Over the past decade, there has been a significant increase in the prevalence of shoulder arthroplasty1. As a result, a wider spectrum of complications associated with shoulder arthroplasty will be encountered. The purpose of this paper was to discuss the management and methods of prevention of the most common complications associated with shoulder arthroplasty.
The reported prevalence of periprosthetic fractures associated with shoulder arthroplasty is between 1.6% and 2.3%2. Potential etiologies include osteopenia, cortical thinning from osteolysis, excess reaming of the humeral cortex, and eccentric placement of the humeral component.
Initially, anteroposterior and axillary radiographs are necessary. It is important that the radiographs include the entire humerus to determine the exact length of the fracture as well as to clearly evaluate for evidence of component loosening. Computed tomography (CT) scans may be very useful in evaluating for component loosening, particularly for the glenoid.
The most widely used classification system was described by Wright and Cofield3. This system is based on the location of the fracture in relation to the tip of the prosthesis. Type-A fractures occur at the tip of the prosthesis and extend proximally. Type-B fractures occur at the tip of the prosthesis without extension. Type-C fractures occur at the prosthetic tip and have distal extension.
The literature indicates that classification of the fracture helps to predict the outcome of treatment. Boyd et al. reported on the outcome of seven periprosthetic fractures, six of which did not heal with nonoperative treatment4. All of the fractures were centered at the tip and were Type-B fractures. Type-B fractures have a high rate of nonunion with nonoperative treatment2. Campbell et al. reported on five fractures that healed with nonoperative treatment, with four fractures distal to the tip of the humeral stem (Type C)5. These Type-C fractures have a high rate of healing with nonoperative treatment5.
Kumar et al. reported on the outcome of sixteen periprosthetic humeral fractures, all followed until union (Figs. 1-A through 1-E)2. The mean interval from arthroplasty to fracture was forty-nine months. None of the patients had an ipsilateral total elbow arthroplasty. The most common mechanism of injury was a fall on the upper extremity. Six fractures healed with nonoperative treatment at a mean of 180 days (range, forty-nine to 332 days). Five fractures were treated surgically after failing to heal with nonoperative management. Five fractures underwent immediate surgery. Excluding one patient who required multiple surgical procedures, including a free vascularized fibular graft to heal, the mean time to healing was 230 days. At the most recent follow-up at a mean of 5.5 years, the average shoulder abduction was 107° and average external rotation was 43°.
Kumar et al.2 recommended the following treatment:
Type C (Loose Humeral Component)
When the humeral component is loose, one can consider placing a long-stemmed component with bone graft at the fracture site.
Type C (Well-Fixed Humeral Component)
When the humeral component is well fixed, the fracture is treated as a closed humeral shaft fracture. A trial of nonoperative treatment using an orthosis is recommended if an acceptable closed reduction can be obtained.
Type B (Loose Humeral Component)
The prosthesis should be revised to a long-stemmed humeral component with allograft at the fracture site. The additional use of a strut allograft or a plate and screws can be considered to improve fracture fixation.
Type B (Well-Fixed Humeral Component)
A trial of nonoperative treatment should be considered initially. However, four of five Type-B fractures treated nonoperatively failed to heal and eventually required surgery2. If surgery is performed, a plate and screws or allograft strut fixation distally and cerclage fixation proximally with or without autogenous bone graft should be considered, as this approach is often an attractive alternative to revising a well-fixed prosthesis.
Type A (Loose Humeral Component)
Revision arthroplasty using a long stem with allograft is necessary, and one should consider a strut allograft or plate and screws to improve fixation.
Type A (Well-Fixed Humeral Component)
The management of this fracture type is debated. However, if there is substantial overlap of the fracture and humeral stem, the humeral component has an increased likelihood of being loose and revision arthroplasty is necessary.
Infection is a rare but devastating complication after shoulder arthroplasty. The prevalence has been reported to range between 0% and 4%6,7. There is minimal information to guide decision making. Therefore, the rationale behind evaluation and treatment is derived in large part from the reported experience in managing infection at the site of total knee arthroplasty and total hip arthroplasty.
