Shoulder Impingement and Associated MRI Findings

Shoulder pain is a common musculoskeletal medical condition affecting 7% to 26% of individuals and is the third most common musculoskeletal-related complaint in the primary care setting.^1,2 Rotator cuff pathology is a common etiology for shoulder pain, with impingement of the rotator cuff often playing an important role. Rotator cuff impingement was first described by Neer et al when he stated that 95% of rotator cuff tears were attributed to impingement and generally occur in patients over age 40.^3,4 Two predominant types of shoulder impingement have been described: intrinsic and extrinsic.

Intrinsic shoulder impingement is relatively uncommon and seen almost exclusively with overhead throwing athletes.⁵ It is a result of extreme abduction and external rotation, which can lead to entrapment of the supraspinatus and/or the infraspinatus tendons between the glenoid.⁶ MRI appearance of intrinsic impingement is varied and includes labral and rotator cuff pathology. The infraspinatus tendon is commonly injured, especially in patients under age 30, with MRI findings ranging from undersurface tears to complete tears.^6,7

Extrinsic, or external, impingement is one of the more common causes of shoulder pain and a frequent source for an orthopedic evaluation.⁸ Extrinsic shoulder impingement is most commonly related to mechanical compression from the acromion, acromioclavicular joint, and the coracoacromial ligament.^3,9 Numerous operative and nonoperative treatment options have been described for extrinsic impingement, ranging from physical therapy and injections to acromioplasty and Mumford procedures.

The purpose of this article is to help understand the relevant anatomy with regard to the subacromial region, review the imaging findings, and discuss the differing etiologies of extrinsic impingement. This knowledge will allow radiologists to effectively communicate with clinicians and help guide appropriate treatment.

Anatomy

The coracoacromial arch provides a safeguard for the shoulder, limiting superior migration of the humeral head. The coracoacromial arch is composed of (from anterior to posterior) the coracoid process, coracoacromial ligament, and the acromion process. Inferior to these structures, and coursing through the arch, are the subacromial/subdeltoid bursa, supraspinatus tendon, and biceps tendon. The humeral head provides the posterior/inferior border of the arch (Figure 1). Processes that decrease the space within the coracoacromial arch presumably may lead to impingement-like symptoms.

The coracoid process is a hook-like osseous structure arising from the superolateral edge of the scapula and extends in an anterolateral orientation. The coracoid is an anchor point for several ligaments and tendons, including the pectoralis minor, coracobrachialis, and short head of the biceps brachii tendons. Also, the coracoid is an attachment site for the coracohumeral, coracoacromial, coracoclavicular, and superior transverse ligaments.¹⁰ The coracoid process can be palpated below and at the lateral edge of the clavicle. Known as the “Surgeon’s Lighthouse,” the coracoid process serves as a landmark to avoid neurovascular injury, as major neurovascular structures traverse medially to the coracoid process.¹¹

The coracoacromial ligament is a thick triangular ligamentous structure extending inferomedially from the anterolateral undersurface of the acromion to the lateral border of the coracoid process. This structure provides an osseo-ligamentous static restraint to superior humeral head displacement. Ligamentous connection of the coracoacromial ligament and the rotator interval capsule is thought to prevent inferior migration of the glenohumeral joint.¹² Coracoacromial ligament thickness is normally 2 to 5.6 mm.¹³ Implicated as a pain generator in impingement syndrome, treatment of the coracoacromial ligament has been controversial. There is uncertainty regarding whether or not to perform a release of the coracoacromial ligament during acromioplasty, as this could increase the risk of superior and anterior glenohumeral translation.⁹

