Impingement Syndrome

The term “impingement syndrome” was popularized by Neer in 1972 as a clinical entity in which the rotator cuff was pathologically compressed against the anterior structures of the coracoacromial arch, the anterior third of the acromion, the coracoacromial ligament, and the AC joint (Fig. 3–41).

Irritation of the rotator cuff muscle compromises its function as a depressor of the humeral head during overhead activities (i.e., less clearance of the humeral head under the arch), which further intensifies the impingement process (Fig. 3–42).

A reactive progression of this syndrome is defined by a narrowing of the subacromial outlet by spur formation in the coracoacromial ligament and on the undersurface of the anterior third of the acromion (Fig. 3–43). All of these factors result in an increase in pressure on the rotator cuff, which can lead to chronic wearing and subsequent tearing of the rotator cuff tendons. Neer also defined three stages of impingement relating patient age, physical findings, and clinical course.

Patients with subacromial impingement often complain of shoulder pain, weakness, and possible paresthesias in the upper arm. It is very important to rule out other causes of these symptoms, such as cervical spine pathology. When subacromial impingement is suspected, it is necessary to differentiate primary from secondary impingement. Correct identification of the etiology of the problem is essential for successful treatment.

Primary Impingement
Primary subacromial impingement is the result of an abnormal mechanical relationship between the rotator cuff and the coracoacromial arch. It also includes other “primary” factors that can lead to narrowing of the subacromial outlet (Table 3–3). Patients with primary impingement are usually older than 40 years, complain of anterior shoulder and upper lateral arm pain, with an inability to sleep on the affected side. They have complaints of “shoulder weakness,” and difficulty performing overhead activities. On physical examination, patients may exhibit a loss of motion or weakness of rotator cuff strength secondary to pain. They will usually have a positive Hawkins sign (see Fig. 3–20) and a positive impingement sign as described by Neer (see Fig. 3–19). The impingement test is performed by injecting 10 ml of 1% lidocaine (Xylocaine) into the subacromial space (see Fig. 3–14). Patients with primary impingement may have associated AC joint arthritis, which may contribute to their symptoms and compression of their rotator cuff. These patients may report additional discomfort in the AC joint area with internal rotation maneuvers, such as scratching their back, or experience pain superiorly with abduction of their shoulder. Findings on physical examination that confirm the diagnosis of AC joint arthritis include “point” tenderness at the AC joint with palpation, worsening of the pain at the AC joint with cross-body adduction (see Fig. 3–32), and resolution of the pain with an injection of lidocaine into the AC joint (Fig. 3–44). Radiologic evaluation including an axillary and supraspinatus outlet view may support the diagnosis of primary or “outlet” impingement by demonstrating an os acromiale or a type III acromion (large, hooked acromial spur), respectively (Fig. 3–45).

Secondary Impingement
Secondary impingement is a clinical phenomenon that results in a “relative narrowing” of the subacromial space. This often results from GH or scapulothoracic joint instability. In patients who have underlying GH instability, the symptoms are those of rotator cuff dysfunction (which occur from an overuse injury of the cuff from the increased work the muscles are performing to stabilize the shoulder). The loss of the stabilizing function of the rotator cuff muscles also leads to an abnormal superior translation of the humeral head (decreased depression of the humeral head during throwing and less “clearance”) and mechanical impingement of the rotator cuff on the coracoacromial arch (see Fig. 3–42). In patients who have scapular instability, impingement results from improper positioning of the scapula with relation to the humerus. The instability leads to insufficient retraction of the scapula, which allows for earlier abutment of the coracoacromial arch on the underlying rotator cuff (Fig. 3–46).

Patients with secondary impingement are usually younger and often participate in overhead sporting activities such as baseball, swimming, volleyball, or tennis. They complain of pain and weakness with overhead motions and may even describe a feeling of the arm going “dead.” On physical examination, the examiner should look for possible associated pathology, including GH joint instability with a positive apprehension (see Fig. 3–23) and relocation (see Fig. 3–25) test or abnormal scapular function such as scapular winging or asymmetrical scapular motion. Patients with tightening of the posterior capsule have a loss of internal rotation. Posterior capsular tightness leads to an obligate translation of the humeral head and rotator cuff in an anterior and superior direction, which contributes to the impingement problem.

In patients with secondary impingement, treatment of the underlying problem should result in resolution of the “secondary impingement” symptoms. Often, the recognition of the underlying GH joint instability or scapular instability is missed, and the “secondary impingement” is incorrectly treated as a “primary” (large spur) impingement. A subacromial decompression here worsens the symptoms because the shoulder is rendered even more “unstable.”

Treatment
The key to the successful treatment of subacromial impingement is defining the underlying cause of the impingement symptoms, whether they are primary or secondary to the pathologic relationship between the coracoacromial arch and the rotator cuff. This factor becomes more critical when conservative management fails and surgical intervention is indicated, because the operative procedures for these two clinical entities may be entirely different. For primary impingement, surgical treatment involves widening the subacromial outlet by performing a subacromial decompression (acromioplasty). The surgical treatment for secondary impingement is directed toward the etiology of the symptoms. For example, if the symptoms of impingement are secondary to anterior GH joint instability, the surgical treatment is an anterior stabilization, not an acromioplasty. Performing an acromioplasty in this setting may provide short-term benefit, but as the activities related to the onset of the problem resume, the instability symptoms will persist.

