Rotator Cuff Disease Medication
- Author: André Roy, MD, FRCPC; Chief Editor: Stephen Kishner, MD, MHA more...
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.
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.
Analgesic effect of acetaminophen is mediated by prostaglandin inhibition.
Nonsteroidal anti-inflammatory drugs
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.
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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|Tendinitis||Partial Tear||Complete Tear|
|Soft tissue calcification(s)||X||X||X|
|Greater tuberosity flattening or hypertrophy||X||X||X|
|Humeral head cysts||X||X||X|
|Acromion type 2 and 3||X||X||X|
|Upward migration of humeral head ( < 6 mm)||X|
|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
|Rupture of the long head of the biceps tendon||Upward migration of humeral head
|Calcifications in the supraspinatus, infraspinatus or teres minor||Bone edema|
|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|
|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|
|Subacromial-subdeltoid bursa effusion|
|Thickening of coracoacromial ligament||X||X||X|
|Greater tuberosity flattening or hyper-trophy||X||X||X|
|Humeral head cysts||X||X||X|
|Anterior acromial spur||X||X||X|
|Acromion type 2 and 3||X||X|
|Upward migration of humeral head||X|
|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|