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|Thoracic Outlet Syndrome|
Inside Thoracic Outlet Syndrome
Thoracic Outlet Syndrome (TOS)
Thoracic outlet or inlet syndrome is a complex of signs and symptoms that result from compression of the neurovascular bundle as it emerges from the thorax and enters the upper limb. Depending on the site of compression and the structure involved, there are a variety of clinical manifestations. The presentation may be confusing, and the complaints and physical findings are often vague. Indeed there is debate as to the existence of such a syndrome; and as a result, the attitude of the clinician dictates whether this syndrome is diagnosed with regularity or not at all.
There are two major components to the syndrome, the first relating to problems with the major vessels and the second to pressure on the nerves. If there is thrombosis of the subclavian artery or vein, it is a clearly defined entity that is easily confirmed and usually presents with dramatic clinical signs. There is no speculation regarding this problem. By contrast, the neural signs and symptoms are more difficult to pin down, even with sophisticated electrophysiologic tests.
The narrow confines of the thoracic outlet may be considered the space between the relatively fixed immobile thorax, particularly the first rib, and the clavicle. Traditionally, this space is extended to include the triangle between the scalenus muscles, which border the roots and trunks of the brachial plexus, en route to the upper limb, within the axillary sheath. During normal development of the human shoulder girdle, the scapula descends from a relatively high position at birth to a low one during adolescence and maturation. These relations are affected by hypertrophy or atrophy of muscles and chronic postural positions. Thus as the configuration of this area changes throughout life, the possibility of a dynamic pathogenesis is possible.
The first potential site of compression is within the
interscalene interval (triangle) between the scalene anterior muscle
anteriorly and the middle scalene posteriorly. Both are attached to the first
rib and serve as a framework for the brachial plexus. This triangle can be
compromised by accessory muscles, hypertrophy of the existing muscles, the
presence of a first rib, or
fibrous bands. Accessory ribs are found in approximately 0.5 percent of the
The second major area of potential compression is between the mobile clavicle and the relatively fixed first rib. Fractures of the clavicle with large callus, congenitally bifid clavicles, a changing posture, a postfixed brachial plexus, or thickened, tight clavipectoral fascia may compromise this space. As has been previously emphasized, many of the problems are congenital rather than acquired, but they are in a dynamic state of changing relations; thus true thoracic outlet compression is rarely found before puberty. The scapula tends to descend more in females than males, which may partly explain the greater incidence of thoracic outlet syndrome in women. With increasing age and changing shoulder posture, particularly in association with excessive body weight and large breasts, this problem may become more manifest. It is worthwhile recalling that the suspension of the mobile scapula is virtually entirely muscular in nature; and the strength and tone of the trapezius muscles, rhomboids, and levator scapulae are particularly important to the possible pathogenesis of the problem as well as when considering treatment. Direct and indirect trauma—a single blow or repetitive, excessive use of the upper limb—may trigger this syndrome. Furthermore, in the young patient or athlete, it is often the particularly heavy muscled individual, with huge trapezius and neck development, who runs into difficulty.
The third potential area of compression for the neurovascular structures is in the subcoracoid region adjacent to the tendon pectoralis minor. Here the thickened clavipectoral fascia, often referred to as the costocoracoid membrane, forms a dense line of fascia. With full circumduction of the arm, the coracoid process almost forms a fulcrum for the subclavian vessels and the neurovascular structures.
Because of the various potential anatomic areas of compression and the variety of structures that can be involved, the clinical manifestations can be inconsistent in nature. The most common clear presenting symptom of the thoracic outlet syndrome arises from compression of the lower trunk of the brachial plexus. The pain extends from the root of the neck to the shoulder and then down the arm in a diffuse fashion. It may be accompanied by paresthesias involving the medial aspect of the hand, particularly the little finger and ring finger, but it may involve the whole of the medial aspect of the arm, particularly from the shoulder to the elbow. Less commonly patients complain of weakness of the affected hand, and there may be detectable wasting. Tennis or baseball players may find difficulty gripping the racket or bat. Occasionally there is only painless intrinsic atrophy of the hand. Ultimately the whole of the hand may be involved, but it usually starts on the ulnar side. Some patients complain mainly of neck and shoulder pain, with vague discomfort extending into the trapezius and suboccipital region, which they may describe as a headache-type sensation.
