- 1 Introduction
- 2 History
- 3 Preferred Classification
- 4 External Impingement
- 4.1 Anatomical Considerations
- 4.2 Etiology
- 4.3 Anamnesis
- 4.4 Physical Examination
- 4.5 Imaging
- 4.6 Treatment of Subacromial and Subclavicular Impingements
- 4.7 Subcoracoid Impingement
- 5 Internal Impingements
- 5.1 Posterosuperior impingement
- 5.1.1 Walch’s theory
- 5.1.2 Frank Jobe’s Theory
- 5.1.3 Christopher Jobe’s Theory
- 5.1.4 Burkhart’s Theory
- 5.1.5 Clinical Examination
- 5.1.6 Imaging
- 5.1.7 Isokinetic assessment
- 5.1.8 Treatment
- 5.2 Anterosuperior Impingement
- 5.3 Frayed Upper Edge Subscapularis Lesion with Impingement (FUSSI) and Subscapularis Abrasion from the Middle glenohumeral ligament (SAM) Lesions
- 5.1 Posterosuperior impingement
“Shoulder impingement” is a vague and elusive entity, which is often misused to label imprecise pain around the shoulder. It was previously thought to be a sole diagnosis itself but is now considered to be a cluster of symptoms and anatomic characteristics. It is associated with 44% to 65% of all shoulder complaints. Many different types of impingements may occur in a native or prosthetic joint, inherently predisposed by translational instability, extreme ranges of motion, contact against the multiple adjacent structures (acromion, glenoid, coracoid process, labrum or conjoined tendon) and repetitive overhead maneuvers that expose the shoulder to significant amounts of stress.
In 1872 Simon Duplay made the classic description of the scapulo-humeral periarthritis. Duplay, a Frenchman, had the merit of being the first to describe the function and pathology of the subacromial space which he called the “second joint” to distinguish it from the “first” one (the glenohumeral joint). One pathology included in the scapulo-humeral periarthritis syndrome is shoulder impingement.
In 1932, Meyer proposed that lesions of the rotator cuff occurred secondary to attrition as a result of friction with the undersurface of the acromion. In 1940, Watson-Jones described the pathologic abutment of the lateral acromion on the rotator cuff during mid-arc shoulder abduction (Figure 1).
In his book “The Shoulder” published in 1934, Codman stated that most degenerative changes occur in the critical zone of vascularization, located one centimeter medial to the insertion of the supraspinatus on the greater tuberosity. He thus introduced the concept of an intrinsic mechanism for the development of rotator cuff tears.
In order to limit attrition and to relieve impingement on the rotator cuff, complete acromionectomy and then lateral acromionectomy were initially proposed. However, the disappointing results of the latter procedures led Neer to focus on the undersurface of the acromion as the offending area. With Neer’s theory, the insertion of the supraspinatus tendon is impinged upon by the anterior one third of the acromion and the formation of the enthesophyte (spur) in the substance of the coracoacromial ligament (Figure 2) leads to chronic wear, and finally tearing of the rotator cuff.
Following Neer’s proposal, open and then arthroscopic anterior acromioplasties became popular. Bigliani later highlighted the importance of acromial morphology (flat, curved or hooked acromion), especially the hooked-type acromion, in the predisposition of patients developing shoulder impingement. However, the concept of acromial shape has been recently questionned.
In 2006, Nyffeler et al. hypothesized that a large lateral extension of the acromion predisposes the supraspinatus tendon to degeneration related to higher abduction force requirements. Finally, Moor et al. introduced the concept of the critical shoulder angle which combined analysis of glenoid inclination and lateral overhanging of the acromion, promoting again lateral rather than anterior acromioplasty. However, the role of acromioplasty is nowadays still not clearly defined, knowing that gliding of the rotator cuff under the acromio-humeral arch is probably part of human evolution since we stand erect to compensate the deficiency of the superior rotator cuff (Figure 3).
External shoulder impingement should be recognized as a clinical entity that is separate from internal impingement. The most basic clinical differentiation between the former and the latter is defined by the rotator cuff as the anatomic boundary of the external and internal forms. External impingement results from a mechanical or physical encroachment of the soft tissue located within the subacromial or subcoracoid spaces. Conversely, internal impingement occurs when the tendons of the rotator cuff encroach between the humeral head and glenoid rim. This impingement may occur as well at numerous locations.
