Supraclavicular reoperation for neurogenic thoracic outlet syndrome

Supraclavicular reoperation for neurogenic thoracic outlet syndrome

ORIGINAL ARTICLES Supraclavicular reoperation for neurogenic thoracic outlet syndrome Stephen W. K. Cheng, MD, and Ronald J. Stoney, MD, San Francisc...

702KB Sizes 0 Downloads 89 Views

ORIGINAL ARTICLES

Supraclavicular reoperation for neurogenic thoracic outlet syndrome Stephen W. K. Cheng, MD, and Ronald J. Stoney, MD, San Francisco, Calif. Thirty-nine reoperations in 38 patients with recurrent symptoms of neurogenic thoracic outlet syndrome were performed by the supraclavicular approach. Scarring around the brachial plexus was the primary cause in 59% of procedures, whereas in 41% of reoperations residual osseous and soft tissue anomalies were identified in the supraclavicular area and were responsible for recurrence of symptoms. Anterior and middle scalenectomy and neurolysis of the brachial plexus were the procedures of choice. Complications included pleural entry (62%), lymphatic leak (10%), brachial plexus and phrenic nerve injuries (5% each), and long thoracic and recurrent laryngeal nerve palsies (3% each). The initial success rate for secondary operations was 74%, and long-term success at 18 months was 45%. Patients who had demonstrable anatomic anomalies had better short- and long-term results than had patients with scarring alone. Compared with the results of primary operations for neurogenic thoracic outlet syndrome, reoperations led to a longer hospital stay and inferior long-term results. Supraclavicular decompression allows maximal exposure of the brachial plexus and identification and correction of causative soft tissue and bony anomalies. For these reasons we recommend this as the approach of choice in both primary and secondary operations for neurogenic thoracic outlet syndrome. (J VAse SURG 1994;19:565-72.)

The controversy surrounding the surgical treatment of neurogenic thoracic outlet syndrome (TOS) has led to a wide variety of operative approaches and a combination of primary procedures, including scalenotomy and scalenectomy, with or without rib resection. The reported success rate of these various operations is in the region of 85% to 90%.1,2 A significant proportion of these patients have recurrent symptoms, usually within a few months after surgery. The management of these patients is at first conservative, but often worsening or persistent symptoms warrant a second operation by a variety of approaches. 3 ,4 This article reviews the cause and results and describes our technique of 39 supraclavicular reoperations in 38 consecutive patients From the Department of Surgery, Division of Vascular Surgery, University of California, San Francisco. Supported in part by the Pacific Vascular Research Foundation. Reprint requests: Ronald J. Stoney, MD, Department of Surgery, Division of Vascular Surgery, M -488, University of California, San Francisco, 505 Parnassus Ave., San Francisco, CA 94143. Copyright © 1994 by The Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter. 0741-5214/94/$3.00 + 0 24/1/48278

treated at the University of California Medical Center, San Francisco.

PATIENTS AND METHODS During a 9-year period from 1983 to 1991, 39 reoperations for recurrent neurogenic TOS were performed by a single surgeon in 38 patients, by the supraclavicular approach. There were 33 women (87%) and 5 men (13%); their ages ranged from 21 to 54 years (mean 40 years). The left upper extremity was the main side of neurologic symptoms in 21 instances (54%). Four of the original operations were performed in this hospital (by the supraclavicular approach); the rest were carried out in other institutions. The initial operations were accomplished by a variety of supraclavicular, transaxillary, or combined approaches and consisted of scalenotomy, and scalenectomy, with or without first rib resection (Table I). Seven patients had undergone prior cervical rib excisions, and one patient had undergone a previous infraclavicular first rib resection. Five patients had undergone a total of 15 previous operations on six sides before they were referred. These multiple procedures invariably con565

566

JOURNAL OF VASCULAR SURGERY April 1994

Cheng and Stoney

Table I. Previous operations for 38 patients with recurrent TOS Procedure Scalenotomy Scalenectomy Scalenectomy, cervical rib excision Scalenectomy, first rib excision Scalenectomy, cervical and first rib excision First rib excision Neurolysis Total

