Vascular Problems and Thoracic Outlet Syndrome




Vascular problems involving the shoulder are relatively uncommon but can result in pain, a profound deleterious effect on an athlete’s performance, and in rare cases, a potentially limb-threatening situation. Acute sports-related vascular injuries are most common in contact sports and can occur as a result of blunt or penetrating trauma. The possibility of penetration of a bone fragment in fractures underscores the need for rapid assessment of vascular status with a physical examination, plain radiography, and arteriography if necessary. Delayed presentation of vascular injuries can be the result of compression or abnormality within the thoracic outlet. The thoracic outlet, which involves the area of the shoulder girdle in which the subclavian artery and vein exit the chest cavity along with the brachial plexus, is vulnerable to injury because of its crowded confines in combination with the high mobility of the glenohumeral and scapulothoracic articulations.


Thoracic outlet syndrome (TOS) generally defines any compression of brachial plexus elements and/or subclavian vessels as they pass from the intrathoracic area through the ribs into the axilla and proximal arm. However, it is important to identify the particular neurovascular structures involved when attempting to diagnose and treat TOS. Variability in the presenting symptoms of TOS provides a challenge for the clinician and highlights the importance of obtaining a careful history and performing a thorough physical examination. The various names referred to as TOS attest to its confusing nature ( Box 59-1 ).



Box 59-1

Synonyms for Thoracic Outlet Syndrome





  • Shoulder-hand syndrome



  • Paget-Schroetter syndrome



  • Cervical rib syndrome



  • First thoracic rib syndrome



  • Scalenus anterior syndrome



  • Brachiocephalic syndrome



  • Scalenus minimus syndrome



  • Scalenus medius band syndrome



  • Costoclavicular syndrome



  • Humeral head syndrome



  • Hyperabduction syndrome



  • Nocturnal paresthetic brachialgia



  • Fractured clavicle syndrome



  • Pneumatic hammer syndrome



  • Cervicobrachial neurovascular compression syndrome



  • Effort vein thrombosis



  • Rucksack paralysis



  • Pectoralis minor syndrome



  • Cervicothoracic outlet syndrome



  • Subcoracoid syndrome



  • Syndrome of the scalenus medius band



  • Naffziger syndrome



  • Acroparesthesia




Historically, the first description of the cervical rib and associated symptoms was by the German anatomist Hunald in 1842. After the advent of radiographs, Thomas and Cushing described a brachial plexopathy called the cervical rib syndrome and a surgical procedure to correct it in 1903. Neurovascular compression in the thoracic outlet area by structures in addition to the cervical rib were first described by Astley Cooper in 1921. In 1927, Adson and Coffey introduced scalenotomy as a treatment option for cervical rib symptoms. While grouping numerous types of neurovascular compression in the thoracic outlet region, Peet et al. first used the term thoracic outlet syndrome in 1956. Surgical management of TOS evolved in 1966, as Roos described the less morbid transaxillary first rib resection. In 1989, Atasoy introduced a combined approach to TOS consisting of transaxillary first rib resection and transcervical anterior and medial scalenectomy. Today, various surgical techniques are used to address any soft tissue or bony structures contributing to compression.


* The views and opinions expressed in this manuscript are those of the authors and do not reflect the official policy of the Department of the Army, the Department of Defense, or the U.S. Government.



Classification


The current classification for TOS focuses on the particular structures that are injured as opposed to the controversial anatomic factors responsible for the injury. In 1984, Wilbourn developed a classification for the TOS disorders based on the vascular or neural elements injured. This classification includes true neurogenic, arterial, venous, traumatic neurovascular, and nonspecific TOS. Clinical features are quite variable between the neurogenic and vascular subtypes of TOS. Neurogenic TOS accounts for more than 90% of all TOS cases, whereas vascular TOS constitutes 3% to 4% of all cases. Most TOS cases are seen in adults between the ages of 20 and 50 years. Vascular TOS is seen equally in nonathletic men and women, but neurogenic TOS is three to four times more likely to occur in women than in men. Among competitive athletes, venous TOS cases predominantly occur in men in their mid-20s. Other neurovascular pathology in the athlete’s shoulder region can be attributed to quadrilateral space syndrome (QSS), scapulothoracic dissociation, shoulder dislocation, and sternoclavicular dislocation.


