The Rotator Cuff–Deficient Arthritic Shoulder: Diagnosis and Surgical Management Craig A. Zeman, MD, Michel A. Arcand, MD, Jeffery S. Cantrell, MD, John G. Skedros, MD, and Wayne Z. Burkhead, Jr, MD Abstract The symptomatic rotator cuffÐdeficient, arthritic glenohumeral joint poses a localized shoulder arthritis associ- complex problem for the orthopaedic surgeon. Surgical management can be facil- ated with a large swelling about itated by classifying the disorder in one of three diagnostic categories: (1) rotator the shoulder, rotator cuff tear, cuffÐtear arthropathy, (2) rheumatoid arthritic shoulder with cuff deficiency, or biceps tendon rupture, and erosion (3) degenerative arthritic (osteoarthritic) shoulder with cuff deficiency. If it is of the superior portion of the not possible to repair the cuff defect, surgical management may include prosthet- humeral head, acromion, and distal ic arthroplasty, with the recognition that only limited goals are attainable, par- clavicle. In his classic 1934 text, ticularly with respect to strength and active motion. Glenohumeral arthrodesis Codman described the case of a 51- is a salvage procedure when other surgical measures have failed. Arthrodesis is year-old woman who had sus- also indicated in patients with deltoid muscle deficiency. Humeral hemiarthro- tained a traumatic rotator cuff tear plasty avoids the complications of glenoid loosening and is an attractive alterna- 6 years prior to surgery. During tive to arthrodesis, resection arthroplasty, and total shoulder arthroplasty. The the operation he found, in addition functionally intact coracoacromial arch should be preserved to reduce the risk of to the large cuff defect, humeral anterosuperior subluxation. Care should be taken not to ÒoverstuffÓ the gleno- head roughening, glenoid oblitera- humeral joint with a prosthetic component. In cases of significant internal rota- tion, intra-articular loose bodies, tion contracture, subscapularis lengthening is necessary to restore anterior and severe atrophy of the surrounding posterior rotator cuff balance. If the less stringent criteria of NeerÕs Ólimited musculature, and a large fluid goalsÓ rehabilitation are followed, approximately 80% to 90% of patients treated accumulation. He believed that with humeral hemiarthroplasty can have satisfactory results. these changes were the final stages J Am Acad Orthop Surg 1998;6:337-348 of a chronically neglected large rotator cuff tear. The patient with a symptomatic must also deal with osteopenic rotator cuffÐdeficient, arthritic bone, severe soft-tissue contrac- Dr. Zeman is in private practice in Oxnard, glenohumeral joint poses a complex tures, and atrophied muscles. It Calif. Dr. Arcand is in private practice in problem for the orthopaedic sur- may be impossible to repair the cuff Norman, Okla. Dr. Cantrell is in private prac- geon. Although this condition has defect. Consequently, many of the tice in Lewisville, Tex. Dr. Skedros is in private been recognized since the early 19th patients who come to surgery are practice in Ogden, Utah. Dr. Burkhead is century, there is no consensus on its treated with prosthetic arthroplasty Clinical Associate Professor of Orthopaedic Surgery, University of Texas Southwestern 1-8 management. One of the difficul- with the recognition that only limit- Medical School, Dallas; and is in private prac- ties is the diverse clinical presenta- ed goals are attainable, particularly tice with W. B. Carrell Memorial Clinic, tion of patients with this disorder: with respect to strength and active Dallas. some have rotator cuffÐtear arthrop- motion.1,7,9-11 athy (RCTA), as defined by Neer et Reprint requests: Dr. Zeman, W. B. Carrell al1; others have end-stage rheuma- Memorial Clinic, 2909 Lemmon Avenue, Dallas, TX 75204. toid arthritis (RA) or degenerative History arthritis with cuff tears. Different Copyright 1998 by the American Academy of surgical solutions may be required Between 1830 and 1860, Smith and Orthopaedic Surgeons. for each presentation.9 The surgeon Adams described several cases of Vol 6, No 6, November/December 1998 337 Rotator Cuff–Deficient Arthritic Shoulder More than a century later, Bur- of the following diagnostic cate- humeral joint.14 For example, the man and co-workers described gories: (1) RCTA, (2) degenerative glenohumeral joint is balanced cases of recurrent spontaneous hem- arthritic (osteoarthritic) shoulder anteriorly and posteriorly by the orrhage into the subdeltoid bursa in with cuff deficiency, and (3) rheu- subscapularis, infraspinatus, and elderly patients with supraspinatus matoid arthritic shoulder with cuff teres minor. Most large rotator cuff tendon tears and glenohumeral deficiency. Categorization is based tears extend posteriorly into the arthritis. In 