External impingement syndrome can be broadly caused by intrinsic changes within the rotator cuff tendons, or by extrinsic compression of the latter between the humerus and the adjacent structures. With dynamic stability compromised, the humeral head migrates superiorly, and the subacromial space decreases in size. It can be further characterized as primary (attributable to abnormal acromion anatomy or acromioclavicular osteophytes) or secondary (result of another process, such as instability or trapezius weakness which lead to cranial translation of the humeral head). Figure 4 summarizes the different types of impingements.
The acromion defines the superior border, the coracoacromial ligament provide the anterior border, and the humeral head serves as the inferior border. Its content is the tendon of the rotator cuff and the subacromial bursa (Figure 5).
Its anatomic borders are defined superiorly by the acromioclavicular joint and the clavicle. The supraspinatus fossa acts as the inferior border. Its content is the musculotendinous junction and the muscle belly of supraspinatus (Figure 6).
The horizontal part of the coracoid process defines the superior border, the tip of the coracoid process and the conjoint tendon form the anterior border, and the anterior humeral head, the glenoid and the middle glenohumeral ligament serve as the posterior border. Its content is the tendon subscapularis (Figure 7).
Interestingly, it is still unknown whether or not the damaged tendons cause impingement, or if the narrowed subacromial, subclavicular or subcoracoid spaces causes the tendinopathy (“chicken or the egg” debate).
All structures such as bone or ligament that are adjacent to musculotendinous unit may provoke a mechanical or physical encroachment of the soft tissue located within the subacromial, subclavicular or subcoracoid spaces. In primary impingement, there is a structural narrowing of these spaces whereas in secondary ones, the anatomy remains normal and onset of impingement appears during shoulder motion, likely secondary to muscle weakness.
Classically, the acromion shape (class I flat acromion, class II curved acromion and class III hooked acromion) was thought to play a role in the development of external, or "outlet-based" impingement syndrome. However, this theory has been recently questioned.
The table 1 summarize the different intrinsic factors responsible for shoulder impingement syndrome.
|Muscle weakness||Overuse of the Shoulder (microtrauma)||Degenerative Tendinopathy||Vascular changes|
Table 1: Intrinsic factors responsible for shoulder impingement syndrome.
Clinicians evaluating patients with acute or chronic shoulder pain should obtain a comprehensive history. Individuals will often present with atraumatic, insidious onset of pain upon lifting the arm or with lying on the affected side. Pain is commonly described as being located over the anterolateral aspect of the shoulder. As symptoms arise from bone and ligaments applying compressive forces to either the rotator cuff, the subacromial bursa, or both structures ("outlet-based" impingement), special attention should be made by the clinician to inquire about symptoms exacerbated by repetitive or overhead activities. Relief may be noted with rest, anti-inflammatory medications, but symptoms often recur upon return to activity.
Physical examination should begin with inspection. Swelling may be observed in the case of subacromial bursitis (Figure 8).
Passive and active range of motion are compared bilaterally and should normally be symmetrical and unlimited. A painful arc of motion, appreciated with abduction of the arm between 70 and 120 degrees and forced overhead movement, is frequently noted in the setting of subacromial impingement.
The Jobe test (empty can test) is performed by placing the patient's arms at 90 degrees of abduction within the scapular plane, maximally internally rotating the arms and resisting further abduction by the patient. In the case of subacromial or subclavicular impingement, a negative test occurs (the patient is able to resist as the tendon is in continuity, there is no weakness) but results in localized pain to the anterolateral shoulder. Special tests (Hawkins test, Neer sign) have low specificity and are not exclusively relied upon by the authors.
Imaging studies have to be performed to confirm the diagnosis and rule out other pathologies.
Standard plain radiographs should be obtained. An anteroposterior view in neutral rotation is used to analyze the acromiohumeral distance (normal range is 7-14 mm, a lower distance suggests rotator cuff pathology) and the critical shoulder angle, and to rule out other pathologies such as calcific tendinitis, arthritic changes or abnormal bone morphology such as malunion (Figures 9-10). The scapular Y view allows for the assessment of the humeral head on the glenoid and the shape of the acromion. The axial view is necessary to rule out an os acromiale (Figure 11).
