Shoulder impingement syndrome was originally described by Dr. Neer in 1972 as shoulder pain, weakness, and dysfunction caused by chronic impingement of the rotator cuff beneath the coracoacromial arch. Repetitive microtrauma of the supraspinatus tendon’s hypovascular area causes progressive inflammation and degeneration of the tendon, resulting in bursitis, tendinopathy, and progressive rotator cuff tearing (partial-thickness tears that progress into full-thickness tears with time). Extrinsic compression of the rotator cuff tendon can occur at the undersurface of the acromion (usually due to subacromial impingement spurs or abnormal morphology of the acromion), the coracoacromial (CA) ligament, and the acromioclavicular (AC) joint.


The acromion, together with the coracoid process and the CA ligament, form the coracoacromial arch. The arch is the rigid structure through which the rotator cuff tendons, subacromial bursa, and humeral head must pass. The primary tendon making up the rotator cuff is the supraspinatus tendon. This is the most common affected tendon in rotator cuff pathology, including subacromial impingement syndrome. The supraspinatus tendon is confined above by the subacromial bursa and coracoacromial arch and below by the humeral head in an area referred to as the “supraspinatus outlet.” On average, there is 9 to 10 mm of space between the undersurface of the acromion and the humeral head in the supraspinatus outlet. This space is narrowed by abnormalities of the coracoacromial arch. Additionally, internal rotation and forward flexion of the arm also decreased the distance between the CA arch and the humeral head, decreasing the space for the supraspinatus tendon and aggravating symptoms associated with impingement syndrome (ex. Hawkins test for impingement). The subacromial bursa tissue overlies the supraspinatus tendon. Its function is to serve as a cushion and lubricate the interface between the rotator cuff and the overlying acromion and AC joint. Importantly, the bursa may become thick and fibrotic in response to progressive subacromial inflammation, further decreasing the volume of the subacromial space while aggravating the symptoms associated with impingement syndrome. Additionally, the supraspinatus tendon has a watershed area of hypovascularity located approximately 1cm medial to the insertion of the rotator cuff on the humeral hand. Due to the lack of blood supply, this area is predisposed to degenerative tearing and tendinopathy as well as tearing from overuse and repetitive microtrauma against the acromion. Together, this is subacromial impingement syndrome.

Acromial morphology most commonly accounts for narrowing of the supraspinatus outlet. Bigliani et al. published a study that described three types of acromial morphology:

  • Type I acromion is flat.

  • Type II acromion is curved.

  • Type III acromion is hooked.

Interestingly, the study also noted that in 70% of cadaver shoulders with rotator cuff tears a type III acromion was present.


Extrinsic or outlet impingement of the rotator cuff is caused by abnormalities of the CA arch, resulting in an overall decreased area for the rotator cuff tendons within the supraspinatus outlet. Other processes or pathologies that narrow the supraspinatus outlet must be considered when assessing a patient for impingement syndrome of the shoulder. These include:

  • Osteophytes of the AC joint, due to progressive osteoarthritis of the AC joint

  • Hypertrophy of the CA ligament

  • Malunion of a greater tuberosity or a clavicle fracture

  • Inflammatory subacromial bursitis

  • Calcific rotator cuff tendinitis

  • A flap from a bursal-sided rotator cuff tear

  • An unstable os acrominale (failure of fusion in one of the acromial ossification centers).

Natural History

Neer classified subacromial impingement into three distinct stages:

  • Stage 1: Lesions occur initially with excessive overhead use in sports or at work. This is a reversible process of edema and hemorrhage that is found in the subacromial bursa and adjacent rotator cuff tissue. This typically occurs in patients younger than the age of 25 years old.

  • Stage 2: In stage II lesions, the subacromial bursa may become irreversibly fibrotic and thickened, and tendinitis develops in the supraspinatus tendon. Typically, this lesion is found in patients 25 to 40 years of age.

  • Stage 3: As subacromial impingement progresses, stage III lesions might occur, with partial or complete tears of the rotator cuff tendon. Changes in the bone architecture at the anterior acromion and greater tuberosity may also develop. These lesions occur almost exclusively to patients older than the age of 40.

In terms of the natural history, stage I and II lesions typically respond to non-operative modalities including rest, activity modification, and nonsteroidal anti-inflammatories (NSAIDs). A subacromial corticosteroid injection may also help treat the subacromial bursitis and relieve refractory symptoms. Refractory stage II lesions and stage III lesions require operative intervention.

Patient History And Physical Finding

Patients with subacromial impingement syndrome of the shoulder typically complain of shoulder pain that is aggravated by overhead activities. The pain is typically localized to the lateral aspect of the acromion, extending distally into the deltoid muscle belly. Patients may also experience pain during the night, especially when lying on the affected shoulder. Most commonly, patients do not complain of a restriction in their range of motion but do experience aggravation of their symptoms with internal rotation and forward flexion of the shoulder that is most common with overhead exercises and activity. Physical examination methods to identify subacromial impingement syndrome include:

  • Palpation over the point of Codman: Palpation just anterior to the anterolateral corner of the acromion may produce tenderness that is a sign of supraspinatus tendinitis, tendinopathy, or an acute tear of the supraspinatus tendon.

