Shoulder Impingement Syndrome

Etiology

Shoulder external 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. The latter occurs secondary to a repetitive impingement in overhead throwers or manual laborers and constitutes articular-sided rotator cuff pathology, glenohumeral internal rotation deficit (GIRD), and superior labrum anterior posterior (SLAP) tears.[4][5][6][7][8]

External impingement, often commonly referred to by clinicians and providers as shoulder impingement, is best described as a painful condition of the shoulder that results from the inflammation, irritation, and degradation of the anatomic structures within the subacromial space.[2][9] Previously, shoulder impingement syndrome was thought to be a sole diagnosis itself but is now considered to be a cluster of symptoms and anatomic characteristics.[10]

Its anatomic borders define the subacromial space. The acromion and coracoacromial ligament provide the anterior border, the acromioclavicular (AC) joint acts as the superior border, and the humeral head serves as the inferior border.[2] The acromion shape is thought to play a role in the development of external, or "outlet-based" impingement syndrome. Bigliani and Morrison classified the shape of the acromion by its three most common morphologies:[6]

• Class I: Flat acromion
• Class II: Curved acromion
• Class III: Hooked acromion

During the actions of shoulder abduction, forward flexion, and internal rotation, normal shoulder girdle movement results in narrowing of the subacromial space. This subacromial space, which is normally 1.0 to 1.5 cm in width, narrows with the superior migration of the humeral head, allowing it to approach the anteroinferior edge of the acromion.[11] The symptom of pain associated with shoulder impingement results with this movement due to the humeral head applying a compressive force to either the rotator cuff, the subacromial bursa, or both structures.[2]

Repetitive pathologic compression, degeneration, and fraying of the rotator cuff tendons are known to contribute to the narrowing of the subacromial space, but it is unknown whether or not the inflamed and damaged tendons cause impingement, or if the narrowed subacromial space causes the tendon inflammation.[2]

Shoulder impingement syndrome can be described according to either the location of the impingement, characterized as external or internal, and/or the underlying cause of the impingement, referred to as primary or secondary impingement.[10][12][13] External, or subacromial impingement, results from a mechanical or physical encroachment of the soft tissue located within the subacromial space. Conversely, internal impingement results when the tendons of the rotator cuff encroach between the humeral head and glenoid rim. Internal impingement is most commonly associated with the supraspinatus and infraspinatus tendons.[10]

In primary impingement, there is a structural narrowing of the subacromial space. Examples of primary shoulder impingement syndrome include those attributable to abnormal acromion anatomy, such as a hooked class III acromion, or swelling of the soft tissues. Secondary shoulder impingement syndrome is characterized by normal anatomy at rest and onset of impingement during shoulder motion, likely secondary to rotator cuff weakness, permitting uncontrolled cranial translation of the humeral head.[10][12][13] Another potential cause of secondary impingement syndrome is a weakness of the trapezius and serratus anterior muscles, limiting the external rotation and rise of the scapula with the abduction of the upper extremity, further narrowing the subacromial space.[2]

Neer classified shoulder impingement in three categories or stages of severity. In stage I, impingement primarily results from edema, hemorrhage, or both and is classically seen with overuse-type mechanisms. Stage II is characterized by greater fibrosis and irreversible tendon changes. A rupture or tear of the tendon may result from chronic, longstanding fibrosis and is seen in stage III shoulder impingement syndrome.[14][15]

Epidemiology

Shoulder impingement syndrome is most commonly seen in individuals who participate in sports and activities that require repetitive overhead activities, including but not limited to handball, volleyball, swimming, carpenters, painters, and hairdressers.[4] Other extrinsic risk factors that may predispose to the development of impingement syndrome include bearing heavy loads, infection, smoking, and fluoroquinolone antibiotics.[2] The incidence of shoulder impingement syndrome rises with age, with peak incidence occurring in the sixth decade of life.[12]

History and Physical

A thorough history and physical examination are key to the diagnosis of shoulder impingement syndrome. Individuals will often present with complaints of pain upon lifting the arm or with lying on the affected side.  They may report loss of motion as the primary reason they come in to be evaluated, or that nighttime pain prevents them from sleeping. Weakness and stiffness often result secondary to the pain.[16] Onset is usually gradual or insidious, typically developing over weeks to months, and patients are often unable to describe a direct trauma or inciting event that resulted in the pain.[12][17] Pain is commonly described as being located over the lateral acromion, frequently with radiation to the lateral mid-humerus. Clinicians should attempt to obtain details regarding the nature of the shoulder pain, such as onset, quality, exacerbating, and remitting factors, and interventions attempted thus far with clinical response and history of prior injuries to the affected extremity. Special attention should be made by the clinician to inquire about overhead activities and repetitive activities. Relief may be noted with rest, anti-inflammatory medications, and ice, but symptoms often recur upon return to activity.

