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 Wylie Traveling Fellowship Final Report 2004

David C. Cassada
Understanding the Treatment of Thoracic Outlet Syndrome

Background

Upper extremity function is critical to human interaction with the environment. Arm strength, sensation and complex function protect and provide for human survival and socialization. Loss of upper extremity function arguably carries higher morbidity than loss of a leg, and there is an unspoken stigma associated with hand loss.

Arm and hand function is governed by a complex set of motor and sensory networks that are controlled by a disproportionately large area of the cerebral homunculus. The amount of central nervous system committed to upper extremity function is evidence of the importance of arm function to human survival. Proper arm function tends to preoccupy humans, as even minor swelling, weakness or numbness can interfere with the myriad of daily activities that require perfect orchestration of neuromuscular function that is generally taken for granted. Clinicians are faced with decisions based on small or major alterations in arm function, determining how much, if any therapy is warranted in response to a patient’s complaints.

Thoracic outlet syndrome (TOS) is defined by a widely varied set of symptoms and clinical findings that vary in description from one authoritative source to the next. TOS as a syndrome contains reference to multiple anatomic sites of neurovascular compression, all generally located at the junction of the first thoracic rib, shoulder girdle, and the clavicle1,2. TOS also contains subsets of end-organ dysfunction, including ischemic and embolic arterial disease, venous-occlusive disease, and neuropathic disease. The vascular components of TOS can have objective measures to specify the diagnosis and describe the pathophysiology, while neurogenic TOS carries the challenge of trying to interpret a location of neuro-compression based upon history, symptoms and often-subjective clinical findings3,4.

After fellowship training, I planned to treat TOS as a junior faculty member at the University of Tennessee Medical Center at Knoxville (UTMCK). My experience entering practice at UTMCK was based upon training from a single institution. To date the majority of our patients at UTMCK with TOS were secondarily referred to another facility with a national reputation of excellence in treating this syndrome. In order for me to offer a reasonable alternative to long distance referral, I wanted to hybridize my experience and not depend on a narrow scope of training, and sporadic literature review. The E.J. Wylie traveling fellowship offered a unique format for pursuing a tailored training under the direction of the best surgeons in the world, who have spent years to develop their expertise.

At the beginning of the academic year, my goal was to use the support of the E. J. Wylie Traveling Fellowship to visit institutions where TOS is routinely treated in a multidisciplinary team-based approach. This experience was intended to provide insight into different methods of evaluating and treating TOS, allowing me to create a similar system within my academic practice at the University of Tennessee. My academic development was to be enriched by visiting the current leaders in the field, understanding what they have learned, and building upon their knowledge as a basic foundation. In return, I would use this experience to create a systematic approach to treating this difficult patient population, collecting data to publish outcomes and ideally create a multicenter registry to direct guidelines for treatment.

My traveling experience was based upon the opportunities to visit four institutions that are recognized as world centers for excellence in the treatment of thoracic outlet syndrome. These sites receive worldwide referrals for the treatment of TOS, and have generated large volumes of these relatively low frequency operations. As such, most were able to plan both clinical activities and operations in anticipation of my visit. Points of interest included the diagnosis, operative and nonoperative therapy for TOS. The body of this report will summarize these observations in the order of the institutions visited.

University of California Medical Center at San Francisco (UCSF)

This institution was an ideal initiation to the fellowship. Arguably UCSF can be considered the origin of the supraclavicular approach for thoracic outlet decompression. My initial interest in pursuing the Wylie fellowship resulted from a long distance telephone conversion with Dr. Ronald Stoney in 2003, prior to my attempt to perform a reoperation for a failed first rib resection. It was after this discussion that I began to understand the reasons for the supraclavicular dissection, and I noticed the academic links between authors using this technique and UCSF training5.