Supraclavicular (n)

Transaxillary (n)

Combined supraclavicular and transaxillary (n)

Parascapular or infraclavicular (n)

5 7 1 2 0

0 0 1 10 2

0 1 0 5 3

0 0 0 1 0

0 2

5 1 19

0 0

0 0

9

1

17

-

Note: The table represented 47 previous operations in the 38 patients. Five patients had undergone more than one previous operation (total of 15, on six sides, usually staged rransaxiUary first-rib resections and supraclavicular scalenectomies). One of these previous operations was a supraclavicular sympathectomy alone and was not listed above.

sisted initially of trans axillary first rib resection, followed later by supraclavicular scalenectomy, or vice versa. The first operations had been performed from 6 months to more than 10 years previously. The symptoms recurred from 1 month to 15 years after the first operation, and the median symptom-free interval was only 4 months. Trauma was the inciting event in 19 instances, nearly half of the group. Most of these were work-related injuries, and flexion-extension injuries of the neck sustained in traffic accidents were reported in only four cases. The recurrent symptoms were similar to the original manifestation of neurologic irritation. The patients were specifically asked about the symptoms of pain, paresthesia, headache, arm weakness, and limitations in motion, and they were all given a standard questionnaire regarding the presence and severity of symptoms. Pain involving the lateral neck and shoulder and paresthesia radiating to the arms and hands were the most common complaints (97%). Unilateral headache was present in 31 % of the patients and weakness of the arm in 8%. The symptoms were aggravated by abduction of the arm in 41 % of cases. Most patients had symptom distributions in the dermatomes of all five roots of the brachial plexus, and we have been unable to separate these into clear-cut groups with symptoms in the upper and lower plexus. The duration of symptoms ranged from 4 months to more than 10 years, with a mean of 62 months. All except one of the patients had undergone prior physical therapy in terms of exercises, nerve blocks, and stellate ganglion injections, all with no effect. Twenty-seven patients (69%) reported that they could not work because of the symptoms, and an additional six patients (15%) had to modify the nature of their job to cope. Physical examination revealed supraclavicular

tenderness in 87% of patients. Results of the elevated arm stress test were positive in 82% of patients, whereas results of the Adson test were positive in only 33% of cases. Small muscle atrophy of the hand was present in two patients. A decreased range of neck motion was detected in 26% of patients. The diagnosis was usually made clinically based on a past history of neurogenic TOS and a return of the previous symptoms. Cervical and chest roentgenograms were taken routinely, and they often showed residual cervical ribs or long posterior stumps of the first rib. Nerve conduction studies were done only when ulnar or median nerve entrapment was suspected and were abnormal in only three instances. Most of the patients were investigated extensively by neurologists before referral by neurophysiologic and imaging studies to rule out alternative diagnoses.

OPERATIVE TECHNIQUE We performed all 39 reoperations through the supraclavicular approach independent of the original operation( s). The procedure consisted of a complete decompression of the thoracic outlet by radical anterior and middle scalenectomy followed by a thorough neurolysis of the brachial plexus. Before mid-1990, we also removed the first rib through the supraclavicular route, whereas afterward the first rib was spared unless a previous attempt at rib resection produced a residual stump with a retained middle scalene muscle, as well as scarring to the brachial plexus. The technique of supraclavicular scalenectomy has been described previously.l In reoperations a similar procedure is adopted. The patient is placed in a semi-Fowler position with the head turned away from the side of the operation. A curvilinear incision

