Thoracic Outlet Compression Syndrome Richard M. Kremer, MD, Spokane, Washington Richard E. Ahlquist, Jr, MD, Spokane, Washington

Neurovascular compression at the base of the neck has been observed by anatomists and surgeons for over a century. During the first half of this century much controversy existed over the compressive mechanisms involved. Numerous terms, such as scalenus anticus syndrome, costoclavicular syndrome, cervical rib syndrome, hyperabduction syndrome, and shoulder-arm syndrome, implicated different anatomic structures as the causative agent, and therapy varied accordingly. Significant contributions were made by Peet and his associates [I] in 1956, who recognized similarity in the symptom pattern of all these syndromes, and by Rob and Standeven [2] in 1958, who suggested grouping all the recognized syndromes of compression of the neurovascular structures to the upper extremities under the term, “thoracic outlet compression syndrome.” Subsequently, the first rib has generally been accepted as the “common denominator” by vascular and thoracic surgeons presented with this difficult problem. The present report outlines our experience in treating forty-nine patients

with the diagnosis

pression

syndrome.

of thoracic

outlet

com-

Material and Methods The forty-nine patients treated surgically for the thoracic outlet compression syndrome averaged thirty-six years of age. Thirty patients (61 per cent) were female. The symptoms encountered were neurologic in 80 per cent, vascular in 4 per cent, and both neurologic and vascular in 16 per cent. At least one of the provocative maneuvers (Adson, military brace or abduction-external rotation) gave positive results in all patients. Thirty per cent had a supraclavicular bruit and 8 per cent had some supraclavicular tenderness. Arteriograms gave positive results in sixteen of twenty-one patients and were equivocal in two. (Figure 1.) Phlebography performed in two patients gave positive results in both. (Figure 2.) Ulnar nerve conduction velocities were measured across the thoracic outlet in five patients and none was positive. Myelograms and electromyograms performed in several Reprint requests should be addressed to Richard M. Kremer, MD. W. 104 5th Avenue. Spokane, Washington 99204.

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patients were useful in excluding those patients with other problems. Sixty-four procedures were performed including forty-nine first rib resections (forty-eight using the transaxillary approach and one the posterior approach), eleven cervical rib resections by the supraclavicular route with and without scalenotomy, two lysis of adhesions, and two scalenotomies alone (the scalenotomies were performed early in the series). Eleven patients had had previous surgical therapy including scalenotomy in five, first rib resection followed by regeneration of the rib in two, first rib resection followed by the development of dense scar along the bed of the ribs in two, and inadequate removal of the first rib in two. Operation is performed in the following way. The patient is placed in a 45 to 90 degree lateral decubitus position. The shoulder, neck, and upper part of the chest and arm are prepared and draped. The arm is draped with stockinette. A curvilinear skin incision is made just inferior to the axillary hair-bearing area. The arm is held by an assistant who has the sole task of maintaining traction at 90 degrees from the chest wall. After the subcutaneous fascia is incised, a satisfactory surgical plane adjacent to the lateral chest wall is entered and developed until the first rib is identified. A consistent small artery (the lateral thoracic artery) seen in the midportion of the field is ligated. An attempt is made to preserve the intercostobrachial cutaneous nerve. The axillary vein is visualized anterior to the anterior scalene muscle. The axillary artery and lower trunk of the brachial plexus are visualized between the insertions of the anterior and middle scalene muscles to the first rib. The anterior and middle scalene muscles are transected adjacent to the superior surface of the first rib. The first rib is dissected free of the pleura extraperiosteally, transected at its midpoint, and removed in two pieces using the Sauerbruch box rongeur for the posterior segment and Bethune rib shears for the anterior segment. If the pleural space is entered, a small Robinson catheter is inserted, the lung is expanded by the anesthesiologist, and closure is carried out around the catheter which is withdrawn at the end of the procedure. Interrupted sutures are used for the subcutaneous fascia and a subcuticular suture for the skin. Operative time approximates fortyfive minutes and blood loss 50 cc. Cervical ribs, when present, are removed through an anterior, supraclavicular approach.

The American Journalol Surgery

Thoracic Outlet Compression Syndrome

Figure 1. Arteriogram showing definite compression of the subciavian artery at the level of the first rib.

Figure 2. Phiebogram showing complete obstruction of the subciavian vein at the level of the first rib.

