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Sport-specific Illness and Injury

Diagnosis and Management of Vascular Injuries in the Shoulder Girdle of the Overhead Athlete

Reeser, Jonathan C. MD, PhD

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Current Sports Medicine Reports: October 2007 - Volume 6 - Issue 5 - p 322-327
doi: 10.1097/01.CSMR.0000306495.46024.c4
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The shoulder joint is the most mobile articulation in the human body, and one of the most vulnerable to injury. Injury epidemiology studies have demonstrated that the shoulder girdle is among the most frequently injured body parts of overhead athletes (eg, baseball pitchers, volleyball attackers, tennis players, and swimmers) [1–4]. The most common injuries to the shoulder girdle in these athletes involve overuse-related pathology of the musculoskeletal soft tissues. In contrast, vascular injuries of the upper limb represent an infrequent cause of pain and functional limitation for athletes who must repetitively perform sport-specific skills overhead [5]. Nevertheless, because a delayed diagnosis could result in considerable morbidity, sports medicine personnel must remain alert to the possibility of vascular pathology in the overhead athlete who presents with complaints of activity- and position-dependent pain, paresthesias, heaviness, fatigue, and/or swelling in the dominant upper limb [6].

The shoulder girdle serves to position and stabilize the upper limb in space, thereby maximizing the functional capacity of the extremity. Anatomically, the shoulder girdle funnels the neurovascular structures emanating from the cervical and upper thoracic regions through the cervicothoracobrachial junction (ie, the “thoracic outlet”) into the proximal upper limb. Although relatively well protected along their course by the clavicle and the overlying pectoral musculature, the subclavian/axillary artery and vein and the brachial plexus are nonetheless vulnerable to blunt trauma as well as to injury secondary to glenohumeral dislocation or clavicular fracture. Perhaps for this reason, neurovascular injuries involving the shoulder girdle are most commonly seen in contact sports, such as American football and wrestling [7]. However, the neurovascular structures that pass through the thoracic outlet are also vulnerable to intermittent compression at several areas within this region (Fig. 1).

Figure 1
Figure 1:
Sites of potential compromise of the subclavian/axillary vessels within the shoulder girdle include the interscalene triangle (A), the costoclavicular space (B), the infrapectoral region (C), the humeral head (D), and the quadrilateral space (E).

Symptomatic dynamic compromise of the neurovascular bundle within the cervicothoracobrachial junction is commonly referred to as “thoracic outlet syndrome” (TOS). While the skeletal boundaries of the thoracic outlet include the first rib, the clavicle, and the scapula, in common usage TOS refers to a symptom complex produced by neurovascular compromise occurring between the neck (proximally) and the axilla (distally) [8]. TOS may be categorized as resulting from either vascular or neurogenic pathology. While neurogenic TOS is reported to be far more prevalent than vascular TOS, there is some debate as to the legitimacy of the former diagnosis [8,9]. There is, however, no disagreement that the subclavian and axillary artery and vein may be susceptible to intermittent compression as they pass through the thoracic outlet. Vascular TOS may therefore be further divided into arterial TOS and venous TOS (Table 1) [10].

Table 1
Table 1:
Typical clinical features of vascular injuries in the shoulder girdle

“Effort Thrombosis” or Paget-Schroetter Syndrome (Venous TOS)

The literature describing the vascular injuries for which overhead athletes are at risk consists almost exclusively of case reports and case series, and thus the incidence and prevalence of vascular-related symptoms in the overhead athlete are not known with any accuracy. Data reported by Arko et al. [11] suggest that venous TOS is more common (or at least diagnosed more frequently) than arterial TOS. “Effort thrombosis,” which is also known as Paget-Schroetter syndrome (PSS), represents the major form of venous TOS [8]. The incidence of PSS has been estimated at two cases per 100,000 persons/year [12]. Men appear to be more frequently diagnosed than women.

As its name aptly describes, effort thrombosis is characterized by subclavian/axillary vein thrombosis associated with overhead activity rather than overt trauma. Compression of the subclavian vein by any one of several structures within the thoracic outlet can potentially result in sufficient stasis to permit thrombus formation. The scalene muscles, the first rib, the subclavius muscle, the clavicle, and the costoclavicular ligament all represent possible sites of subclavian vein compression. Less commonly, the axillary vein may be symptomatically compressed as it passes beneath the tendon of the pectoralis minor muscle. Anatomic variants, such as the axillary arch of Langer [13], also can impinge upon the axillary vein. Mechanistically, it is believed that repetitive hyperabduction (combined with external rotation) of the upper limb at the shoulder persistently compresses the subclavian and/or axillary vein at one of these sites, resulting in cumulative damage to the intima and transiently restricting venous flow. This satisfies two of Virchow's classic triad (vascular injury and stasis), thereby creating an environment conducive to thrombosis. Once PSS has been diagnosed, it is important to screen for reversible risk factors that may satisfy Virchow's third criteria (ie, the hypercoaguable state) [14]. Concurrent systemic illness, significant dehydration, smoking, and oral contraceptive use represent common examples of such reversible risk factors.

