Supraspinatus Tendonitis

Updated: Dec 03, 2018
Author: Thomas M DeBerardino, MD; Chief Editor: Sherwin SW Ho, MD 


Practice Essentials

Supraspinatus tendonitis is often associated with shoulder impingement syndrome. The common belief is that impingement of the supraspinatus tendon leads to supraspinatus tendonitis (inflammation of the supraspinatus/rotator cuff tendon and/or the contiguous peritendinous soft tissues), which is a known stage of shoulder impingement syndrome (stage II) as described originally by Neer in 1972.[1]

The causes of supraspinatus tendonitis can be broken down into extrinsic and intrinsic factors.[2, 3]  Extrinsic factors are further broken down into primary impingement, which is a result of increased subacromial loading, and secondary impingement, which is a result of rotator cuff overload and muscle imbalance. In athletes whose sport involves stressful repetitive overhead motions, a combination of causes may be found.



United States

Supraspinatus tendonitis is a common cause of shoulder pain in athletes whose sports involve throwing and overhead motions.

Functional Anatomy

The shoulder consists of 2 bones (ie, humerus, scapula), 2 joints (ie, glenohumeral, acromioclavicular), and 2 articulations (ie, scapulothoracic, acromiohumeral). Several interconnecting ligaments and layers of muscles join these bones. The relative lack of bony stability in the shoulder permits a wide range of motion. Soft tissue structures are the major glenohumeral stabilizers.

The static stabilizers consist of the articular anatomy, glenoid labrum, joint capsule, glenohumeral ligaments, and inherent negative pressure in the joint. The dynamic stabilizers include the rotator cuff muscles, long head of the biceps tendon, scapulothoracic motion, and other shoulder girdle muscles such as the pectoralis major, latissimus dorsi, and serratus anterior.

The rotator cuff consists of 4 muscles, which control 3 basic motions: abduction, internal rotation, and external rotation. The supraspinatus muscle is responsible for initiating abduction, the infraspinatus and teres minor for controlling external rotation, and the subscapularis for controlling 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. It is responsible for 45% of abduction strength and 90% of external rotation strength.

The supraspinatus outlet is a space formed by the acromion, coracoacromial arch, and acromioclavicular joint on the upper rim and the humeral head and glenoid below. It accommodates passage and excursion of the supraspinatus tendon. Abnormalities of the supraspinatus outlet have been identified as a cause of impingement syndrome and rotator cuff tendonitis.

Impingement implies extrinsic compression of the rotator cuff in the supraspinatus outlet space. Bigliani and associates discovered and described that variations in acromial size and shape can contribute to impingement. From cadaveric studies, 3 different variations in the morphology of the acromion are described. Type I is flat, type II is curved, and type III is anteriorly hooked. Although the curved configuration is the most common (43% prevalence, compared with 17% for flat and 40% for hooked), the hooked configuration is associated most strongly with rotator cuff pathology.

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. Only rarely is the medial coracoid 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 can also occur. The causes may be loss of normal humeral head depression either from a large rotator cuff tear or weakness of the rotator cuff muscles from a C5/C6 neural segmental lesion or a suprascapular mononeuropathy. Another way this may occur is with 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 tendonitis. Shoulder pain and rotator cuff tendonitis are common in athletes involved in sports requiring repetitive overhead arm motion (eg, swimming, baseball, tennis).

Secondary impingement

Supraspinatus tendonitis is often attributed to impingement, which is seldom mechanical in athletes. Rotator cuff tendonitis in this population may be related to subtle instability and therefore may be secondary to such factors as eccentric overload, muscle imbalance, and 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 use overhead motions and who frequently place repetitive large stresses on the static and dynamic glenohumeral stabilizers, resulting in microtrauma and attenuation of the glenohumeral ligamentous structures and leading to subclinical glenohumeral instability. Such instability places increased stress on the dynamic stabilizers of the glenohumeral joint, including the rotator cuff tendon. These increased demands may lead to rotator cuff pathology such as partial tearing or tendonitis, and, as the rotator cuff muscles fatigue, the humeral head translates anteriorly and superiorly, impinging on the coracoacromial arch, which leads to rotator cuff inflammation. In these patients, treatment should be directed at the underlying instability.

Glenoid impingement

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

Arthroscopic studies of these patients have noted 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 are 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 and rotator cuff tendonitis.