Visualizing the impingement itself through dynamic analysis is more challenging. Dynamic analysis of an external impingement involves abduction of the shoulder during imaging. Four signs have been described, including “bunching” of the subacromial-subdeltoid bursa or of the supraspinatus tendon beneath the acromion, “bulging” of the acromioclavicular ligament, and rarely “blocking” of the supraspinatus tendon.
Magnetic Resonance Imaging (MRI) / Magnetic Resonance Arthrography (MRA)
Consideration for advanced imaging with magnetic resonance imaging with or without arthrography is always recommended before planning for a surgery. It will allow for a detailed evaluation of bony and soft tissue structures and will confirm the isolated character of the impingement (Figures 12 and 13). Relevant bursitis can be defined as 3 mm or more of fluid above the rotator cuff (Figure 14).
Treatment of Subacromial and Subclavicular Impingements
Conservative (Nonoperative) Treatment
Classically, the foundation of management for subacromial and subclavicular impingement has been adaptation, rest, NSAIDs, subacromial injection and rehabilitative exercise programs for the first 6 months of treatment. Physiotherapy should include reinforcement of scapula stabilizers and muscles that lower the humerus. An isokinetic evaluation will help to precise muscular imbalance. Ultrasound guided cortisone subacromial injection is advised at least once before surgery to confirm temporary relief, otherwise the diagnosis is highly unlikely. Injection thus plays both a diagnostic and therapeutic role.
A clear distinction has to be made between isolated acromioplasty performed for subacromial impingement syndrome (pain, impingement, rotator cuff tendinopathy, snapping) and acromioplasty realized as an adjuvant procedure to rotator cuff repair, acromioclavicular joint osteoarthritis, or biceps pathology. An indication for isolated acromioplasty is rare, representing around 0.5 to 1% of shoulder surgeries in our experience. For such surgical indication, an acromioplasty with detachment of the coracoacromial ligament is indicated. Acromioplasty associated with rotator cuff repair serves a completely different purpose, dealing with working space necessary for arthroscopic repair or access to acromioclavicular joint, decreasing load on repaired tendons, and perhaps aiding the healing process by providing growth factors from bleeding bone, etc. In the rotator cuff repair scenario, a more lateral acromioplasty with preservation of the acromioclavicular ligament is emphasized.
Patients will most likely benefit from surgery if they have the following criteria: shoulder pain with overhead activities, persistent symptoms for more than 6 months, improvement after subacromial steroid injection, symptoms persist after at least 1 course of supervised physiotherapy, painful arc of motion, and radiologic evidence of impingement.
Subacromial decompression includes nowaday a bursectomy, a release or excision of the coracoacromial ligament and the removal of the acromial undersurface (acromioplasty) with improved arthroscopic visualization, as well as an increase in the local concentrations of growth and angiogenic factors, potentially improving the healing environment. Subclavicular decompression includes a coplanning of the inferior clavicle or a resection of the distal resection in case of painful acromioclavicular arthropathy.
Following subacromial or subclavicular decompression without rotator cuff repair, patients do not need to wear a sling and early passive range of motion rehabilitation exercises are recommended. Initially, patients are instructed to avoid heavy lifting and sports to facilitate soft tissue healing. Cryotherapy devices are often applied for the first 10 to 14 days postoperatively. Physical therapy, if required, is started postoperatively. Full active range of motion should be achieved by 2 weeks. If applicable, return to sport is allowed at 6 weeks as tolerated.
Few long-term series had confirmed that in selected and rare patients, surgery is usually saving, provides complete relief a few days/weeks and has a long-term protective role. Conversely, several recent studies have called into question the role of acromioplasty. However, these small series tried to analyze the role of acromioplasty with short-term follow-up which is insufficient to confirm or refute whether the procedure prevents abrasive wear and tear. Degeneration of rotator cuff tendons due to impingement against an acromial spur is a process that depends on acromial morphology and shoulder movements, and can extend over several decades. It is thus logical according to these studies' methodology that no differences were found. Moreover, it is still unknown if postoperative improvement is only related to relief of impingement, bursectomy, decreaseed of stress on the supraspinatus tendon, or improvement of shoulder kinematics after repair.
Due to the underlying etiology of subacromial and subclavicular impingement syndrome, complications that may arise predominantly result from structural damage within the subacromial or subclavicular spaces, altered biomechanics, or avoidance of use with subsequent atrophy.