Patients with neurogenic TOS commonly report a history of neck trauma, such as a motor vehicle accident, a violent collision in a sporting event, or repetitive heavy lifting. Complaints consist of paresthesias or weakness of the hand and arm, as well as pain involving the head, neck, shoulder, and back. Symptoms may also include loss of dexterity, muscle spasm, and a feeling of heaviness of the upper extremity. These clinical findings almost never solely involve pain or weakness in the dermatomes and myotomes associated with C8 or T1 compression. Patients may also report cold intolerance, Raynaud phenomenon, coldness of the hand, and color changes as a result of sympathetic overactivity as opposed to ischemia. Finally, nonspecific complaints such as headaches, tinnitus, and vertigo also may be present. Generally speaking, patients with true neurogenic TOS have objective motor and/or sensory deficits, whereas patients with nonspecific neurogenic TOS typically have subjective weakness and/or numbness in the upper extremity. Otherwise, these two entities share the same clinical presentation but may have vastly different treatment protocols.


Venous thoracic outlet syndrome, also known as Paget-Schroetter syndrome, has a variety of clinical presentations. This syndrome often occurs in healthy young men who have participated in excessive upper extremity activities and is caused by a spontaneous thrombosis of the subclavian or axillary vein. Usually no underlying compressive abnormality exists that predisposes the patient to the thrombosis. After the venous occlusion occurs, the limb feels heavy and becomes edematous and possibly even cyanotic. The patient may have neurologic features such as pain and paresthesias because of the vascular insult rather than injury to the nerve itself. The three most important factors that lead to venous TOS in athletes are hypertrophy of the pectoral muscle, fibrosis and thickening of the damaged vessel wall from repetitive activity, and damage to the intima of the vein leading to a thrombogenic surface. The term effort thrombosis has been used to describe this clinical entity, and this diagnosis has been reported in participants in sports such as swimming, tennis, and weight lifting.


Arterial TOS is the least common form of TOS but may have the most serious potential consequences to life or limb. Flow in the subclavian or axillary artery is obstructed, most likely from compression between the anterior scalene muscle or a bony anomaly such as a cervical rib or deformed first thoracic rib. The downstream effects of this arterial compression include vessel damage, turbulent blood flow, aneurysm formation, and thrombus formation. Later consequences can include embolization and ischemia of the digits. Importantly, aneurysm or thrombosis formation may not always be explained by direct arterial vessel compression via nearby structures. Kee et al. reported on ischemia of the throwing hand in professional baseball pitchers because of an embolic occlusion from an axillary artery branch aneurysm. These investigators did not detect any direct inducible compression of the artery but attributed the lesion to repetitive injuries to the artery during the throwing movement. Rohrer et al. showed that the subclavian or axillary artery can undergo considerable compression in arms that were hyperextended into a throwing position. These investigators reported at least a 20 mm Hg increase in arterial blood pressure in athletes and nonathletes when the arm was placed in that position. This condition may be underdiagnosed because its symptoms can mimic fatigue and musculoskeletal pathology in overhead throwing athletes. Rarer still, arterial TOS can present in children, in which case making a correct diagnosis often involves a lengthy workup.


QSS in athletes is most commonly diagnosed in baseball pitchers and volleyball players. The quadrilateral space is defined as the area enclosed by the teres minor superiorly, the humeral shaft laterally, the teres major inferiorly, and the long head of the triceps medially. The axillary nerve and posterior humeral circumflex artery traverse this space and are subjected to an often overlooked and position-dependent compressive entrapment. Hypertrophy of any one of the three muscular borders may reduce the space available for the neurovascular bundle, leading to QSS symptoms. Fibrous bands within this space, most commonly between the teres major and long head of the triceps, may contribute to the decreased cross-sectional area of the quadrilateral space. Additionally, the circumflex course of these structures predispose them to tethering and stretch injuries when the arm is abducted and rotated. Symptoms can be quite vague and overlap with other causes of posterior shoulder pain, such as posterior labral injury, rotator cuff tendinosis, and suprascapular nerve entrapment. Generally, no motor or sensory deficits are noted on physical examination. A lidocaine block has been described and is positive if the patient no longer has tenderness to palpation or pain with activity after the injection. A clinician must have a high index of suspicion and should rule out other sources of shoulder pathology before making this diagnosis.