  • Range of motion (ROM) Testing: patients with impingement often have limited internal rotation due to contracture of the posterior shoulder capsule. Active motion is typically more painful than passive motion especially during the eccentric phase of the motion arc.

  • Neer Impingement Sign.

  • Neer Impingement Test:  an injection of local anesthetic into the subacromial space followed by relief of pain on clinical impingement tests.

  • Hawkins Sign

A complete physical examination of the shoulder should be performed to evaluate and rule out other associated pathologies and other processes in the differential diagnosis. These include:

  • Acromioclavicular (AC) Osteoarthritis

  • Rotator Cuff Tears

  • Glenohumeral Instability

  • Biceps Pathology

  • Glenohumeral osteoarthritis

Imaging/ Diagnostic Studies

Standard radiographs of the shoulder should be taken that include standard anteroposterior (AP) orientations including internal and external rotation views as well as a supraspinatus outlet view. Acromiohumeral distance is the minimal distance between the undersurface of the acromion and the uppermost point of the humeral head. An acromiohumeral distance of less than 7 mm is considered abnormal and a potential cause of subacromial impingement.  An AP radiograph of the contralateral normal shoulder might be taken and used as a comparison view for the acromiohumeral distance.

Other studies, including MRI, CT scan, arthrography, and ultrasonography might be indicated based on the patient’s presentation and clinical examination as well as the findings on plain radiographs. Typically, these tests are reserved for patients whose diagnosis of impingement syndrome is not completely clear or understood from the history, physical examination, and plain radiographs. Additionally, these other modalities may help diagnose associated pathology of the soft tissues around the shoulder including the long head of biceps tendon, labrum, and rotator cuff tendon.

Differential DIagnosis

  • Rotator cuff pathology, including partial and full-thickness tears

  • AC joint osteoarthritis

  • Glenohumeral instability

  • Posterior glenoid and rotator cuff (internal) impingement

  • Glenohumeral osteoarthritis

  • Biceps tendon pathology (biceps tenosynovitis)

  • Adhesive capsulitis (aka. Frozen shoulder)

  • Cervical spine disease

  • Viral brachial plexopathy

  • Thoracic outlet syndrome

  • Neoplasm of the proximal humerus or shoulder girdle

  • SLAP tear

Nonoperative Management

All patients with subacromial impingement syndrome should undergo a course of non-operative management for at least 3 to 6 months. Non-operative treatment  modalities include:

  • Subacromial corticosteroid injections

  • NSAIDs (Nonsteroidal anti-inflammatory drugs)

  • Hot and cold therapies

  • Ultrasound

  • Physical Therapy

Approximately 70% of patients will respond to a conservative treatment protocol with success. The goal of therapy is to regain or improve ROM while improving symptoms of pain. Therapy should be advanced as the pain and inflammation subside. Posterior capsular contracture should also be addressed in physical therapy with progressive adduction and internal rotation stretching. Modalities to control pain are indicated in the acute setting.

Surgical Management

Operative intervention is indicated in patients that continue to have symptoms of impingement syndrome that are refractory to a progressive rehabilitation protocol of stretching and strengthening over a minimum 3- to 6-month period. If the diagnosis is not completely clear based on the initial tests, a more extensive diagnostic workup is warranted before surgical intervention. This will usually include an MRI or an MR arthrography (MRA) of the shoulder to rule out rotator cuff pathology and other internal derangement of the shoulder. Particular attention should be  paid to the acromial morphology, the status of the AC joint, and evidence of rotator cuff disease, as these disease processes often coexist in subacromial impingement syndrome. The mainstay of surgical management is subacromial decompression and acromioplasty in order to increase the acromiohumeral distance and supraspinatus outlets for the rotator cuff to pass without further impingement.

Subacromial Decompression / Acromioplasty

During subacromial decompression, an arthroscopic burr is introduced into the subacromial space and is used to resect abnormal, pathologic bone from the undersurface of the acromion. Resection begins at the anterolateral corner of the acromion and the desired depth of resection is estimated based on the diameter of the burr (usually 5.5mm). The depth of resection is achieved anteriorly from the anterolateral corner of the acromion to the medial acromial facet of the AC joint. All abnormal subacromial spurs are removed during the resection. AC joint bone spurs are also removed. Dr. Dold will also resect and release the coracoacromial (CA) ligament completely and visualize the undersurface of the deltoid at least 15mm posterior to the anterolateral corner of the acromion to ensure a complete subacromial decompression. The entirety of the procedure is done arthroscopically through small keyhole incisions. The patient is placed in a sling for comfort post-operatively and begins passive and active range of motion in physical therapy immediately following surgery. The physical therapy protocol is advanced as rapidly as motion and pain will allow. Full recovery is generally achieved by approximately 3 months postoperatively. However, patients with significant rotator cuff pathology or full thickness tears me take much longer to improve. The success rate of arthroscopic subacromial decompression ranges from 73% to 95%.

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