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Sports Medicine > Shoulder
Supraspinatus Tendonitis
Article Last Updated: Jun 8, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 10
Author: Thomas M DeBerardino, MD, Director, John A Feagin Jr West Point Sports Medicine Fellowship, Orthopedic Surgery Service, Clinical Instructor in Surgery, Keller Army Community Hospital at West Point
Thomas M DeBerardino is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Medical Association, American Orthopaedic Association, and American Orthopaedic Society for Sports Medicine
Coauthor(s):
Wing K Chang, MD, Musculoskeletal Spine Fellow, Department of Physical Medicine and Rehabilitation, University of Michigan Medical Center
Editors: Craig C Young, MD, Medical Director of Sports Medicine, Departments of Orthopedic Surgery and Community and Family Medicine, Sports Medicine Fellowship Director, Associate Professor, Medical College of Wisconsin; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Russell D White, MD, Professor of Medicine, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center Lakewood; Jon Whitehurst, MD, Consulting Staff, Rockford Orthopedic Associates; William Jay Bryan, MD, Clinical Professor, Department of Orthopedic Surgery, Baylor University College of Medicine
Author and Editor Disclosure
Synonyms and related keywords:
rotator cuff tendonitis, rotator cuff tendinopathy, rotator cuff tendinosis, shoulder impingement syndrome, shoulder pain, rotator cuff injury, rotator cuff tear, torn rotator cuff, shoulder injury, rotator cuff pathology, shoulder pathology, pitching injury, throwing injury
Background
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.
The causes of supraspinatus tendonitis can be broken down into extrinsic and intrinsic factors. 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.
Frequency
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.
History
- Age
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- 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
Physical
- 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)
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- 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
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- 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.
Causes
- 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
Acromioclavicular Joint Injury
Bicipital Tendonitis
Brachial Plexus Injury
Cervical Disc Injuries
Cervical Discogenic Pain Syndrome
Cervical Radiculopathy
Cervical Spine Sprain/Strain Injuries
Clavicular Injuries
Contusions
Infraspinatus Syndrome
Myofascial Pain in Athletes
Rotator Cuff Injury
Shoulder Dislocation
Shoulder Impingement Syndrome
Superior Labrum Lesions
Swimmer's Shoulder
Other Problems to Be Considered
Os Acromiale
Imaging Studies
- 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.
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.
Other Treatment
During the acute to subacute phase, when pain and inflammation predominate, a subacromial injection may be diagnostic and therapeutic as an adjunct to the rehabilitation program. Injecting 10 mL of a 1% lidocaine solution without epinephrine into the subacromial space may relieve the shoulder pain if the pain and inflammation are truly originating from the supraspinatus outlet/subacromial space. Adding a low-dose, intermediate-acting, injectable corticosteroid may provide a therapeutic effect. Betamethasone, triamcinolone, and methylprednisolone are used commonly. The common dose is 1 mL of any of these available injectable corticosteroids mixed with 9 mL of a 1% lidocaine solution without epinephrine. - Technique
- Have patients sit with their arms hanging by their side to distract the humerus from the acromion.
- Identify the lateral edge of the acromion.
- Insert a needle at the midpoint of the acromion, and angle it slightly upward under the acromion to its full length.
- Slowly withdraw the needle while simultaneously injecting fluid in a bolus (wherever resistance is not present). Continue aspirating before injecting. Sometimes, a swelling caused by the 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. Failing this, surgical evaluation may be necessary.
- Aftercare
- Inform the patient that once the effect of the lidocaine wears off, a local reaction to the corticosteroid may occur in the next 24-72 hours. If this occurs, instruct the patient to apply ice (wrapped in a towel) to the affected shoulder for 20 minutes, remove it for 20 minutes, and then repeat (ie, 20 min on, 20 min off) 3 times in the beginning and at the 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.
- The patient may resume a symptom-limited therapy program in the first week postinjection and then resume the full course thereafter.
- Adverse effects in general
- Although uncommon with this injection procedure when performed correctly, adverse effects may occur. The clinician and the patient must be educated about them, and the clinician must know how to manage any related complications.