Vascular injuries in the area of the shoulder can be potentially life- or limb-threatening conditions. A high level of awareness should be maintained for athletes who sustain clavicle fractures, proximal humerus fractures, glenohumeral joint dislocations, and other blunt or penetrating shoulder trauma. Most vascular injuries to the shoulder region occur as a result of penetrating bone fragments or a foreign object. However, Carli et al. reported a case of isolated axillary artery dissection due to blunt trauma in an ice hockey player. Vascular injuries after dislocations are also relatively uncommon, with an incidence of 0.97% after shoulder dislocation. Signs and symptoms of axillary artery injury after shoulder dislocation may be subtle, develop slowly, or be absent altogether. Pulses are absent in 93% of cases, but because of an extensive network of collateral vessels, distal pulses may still be present. Pain, swelling, an axillary mass, and a neurologic deficit are other findings to note on physical examination. The clinician must carefully evaluate the potential for injury to the axillary artery or its branches when managing cases of shoulder trauma in an athlete.




Anatomy


A thorough understanding of the proximal upper extremity vascular anatomy is essential when evaluating and treating potential neurovascular injuries in the area of the shoulder ( Fig. 59-1 ). Blood flows from the heart into the subclavian arteries in each upper extremity, with a short traverse through the innominate artery first on the right. The left subclavian artery arises directly from the arch of the aorta. The subclavian artery then enters the thoracic outlet, confined by the upper border of the first rib, the lower border of the clavicle, and the anterior and middle scalene muscles, and extends to the lateral border of the first rib. The artery becomes the axillary artery as it exits from the lateral border of the first rib to the inferior border of the latissimus dorsi. The axillary artery is divided into three anatomic sections by the pectoralis minor tendon, with the first section being above the superior border of the pectoralis minor and giving off the superior thoracic artery inferiorly. The second section of the axillary artery lies deep to the pectoralis minor and gives off the lateral thoracic branch and the thoracoacromial artery, which further divides into the clavicular, acromial, deltoid, and pectoral branches. The third and final section of the axillary artery lies distal to the pectoralis minor and contributes the subscapular artery and the anterior and posterior circumflex arteries. The subscapular artery further divides into the scapular circumflex and thoracodorsal arteries. The anterior circumflex artery provides the majority of blood supply to the humeral head near the intertubercular groove through the arcuate artery, which is an anterolateral ascending branch of the anterior circumflex humeral artery.




FIGURE 59-1


Vascular anatomy of the shoulder.

(From Drake RL, Vogl AW, Mitchell AWM: Gray’s anatomy for students , Philadelphia, 2010, Elsevier.)


The basilic vein drains the ulnar portion of the hand and forearm and the medial portion of the arm before becoming the axillary vein at the inferior border of the latissimus dorsi. It then becomes the subclavian vein at the lateral border of the first rib before draining into the brachiocephalic vein medially. The cephalic vein is the more lateral superficial vein in the arm and enters the clavipectoral fascia before emptying into the axillary vein. Together, the axillary and cephalic veins account for the majority of the venous drainage in the shoulder. The shoulder lymphatics end in the thoracic and right lymphatic ducts.


Anatomically, the thoracic outlet spans the general area from the supraclavicular fossa to the axilla and includes the area between the clavicle and the first rib. More specifically, the thoracic outlet includes three confined spaces in which compression can occur ( Fig. 59-2 ). These compartments include the interscalene triangle, the costoclavicular space, and the retropectoralis minor space. The interscalene triangle is bordered anteriorly by the anterior scalene muscle, posteriorly by the middle scalene muscle, and inferiorly by the medial surface of the first rib. The interscalene triangle contains the vast majority of neurovascular compression cases of TOS. The trunks of the brachial plexus and subclavian artery pass through the interscalene triangle, whereas the subclavian vein actually passes anterior to the anterior scalene muscle ( Fig. 59-3 ). The costoclavicular space lies between the clavicle and the first rib posteromedially and the upper border of the scapula posterolaterally. The retropectoralis space lies inferior to the coracoid process beneath the pectoralis minor tendon.




FIGURE 59-2


Three spaces in the thoracic outlet that may be responsible for thoracic outlet syndrome.



FIGURE 59-3


Normal bony anatomy and neurovascular relationships of the thoracic outlet. a, Artery; m, muscle; v, vein.