A study by Millar et al suggested proinflammatory cytokines may have a role in supraspinatus tendinopathy.[4] The investigators used custom micro-arrays to assess rat supraspinatus tendinopathy produced by running overuse. In addition, samples of torn supraspinatus tendon and matched intact subscapularis tendon from patients undergoing shoulder surgery for rotator cuff tears, as well as control samples of subscapularis tendon from 10 individuals with normal rotator cuffs undergoing arthroscopic shoulder stabilization, were collected and examined with semiquantitative reverse transcription polymerase chain-reaction (RT-PCR) and immunohistochemistry.[4] The presence of significant upregulation of proinflammatory cytokines and apoptotic genes was found in the rat samples (P = 0.005) as well as in the supraspinatus and subscapularis tendons obtained from the patients with rotator cuff tears (P = 0.0008).




See the list below:

  • Age

    • Younger than 40 years: It is usually glenohumeral instability. The cause is acromioclavicular joint disease or injury.

    • Older than 40 years: Consider glenohumeral impingement syndrome or rotator cuff tendonitis. Additionally, consider degenerative joint disease of the glenohumeral joint.

  • Occupation

    • Laborers and persons with jobs that require repetitive overhead activity (most at risk).

    • Athletes (eg, swimmers, those participating in throwing sports, tennis players, volleyball players)

  • Athletic activity

  • Onset of symptoms related to specific phases of the athletic event performed

  • Duration and frequency of play

  • Duration and frequency of practice

  • Level of play (Little League [elementary school], middle school, high school, college, professional)

  • Actual playing time (starter, backup, bench player)

  • Position played

  • Symptom onset

    • Sudden onset of sharp pain in the shoulder with tearing sensation - More suggestive of a rotator cuff tear

    • Gradual increase in shoulder pain with overhead activities - More suggestive of an impingement problem

  • Chronicity of symptoms

  • Location of symptoms (ie, pain)

    • Usually lateral, superior, anterior shoulder; occasionally referred to deltoid region

    • Posterior shoulder capsule - Usually consistent with anterior instability causing posterior tightness

  • Setting during which symptoms appear (eg, pain during sleep or various sleeping positions, at night, with activity, types of activities, at rest)

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

  • Severity of pain (ie, on a scale of 1-10, with 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, change in position played)

  • Associated manifestations (eg, chest pain, dizziness, abdominal pain, shortness of breath) - May indicate a more ominous problem than supraspinatus tendonitis

  • Provocative positions

    • Pain with humerus in forward flexed and internally rotated position - Suggestive of rotator cuff impingement

    • Pain with humerus in abducted and externally rotated position - Suggestive of anterior glenohumeral instability and laxity

  • Other history - Previous or recent trauma, stiffness, numbness, paresthesias, clicking, catching, weakness, crepitus, symptoms of instability, neck symptoms


See the list below:

  • Inspection

    • Men should wear no shirt; women are instructed to wear a tank top to the visit.

    • Visualize the entire shoulder girdle and scapular area, noting muscle mass asymmetry/atrophy or bony asymmetry.

  • Active range of motion:

    • Test this if possible; if not, then test passive range of motion.

    • Test forward flexion. The average range is 150-180°.

    • Test abduction. The average range is 150-180°.

    • Test external rotation. The average range with the arm in adduction is 30-60°, and the average range with the arm in abduction is 70-90°.

    • Test internal rotation. The average range is measured by how high the patient can reach up his or her back with the ipsilateral thumb (ie, ipsilateral hip, T12, L5). The average range is above T8.

    • Test adduction. The average range is 45°.

    • Test extension. The average range is 45°.

    • Note that stiffness with external/internal rotation is best tested with the arm in 90° of abduction. Also, for an optimal evaluation, test external and internal rotation in the supine position with the scapulothoracic articulation stabilized. Moreover, most high-level pitchers have increased external rotation and decreased internal rotation in the pitching arm compared with the nonpitching arm. However, the overall absolute arc of motion when measured in degrees is usually equal. This may not be pathologic in the high-level athletic population. Finally, a painful arc of motion may be experienced with elevation above the shoulder level in patients with impingement (typically 80-150°).

  • Palpation

    • Areas that are palpated include the joints, biceps tendons, supraspinatus and subscapularis tendons, and anterolateral corner of the acromion.

