Shoulder Impingement Syndrome

Updated: Oct 19, 2023
Author: Thomas M DeBerardino, MD, FAAOS, FAOA; Chief Editor: Craig C Young, MD 


Practice Essentials

In 1972, Neer first introduced the concept of rotator cuff impingement to the literature, stating that it results from mechanical impingement of the rotator cuff tendon beneath the anteroinferior portion of the acromion, especially when the shoulder is placed in the forward-flexed and internally rotated position.[1]

Neer describes the following 3 stages in the spectrum of rotator cuff impingement:

  • Stage 1, commonly affecting patients younger than 25 years, is depicted by acute inflammation, edema, and hemorrhage in the rotator cuff. This stage usually is reversible with nonoperative treatment.

  • Stage 2 usually affects patients aged 25-40 years, resulting as a continuum of stage 1. The rotator cuff tendon progresses to fibrosis and tendonitis, which commonly does not respond to conservative treatment and requires operative intervention.

  • Stage 3 commonly affects patients older than 40 years. As this condition progresses, it may lead to mechanical disruption of the rotator cuff tendon and to changes in the coracoacromial arch with osteophytosis along the anterior acromion. Surgical l anterior acromioplasty and rotator cuff repair is commonly required.

In all Neer stages, etiology is impingement of the rotator cuff tendons under the acromion and a rigid coracoacromial arch, eventually leading to degeneration and tearing of the rotator cuff tendon.

Although rotator cuff tears are more common in the older population, impingement and rotator cuff disease are frequently seen in the repetitive overhead athlete. The increased forces and repetitive overhead motions can cause attritional changes in the distal part of the rotator cuff tendon, which is at risk due to poor blood supply. Impingement syndrome and rotator cuff disease affect athletes at a younger age compared with the general population.[2]

Signs and symptoms

Sudden onset of sharp pain in the shoulder with tearing sensation is suggestive of a rotator cuff tear. Gradual increase in shoulder pain with overhead activities is suggestive of an impingement problem.

See Presentation for more detail.


Magnetic resonance imaging (MRI) is considered the imaging study of choice for evaluation of shoulder pathology.

See Workup for more detail.


In general, conservative measures for shoulder impingement syndrome are applied for at least 3-6 months or longer if the individual is improving, which is usually the case in 60-90% of patients. If the patient remains significantly disabled and has no improvement after 3 months of conservative treatment, the clinician must seek further diagnostic workup, as well as reconsider other etiologies or refer the person for surgical evaluation.

See Treatment and Medication for more detail.


Primary impingement

Causes of primary impingement are as follows:

  • Increased subacromial loading

  • Acromial morphology (A hooked acromion, presence of an os acromiale or osteophyte, and/or calcific deposits in the subacromial space make patients more predisposed for primary impingement.)

  • Acromioclavicular arthrosis (inferior osteophytes)

  • Coracoacromial ligament hypertrophy

  • Coracoid impingement

  • Subacromial bursal thickening and fibrosis

  • Prominent humeral greater tuberosity

  • Trauma (direct macrotrauma or repetitive microtrauma)

  • Overhead activity (athletic and nonathletic)

Secondary impingement

Causes of secondary impingement are as follows:

  • Rotator cuff overload/soft tissue imbalance

  • Eccentric muscle overload

  • Glenohumeral laxity/instability

  • Long head of the biceps tendon laxity/weakness

  • Glenoid labral lesions

  • Muscle imbalance

  • Scapular dyskinesia

  • Posterior capsular tightness

  • Trapezius paralysis


United States statistics

No documented information on the occurrence of shoulder impingement syndrome exists.

International statistics

From 23% to 38% of swimmers experience shoulder injuries within a 1-year period, and 23% of volleyball players have dominant shoulder pain during the season. Among elite handball players, up to 52% have current shoulder pain, and the weekly prevalence of significant shoulder injuries among these athletes is 12%.[3]

In the general population, subacromial impingement syndrome is responsible for up to 65% of all shoulder complaints.[4]

Functional Anatomy

The shoulder consists of 2 bones (humerus, scapula), 2 joints (glenohumeral, acromioclavicular), and 2 articulations (scapulothoracic, acromiohumeral) that are joined by several interconnecting ligaments and layers of muscles. Minimal bony stability in the shoulder permits a wide range of motion (ROM). Soft tissue structures are the major glenohumeral stabilizers. Static stabilizers consist of the articular anatomy, glenoid labrum, joint capsule, glenohumeral ligaments, and inherent negative pressure in the joint. Dynamic stabilizers include the rotator cuff muscles, long head of the biceps tendon, scapulothoracic motion, and other shoulder girdle muscles (eg, pectoralis major, latissimus dorsi, serratus anterior).

The rotator cuff consists of 4 muscles that control 3 basic motions, abduction, internal rotation, and external rotation. The supraspinatus muscle is responsible for initiating abduction, the infraspinatus and teres minor muscles control external rotation, and the subscapularis muscle controls internal rotation. The rotator cuff muscles provide dynamic stabilization to the humeral head on the glenoid fossa, forming a force couple with the deltoid to allow elevation of the arm. This force couple is responsible for 45% of abduction strength and 90% of external rotation strength.