JOURNAL OF VASCULAR SURGERY Volume 19, Number 4

is made at the base of the neck, two finger breadths above the clavicle, and curved posteriorly for about 10 cm. Subplatysmal flaps are raised and the clavicular head of the sternocleidomastoid is divided if necessary. Exposure is facilitated with a self-retaining miniframe retractor, and headlight illumination is enhanced visibility. The scalene fat pad is then reflected on a laterally based pedicle. If the patient had undergone a previous supraclavicular operation, scar tissue will be encountered from the level of the platysma down to and encasing the roots and trunks of the brachial plexus. Parts of the anterior and middle scalene muscle are often retained as well, which may be fixed to the first rib bed or the Sibson's fascia. Remnants of cervical ribs, long transverse process of the C7 vertebra, and stumps of the first rib may pose additional pressure on the brachial plexus. These should be recognized on a preoperative roentgenogram and defined accurately during the dissection. A careful, methodic dissection is begun to define the anatomy around the nerves of the brachial plexus. Care is taken to avoid the phrenic nerve, which is often incorporated into the scar tissue and not easily identified. The residual anterior scalene muscle is mobilized, separated from the phrenic nerve, and completely removed by dividing its origins from the transverse processes of the cervical vertebrae. All five roots and three trunks of the brachial plexus are carefully mobilized. Any residual bony or soft tissue anomalies that were overlooked in the first operation can now be detected and removed. Frequently anomalous scalene muscle interdigitations or a small scalene muscle is encountered, especially if the original operation was performed through the transaxillary route. The plexus is elevated gently and the middle scalene muscle is identified next, with the long thoracic nerve emerging at its lateral border. The middle scalene muscle is transected on a line parallel and inferior to the course of the long thoracic nerve down to its attachment to the scar tissue on the residual stump of the first rib and excised in its entirety. The lower roots (C8 and Tl) of the plexus are often adherent to the posterior stump of the firstrib, which in some instances may be a calcified fibrocartilaginous mass. Further dissection of the nerves is necessary to allow complete mobilization of the vital structures away from the remnants of the first rib segment. The rib is sectioned at the level of the neck with a sagittal saw and extraperiosteal dissectors are used to free the residual bone from the intercostal muscles, and the stump of the rib is removed. The

Cheng and Stoney

567

subclavian artery is cleared from its first portion through its third portion, and all the scar tissue surrounding the vessel and overlying the dome of the pleura is removed. With sharp dissection with scissors a thorough neurolysis of the brachial plexus is performed from the intervertebral foramina down to the clavicle until all the nerves are skeletonized. Since mid-1990, we have preserved the first rib in the only six instances in which a rib resection was not performed at the initial operation. It is our experience that the first rib rarely if ever causes actual compression of the plexus. If the medial neck of the first rib displaces the course of the Tl root, a bone rongeur can be used to remove a small rim of the medial border (sagittal osteotomy) to allow the root to ascend and cross the rib unrestricted. A cervical sympathectomy may be included for those patients with prominent vasomotor symptoms by displacing the pleura inferiorly and laterally to gain access to the sympathetic chain. Hemostasis is achieved and the wound is inspected carefully for any chylous or lymphatic leakage. If the pleura is disrupted, a small catheter is placed through the pleurotomy and the air is evacuated by suction before closure. The catheter is then withdrawn. A chest drain would be used for a large pleural rent and air leak. The previously mobilized prescalene fat pad is then positioned loosely over the trunks of the brachial plexus as an extra insulating layer to protect the nerves from adjacent soft tissues and provide a vascularized pedicle to promote healing. The platysma is reapproximated and the skin closed with a subcuticular suture around a closed suction drain. A fine catheter placed adjacent to the brachial plexus roots before closure allows instillation of topical anesthetic agents after surgery for relief of pain and steroids for the prevention of excessive scar formation. Passive arm movements are allowed immediately after the operation. The drain is usually removed after 48 hours, and the catheter is removed at the time of discharge. A supervised physical therapy program guided by brachial plexus tension testingS is prescribed for 8 weeks.

OPERATIVE FINDINGS The supraclavicular route allows an unrestricted exposure of the entire course of the brachial plexus and direct visualization of the anatomy of the interscalene space. The operative findings are listed in Table II. Scarring around the brachial plexus was almost universal on reoperations. Usually more than one source of recurrent brachial plexus irritation was