    • The entire shoulder girdle is palpated (noting tenderness, deformities, or atrophy) from the 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 the shoulder girdle muscles (especially external and internal rotation, abduction).

    • The supraspinatus may be isolated by having the patient rotate the upper extremity so that the thumbs are away from the floor and resistance is applied with the arms at 30° of forward flexion and 90° of abduction.

    • Note that pain is felt with tendonitis or partial injury to the supraspinatus tendon with the supraspinatus isolation test, but weakness can also be found accompanying partial- or full-thickness disruption of the supraspinatus tendon. Also, weakness may be found with tendonitis because of muscle inhibition from the pain stimulus.

  • Special tests (impingement signs)

    • For the Neer test, the examiner forcefully elevates an internally rotated arm in the scapular plane, causing the supraspinatus tendon to be impinged against the anterior inferior acromion.

    • For the Hawkins-Kennedy test, the examiner forcefully internally rotates a 90° forwardly flexed arm, causing the supraspinatus tendon to be impinged against the coracoacromial ligamentous arch. Pain and a grimacing facial expression indicate impingement of the supraspinatus tendon, and this is a positive Neer/Hawkins-Kennedy impingement sign.

    • For the impingement test, the examiner injects 10 mL of a 1% lidocaine solution into the subacromial space and then repeats the tests for the impingement sign. Elimination or significant reduction of pain constitutes a positive impingement test result.

    • With the 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.

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

  • Tests for instability

    • To elicit the sulcus sign, the examiner grasps the patient's elbow and applies inferior traction. Dimpling of the skin subjacent to the acromion (the sulcus sign) indicates inferior humeral translation, which suggests multidirectional instability.

    • The apprehension test is performed most effectively with the patient supine, stabilizing the scapulae. The examiner gently brings the affected arm into an abducted and externally rotated position. The patient's apprehension and guarding by not allowing further motion by the examiner denotes a positive test result, which is consistent with anterior shoulder instability.

    • The relocation test is usually performed in conjunction with the apprehension test. After placing the patient in an apprehensive position, posteriorly directed pressure is applied to the anterior proximal humerus, simulating a relocation of the glenohumeral joint that was presumably partially dislocated from the apprehension test. The adept examiner may feel posterior translation of the humeral head on the glenoid. A positive test result is when the patient's apprehension is relieved by the application of pressure on the anterior proximal humerus, which suggests anterior shoulder instability.

  • Note: Any tests completed should compare both shoulders in order to detect bilateral pathology or have a control for comparison with the affected shoulder.

  • Other tests: These should be performed during the shoulder examination 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 range of motion should also be performed to assess for generalized ligamentous laxity.

  • Neurovascular examination

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

    • The neurologic examination should include all neurologic segments from C5 through T1 myotome and dermatome, with the corresponding stretch reflexes.

    • Lewis et al demonstrated the presence of neovascularity in individuals with a clinical diagnosis of rotator cuff tendinopathy and, to a lesser extent, in asymptomatic shoulders. Twenty patients (mean age, 50.2 y; range 32-69 y) with a clinical diagnosis of unilateral rotator cuff tendinopathy received a clinical examination then underwent bilateral grey scale and color Doppler ultrasound assessment.

      Neovascularity was found in the symptomatic shoulder in 13 of 20 patients (35%) as well as in the asymptomatic shoulder in 5 of the 20 patients (25%).[5] Of 6 other patients who withdrew from the study before entering the trial, 1 withdrew due to cessation of symptoms and did not have neovascularity in either shoulder; 5 withdrew due to bilateral symptoms, of whom 2 had signs of bilateral neovascularity, 1 had unilateral neovascularity, and the remaining 2 did not have neovascularity in either shoulder.[5] No association was identified between the presence of neovascularity and pain, duration of symptoms, and neovascularity and shoulder function. The investigators noted more research is needed to evaluate the relevance of their findings.