The supraspinatus outlet is a space formed on the upper rim, humeral head, and glenoid by the acromion, coracoacromial arch, and acromioclavicular joint. This outlet accommodates passage and excursion of the supraspinatus tendon. Abnormalities of the supraspinatus outlet have been attributed as a cause of impingement syndrome and rotator cuff disease, though other causes have been discovered. Impingement implies extrinsic compression of the rotator cuff in the supraspinatus outlet space. Bigliani and associates discovered and described how variations in acromial size and shape can contribute to impingement.[5]

Cadaveric studies show 3 variations in acromion morphology, as follows: type 1 is flat, type 2 is curved, and type 3 is hooked anteriorly. Although the curved configuration was the most common (43% prevalence, compared to 17% flat and 40% hooked), the hooked configuration most strongly was associated with full-thickness rotator cuff tears. Other sites of impingement in the supraspinatus outlet space include the coracoacromial ligament (where thickening can occur) and the undersurface of the acromioclavicular joint (where osteophytes can form). The medial coracoid rarely is involved. These impingement sites in the supraspinatus outlet are compressed further when the humerus is placed in the forward-flexed and internally rotated position, forcing the greater tuberosity of the humerus into the undersurface of the acromion and coracoacromial arch.

Nonoutlet impingement also can occur. Causes may be loss of normal humeral head depression from either a large rotator cuff tear or weakness in the rotator cuff muscles from a C5/C6 neural segmental lesion or a suprascapular mononeuropathy. This condition also may occur because of thickening or hypertrophy of the subacromial bursa and rotator cuff tendons.

Sport-Specific Biomechanics

Overuse or repetitive microtrauma sustained in the overhead position may contribute to impingement and rotator cuff pathology. Shoulder pain and rotator cuff disease are common in athletes involved in sports requiring repetitive overhead arm motion (eg, swimming, baseball, volleyball, tennis).

Secondary impingement often is attributed to impingement, which seldom is mechanical in nature in young athletes. Rotator cuff disease in this population may be related to subtle instability, and, therefore, may be secondary to such factors as eccentric overload, muscle imbalance, glenohumeral instability, or labral lesions. This has led to the concept of secondary impingement, which is defined as rotator cuff impingement that occurs secondary to a functional decrease in the supraspinatus outlet space due to underlying instability of the glenohumeral joint.

Secondary impingement may be the most common cause in young athletes who frequently place large, repetitive overhead stresses on the static and dynamic glenohumeral stabilizers, resulting in microtrauma and attenuation of the glenohumeral ligamentous structures, which leads to subclinical glenohumeral instability. Such instability places increased stress on the dynamic stabilizers of the glenohumeral joint, including the rotator cuff tendons.

These increased demands may lead to rotator cuff pathology (eg, partial tearing, tendonitis). Furthermore, as the rotator cuff muscles fatigue, the humeral head translates anteriorly and superiorly, impinging upon the coracoacromial arch. This leads to rotator cuff inflammation. In these patients, treatment should address underlying instability.

The concept of glenoid impingement has been advanced as an explanation for partial-thickness tears in throwing athletes, particularly those involving the articular surface of the rotator cuff tendon. Such tears may occur in the presence of instability due to increased tensile stresses on the rotator cuff tendon from abnormal motion of the glenohumeral joint or increased forces on the rotator cuff necessary to stabilize the shoulder.

Arthroscopic studies of these patients note impingement between the posterior superior edge of the glenoid and the insertion of the rotator cuff tendon with the arm placed in the throwing position (abducted and externally rotated). Lesions were noted along the area of impingement at the posterior aspect of the glenoid labrum and articular surface of the rotator cuff. This concept is believed to occur most commonly in throwing athletes and must be considered when assessing for impingement.


In general, prognosis for prompt and correct diagnosis and treatment of shoulder impingement syndrome is good, and 60-90% of patients improve and are symptom-free with conservative treatment. Surgical outcomes are promising in patients who fail conservative therapy.


If shoulder impingement syndrome is not diagnosed and treated promptly and correctly, it can progress to rotator cuff degeneration and eventual tear. A study by Quinlan et al found that in patients treated conservatively for rotator cuff tendinopathy, the rates of progression to full or partial tear at 1-2 years, 2-5 years, and over 5 years between MRI scans were 32%, 37%, and 54%, respectively.[6]

Other complications may include progression to adhesive capsulitis, cuff tear arthropathy, and reflex sympathetic dystrophy. Complications also may result from surgery, injection, physical therapy, or medication. 

Patient Education

Patient education may improve the outcome if the patient is educated regarding avoidance of provocative activities, pathology, and proper shoulder arthrokinematics. Education also should stress proper warm-up techniques, specific strengthening techniques, and warning signs of early impingement. A proper home exercise program should be formulated and encouraged to prevent recurrence of symptoms.





Patients younger than 40 years - Usually glenohumeral instability, and acromioclavicular joint disease/injury

Patients older than 40 years - Consider glenohumeral impingement syndrome/rotator cuff disease and glenohumeral joint degenerative disease


Individuals at highest risk for shoulder impingement are laborers and those working in jobs that require repetitive overhead activity.