The acromion process is a triangular-like extension of the scapular spine, and anteriorly articulates with the clavicle. The acromioclavicular articulation is a synovial joint, connecting the scapula and clavicle, allowing the scapula to have multidirectional motion with relation to the rest of the body. The coracoacromial ligament forms the ligamentous attachment between the acromion and coracoid process (Figure 2). The deltoid and trapezius muscle groups have attachments on the acromion. The deltoid muscle abducts the arm at the shoulder and contraction of the trapezius rotates the scapula, providing stability to the scapular body. At birth, the distal acromion and clavicle are cartilaginous structures, but maintain the shape of the fully matured ossified bone. With maturation, the primary ossification center ossifies and proceeds to fuse with smaller secondary ossification centers to form a single fused plate. Most literature suggests these ossification centers normally ossify between 18 to 25 years of age.¹⁴ Unfused secondary ossification centers may be mistaken for avulsion fractures, and primary and secondary fusion scars can mimic an incompletely healed fracture on radiographs and MRI, respectively (Figure 3). The presence of marrow edema on MR images should portend a diagnosis of fracture.¹⁵

As stated earlier, Neer proposed that tears of the cuff tendons (specifically the supraspinatus) are often a result of impingement by structures forming the coracoacromial arch. Extrinsic impingement syndrome is clinically characterized as acute or chronic pain induced by abduction and external rotation or elevation with internal rotation of the shoulder. Impingement typically occurs in young athletes who participate in sports involving repetitive movements of elevation and abduction of the shoulder, or in the elderly population with degenerative joint disease.¹⁶ Numerous anatomical etiologies have been suggested as a contributor of impingement syndrome including variant acromion shape, slope of the acromion, acromioclavicular arthropathy, acromion positioning, coracoacromial ligament thickening, and os acromiale. However, it is worth noting that many of the aforementioned anatomical factors can be seen in the asymptomatic patient, and ultimately the diagnosis is one of a clinical nature.¹⁷

Three predominant shapes of the lateral acromion have been described by Bigliani et al and are based on the scapular-Y view radiograph.¹⁸ Type I acromion has a flat undersurface (Figure 4). Type II acromion is more concave along the undersurface with the inferior acromial cortex parallel to the cortex of the humeral head (Figure 5). Type III acromion has an inferiorly projecting anterior hook, narrowing the space between the acromion and humeral head (Figure 6). Some theories suggest type II and III acromions have an increased incidence of cuff disease, but this remains controversial among most surgeons.¹⁷ Type IV acromion has also recently been described as having a convex undersurface, although correlation with extrinsic impingement has not been shown.^19,20

Normal orientation of the lateral aspect of the acromion is horizontal or slightly downsloping posteriorly on the sagittal images. An abnormally sloped acromion occurs in an anteriorly downsloped and inferolateral sloped orientation (Figure 7). These anomalous acromial sloping positions can impinge on the subacromial space and cause mechanical trauma to the subjacent supraspinatus tendon.¹⁷

Normal positioning of the acromion has an inferior cortex running parallel with the inferior cortex of the clavicle. When the acromion is low-lying, the inferior cortex of the acromion lies below the inferior cortex of the clavicle (Figure 8). This low position causes narrowing of the subacromial space.¹⁷

Os acromiale represents an accessory ossification center that has not fused by age 25 years. This normal variant occurs in 15% of the population. Failure of fusion occurs between 1 of the 3 ossification centers: pre-acromion (Figure 9A), meso-acromion (Figure 9B), and meta-acromion. A classification scheme was proposed by Park et al with subtypes A-G. Type A, also known as the meso-acromial or meso-type, is the most common and is a failure of fusion between the meso-acromion and meta-acromion.²¹ The presence of an os acromiale has been associated with increased incidence of impingement and rotator cuff disease, although is controversial in the literature.^21,22 There is suggestion that the os is mobile, and thus reduces the size of the coracoacromial arch during motion. Os acromiale can cause impingement in 2 separate manners: Contraction of the deltoid muscle will force the os acromiale inferiorly, leading to narrowing of the rotator cuff outlet. The other mechanism occurs when osteophytes develop at the margin of the acromial gap, often directly impinging on the rotator cuff.