See the list below:

  • Extrinsic causes

    • Primary impingement

      • Increased subacromial loading

      • Trauma (direct macrotrauma or repetitive microtrauma)

      • Overhead activity (athletic and nonathletic)

    • Secondary impingement

      • 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

  • Intrinsic causes

    • Acromial morphology (ie, hooked acromion, presence of an os acromiale or osteophyte, calcific deposits in the subacromial space, all of which predispose to primary impingement)

    • Acromioclavicular arthrosis (inferior osteophytes)

    • Coracoacromial ligament hypertrophy

    • Coracoid impingement

    • Subacromial bursal thickening and fibrosis

    • Prominent humeral greater tuberosity

    • Impaired cuff vascularity

    • Aging (primary)

    • Impingement (secondary)

    • Primary tendinopathy

    • Intratendinous

    • Articular side partial-thickness tears

    • Calcific tendinopathy





Imaging Studies

See the list below:

  • Standard radiographic studies are used to rule out glenohumeral/acromioclavicular arthritis and Os Acromiale.

    • Anteroposterior view of the glenohumeral joint

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

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

    • Stryker notch view - Potential os acromiale is easily visualized and assessed when viewed through the humeral head

    • Supraspinatus outlet view - Most useful to assess the supraspinatus outlet space (If < 7 mm, the patient is more at risk for impingement syndrome.) and helps assess morphology of the acromion (A hooked acromion is more at risk for impingement.)

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

    • Advantages

      • Noninvasive

      • No radiation

      • Can detect intrasubstance tendon degeneration or partial rotator cuff tears

      • Can detect inflammation, edema, hemorrhage, and scarring

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

    • Disadvantages

      • Often cannot accommodate patients with claustrophobia

      • Often cannot accommodate larger patients

      • Cannot accommodate patients with pacemakers, other metal implants, or particles

      • Dependent on quality of the MRI machine

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

      • High cost

  • For arthrography, dye is injected into the glenohumeral joint and postinjection radiographs are taken to assess the integrity of the glenohumeral joint.

    • Can be used to evaluate rotator cuff tears (A finding of dye escaping out of the joint and into the subacromial space is diagnostic of a full-thickness rotator cuff tear.)

    • Advantages - Can be used in conjunction with a CT scan to evaluate intra-articular pathology (eg, Bankart tears) and has a low cost

    • Disadvantages - Size of the tears cannot be quantified, patient is exposed to radiation and contrast dye, procedure is invasive

  • Diagnostic arthroscopy

    • Minimally invasive, visual, surgical procedure to assess shoulder pathology

    • Can visualize and assess most shoulder pathology

    • May afford the patient and physician a chance to diagnose and treat the pathology with one procedure

    • Disadvantage - May miss capsular-sided, partial-thickness tears

  • Note: A workup for other, more systemic processes may be included as clinically indicated.

Sonoelastography (SE) is a new technique that can assess differences in tissue stiffness. A study investigated the performance of sonoelastography (SE) for the differentiation of supraspinatus (SSP) tendon alterations of tendinopathy compared to magnetic resonance imaging (MRI) and conventional ultrasonography (US). The study concluded that SE is valuable in the detection of the intratendinous and peritendinous alterations of the SSP tendon and has excellent interobserver reliability and excellent correlation with MRI findings and conventional ultrasonography findings.[6]  

A study by Lee et al evaluated the relationship between tendon stiffness on sonoelastography and the MRI tendinosis grade in patients with rotator cuff tendinopathy. The study found that the MRI tendinosis grade is associated with stiffness assessed using sonoelastography in patients with rotator cuff tendinopathy.[7]



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.

Recovery Phase

Rehabilitation Program

Physical Therapy

The initial goals of this phase are to normalize range of motion and shoulder arthrokinematics, perform symptom-free activities of daily living, and improve neuromuscular control and muscle strength. Range-of-motion exercises are progressed to active exercises in all planes and self-stretches, concentrating on the joint capsule, especially posteriorly.

Strengthening includes isotonic 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.

Other important goals include maintaining joint motion and neuromuscular re-education. Upper extremity ergometry exercises, trunk exercises, and general cardiovascular conditioning for endurance are also recommended. Therapies may be continued if necessary. Guidelines to advance are full, nonpainful range of motion when manual muscle testing of strength is 70% of the contralateral side.

The final goal of this phase is to progress to the point at which the athlete is again throwing and includes improving strength, power, 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 and internal rotation. Initiate plyometrics, sports-specific exercises, proprioceptive neuromuscular facilitation, and isokinetic exercises.

Other Treatment (Injection, manipulation, etc.)