Athletes (eg, swimming, throwing sports, tennis, volleyball)

Athletic activity

Onset of symptoms in relation to specific phases of the athletic event performed

Duration and frequency of play

Duration and frequency of practice

Level of play (eg, little league, high school, college, professional)

Actual playing time (eg, starter, backup, bench player) and position played

Lack of periodization in training - Athlete participating in same overhead sport year-round


Onset: Sudden onset of sharp pain in the shoulder with tearing sensation is suggestive of a rotator cuff tear. Gradual increase in shoulder pain with overhead activities is suggestive of an impingement problem.

Chronicity of symptoms

Location: Pain usually is reported over the lateral, superior, anterior shoulder; occasionally refers to the deltoid region. Posterior shoulder capsule pain usually is consistent with anterior instability, causing posterior tightness.

Setting during which symptoms arise (eg, pain during sleep, in various sleeping positions, at night, with activity, types of activities, while resting)

Quality of pain (eg, sharp, dull, radiating, throbbing, burning, constant, intermittent, occasional)

Quantity of pain (on a scale of 0-10, 10 being the worst)

Alleviating factors (eg, change of position, medication, rest)

Aggravating factors (eg, change of position, medication, increase in practice, increase in play, change in athletic gear/foot wear, change in position played)

Functional symptoms - Patient changed mechanics (eg, throwing motion, swim stroke) to compensate for pain

Associated manifestations (eg, possibly chest pain, dizziness, abdominal pain, shortness of breath)

Provocative position: Pain with humerus in forward-flexed and internally rotated position suggests rotator cuff impingement. Pain with humerus in abducted and externally rotated position suggests anterior glenohumeral instability and laxity.

Other history

Inquire about previous or recent trauma, stiffness, numbness, paresthesias, clicking, weakness, crepitus of instability, and neck syndromes.

Physical Examination


Men should have their shirts off, and women should wear a tank top for the examination.

Visualize entire shoulder girdle and scapular area. Inspect for scapular winging (long thoracic nerve palsy) by having the patient perform a wall push-up.

Note muscle mass asymmetry/atrophy and bony asymmetry.

Active range of motion (AROM) is tested if possible. If not possible, passive range of motion (PROM) is performed, as follows:

  • Forward flexion (average range is 150-180°)

  • Abduction (average range is 150-180°)

  • External rotation (average range with arm in adduction is 30-60°)

  • External rotation (average range with arm in abduction is 70-90°)

  • Internal rotation (average range, which is measured by how high the patient can reach around the back with the ipsilateral thumb [ie, ipsilateral hip, T12, L5], is above T8)

  • Adduction (average range is 45°)

  • Extension (average range is 45°)

Note the following:

  • Stiffness with external/internal rotation is best tested with arm in 90° of abduction.

  • External and internal rotation are best tested in the supine position with the scapulothoracic articulation stabilized.

  • Most high-level pitchers have increased external rotation and decreased internal rotation in the pitching arm compared to the nonpitching arm. This may not be pathologic in the high-level athletic population.

  • A painful arc of motion may be experienced with elevation above the shoulder level in patients with impingement.


Palpate along the joints, noting the biceps tendons, supraspinatus and subscapularis tendons, and anterolateral corner of the acromion. Check for bony pain over anterior portion of acromion in region of potential os acromiale.

The entire shoulder girdle is palpated (noting tenderness, deformities, and atrophy) from acromioclavicular joint, clavicle, glenohumeral joint, scapula, scapulothoracic articulation, anterior/posterior shoulder capsule, supraspinous fossa, infraspinous fossa, and humerus (especially proximally).

Manual muscle testing

Concentrate on assessing the shoulder girdle muscles, especially external/internal rotation and abduction.

Supraspinatus may be isolated by having the patient rotate the upper extremity so that the thumbs are pointing toward the floor and apply resistance with the arms at 30° of forward flexion and 90° of abduction (called the supraspinatus isolation test or empty can test because the position assimilates emptying a can).

Pain is felt with tendonitis or partial injury to the supraspinatus tendon in the supraspinatus isolation test, but weakness also may be found accompanying partial-thickness or full-thickness disruption of the supraspinatus tendon.

Weakness also may be found with tendonitis, due to muscle inhibition from painful stimuli.

Special tests

Any test performed should compare both shoulders either to detect bilateral pathology or to establish a control for comparison with the affected shoulder.

  • Neer test: Forcefully elevate an internally rotated arm in the scapular plane, causing the supraspinatus tendon to impinge against the anterior inferior acromion.

  • Hawkins-Kennedy test: Forcefully internally rotate a 90° forwardly flexed arm, causing the supraspinatus tendon to impinge against the coracoacromial ligamentous arch. Note: Pain and a grimacing facial expression indicate impingement of the supraspinatus tendon, indicating a positive Neer/Hawkins impingement sign.

  • Impingement test: Inject 10 mL of 1% lidocaine solution into the subacromial space. Repeat testing for an impingement sign. Elimination or significant reduction of pain constitutes a positive impingement test.