568

JOURNAL OF VASCULAR SURGERY April 1994

Cheng and Stoney

Table II. Problems encountered during 39 supraclavicular reoperations for neurogenic TOS Anomaly Scar formation Anterior scalene reattachment to first rib bed Middle scalene reattachment Bony abnormalities Long residual stump of first rib Long residual stump of cervical rib Long transverse process of C7 Calcified/cartilaginous first rib mass Intact (missed) cervical rib Soft tissue anomalies Anterior scalene anomalies Middle scalene anomalies Small scalene anomalies Fibrous bands

n 20 9 16 2 1 4 3 2 5 6 7

evident. Based on these observations, we have been able to classifY the patients into two subgroups according to the anatomic structures responsible for the neurologic compression: The first group is comprised of 23 patients who are considered "true recurrences," in which the initial operation was deemed adequate and the cause of recurrent symptoms was attributed primarily to scarring around the brachial plexus. There may be associated reattachment of the residual anterior scalene muscle to the first rib bed or a fibrotic posterior stump of the first rib. In the second group of 16 patients, in addition to the scarring described, bony or soft tissue anomalies were found that appeared to be the responsible structures entrapping and compressing the nerves during the second operation. The original procedure was therefore considered "inadequate" in the sense that the anatomic structure responsible for the brachial plexus irritation was overlooked or incompletely removed. Among the offending structures were the small scalene muscle, anomalous fibrous bands, missed cervical ribs, or definite abnormalities in the anterior and middle scalene muscles themselves. Seventeen patients from group 1 (74%) and 12 patients from group 2 (75%) had undergone previous supraclavicular explorations at other institutions. RESULTS Complications Complications were not infrequent in this group of patients undergoing reoperation in whom the dissection was made difficult by scarring. The most common complication was pleural disruption, which occurred in 24 cases (62%). A chest tube was placed

during surgery in nine procedures (23%) to evacuate air and a pneumothorax occurred in another three patients after surgery (8%), two of whom subsequently required insertion of a chest tube. Fifteen other complications occurred in nine patients. There were four lymphatic leakages or collections in the neck wound (10%). In one patient the leak failed to subside with conservative treatment, and she required a reexploration and ligation of an anomalous right-sided duct and 1 month of total parenteral nutrition until this was healed. A hypoplastic T1 root of the brachial plexus was accidentally divided during one procedure. The nerve was repaired primarily and the patient had a near-complete recovery. Two patients had asymptomatic elevations of the ipsilateral hemidiaphragm, detected after surgery. One patient had a winged scapula caused by a previous long thoracic nerve injury. One patient had a recurrent laryngeal nerve damage and resultant hoarseness. Two patients suffered from a postoperative Horner's syndrome. Other complications included one hemopneumothorax, one pleural effusion necessitating drainage, and one self-limited aspiration pneumonia. In one patient who had dense scarring imprisoning the brachial plexus from a recent supraclavicular first rib resection, an expanded polytetrafluoroethylene patch was placed around the plexus at the end of the second operation in an attempt to protect the nerves. However, she had severe persistent wound pain afterward and had to undergo reexploration 6 weeks later. Heavy fibrosis was found around the patch binding down the nerves and the patch was removed and a second neurolysis completed. Compared with 195 primary supraclavicular operations performed by the same surgeon during the same period, the group undergoing reoperation had a significantly higher incidence of brachial plexus injury (p < 0.05, X2 test). They also suffered a slightly higher rate of other complications, especially pleural injury, although these are not statistically significant. The mean hospital stay required for patients who underwent reoperation was 51f2 days, which was significantly longer than that for primary operations (4.6 days; p < 0.05, unpaired Student t test). These patients tended to have a longer symptomatic period (mean 62 months) before they underwent surgery compared with a mean duration of symptoms of 39 months in the group undergoing primary operation (p < 0.05, Student t test). Contrary to a previous report, 6 the presence or ~bsence of trauma before recurrence of symptoms had no effect on the outcome in our series.