The athlete with acute PSS usually presents within 24 hours of the inciting activity with complaints of diffuse effort-dependent pain in the dominant upper limb, fatigue and/or weakness with functional limitation, and deteriorating athletic performance. Initial symptoms and signs may also include heaviness, paresthesias, venous distension, and diffuse upper limb swelling. Doppler ultrasonography serves to identify both the location and extent of the thrombus, but contrast venography combined with cross-sectional imaging provides superior detail of the sites of any external venous compression. Conservative treatment options include rest and systemic heparinization, followed by long-term oral anticoagulation [15], but catheter-directed thrombolytic therapy represents the current standard of care for the treatment of acute PSS [16,17•]. However, thrombolysis may be less successful in cases of chronic subclavian vein thrombosis. Angioplasty (with or without stent placement) has been employed to restore vessel patency and maintain venous flow in some cases [18], although the long-term utility of this intervention without concomitant surgical decompression has been questioned [17•,19].

The fact that upper limb venous thrombi can (not infrequently) embolize to the lungs reinforces the importance of making an accurate diagnosis and initiating definitive treatment. Molina et al. [20••] tout prompt surgical decompression of the subclavian vein as critical to a favorable clinical outcome for the treatment of PSS. Their protocol (consisting of first rib resection, scalenectomy, and subclavius muscle resection within hours after successful thrombolysis), resulted in a good outcome in all 97 subjects treated within 2 weeks of symptom onset. Similar protocols have permitted major league baseball players to successfully return to competition [21,22]. Conversely, delays in diagnosis and surgical decompression tend to be associated with less favorable outcomes [17•,20••]. Molina et al. [20••] report that of the 17 patients evaluated more than 2 weeks after the initial onset of symptoms, only five (29%) were subsequently felt to be surgical candidates. The remaining 12 were deemed inoperable since the subclavian vein had developed extensive fibrosis. Postoperative rehabilitation should emphasize correction of postural maladaptations that may predispose the individual to TOS (eg, head forward and rounded shoulders), strengthening the scapular stabilizers, correction of muscle imbalances, and modification of overhead sport skill mechanics [23•]. Identification of both heritable and acquired risk factors, and elimination of those deemed reversible, are integral to secondary prevention.

Subclavian/Axillary Arterial Injury (Arterial TOS)

The subclavian/axillary artery is also vulnerable to compression injury within the thoracic outlet. Epidemiologic data is limited, but it appears that the incidence of subclavian injury may slightly exceed that of axillary injury [24]. In addition, the available data suggest that while the gender distribution of subclavian injury appears to be essentially equal, male athletes may be at greater risk of axillary injury than female athletes [24]. Whether gender represents a true risk factor for axillary injury must await more definitive epidemiologic investigation. Documented structural factors related to subclavian arterial compression include cervical ribs [25] and anomalous first ribs. These anatomic variants were implicated by Durham et al. [24] in 20 of 27 cases of subclavian arterial compromise. As was the case with the subclavian vein, overdeveloped scalene muscles have also been described to compromise blood flow through the subclavian artery as it traverses the interscalene triangle proximally. More distally, the axillary artery may undergo compression as it passes beneath the tendon of the pectoralis minor muscle. In addition, the close anatomic relationship between the humeral head and the axillary artery [26] may predispose the throwing athlete to developing axillary arterial injury.

Rohrer et al. [27] documented that when the upper limb is placed in a “cocked” position the humeral head becomes a fulcrum over which the distal third of the axillary artery may be transiently compressed. The authors detected ultrasonographic evidence of axillary arterial compromise in 83% of the shoulders evaluated in a position of abduction and external rotation, with nearly 8% of subjects experiencing greater than 50% stenosis of the axillary artery in this position. Rohrer et al. [27] also documented a drop in blood pressure of 20 mm Hg or greater in 56% of subjects tested, with complete loss of detectible ipsilateral blood pressure in 13% of the participants. Because the authors did not report what percentage of the athletes who experienced a drop in blood pressure also became symptomatic (if any), it is unclear if this mechanism is by itself sufficient to produce the observed clinical symptom complex. It seems likely that other risk factors (such as abnormal scapular dynamics and/or glenohumeral laxity) also play a role in the position-dependent onset of symptoms. Indeed, there are several reported cases of axillary arterial injury (and associated aneurysm formation) following anterior dislocation of the humeral head [28,29]. Sports medicine clinicians should, therefore, carefully assess the neurovascular status of the affected upper limb both before and after reduction of an anterior shoulder dislocation [30].