Subacromial injection of platelet rich plasma (PRP) was reviewed in a retrospective trial.[8] The authors concluded that most patients reported a moderate (>50%) improvement in symptoms of pain; 85% were satisfied with the ultrasound-guided PRP injection.[8] Further studies are needed as a recent Cochrane review concluded that there is currently insufficient evidence to recommend the use of platelet-rich therapies (PRT) to treat musculoskeletal soft tissue injuries.[9]

A study by Flores et al reported that subacromial hyaluronic acid injections combined with physical therapy were effective in the treatment of supraspinatus tendinopathy.[10]

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 and more intense workouts, proper arthrokinematics of the shoulder, and analysis and modification of techniques and mechanics that may reexacerbate symptoms. Make refinements in intensity and coordination.

Patient education is again reemphasized, maintaining proper mechanics, strength, and flexibility, and having a good understanding of the pathology. The patient should also show an understanding of a home exercise program with the proper warm-up, strengthening techniques, and warning signs of early impingement.

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 perform a more extensive diagnostic workup, reconsider other etiologies, or refer the patient for surgical evaluation.

Appropriate surgical referrals are patients with rotator cuff tendonitis refractory to 3-6 months of appropriate conservative treatment. Surgery may be particularly beneficial in patients with full, unrestricted passive range of motion; a positive response to injection of lidocaine into the subacromial space; or a type III acromion with a large subacromial spur and in those in whom changes are noted in the rotator cuff tendon after MRI.

  • Surgical evaluation

    • Initially, perform the examination with the patient under anesthesia (general anesthesia vs regional block) and include diagnostic arthroscopy.

    • Evaluate shoulder range of motion and stability.

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

    • Document any instability.

    • Perform an 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 evaluated using arthroscopy.

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

    • Also note any signs of fraying or wear changes on the undersurface of the coracoacromial ligament.

    • If no evidence of rotator cuff disruption is noted and 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 perform glenohumeral debridement of this tear.

    • If the patient has changes suggestive of impingement syndrome, arthroscopic subacromial decompression (acromioplasty, ie, resection of the anterior inferior portion of the acromion) is also performed.

    • If, following subacromial decompression, a rotator cuff repair is necessary, it may be continued under arthroscopic assistance or it may require conversion of the rotator cuff repair to an open procedure.

  • Postoperative care

    • A postoperative radiograph (supraspinatus outlet view) is 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 active and passive range-of-motion exercises. When pain has decreased significantly and range of motion has returned toward normal, a program of strengthening, similar to the previously mentioned conservative management, is instituted. Patients cannot begin sports-specific activities until they have full, active range of motion in the operated shoulder and normal strength, generally a period of approximately 3-4 months.

  • Surgical outcome

    • Subacromial decompression results generally are poor in young, high-performance athletes with injuries from overhead motions.

    • Results generally are good for properly selected middle-aged patients with evidence of impingement in history and physical examination findings 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.



Medication Summary

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

NSAIDs mechanism of action

The major mechanism of action of NSAIDs is inhibition of the synthesis of prostaglandin (PG), specifically PGE2, via blocking cyclooxygenase (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). In soft tissue, PGE2 causes pain and inflammation. In the GI tract, it is cytoprotective and increases the secretion of mucus and bicarbonates and decreases the secretion of gastric acids and digestive enzymes. In the renal system, PGE2 enhances renal salt and water excretion by acting as a vasodilator of small arterial blood vessels.

The COX pathway is subdivided into COX-1, which is responsible for PGE2 production in the GI tract and kidneys, and COX-2, which is responsible for inflammatory PG synthesis during soft tissue injury. NSAIDs serve as competitive inhibitors of COX activity and either selectively inhibit the COX-2 enzymes or nonselectively inhibit both the COX-1 and the COX-2 enzymes, making the nonselective NSAIDs a higher risk for potential ulcerogenic and other adverse effects.

Adverse drug reactions

All NSAIDs have similar adverse drug reactions. The first is hepatotoxicity. The liver function profile should be monitored periodically, especially in high-risk individuals. The second is renal toxicity. The renal function profile should be monitored periodically, especially in high-risk individuals. The third is GI toxicity. Symptoms may include nausea, diarrhea, acid reflux, and periumbilical cramping. 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 patients have evidence of complications (eg, iron deficiency anemia, GI bleeding, unexplained weight loss, dysphagia), an endoscopic evaluation is indicated. The fourth is aplastic anemia. Monitor the complete blood count, especially platelets, periodically for 1-2 months. The fifth is anaphylaxis. Inquire about and check medical records for a history of allergic reactions.