JOURNAL OF VASCULAR SURGERY Volume 19, Number 4

Follow-up results The patients were examined and followed up after discharge from the hospital. All but two of the patients were also reassessed at regular intervals between 3 months and 9 years after surgery (mean 18 months). The results are graded according to the percentage improvement of their preoperative symptoms. With a standard scoring system, five symptoms were evaluated: pain, paresthesia, headache, weakness, and limitation of motion. If all of the symptoms were consistently relieved, the patients were considered cured. If there was a greater than 75% symptomatic improvement of all symptoms at follow-up, the patients were classified as markedly improved. Fifty percent to 75% improvement was graded improved, and less than 50% improvement was graded as fair or worse. We consider a less than 50% improvement of symptoms a failure of the operation. The initial postoperative results were obtained after 2 to 3 months when the wound was healed and the patients had undergone the course of physical therapy. The early success rate for patients in group 2 (those with residual anatomic anomalies) was significantly better than that for patients in group 1 (without anomalies) (p < 0.005, x2 test; Table III). The overall initial success rate for reoperation was 75%. The long-term follow-up results are reported by life-table methods. In the analysis, patients with less than 50% improvement were considered failures (Table IV). The results of reoperations were compared within the two subgroups (Fig. 1) and with 195 primary operations performed during the same period (Fig. 2). The differences are evaluated by the log-rank test and the Lee-Desu statistic? Relief of symptoms in patients in group 2 was consistently better than that for patients in group 1, although statistically they were not significantly different. The long-term clinical results of patients who underwent primary operations, however, were significantly better than those of the patients who underwent reoperation (p < 0.01). DISCUSSION The causes of recurrence of neurologic symptoms after previous thoracic outlet decompression are multiple, and many offending structures have been identified based on observations made during secondary operations.3~8,9 Among the many factors, an inappropriate first operation was often blamed. From our previous experience of trans axillary rib resection, failure rates were high (21%),10 and supraclavicular reoperation in these patients frequently revealed soft

Cheng and Stoney 569

tissue or bony anomalies that were not identified and removed adequately at the first operation. This finding has prompted us to adopt the supraclavicular route for all primary operations for TOS.l With further experience we have extended this approach to reoperations in patients with symptomatic recurrences after all thoracic outlet operations, including previous supraclavicular procedures. From our findings during supraclavicular reoperation, we have been able to identify a group of patients who had residual anomalies in the brachial plexus region apart from scarring. These included missed cervical ribs, persistent fibrous bands, and anomalous interdigitations between the scalene muscles and the small scalene muscles. These anomalies would at least contribute to, if not totally account for, irritation of the roots and trunks of the brachial plexus and a recurrence of neurologic symptoms. Precise identification of these anatomic anomalies would be difficult in the presence of scarring by any approach other than supraclavicular, which offers a full unrestricted exposure of the brachial plexus from the intervertebral foramina to the clavicle. In this group of patients, once the anomalies were removed successfully, the results of reoperation had been good (Fig. 1) and often comparable to results after primary operations. The frequency of some of these anomalies (especially the small scalene muscle and fibrous bands) may indicate that they were in fact anatomic variations common in the population. A thorough exposure and careful dissection to locate these structures during the primary operation is therefore mandatory for the success of brachial plexus decompression. In the group of patients in whom scarring alone was considered the primary cause of recurrence ("true" recurrences), supraclavicular reoperation provides adequate removal of all adhesions and a complete neurolysis of the brachial plexus. The results of this group of patients, however, were significantly worse than those of the group in whom residual anomalies were identified and removed. Perhaps they represent those who had an inherent predilection for excessive scar formation in the postoperative period. In these patients prevention would be important. Attempts to minimize scar formation after surgery with the expanded polytetrafluoroethylene patch and postoperative steroid infusion were disappointing. Infusion of heparin or other agents that are known to reduce scarring such as hyaluronic acid may playa future role. Currently we prefer to preserve the mobilized prescalene fat pad and use it to cover the brachial plexus to protect the

JOURNAL OF VASCULAR SURGERY April 1994

570 Cheng and Stoney

Table III. Early postoperative results of 39 reoperations for neurogenic TOS Very good

Good

Excellent (cured) (n)

(75%-100%

(50%-75%

«50%

improved) (n)

improved) (n)

improved) (n)

Poor (worse) (n)

Total (n)

3 3

6 7

3 6

8 0

1 0

21 16

Group 1 (recurrent scar) Group 2 (inadequate operation)

Fair

Success

Failure

(?50%

«50%

improved)

improved)

n

%

n

%

12 16

57 100

9 0

43

Total (n) 21 16

Two patients were lost before 3 months' follow-up.

p < 0.005, X2 test.