Although described over a century ago, subcoracoid impingement remains an underreported source of anterior shoulder pain, because of its high association with other pathologies and its non-specific clinical findings. It was initially described to be caused by entrapment of the superior tendon of the subscapularis between the coracoid process and the lesser tuberosity. Similar to subacromial impingement, it is the result of any condition that impairs proper gliding of the tendon in its sheath, and reported etiologies are multiple. Underlying causes are usually classified as idiopathic, iatrogenic, pathologic, and traumatic. They can however also be regrouped in two categories based on a biomechanical approach: a) subcoracoid space filling, including subscapularis tendon calcification or ossification, thickening of the subcoracoid bursa and glenohumeral ligaments, soft-tissue tumors such as ganglion cysts or lipoma, or suture material or other surgical hardware, and b) subcoracoid space narrowing, including anterosuperior migration of the humeral head in cuff deficient shoulders, anatomic variations of the coracoid or lesser tuberosity and bicipital groove, coracoid or proximal humerus malunion (Figure 15), posterior opening glenoid osteotomy (Scott glenoplasty), or bony tumors. Narrowing of the subcoracoid space may lead to stenosis, a condition defined as less than 6 mm distance between the coracoid and the lesser tuberosity, eventually causing subscapularis tendon failure.
Occasionally impingement can be lower, involving the conjoined tendon (Figure 16), or an accessory coracobrachialis muscle. The impingement occurs lower on the anterior to anteroinferior border of the subscapularis, and needs a specific exploration and release during surgery through an anterolateral arthroscopic portal, while avoiding damaging the subscapular nerves and anterior circumflex vessels.
Clinical manifestations of subcoracoid impingement include anterior shoulder pain located around the coracoid exacerbated by overhead activities, associated with snapping during internal or external rotation of the arm. Clinical diagnosis is thus challenging, as this condition is rarely isolated and the non-specific findings may mimic other shoulder pathologies such as acromioclavicular pain or subacromial impingement.
Dynamic ultrasound is useful because it is cost-effective, allows direct visualization of the snapping tendon, and helps in discriminating this particular entity from other sources of anterior painful snapping in the shoulder, such as biceps pulley lesions, glenohumeral instability, or loose bodies. Moreover, it also offers guidance for diagnostic and pain-relieving injections of the subcoracoid bursa. Magnetic resonance arthrography (MRA) scans are still warranted to further identify the underlying cause and associated conditions. With the arm in maximal internal rotation, these modalities allow measurement of the coracohumeral interval.
Treatment of Subacromial Impingement
Initial treatment consists of conservative measures, including physical therapy and guided injections. Arthroscopy has become the favored treatment because it offers a better visualization and dynamic assessment of the subcoracoid space, as well as a better identification and treatment of concomitant shoulder lesions, such as capsulolabral tears, anterosuperior rotator cuff tears, biceps pulley lesions, or arthrosynovial cysts. Additionally, coracoplasty can be performed safely while staying well away of the medial neurovascular structures. Although surgical techniques seem to yield satisfactory results, they remain poorly interpretable as reported results are rare and consist mainly in level IV series, where subcoracoid impingement is associated with other conditions.
Posterosuperior impingement occurs when the supraspinatus and infraspinatus become entrapped between the greater tuberosity and posterosuperior aspect of the glenoid labrum. The precise causes for this impingement remained unclear, but certain surgeons made theories, stating that repetitive contact, glenohumeral instability, scapular orientation, rotator cuff dysfunctions, posteroinferior capsular contracture with resultant glenohumeral internal rotation deficit (GIRD) may play a role in the development of symptomatic impingement.
Walch et al. developed the theory of isolated posterosuperior impingement by publishing a series of 17 arthroscopies performed in athletes who demonstrated pain in the cocking phase but lacked concomitant instability. He explain this symptomatology by mechanical impingement repeated at 90 degrees of abduction, maximum external rotation and retropulsion (maximum extension), between the greater tubercle and the posterosuperior glenoid rim, causing partial tears in the posterosuperior rotator cuff and the facing glenoid labrum (Figure 17). The appeal of this theory is that it is validated by simple observation when reproducing cocking and retropulsion movements under arthroscopic control, revealing the tears by repeated contact.