A humeral component that has become loose is considered to be associated with infection until proven otherwise. First, one must determine the time course of the pain and whether the patient had a recent procedure, such as dental work, that may have caused bacterial seeding of the joint. Did the patient have wound-healing problems or prolonged antibiotic use at the time of the initial shoulder arthroplasty? The prior operative reports should be reviewed and the indication for the original procedure determined. All prior radiographs should be reviewed.
Diagnosis of infection can be challenging. The majority of patients do not present with overt signs of infection. Topolski et al. evaluated the outcome of seventy-five patients with positive cultures at the time of revision shoulder arthroplasty without overt signs of infection8. The white blood-cell count was normal in 93% (sixty-seven) of seventy-two patients, polymorphonuclear cell or neutrophil distribution was normal in 91% (sixty-four) of seventy patients, erythrocyte sedimentation rate was normal in 86% (thirty-six) of forty-two patients, and C-reactive protein was normal in 75% (twelve) of sixteen patients. For these patients, the intraoperative histological studies were negative for acute inflammation in 92% (sixty-seven of seventy-three patients). Propionibacterium acnes is the most common organism responsible for infection after shoulder arthroplasty7. However, as shown by Topolski et al., the first culture to become positive required an average of 5.1 days8, so reviewing culture data after shoulder aspiration is necessary for at least a week.
Coste et al. reported on eight shoulders that had debridement for infection6. Each of two arthroscopic debridements failed, and four of six open debridements failed. Sperling et al. noted that three of six open debridements failed7. Ince et al. reported on nine patients with a one-stage reimplantation without any recurrent infection9. Strickland et al. reported on the outcome of two-stage reimplantation in nineteen patients10. At the time of the most recent follow-up of these patients, the mean shoulder elevation was 89° and mean external rotation was 48°. There were a substantial number of complications, including the need for secondary surgical procedures in five patients and for chronic antibiotic treatment for infection suppression in six patients.
Type I: Positive Cultures at Time of Revision Surgery
Organism-specific antibiotic treatment is instituted with close clinical observation. There are no good data to determine the optimal length of antibiotic treatment.
Type II: Acute Infection within Thirty Days After Surgery
Surgical debridement and prosthetic retention is utilized, although there are minimal data available on the outcomes of this approach.
Type III: Acute Hematogenous Infection More Than Thirty Days After Surgery
Surgical debridement with retention of the implants or two-stage treatment with use of an antibiotic spacer impregnated with gentamycin and vancomycin between explantation and reimplantation is recommended.
Type IV: Chronic Infection
Surgical debridement with implant removal, temporary placement of an antibiotic spacer impregnated with gentamycin and vancomycin, and reimplantation approximately eight weeks later are recommended.
There are different patterns of shoulder instability after arthroplasty. Superior instability is usually associated with a deficient rotator cuff and/or coracoacromial arch. Although superior instability is characterized by a loss of contact between the glenoid and the proximal part of the humerus, this pattern of instability is a separate topic. The focus of this section is anterior and posterior instability after shoulder arthroplasty. The causes, characteristics, and treatment of prosthetic instability are different after nonconstrained anatomic arthroplasty or semiconstrained reverse arthroplasty and are discussed separately.
The reported frequency of anterior instability after total shoulder arthroplasty with an anatomic prosthesis has ranged from 0.9% to 1.8%11,12. There are two main causes: soft-tissue abnormality (subscapularis rupture or insufficiency) or component malposition (humeral and/or glenoid anteversion). Some patients may have both.
Treatment results are generally discouraging when an anatomic prosthesis is revised to another anatomic prosthesis. Sanchez-Sotelo et al. reported that after subscapularis repair, component revision, and humeral head exchange was performed in nineteen shoulders, stability was obtained in only five13. Ahrens et al. repaired the subscapularis, transferred the pectoralis major tendon, and reoriented the humeral and glenoid components in thirty-five shoulders11. There was recurrent instability in more than half of the shoulders. However, all three shoulders that underwent a revision to a reverse shoulder arthroplasty were stable. Moeckel et al. described repair of the subscapularis in seven patients with anterior instability14. Three of the patients continued to have instability and underwent subsequent reconstruction with an Achilles tendon allograft with successful results.
The rate of posterior instability after arthroplasty with an anatomic prosthesis has been reported to range from 1% to 1.3%11,12. There are two primary causes: soft-tissue abnormality (excess posterior capsular laxity) or component malposition (humeral and/or glenoid retroversion). The patient with preoperative posterior static instability with an associated biconcave glenoid is predisposed to posterior instability after arthroplasty with an anatomic prosthesis.