  • Drop arm test: The patient places the arm in maximum elevation in the scapular plane and then lowers it slowly (the test can be repeated following subacromial injection of lidocaine). Sudden dropping of the arm suggests a rotator cuff tear.

  • Supraspinatus isolation test/empty can test: The supraspinatus may be isolated by having the patient rotate the upper extremity so that the thumbs are pointing to the floor and apply resistance with the arms in 30° of forward flexion and 90° of abduction (assimilates emptying of a can). This test is positive when weakness is present (compared to the unaffected side), suggesting disruption of the supraspinatus tendon.

  • A systematic review and meta-analysis used the PRISMA (preferred reporting items for systematic reviews and meta-analyses) guidelines, and 10 studies met the criteria to be included in the final analysis and review. The Hawkins-Kennedy test, Neer sign, and empty can test were determined to be best to negate the diagnosis of impingement. A negative Neer sign reduced the probability of subacromial impingement from 45% to 14%. The drop arm test and lift-off test were thought to be more useful for confirming the diagnosis of impingement if the test results were positive.[7]

Tests for instability

Tests for instability are as follows:

  • Sulcus sign: Grasp the patient's elbow and apply inferior traction. Dimpling of the skin subjacent to the acromion (the sulcus sign) indicates inferior humeral translation, suggesting multidirectional instability.

  • Apprehension test: Most effectively performed with the patient in the supine position stabilizing the scapula. Gently bring the affected arm into an abducted and externally rotated position. Patient apprehension and guarding by not allowing further motion by the examiner denotes a positive test that is consistent with anterior shoulder instability.

  • Relocation test: Usually, this test is performed in conjunction with the apprehension test. After putting patient in an apprehensive position, apply a posteriorly directed pressure to the anterior proximal humerus, simulating a relocation of the glenohumeral joint that presumably was dislocated partially from the apprehension test. Posterior translation of the humeral head on the glenoid may be felt. A positive test may be noted when the patient becomes at ease with application of pressure on the anterior proximal humerus, suggesting anterior shoulder instability.

Other tests may be performed on the shoulder to rule out other pathology affecting the biceps tendon, glenoid labrum, cervical spine, sternoclavicular joint, acromioclavicular joint, and scapulothoracic joint. A survey of other joint ROM also should be performed to assess for generalized ligamentous laxity.

Neurovascular examination

To complete the shoulder examination, a full neurologic examination must be performed, along with assessment of all upper extremity vascular pulses.

Neurologic examination should include all neurologic segments from C5 through T1 myotomes (dermatomes with the corresponding stretch reflexes).





Imaging Studies

Standard radiographic studies (4 views to rule out glenohumeral/acromioclavicular arthritis)

The following are the standard radiographic studies:

  • Anterior-posterior (AP) view of the glenohumeral joint

  • Internal rotation view of the humerus with 20° upward angulation to show acromioclavicular joint

  • Axillary view is most useful to rule out subtle signs of instability (eg, glenoid avulsion, Hill-Sachs lesion) and to visualize presence of an os acromiale.

  • Supraspinatus outlet view is most useful to assess the supraspinatus outlet space. If the space is less than 7 mm, then an increased risk for impingement syndrome exists. Also, assess morphology of the acromion (hooked acromion more at risk for impingement).

MRI is considered the imaging study of choice for shoulder pathology.

Advantages include the following:

  • Noninvasive

  • No radiation

  • Able to detect intrasubstance tendon degeneration or partial rotator cuff tears

  • Able to detect inflammation, edema, hemorrhage, or scarring

  • Able to be used with an intra-articular contrast agent (eg, gadolinium), improving the MRI ability to detect partial rotator cuff tears

Disadvantages include the following:

  • Not able to accommodate patients with claustrophobia

  • Not able to accommodate larger patients

  • Not able to accommodate patients with pacemakers or other metal implants or particles

  • Dependent on quality of the MRI machine

  • Dependent on skill of technician performing the imaging and the radiologist interpreting the images

  • Expensive


Dye is injected into the glenohumeral joint and postinjection radiographs are filmed to assess the integrity of the glenohumeral joint.

This study frequently is used in evaluating rotator cuff tears.

If dye escapes out of the joint and into the subacromial space, it is diagnostic of a full-thickness rotator cuff tear.

Advantages include the following:

  • Can be used in conjunction with CT scan or MRI to evaluate intra-articular pathology (eg, Bankart tears)

  • Low cost

Disadvantages include the following:

  • Size of the tears cannot be quantified.

  • Patient is exposed to radiation.

  • Contrast dye exposure

  • Invasive procedure

Diagnostic arthroscopy includes the following:

  • Minimally invasive visual surgical procedure to assess shoulder pathology

  • Able to visualize and assess majority of shoulder lesions

  • May give the patient and physician a chance to diagnose and treat the pathology in one procedure

Workup for other more systemic processes may be included as clinically indicated.



Acute Phase

Rehabilitation Program

Physical Therapy

The goals of the acute phase are to relieve pain and inflammation, prevent muscle atrophy without exacerbating the pain, reestablish nonpainful range of motion, and normalize the arthrokinematics of the shoulder complex. This includes a period of active rest, eliminating any activity that may cause an increase in symptoms.