For the bilateral operation, only one side was chosen by random for statistical analysis.

Table IV. Follow-up results of 39 reoperations for neurogenic TOS Interpal starting time (mo)

No. at risk

No. withdrawn during interpal*

No. exposed to risk

No. of failurest

Proportion failedt

Cumulative success rate (%)

0 3 6 9 12 18

37 23 15 11 8 5

5 7 3 1 2 1

34.5 19.5 13.5 10.5 7 4.5

9 1 1 2 1 0

0.26 0.05 0.07 0.19 0.14 0.00

74 70 65 53 45 45

*Number withdrawn equals patients lost or not followed up to that time interval. tFailures defined as those who had less than 50% symptomatic improvement or worse. :j:By litt-table method, proportion failed = No. of failures during intervaljNo. at risk at start of interval-V2 (No. withdrawn).

nerve roots from adjacent fibrosis. Similar techniques involving ''wrapping'' the plexus by the fat pad have been described. 4 Staged reoperation has been advocated6 based on the disease and identification of the cause of symptoms as upper plexus (scalene musculature) or lower plexus (first rib and scarring). 3 A supraclavicular scalenectomy would be performed for patients with predominantly upper plexus symptoms and trans axillary first rib resection for those with lower plexus symptoms; the opposite route is reserved for recurrences. Most of the patients in our series had mixed symptoms and could not be classified accurately into groups with upper or lower plexus symptoms. Whether the site of symptoms, or the site of pathologic scarring, dictates the approach is not certain. In a significant proportion of our patients (41 %) residual anomalies were demonstrated on reoperation. Most of these were soft tissue anomalies and were not evident on a routine roentgenogram. Magnetic resonance imaging scans may prove useful in demonstrating these abnormalities. These were either not accessible at the first operation because of limited exposure or they were overlooked. Seventyfive percent of these patients had undergone previous supraclavicular explorations. If the second operation is performed through the trans axillary route, a

persistent anatomic anomaly not removed at the first operation may not be detected, especially when it is performed by surgeons who are less experienced in this field, and it will not permit adequate exposure of the upper plexus and the scalene musculature. When the reoperation is supraclavicular, there are no restrictions on exposure to display the entire brachial plexus and the site of the previous surgical scarring. A second reoperation is therefore unnecessary. The importance of the middle scalene muscle in recurrences is also being recognized increasingly. Nine of our patients (23%) were found to have middle scalene reattachments. An adequate middle scalenectomy can be done only through the supraclavicular route. We therefore regard the supraclavicular approach as the best choice for reoperations irrespective of the original procedure. We have not favored the posterior approach for reoperations. Although it avoids the scars of a previously operated field, and good results have been reported,l1 this approach necessitates extensive muscular divisions and would not allow the exposure required for a complete decompression and removal of all the remaining offending structures. It is our experience that, on the whole, the results of reoperations in neurogenic TOS are less favorable than those of primary operations (Fig. 2). It has been

JOURNAL OF VASCULAR SURGERY Volume 19, Number 4

Cheng and Stoney

571

100

75

,,

,,

,, ,.... _.... _- ...

50

-

,,

Inadequate op Recurrent scar

o 9

3

12

36

Follow up (IDOnths)

Fig. 1. Results of reoperations for patients with recurrent neurogenic TOS. Long-term success rates of patients in group 2 (inadequate first operation) were slightly better than those of patients in group 1 (recurrent scarring), although difference is not statistically significant (p > 0.05).

