Subacromial Impingement Syndrome

Subacromial impingement is one of the most common causes of shoulder pain encountered in clinical practice.

Subacromial Impingement Causes

In the past, some authors believed impingement was the result of extrinsic factors, citing various potential sources of external cuff compression. Others believed the disorder was related to intrinsic cuff degeneration, leading to cuff weakness and proximal humeral migration followed by cuff abrasion under the acromion.

However, recent thinking suggests that subacromial impingement is likely multifactorial involving a combination of both intrinsic and extrinsic factors that ultimately lead to rotator cuff disease.

See Also: Rotator Cuff of the Shoulder

Pathogenesis Involving Extrinsic Factors

Neer originally described subacromial impingement as the repeated contact between the greater tuberosity and the undersurface of the acromion and coracoacromial ligament. He hypothesized that this repetitive mechanical impingement led to the development of proliferative anterolateral acromial spurs.

Coracoacromial Ligament

The coracoacromial ligament originates from the distal-lateral extension of the coracoid process and travels posterosuperiorly to insert upon the anterolateral margin of the acromion. As part of the coracoacromial arch, this ligament is commonly described as being involved with subacromial impingement lesions due to the proximity of the cuff tendons that pass closely beneath, especially as the arm is elevated.

The coracoacromial ligament has a number of anatomic variations; however, only those variations that involve a distinct anterolateral and posteromedial bundle are likely to be related to rotator cuff impingement and subsequent tearing.

Os Acromiale

The acromion is also subject to developmental abnormalities as a result of failed fusion of secondary ossification centers. This failed fusion results in a defect known as an “os acromiale” and occurs in approximately 8 % of the population where 1/3 of these individuals are affected bilaterally . Os acromiale is a mobile accessory ossicle that, when unstable and pulled inferiorly by contraction of the deltoid with arm elevation, has been associated with the development of identifiable impingement lesions and pain at the top of the shoulder.

Acromial Morphology and Glenoid Version

The anterior aspect of the acromion may, in itself, be a potential site of rotator cuff abrasion and subsequent tearing regardless of the presence or absence of space-occupying traction spurs associated with the coracoacromial ligament.

In 1991, Bigliani et al. described the three most common acromial morphologies as flat (type I), curved (type II), and hooked (type III), citing the hooked acromion as most relevant to the development of subacromial impingement.

Some investigators report that decreased coverage of the humeral head by the acromion (i.e., a decreased acromial index) may allow the humeral head to utilize the anterolateral acromion as a fulcrum or lever to aid in glenohumeral elevation, possibly causing abrasion of the cuff tendons and subsequent rotator cuff tearing.

Inclination of the glenoid in the coronal plane has also been associated with the development of rotator cuff tears on several occasions. The critical shoulder angle (CSA) is another radiographic measurement purported to have an association with rotator cuff tears or osteoarthritis. The CSA is obtained from true anteroposterior (AP) radiographs and takes into account both the acromial index and the degree of glenoid inclination in the scapular plane. The original developers of this measurement have suggested that the CSA may have an ability to predict the future development of degenerative rotator cuff tears (when the CSA > 35°) and glenohumeral osteoarthritis (when the CSA < 30°).

Pathogenesis Involving Intrinsic Factors

While extrinsic factors probably have some role in the development of subacromial impingement, many authors believe that the initiation and progression of rotator cuff disease primarily occurs as a result of intrinsic cuff degeneration. They argue that degenerative changes and/or traumatic injuries weaken the contractile strength of supraspinatus muscle which predictably leads to superior humeral head migration and cuff impingement beneath the acromion with humeral elevation.

Spurring of the anterolateral acromion and erosion of the greater tuberosity are then observed (due to repeated reciprocal contact) along with rotator cuff degeneration. The deterioration of tendon quality due to advanced age is often implicated as one of the primary causes of rotator cuff weakness, potentially resulting in proximal humeral head migration, subsequent bursal irritation and cuff tendinopathy.

The tenuous microvascular blood supply to the supraspinatus and infraspinatus tendons has also been suggested as a possible intrinsic factor related to the development and progression of certain rotator cuff tears.