Range-of-motion exercises may include pendulum exercises and symptom-limited, active-assisted range-of-motion exercises. Joint mobilization may be included with inferior, anterior, and posterior glides in the scapular plane. Strengthening exercises should be isometric in nature and work on the external rotators, internal rotators, biceps, deltoid, and scapular stabilizers (ie, rhomboids, trapezius, serratus anterior, latissimus dorsi, pectoralis major). Neuromuscular control exercises also may be initiated.

Modalities that also may be used as an adjunct include cryotherapy, transcutaneous electrical nerve stimulation, high-voltage galvanic stimulation, ultrasound, phonophoresis, or iontophoresis.

Patient education regarding activity; pathology; and the avoidance of overhead activity, reaching, and lifting is particularly important for this acute phase. The general guidelines to progress from this phase are decreased pain or symptoms, increased range of motion, painful arc in abduction only, and improved muscular function.

A systematic review and meta-analysis by Steuri et al found that although the quality of evidence was low, exercise interventions should be considered for all patients with shoulder impingement symptom.[8]

A study of 97 patients on the waiting list for subacromial decompression reported that an exercise program that included eccentric exercises for the rotator cuff and a combination of concentric and eccentric exercises for scapula stabilizers, lowered surgical rate and resulted in decreased symptoms. These results were also maintained on 1 year follow-up.[9]

Extracorporeal shock wave therapy has also been used in subacromial impingement syndrome. A study by Santamato et al indicated that a combination of extracorporeal shock wave therapy and isokinetic exercise is more effective than shock wave therapy alone for treatment of the condition.[10]

A study by Keenan et al indicated that kinesiology taping in subacromial shoulder impingement syndrome neither improves nor impairs shoulder strength, shoulder proprioception, or scapular kinematics.[11]  Similarly, a meta-analysis by Araya-Quintanilla et al found that kinesiotaping was no more effective than other interventions for reducing shoulder pain intensity and improving function and range of motion in persons with subacromial impingement syndrome.[12]

Subacromial injection

During the acute to subacute phase, when pain and inflammation are predominant, a subacromial injection may be diagnostic and therapeutic as an adjunct to a rehabilitation program. Injection of 10 mL of 1% lidocaine solution (without epinephrine) into the subacromial space should relieve shoulder pain if pain and inflammation truly is originating from the supraspinatus outlet/subacromial space. Adding a low dose intermediate-acting injectable corticosteroid may provide a therapeutic effect. Betamethasone, triamcinolone, and methylprednisolone commonly are used. One mL of any of these available injectable corticosteroids mixed with 9 mL of 1% lidocaine solution (without epinephrine) commonly is used.

One clinical trial found that subacromial injection of corticosteroid provided effective relief of symptoms and normalized function in patients with impingement syndrome. The authors noted that ultrasound-guided injections were not significantly better than a standard clinical injection when performed by an experienced individual. Injection accuracy, measured by post-injection MRI, was unexpectedly low for both blind and ultrasound-guided techniques (65% versus 70% respectively).[13]

A Cochrane review concluded that there is currently insufficient evidence to recommend the use of platelet-rich therapy (PRT) preparations for the treatment of impingement syndrome.[14]

Technique: Have the patient sit with the arm hanging by his/her side to distract the humerus from the acromion. Identify the lateral edge of the acromion. Insert the needle at midpoint of acromion and angle slightly upward under the acromion to full length. Slowly withdraw needle while simultaneously injecting fluid in a bolus wherever resistance is not present. Continue aspirating before injecting. Sometimes a swelling caused by fluid is visible around the edge of the acromion. Occasionally, calcification occurs within the bursa and hard resistance is encountered. In this case, aspiration and infiltration with a large bore needle and local anesthetic may be helpful. Failure of this injection may necessitate surgical evaluation.

Aftercare: Patient is informed that a local reaction may occur to the corticosteroid in the next 24-72 hours once the effect of the lidocaine wears off. If this happens, the patient is recommended to apply ice (wrapped in a towel) to the affected shoulder 20 minutes on and 20 minutes off, 3 times at the beginning and end of the day. Relief of pain after one injection is usual, but the patient must be advised to maintain correct posture with retraction and depression of the shoulder and to avoid the painful arc of elevation for 1 week. Patient may resume a symptom-limited therapy program in the first week postinjection, and then resume the full course.

Adverse effects of medications may be minimized when dosed as recommended. Adverse reactions are uncommon; however, they may occur, even when the injection is administered correctly. The clinician and patient must be educated about possible reactions, and the clinician must know how to manage any related complications. Absolute contraindications include documented allergy to any corticosteroid or local anesthetics. Relative contraindications include diabetes, hypertension, immunosuppression, cardiac arrhythmias, and heart blocks.

Adverse effects of injectable corticosteroids

  • Systemic effects include flushing, menstrual irregularity, impaired glucose tolerance, osteoporosis, psychological disturbance, steroid arthropathy, steroid myopathy, and immunosuppression.

  • Local effects include postinjection flare.

Adverse effects of local anesthetics

  • Usually, adverse effects are due to overdose and allergic reactions, which definitively can be minimized by double-checking the administered dose and inquiring about and checking on medication records for medication allergies.