The clinical symptoms and signs characteristic of either subclavian or axillary arterial compromise include cyanosis, a cool limb, early fatigability, claudication, and position-dependent decrement in the peripheral radial pulse and blood pressure as well as delayed capillary refill. A bruit may also be heard. However, unless the clinician maintains a high index of suspicion, it is entirely possible that the affected athlete may be initially misdiagnosed with musculoskeletal shoulder pain [10,31]. Only rarely will the athlete with arterial TOS have demonstrable weakness or sensory deficit, but if present the distribution of these findings may provide a diagnostic clue as to the location of neurovascular compromise. Although several different physical examination techniques have been developed in an effort to reproduce the athlete's symptoms through positional compression, (including the Adson test, the Wright [hyperabduction] test, and the elevated arm stress test) [32], none is sufficiently sensitive or specific to be diagnostic when used in isolation [33].

Due to the diagnostic uncertainty inherent in these physical examination techniques, and in light of the variability in reported symptoms, the definitive diagnosis of arterial TOS rests upon radiographic documentation of dynamic circulatory compromise. Available imaging modalities include Doppler ultrasonography, conventional or CT angiography, and magnetic resonance angiography [34•]. The anatomical detail afforded by MRI often provides clinically useful information not obtainable via other modalities. Conventional radiography should always be included as part of the diagnostic evaluation to identify/rule out other bony abnormalities, particularly if the individual provides a history of trauma to the shoulder girdle (TOS has been reported to occur as a late sequela of a fractured clavicle) [35,36]. The diagnostic finding on imaging is a position-dependent interruption of blood flow (ie, vascular compromise in the abducted and externally rotated upper limb that resolves when the limb is in a dependent position). Other relevant radiographic findings include poststenotic vascular dilatation and aneurysms. Aneurysm formation increases the risk of peripheral emboli, signs of which include selective digital ischemia, splinter hemorrhages, and/or ulceration on the tips of the digits [37].

Once the site of arterial compression has been identified, surgical intervention is generally recommended to relieve the compression and restore distal flow. In their case series, Durham et al. [24] report on 34 patients who were treated for arterial TOS over an 11-year period. Twenty-two patients underwent resection of a cervical rib or anomalous first rib. Reported outcomes were generally favorable, although not everyone in the series had returned to their premorbid level of function at the time of the report. The outcome of treatment depends not only on providing the appropriate intervention, but also upon making an accurate clinical diagnosis in a timely manner. Delayed treatment may increase the athlete's risk of developing a chronic pain syndrome, such as sympathetically maintained pain [17•].

Compromise of the Posterior Circumflex Humeral Artery within the Quadrilateral Space

The posterior circumflex humeral artery (PCHA) arises from the distal third of the axillary artery and travels with its fellow nerve (the axillary nerve, C56) posteriorly through a space bounded by the teres minor (superiorly), the long head of the triceps (medially), the teres major (inferiorly), and the humerus (laterally). The neurovascular bundle is vulnerable to position-dependent entrapment within this “quadrilateral space.” The affected athlete usually gives a history of repetitively placing the upper limb in extreme abduction combined with external rotation (ie, the “cocked” position). Not surprisingly, therefore, “quadrilateral space syndrome” (QSS) is most frequently diagnosed in baseball pitchers and volleyball athletes [38]. Hypertrophy of any of the three muscular borders of the quadrilateral space may reduce the room available for the PCHA and axillary nerve, thereby contributing to the gradual functional compromise and onset of symptoms. It has been suggested that since the PCHA and the axillary nerve follow a similar course through the quadrilateral space, intermittent obstruction of the PCHA might interrupt flow to the vasa nervorum, thereby precipitating symptoms of axillary nerve ischemia. The incidence of electrodiagnostically confirmed axillary neuropathy coincident with radiographically documented PCHA stenosis is not known.

Other potential mechanisms involved in producing symptomatic QSS include traction on the PCHA by the pectoralis major muscle [39]. In addition, the circumflex nature of the PCHA may serve to “tether” it to the proximal humerus, placing the artery at increased risk for traction-related intimal injury as the upper limb is moved into a position of extreme abduction and external rotation in preparation for delivering a pitch or attempting a spike [24]. In support of this mechanism, Durham et al. [24] report that all patients in their series who were documented to have positional axillary arterial compression also experienced concomitant PCHA occlusion. Other potential risk factors for QSS may include glenohumeral instability or the presence of a glenoid labral cyst (which may intermittently compress the PCHA). Finally, chronic overuse may result in the formation of fibrotic bands that are thought to contribute to the position-dependent compression within the quadrilateral space [40].

