Updated: Jun 8, 2006
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.
Supraspinatus tendonitis is a common cause of shoulder pain in athletes whose sports involve throwing and overhead motions.
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.
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.
| Acromioclavicular Joint Injury | Contusions |
| Bicipital Tendonitis | Infraspinatus Syndrome |
| Brachial Plexus Injury | Myofascial Pain in Athletes |
| Cervical Disc Injuries | Rotator Cuff Injury |
| Cervical Discogenic Pain Syndrome | Shoulder Dislocation |
| Cervical Radiculopathy | Shoulder Impingement Syndrome |
| Cervical Spine Sprain/Strain Injuries | Superior Labrum Lesions |
| Clavicular Injuries | Swimmer's Shoulder |
Os Acromiale
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.
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.
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.
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.
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.
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.
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.
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.
400-800 mg PO tid/qid; not to exceed 3200 mg/d
<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
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
Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding
B - Usually safe but benefits must outweigh the risks.
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
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.
100-200 mg/d PO divided doses tid/qid
Not established; 25 mg PO bid/tid suggested if >6 mo
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
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
B - Usually safe but benefits must outweigh the risks.
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
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.
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
<14 years: Not established
>14 years: Administer as in adults
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
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
C - Safety for use during pregnancy has not been established.
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
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.
250-500 mg PO bid; not to exceed 1000 mg/d
Not established; 10 mg/kg/d PO divided bid suggested if >6 mo
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
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
B - Usually safe but benefits must outweigh the risks.
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
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.
600-1200 mg PO qd; not to exceed 1800 mg/d
<14 years: Not established
>14 years: Administer as in adults
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
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
C - Safety for use during pregnancy has not been established.
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
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.
1000 mg/d PO; not to exceed 2000 mg/d in 1-2 divided doses
<14 years: Not established
>14 years: Administer as in adults
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
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
C - Safety for use during pregnancy has not been established.
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
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).
10-20 mg PO qd/bid
<14 years: Not established
>14 years: Administer as in adults
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
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
C - Safety for use during pregnancy has not been established.
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
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.
100-200 mg PO bid; not to exceed 600 mg/d
<18 years: Not established
>18 years: Administer as in adults
Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration with rifampin may decrease celecoxib plasma concentrations
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks.
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 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 warmup 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 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.
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Hawkins RJ, Kennedy JC. Impingement syndrome in athletes. Am J Sports Med. May-Jun 1980;8(3):151-8. [Medline].
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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].
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
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, MD 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
Disclosure: Nothing to disclose.
Wing K Chang, MD, Musculoskeletal Spine Fellow, Department of Physical Medicine and Rehabilitation, University of Michigan Medical Center
Wing K Chang, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, and Physiatric Association for Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.
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
Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, Phi Beta Kappa, and Wilderness Medical Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
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
Disclosure: Nothing to disclose.
Jon Whitehurst, MD, Consulting Staff, Rockford Orthopedic Associates
Disclosure: Nothing to disclose.
William Jay Bryan, MD, Clinical Professor, Department of Orthopedic Surgery, Baylor University College of Medicine
William Jay Bryan, MD is a member of the following medical societies: Texas Orthopaedic Association
Disclosure: Nothing to disclose.
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