I spent the better part of an afternoon discussing TOS with Dr. Stoney, and learning his philosophy on the pathophysiology of TOS, which centers largely on degenerative changes in the anterior scalene muscle. Chronic or acute injury of the neck can result in scarring and tightening of the anterior scalene muscle over the trunks of the brachial plexus. This results in direct compression of the neural and arterial components of the thoracic outlet, as well as elevation of the first rib, further closing the anterior scalene triangle. The addition of a cervical rib serves to reduce the spatial tolerances and create a “fulcrum” over which the lower trunk of the brachial plexus and the subclavian artery are leveraged, creating ulnar distribution neuropathy with pulse diminution and even aneurysmal degeneration. Understanding of these basic tenants of the syndrome created a conceptual framework for understanding the diagnosis and treatment of TOS. 

There appears to be no “definitive” test for TOS outside of a thorough history and physical examination. Nerve conduction studies are of little value as they can produce falsely negative readings in the presence of severe symptoms or localize the lesion to multiple levels along the extremity, giving credence to the theory of the “double crush” syndrome, or the observation of different levels of nerve compressive symptoms in patients with TOS. Further supporting the notion of “double crush” is the observation of prior carpal tunnel release in patients with clear-cut TOS, where a prior surgeon has not considered TOS as the index site of nerve compression.

At UCSF, the diagnosis of TOS followed a thoughtful history and physical examination where a chronic repetitive or acute traumatic neck injury preceded the neuropathic, arterial embolic, or positional ischemic symptoms. The diagnosis is reached after independent examinations by both the vascular surgeon (Dr Louis Messina or Dr Darren Schneider) and Peter Edgelow, a recognized leader in the treatment of TOS. Repetitive upper extremity use, particularly at the level of the shoulder was commonly associated with pain in the extremity and tenderness over the anterior scalene muscle, which is often quite spasmed. Other signs included decreased capacity to passively abduct the extremity, ulnar distribution weakness, and grip strength improved by off loading the scalene muscle though isometric strengthening of the longus coli muscle (Thinker’s position). Twenty seconds of Thinker’s position would result in the immediate observation of improved ulnar nerve based strength, and was a good predictor of improvement with physical therapy. Emboli to the fingers and thenar or hypothenar muscle compartment wasting were early indicators for surgery, and generally reflected anatomic abnormalities not improved by physical therapy, related to longstanding untreated disease.

Physical therapy prescribed at UCSF generally followed the Edgelow theories for the basis of TOS. The degree of symptoms related directly to spasm within the anterior scalene muscle, and exercises were directed at improving this particular abnormality. The therapy centered on diaphragmatic breading that would not recruit and tense the anterior scalene, an accessory ventilatory muscle. Different positions and exercises were intended to stretch and improve the compliance of the anterior scalene muscle, while strengthening other axial muscles of the neck. Importantly, these exercises are self-paced and done independently, thereby providing convenient access for the patient, as well as self-reliance6. As with other chronic pain syndromes, TOS tends to make patients reliant on the touch of the clinician as well as narcotics. The Edgelow protocol is suited to allow the patient to have dominion over the pain through self-paced exercises; to this end, the patient tends to regain control and become less dependent on others. In the vast majority of cases, neurogenic TOS responded favorably to this approach without the need for surgical decompression. Failure of the this nonoperative approach generally related to longstanding disease with severe fibrous changes in the anterior scalene, or the presence of an osseous abnormality which would have no rational response to the Edgelow protocol.