Symptoms associated with QSS tend to be intermittent, and are typically provoked by the aforementioned positioning of the upper limb. The affected athlete may complain of poorly localized discomfort throughout the shoulder girdle, although classically the individual is tender to direct palpation over the quadrilateral space. He or she may also experience paresthesias or numbness in an axillary nerve distribution, and may demonstrate weakness of shoulder abduction. Complaints of more distal embolic symptoms suggest an associated aneurysm with thromboembolism [41]. Definitive confirmation of the clinical diagnosis can be achieved by demonstrating a position-dependent occlusion of blood flow to the PCHA on arteriography. Occasionally QSS will be diagnosed incidental to the finding of fatty replacement and atrophy of the teres minor on shoulder MRI [38]. Optimal treatment consists of identifying and attempting to correct any reversible risk factors that may exist (eg, faulty biomechanics) while attempting to conservatively rehabilitate the affected shoulder girdle. However, if symptoms persist, surgical decompression of the quadrilateral space is indicated [22]. Postoperatively, the athlete should engage in a structured rehabilitation program prior to attempting to return to overhead sporting activity.

Other Conditions

Other neurovascular conditions for which the overhead athlete should be considered at risk include suprascapular neuropathy (SSN), long thoracic neuropathy, and (in volleyball and baseball players) posttraumatic aneurysmal dilatation of the palmar arteries. SSN is frequently diagnosed among volleyball players. In fact, SSN is sufficiently prevalent in this population that it has come to be known as “volleyball shoulder” [42]. However, the prevailing opinion is that SSN represents a peripheral mononeuropathy without a vascular component. The same may be said for long thoracic neuropathy [43]. While cumulative traumatic injury to the palmar arteries clearly represents a vascular injury [31], the mechanism of injury (repetitive impact) is not intrinsically related to the kinematics of the overhead throwing motion.


Each of the vascular conditions considered in this review is thought to result from the repetitive position-dependent compression of vessels within the shoulder girdle. Considering the widespread popularity of the many different sporting disciplines that require overhead skills, and given the load placed upon the shoulder girdle by the overhead athlete, it is perhaps somewhat surprising that these vascular pathologies are not more frequently diagnosed, particularly among elite overhead athletes. Accordingly, it seems reasonable to posit three potential reasons for the relatively low incidence of vascular injuries in this population: 1) a lack of diagnostic accuracy among treating sports medicine clinicians; 2) insufficient interaction between intrinsic and extrinsic risk factors; and 3) the inherent resiliency and adaptability of the human body.

The frequency with which the first condition contributes to underdiagnosis of vascular injury in the shoulder girdle cannot be known with any certainty, but in light of the often vague presentation of these vascular conditions it almost certainly represents a real and significant factor. The third factor (which is related to the second) is undeniable, but cannot be readily quantified. The second factor seems worthy of additional brief discussion.

Cervical ribs are found in 0.5% to 1.0% of the general population, yet more than three fourths of the patients diagnosed with subclavian arterial injury in Durham's case series were found to have them [24]. Although cervical ribs occur bilaterally in 50% of cases, the incidence of vascular symptoms on the nondominant side appears to be considerably lower than on the dominant side. Why? The most likely explanation for such side-to-side variation in symptoms is, of course, overload of the dominant shoulder girdle due to throwing (or other overhead skills). But can we be confident that throwing (and the attendant positional compromise in vascular flow) is truly the source of symptoms in these overhead athletes? Certainly, the reported results would lead us to that conclusion. Each of the 12 cases of axillary arterial injury reported by Durham et al. [24] could be considered an overhead athlete (either sporting or industrial), and the majority of the cases responded favorably to operative intervention. Yet Rohrer et al. [27] documented position-dependent compression of the axillary artery by the humeral head with essentially equal frequency in throwers and nonthrowers alike. Because the study subjects were apparently asymptomatic, it is difficult to derive any clinical application from those intriguing data. The results do, however, suggest that additional risk factors (beyond periodic circulatory interruption) must exist to precipitate symptoms. Collectively, then, these observations imply that vascular pathology in the upper limb is most often the result of an anatomical predisposition exposed to environmental stimuli that have yet to be fully defined or quantified. While our understanding of the natural history of, risk factors for, and optimal treatment of both arterial and venous TOS is improving, it would undoubtedly be further enhanced by well-designed, systematic prospective longitudinal data collection efforts. Such studies could also provide valuable insight into the immediate, short-term, and long-term impact of these conditions on the athletes' quality of life and functional status.

References and Recommended Reading

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© 2007 American College of Sports Medicine