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Rotator Cuff Disease Medication

  • Author: André Roy, MD, FRCPC; Chief Editor: Stephen Kishner, MD, MHA  more...
 
Updated: Apr 21, 2016
 

Medication Summary

Oral medications for the treatment of degenerative rotator cuff disease include simple analgesics and nonsteroidal anti-inflammatory drugs. Because rotator cuff disease is a chronic condition, opioid analgesics are not recommended.

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Simple analgesics

Class Summary

While NSAIDs are known to be effective in reducing pain and improving function and ROM, they may exert their effect through their analgesic rather than their anti-inflammatory properties. One study with poor methodological quality did not show short-term superiority of NSAIDs as compared to acetaminophen in the treatment of painful shoulder syndrome. Long-term and short-term studies comparing the efficacy of NSAIDs with acetaminophen in osteoarthritis of the knee exist and showed similar efficacy. Moreover, even the presence of inflammatory signs did not predict a better response to treatment with NSAIDs than acetaminophen, suggesting that improvements are not necessarily dependent on an anti-inflammatory effect.

Considering the toxicity of NSAIDs, the need for an analgesic rather than anti-inflammatory effect, the lower cost of a simple analgesic, and the chronicity of degenerative rotator cuff disease, it is indicated to prescribe acetaminophen (APAP) as an initial treatment.

Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)

 

Analgesic effect of acetaminophen is mediated by prostaglandin inhibition.

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Nonsteroidal anti-inflammatory drugs

Class Summary

Numerous studies on the efficacy of NSAIDs for different shoulder conditions have been published; however, because of the factors previously mentioned, most of them have poor methodological quality and, therefore, no conclusions can be drawn about the efficacy of NSAIDs.

Recent review articles, using strict inclusion criteria based on the quality of the methodology, concluded that the trials with the best methodology show a superior short-term efficacy (2 weeks) of NSAIDs compared with placebo; however, at 4 weeks, results did not show any statistical differences. Therefore, it is indicated to prescribe a short course of 10-14 days of NSAIDs as a second-line treatment. No evidence supports a longer use. In case of persistent pain, other therapeutic modalities should be sought. Comparison between different types of NSAIDs didn't show evidence of the superiority of one NSAID with respect to efficacy. Therefore, NSAIDs with the fewest side effects like the newer Cox-2 selective molecules or NSAID with a combination of prostaglandin E1 analog (diclofenac/misoprostol) should be the drug of choice.

In an aging population taking additional medication that may interact with NSAIDs, drug interactions must be avoided. Forty to sixty percent of drugs consumed are over-the-counter (OTC) medications, most often analgesics and NSAIDs, increasing the risk of potential gastrointestinal side effects. The patient should be asked whether he/she is taking any medications concomitantly, such as anticoagulants (hemorrhage), corticosteroids (peptic ulcer), diuretics and antihypertensives (decreased blood pressure control), ACE inhibitors (acute renal failure), high dose methotrexate (increased MTX toxicity), lithium, digoxin, aminoglycosides (decreased renal clearance), phenytoin (decreased albumin binding), and antacids (decreased NSAID levels). NSAIDs should be avoided, if possible, in elderly patients with congestive heart failure or renal or hepatic dysfunction and who are taking other medications.

Celecoxib (Celebrex)

 

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.

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Contributor Information and Disclosures
Author

André Roy, MD, FRCPC Consulting Staff, Department of Physiatry, Montreal University Hospital Center and Montreal Rehabilitation Institute

André Roy, MD, FRCPC is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Coauthor(s)

Thierry HM Adahan, MD LMCC, CCFP, FRCPC, FABPMR, Head, Pain Rehabilitation Center, Haim Sheba Medical Center, Tel Hashomer, Israel

Thierry HM Adahan, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Benjamin Dahan University of Montreal, Canada

Disclosure: Nothing to disclose.

Manon Bélair, MS Consulting Staff, Hospital Notre-Dame, Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Patrick M Foye, MD Director of Coccyx Pain Center, Professor and Interim Chair of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School; Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, University Hospital

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, International Spine Intervention Society, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans

Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM President and Director, Georgia Pain Physicians, PC; Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Emory University School of Medicine

Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Medical Association, International Association for the Study of Pain, Texas Medical Association

Disclosure: Nothing to disclose.