Results

side and underwent a similar procedure with the same findings. One year postoperatively he is completely asymptomatic, with negative military brace and abduction-external rotation maneuvers.

We have achieved good to excellent relief of symptoms in 86 per cent of patients with a followup study of at least six months. The average hospital stay was 3.2 days, with a range of two to eight days. Postoperative complications were few and included numbness of the medial upper arm due to transection of the intercostobrachial cutaneous nerve, hematoma, pleuritis; and pneumothorax. There have been no deaths or serious postoperative complications. Two case reports are presented to illustrate the problems we have encountered. Case I. An eighteen year old man (DKM) was discharged from the service with a diagnosis of bilateral Raynaud’s syndrome. He had weakness and coldness of the hands. He was unable to work above his head, and his arms would go to sleep or become painful with elevation. He had positive military brace and abduction-external rotation maneuvers bilaterally. Arteriograms demonstrated an 85 per cent obstruction of the left subclavian artery; the right subclavian artery was normal. Bilateral transaxillary first rib resections were performed at one month intervals. Initially, he had complete relief of symptoms; however, three months subsequently he was again symptomatic on the right side and had converted back to positive military brace and abduction-external rotation maneuvers. Exploration of the right supraclavicular area was performed with resection of dense fibrous tissue in the bed of the first rib and decompression of the subclavian vessels and brachial plexus. He subsequently became symptomatic on the left

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Comment: We have had four instances in which patients have had either regeneration of the rib or the appearance of dense fibrous scar tissue in the bed of the first rib with recurrence of symptoms. Case II. A thirty-five year old man (JHE) presented with bilateral shoulder pain. An arteriogram showed narrowing of the left subclavian artery. A myelogram was negative for abnormalities. He underwent left scalenotomy in 1967 with an initial good result. One year later symptoms recurred as did a positive abductionexternal rotation maneuver and supraclavicular bruit. He underwent transaxillary first rib resection with some improvement in the symptoms postoperatively. One year postoperatively he had negative abduction-external rotation and military brace maneuvers. Subsequently, he had recurrent symptoms, and a roentgenogram revealed regeneration of the first rib. During re-resection of the first rib, refusion of the scalene muscles to the first rib was identified. Postoperatively, the patient did not experience relief of symptoms. A complete neurologic, orthopedic, and vascular work-up, including arteriography and myelography, gave normal results. Incidentally, the patient exhibits signs of compression of the right subclavian artery, which has not been approached surgically. The patient continues to have bilateral shoulder and arm pain. Comment: This patient, although undergoing extensive pre- and postoperative evaluations, continues to have poor results from his treatment.

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Comments

A thorough understanding of the anatomy of the base of the neck is mandatory in the evaluation and treatment of this syndrome. Knowledge of the mechanisms of neurovascular compression was slow to develop. Hilton [3] in 1853 first described gangrene from compression caused by exostosis of the first thoracic rib. Coote [4] in 1861 removed a cervical rib and exostosis with relief of symptoms caused by compression. Bramwell [5] suggested the possibility of neurovascular compression at the level of the first thoracic rib in patients without a cervical rib. Todd [6] in 1912 suggested that hyperabduction was a cause of arterial insufficiency; he identified the symptoms in himself while sleeping with his hands above his head and was able to reproduce them with hyperabduction. Adson and Coffey [7] in 1927 advanced the mechanism of the scalene anticus syndrome and suggested scalenotomy for decompression. In 1934 Lewis and Pickering [8] described a patient with severe compression of the subclavian artery between the clavicle and the first rib, which they recognized at operation. Falconer and Weddell [9] in 1943 added several more cases of neurovascular symptoms among military personnel and introsyndrome.” duced the term, “costoclavicular Wright [IO] in 1945 proposed the term, “hyperabduction syndrome,” which he thought was caused’ by traction on the axillary artery and brachial plexus when stretched under the tendinous insertion of the pectoralis minor muscle into the coracoid process of the scapula. Two more recent events have helped capsulize the preceding one hundred years and advance the understanding and treatment of these problems. Peet and associates [I] in 1956 recognized that the symptom pattern of all of these syndromes was similar and suggested the term, “thoracic outlet Rob and Standeven [2] suggested syndrome.” grouping all the recognized syndromes of compression of the neurovascular structures to the upper extremity under the term, “thoracic outlet compression syndrome.” Some of the difficulties encountered in treating these problems involve the evaluation of the symptoms and the paucity of objective findings. Naffziger and Grant [II] in 1938 stated that, “The bizarre symptoms and insidious onset render early diagnosis difficult, as does the fact that objective signs may be relatively late.” Also, the majority of signs and objective findings are related to vascular