Imaging Appearance of Extrinsic Impingement

The imaging findings of external impingement are varied, ranging from subacromial/subdeltoid bursitis to full-thickness rotator cuff tears. In 1972, Charles Neer classified impingement into 3 distinct stages. Stage I impingement is characterized by edema and/or hemorrhage in the subacromial/subdeltoid bursa and is generally seen in patients less than 25 years-old. Stage II demonstrates chronic changes such as fibrosis and tendinitis of the rotator cuff and is generally seen in those 25 to 40 years. Stage III is characterized by partial or complete rotator cuff tears, and is usually seen in patients > 40 years.^4,23

Subacromial/subdeltoid bursitis is a finding seen with considerable frequency on MRI examinations of the shoulder (Figure 10). This diagnosis is characterized by fluid-like signal in the bursa that extends 2 cm medial to the acromioclavicular joint with distension of the bursa > than 3 mm thick. Fluid also commonly extends into the anterior aspect of the bursa.²⁴

Rotator cuff tendinopathy (or tendinosis) is depicted by thickening and increased signal within the tendons. With tendinopathy, there is no visible discontinuity of tendon fibers and signal does not extend to the articular or bursal surface. Also, signal seen within tendinopathy is hyperintense on fluid-sensitive sequences, but is hypointense compared to nearby intra-articular fluid signal (Figure 11). Fluid-like hyperintense signal within the tendon suggests an intrasubstance partial tear.

Partial thickness tears of the rotator cuff are characterized by fluid-like signal in the tendons that does not involve the entire tendon bulk. These tears can be further characterized by whether they involve the bursal surface, intrasubstance portion of the tendon, or articular surface of the tendon fibers (Figures 12-14). Partial thickness tears occur more frequently along the articular surface of the tendon.²⁵ Ellman developed a classification system for partial rotator cuff tears based on the tendon tear depth. This system classifies partial thickness tears into grade I (< 3 mm), grade II (3 to 6 mm), or grade III (> 6 mm).²⁶ As grade III tears comprise > 50% of the rotator cuff, these are generally considered significant and are typically repaired surgically.²⁷

Full-thickness rotator cuff tears are manifested by fluid-like signal within the tendon, which extends throughout the entire substance of the tendon from the articular to the bursal surface (Figure 15). These can be further classified according to size. A widely used system created by DeOrio and Cofield classifies full thickness tears based on their greatest dimension. These are classified as small (< 1 cm), medium (1 to 3 cm), large (3 to 5 cm), or massive (> 5 cm).²⁸ Other important features of full-thickness tears are the degree of tendon retraction and presence or absence of muscle atrophy. A tendon retracted medial to the glenoid has historically indicated that the tendon tear is not amenable to repair (Figure 16).²⁹ Muscle atrophy in association with a full-thickness tear of the supraspinatus or infraspinatus tendons suggests that the muscle has lost its ability to contract and may not be successfully treated with surgery.³⁰ This information is of clinical value to the surgeon when deciding whether to repair the tear.

MR characteristics of impingement have been subsequently grouped into subtypes by Seeger et al.³¹ Type I impingement is noted as the least severe and includes subacromial bursitis and bursal thickening with normal signal intensity of the supraspinatus tendon. Type II impingement is classified as abnormally high-signal in the supraspinatus tendon without abnormal intramuscular signal or tendon retraction. Type III impingement findings include full-thickness abnormal signal intensity with muscle retraction, indicating a full-thickness tear.

Acromion morphology and acromion-related pathology is easily identified on MR. Acromial spurs have been described with numerous morphologic subtypes including acromial hook and keel osteophytes. The acromial hook lies within the origin of the coracoacromial ligament and projects toward the coracoid. This is located at the anterior inferior acromion.³² A subacromial keel osteophyte is an acromial spur that causes severe damage to the bursal cuff and is shaped like the keel of a sailboat. The spur is found along the anterior lateral edge of the acromion, between the lateral border of the acromion and the acromioclavicular joint, and extends posteriorly to the middle of the acromion undersurface.³³

Location of the acromial spur is also important, occurring along the medial, lateral, and anterior aspects of the acromion with anterolateral spurs having a closer association with cuff pathology.³⁴ Subacromial spurs are contiguous with the cortex of the acromion undersurface with signal isointense to adjacent bone marrow on MRI (Figure 17). Acromion shape has been implicated in impingement with a classification scheme devised by Bigliani et al, as described previously. Only type III has shown a common association with impingement and rotator cuff tears, by most authors. Impingement and rotator cuff tears attributed to a type III acromion are best appreciated on the coronal and sagittal sequences.^20,35 The slope and angle of the acromion is also associated with extrinsic impingement. Studies have indicated that low lateral acromial angle was seen with a higher incidence of impingement. Lateral acromial angle is calculated by a vertical line lateral to the glenoid and a horizontal line parallel to the acromion surface (Figure 18). Lateral acromial angle can be seen effectively on the coronal MR image with an angle < 70 degrees associated with cuff pathology.^20,36