There are a variety of strategies to restore stability in shoulders with posterior instability. It is critical to address all potential causes of instability including restoration of normal retroversion of the components, posterior capsular tightening, and potential immobilization in neutral rotation. Sanchez-Sotelo et al. reported that the outcome after the treatment of fourteen patients with posterior instability was categorized as good for nine patients and as a failure for five13. Ahrens et al. reported that, after twenty-nine patients had a revision, fifteen patients had a good result and fourteen had a failure11. All four patients who had revision to a reverse arthroplasty had a stable shoulder.
Instability after a reverse arthroplasty is more frequent in revision arthroplasty and primary arthroplasty for posttraumatic arthritis. The causes are soft-tissue abnormalities (inadequate deltoid tension), component malposition, or both. The key to avoiding instability after reverse arthroplasty is to restore the humeral length. The surgical approach may influence the rate of instability. A superior approach has been noted to have a lower prevalence of instability compared with a deltopectoral approach15. Additionally, there is increasing interest in repairing the subscapularis and then protecting this repair with limitation of shoulder motion for four to six weeks.
It is necessary to carefully assess the humeral length in a patient with unstable reverse arthroplasty components. It may be helpful to obtain a CT scan to evaluate the glenosphere position to ensure proper version. In the acute setting, a closed reduction can be attempted. If open reduction is done, it is essential to have the appropriate instrumentation available to place a thicker humeral bearing surface, to increase the diameter and/or thickness of the glenosphere, or to place a retentive insert.
There are a variety of different presentations of rotator cuff tearing after shoulder arthroplasty12,16. Rupture of the subscapularis is the most frequent and may present with anterior subluxation of the humeral head on the axillary radiograph12. The rate of postoperative rupture of the subscapularis is likely underestimated12. There may be a traumatic or an atraumatic onset. Often, the tear is asymptomatic with a loss of strength discovered at clinical examination, including excessive external rotation with the elbow at the side or a positive belly-press test.
The rate of rotator cuff tearing after shoulder arthroplasty has been reported to range from 1.3% to 7.8%12,17-20. Rupture of the posterosuperior aspect of the cuff (the supraspinatus and/or the infraspinatus and/or the teres minor) may occur and typically presents with upward migration of the humeral head with a decreased acromiohumeral distance on anteroposterior radiographs.
There are several important factors to consider so as to avoid this complication. Because subscapularis fatty infiltration may be associated with a high risk for nonhealing and secondary insufficiency, knowing that it exists before surgery may reduce the risk. This may be determined by physical examination as well as possible imaging studies including magnetic resonance imaging (MRI). Key technical steps at the time of surgery include intraoperative mobilization of the superior tendon with release of subcoracoid adhesions, release of the middle and inferior glenohumeral ligaments, and sparing the innervation of the subscapularis. It is important to avoid overstuffing the joint. A secure repair of the subascapularis is critical as is postoperative protection of this subscapularis repair. The postoperative safe range of motion for physical therapy is determined at the time of surgery.
Treatment of the postoperative subscapularis tear is challenging. Miller et al. reported on early repeat repair with gentle mobilization in patients with symptomatic rupture21. For patients with a chronic rupture, we recommend consideration of an augmentation of the repair with a pectoralis major tendon transfer.
Deprey described attempted tendon repair with placement of a smaller prosthetic humeral head, as well as possible pectoralis major transfer19. In that report of twenty-two shoulders, the functional gain was minimal.
In patients with a traumatic acute subscapularis rupture with good quality tendon and muscle, an immediate revision to repair the tendon is likely the best treatment. In patients with a chronic tear with fatty infiltration, nonoperative treatment is preferred if there are minimal symptoms because repair with or without pectoralis major transfer does not provide good results22. For the patients with symptoms, a reverse arthroplasty may also be considered.
The frequency of postoperative rupture of the posterosuperior aspect of the rotator cuff has been reported to be variable, but is usually associated with rheumatoid arthritis23-26. It may occur secondary to trauma or degeneration without trauma but increases with time from surgery. Young et al. reported on the outcome of 518 total shoulder arthroplasties for primary osteoarthritis with a mean follow-up of 8.7 years20. The survivorship free of secondary cuff failure was 100% at five years, 84% at ten years, and 43% at fifteen years following surgery.