Stages

Later, realizing that subacromial impingement likely involves a continuum of disease processes, Neer described three basic stages in the development of impingement syndrome:

Stage I:

This stage consists of localized inflammation, slight bleeding, and edema of the rotator cuff. This stage is typically observed in patients under 25 years of age, although it can also be seen in older populations due to overuse. The patient reports pain in the shoulder and a history of acute trauma or repetitive microtrauma.

The physical examination during this stage reveals tenderness at the supraspinatus insertion and anterior acromion, a painful arc, and weakness of the RC secondary to pain, particularly when tested at 90-degree abduction or flexion.

In addition to the rest and modification of activities, pain and inflammation may be controlled with the use of electrotherapeutic modalities, cryotherapy, and NSAIDs prescribed by the physician.

Stage II:

Stage II represents a progressive process in the deterioration of the tissues of the rotator cuff. This stage is generally seen in the 26–40-year-old age group. Irritation of the subacromial structures continues as a result of the abnormal contact with the acromion. The subacromial bursa loses its ability to lubricate and protect the underlying RC, and tendinitis of the cuff develops. The patient often reports that a specific activity brings on their symptoms, especially an overhead activity. Pain is generally located on the top of the shoulder and will radiate to the midbrachium in the region of the deltoid insertion.

The physical examination reveals crepitus or catching at approximately 100 degrees and restriction of PROM (due to fibrosis)

This stage is no longer reversible with just rest. Although this stage often responds to long-term conservative care, it can progress to a partial thickness tear. If the level of symptoms is severe enough, surgery is often required. Surgical intervention is usually reserved for those who have failed to make satisfactory improvement over a period of 6 months.

Stage III:

Subacromial impingement Stage III is the end stage, common in the over-40 age group, where destruction of the soft tissue and rupture, or macrotrauma of the rotator cuff, is seen. Localized atrophy can occur with this stage. Osteophytes of the acromion and A-C joint develop. The wear of the anterior aspect of the acromion on the greater tuberosity and the supraspinatus tendon eventually results in a full-thickness tear of the rotator cuff.

The physical examination reveals atrophy of the infraspinatus and supraspinatus, and more limitation in AROM and PROM than the other stages.

Subacromial Impingement Special Tests

The most useful and most widely utilized tests for the detection of subacromial impingement include:

1. Neer impingement sign
2. Hawkins–Kennedy test
3. Painful arc sign

When the diagnosis is in question, it is often useful to inject a local anesthetic into the subacromial space before repeating each test. This method is typically used to identify whether the patient’s subjective weakness is primarily due to guarding or due to actual muscle weakness. The relief of impingement-like signs and symptoms that were present before the injection usually confirms the diagnosis.

See Also: Subacromial Injection Test

Radiology

Findings on radiograph may include one or more of the following:

1. proximal migration of the humerus.
2. traction osteophytes
3. calcification of the coracoacromial ligament
4. cystic changes within the greater tuberosity
5. Type III-hooked acromion.
6. os acromiale: best seen on axillary lateral.

MRI to evaluate the degree of rotator cuff pathology.

Ultrasound can be used to detect the rotator cuff tears.

Shoulder Impingement Treatment

Non-operative treatments of rotator cuff impingement is the first line of treatment, these include:

1. Physical therapy,
2. Anti-inflammatory medication,
3. Cortisone subacromial injections.

Subacromial Impingement operative treatment is indicated if non-operative treatment failed for a minimum of 4-6 months.

Operative treatments include:

1. Subacromial decompression.
2. Acromioplasty.

Shoulder Impingement Physical Therapy include many protocols. A progression from isometric exercises to close chain, and finally to open-chain activities beginning with scapulothoracic strengthening and scaption retraining, and then proceeding to RC strengthening, is generally recommended.

• Scapulothoracic strengthening and scaption retraining exercises include isometric scapular pinches and shrug exercises, rowing, press ups, and the push-up plus. Exercises to improve the scapulohumeral rhythm include the PNF D2 pattern, alternating serratus punches with tubing, and latissimus dorsi pull downs.
• Rotator cuff strengthening exercises include the empty can, biceps curl, IR and ER of the shoulder against resistivetubing, elbow extension, prone ER of the shoulder, and shoulder flexion and abduction (performed below 90 degrees).

References

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