Frank Jobe’s Theory
For Frank Jobe, lesions observed in throwing athletes are related to subtle anterior instability (Figure 18).
Christopher Jobe’s Theory
Christopher Jobe, Frank’ son, postulated that posterosuperior impingement was mainly due to hyperextension of the humerus relative to the scapula (Figure 19). In 1995, Davidson et al. took up this theory and showed how hyper-rotation (hyperabduction) and anterior humeral translation act as the trigger mechanism for pain, and explain how the shoulder relocation test reduces pain by releasing the internal impingement.
Burkhart et al. proposed a posteroinferior capsular contracture occurs in throwers, associated or not to a stretching of the anterior structures. This essential lesion secondarily results in increased external rotation. When the posterior capsule shortens, the glenohumeral contact point shifts posterosuperiorly (static posterosuperior glenohumeral instability), allowing hyperexternal rotation and repetitive hypertwisting of the rotator cuff fibers and of the long head of the biceps. Furthermore, a torsional force known as the peelback phenomenon is applied to the biceps anchor during the late cocking phase of throwing, leading to the development of lesion of the deep surface of the posterosuperior rotator cuff and to superior labral anterior posterior (SLAP) lesion.
Despite the theories of Frank Jobe et al. and Burkhart et al., Lädermann et al., using a precise and dynamically in-vivo motion analysis of the entire kinematic chain of the shoulder, could not confirm any form of dynamic antero-inferior or static posterosuperior micro-instability, respectively. Consequently, it seems that posterosuperior at least in tennis players is due to a repetitive contact between the rotator cuff and the glenoid favorized by movements of abduction, external rotation and hyperabduction and not instability.
The shoulder can exhibit increased external rotation and decreased internal rotation compared to the contralateral side. In abduction and maximal external rotation, the patient can experience the feeling of a dead arm. The Jobe test (empty can test), performed by placing the patient's arms at 90 degrees of abduction within the scapular plane, maximally internally rotating the arms and resisting further abduction by the patient is usually negative but results in pain. Similarly, an anterior apprehension maneuver is negative for instability but reproduces pain and the disagreeable feeling known by the patient. Finally, the relocation test (Figure 20) has the tendency to relieves the patient's symptoms.
Simple radiographic examination is comprised of three views (anteroposterior, Lamy and Bernageau views) to assess for glenoid thrower’s exostosis (Figure 21) and bone cyst (Figure 22).
Posterior internal impingement occurs often in overhead athletes and involves pinching of the supra- and infraspinatus tendons with the posterosuperior portion of the glenoid labrum when the shoulder is in abduction/external rotation/hyperextension (Figure 23 and 24). Dynamic imaging of this pathological impaction is carried out with the patient’s arm adducted and making external and internal rotation movements.
Computed tomography (CT) arthrography
Computed tomography using intra-articular injection of a contrast is reliable to visualize labral lesions, articular rotator cuff lesions and glenoid bone formation (Figure 25).
Magnetic Resonance Imaging (MRI) and Magnetic Resonance Arthrography (MRA)
Magnetic resonance imaging (MRI), enhanced or not with gadolinium contrast to increase the diagnostic value, is the most utilized imaging modality to confirm posterosuperior impingement. This modality will confirm articular-sided rotator cuff tears found in up to 40% of professional baseball pitchers and in up to 60% of professional tennis players, cystic changes in the posterior aspect of the humeral head (Figure 26), posterosuperior labral pathology (Figure 27), possible presence of a spinoglenoid cyst (Figure 28) and mature periosteal glenoid formation. Jung et al. report a sensitivity of 85% and a specificity of 86% for superior labral tears. Sequences with the shoulder in both the abducted and abducted and externally rotated position (ABER) appear to improve the diagnostic accuracy of soft tissue anterior and posterior labral tears, SLAP tears, and bony glenoid lesions.
Isokinetic studies (Figure 29) now permit objective quantification of internal and external rotational forces, and especially the definition of ratios for comparative purposes. Such assessment, while not perfectly simulating throwing conditions, does ensure a reliable, reproducible method for analyzing ratios and their imbalance, with linear tracking over time (to track progress, etc.). It is of major interest because it must be standardized, just as the articular amplitudes must be perfectly symmetrical before considering surgery or return to sports (with or without surgery).