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Normal plain radiograph of the shoulder in internal, external, and neutral positions.
Subchondral sclerosis of the humeral head as seen in chronic tendinopathy.
Calcification at the insertion of the rotator cuff, another sign of chronic tendinopathy.
Presence of a bony spur on the inferior surface of the acromion.
Superior migration of the humeral head in chronic, complete rotator cuff tear. Note the reduced space between the acromion and the humeral head.
Normal double-contrast arthrography of the shoulder.
This image depicts the channel between the articular capsule and the subacromial-subdeltoid bursa in a complete rotator cuff tear.
Even if the channel cannot be always identified, the presence of contrast medium in the subdeltoid-subacromial bursa signs the presence of a complete rotator cuff tear.
Complete rotator cuff tear with presence of contrast medium in the subacromial-subdeltoid bursa. Also note the multiple irregularities in the synovial fluid showed as multiples filling defects.
Computed tomography (CT)-arthrography scan of the shoulder in the axial plane. Note the presence of air and contrast in the subacromial-subdeltoid bursa.
Full-thickness tear of the supraspinatus seen as a hyperintensity line through the full thickness of the tendon (as viewed in a flash 2-dimensional magnetic resonance imaging [MRI] sequence in the coronal oblique plane).
Slight hyperintensity signal within the tendon without transsectional hyperintensity throughout the tendon is compatible with tendinopathy without complete tear. Additionally, note the presence of the hyperintensity signal in the region of the subdeltoid-subacromial bursa, which indicates bursitis.
Calcifications are seen as hypointense foci in flash 2-dimensional.
Arthro–magnetic resonance imaging (MRI) can help to identify labral tears, as seen in this image. The contrast medium penetrates between the labrum and the articular surface.
Ultrasonography is another modality that can demonstrate a complete rotator cuff tear. This image reveals a gap of more than 2 cm between both extremities of the torn tendon.
Table 1: Radiological Findings on Plain Film
  Tendinitis Partial Tear Complete Tear
Normal X X X
Soft tissue calcification(s) X X X
Greater tuberosity flattening or hypertrophy X X X
Humeral head cysts X X X
Acromial sclerosis X X X
Acromial spurs X X X
Acromion type 2 and 3 X X X
Acromioclavicular osteoarthritis X X X
Upward migration of humeral head ( < 6 mm)     X
Table 2: Radiological Findings on MRI
Tendons Soft tissues Bone structures
Thickening of rotator cuff tendon (RCT) Intra-articular effusion Greater tuberosity flattening or hypertrophy
Grey signal intensity within the RCT Subacromial-subdeltoid bursal effusion Humeral head cysts
Fluid-filled gap across the tendon Muscle atrophy Acromial sclerosis
Retraction Thickening of coracoacromial ligament Anterior acromial spur
Grey signal intensity in the long head of biceps tendon   Acromion type 2 and 3



Acromioclavicular osteoarthritis



Rupture of the long head of the biceps tendon   Upward migration of humeral head



Os acromiale



Calcifications in the supraspinatus, infraspinatus or teres minor   Bone edema
Table 3: Radiological Signs of Specific Disorders
  Tendinitis Partial Tear Complete Tear
Thickening of RCT X X  
Grey signal intensity within the RCT X X  
High signal intensity crossing only 1 surface of the tendon   X  
Fluid-filled gap across the tendon     X
Retraction     X
Grey signal intensity in the long head of the biceps tendon X X X
Rupture of the long head of the biceps tendon X X X
Calcifications in the supraspinatus, infraspinatus or teres minor tendon X X X
Intra-articular effusion X X X
Subacromial-subdeltoid bursa effusion      
Muscular atrophy     X
Thickening of coracoacromial ligament X X X
Greater tuberosity flattening or hyper-trophy X X X
Humeral head cysts X X X
Acromial sclerosis X X X
Anterior acromial spur X X X
Acromion type 2 and 3   X X
Acromio-clavicular osteoarthritis X X X
Upward migration of humeral head     X
Table 4: Ultrasonographic Signs of Rotator Cuff Disease
Primary signs Accessory findings
Focal interruption of tendon Retraction of the muscle
Presence of fluid in the gap Synovial cysts in the humeral head
Lost of convexity of the tendon and bursa Hyperechoic foci + shadowing (calcium)
Uncovered cartilage sign Fluid effusion in the bursa
Diffusely hypoechoic tendon articulation Fluid effusion in the Ganglion cysts
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