James E. Moravek

Reverse total shoulder arthroplasty for the management of failed shoulder arthroplasty with proximal humeral bone loss: is allograft augmentation necessary?

BACKGROUND Patients undergoing revision shoulder arthroplasty frequently have deficient proximal humeral bone stock. Proximal humeral allograft has been recommended to augment reverse total shoulder arthroplasty (RTSA) to improve stability and function. This study reports the results of RTSA without proximal humeral allograft in patients with proximal humeral bone loss secondary to failed shoulder arthroplasty. MATERIALS AND METHODS From 2005 to 2008, 251 patients were enrolled in a prospective RTSA cohort study. Significant humeral bone loss was demonstrated in 15 of 56 undergoing revision for failed arthroplasty. Average age was 67 years. Average bone loss measured 38.4 mm (range, 26-72 mm). Patients were followed up for a minimum of 2 years with American Shoulder and Elbow Surgeons (ASES), Subjective Shoulder Value (SSV), Constant Score (CS), and visual analog scale (VAS) pain scores, as well as self-reported satisfaction and radiographs. RESULTS Patients demonstrated significant improvement in mean CS (23.0 to 44.2), ASES (38.2 to 68.3), ASES activities of daily living (7.0 to 15.9), SSV (19.2 to 75.8), and VAS pain (4.6 to 1.6) scores. Thirteen of 15 patients reported satisfaction (87%). Range of motion improved in forward flexion (38.3° to 103.2°) and external rotation (-0.5° to 11.9°). Radiographs demonstrated notching in 3 patients (20%), no humeral subsidence or loosening, and prosthetic fracture of 1 modular humeral stem. CONCLUSIONS Use of RTSA for failed shoulder arthroplasty and deficient humeral bone stock provides a significant clinical benefit without the need for allograft augmentation. Monoblock humeral component use may diminish risk for prosthetic fracture.

The evaluation of the failed shoulder arthroplasty

As the incidence of shoulder arthroplasty continues to rise, the orthopedic shoulder surgeon will be increasingly faced with the difficult problem of evaluating a failed shoulder arthroplasty. The patient is usually dissatisfied with the outcome of the previous arthroplasty as a result of pain, but may complain of poor function due to limited range of motion or instability. A thorough and systematic approach is necessary so that the most appropriate treatment pathway can be initiated. A comprehensive history and physical examination are the first steps in the evaluation. Diagnostic studies are numerous and include laboratory values, plain radiography, computed tomography, ultrasound imaging, joint aspiration, nuclear scans, and electromyography. Common causes of early pain after shoulder arthroplasty include technical issues related to the surgery, such as malposition or improper sizing of the prosthesis, periprosthetic infection, neurologic injury, and complex regional pain syndrome. Pain presenting after a symptom-free interval may be related to chronic periprosthetic infection, component wear and loosening, glenoid erosion, rotator cuff degeneration, and fracture. Poor range of motion may result from inadequate postoperative rehabilitation, implant-related factors, and heterotopic ossification. Instability is generally caused by rotator cuff deficiency and implant-related factors. Unfortunately, determining the cause of a failed shoulder arthroplasty can be difficult, and in many situations, the source of pain and disability is multifactorial.

The impact of rotator cuff deficiency on structure, mechanical properties, and gene expression profiles of the long head of the biceps tendon (LHBT): Implications for management of the LHBT during primary shoulder arthroplasty

The long head of the biceps tendon (LHBT) occupies a unique proximal intra‐articular and distal extra‐articular position within the human shoulder. In the presence of a rotator cuff (RC) tear, the LHBT is recruited into an accelerated role undergoing potential mechanical and biochemical degeneration. Intra‐articular sections of the LHBT were harvested during primary shoulder arthroplasty from patients with an intact or deficient RC. LHBTs were stained (H&E, Alcian Blue) and subjected to histologic analysis using the semiquantitative Bonar scale and measurement of collagen orientation. LHBTs (n = 12 per group) were also subjected to gene‐expression analyses via an RT2‐PCR Profiler Array quantifying 84 genes associated with cell‐cell and cell‐matrix interactions. LHBTs (n = 18 per group) were biomechanically tested with both stress‐relaxation and load‐to‐failure protocols and subsequently modeled with the Quasilinear Viscoelastic (QLV) and Structural‐Based Elastic (SBE) models. While no histologic differences were observed, significant differences in mechanical testing, and viscoelastic modeling parameters were found. PCR arrays identified five genes that were differentially expressed between RC‐intact and RC‐deficient LHBT groups. LHBTs display signs of pathology regardless of RC status in the arthroplasty population, which may be secondary to both glenohumeral joint arthritis and the additional mechanical role of the LHBT in this population.

Exploring Failure of Total Shoulder Arthroplasty Systems Through Implant Retrieval, Radiographic, and Clinical Data Analyses:

Background Retrieved clinically failed anatomic total shoulder arthroplasty (TSA) components as well as associated radiographs and medical records were analyzed in order to investigate the origins of clinical failure(s) of TSA components. Methods Fifty TSA systems were retrieved from 48 patients including 27 females and 21 males; components were implanted for an average of 68 months (range, 2–267). Data obtained through radiographic analysis, medical records review, and damage mode analysis of each component were performed and statistically analyzed. Results Significant correlations were found between glenoid loosening and preoperative pain (r = 1.00, P < .001), humeral stem scratching and humeral loosening (Zone 1: r = .60, P < .01; Zone 2: r = .45, P = .03; Zone 3: r = .45, P = .03) , as well as glenoid damage and rotator cuff tears (r = .36, P = .02). Discussion Wear and damage of the glenoid and humeral components, which may result from rotator cuff tearing, may lead to accelerated loosening, clinical failure, and early revision arthroplasty. Improved implant design and/or surgical indications may improve implant performance, thereby reducing the incidence of implant damage and wear, and result in improved clinical outcomes.

Current concepts in subacromial impingement and the role of acromioplasty

The treatment of subacromial impingement syndrome remains a controversial entity among both primary care physicians and orthopaedic surgeons. The initial management of this disorder is usually conservative with directed physiotherapy, subacromial corticosteroid injections and nonsteroidal anti-inflammatories representing the mainstays of treatment. Surgery in the form of arthroscopic bursectomy or acromioplasty is reserved for those patients who fail at least 6 months of conservative management. Traditionally, there have been few high-level studies to guide the practitioner concerning when conservative treatment has failed, which patients are candidates for surgical intervention or which surgical intervention may be most appropriate for a particular patient. However, recent studies have improved our knowledge base of the pathophysiology underlying this disorder and they provide some useful guidance on the conservative and operative management of this complex problem.