Conservative (Nonoperative) Treatment
Conservative treatment should always be the first line of treatment for patients with posterosuperior impingement. Patients, athletes or not, will improve with cessation of activities and focused therapy modalities. Patients with new-onset impingement symptoms should be initially treated with activity modification, initiation of short-term routine NSAID use, and enrollment into a formal throwing therapy program. Rehabilitation should contain three key components: application of kinetic chain exercises, shoulder mobility, and shoulder strengthening. All ranges of movement must be recovered, especially internal rotation at 90 degrees of abduction, by teaching the patient self-stretching exercises such as ‘sleeper-stretching’ (Figure 30).
Another tenet of nonoperative treatment is specific strengthening through restoration of scapular motor control, initiation of a scapular feedback program, and promotion of eccentric control through an increased number of repetitions throwing cycles. Strengthening of the external rotators should be concentric and eccentric using elastics or weights, as described in some protocols depending on the results of the isokinetic analysis (Figure 31). Proprioception can be worked on with ball exercises (Figure 32). If the patient fails in a 6-month range and cannot return to activities, then the patient may be considered for surgical intervention.
Operative (Surgical) Treatment
Depending on patient’s expectations and underlying conditions, surgical options include arthroscopic debridement, arthrolysis, posterosuperior glenoidplasty as described by Lévigne et al. (Figures 33) and derotational osteotomy (Figure 34). The later technique has largely been abandoned.
Anterosuperior impingement was first described by Gerber and Sebesta who reported that repetitive friction led to partial articular subscapularis tendon and biceps pulley tears. It is caused by entrapment of the subscapularis tendon between the anterior humeral head and anterior glenoid labrum with the arm in forward flexion, adduction, and internal rotation. It mirrors Walch’s posterosuperior impingement that involves the posterosuperior rotator cuff. It should not be mistaken with anterolateral impingement which is a synonym for the far more frequent subacromial impingement. Pain in anterosuperior impingement seems to be specifically located to the anterior aspect of the shoulder, and has been frequently observed in patients with activities implying this repetitive movement, typically such as tennis players.
Frayed Upper Edge Subscapularis Lesion with Impingement (FUSSI) and Subscapularis Abrasion from the Middle glenohumeral ligament (SAM) Lesions
From Brady et al., with permission.
In some cases, the middle glenohumeral ligament or even the anterior glenoid abrades against the upper edge of the subscapularis medial to its insertion at the lesser tuberosity. The middle glenohumeral ligament compresses into the upper edge of the subscapularis causing pain and intraarticular pathology. The acronym of the SAM lesion (for Subscapularis Abrasion from the Middle glenohumeral ligament) or the FUSSI lesion described by Snyder (for Frayed Upper SubScapularis with Impingement) have been used. The SAM and FUSSI lesion may differ in some ways. First, the FUSSI lesion is described as a capsular reflection causing abrasion whereas the SAM lesion describes the middle glenohumeral ligament as being the offending structure. Second, the lesion caused by the capsular reflection is typically quite medial and often not visible from the posterior portal with a standard arthroscope whereas the condition the SAM lesion is always visible from the posterior portal as the pathology lies at the level (or lateral to) the middle glenohumeral ligament. Third, the abrasion of the subscapularis caused by the capsular reflection is noted to be worse with external rotation. However, with the SAM lesion the middle glenohumeral ligament compresses the upper subscapularis with internal rotation.
Preoperatively these patients have presented somewhat of a diagnostic conundrum. They frequently have vague and nondescript anterior shoulder pain. Symptoms are primarily reproduced with resisted internal rotation of the shoulder however the patients have good strength with subscapularis testing including negative bear hug, belly press, lift off, and Napoleon exams. Biceps exam is typically equivocal and often biceps pathology is suspected in these patients secondary to their symptoms of primarily anterior shoulder pain with activities. Patients have failed exhaustive conservative treatments and even failed previous operative intervention.
Imaging studies including MRI and radiographs are typically non-diagnostic.
Typically, with internal rotation of the humerus the middle glenohumeral ligament is seen “cutting” into the upper boarder of the subscapularis (Figure 35) or creating a superior abrasion on the upper part of the tendon (Figure 36). The middle glenohumeral ligament must be divided with electrocautery. Eventually anterior glenoplasty or coracoplasty, in order to allow proper gliding of the superior border of the tendon, is performed.
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