Updated: Apr 15, 2009
Rotator cuff injuries are problems commonly encountered in athletic and nonathletic patients. Symptoms include pain, weakness, and decreased range of motion. Early diagnosis is important for identifying causes, implementing effective treatment, and preventing further injury.
Knowledge of the mechanical and normal anatomical structure allows for understanding of rotator cuff injuries (see Rotator Cuff Pathology). The rotator cuff muscles are the supraspinatus, infraspinatus, subscapularis, and teres minor.
Microscopically, all of the tendons of the rotator cuff fuse to form one continuous band, which is composed of a 5-layer structure. Because of this structure, none of the individual muscles have a higher incidence of tear, per se. However, the joint-side portion of the supraspinatus tendon is more susceptible to mechanical failure than the bursal side.
Most of the tears of the cuff are the result of chronic degeneration, which makes them susceptible to rupture. The chronic deterioration of the cuff results from the coracoacromial arch, which is composed of the bony acromion, the coracoacromial ligament, and coracoid process. Because of its position above the rotator cuff, the coracoacromial arch forms the roof through which the supraspinatus tendon must pass (ie, supraspinatus outlet). Repetitive microtrauma and anatomical variations lead to most of the rotator cuff injuries.
The precise incidence of symptomatic rotator cuff injuries is not known. Many individuals with full-thickness cuff tears are not only asymptomatic but they have minimal functional disability. The most accepted figure is 20-30%. Cadaver studies of elderly persons have estimated full-thickness tears as high as 30%.1
An estimated 4% of cuff ruptures develop a cuff arthropathy. Various authors report a rate of success with conservative treatment ranging from 33-90%, with longer recovery time in older patients. Surgery results in improved function regardless of the patient's age.2,3,4
Rotator cuff injuries and tears usually do not occur in persons younger than 40 years (5-30%). The great majority is found in persons aged 55-85 years. Approximately 15% of patients with shoulder pain who are older than 70 years have rotator cuff injuries.1
Assess any patient with shoulder pain with respect to the patient's age and occupation. Characterize pain according to its duration of onset, location, radiation, timing, and quality. In addition, investigate pain for its relationship to activities and sport.
Approach the shoulder examination systematically in every patient with inspection, palpation, range of motion, strength testing, neurologic assessment, and performances of special shoulder tests. Also, include evaluation of the cervical spine and upper extremity.
An emerging consensus suggests that the etiology of rotator cuff disease is multifactorial. Extrinsic factors exist, such as the morphology of the coracoacromial arch, tensile overload, repetitive use, and kinematics abnormalities. Intrinsic factors also exist, such as altered tendon vascular supply, microstructural collagen fiber abnormalities, and regional variations.
Cervical Strain
Dislocations, Shoulder
Myocardial Infarction
Myopathies
Avascular necrosis of humerus
Acromioclavicular injury
Neurologic injuries (C5-C6) caused by repetitive trauma
Septic arthritis
Spleen rupture
(Only the last 2 points were found to have 78% sensitivity and 98% specificity.)
Stabilization with a shoulder sling and an ice pack are sufficient for prehospital care.
Consider an orthopedic consultation in primarily acute injuries or even severe extension of chronic rotator cuff injuries. An orthopedic consultation for possible surgical intervention is required under the following conditions:
The goal of pharmacotherapy is to reduce pain and inflammation.
Pain control is essential to quality patient care, ensuring patient comfort, promoting pulmonary toilet, and enabling physical therapy regimens. Most analgesics have sedating properties, which are beneficial for patients who have sustained painful skin lesions.
Usually the DOC for the treatment of mild to moderate pain if no contraindications exist. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
400 mg PO q4-6h, 600 mg PO q6h, or 800 mg PO q8h while symptoms persist; not to exceed 3.2 g/d
<6 months: Not established
6 months to 12 years: 10-70 mg/kg/d PO divided tid/qid; begin at lower end of dosing range and titrate upward; not to exceed 2.4 g/d
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (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; high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain and inflammation.
Small dosages initially are indicated in small and elderly patients and in persons with renal or liver disease. Doses more than 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patients for response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 14 years: 0.1–1 PO mg/kg q6-8h
>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 of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; GI disease
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
DOC for the treatment of pain in patients with documented hypersensitivity to aspirin or NSAIDs, persons with upper GI disease, or those taking oral anticoagulants.