I observed two thoracic outlet decompressions performed by Dr Darren Schneider, a junior faculty member of the vascular division who completed his training the same year as myself (Image 1). The technique was stepwise and systematic as with any well-performed surgery. The first observation was that the exposure was facilitated to a large degree by the use of the pediatric Omnitract retractor (which I learned was developed by Dr. Stoney) 7. This opened the space considerably more than perpendicular Weitlander retractors, and I was able to imitate the exposure upon return to UTMCK. The operation had three basic steps 1) Complete resection of the anterior scalene muscle from the first rib to the transverse processes 2) Assessment of the significance of the first rib compression of the brachial plexus 3) Neurolysis and hemostasis (Image 2). Dr. Stoney had explained to me that the anterior scalene muscle could alone be accredited for the TOS symptoms in the majority of patients, and that rib resection may not be important to long-term results. Furthermore, muscle remnants left behind could be the basis for reconstitution of the bands that course along the normal anatomic position of the anterior scalene, so a complete removal and debridement of the muscle was needed to treat this aspect of the compression. Bleeding also potentially causes severe perineural scarring and a dry surgical field is considered critical to long-term results. The use of film hyaluronidase inhibitors also were considered important to reducing adhesions, and on reoperation has appeared to have some benefit. These last concepts are echoed at other institutions, although most resect the rib primarily.

Swedish Providence Hospital, Seattle, Washington

Dr. Kaj Johanssen has developed an efficient clinical system for providing care to patients who suffer TOS. The foundation for this program is based upon the efforts of Dr. George Thomas (Image 3), a cardiothoracic surgeon who has greater than 50 years of clinical experience in the management of TOS. Dr. Johanssen took extraordinary efforts to provide an organized clinical curriculum that covered every aspect of his approach to TOS. This was organized into patient evaluation and diagnosis, nonoperative treatment, surgical technique and postoperative care. He was a gracious host who opened his practice to my inspection, and engaged me in thought-provoking conversation, even taking the effort to generate a panel of Seattle-based physicians under the heading of the “George Thomas Thoracic Outlet Mini-Symposium.”

This weeklong adventure began at the Western Vascular Society meeting at Victoria, B.C. Many vascular and endovascular topics were discussed at an open session, including a review of outcomes for surgical treatment of neurogenic TOS from the University of California at Los Angeles. After the meeting, the events moved to his hometown of Seattle for a rich clinical experience headed by observations of Dr. Thomas evaluating patients for thoracic outlet syndrome.

Dr. Thomas approached these patients by compiling a very precise clinical history, looking at the key risk factors and events that create a susceptibility to neurogenic TOS8. I gained an understanding of the association between chronic repetitive tasks and the development of spasm within the anterior scalene muscle9,10. Unlike discrete traumatic events, repetitive tasks seem to set in motion the cycle of inflammation within the anterior scalene triangle, tightening of the muscle with first rib elevation, and recruitment of secondary muscles of the shoulder girdle to “protect “ the neurovascular structures from ongoing irritation. Early intervention may serve to break this cycle through muscle relaxation, providing nonoperative decompression as the anterior scalene becomes more compliant, respecting the spatial parameters of the tight space that the brachial plexus traverses as it exits the neck. His history and physical examination was thorough, often exceeding two hours of thought and observation. Different physical findings were demonstrated by maneuvers that Dr. Thomas had acquired over a lifetime of experience in this field. This altered my understanding of this examination, and objectified many of the anatomic changes associated with TOS.

Pharmacological relaxation of the anterior scalene muscle with local anesthetic is described in the literature as an evocative test that may confirm the presence of TOS. Anterior scalene muscle block has technical points that are critical to its accuracy, as inadvertent bathing of the brachial plexus in lidocaine can provide relief as a nerve block, while the real objective is to relax the anterior scalene, releasing its grip on the trunks of the brachial plexus. Dr. Johanssen advocates a rational improvement in the accuracy in anterior scalene block by attaching the infusion needle to monitor to detect muscle action potentials11. The spastic muscle emits a very clear discharge signal as it is accessed percutaneously, and guides infusion of a small amount of lidocaine into the muscle belly. Any relief experienced by patient can then be reliably attributed treatment of the anterior scalene, rather than nerve anesthesia, which may falsely guide the clinician to the diagnosis of TOS. An additional benefit may be the decreased incidence of Horner’s syndrome and temporary arm paralysis.