Several bony abnormalities may play a role in compressing structures in the thoracic outlet and causing neurovascular symptoms ( Fig. 59-4 ). Cervical ribs can originate from the seventh cervical vertebra in approximately 1% of the population, with about 10% of those persons having symptoms related to this condition. Various types of cervical ribs can exist, ranging from short bars of bone, incomplete ribs with fibrous bands, and full ribs articulating with the first rib, manubrium, or sternum. In addition, an elongated C7 transverse process can cause compression. Abnormalities such as exostosis, tumor, callus, or fracture of the first rib or clavicle may also be responsible for compressive symptoms. Complications of clavicular fractures such as malunion, fragmentation, and retrosternal dislocation can also increase the risk of developing TOS.




FIGURE 59-4


Common bony anomalies in persons with thoracic outlet syndrome.


Soft tissue abnormalities such as anomalous fibrous bands and anatomic variations of the scalene muscles can create compression in the thoracic outlet. Roos classified 10 types of fibrous bands in the area of the thoracic outlet that may act to compress its neurovascular structures through direct contact or by compromising the space available within the outlet. Scalene muscle variations that may contribute to TOS include anterior scalene hypertrophy, passage of the brachial plexus through the substance of the anterior scalene muscle, and a broad, anterior insertion of the middle scalene onto the first rib. Potential loading of the neural tissue may also occur if clavicular motion during upper extremity elevation is compromised, particularly with injuries to the acromioclavicular or sternoclavicular joints. Repetitive trauma to the more vulnerable lower brachial plexus trunk and C8–T1 spinal nerve roots can play a role in the pathogenesis of TOS.




History


The patient’s history prior to the onset of symptoms is often the most helpful tool in diagnosing TOS. The history may include a neck injury, clavicle fracture, presence of a cervical rib, unusual postural requirements, or strenuous overhead activities. Patients typically report an aching pain radiating from the back of the shoulder region down into the upper extremity. Pain may be accompanied by numbness, tingling, weakness, swelling, coolness, and discoloration. Occasionally pain spreads up the back and into the side of the neck, with an associated ipsilateral hemicranial headache. These symptoms are often exacerbated by arm elevation and by carrying heavy loads. Furthermore, these symptoms progress despite various conservative treatment modalities, such as physical therapy, medications, injections, biofeedback, and psychotherapy.


The differential diagnoses for TOS include any pathology creating pain or weakness in the neck, arms, or shoulders. The differential can include cervical radiculopathy or arthritis, brachial plexus neuritis, shoulder pathology, peripheral nerve compression, neoplasm, vasculitis or thromboangiitis, rheumatologic conditions, multiple sclerosis, or acute coronary syndrome. In most situations, TOS is a diagnosis of exclusion. For true neurologic TOS, any disorder involving the sensory or motor nerve fibers of the C8 or T1 spinal cord segment must first be investigated and can include anterior horn cell disorders, brachial plexopathies, radiculopathies, or mononeuropathies of the median, ulnar, and radial nerve. Furthermore, traumatic factors such as clavicle fractures, clavicle malunions/nonunions, injuries to the cervical spine, dislocation of the humeral head, and atherosclerosis of the major arteries near the humerus must be considered.


TOS can be seen in athletes who engage in overhead motions, such as pitchers, tennis players, and swimmers. Muscular athletes may be especially susceptible because of hypertrophy of neck, shoulder, and scapular musculature. Athletes in contact sports may sustain traction injuries to the upper arm and chest. Direct trauma that results in rib fractures, transverse process fractures, clavicle fractures, and shoulder injuries may lead to TOS. Effort thrombosis caused by compression of the subclavian vein between the clavicle and first rib is probably the most frequently encountered vascular disorder in young athletes. Hypertrophy of the anterior scalene muscle may be a contributing cause of this compression. Axillary artery lesions are rarely the cause of nontraumatic etiology, although a distinctive lesion can occur in baseball pitchers. Compression and stretching of the axillary artery by the humeral head as it shifts forward during the late cocking phase of pitching may lead to aneurysms and occlusions of the artery itself.




Physical Examination


After a thorough history has been obtained that details timing aspects of symptoms and precipitating causes, both upper extremities should be carefully examined for evidence of swelling, discoloration, temperature changes or cold intolerance, ulcerations, muscle atrophy, or nail bed deformities. General range of motion, strength testing (including hand intrinsic muscles), and pulse palpation from the wrist to the shoulder should be documented. A classic finding in true neurogenic TOS is wasting of the abductor pollicis brevis and mild wasting of the interossei and hypothenar muscles, presenting as the Gilliatt-Sumner hand. Blood pressure and an Allen test should be evaluated. The cervical spine, clavicle, and scapula must be thoroughly examined to evaluate for cervical disk pathology, clavicular trauma, scapular winging, or other abnormalities. Sensation should be tested statically and dynamically with two-point discrimination. Muscles and bones should be palpated for areas of tenderness and possible anatomic abnormalities, such as cervical ribs. The extremities also should be examined for evidence of distal nerve compression, especially near common problematic areas such as the carpal tunnel, pronator teres, and cubital and radial tunnels.