  • Effects of overdose and allergic reactions may be catastrophic and may include cardiac, respiratory, and cerebral compromise.

Adverse reaction to the injection: Occasionally, a patient may experience a vasovagal reaction (faint) due to pain, apprehension, or needle phobia. In such cases, treatment should consist of the following:

  • Lie the patient down in the supine position. Elevate the patient's legs.

  • Strongly reassure patient that recovery is fast.

  • If patient briefly loses consciousness, protect the airway and give oxygen at 35% concentration.

High-intensity laser therapy

Santamato et al evaluated the short-term effects between high-intensity laser therapy (HILT) and sonographic therapy in 70 patients with subacromial impingement syndrome.[15] The patients were randomized to receive 10 treatments of HILT or ultrasound over 2 consecutive weeks. After 2 weeks, patients in the HILT group showed statistically significant improvements in pain reduction, articular movement, functionality, and muscle strength as measured by 3 outcome measure scores.[15] However, further investigation is warranted, as the study was limited by its small size, lack of control or placebo groups, and follow-up period.

Surgical Intervention

In general, conservative measures are continued for at least 3-6 months or longer if the patient is improving, which is usually the case in 60-90% of patients. If the patient remains significantly disabled and has no improvement after 3 months of conservative treatment, the clinician must seek further diagnostic work-up, as well as reconsider other etiologies or refer for surgical evaluation.

Appropriate surgical referrals are patients with subacromial impingement syndrome refractory to 3-6 months of appropriate conservative treatment. Surgery may be particularly beneficial in patients with full unrestricted PROM, positive response to injection of lidocaine into the subacromial space, a type III acromion having a large subacromial spur and those in whom changes are noted in the rotator cuff tendon on MRI scanning.

In a systematic review, Dorrestijn et al attempted to compare the effects of conservative and surgical treatment for subacromial impingement syndrome with regard to improvement of shoulder function and reduction of pain.[16] Of 4 randomized controlled trials that met the investigators' criteria, 2 were of medium methodologic quality and 2 were of low methodologic quality, but there were no differences in outcome between the treatment groups. Their findings led Dorrestijn et al to note the scarcity of high-quality randomized controlled trials does not allow conclusive evidence for differences in pain outcomes and shoulder function in conservatively and surgically treated patients with subacromial impingement syndrome.[16]

In another study, Ketola et al found no evidence that arthroscopic acromioplasty provides any additional value in the treatment of shoulder impingement syndrome.[17] In a randomized, controlled trial in 140 patients, follow-up at 24 months showed no statistically significant difference in self-reported pain between patients who received only a supervised exercise program and those who underwent acromioplasty followed by an exercise program. In addition, acromioplasty added considerably to the cost of treatment.[17] A review article found no significant difference between outcomes of formal bony subacromial decompression compared with an isolated subacromial bursectomy.[18]

Surgical evaluation

Initial examination under anesthesia (general anesthesia vs. regional block) and diagnostic arthroscopy

Evaluation of shoulder ROM and stability

In patients with limited motion, manipulation of the shoulder is performed. Diagnostic arthroscopy also may be performed, but arthroscopic subacromial decompression is generally not performed in patients with significant preoperative stiffness due to the increased risk of postoperative adhesive capsulitis.

Document any instability.

Arthroscopic evaluation

Particular attention is directed to the rotator cuff, especially the supraspinatus tendon near its insertion onto the greater tuberosity

Visualize the subscapularis tendon.

Assess for labral pathology or changes suggesting glenohumeral instability.

A partial tearing of the supraspinatus tendon along its articular surface is a common finding in symptomatic throwing athletes. The fragmented and torn tissue is debrided, leaving all intact rotator cuff tendon. This allows a more accurate determination of the size and thickness of the tear on the articular side of the rotator cuff and may help reduce symptoms of catching and pain.

Following glenohumeral arthroscopy, the bursal side of the rotator cuff is then evaluated with arthroscopy

The bursal surface of the rotator cuff is assessed for evidence of fraying as well as the amount of clearance between the anterior inferior acromion and the supraspinatus tendon.

Also noted are any signs of fraying or wear changes on the undersurface of the coracoacromial ligament.

If no evidence of rotator cuff disruption is noted, the coracoacromial ligament is smooth with adequate space between the anterior inferior acromion and rotator cuff, then the diagnosis of subacromial impingement is unlikely. In this case, subacromial decompression is not performed.

In case of a small partial-thickness rotator cuff tear on the articular surface, without evidence of impingement, only glenohumeral debridement of this tear is performed. However, if the patient has changes suggestive of impingement syndrome, arthroscopic subacromial decompression (acromioplasty- resection of the anterior inferior portion of the acromion) is performed as well.

If following subacromial decompression, a rotator cuff repair is necessary, it may be continued with arthroscopic assistance or it may be necessary to convert the rotator cuff repair to an open procedure.

Postoperative care

Postoperatively, a radiograph (supraspinatus outlet view) should be obtained to document the adequacy of the subacromial decompression. The appearance on this radiographic view should be of a type I acromial arch without any residual spurring.