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compression whereas the majority of symptoms relate to neural compression. A clear, concise history is the most important diagnostic factor in the thoracic outlet compression syndrome. Symptoms may be related to neural, arterial, or venous compression and will vary depending on the point at which compression occurs. Neurologic symptoms are produced by stretching or compressing the lower trunk or medial cord of the brachial plexus which is formed by the anterior rami of the eighth cervical and first thoracic nerve roots. These consist of pain, numbness, paresthesia, and weakness, generally of the ulnar portion of the arm and hand. Arterial compression is manifest clinically by pain, numbness, coolness, pallor, weakness, and claudication. Late evidence of arterial involvement may include ulceration and gangrene. The concomitant occurrence of Raynaud’s phenomenon is poorly understood. Venous compression may cause intermittent edema, venous distention, discoloration, and fatigue. Late manifestations may consist of axillary vein thrombosis with edema and gangrene. Symptoms may frequently present at night when sleeping with the arms over the head. They are related to arm position and use and are aggravated by sustained activity that stresses the shoulder girdle such as driving a car, hanging laundry, putting packages on a shelf, and hammering. Early cases of neural compression may not exhibit any definite signs, although supraclavicular tenderness, which has been noted, is thought to be due to irritation of the brachial plexus. Late signs may be manifest by weakness, muscle atrophy, and decreased sensation in the distribution of the ulnar nerve. Vascular compression may be elicited by a number of maneuvers including the Adson, abduction-external rotation, military brace, and claudication test. Unfortunately, Telford and Mottershead [12] found that in 120 healthy medical students, 38 ,per cent had obliteration of the radial pulse with shoulder depression, 68 per cent with shoulder retraction, and 54 per cent with shoulder abduction. A supraclavicular bruit has been found in approximately 30 per cent of patients with the thoracic outlet compression syndrome. Color and temperature changes as well as edema and venous engorgement may be seen with venous compression. Ulceration and gangrene may be late consequences. The differential diagnosis of the thoracic outlet compression syndrome must include lesions of the

The Anwlcan

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Thoracic Outlet Compression Syndrome

cervical spine such as osteoarthritis, spondylitis, intervertebral disk disease, or tumors, lesions of the brachial plexus such as birth injuries, superior sulcus tumors, and trauma, and lesions of the peripheral nerves such as the carpal tunnel syndrome, ulnar compression at the elbow, medical neuropathies, trauma, and tumors. The differential diagnosis must also include vasospastic diseases, arteriosclerosis, and thrombophlebitis and venous obstruction from obstruction of the superior vena cava. However, none of these entities has signs and symptoms of neurovascular compression related to arm position. Complete evaluation of the patient suspected of having the thoracic outlet compression syndrome should include x-ray films of the chest, shoulder, and cervical spine. Arteriograms, phlebograms, and myelograms may be performed when indicated. Nelson and Davis [13] have stated that a positive arteriogram has been interpreted as confirmatory evidence of the thoracic outlet compression syndrome; however, they admit that significant neural compression may exist without concomitant arterial compression. We believe that an arteriogram should be taken in the patient with an atypical history or equivocal physical findings. All but one of our patients who had a positive arteriogram had favorable results from surgery. We had hoped that ulnar nerve conduction velocity across the thoracic outlet would provide an objective test for diagnosing the thoracic outlet compression syndrome. To date, however, we have not been able to reproduce the success reported by Urschel, Paulson, and McNamara [14] and have recently abandoned its use. According to Urschel, Paulson, and McNamara [14] and Rosati and Lord [15], management of the thoracic outlet compression syndrome was conservative in 50 to 70 per cent of their patients and consisted of exercises to strengthen the trapezius muscle, improved posture, and muscle relaxants when spasm is apparent in the neck muscles. This form of therapy is used when the symptoms are mild, not disabling, and of short duration and when there is no history of recent trauma, whiplash, or other cervical injury. Surgery is indicated when symptoms are severe, disabling, or persistent. Because of the high failure rate of scalenotomy and the unacceptable disfiguration and complication of other procedures, operative management at the present time focuses on removal of the first thoracic rib, or a cervical rib if present. Controver-

Mume 130, November 1975

sy exists as to the best surgical approach. Falconer and Li [16] in 1962 recommended an anterior supraclavicular approach and Clagett [17] that same year reported the use of the posterior approach; each reported good initial results in their series of first rib resections for severe thoracic outlet compression syndrome. More recently, Hamlin and Pecora [18] suggested the anterior subclavicular approach. In 1966 Roos [19] formally proposed the “common denominator” theory as a rationale for first rib resection in all cases of neurovascular compression in this region and described the transaxillary approach.