During the history it is important to elicit that the patient or athlete relates the symptoms to upper limb motion in the arc where the nerves are either stretched or compressed. Adopting the posture that either narrows the costoclavicular interval or allows compression of the underlying structures should reproduce the symptoms. Numbness and tingling in the hand with overhead movements must be distinguished from the dead arm syndrome of shoulder instability, where rapid movements are involved. Some patients complain of nocturnal paresthesias, waking to find that they have slept with their arms in an overhead position.
Symptoms of arterial compression are usually related to numbness of the whole arm with rapid fatigue during overhead exercises. These symptoms may be an isolated finding or occur in association with some neural symptoms. When there is significant arterial compression, the hand may be obviously cool and pale compared to that on the contralateral side when both are held above the head. In addition, the radial pulse may disappear only to return when the arm is replaced at the side. However, this phenomena is frequently seen in the general population, and so great care should be taken when drawing any conclusions from a weakening or a disappearing pulse with the arms above the level of the shoulder. Rarely there are signs of acute arterial insufficiency with major vascular compromise to the hand or even the entire limb.
When venous compression in the thoracic outlet is the presenting problem, the patient may arrive with a swollen, discolored limb several hours after a bout of intense exercise. In the general population unaccustomed activity such as a building project may cause the problem, but with the patient or athlete it is usually a sudden change in exercise pattern, either different activity or an intense increase in volume of a specific overhead movement. Occasionally, this obvious swelling and color change disappears over several hours so by the time the patient is examined by the physician there is little to see; thus a careful history is important. When Venous compromise is sufficiently severe or there is also occlusion of the subclavian vein, a visible venous collateral pattern may become evident across the patient’s shoulder, chest, and ipsilateral breast.
In addition to a detailed history, it is essential to evaluate the cervical spine, shoulder, elbow, and hand for evidence of neural compression. It is mandatory to distinguish the classic ulnar and median nerve compression syndromes and cervical radicular signs. Instability of the shoulder should be ruled out and posture evaluated. Inasmuch as the diagnosis of the thoracic outlet compression is usually one of exclusion, this initial screening is mandatory.
1. Inspection of posture:
A. Shoulder asymmetry.
B. Poorly developed musculature/drooping shoulders.
C. Unusually large breasts.
2. Palpation: Reveals tenderness over supraclavicular fossa, check for increased tone of the scalene muscles.
3. Listen for bruits: Over supraclavicular fossa while arm is in a provocative position.
4. Provocative maneuvers: Examiner looks for obliteration of radial pulse and/or exacerbation of symptoms.
A. Costoclavicular maneuver. Patient shrugs shoulders with deep inhalation while drawing the shoulders backward in an exaggerated military position.
B. Scalenus anticus maneuver. Patient turns the head away from the involved side and opens and closes the involved hand 5 times and is then examined for blanching of the hand. This may also be done by turning the head toward the involved side.
C. Adson’s maneuver. Patient extends and turns head toward involved side with deep inhalation, and the examiner laterally rotates and extends the shoulder.
D. Wright’s hyperabduction. Patient turns head away from involved side, and with deep inhalation the arm is abducted and externally rotated. The pectoralis minor muscle forces compression against the fulcrum of the coracoid process.
E. Arm elevation stress test (AEST). With arms overhead, patient rapidly flexes and extends fingers. Reproduction of symptoms or fatigue is a positive sign.
The hyperabduction test is performed by taking the arm into gradual abduction and extension of the shoulder while monitoring the pulse. This test is considered positive only if it reproduces all the clinical signs; it is also helpful if there is confirmatory bruit over the subclavian arterial at the time of pulse diminution and reproduction of the symptoms.
The Arm Elevation Stress Test (a/k/a ROOS' test) is performed by having the patient take the arms into full elevation and then rapidly flex and extend the fingers. In susceptible individuals a feeling of fatigue or even cramping of the forearm muscles may be experienced within about 20 seconds. The elevated arm may also become pale compared to the normal side, and the obliteration or diminishing of a pulse assists in confirming the diagnosis. A variation of this test is the 3-minute elevated arm exercise test.
