Despite a well-placed reverse prosthesis, there is increased reliance on surrounding glenohumeral musculature, resulting from poor rotator cuff function and biomechanical differences compared with a native shoulder. Both our patients were found to have relatively small body habitus. It is possible that, by nature of their smaller statures, they were more susceptible to consequences of excessive joint and soft-tissue tension after RTSA. One explanation for acromial fractures after RTSA is that, by excessively lengthening and/or lateralizing the deltoid, the tension on the acromion in these elderly patients may be sufficient to cause a fracture. A similar mechanism may explain their coracoid fractures. As the arm is lengthened and the prosthesis is tightened, the conjoint tendon is significantly tensioned. We routinely check the tension of these muscles as an extra confirmation of joint stability. However, excessive tension for a significant duration may provide too much stress for bone turnover to match with the inherent repair process, potentially causing a fracture. Recent evidence has also found that bone mineral density of the coracoid diminishes with age, suggesting some predisposition to fracture with lower-energy mechanisms.22
Another possible cause for coracoid fractures may be the orientation of the implants. While we did not have mechanistic evidence, it is possible that, with adduction and internal rotation, prosthetic impingement against the coracoid is feasible, particularly in patients of small stature. Although a glenoid implant placed high can increase the chance for coracoid–implant impingement, the fact that the patients improved without revision makes chronic mechanical impingement less likely. Drill holes, especially multiple ones, placed throughout the base of the coracoid may also predispose to coracoid fractures.
Patients with periscapular fractures (acromion, scapular spine, or coracoid) after RTSA often present with pain and occasional deficits in function. Both patients in this series noted pain out of proportion to examination. The onset of this pain differed, with 1 patient noting pain within the first 3 months and 1 noting discomfort later. Neither patient had any trauma. In the presence of significant symptoms, negative radiographs, and a poor response to conservative treatment, we recommend advanced imaging to rule out fracture. However, prior to obtaining advanced imaging, proper radiographic techniques should be utilized. Eyres and colleagues,23 in a series of 12 fractures of the coracoid process, relied primarily on coracoid views directed 45° in a cephalic direction and thin-slice CT. An isotope bone scan identified 1 case not initially found on radiographs.23
Conservative management with use of a sling until resolution of symptoms was successful in our series. If symptoms persist, a bone stimulator can be used prior to implementing a surgical solution; however, current evidence does not expound on timing and utility of such modalities. Perhaps as important as treatment is education of the patient and the rehabilitation team about the importance of identifying increasing pain as a potential sign of impending fracture in this population. Subsequent activity modification until the pain resolves can help avoid the setback in postoperative recovery that this complication may cause.
Conclusion
We present 2 patients with coracoid fractures encountered at 3 months and 15 months after RTSA. Nonoperative management proved adequate in treating both cases. We suggest a high level of suspicion for possible fracture in the patient who comes in with new-onset pain in a localized region with or without functional deficits.