Summary Forty-nine patients underwent sixty-four procedures for the treatment of the thoracic outlet compression syndrome. Detailed history and careful physical examination are of paramount importance in diagnosing this disease. Our findings strongly suggest that a positive arteriogram is confirmatory evidence of the thoracic outlet compression syndrome. Two problems are identified as the source of unsatisfactory results in this series: poor selection of patients and the regeneration of rib and dense scar tissue with recurrence of compression symptoms. We favor the transaxillary approach to resection of the first rib because it provides satisfactory exposure for removal of the entire rib and utilizes a more cosmetically pleasing incision. Division of muscles, traction on nerves, and entrance into a body cavity are not required, operating time and hospital stay are shortened, and blood loss is minimized. Favorable long-term results were seen in 86 per cent of the patients treated. References 1. Peet FM, Hendriksen JD, Anderson TP, Martin GM: Thoracicoutlet syndrome: evaluation of a therapeutic exercise program. Mayo Cl/n Proc 31: 281, 1956. 2. Rob CG, Standeven A: Arterial occlusion complicating thoracic outlet compression syndrome. Br A&d J 2: 709. 1958. 3. Hilton J: On Rest and Pain, 2nd ed. New York, William Wood, 1879. 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 Gaz 2: 108.1861. 5. Bramwell E: Lesion of the first dorsal nerve root. Rev Neural 1: 236, 1903. 6. Todd TW: The descent of the shoulder after birth: its signifii cance in the production of pressure symptoms on the lowest brachiil trunk. Anat Anz 41: 385, 1912.

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7. Adson AW, Coffey JR: Cervical rib: a method for relief of symptoms by division of the scalene anticus. Ann Surg 85: 839, 1927. 8. Lewis T. Pickering GW: Observation upon maladies in which the blood supply to digits ceases intermittently or permanently, and upon bilateral gangrene of digits: observations relevant to so-called “Raynaud’s disease.” C/in Sci 1: 327, 1934. 9. Falconer MA, Weddell G: Costoclavicular compression of the subclavian artery and vein. Relation to the scalenus antii cus syndrome. Lancet 2: 539, 1943. 10. Wright IS: Neurovascufar syndrome produced by hyperabduction of the arms. Am Heart J 29: 1, 1945. 11. Naffziger HC, Grant MT: Neuritis of the brachhl plexus mechanical in origin: the scalenus syndrome. Surg Gynecol Obstet 67: 722, 1938. 12. Telford ED, Mottershead S: Pressure at the cervico-brachiil junctions: an operative and anatomical study. J Bone Joint

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Surg(Btj 30: 249, 1948. 13. Nelson RM, Davis RW: Thoracic outlet compression syndrome. Ann Thorac Surg 8: 437, 1969. 14. Urschel HC Jr, Paulson DL, McNamara JJ: Thoracic outlet syndrome. Ann Thorac Surg 6: 1, 1968. 15. Rosati LM, Lord JW: Neurovascular compression syndromes of the shoulder girdle, p 168. Modern Surgical Monograph. New York, Grune 8 Stratton, 1961. 16. Falconer MA, Li FWP: Resection of the first rib in costoclavtcular compression of the brachial plexus. Lancet 1: 59, 1962. 17. Clagett OT: Presidential address: research and prosearch. J Thorac Cardiovasc Surg 44: 153, 1962. 18. Hamlin H, Pecora D: Subclavicutar segmental resection of first rib for correction of subjacent neurovascular compression. Am J Surg 117: 754, 1969. 19. Roos DB: Transaxillary approach for first rib resection to relieve thoracic outlet syndrome. Ann Surg 163: 354, 1966.

Tha American Journal

of Surgery

Thoracic outlet compression syndrome.

Forty-nine patients underwent sixty-four procedures for the treatment of the thoracic outlet compression syndrome. Detailed history and careful physic...
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