The arthritic shoulder with irreparable massive cuff deficiency is one of the most difficult and challenging issues in shoulder practice because of the combination of severe articular and periarticular soft-tissue damage. This entity is the common end-stage result of several disease processes such as rheumatoid arthritis, rotator cuff tear arthropathy, and Milwaukee shoulder syndrome. By creating a substantial defect in the rotator cuff tendons, these disease processes lead to destabilization of the glenohumeral joint with subsequent superior migration of the humeral head and secondary severe damage to both the intraarticular and extraarticular elements. The result is a painful, dysfunctional shoulder that necessitates, in many cases, a surgical solution to be carried out to decrease patient morbidity. The lack of adequate stability and the insufficient bone stock make the task of replacing the damaged joint with a stable construct a very difficult task. The aims of this chapter are to review the pathomechanics of this disorder, to evaluate the different treatment options, to discuss the indications for surgical treatment, to elaborate on the different surgical options, and to establish a decision-making
algorithm for the patient with a rotator cuff-deficient arthritic (RCDA) shoulder (Fig. 8-1).

The glenohumeral joint lacks significant intrinsic bony stability and thus relies to a great extent on its soft-tissue components. The rotator cuff tendons provide a major contribution to the dynamic stabilization of the glenohumeral joint by increasing the concavity-compression force in the joint (1, 2, 3, 4, 5). By their synchronous action, they oppose the displacing effect of the strong deltoid muscle, keeping the humeral head centered in the glenoid fossa throughout its movement (6, 7, 8). The coupled work of the infraspinatus and subscapularis has been shown to be a major factor in superior glenohumeral stability, whereas the contribution of supraspinatus is less significant (9,10). A massive tear, consisting of the supraspinatus and at least one of the other rotator cuff tendons (11) (in most cases the infraspinatus), may render the rotator cuff’s anterior and posterior force couple ineffective in both the vertical and the transverse planes. The result is a diminution of joint reaction force and a change in the overall direction of the joint force that leads to the destabilization of the glenohumeral joint (12). In cases where the long head of biceps is still functional, it may oppose, to some extent, to the superior migration of the humeral head (13,14).

Once the proximal pull of the deltoid is left unopposed, the humeral head migrates superiorly toward the coracoacromial arch. The deltoid, which has lost its fulcrum, is left with a smaller mechanical advantage and therefore must generate more force to perform its function (15). The humeral head then articulates with the coracoacromial arch superiorly and the superior glenoid rim inferiorly, leading to flattening of the superior part of the humeral head and tuberosities (“femoralization”), rounding and thinning of the coracoacromial arch (“acetabularization”), and destruction of the superior glenoid region (Fig. 8-2). The acromioclavicular joint is also frequently involved in the process, joining its cavity with that of the now joined synovial intraarticular and subacromial bursal spaces. The end result is an incongruous, unstable joint with a higher joint friction and superiorly malpositioned center of rotation.

A pathomechanistic and pathomorphologic classification of RCDA, based on the position and stability of the humeral head, is presented in Fig. 8-3 (16). The classification is independent of the underlying pathologic conditions and is based on two critical issues for the function of the deltoid muscle: The glenohumeral center of rotation and the degree of anterior-superior instability.

Although sharing a common end result, it is important to recognize the various disease processes leading to glenohumeral RCDA joint.

Rheumatoid arthritis (RA) is the most common cause of RCDA. Between 48% and 65% of patients with RA have significant glenohumeral joint involvement. Approximately 24% of those with glenohumeral arthritis will have a simultaneous rotator cuff tear (17,18). Superimposed on the aforementioned changes are severe osteopenia, erosions of the entire glenoid without osteophyte formation, and medialization of the glenohumeral joint.

Cuff tear arthropathy (CTA) is the extreme end result of a massive rotator cuff tear. The term coined by Neer in 1983 (19) refers to a primary massive rotator cuff tear that, by virtue of mechanical superior instability and nutritional effects, leads to a secondary glenohumeral joint destruction (21). It is believed that between 0% and 25% of massive rotator cuff tears will end up as CTA, but it is difficult, if not impossible, to predict which of the massive tears will result in CTA.

The Milwaukee shoulder syndrome was originally described by McCarty in 1981 (20). This is an uncommon entity affecting shoulders of elderly people, predominantly women. It consists of a massive rotator cuff tear, joint instability, bony destruction, and a large blood-stained joint effusion containing basic calcium phosphate crystals, detectable protease activity, and minimal inflammatory elements. Its relation to rotator cuff arthropathy is not clear, and it might represent one spectrum of the disease. The role of the basic calcium phosphate crystals in creating this syndrome is still controversial. Whether it is the cause of the articular damage, through macrophage spillage of proteases, or just the result of the osteoarthritic process is still unknown (21).

Primary glenohumeral osteoarthritis is the most common reason for shoulder joint replacement. However, it is associated with rotator cuff tear in only 5% of patients, most of which are reparable. It is therefore uncommon for primary osteoarthritis to end up as RCDA.

Patients with an arthritic shoulder and an irreparable, massive cuff deficiency are primarily elderly people, with female gender predominance. Their main complaints are of severe shoulder pain; limited range of movement; and, in some cases, recurrent swelling of the shoulder. The pain is constant, aggravated by shoulder motion, and felt at the periacromial region and the glenohumeral joint line. On physical examination the examiner can observe wasting of the infraspinatus and supraspinatus muscles, a decrease in active and passive glenohumeral motion, and crepitus while moving the patient’s shoulder (21). The x-ray image is typical and consists of a superiorly positioned humeral head, an “acetabularized” socket built up from a thinned, sclerotic acromion, and the eroded upper glenoid fossa (Fig. 8.2). Occasionally, the acromioclavicular joint and distal clavicle are also damaged and are thus included in the “socket.” Cases of secondary stress fractures of the thinned acromion have also been published (22).

The combination of the clinical and radiologic information is, in most cases, sufficient to make the proper diagnosis, although other modalities such as computed tomography and magnetic resonance imaging may be needed for treatment planning.

RCDA shoulder combines severe articular damage, bone destruction, osteoporosis, and rotator cuff tendon deficiency resulting in glenohumeral destabilization. In contrast to the more common primary degenerative shoulder arthrosis, the inherent instability of the rotator cuff-deficient shoulder necessitates specific consideration. Severe pain and shoulder dysfunction lead many of these patients to seek medical advice. The treatment armamentarium available is variable and includes both conservative, nonsurgical treatment and surgical procedures such as humeral head replacement, total shoulder arthroplasty, and even arthrodesis and resection arthroplasty. The responsibility of the orthopedic surgeon is to tailor the best treatment option for the particular patient, taking into account the patient’s symptoms, functional needs, and the bone and soft-tissue conditions of the shoulder joint.