Nonsteroidal anti-inflammatory drugs

Class Summary

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

Ibuprofen (Ibuprin, Advil, Motrin)

Arylpropionic acid prototypical NSAID that has the advantage of causing less epigastric pain, GI occult blood loss, and less hepatotoxicity. Mostly indicated for rheumatoid arthritis and osteoarthritis for mild to moderate pain. Compared with other available NSAIDs, it has a short half-life.

Diclofenac sodium/diclofenac potassium (Voltaren, Cataflam)

Chemical composition is heteroaryl acetic acid with a short half-life. Delayed-release enteric-coated form is diclofenac sodium, and immediate-release form is diclofenac potassium. Both are primarily indicated for rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis. Diclofenac can cause hepatotoxicity; hence, monitor liver enzymes in the first 8 wk of treatment. Diclofenac has a relatively low risk for bleeding GI ulcers.

Etodolac (Lodine, Lodine XL)

Indole NSAID with an intermediate half-life, indicated for rheumatoid arthritis and osteoarthritis. Short-acting form is approved for analgesic use, comparable to aspirin/acetaminophen with codeine. Etodolac has a lower risk of producing GI complications and, as a result, is especially well tolerated in elderly patients.

Naproxen (Aleve, Anaprox, Naprelan, Naprosyn)

Probably the most potent of the arylpropionic acids, with a long half-life. Indicated for rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, juvenile arthritis, acute gout, and mild to moderate pain. Available in a controlled-release form, which is also used for acute pain, and an enteric-coated form, which is not used for acute pain.

Oxaprozin (Daypro)

An arylpropionic acid with a 40-50 h half-life and can be given once daily. Used for relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of COX, which results in a decrease in PG synthesis.

Nabumetone (Relafen)

Alkanone NSAID with a long (24 h) half-life and can be given once daily. Has a lower risk of producing GI complications and is indicated for rheumatoid arthritis and osteoarthritis.

Piroxicam (Feldene)

Enolic acid, piroxicam with long half-life (50 h) that can be given once daily. Indicated for use in rheumatoid arthritis and osteoarthritis. Has high GI toxicity (greater than aspirin).

Celecoxib (Celebrex)

Selective COX-2 inhibitor NSAID. Approved by FDA on December 31, 1998 and indicated for use in osteoarthritis and rheumatoid arthritis and for moderate to severe pain. Potentially presents less GI complications and platelet aggregation problems than the nonselective COX-inhibitor NSAIDs. Renal complications are comparable. Has a sulfonamide chain and is primarily dependent on cytochrome P-450 enzymes (a hepatic enzyme) for metabolism.



Return to Play

Return to play is restricted until full, painless range of motion is restored; both rest- and activity-related pain are eliminated; and provocative impingement signs are negative. Isokinetic strength testing must be 90% compared with the contralateral side. Resumption of activities is completed gradually, first during practice, to build up endurance, work on modified technique/mechanics, and simulate a game situation. Patients must be free of symptoms. To prevent recurrence, the patient should continue flexibility and strengthening exercises after returning to sports activities.


If rotator cuff tendonitis is not diagnosed and treated promptly and correctly, it can progress to rotator cuff degeneration and eventual tear. Other complications may include progression to adhesive capsulitis, cuff tear arthropathy, and reflex sympathetic dystrophy. Other complications may result from surgery, injections, physical therapy, or medications.



Primary prevention should be considered an integral part of the treatment of rotator cuff tendonitis. Educating patients at risk can circumvent the development of rotator cuff tendonitis. Athletes, particularly those involved in throwing and sports involving overhead actions, and laborers with repetitive shoulder stress should be instructed in proper warm-up techniques, specific strengthening techniques, and warning signs of early impingement.


In general, the prognosis is good for rotator cuff tendonitis that is promptly and correctly diagnosed and treated. Of patients, 60-90% improve and are free of symptoms with conservative treatment. Surgical outcomes are also very promising for patients in whom a full trial of conservative therapy fails.


Patient education may improve the outcome because the patient is educated regarding avoidance of provocative activities, pathology, and proper shoulder arthrokinematics. Education should also 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.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Tendinitis and Rotator Cuff Injury.


Questions & Answers


What is supraspinatus tendonitis?

What are the causes of supraspinatus tendonitis?

Which athletes are at highest risk for supraspinatus tendonitis?

