jr: The John H. Gibbon, Jr., Memorial Lecture: Thoracic outlet syndromes. Annual Meeting of the American College of Surgeons, San Francisco, October 10–15, 1993. 

29. Novak C, MacKinnon S: Thoracic outlet syndrome. Orthop Clin North Am 27:747–62, 1996.[PubMed: 8823394]

30. Urschel HC Jr, Paulson D, McNamarra J: Thoracic outlet syndrome. Ann Thorac Surg 6:1–10, 1968.[PubMed: 5748008]

31. Swank R, Simeone F: The scalenus anticus syndrome. Arch Neurol Psychiatry 51:432, 1944. 

32. Urschel HJ, Razzuk MA: Thoracic outlet syndrome. In Glenn WL, Baue AE, Geha AF (eds): Thoracic and Cardiovascular Surgery. Norwalk, CT, Appleton-Century-Crofts, 1995.

33. Urschel HJ, Cooper J: Atlas of Thoracic Surgery. New York, Churchill-Livingstone, 1995.

34. Stoney WS, Addlestone RB, Alford WC , Jr., et al: The incidence of venous thrombosis following long-term transvenous pacing. Ann Thorac Surg 22:166, 1976.

35. Urschel HC Jr, Razzuk MA: Upper plexus thoracic outlet syndrome: Optimal therapy. Ann Thorac Surg 63:935–9, 1997.[PubMed: 9124966]

36. Wood VE, Ellison DW: Results of upper plexus thoracic outlet syndrome operation. Ann Thorac Surg 58:458–61, 1994.[PubMed: 8067849]

37. Sanders R: Thoracic Outlet Syndrome: A Common Sequela of Neck Injuries. Philadelphia, Lippincott, 1991.

38. Urschel HC Jr, Razzuk MA: Paget-Schroetter syndrome: What is the best management? Ann Thorac Surg 69:1663–8; discussion 1668–9, 2000. 

39. Paget J: Clinical Lectures and Essays. London, Longmans Green, 1985.

40. Von Schroetter L: Erkrankungen der Fegasse. Vienna, Holder, 1884. 

41. Adams JT, DeWeese JA: "Effort" thrombosis of the axillary and subclavian veins. J Trauma 11:923–30, 1971.[PubMed: 5160553]

42. Urschel HC Jr, Razzuk MA: Improved management of the Paget-Schroetter syndrome secondary to thoracic outlet compression. Ann Thorac Surg 52:1217–21, 1991.[PubMed: 1755673]

43. Azakie A, McElhinney DB, Thompson RW, et al: Surgical management of subclavian vein effort thrombosis as a result of thoracic outlet compression. J Vasc Surg 28:777–86, 1998.[PubMed: 9808844]

44. Lord J, Urschel HJ: Total claviculectomy. Surg Rounds 11:17, 1988. 

45. Urschel HC Jr: Dorsal sympathectomy and management of thoracic outlet syndrome with VATS. Ann Thorac Surg 56:717–20, 1993.[PubMed: 8379779]

46. Urschel HC Jr: Video-assisted sympathectomy and thoracic outlet syndrome. Chest Surg Clin North Am 3:299, 1993. 

47. Urschel HC Jr, Razzuk M: Thoracic outlet syndrome. In Shields TW (ed): General Thoracic Surgery. Philadelphia, Lea & Febiger, 1994.

48. Hempel GK, Rusher AH Jr, Wheeler CG, et al: Supraclavicular resection of the first rib for thoracic outlet syndrome. Am J Surg 141:213–5, 1981.[PubMed: 7457739]

49. Urschel HC Jr, Razzuk M: Posterior thoracic sympathectomy. In Malt RA (ed): Surgical Techniques Illustrated: A Comparative Atlas. Philadelphia, Saunders, 1958.

50. Atkins HJ: Sympathectomy by the axillary approach. Lancet 266:538–9, 1954.[PubMed: 13143720]

51. Martinez B: Thoracic outlet syndrome. In Cameron JL (ed): Current Surgical Therapy. St Louis, Mosby, 1992:753–7.

52. Urschel HC Jr, Razzuk MA: The failed operation for thoracic outlet syndrome: The difficulty of diagnosis and management. Ann Thorac Surg 42:523–8, 1986.[PubMed: 3778002]

53. Cheng SW, Stoney RJ: Supraclavicular reoperation for neurogenic thoracic outlet syndrome. J Vasc Surg 19:565–72, 1994.[PubMed: 8164270]

54. Dale WA: Thoracic outlet compression syndrome: Critique in 1982. Arch Surg 117:1437–45, 1982.[PubMed: 7138303]

55. Lepantalo M, Lindgren KA, Leino E, et al: Long term outcome after resection of the first rib for thoracic outlet syndrome. Br J Surg 76:1255–6, 1989.[PubMed: 2605466]

56. Goff CD, Parent FN, Sato DT, et al: A comparison of surgery for neurogenic thoracic outlet syndrome between laborers and nonlaborers. Am J Surg 176:215–8, 1998.[PubMed: 9737636]

57. Horowitz SH: Brachial plexus injuries with causalgia resulting from transaxillary rib resection. Arch Surg 120:1189–91, 1985.[PubMed: 4038064]

If you find an error or have any questions, please email us at Thank you!