Evaluating an os acromiale and its contribution to impingement can be challenging. On coronal and sagittal planar imaging, an os acromiale may be mistaken for a normal acromioclavicular joint. Axial imaging, usually the most cephalad image, is ideal for identifying an os acromiale. High-signal intensity on T2-weighted images may be appreciated at the synchondrosis, which may represent degenerative changes and/or instability of the os acromiale (Figure 19).^21,37

Acromioclavicular joint osteoarthritis may result in inferior projecting osteophytes or fibrosis around the joint capsule, potentially causing impingement. Inferior spurring of the distal clavicle and acromion can also cause impingement, with an inferior acromial spur associated more often with clinical symptoms. MRI appearance varies and acromioclavicular arthrosis may demonstrate marrow edema (which will have high signal intensity on T2-weighted sequences), subchondral cysts, sclerosis, and/or erosions.³⁸

Coracoacromial ligament (CAL) pathology has been extensively studied with regard to impingement syndrome.³⁹ The CAL is susceptible to pathological degeneration, which can thicken the ligament, greater than its normal thickness of 2 to 5.6 mm. This thickening, and associated subacromial osteophytes at the ligamentous attachment, can cause impingement on the supraspinatus tendon (Figures 20, 21).⁴⁰

Treatment

Of the nonoperative treatment options, studies have shown that exercise therapy combined with other noninvasive treatments have higher efficacy with regard to pain score.⁴¹ Exercise therapy and localized drug injections showed better positive effects on pain score than any other nonoperative treatment options.^41,42

Operative treatment options for extrinsic shoulder impingement are usually related to the underlying etiological cause, and are usually reserved for cases of failed conservative treatments. One of the more common surgical procedures is subacromial decompression, which involves a subacromial bursectomy, release or retraction of the coracoacromial ligament, and removal of the subacromial spurs (Figure 22). This can be performed either as open surgery or arthroscopically. Some studies have shown that an arthroscopic approach has a better efficacy, while others show no significant difference in long-term outcome. However, it is generally accepted that arthroscopy has less of an economic burden and should be the preferred method.^43,44

CAL release is a controversial topic and resection can lead to biomechanical alteration with regard to humeral head movement. Therefore, partial release has been advocated with good long-term outcomes.^39,45 Limited studies have evaluated bursectomy alone vs. standard subacromial decompression, with no significant difference in clinical results between the procedures.⁴⁶ Acromioclavicular joint arthritis alone can be a source of pain, but has also been implicated as a cause of impingement. Distal clavicular resection, or the Mumford procedure, has been shown to improve symptomatic impingement with related acromioclavicular arthropathy as an adjunct to subacromial decompression.^47,48 Os acromiale treatment includes conservative measures, although patients with persistent symptomatic or functional deficits can benefit from surgical options. One of the more common procedures is an osseous fusion of the os acromiale combined with internal fixation and tension banding. This is usually followed by acromioplasty of the new acromio-acromion joint, ie, a 2-stage fusion.⁴⁹

Conclusion

Extrinsic shoulder impingement is a common cause of shoulder pain and frequently seen in clinical practice. Imaging plays an important role in identifying the cause of impingement and also in guiding clinicians with treatment planning. Understanding the anatomy, underlying mechanics, and MRI characteristics of rotator cuff impingement will allow for prompt recognition and ultimately improve outcomes.

