Radiographs of the involved shoulder provide the basis for an evaluation of the bony anatomy. A complete radiographic assessment consists of four standard views: a true anteroposterior (AP) of the glenohumeral joint with internal and external rotation of the proximal humerus, scapular Y, and axillary view. The bony structures should be evaluated for “quantity, quality, and deformity.” Bone quantity refers to the degree of bone loss that may be present as a result of inflammatory, degenerative, or traumatic processes. This most commonly applies to the humeral head and glenoid, but the acromion, distal clavicle, and coracoid may be affected as well. Bone quality refers to the structure of the available bone. The presence of both osteopenia and sclerosis should be noted, as each may present distinctly different challenges. Bone deformity is especially important in the posttraumatic patient and those with end-stage degenerative disease. In patients with a history of trauma, the greater and lesser tuberosities should be scrutinized for malunion, nonunion, and displacement. Similarly, any deformity of the humeral head and its relationship with the proximal humeral shaft must be considered when planning to insert a stemmed humeral prosthesis.

The added value of computed tomography (CT) for the evaluation of bone loss and deformity cannot be overstated. This is especially true for the glenoid. Both CT and three-dimensional (3D) CT reconstructions are particularly effective in understanding pathoanatomy, for the assessment of glenoid wear, scapular and glenoid vault morphology, as well as humeral head alignment and subluxation. This information is essential for preoperative planning and is discussed in detail in Chapter 6.

Assessment of the soft tissues is imperative when treating patients with glenohumeral arthritis. The degree of attainable motion and postoperative function following shoulder arthroplasty is largely dependent upon the integrity of the rotator cuff and deltoid muscles, as well as the overall balance of the shoulder’s dynamic
stabilizers. Muscle denervation and nerve injury must also be considered, as this too will influence surgical decision-making. History of trauma, prior surgery, and the type of glenohumeral arthritis each impact the status of the surrounding soft tissues, warranting preoperative attention and intraoperative preparedness for an array of technical challenges.

Magnetic resonance imaging (MRI) is particularly valuable for the assessment of concomitant rotator cuff pathology, which has implications for surgical planning, implant selection, and alignment of patient expectations regarding postoperative range of motion. In addition to evaluating for partial and complete rotator cuff tears, both MRI and CT can be used to determine the quality of remaining rotator cuff tissue.¹ The location and extent of rotator cuff fatty infiltration has been associated with specific patterns of glenoid wear, underscoring the interplay of bony and soft-tissue anatomy on the development of glenohumeral arthritis.²

Associated degenerative problems of the affected upper extremity require detailed assessment during the preoperative period. Foresight is particularly prudent in patients with polyarticular inflammatory arthritis who have ipsilateral elbow, wrist, and hand involvement; these issues may require staging of surgical procedures.³ Intervening on hand and wrist pathology prior to shoulder reconstruction may optimize overall function and ease surgical recovery. Patients using antibiologic medications for inflammatory conditions are likely to require a regimen holiday during the perioperative window to minimize risks of infection and delayed wound healing.⁴ Careful coordination among the patient, surgeon, rheumatologist, and all relevant medical providers is necessary to optimize the patient’s biologic environment for surgery while continuing to mitigate the symptoms of ongoing systemic disease throughout the initial postoperative recovery.

Associated degenerative problems of the lower extremities, as well as the dependence on assistive devices for ambulation, must also be considered. Load bearing on assistive walking devices after shoulder arthroplasty may prematurely stress implant fixation or subscapularis repair, increasing the risk of early postoperative complications.⁵,⁶ A patient with advanced glenohumeral arthritis who is also in need of a total hip or knee arthroplasty should completely recover from the lower extremity operation before shoulder arthroplasty is performed. It is our preference to wait at least 3 months and preferably closer to 6 months after shoulder arthroplasty before allowing the use of assistive devices for ambulation. Some individuals may require ambulatory aids for baseline function, independent of coexisting lower extremity conditions. The patient’s care team should implement preventative measures such as preoperative rehabilitation for adaptive gait training with the goal of using the assistive device in the nonoperative extremity postoperatively until the patient has sufficiently recovered and can resume use of the operative extremity. Modifications to the home environment may also be necessary along with a plan for assistance at home.

RA is a chronic systemic inflammatory disorder of unclear etiology characterized by a progressively debilitating, erosive, symmetrical polyarthritis. The estimated prevalence is 1% worldwide, with a female-to-male ratio of 3 to 5:1 that diminishes with age.²³ Prevalence increases starting in the third decade of life, and the disease affects more than 5% of the population older than 70 years.²⁴ Shoulder involvement remains a common finding in patients with long-standing RA (>5-year duration).²⁵ The incidence of end-stage shoulder RA has decreased considerably with the advent and improvement of antibiologic medication. The disease process is triggered by exposure of a genetically susceptible host to an arthritogenic antigen resulting in a breakdown of immunological self-tolerance and a chronic inflammatory reaction.²³ Acute arthritis is initiated in this manner. Ongoing autoimmune reaction, CD4+ helper T cell activation, and local release of inflammatory mediators and cytokines ultimately destroy the joint. Microvascular injury, synovial cell proliferation, and perivascular lymphocytosis result in the formation of an erosive, hyperplastic synovium (pannus) that grows over the articular surface. Immune complex deposition, complement activation, and production of cartilage matrix metalloproteinases cause proteoglycan and collagen degradation at the joint surface. The release of proinflammatory cytokines results in continued cartilage damage and increased osteoclast activity. This process yields bone erosion and soft-tissue degradation that frequently involves the insertion of the rotator cuff.²³

