Rotator Cuff Failure.

Figure 13 - "Boutonniere" deformity

Figure 14 - Cuff tear arthropathy

Figure 15 - Acute extension of the defect

Conclusion

Effects of cuff failure

The concavity compression mechanism is compromised by cuff disease. Beginning with the early stages of cuff fiber failure, the compression of the humeral head becomes less effective in resisting the upward pull of the deltoid. Partial thickness cuff tears cause pain on muscle contraction similar to that seen with other partial tendon injuries (such as those of the Achilles tendon or extensor carpi radialis brevis). This pain produces reflex inhibition of the muscle action. In turn, this reflex inhibition along with the absolute loss of strength from fiber detachment makes the muscle less effective in balance and stability. The weakened cuff function allows the humeral head to rise under the pull of the deltoid, squeezing the cuff between the head and the coracoacromial arch. Under these circumstances, abrasion occurs with humeroscapular motion, further contributing to cuff degeneration. Degenerative traction spurs develop in the coracoacromial ligament which is loaded by pressure from the humeral head (analogous to the calcaneal traction spur that occurs with chronic strains of the plantar fascia). Upward displacement of the head also wears on the upper glenoid lip and labrum, reducing their contributions to the effective depth of the upper glenoid and to glenohumeral stability from concavity compression.

Further deterioration of the cuff allows the tendons to slide down below the center of the humeral head, producing a "boutonniere" deformity. The cuff tendons become head elevators rather than head compressors. Once the full thickness of the cuff has failed, abrasion of the humeral articular cartilage against the coracoacromial arch may lead to a secondary degenerative joint disease known as cuff tear arthropathy.

The progression from partial thickness tear toward cuff tear arthropathy can take place as a subtle and even subclinical degenerative process, with a few fibers giving way at a time. It can also progress as a series of episodes interpreted as "tendinitis," "bursitis," or "impingement syndrome." A more significant injury can produce an acute extension of the defect. It is important to note that cuff defects arising with minimal or no injury suggest that the cuff tissue is of poor quality and thus is more likely to fail again after surgical repair. By contrast, acute tears resulting from major injuries are more likely to involve robust tissue that is more amenable to a durable repair.

The disuse of torn tendon leads to scarring and atrophy of tendon and muscle. Loss of cuff material from the degenerative process limits what is available for repair. Local injections of steroids may further compromise the healing potential of failed cuff fibers. Once the humeral head has started to subluxate superiorly, increased stretching loads are placed on the residual tendons, tending to exacerbate the cuff defect. Long-standing superior subluxation leads to erosion of the upper glenoid lip, favoring continued superior subluxation even after cuff repair. Once the process of superior subluxation is established, stabilization of the humeral head in its normal position is difficult even if a cuff repair is achieved.

In summary

Disclaimer

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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