References

1. Luime JJ, Koes BW, Hendriksen IJM, et al. Prevalence and incidence of shoulder pain in the general population; a systematic review. Scand J Rheumatol 2004;33(2):73-81.
2. Urwin M, Symmons D, Allison T, et al. Estimating the burden of musculoskeletal disorders in the community: the comparative prevalence of symptoms at different anatomical sites, and the relation to social deprivation. Ann Rheum Dis 1998;57(11):649-655.
3. Neer CS. Impingement lesions. Clin Orthop Relat Res 1983;173:70.
4. Wolff AB, Sethi P, Sutton KM, et al. Partial thickness rotator cuff tears. J Am Acad Orthop Surg 2006;14(13):715.
5. Budoff JE, Nirschl RP, Ilahi OA, et al. Internal impingement in the etiology of rotator cuff tendinosis revisited. Arthroscopy 2003;19(8):810-814.
6. Giaroli EL, Major NM, Higgins LD. MRI of internal impingement of the shoulder. Am J Roentgenol 2005;185(4):925-929.
7. Muto T, Inui H, Ninomiya H, et al. Characteristics and clinical outcomes in overhead sports athletes after rotator cuff repair. J Sports Med 2017;2017:5476293.
8. Seitz AL, McClure PW, Finucane S, et al. Mechanisms of rotator cuff tendinopathy: intrinsic, extrinsic, or both? Clin Biomech 2011;26(1):1-12.
9. Neer CS 2nd. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg Am 1972;54(1):41-50.
10. Standring S. Gray’s Anatomy E-Book: The Anatomical Basis of Clinical Practice. Amsterdam, Netherlands: Elsevier Health Sciences; 2015.
11. Matsen FA. Shoulder Surgery: Principles and Procedures. Philadelphia, PA: Saunders; 2004.
12. Edelson JG, Luchs J. Aspects of coracoacromial ligament anatomy of interest to the arthroscopic surgeon. Arthroscopy 1995;11(6):715-719.
13. Gallino M, Battiston B, Annaratone G, et al. Coracoacromial ligament: a comparative arthroscopic and anatomic study. Arthroscopy 1995;11(5):564-567.
14. Scheuer L, Black S, Christie A. The pectoral girdle. San Diego, CA: Elsevier Academic Press; 2000.
15. Flecker H. Roentgenographic observations of the times of appearance of epiphyses and their fusion with the diaphyses. J Anat 1932;67(Pt 1):118-164.3.
16. Rockwood CA, Lyons FR. Shoulder impingement syndrome: diagnosis, radiographic evaluation, and treatment with a modified Neer acromioplasty. J Bone Joint Surg Am 1993;75(3):409-424.
17. Michener LA, McClure PW, Karduna AR. Anatomical and biomechanical mechanisms of subacromial impingement syndrome. Clin Biomech 2003;18(5):369-379.
18. Bigliani LU, D’Alessandro DF, Duralde XA, et al. Anterior acromioplasty for subacromial impingement in patients younger than 40 years of age. Clin Orthop Relat Res 1989;(246):111-116.
19. Farley TE, Neumann CH, Steinbach LS, et al. The coracoacromial arch: MR evaluation and correlation with rotator cuff pathology. Skeletal Radiol 1994;23(8):641-645.
20. Balke M, Schmidt C, Dedy N, et al. Correlation of acromial morphology with impingement syndrome and rotator cuff tears. Acta Orthop 2013;84(2):178-183.
21. Park JG, Lee JK, Phelps CT. Os acromiale associated with rotator cuff impingement: MR imaging of the shoulder. Radiology 1994;193(1):255-257.
22. Rovesta C, Marongiu MC, Corradini A, et al. Os acromiale: frequency and a review of 726 shoulder MRI. Musculoskelet Surg February 2017. doi:10.1007/s12306-017-0463-2.
23. De Yang Tien J, Tan AHC. Shoulder impingement syndrome, a common affliction of the shoulder: a comprehensive review. Proc Singapore Healthcare 2014;23(4):297-305.
24. Umer M, Qadir I, Azam M. Subacromial impingement syndrome. Orthop Rev 2012;4(2):e18.
25. Vinson EN, Helms CA, Higgins LD. Rim-rent tear of the rotator cuff: a common and easily overlooked partial tear. Am J Roentgenol 2007;189(4):943-946.