The initial presentation of RA is highly variable; however, greater than 90% of patients report generalized symptoms of fatigue, musculoskeletal pain, variable
fever, and weight loss.²⁴,²⁵ During the initial phases of disease, the clinical course may be characterized by quiescence during periods of remission. Early involvement typically affects the small joints of the hand and foot, while larger joints are affected later. Rheumatoid involvement of the shoulder may present with an insidious onset of pain, swelling, and progressive loss of motion reflective of both articular and periarticular involvement. Unlike other joints involved, glenohumeral RA commonly contributes to nocturnal symptoms. All synovial joints around the shoulder may be affected, including the glenohumeral, acromioclavicular, and sternoclavicular articulations. Seventy-five percent of RA patients eventually develop rotator cuff pathology, with 20% to 50% developing full-thickness tears.²⁶,²⁷ Findings on shoulder examination include those related to inflammation: tenderness, often diffuse but occasionally localized to the joint line; cutaneous warmth compared to surrounding areas; and variable swelling either due to glenohumeral effusion, or more often subacromial and subdeltoid fluid accumulation in the presence of a full-thickness rotator cuff tear. Erythema is not a typical symptom. Atrophy of the shoulder musculature due to rotator cuff pathology and/or disuse is usually present, though may be difficult to recognize due to generalized swelling or effusion. Active motion is typically compromised first, followed by both active and passive motion limitations. This can lead to fixed contractures in all three important planes of motion. Signs and symptoms of systemic involvement should also be noted in both the history and physical examination.

Laine has classified the progression of RA of the glenohumeral joint into three stages based on clinical and radiographic findings.²⁸ Stage I is characterized clinically by slight limitation of shoulder motion with mild to moderate pain, tenderness to palpation, and variable crepitation on range of motion; radiographs reveal only generalized osteopenia. Stage II describes moderate limitation of motion with crepitus and moderate to severe pain. Radiographic findings include osteopenia, erosive bony changes, and joint space narrowing. In stage III, severe functional deficits are present; range of motion is painful and limits activities of daily living. Radiographs show advanced erosive changes of both the humeral head and glenoid.²⁸

The nature of radiographic lesions in glenohumeral RA vary considerably based on the duration and extent of disease, as well as the quality of medical management. Radiographic hallmarks of the disease include joint effusion, juxta-articular osteopenia with marginal erosions and cyst formation, concentric joint space narrowing with medialization of the glenohumeral joint line, and a lack of osteophyte formation (FIGURE 5.3). A decreased acromiohumeral interval is frequently present due to rotator cuff tear compromise, and acromioclavicular (synovial) joint destruction is also commonly present. Numerous radiographic classifications of RA have been suggested in addition to that previously mentioned by Laine.²⁸ The most widely used system by Larsen et al describes six radiographic stages of RA (0-5) defined by the severity of the osteoarticular lesions and joint space narrowing; however, this method was not specifically designed for glenohumeral disease.²⁹ Specific to the shoulder, the four-stage classification by Walch et al describes earlier stages of rheumatoid involvement and provides prognostic information, where type C is the turning point beyond which destruction of the glenohumeral joint (type D) occurs inevitably within several months to 2 years.³⁰ The three-pattern scheme based on the sphericity of the humeral head and the upward migration of the humeral head in relation to the glenoid described by Lévigne and Franceschi (FIGURE 5.4) completes Walch’s classification after the development of glenohumeral joint space loss.³¹ The ascending form is the most common, which is encountered predominantly in older patients with rotator cuff lesions and leads to asymmetric wear of the superior portion of the glenoid with eventual pseudoarticulation between the humeral head and acromion (FIGURE 5.5A). In the centered form, rotator cuff tears are relatively rare and disease progression is slow; concentric glenoid erosion occurs medially (FIGURE 5.5B). In the destructive form, haphazardly distributed lesions of the joint surfaces lead to extensive erosions or “arthritis mutilans” (FIGURE 5.5C).