Dr Johansen’s operative approach to brachial plexus relief involved a standard supraclavicular approach with anterior scalene muscle resection brachial plexus neurolysis and segmental first rib resection12. He also advocated the addition of the release of the pectoralis minor muscle to divest the cords of the brachial plexus as they pass under the corocoid process, a second sight of nerve compression associated historically with the upper extremity “hyperabduction syndrome.”  His experience with this technique was first developed as an adjunct to reoperation for TOS and he has now selectively incorporated it as a part of the primary operation for neurogenic TOS. His is currently collecting outcomes data relating to this combination therapy.

University of Colorado Medical Center at Denver

Dr. Richard Sanders may have the single largest clinical experience in thoracic outlet decompression in the world. Much of my prior knowledge of TOS was based upon his contributions to the literature regarding his patient series13. Informally, his patient series approaches 5000 over his long career in this field, and observing his clinical techniques revealed many details about his practice that may not be available in the literature.

His algorithm for evaluation includes a detailed history with precise temporal relationships established between potentially causal events and the onset of symptoms14. This has obvious clinical value, but also becomes important during legal discovery, as many of these patients are involved in litigation. His documentation often becomes that platform for the patient’s argument, and potentially a point of contention for a challenging attorney.

His physical examination is a detailed one, involving unique and “standard” maneuvers seen at other institutions. In conversation it was revealed that he has had ongoing collaboration with other surgeons in this field, and tailored his approach over years of practice. He personally does the anterior scalene block in the office as a concluding test for neurogenic TOS, completing the workup for a patient who may have traveled a long distance to obtain his medical opinion.

His operative approach for neurogenic TOS is a supraclavicular dissection with a thorough resection of the anterior scalene muscle, and he examines the anterior scalene space to determine the need for first rib resection15.  In this detail he agrees with the underlying importance of the muscle alone in the pathophysiology of brachial plexus compression described by Dr. Stoney. A case was performed where he evaluated the anatomy intraoperatively, and clarified some of the key observations that help him determine the extent of dissection. The brachial plexus neurolysis was a thoughtful and time intensive exercise that completely cleaned the nerves of any investing tissue that could potentially serve as a source for recurrent symptoms after thoracic outlet release. He also advocated the value of the transaxillary approach for access to the anterior aspect of the first rib. This may be critical to subclavian vein decompression, where the anterior portion of the first rib cannot be accessed through a standard supraclavicular dissection16. In conference, two cases of Paget-Schroetter syndrome were discussed where immediate internal jugular vein transposition was employed to improve venous outflow in the presence of a severely diseased subclavian vein. An axillary arteriovenous fistula was created to improve graft patency during the healing period.

Washington University Medical Center, St. Louis, Missouri

Dr. Robert Thompson has a busy practice at Barnes Jewish Hospital, with a focused clinical interest in TOS. He has treated a large number of athletes with TOS, particularly Paget-Schroetter syndrome, and has been a referral destination for our own University of Tennessee athletes. His training in TOS occurred largely during his fellowship training at UCSF, and much of his clinical evaluation and treatment routine is based upon the principles and practice described by Dr. Stoney. Dr. Thompson has an interest in outcomes data for TOS, and employs a research coordinator to assist in evaluating his TOS patient series.

Of particular interest is his developing surgical approach to the treatment of the subclavian vein for Paget-Schroetter syndrome17. A basic tenant is that the vein has intrinsic disease that exceeds what is visible angiographically. Trabeculations and mural scarring may often render the native subclavian vein too diseased to adequately decrease venous hypertension in the extremity. This correlates with the observation that many of these patients require postoperative venoplasty to maintain patency and decrease persistent arm swelling18. He therefore routinely opens the vein after”paraclavicular” decompression and will perform a bypass using tailored Saphenous vein conduit. In his patient series this produces a consistent and durable relief of swelling symptoms.