1968, DeSeze called this on specific clinical, radiographic, infraspinatus and teres minor, leav- condition l'Žpaule sŽnile hŽmorragique and laboratory findings. These des- ing the subscapularis unbalanced. (Òhemorrhagic shoulder of the ignations help the surgeon antici- Due to unbalanced force couples, elderlyÓ). In 1977, Neer introduced pate the quality of tissues, the natural volitional attempts to elevate the term Òcuff-tear arthropathyÓ to history of the disease, and the ulti- and/or rotate the arm can produce describe findings associated with a mate surgical outcome. destructive forces in the gleno- chronic full-thickness rotator cuff humeral joint. A deficient cuff may tear, which include restricted shoul- Rotator Cuff–Tear Arthropathy allow excessive upward migration der motion, erosions of the osseous In a 1983 landmark review arti- of the humeral head, resulting in structures of the shoulder, and an cle, Neer et al1 expounded on NeerÕs abrasion and erosion of the superi- arthritic, osteopenic, and collapsed original description of RCTA. or glenoid, acromioclavicular joint, humeral head.1 In the early 1980s, Because RCTA was found not to be and acromion. Because only about Halverson et al12,13 described the associated with degenerative arthri- 4% of shoulders with full-thickness ÒMilwaukee shoulder syndrome,Ó tis in other joints, they suggested rotator cuff defects progress to which is in many ways similar to that a massive rotator cuff tear is the RCTA,1 mechanical factors do not RCTA. initial event in the pathogenesis. appear to be wholly responsible for They also described mechanical and the pathologic features of RCTA nutritional factors that may precipi- described by Neer. Types of Rotator Cuff tate development of RCTA (Fig. 1). Problems in Arthritic Nutritional Factors Shoulders Mechanical Factors As in other diarthrodial joints, The concept of Òforce couplesÓ the articular surfaces of the shoul- Surgical management of a rotator in the shoulder emphasizes the crit- der receive nutrition from synovial cuffÐdeficient arthritic shoulder can ical nature of mechanical factors in fluid. A full-thickness rotator cuff be facilitated by assigning it to one the dynamic stability of the gleno- tear violates the closed joint space, Mechanical Factors Nutritional Factors Massive cuff defect Massive cuff defect Reduced motion and function Loss of “water-tight” joint space Head migrates upward Gross instability Disuse osteoporosis and Loss of pressure and Wear into acromion, acromio- Recurrent dislocations via biochemical changes in diminished quantity of clavicular joint, and coracoid “posterior mechanism” water and glycosamino- glycan content of cartilage joint fluid Cartilage atrophy Abnormal trauma and subchondral collapse Cuff-tear arthropathy Cuff-tear arthropathy Fig. 1 Mechanical factors (left) and nutritional factors (right) that contribute to joint destruction in RCTA, according to Neer et al.1 (Adapted with permission from Neer CS II, Craig EV, Fukuda H: Cuff-tear arthropathy. J Bone Joint Surg Am 1983;65:1232-1244.) 338 Journal of the American Academy of Orthopaedic Surgeons Craig A. Zeman, MD, et al allowing synovial fluid, with its particular seem to occur in the increasing pain that is worse at nutrients and other biochemical more destructive atrophic situa- night and is intensified by gleno- constituents, to leak into the subdel- tions. Consequently, they speculat- humeral motion. They also report toid and subacromial spaces and ed that BCP crystals may be a prod- loss of active shoulder motion. The surrounding soft tissues. In addi- uct of articular surface wear, and observation by Neer et al1 that 10 tion, pain leads to shoulder inactivi- that the crystals are produced by of 26 patients with RCTA had not ty, which reduces the delivery of processes that are secondary to joint received antecedent corticosteroid synovial nutrients and produces destruction and are not the inciting injections diminishes their impor- disuse osteopenia and joint stiff- cause. They proposed crystal depo- tance as an etiologic factor. ness. All of these factors contribute sition as an opportunistic event in Patients with OA and rotator to articular cartilage destruction. OA, with the joint damage predis- cuff tears also relate a history of posing to deposition, and the de- progressive pain and stiffness. It is Inflammatory Factors posits in turn modifying the under- not uncommon for these patients to The rheumatology literature con- lying disease. If this interpretation relate an acute traumatic event fol- tains an abundance of clinical cases is correct, Milwaukee shoulder syn- lowed by increased shoulder weak- that appear grossly similar to drome may be a localized form of ness and symptoms. Patients with RCTA.12-17 However,