- Absolute contraindications include documented allergy to any corticosteroid or local anesthetics, overlying skin infection, or cellulitis.
- Relative contraindications include diabetes, hypertension, immunosuppression, cardiac arrhythmias, and heart blocks.
- Note that adverse effects of the medications may be minimized when the medication is administered in the recommended dose.
- 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, which may include local injection site erythema, mild swelling, ecchymoses, and pain.
- Adverse effects of local anesthetics
- These usually result from an overdose or allergic reactions, which definitely can be minimized by double-checking the dose before administering and inquiring about and checking on the records for medication allergies.
- Overdose and allergic reactions may be catastrophic and may include cardiac, respiratory, and cerebral compromise.
- Adverse reaction to the injection
- Aside from the one mentioned, occasionally a patient may have a vasovagal reaction (fainting episode) due to pain, apprehension, or needle phobia.
- Treatment involves placing the patient supine, elevating the legs, and strongly reassuring him or her that recovery is forth coming shortly. If the patient loses consciousness briefly, protect the airway and give oxygen at 35% concentration.
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.
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 warmup, 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.
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.
Drug Category: Nonsteroidal anti-inflammatory drugs
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.
| Drug Name | Ibuprofen (Ibuprin, Advil, Motrin) |
| Description | 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. |
| Adult Dose | 400-800 mg PO tid/qid; not to exceed 3200 mg/d |
| Pediatric Dose | <6 months: Not established >6 months <20 kg: Up to 400 mg/d PO in divided doses 20-30 kg: Up to 600 mg/d PO in divided doses 30-40 kg: Up to 800 mg/d PO in divided doses |
| Contraindications | Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding |
| Interactions | Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
| Pregnancy | B - Usually safe but benefits must outweigh the risks.
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| Precautions | Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy |
| Drug Name | Diclofenac sodium/diclofenac potassium (Voltaren, Cataflam) |
| Description | 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. |
| Adult Dose | 100-200 mg/d PO divided doses tid/qid |
| Pediatric Dose | Not established; 25 mg PO bid/tid suggested if >6 mo |
| Contraindications | Documented hypersensitivity; do not administer into CNS or to patients with peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding |
| Interactions | Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
| Pregnancy | B - Usually safe but benefits must outweigh the risks.
|
| Precautions | Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low WBC counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs |
| Drug Name | Etodolac (Lodine, Lodine XL) |
| Description | 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. |
| Adult Dose | 600-1200 mg/d PO divided doses bid/qid; not to exceed 1200 mg or 20 mg/kg for patients <60 kg Extended-release form: 400-1000 mg PO qd |
| Pediatric Dose | <14 years: Not established >14 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; do not administer into CNS or to patients with peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding |
| Interactions | Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
| Pregnancy | C - Safety for use during pregnancy has not been established.
|
| Precautions | Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low WBC counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs |
| Drug Name | Naproxen (Aleve, Anaprox, Naprelan, Naprosyn) |
| Description | 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. |
| Adult Dose | 250-500 mg PO bid; not to exceed 1000 mg/d |
| Pediatric Dose | Not established; 10 mg/kg/d PO divided bid suggested if >6 mo |
| Contraindications | Documented hypersensitivity; do not administer into CNS or to patients with peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding |
| Interactions | Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
| Pregnancy | B - Usually safe but benefits must outweigh the risks.
|
| Precautions | Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug |
| Drug Name | Oxaprozin (Daypro) |
| Description | 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. |
| Adult Dose | 600-1200 mg PO qd; not to exceed 1800 mg/d |
| Pediatric Dose | <14 years: Not established >14 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; do not administer into CNS or to patients with peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding |
| Interactions | Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
| Pregnancy | C - Safety for use during pregnancy has not been established.
|
| Precautions | Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug |
| Drug Name | Nabumetone (Relafen) |
| Description | 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. |
| Adult Dose | 1000 mg/d PO; not to exceed 2000 mg/d in 1-2 divided doses |
| Pediatric Dose | <14 years: Not established >14 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; do not administer into CNS or to patients with peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding |
| Interactions | Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
| Pregnancy | C - Safety for use during pregnancy has not been established.