Following subacromial decompression, the patient is placed in a sling but is encouraged to remove the sling when comfortable and begin AROM and PROM exercises. When pain has decreased significantly and ROM has returned toward normal, a program of strengthening similar to the previously mentioned conservative management may be instituted. Patients cannot begin sports-specific activities until they have full AROM in the operated shoulder and normal strength, generally a time course of approximately 3-4 months.

Surgical outcome

Results are generally good for properly selected middle-aged patients with evidence of impingement on history and physical examination and at the time of arthroscopy.

General consensus in the literature is that arthroscopic subacromial decompression results in a good return to the previous level of function in approximately 85-90% of patients; however, results are generally poor in young high-performance athletes who participate in overhead activities.

Evidence in the literature reveals the limited utility of isolated subacromial decompression for the treatment of recalcitrant shoulder impingement syndrome.[19]

Recovery Phase

Rehabilitation Program

Physical Therapy

Initial goals of this phase are to normalize ROM and shoulder arthrokinematics, perform symptom-free daily activities, and improve neuromuscular control and muscle strength. ROM exercises should progress to active exercises in all planes and self-stretches, concentrating on the joint capsule, especially the posterior capsule.

Strengthening exercises should include isotonic dumbbell resistance exercises with the supraspinatus, internal rotators, external rotators, prone extension, horizontal abduction, forward flexion to 90°, upright abduction to 90°, shoulder shrugs, rows, push-ups, press-ups, and pull-downs to strengthen the scapular stabilizers. Joint mobilization and neuromuscular reeducation also should be maintained. Upper extremity ergometry exercises, trunk exercises, and general cardiovascular conditioning should be maintained for endurance. Use of modalities may be continued if necessary. Guidelines to advance from this phase are full pain-free ROM and when manual muscle strength testing is 70% of the contralateral side.

The final goal of this phase is to get the athlete back to throwing and should include improving strength, power and endurance, and sports-specific neuromuscular control. Emphasis is placed on high-speed, high-energy strengthening exercises, and eccentric exercises in diagonal patterns. Continue isotonic strengthening with increased resistance in all planes, allowing resistance in the throwing position, 90° of abduction, and 90° of external rotation. Initiate plyometrics, sports-specific exercises, proprioceptive neuromuscular facilitation, and isokinetic exercises.

Maintenance Phase

Rehabilitation Program

Physical Therapy

The goal of this phase is to maintain a high level of training and prevent reoccurrence. Emphasis is placed on longer, more intense workouts and proper arthrokinematics of the shoulder. Analysis and modification of techniques and mechanics may reexacerbate symptoms. Make refinements in intensity and coordination. Patient education again is reemphasized, maintaining proper mechanics, strength, and flexibility and understanding the pathology. The patient also should have a good understanding of the warnings signs of early impingement and continue with a home exercise program with proper warm-up and strengthening techniques.

Return to Play

Return to play is restricted until full pain-free ROM is restored, both rest and activity-related pain are eliminated, and provocative impingement signs are negative. Isokinetic strength testing must be 90% compared to the contralateral side. When the patient is symptom-free, resuming activities is gradual, first during practice to build up endurance while working on modified techniques/mechanics, and then in simulated game situations. The athlete should continue flexibility and strengthening exercises after returning to his/her sport to prevent recurrence.


Primary prevention should be considered an integral part in the treatment of impingement syndrome. Education of patients at risk can do much to circumvent the development of impingement syndrome. Athletes, particularly those involved in throwing and overhead sports, and laborers with repetitive shoulder stress should be instructed in proper warm-up techniques, specific strengthening techniques, and have a good understanding of the warning signs of early impingement.



Medication Summary

During the acute and subacute phases of shoulder impingement syndrome, it is appropriate to use a short course of nonsteroidal anti-inflammatory drugs (NSAIDs) for analgesic and anti-inflammatory effects as an adjunct to the therapy program and other treatment modalities. Choices in this drug classification are extensive, so only selected examples are discussed. Patient response to differing NSAIDs may vary. For information on the full array of NSAIDs available, dosing, and schedule, please refer to the latest edition of the Physician's Desk Reference.

The major mechanism of action of NSAIDs is inhibition of the synthesis of prostaglandin (PG), specifically PGE2 via blocking of cyclo-oxygenase (COX), which is the enzyme that converts arachidonic acid into PG. PGs lower the threshold to noxious stimuli by sensitizing the nociceptors to the actions of other noxious endogenous substances (eg, bradykinin, histamine, substance P, serotonin). PGE2 causes pain and inflammation in soft tissues, is cytoprotective in the GI tract by increasing secretion of mucus and bicarbonates and decreasing secretion of gastric acids and digestive enzymes, and enhances renal salt and water excretion in the renal system by acting as a vasodilator of small arterial blood vessels.

The COX pathway is subdivided into COX1, which is responsible for PGE2 production in the GI tract and kidneys, and, COX2, which is responsible for inflammatory PG synthesis during soft tissue injury. NSAIDs serve as competitive inhibitors of COX activity, and either selectively inhibit the COX2 enzymes or nonselectively inhibit both COX1 and COX2 enzymes, making the nonselective NSAIDs potentially ulcerogenic and renal toxic.

