Rotator Cuff Clinical Presentation.

Figure 10

Figure 11

Figure 12

Figure 13

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Figure 15

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Figure 17

Roughness

More about rougness

Bursal hypertrophy, secondary changes in the undersurface of the coracoacromial arch, loss of the integrity of the upper aspect of the cuff tendons, degenerative changes of the tuberosities may all contribute to subacromial abrasion. Crepitus from subacromial abrasion is easily detected by placing the examiner's thumb and fingers on the anterior and posterior aspects of the acromion while the humerus is moved relative to the scapula (see figures 10 and 11). In that many shoulders demonstrate asymptomatic subacromial crepitus, it is important during the examination to ask whether the crepitus noted by the examiner is directly related to the patient's complaints.

Rotator cuff tear arthropathy is another cause of roughness associated with cuff disease. This term, coined by Neer and coworkers (Neer, Craig, 1983), denotes the loss of the glenohumeral articular surface in association with a massive rotator cuff deficiency (see figure 12). These authors described 26 shoulders of which over 75% were in female patients. The average age was 69 years; 20 per cent had evidence of contralateral cuff arthropathy, and 75 per cent had no history of trauma. Typically the shoulders were swollen, the muscles atrophic, and the long head biceps ruptured; passive elevation was limited to an average of 90 degrees of elevation and 20 degrees of external rotation (a degree of limitation atypical of uncomplicated cuff tears). Often the shoulder demonstrated anteroposterior instability. Collapse of the proximal humeral subchondral bone was a common observation. Glenoid, greater tuberosity, acromial, and lateral clavicular erosion were also commonly observed. The authors hypothesized that the arthropathy resulted from both mechanical factors (such as anteroposterior instability and superior migration of the humeral head) (see figures 13-17) and nutritional factors (such as loss of a closed joint space, lack ofnormal diffusion of nutrients to the joint surface, and disuse). To this list could be added the disruption of the tendinous--osseous circulation entering through the subscapular, anterior humeral circumflex, and suprascapular vessels. This condition is distinct from osteoarthritis, rheumatoid arthritis, avascular necrosis, and neurogenic arthropathy. (Neer, 1983)

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This resource has been provided by the University of Washington Department of Orthopaedics and Sports Medicine as general information only. This information may not apply to a specific patient. Additional information may be found at http://www.orthop.washington.edu or by contacting the UW Department of Orthopaedics and Sports Medicine.

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