While at Washington University, I gained an appreciation of the variation in clinical evaluation and treatment of TOS. My discussions with Dr Thompson centered on the need for a multicenter registry to look critically at patient data, and help direct surgeons to determine the best treatment course for these difficult patients.

Conclusions

The E.J Wylie Memorial Traveling Fellowship has provided me with a profound extended training in TOS by allowing access to superb clinicians who have had a direct hand in describing the pathophysiology of upper extremity dysfunction caused by neurovascular compression at the thoracic outlet. Without the financial and academic support of this training grant funded by W.L. Gore and sponsored by the American Vascular Association, this hybridized academic exposure to TOS would be impossible. Additionally the traveling experience has helped me to create friendships and inter-institutional bonds that embody the spirit of Dr. Wylie, who valued worldwide collaboration during his prolific surgical career. It is my intention to maintain these valuable contacts to help me provide the best possible care In my practice at UTMCK, and to contribute to the body of surgical literature relating to the treatment of TOS.

References

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  2. Pollak EW. Thoracic outlet syndrome: diagnosis and treatment. Mount Kisco, N.Y.: Futura Pub. Co.; 1986.
  3. Pascarelli EF, Hsu YP. Understanding work-related upper extremity disorders: clinical findings in 485 computer users, musicians, and others. J Occup Rehabil 2001;11(1):1-21.
  4. Ritter A, Sensat ML, Harn SD. Thoracic outlet syndrome: a review of the literature. J Dent Hyg 1999;73(4):205-7.
  5. Reilly LM, Stoney RJ. Supraclavicular approach for thoracic outlet decompression. J Vasc Surg 1988;8(3):329-34.
  6. Edgelow P. Neurovascular Consequences of Cumulative Trauma Disorders Affecting the Thoracic Outlet: A Patient Centered Treatment Approach. Physical Therapy of the Shoulder, 4th edition, New York: Church Livingston,2004.
  7. Veith FJ, Stoney RJ. Self-retaining retraction in vascular surgery. J Vasc Surg 1986;3(5):824.
  8. Guidotti TL. Occupational repetitive strain injury. Am Fam Physician 1992;45(2):585-92.
  9. Thomas GI, Jones TW, Stavney LS, Manhas DR. The middle scalene muscle and its contribution to the thoracic outlet syndrome. Am J Surg 1983;145(5):589-92.
  10. Thomas GI. Thoracic outlet syndrome. Neurology 1993;43(6):1270-1.
  11. Jordan SE, Machleder HI. Diagnosis of thoracic outlet syndrome using electrophysiologically guided anterior scalene blocks. Ann Vasc Surg 1998;12(3):260-4.
  12. Ambrad-Chalela E, Thomas GI, Johansen KH. Recurrent neurogenic thoracic outlet syndrome. Am J Surg 2004;187(4):505-10.
  13. Sanders RJ, Haug CE. Thoracic outlet syndrome: a common sequela of neck injuries. Philadelphia: Lippincott; 1991.
  14. Sanders RJ, Hammond SL. Etiology and pathology. Hand Clin 2004;20(1):23-6.
  15. Sanders RJ, Monsour JW, Gerber WF, Adams WR, Thompson N. Scalenectomy versus first rib resection for treatment of the thoracic outlet syndrome. Surgery 1979;85(1):109-21.
  16. Sanders RJ, Hammond SL. Subclavian vein obstruction without thrombosis. J Vasc Surg 2005;41(2):285-90.
  17. Thompson RW, Schneider PA, Nelken NA, Skioldebrand CG, Stoney RJ. Circumferential venolysis and paraclavicular thoracic outlet decompression for "effort thrombosis" of the subclavian vein. J Vasc Surg 1992;16(5):723-32.
  18. Schneider DB, Dimuzio PJ, Martin ND, et al. Combination treatment of venous thoracic outlet syndrome: open surgical decompression and intraoperative angioplasty. J Vasc Surg 2004;40(4):599-603.

Posted June 2010

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