Adson’s maneuver is performed with the arm at the side and externally rotated and the examiner monitoring the pulse while the patient rotates the head toward the involved side, elevates the chin, pushes into full rotation, and takes a deep breath to fix the upper rib. Unfortunately, this test for thoracic outlet compression produces many false-positive findings.
With Wright’s maneuver, the pulse of the abducted and laterally rotated arm is monitored while the neck is rotated to the opposite side. The patient takes a deep breath while adopting the so-called military brace position with the shoulders retracted and pulled down.
Plain cervical spinal roentgenograms (x-rays) may help to rule out certain intrinsic conditions, e.g., cervical spondylosis, narrowed intervertebral discs, and osteophytic impingement (bone spurs). The presence of cervical ribs or long C7 transverse processes may fit in with the findings of thoracic outlet compression. All patients should have adequate studies of the apex of the lung on the affected side.
There is a discrepancy of opinion regarding the value of electrodiagnostic studies. There is considerable difficulty accurately determining the nerve conduction velocity through the thoracic outlet. In many ways, the biggest value of electrodiagnostic studies is to rule out peripheral entrapment, e.g., ulnar neuropathy at the elbow or hand or carpal tunnel syndrome of the median nerve at the wrist.
If there is significant evidence of arterial venous
involvement suggesting either thrombosis, aneurysm or compression, it may be
prudent to obtain Doppler, Angiographic,
or venographic studies.
Because there are few definite indicators of the thoracic outlet syndrome, its diagnosis is one of exclusion. Thus the differential diagnosis assumes significance.
Cervical spinal pathology is the most common cause of paresthesia in the upper limb, and efforts should be made to distinguish radicular pain in the C8 and T1 distribution. Most disc diseases affect the C5—C6 level and to somewhat lesser extent the C7 level. Thus paresthesias in the ulnar side of the hand are more likely to be of distal origin.
Any space-occupying lesion within the thoracic outlet, particularly the Pancoast’s tumor at the apex of the lungs, may mimic the symptoms of the thoracic outlet syndrome. Although it is believed that the pursuit of health and fitness is not compatible with smoking, a large number of patients and athletes do indeed smoke on a regular basis. The incidence of lung cancer parallels this habit, and so the middle-aged and elderly pateint is not immune from lung tumors.
Peripheral entrapment of the ulnar nerve at the elbow and in the cubital tunnel, or in the hand in Guyon’s canal, can produce typical dysesthesia in the ring and little fingers. Similarly, compression of the median nerve and the carpal tunnel may produce paresthesias in the distribution of that nerve, typically in the thumb and index and middle fingers, with wasting of the hyperthenar eminence. In previously reported series of cervical rib resection for thoracic outlet, there was an uncomfortably large percentage of individuals who subsequently required release of the ulnar or medial nerve peripherally. It is tempting to postulate a double-crush syndrome, with irritation at a subclinical level in both sites, combining to produce a significant clinical entity. One should remain pragmatic, however, and assume that in many of these instances an incorrect diagnosis has been made.
Reflex Sympathetic Dystrophy
Like the thoracic outlet syndrome, reflex sympathetic dystrophy presents as a constellation of peripheral symptoms, including dysesthesias, hypersensitivity, and muscle wasting. The key to diagnosing reflex sympathetic dystrophy is awareness of the possibility of this syndrome. A key feature is the disassociation between the sensations of touch, pressure, and pain. It may be particularly difficult to distinguish the two syndromes if there is appreciable swelling within the
It may have a blood vessel (vascular) vascular origin or a nerve (neural) origin.
• Vascular origin
- Dull aching
- Venous distension
- Peripheral edema
- Occasional ulceration
• Nerve Origin
- Usually ulnar abnormal sensation (dysesthesia) - T1 dermatome usually
- Aggravated by overhead activity
- Generalized upper limb ache
POTENTIAL SITES OF NEUROVASCULAR COMPRESSION
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