100

I

75

,,

... -

"-

.... -. ,

,,

. , -\

50

25

-

Primary op

- - Re-operations

o 3

Follow up (months)

Fig. 2. Results of 39 reoperations compared with 195 primary supraclavicular operations for neurogenic TOS. Primary operations have significantly better long-term results (p < 0.01).

shown that in general the patients who were referred for reoperation had a longer symptomatic period than their counterpart undergoing primary TOS decompression. This is explainable by the reluctance on the part of the referring physician to subject these patients to a second operation. The majority of the patients who were referred for recurrent symptoms after previous TOS surgery were operated on because they usually had tried, in vain, extended periods of physical therapy. Occasionally some patients with

minor recurrent symptoms associated with a specific factor such as another injury or work-associated micros tress can be managed successfully by conservative measures. However, for most of the patients the hesitation of their physicians to offer surgery for recurrences may have encouraged extensive scar formation around the brachial plexus, and the protracted compression of the nerve roots by fibrosis would result in irreversible neurologic injury and diminish the chance of a full recovery.

JOURNAL OF VASCULAR SURGERY

572 Cheng and Stoney

Prevention remains the most important factor for a successful TOS operation. During reoperations, previous scars often encase the brachial plexus and render the precise identification of the anatomy difficult and dissection tedious and prolonged. Although reoperation poses only a slightly higher risk of complications than primary procedures, it does carry a longer period of hospital stay. An adequate total decompression of the brachial plexus during the first operation by radical anterior and middle scalenectomy and neurolysis, performed with the precise exposure of the supraclavicular route, appear to be the only ways to ensure that all sources of future plexus irritation are identified and removed and the morbidity of unnecessary reexplorations avoided. Postoperative scarring can be minimized by careful hemostasis and coverage of the nerves with the vascularized supraclavicular fat pad. In the past, first rib excision has been considered crucial in thoracic outlet decompression, and a long retained stump of the first rib after trans axillary rib resection has been blamed as a cause of recurrence. In our experience the first rib seldom if ever is in actual mechanical contact with the brachial plexus, and it serves only as a passive matrix on which soft tissue elements attach. Routine resection of the first rib is unnecessary and, if the practice persists, only creates a fibrous tissue bed where muscle remnants and scars adhere and exert pressure on the plexus, resulting in recurrence of symptoms. Once we adopted the first rib-sparing policy, all primary operations have been carried out by the supraclavicular approach alone. The problem of scarring after rib resection is minimized, in case a reoperation is needed. To date there

April 1994

have been no recurrent symptoms requiring reoperation among 45 consecutive patients who have undergone a rib-sparing primary decompressive operation for neurogenic TOS.

REFERENCES 1. Reilly LM, Stoney RJ. Supraclavicular approach for thoracic outlet decompression. J VASC SURG 1988;8:329-34. 2. Roos DB. The place for scalenectomy and first rib resection in thoracic outlet syndrome. Surgery 1982;92:1077-85. 3. Roos DB. Recurrent thoracic outlet syndrome after first rib resection. Int AngioI1984;3:169-77. 4. Sanders RJ, Monsour ]W, Gerber WF. Recurrent thoracic outlet syndrome following first rib resection. Vasc Surg 1979;13:325-30. 5. Kenneally M, Rubenach H, Elvey R. The upper limb tension test: the SLR test of the arm. In: Grant R, ed. Physical therapy of the cervical and thoracic spine. New York: Churchill Livingstone, 1988:167-94. 6. Sanders RJ, Haug CE, Pearce WH. Recurrent thoracic outlet syndrome. J VASC SURG 1990;12:390-400. 7. Lee E, Desu M. A computer program for comparing k samples with right censored data. Comput Prog Biomed 1972;2:31521. 8. Sessions RT. Recurrent thoracic outlet syndrome: causes and treatment. South Med J 1982;75:1453-62. 9. Sessions RT. Reoperation for thoracic outlet syndrome. J Cardiovasc Surg 1989;30:434-44. 10. Qvarfordt PG, Ehrenfeld WK, Stoney RJ. Supraclavicular radical scalenectomy and transaxillary first rib resection for the thoracic outlet syndrome: a combined approach. Am J Surg 1984;148:111-6. 11. Urschel HC Jr, Razzuk MA, Albers JE, Wood RE, Paulson DL. Reoperation for recurrent thoracic outlet syndrome. Ann Thorac Surg 1976;21:19-25.

Submitted Feb. 4, 1993; accepted April 28, 1993.