|
| Precautions | Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug |
| Drug Name | Piroxicam (Feldene) |
| Description | 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). |
| Adult Dose | 10-20 mg PO qd/bid |
| Pediatric Dose | <14 years: Not established >14 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; do not administer into CNS or to patients with peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding |
| Interactions | Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
| Pregnancy | C - Safety for use during pregnancy has not been established.
|
| Precautions | Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug |
| Drug Name | Celecoxib (Celebrex) |
| Description | 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. |
| Adult Dose | 100-200 mg PO bid; not to exceed 600 mg/d |
| Pediatric Dose | <18 years: Not established >18 years: Administer as in adults |
| Contraindications | Documented hypersensitivity |
| Interactions | Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration with rifampin may decrease celecoxib plasma concentrations |
| Pregnancy | B - Usually safe but benefits must outweigh the risks.
|
| Precautions | May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, and conditions predisposing to fluid retention; caution in severe heart failure and hyponatremia because may deteriorate circulatory hemodynamics; may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction or in abnormal liver lab results |
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.
Complications
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.
Prevention
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 warmup techniques, specific strengthening techniques, and warning signs of early impingement.
Prognosis
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.
Education
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 warmup 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 eMedicine's Breaks, Fractures, and Dislocations Center and Sports Injury Center. Also, see eMedicine's patient education articles Tendinitis and Rotator Cuff Injury.
Medical/Legal Pitfalls
- If the diagnosis of a rotator cuff tendonitis is missed, no immediate catastrophic sequela occurs; although, without prompt and correct diagnosis and treatment, the patient may become progressively disabled. Other complications may include progression to adhesive capsulitis, cuff tear arthropathy, and reflex sympathetic dystrophy. Other complications may result from surgery, injection, physical therapy, or medications.
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- With any complaint of shoulder pain, the clinician must rule out disorders that may have catastrophic consequences if action is not taken immediately, such as infection, cardiac etiologies, tumor, dislocation, fracture, vascular injury, peripheral neurologic injury, and cervical spine neurologic injury. These diagnoses must be kept in mind in the differential and tested for when assessing a shoulder problem in any patient.
Special Concerns
- Supraspinatus tendonitis is managed similarly in all populations. Whether it is managed more or less aggressively depends on the patient's activity level, reliance on the shoulder for an occupation or athletics (recreational or competitive), age, and comorbid medical illnesses.
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- In pregnant women, nursing mothers, young children, and patients with comorbid medical illnesses, caution should be used when administering medications to ensure the medication chosen is compatible with the patient. Age, accompanying medical illnesses, low activity level, poor healing potential, poor anesthetic candidacy, and pregnancy status may preclude the patient from being a surgical candidate.
- Andrews JR, Harrelson GL, Wilk KE, Lampert R, eds. Physical Rehabilitation of the Injured Athlete. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1998:478-553.
- Bigliani LU, Morrison DS, April EW. The morphology of the acromion its relationship to rotator cuff tears. J Orthop Trans. 1986;10:228.
- Brotzman SB, ed. Clinical Orthopaedic Rehabilitation. First ed. London, England: Mosby; 1995:92-98.
- Fu FH, Stone DA, eds. Sports Injuries: Mechanisms, Prevention, Treatment. First ed. Philadelphia, Pa: Lippincott, Williams & Wilkins; 1994:895-923.
- Hawkins RJ, Kennedy JC. Impingement syndrome in athletes. Am J Sports Med. May-Jun 1980;8(3):151-8. [Medline].
- Miller MD, Cooper DE, Warner JJ, eds. Review of Sports Medicine and Arthroscopy. First ed. Philadelphia, Pa: WB Saunders Co; 1995:113-164.
- Neer CS 2nd. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg Am. Jan 1972;54(1):41-50. [Medline].
- Schmitt J, Haake M, Tosch A, Hildebrand R, Deike B, Griss P. Low-energy extracorporeal shock-wave treatment (ESWT) for tendinitis of the supraspinatus. A prospective, randomised study. J Bone Joint Surg Br. Aug 2001;83(6):873-6. [Medline].
Supraspinatus Tendonitis excerpt Article Last Updated: Jun 8, 2006
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