There are several potential predisposing factors20,27, including preoperative fatty infiltration of the rotator cuff muscles as detected on MRI (p < 0.05), superior tilt of the glenoid component on immediate postoperative radiographs (p < 0.01), and a longer duration of follow-up (p < 0.001).
Weakness in shoulder forward elevation and external rotation is the common symptom. Patients with a postoperative tear have a worse clinical outcome with respect to the Constant score, subjective results, and shoulder motion20. Results using radiographic criteria are also worse. However, Young et al. reported that the revision rate was not significantly different between patients with and those without secondary rotator cuff failure20.
Patients with minimal symptoms can be treated without surgery because attempts at repair have not been very successful. In the series by Hattrup et al.24, repair was successful in only four of eighteen shoulders. For the patient with symptoms, the use of revision to reverse arthroplasty with or without latissimus dorsi transfer appears to be the best treatment.
Glenoid components remain a primary concern in shoulder arthroplasty. The presence of radiolucent lines around the glenoid component may not be clinically important. Miller and Bigliani reported that radiolucent lines were common, but there was no direct correlation to the level of clinical symptoms28. Brems reported on the association between lucent lines and revision procedures with an analysis of twenty reported series of total shoulder arthroplasties29. At a mean follow-up of five years, radiolucent lines were seen around 39% of all total shoulder replacements. For all of the shoulders with periprosthetic lucency, the rate of revision surgery was 8%. We found that lucent lines may be reflective of the operative technique, glenoid bone quality, and changes that may result from stress-shielding or disuse osteoporosis. We believe that careful preparation of the glenoid bone and the use of a minimal amount of cement reduce the prevalence of glenoid loosening. Loosening of the glenoid component is associated with rotator cuff deficiency, as Franklin et al. reported seven patients with glenoid component loosening associated with rotator cuff insufficiency30.
Evaluation of glenoid loosening requires proper radiographs, preferably made with use of fluoroscopically positioned views. If it is difficult to determine whether the glenoid component is loose, a CT scan is useful.
Prevention of loosening is critical. The surgeon must have a clear understanding of the glenoid anatomy including the specific wear pattern. Careful review of preoperative radiographs is essential. A CT scan will aid in planning if the wear pattern is not determined with radiographs. Key technical steps to prevent loosening include preserving as much native glenoid bone stock as possible during preparation and removal of only that amount of bone essential to place the implant, including minimal reaming. Additional preparation includes pulsatile saline solution lavage, careful drying of the glenoid bone, mixing the bone cement to diminish porosity, and pressurizing the bone cement.
Overall, a substantial number of glenoid components that have loosened do not require revision surgery. If a patient becomes symptomatic, it is imperative to rule out other problems as a reason for the symptoms, including a rotator cuff insufficiency or a low-grade infection. Each of these may occur alone or together with loosening of the glenoid.
The largest series, as far as we know, on revision for glenoid component loosening was reported by Cheung et al.31. Those authors reviewed the results after revision for glenoid loosening in sixty-eight shoulders in sixty-six patients. In the study, thirty-three shoulders underwent placement of a new glenoid component, and thirty-five shoulders had removal and bone-grafting without glenoid reimplantation. The authors noted significant overall improvement with regard to pain in both groups. Twenty-four (73%) of thirty-three patients who received a new glenoid component were satisfied compared with nineteen (54%) of thirty-five who had only bone-grafting. Nine shoulders with a new glenoid component and three with bone-grafting had an excellent or satisfactory result (p = 0.0432). Interestingly, twenty shoulders had positive cultures, with Propionibacterium acnes detected most frequently.
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Disclosure: None of the authors received payments or services, either directly or indirectly (i.e., via his or her institution), from a third party in support of any aspect of this work. One or more of the authors, or his or her institution, has had a financial relationship, in the thirty-six months prior to submission of this work, with an entity in the biomedical arena that could be perceived to influence or have the potential to influence what is written in this work. No author has had any other relationships, or has engaged in any other activities, that could be perceived to influence or have the potential to influence what is written in this work. The complete Disclosures of Potential Conflicts of Interest submitted by authors are always provided with the online version of the article.