26. Ellman H. Diagnosis and treatment of incomplete rotator cuff tears. Clin Orthop Relat Res 1990;254:64.
27. Weber SC. Arthroscopic debridement and acromioplasty versus mini-open repair in the treatment of significant partial thickness rotator cuff tears. Arthroscopy 1999;15(2):126-131.
28. DeOrio JK, Cofield RH. Results of a second attempt at surgical repair of a failed initial rotator-cuff repair. J Bone Joint Surg Am 1984;66(4):563-567.
29. Thomazeau H, Boukobza E, Morcet N, et al. Prediction of rotator cuff repair results by magnetic resonance imaging. Clin Orthop Relat Res 1997;(344):275-283.
30. Maughan RJ, Watson JS, Weir J. Strength and cross-sectional area of human skeletal muscle. J Physiol 1983;338:37-49.
31. Seeger LL, Gold RH, Bassett LW, et al. Shoulder impingement syndrome: MR findings in 53 shoulders. Am J Roentgenol 1988;150(2):343-347.
32. Ogata S, Uhthoff HK. Acromial enthesopathy and rotator cuff tear. A radiologic and histologic postmortem investigation of the coracoacromial arch. Clin Orthop Relat Res 1990;(254):39-48.
33. Snyder JS. Rotator cuff: introduction, evaluation, and imaging. Shoulder arthroscopy, 2nd ed Lippincott Williams & Wilkins. 2003.
34. Oh JH, Kim JY, Lee HK, et al. Classification and clinical significance of acromial spur in rotator cuff tear: heel-type spur and rotator cuff tear. Clin Orthop Relat Res 2010;468(6):1542-1550.
35. Bigliani LU, Ticker JB, Flatow EL, et al. The relationship of acromial architecture to rotator cuff disease. Clin Sports Med 1991;10(4):823-838.
36. Tuite MJ, Toivonen DA, Orwin JF, et al. Acromial angle on radiographs of the shoulder: correlation with the impingement syndrome and rotator cuff tears. Am J Roentgenol 1995;165(3):609-613.
37. Kurtz CA, Humble BJ, Rodosky MW, Sekiya JK. Symptomatic os acromiale. J Am Acad Orthop Surg 2006;14(1):12-19.
38. Stoller DW. Magnetic Resonance Imaging in Orthopaedics and Sports Medicine. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.
39. Rothenberg A, Gasbarro G, Chlebeck J, et al. The coracoacromial ligament: anatomy, function, and clinical significance. Orthop J Sports Med 2017;5(4):2325967117703398.
40. Burns WC 2nd, Whipple TL. Anatomic relationships in the shoulder impingement syndrome. Clin Orthop Relat Res 1993;(294):96-102.
41. Dong W, Goost H, Lin X-B, et al. Treatments for shoulder impingement syndrome: a PRISMA systematic review and network meta-analysis. Medicine 2015;94(10):e510.
42. Rob J. Does the addition of a corticosteroid injection to exercise therapy improve outcomes in subacromial impingement syndrome? Clin J Sport Med 2011;21(5):463-464.
43. Sachs RA, Stone ML, Devine S. Open vs. arthroscopic acromioplasty: a prospective, randomized study. Arthroscopy 1994;10(3):248-254.
44. Davis AD, Kakar S, Moros C, et al. Arthroscopic versus open acromioplasty. Am J Sports Med 2010;38(3):613-618.
45. Su W-R, Budoff JE, Luo Z-P. The effect of coracoacromial ligament excision and acromioplasty on superior and anterosuperior glenohumeral stability. Arthroscopy 2009;25(1):13-18.
46. Donigan JA, Wolf BR. Arthroscopic subacromial decompression: acromioplasty versus bursectomy alone—does it really matter? A systematic review. Iowa Orthop J 2011;31:121-126.
47. Lesko PD. Arthroscopic Mumford procedure variation of technique. Iowa Orthop J 1999;19:93-98.
48. Daluga DJ, Dobozi W. The influence of distal clavicle resection and rotator cuff repair on the effectiveness of anterior acromioplasty. Clin Orthop Relat Res 1989;(247):117-123.
49. Barbier O, Block D, Dezaly C, et al. Os acromiale, a cause of shoulder pain, not to be overlooked. Orthop Traumatol Surg Res 2013;99(4) :465-472.