Physical examination should consist of inspection, palpation, passive, and active range of motion, and strength testing of the neck and shoulder, all of which are compared bilaterally. Often, patients will have weakness of abduction and/or external rotation of the affected side.[10][12] Scapular dyskinesis can be seen with forward elevation of the arm. Tenderness to palpation is usually present over the coracoid process of the affected arm.

Special tests are key components of the physical examination.[8] Those tests specific to shoulder impingement syndrome include the Hawkins test, Neer sign, Jobe test, and a painful arc of motion. Individually, these tests have low sensitivity and specificity, but when combined, they can help complete the picture of shoulder impingement syndrome.[10]

Hawkins test: The Hawkins test is performed when the patient's arm is passively internally rotated with the shoulder in 90 degrees of shoulder forward flexion and elbow flexion. Pain over the acromion indicates subacromial impingement but may be negative in internal impingement.[10]

Neer sign: With the scapula fixed into a depressed position, this test is performed by the examiner maximally forward flexing the patient's arm (passive range of motion testing). Localized pain on the anterior shoulder suggests subacromial impingement, whereas posterior shoulder pain suggests internal impingement.

Jobe test: Also known as the empty can test, this 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. A positive test occurs with localized pain to the affected arm.[10]

Painful arc of motion: The painful arc is a physical exam finding in which pain is appreciated with abduction of the arm between 70 and 120 degrees and forced overhead movement.[12]

Special tests to evaluate for shoulder instability include the sulcus sign, anterior apprehension, and relocation. Classically, these tests are negative in shoulder impingement syndrome.

Sulcus sign: With the patient sitting upright with arm resting at their side, the clinician stabilizes the shoulder proximally and applies an inferiorly-directed force at the elbow. A positive test is noted based on the inferior displacement of the humeral head.[18]

Anterior apprehension: With the patient lying supine, this test is performed by placing the patient's shoulder in 90 degrees of abduction and 90 degrees of external rotation. While supporting the proximal shoulder, the clinician then applies greater gentle external rotation movement. The exam is considered positive when the patient reports a subjective feeling of impending subluxation or near dislocation.[18]

Relocation test: This test for shoulder instability requires a positive anterior apprehension test. After the patient reports the prodrome of dislocation or subluxation described above, the clinician applies a posteriorly directed force on the anterior humeral head, which relieves the patient's symptoms.[18]

Evaluation

While the overall diagnostic sensitivity of the physical exam is reportedly as high as 90%, imaging studies are often performed to confirm the diagnosis and rule out other pathologies.[12] If the decision to obtain radiographs is made, they should be obtained bilaterally, rather than only on the affected side, to evaluate potential anatomic differences and to rule out other pathologies such as calcific tendinitis or arthritic changes.

Plain radiograph standard shoulder films include 2 views (AP and lateral/scapular Y) The AP view of the shoulder can be used to determine the critical shoulder angle (CSA), which involves the extent of lateral coverage by the acromion and the inclination of the glenoid. At CSAs greater than 35 degrees, there is an increased likelihood that a rotator cuff is contributing to impingement syndrome. Similarly, measurements such as the acromiohumeral distance (AHD) can help to detect rotator cuff pathologies and defects. The AHD is measured from the inferior edge of the acromion to the humeral head. The normal range is approximately 7 to 14 mm in men and 7 to 12 mm in women. A lower AHD suggests rotator cuff pathology. The scapular Y view allows for the assessment of the humeral head on the glenoid. Additional plain radiographs featuring the outlet view will best visualize and evaluate the shape of the acromion.[12]

Other imaging modalities to consider include ultrasound and magnetic resonance imaging (MRI). Consideration for advanced imaging with MRI is recommended after 6 weeks of therapy without clinical improvement.[19] MRI allows for a detailed evaluation of bony and soft tissue structures within the shoulder girdle. Ultrasound is a bedside imaging option that primarily enables assessment of the soft tissue contributing factors such as bursitis, tendinopathy, and/or tendon ruptures.[12][20]