Vascular TOS is usually readily identified and differentiated from neurogenic TOS via symptoms, physical examination findings, and diagnostic studies. Arterial TOS commonly involves symptoms and findings distally in the forearm and hand and is less often provoked by scalene palpation, neck rotation, or head tilting. Arterial emboli can produce distal findings of subungual petechiae, digital ischemia, claudication, pallor, coldness, pain, and paresthesias in the hand. Emboli can also lead to obliteration of the radial pulse at rest, and abduction of the arm is unnecessary to detect it. Venous TOS is usually associated with arm swelling, cyanosis, and distended superficial veins not usually seen in arterial or neurogenic TOS.


Neurogenic TOS is classically associated with certain provocative tests, although they display high rates of false-positives. All tests are positive if they increase symptoms such as pain, paresthesias, or attenuation of the radial pulse. Tests that more specifically delineate compromise in the interscalene triangle are the Adson test and the supraclavicular pressure test. The costoclavicular or military brace maneuver narrows and emphasizes possible compression in the costoclavicular space. The Wright test compresses and stretches structures in the retropectoral space. The elevated arm test (Roos) evaluates for neural compromise throughout the thoracic outlet. Upper limb tension testing indicates brachial plexus compression; however, it may be in the retropectoral space, interscalene triangle, or cervical spine.


The Adson test is performed with the patient’s affected arm extended and slightly abducted, the neck tilted toward the affected side, and the patient inhaling deeply ( Fig. 59-5 ). The physician feels the radial pulse before and during the test and looks for obliteration due to compression of the subclavian artery by the anterior scalene. This test can be positive in a healthy person and can be unreliable for arterial TOS if the pulse is already absent as a result of emboli. Tilting the neck to the opposite side (the reverse Adson test) may be a more reliable test that can produce arm heaviness, fullness, pain, and distal numbness in symptomatic patients. The supraclavicular pressure test is performed by placing compression in the retroclavicular space with the thumb in an attempt to compress the brachial plexus and vascular structures ( Fig. 59-6 ). During the costoclavicular maneuver, the patient retracts the shoulders backward and downward to bring the clavicle closer to the first rib in an attempt to elucidate neurogenic or vascular symptoms ( Fig. 59-7 ). The Wright test has the physician hyperabduct and externally rotate the affected extremity of the patient while looking for arm, hand, or pulse changes ( Fig. 59-8 ). The Roos elevated arm test is performed by abducting and externally rotating each of the shoulders 90 degrees while opening and closing the hands rapidly ( Fig. 59-9 ). The test lasts 3 minutes and is positive if the patient feels fatigue, pain, paresthesias, or numbness. Upper limb tension testing is a good screening test for sensitization of neural tissue in the cervical spine, brachial plexus, and upper limb but is not specific. The following three positional instructions are performed: (1) abduct both arms to 90 degrees with the elbows straight; (2) dorsiflex both wrists; and (3) tilt the head to one side with the ear to the shoulder, and then to the other side. Ipsilateral symptoms are seen in positions 1 and 2. Contralateral symptoms are seen in position 3. A strong positive test is onset of pain and/or paresthesias in position 1 that increases in positions 2 and 3.




FIGURE 59-5


The Adson test is performed with the head tilted to the affected side and the patient’s affected arm extended and slightly abducted.



FIGURE 59-6


The supraclavicular pressure test is performed by placing compression in the retroclavicular space with the thumb in an attempt to compress the brachial plexus and vascular structures.



FIGURE 59-7


In the costoclavicular maneuver, the patient retracts the shoulders backward and downward to bring the clavicle closer to the first rib in an attempt to elucidate neurogenic or vascular symptoms.



FIGURE 59-8


The Wright test has the physician hyperabduct and externally rotate the affected extremity of the patient while looking for arm, hand, or pulse changes.

Feb 25, 2019 | Posted by in SPORT MEDICINE | Comments Off on Vascular Problems and Thoracic Outlet Syndrome
Premium Wordpress Themes by UFO Themes