Nonoperative Treatment
Nonoperative treatment is very successful and involves a combination of treatment modalities including anti-inflammatory medications and a well-organized rehabilitation program. In general, the comprehensive rehabilitative protocols for both primary and secondary impingement syndrome are similar and follow the postoperative rehabilitation plan for patients who have had a subacromial decompression with a normal rotator cuff. The initial goals of the rehabilitative process are to obtain pain relief and regain motion. Along with oral medications, judicious use of subacromial injections with a corticosteroid may help to control the discomfort in the acute stages of the inflammatory process. Other modalities such as cryotherapy and ultrasound are also effective in controlling pain. Improving comfort will allow more successful advances in motion and strengthening. Because the rotator cuff tendon is intact, ROM exercises can be both passive and active. Initially, these are done with the arm below 90 degrees of abduction to avoid impingement of the rotator cuff. As symptoms improve, the ROM is increased.

Initially, strengthening exercises begin with the arm at the side. The program begins with closed-chain exercises (see Fig. 3–36), with open-chain exercises initiated after advancing the closed-chain exercises without aggravating shoulder discomfort (see Fig. 3–39). These exercises help restore the ability of the rotator cuff to dynamically depress and stabilize the humeral head, resulting in a gradual relative increase in the subacromial space. In patients with secondary impingement, strengthening is started with the arm comfortably at the patient’s side to avoid positions that provoke symptoms of instability, such as abduction combined with external rotation. As the dynamic stabilizers respond to the strengthening program, exercises can be added in higher planes of abduction. In general, strengthening of the deltoid muscle is not emphasized early in the rehabilitation program to avoid a disproportionate increase in the upward force on the humerus.

Scapula stabilizing exercises are important for patients with primary or secondary impingement (see Figs. 3–37 and 3–38). The scapula forms the base from which the rotator cuff muscles originate. Reciprocal motion is required between the GH and scapulothoracic joint articulations for proper cuff function and correct positioning of the coracoacromial arch.

Abnormal scapular movement or dyskinesia can be treated with a scapular taping program as part of the exercise regimen (Fig. 3–47). Scapular taping can improve the biomechanics of the scapulohumeral and scapulothoracic joints, helping to relieve patient’s symptoms.

Historically, nonoperative treatment was considered unsuccessful if no improvement occurred after a year of proper conservative management. Today, nonoperative treatment should be considered unsuccessful if the patient shows no improvement after 3 months of a comprehensive and coordinated medical and rehabilitative program. Furthermore, after 6 months of appropriate conservative treatment, most patients have achieved maximal improvement from the nonoperative treatment program. Failed conservative management or a plateau in recovery at an undesirable level of function is an indication for surgical intervention.

Operative Treatment
The success of operative treatment is determined by the choice of an appropriate operative procedure and the technical skill of the surgeon. For primary impingement, the current procedure of choice is arthroscopic subacromial decompression, although comparable long-term results can be obtained with a traditional open acromioplasty. Rehabilitation after the surgery focuses on pain control, improved ROM, and muscle strengthening.

When GH joint instability is the reason for secondary impingement, surgical treatment is a stabilization procedure. In our practice, we see numerous patients whose impingement was secondary (due to underlying GH joint instability) but were incorrectly treated with subacromial decompression. This only worsens the underlying instability.

The most commonly performed procedure is an open stabilization, with either a repair of a torn or avulsed labrum or a capsular shift (capsulorrhaphy), depending on the etiology. With technologic advances in arthroscopic instrumentation, fixation devices, and electrothermal technology, many surgeons are now performing arthroscopic stabilization procedures. The potential advantages of arthroscopic procedures include decreased operative time, less operative morbidity, less loss of motion, and a quicker recovery. Currently, the literature reflects a higher failure rate after arthroscopic stabilization than after open stabilization. Arthroscopic procedures require advanced arthroscopic skills, complete recognition of the pathoanatomy, challenging fixation techniques, and appropriate diagnosis-related rehabilitation programs. The rehabilitation principles after an arthroscopic stabilization procedure that includes a labral repair or suture capsulorrhaphy are similar to those after an open stabilization. The biology of healing tissue is the same whether the procedure is done open or arthroscopically, unless the tissue has been treated with thermal energy. Electrothermal arthroscopic capsulorrhaphy, or “shrinking” the shoulder capsule, requires a protective period of approximately 3 weeks after the treatment. If the rehabilitation program is advanced too early, before the healing response has been adequately initiated, there is a high risk that the capsule will be “stretched” and the procedure will not correct the capsular laxity. The rehabilitation protocol after an open or arthroscopic Bankart repair for anterior shoulder instability is fundamentally the same, except for the 3-week delay for patients who have been treated with an electrothermal capsulorrhaphy.