Treatment / Management

Classically, the foundation of management for shoulder impingement syndrome has been rehabilitative exercise programs with subsequent surgical intervention if indicated by underlying anatomy, pathology, or failure of response to physiotherapy. Without known structural damage, non-operative therapies with a controlled exercise program, nonsteroidal anti-inflammatory drugs (NSAIDs), and subacromial injections are considered the treatment of choice for the first 3 to 6 months of treatment.[2]

In one study, exercise therapy was found to have better results when compared to a control/placebo in the sub-acute injury phase.[21] Physiotherapy for shoulder impingement syndrome should consist of exercises that focus on rotator cuff strengthening, with a special focus on the supraspinatus and infraspinatus rotator cuff muscles, the trapezius, and serratus anterior strengthening and retraining exercises to minimize scapular dyskinesia, and other exercises to correct strength imbalances of the upper extremities. The combination of exercise with other conservative therapy lead to greater improvements in pain score compared to either treatment alone. Physiotherapy plus localized injection resulted in a maximized treatment effect compared to solitary localized injection.[15] Further, moderate strength evidence supports the effective addition of hyperthermia to physical therapy, though symptom relief was only noted to be short-term.[21](A1)

Numerous methodologies and approaches for corticosteroid injections exist, but the commonly used posterior subacromial approach requires less precision and is often viewed as most straightforward.[22] A 1.5 inch, 21, or 22 gauge needle with lidocaine and corticosteroid is commonly used. In this approach, the clinician locates the posterior shoulder portal, located 1 cm medial and inferior to the posterior corner of the acromion. While angling the needle in the direction of the underside of the acromion, the clinician advances the needle toward the acromion in an anterosuperior direction. Injection flow should be easy, without resistance, otherwise, the needle should be redirected slightly inferiorly to avoid directly injecting a rotator cuff tendon. While landmark-based approaches provide clinical benefit, ultrasound-guided injections may be superior in symptom relief.[23]

A systematic review of randomized controlled trials comparing surgical intervention versus conservative therapy yielded moderate evidence that surgical intervention was not more effective for reducing pain than impingement-directed physical therapy.[24] Arthroscopic subacromial decompression (ASD) consists of acromioplasty at the anterolateral edge, bursal debridement, and resection of the coracoacromial ligament.[2] The ASD or other similar procedure is recommended when a patient has severe, persistent subacromial shoulder pain with functional impairments that have not improved despite conservative therapy.[1][12][17]  Combined ASD and treatments such as radiofrequency ablation and arthroscopic bursectomy have more beneficial effects than open subacromial decompression (OSD) plus platelet-leukocyte gel injection.[15]  However, a 2018 systematic review found there was no additional benefit in pain reduction when comparing the results of ASD surgery to placebo surgery at 12 months.[25] Alternative surgical options include acromioplasty or bursectomy alone, though, like ASD, these surgical interventions appear to provide minimal benefit to patients.[26] (A1)

When comparing surgical intervention with physiotherapy to that of surgery alone, no statistically significant or clinically significant difference between the two arms was observed with respect to pain at 3 months, 6 months, 5 years, and 10 years. Further, no statistical or clinically significant difference in function was noted at 3 months, 6 months, and 1 year follow-up between the groups.[1](A1)

Differential Diagnosis

• Adhesive capsulitis
• Rotator cuff tear
• Acromioclavicular joint arthritis
• Acromioclavicular joint sprain
• Trapezius muscle spasm
• Biceps tendonitis
• Biceps tendon rupture
• Calcific tendonitis
• Glenohumeral arthritis
• Distal clavicle osteolysis
• Cervical radiculopathy
• Thoracic outlet syndrome

Prognosis

In 60% of patients, physical therapy, NSAIDs, corticosteroid injections, and other means of conservative therapy yield satisfactory results within two years.[2][12]

Complications

Due to the underlying etiology of shoulder impingement syndrome, complications that may arise predominantly result from structural damage within the subacromial space, altered biomechanics, or avoidance of use with subsequent atrophy. Potential pathologies that may result include rotator cuff tendonitis or tear, bicipital tendonitis or tear, or adhesive capsulitis.