All NSAIDs have similar adverse drug reactions, as follows:

  • Hepatotoxicity: Liver function profile must be monitored in patients taking NSAIDs, periodically every 1-2 months, especially in high-risk individuals.

  • Renal toxicity: Renal function profile must be monitored periodically every 1-2 months, especially in high-risk individuals.

  • GI toxicity: Symptoms may include nausea, diarrhea, acid reflux, and periumbilical cramping. The physician may consider administering NSAIDs in conjunction with GI protective medications (eg, misoprostol, omeprazole, H2-blockers) and instruct patients to take NSAIDs with food. If GI symptoms persist for more than 2 weeks or if the patient has evidence of complication (eg, iron deficiency anemia, GI bleeding, unexplained weight loss, dysphagia), endoscopic evaluation is indicated

  • Aplastic anemia: Monitor CBC, especially platelets, periodically for 1-2 months.

  • Anaphylaxis: Inquire about and check medical records for history of allergic reactions.

Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

Class Summary

NSAIDs are the most widely used drugs in the world, exhibiting anti-inflammatory, antipyretic, and analgesic activities. They primarily are used for treating inflammatory conditions that are musculoskeletal in origin. Numerous drugs are available in this category and all have similar drug profiles.

Ibuprofen (Ibuprin, Advil, Motrin)

An arylpropionic acid, it is the prototypical NSAID and causes less epigastric pain, GI occult blood loss, and less hepatotoxicity. Mostly indicated for rheumatoid arthritis and osteoarthritis for mild to moderate pain. Compared to other available NSAIDs, it has a short half-life.

Diclofenac sodium/potassium (Voltarem, Cataflam)

Chemical composition is heteroaryl acetic acid with a short half-life. The delayed-release enteric-coated form is diclofenac sodium and the immediate release form is diclofenac potassium. Both primarily are indicated for rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis. Can cause hepatotoxicity; hence liver enzymes should be monitored in the first 8 weeks of treatment. Has a relatively low risk for bleeding GI ulcers.

Etodolac (Lodine, Lodine XL)

Indole NSAID with intermediate half-life indicated for rheumatoid arthritis and osteoarthritis. The short-acting form is approved for analgesic use comparable to aspirin/Tylenol (with codeine). Lower risk of GI complications and is especially well tolerated by elderly patients.

Naproxen (Aleve, Anaprox, Naprelan, Naprosyn)

Probably most potent arylpropionic acid with a long half-life. Indicated for rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, juvenile arthritis, acute gout, and mild to moderate pain. Comes in a controlled release form (also used for acute pain) and an enteric-coated form (not used for acute pain).

Oxaprozin (Daypro)

Arylpropionic acid with 40-50 h half-life. Can be administered qd.

Nabumetone (Relafen)

An alkanone NSAID with long half-life (24 h) that can be administered qd. Lower risk of GI complications and is indicated for rheumatoid arthritis and osteoarthritis.

Piroxicam (Feldene)

Enolic acid with a long half-life (50 h) that can be administered qd. Indicated for rheumatoid arthritis and osteoarthritis. Has high GI toxicity, greater than ASA.

Cyclooxygenase-2 (COX-2) Inhibitors

Class Summary

Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.

Celecoxib (Celebrex)

Selective COX-2 inhibitor, NSAID approved by the FDA on 12/31/98. Indicated for osteoarthritis and rheumatoid arthritis and moderate to severe pain. Potentially presents less GI complications and platelet aggregation problems than nonselective COX-inhibitor NSAIDs. Renal complications are comparable. Celecoxib has a sulfonamide chain and is primarily dependent upon cytochrome P450 enzymes (a hepatic enzyme) for metabolism.

Analgesic Combinations

Class Summary

May offer improved relieve over either agent alone.

Tramadol 37.5 mg and acetaminophen 325 mg (Ultracet)

Centrally acting pain medication that combines tramadol hydrochloride with acetaminophen. Clinical trials demonstrated that the combination offers better pain relief over either medication alone. Indicated for the short-term (5 d or less) management of acute pain.


Questions & Answers


What is rotator cuff impingement?

Which patients are at highest risk for shoulder impingement syndrome?

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Which special tests are performed in the physical exam of suspected shoulder impingement syndrome?

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What are the differential diagnoses for Shoulder Impingement Syndrome?


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What is included in treatment during the acute phase of shoulder impingement syndrome?

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What is the prognosis following arthroscopic subacromial decompression for shoulder impingement syndrome?

What is the role of physical therapy during the recovery phase of shoulder impingement syndrome treatment?

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What is the role of NSAIDs in the treatment of shoulder impingement syndrome?

What are possible adverse effects of NSAIDs for treatment of shoulder impingement syndrome?

Which medications in the drug class Analgesic Combinations are used in the treatment of Shoulder Impingement Syndrome?

Which medications in the drug class Cyclooxygenase-2 (COX-2) Inhibitors are used in the treatment of Shoulder Impingement Syndrome?

Which medications in the drug class Nonsteroidal Anti-inflammatory Drugs (NSAIDs) are used in the treatment of Shoulder Impingement Syndrome?