325-650 mg PO q4-6h or 1000 mg PO tid/qid; not to exceed 4 g/d; Alternately, 1000 mg PO tid/qid; not to exceed 4 g/d
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 5 dose/d
Rifampin can reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity; G-6-PD deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible in chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products, and combined use with these products may result in cumulative acetaminophen doses exceeding recommended maximum dose
Moosmayer S, Smith HJ, Tariq R, Larmo A. Prevalence and characteristics of asymptomatic tears of the rotator cuff: an ultrasonographic and clinical study. J Bone Joint Surg Br. Feb 2009;91(2):196-200. [Medline].
Ecklund KJ, Lee TQ, Tibone J, Gupta R. Rotator cuff tear arthropathy. J Am Acad Orthop Surg. Jun 2007;15(6):340-9. [Medline].
Fongemie AE, Buss DD, Rolnick SJ. Management of shoulder impingement syndrome and rotator cuff tears. Am Fam Physician. Feb 15 1998;57(4):667-74, 680-2. [Medline].
Hayes K, Ginn KA, Walton JR, Szomor ZL, Murrell GA. A randomised clinical trial evaluating the efficacy of physiotherapy after rotator cuff repair. Aust J Physiother. 2004;50(2):77-83. [Medline].
SooHoo NF, Rosen P. Diagnosis and treatment of rotator cuff tears in the emergency department. J Emerg Med. May-Jun 1996;14(3):309-17. [Medline].
Fuchs S, Chylarecki C, Langenbrinck A. Incidence and symptoms of clinically manifest rotator cuff lesions. Int J Sports Med. Apr 1999;20(3):201-5. [Medline].
Miniaci A, Salonen D. Rotator cuff evaluation: imaging and diagnosis. Orthop Clin North Am. Jan 1997;28(1):43-58. [Medline].
Millstein ES, Snyder SJ. Arthroscopic evaluation and management of rotator cuff tears. Orthop Clin North Am. Oct 2003;34(4):507-20. [Medline].
Hashefi M. Ultrasound in the diagnosis of noninflammatory musculoskeletal conditions. Ann N Y Acad Sci. Feb 2009;1154:171-203. [Medline].
Dalton SE. The conservative management of rotator cuff disorders. Br J Rheumatol. Jul 1994;33(7):663-7. [Medline].
Hanusch BC, Goodchild L, Finn P, Rangan A. Large and massive tears of the rotator cuff: functional outcome and integrity of the repair after a mini-open procedure. J Bone Joint Surg Br. Feb 2009;91(2):201-205. [Medline].
Zumstein MS, Jost B, Hempel J, Hodler J, Gerber C. The clinical and structural long-term results of open repair of massive tears of rotator cuff. J Bone Joint Surg Am. Nov 2008;90(11):2423-31.
Morse K, Davis AD, AFra R, Kaye EK, Schepsis A, Voloshin I. Arthroscopic versus mini-open rotator cuff repair: a comprehensive review and meta-analysis. Am J Sports Med. Sept 2008;26(9):1824-1828. [Medline].
Tonino PM, Gerber C, Itoi E, Porcellini G, Sonnabend D, Walch G. Complex shoulder disorders: evaluation and treatment. J Am Acad Orthop Surg. Mar 2009;17(3):125-36. [Medline].
Rudzki JR, Shaffer B. New approaches to diagnosis and arthroscopic management of partial-thickness cuff tears. Clin Sports Med. Oct 2008;27(4):691-717. [Medline].
Barr KP. Rotator cuff disease. Phys Med Rehabil Clin N Am. May 2004;15(2):475-91. [Medline].
Quillen DM, Wuchner M, Hatch RL. Acute shoulder injuries. Am Fam Physician. Nov 15 2004;70(10):1947-54. [Medline].
Rokito AS, Cuomo F, Gallagher MA, Zuckerman JD. Long-term functional outcome of repair of large and massive chronic tears of the rotator cuff. J Bone Joint Surg Am. Jul 1999;81(7):991-7. [Medline].
Soslowsky LJ, Carpenter JE, Bucchieri JS, Flatow FL. Biomechanics of the rotator cuff. Orthop Clin North Am. Jan 1997;28(1):17-30. [Medline].
rotator cuff tears, shoulder pain, rotator cuff dysfunction, rotator cuff disease, glenohumeral instability, impingement syndrome, rotator cuff injury
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