What is the relevant anatomy of supraspinatus tendonitis?

What is the anatomy of static and dynamic stabilizers relative to supraspinatus tendonitis?

What is the functional anatomy of the rotator cuff relative to supraspinatus tendonitis?

What is the functional anatomy of the supraspinatus outlet relative to supraspinatus tendonitis?

What is the functional anatomy of impingement relative to supraspinatus tendonitis?

What are the possible sites of impingement in supraspinatus tendonitis?

What causes nonoutlet impingement in supraspinatus tendonitis?

What is the role of overuse and repetitive microtrauma in the etiology of supraspinatus tendonitis?

What is secondary impingement in supraspinatus tendonitis?

What is the role of secondary impingement in the etiology of supraspinatus tendonitis?

What are the indications of glenoid impingement in supraspinatus tendonitis?

What are the effects of glenoid impingement in supraspinatus tendonitis?

What is the role of proinflammatory cytokines in the pathogenesis of supraspinatus tendonitis?


What should be the focus of patient history in the evaluation of supraspinatus tendonitis?

How is the physical exam for supraspinatus tendonitis performed?

How is active range of motion tested in the physical exam of supraspinatus tendonitis?

What is the role of palpation in the physical exam of supraspinatus tendonitis?

What is the role of manual muscle testing in the physical exam of supraspinatus tendonitis?

Which tests are performed for impingement signs in supraspinatus tendonitis?

Which tests are performed for signs of instability in supraspinatus tendonitis?

Why should both shoulders be tested in the evaluation of supraspinatus tendonitis?

How is a neurovascular exam performed in the evaluation of supraspinatus tendonitis?

What are the extrinsic causes of primary impingement in supraspinatus tendonitis?

What are the extrinsic causes of secondary impingement in supraspinatus tendonitis?

What are the intrinsic causes of supraspinatus tendonitis?


What are the differential diagnoses for Supraspinatus Tendonitis?


What is the role of radiography in the workup of supraspinatus tendonitis?

What are the advantages of MRI in the diagnosis of supraspinatus tendonitis?

What are the limitations of MRI in the evaluation of supraspinatus tendonitis?

What is the role of arthrography in the workup of supraspinatus tendonitis?

What are the advantages and disadvantages of arthroscopy for the diagnosis of supraspinatus tendonitis?

What is the role of sonoelastography (SE) in the workup of supraspinatus tendonitis?


What are the goals of acute phase physical therapy (PT) in the treatment of supraspinatus tendonitis?

Which exercises are included in acute phase physical therapy (PT) for supraspinatus tendonitis?

What adjunct modalities used in acute phase physical therapy (PT) for supraspinatus tendonitis?

What is the role of patient education in acute phase physical therapy (PT) for supraspinatus tendonitis?

What are the initial goals of recovery phase physical therapy (PT) for supraspinatus tendonitis?

Which exercises are included in recovery phase physical therapy (PT) for supraspinatus tendonitis?

What are secondary goals of recovery phase physical therapy (PT) for supraspinatus tendonitis?

What is the final goal of recovery phase physical therapy (PT) for supraspinatus tendonitis?

What is the role of injections in the treatment of supraspinatus tendonitis?

What is the goal of the maintenance phase physical therapy (PT) for supraspinatus tendonitis?

What is the role of patient education in the maintenance phase of physical therapy (PT) for supraspinatus tendonitis?

When is surgery considered for the treatment of supraspinatus tendonitis?

What are the indications for surgery for supraspinatus tendonitis?

What is included in the surgical evaluation of supraspinatus tendonitis?

What is included in the postoperative care of supraspinatus tendonitis?

What is the prognosis of supraspinatus tendonitis following surgery?


Which medications are used in the treatment of supraspinatus tendonitis?

What is the mechanism of action of NSAIDs for the treatment of supraspinatus tendonitis?

What are possible adverse drug reactions of NSAIDs in the treatment of supraspinatus tendonitis?

Which medications in the drug class Nonsteroidal anti-inflammatory drugs are used in the treatment of Supraspinatus Tendonitis?


What are the return to play protocols following treatment of supraspinatus tendonitis?

What are possible complications of supraspinatus tendonitis?

How is supraspinatus tendonitis prevented?

What is the prognosis of supraspinatus tendonitis?

What are the benefits of patient education for supraspinatus tendonitis?