MRI is useful to determine the extent of joint effusion, synovial proliferation, pannus formation, bone and cartilage lesions, and rotator cuff pathology. It is particularly valuable for the evaluation of shoulder weakness and pain, not fully explained by bony changes visible on standard radiographs.³² In addition to the assessment of glenoid erosion, CT allows for the characterization of humeral head defects that are not as easily detected on x-ray (FIGURE 5.6).³³

Crystalline arthropathy may represent gout, pseudogout, or hydroxyapatite deposition disease (“Milwaukee shoulder syndrome”) and is uncommon about the glenohumeral joint. Gout is characterized by hyperuricemia and resultant precipitation of monosodium urate crystals into joints and surrounding soft tissues. Lower temperatures facilitate monosodium urate crystal formation, causing gout to primarily manifest in small peripheral joints—shoulder involvement is only encountered with advanced, uncontrolled disease.²³ Gout has a strong predisposition toward men (20:1) and is the most common inflammatory arthropathy in males older than 40 years.³⁴ Pseudogout is also known as calcium pyrophosphate dihydrate (CPPD) deposition disease or chondrocalcinosis. Half as common as gout, it is characterized by CPPD crystal deposition into fibrocartilage
and hyaline cartilage via unclear mechanisms. There is no associated metabolic disturbance or gender predisposition.²³ The shoulder is the third most commonly involved joint after the knee and wrist.²³

Intra-articular accumulation of both monosodium urate and CPPD crystals incite a common synovial inflammatory response in which chemotactic factors are released and propagated by polymorphonuclear phagocytosis.²³ Following repeated acute attacks, synovial hyperplasia and pannus formation can ensue—this perpetuates underlying cartilage damage, juxta-articular bone erosion, and joint destruction. Hydroxyapatite crystals do not incite the same degree of synovial response as seen in the other forms of crystalline arthropathy.³⁵ There has been some disagreement as to whether “Milwaukee shoulder syndrome” and rotator cuff arthropathy (RCA) represent the same or different disease entities. As Milwaukee shoulder and CTA have a unique clinical presentation that differs from gout and pseudogout, this entity will be discussed further in the subsequent section on CTA.

End-stage crystalline arthropathy is generally found in patients older than 70 years, with men more commonly affected than women. The degree of bony involvement as well as soft-tissue involvement is variable, ranging from the appearance of a mild inflammatory arthritis to one of extensive soft-tissue and bone destruction. Radiographically, late stages of disease may appear indistinguishable either from primary OA or RA. Chondrocalcinosis is often visible but is nonspecific, while gouty tophi are generally rare about the shoulder. Juxta-articular osteopenia and sharply outlined erosions, punched out with sclerotic margins, are classic x-ray findings (FIGURE 5.7).

Hemophiliac arthropathy is a rare form of inflammatory arthropathy that is primarily encountered in patients with hemophilia A (factor VIII deficiency) and hemophilia B (factor IX deficiency). von Willebrand disease and other factor deficiencies have also been implicated but are much less common. Hemophilia is classified as mild, moderate, or severe based on the clotting activity level. Spontaneous bleeding episodes are frequent in patients with severe disease, while those with mild deficiencies only experience bleeding episodes after trauma, surgery, or dental procedures. Greater than 60% of spontaneous bleeding events occur in joints, of which the shoulder is the fourth most common site.³⁶ The reported incidence of shoulder arthropathy among hemophiliacs ranges from 11% to 37% and increases with age and severity of the disease.³⁷,³⁸,³⁹ Men are much more commonly affected than women due to the sex-linked recessive nature of the disease. In hemophiliac arthropathy, hemosiderin deposition from recurrent hemarthroses leads to a chronic cycle of inflammatory synovitis and synovial hypertrophy.⁴⁰ Progressive cartilage destruction from synovial invasion and enzymatic degradation results in bony erosions, soft-tissue deterioration, and end-stage arthropathy over time.⁴⁰,⁴¹

Contrary to the juvenile onset of lower extremity involvement (ie, ankle, knee), hemarthrosis and chronic synovitis of the shoulder typically occurs in adulthood. Nonetheless, hemophiliac arthropathy of the shoulder can result in intractable pain and severe functional impairment, with progression to end-stage disease by the fourth or fifth decade.⁴² Age, lack of prophylactic therapy, and higher frequency of crutch use (typically from lower extremity involvement) are the most significant risk factors associated with recurrent shoulder bleeds.³⁹ Muscle atrophy and loss of motion occur early, often before the patient is aware of a significant problem. Impaired elbow motion can make the loss of shoulder function even more consequential. Oftentimes, early rehabilitation efforts may be thwarted by recurrent hemorrhage despite appropriate factor replacement therapy. Progression to end-stage arthropathy and arthrofibrosis requires many years but is the usual course, particularly in those with moderate to severe disease.⁴¹ Concomitant soft-tissue pathology such as tendonitis of long head of the biceps and rotator cuff tears are common (up to 50% of patients with shoulder symptoms) but may be difficult to assess secondary to generalized pain on physical examination.³⁸,³⁹ Clinical presentation correlates well with findings on imaging studies.³⁹

Radiographically, hemophiliac arthropathy can appear similar to RA. A spectrum of changes may be seen beginning with mild subchondral irregularity and cyst formation progressing to osteopenia, joint space narrowing, marginal erosion, osseous deformity, and thinning of the glenoid (FIGURE 5.8).³⁷ The Modified Arnold-Hilgartner arthropathy classification describes the general radiographic progression of hemophiliac arthropathy, though it is not specific to the shoulder.⁴³ Aside from rotator cuff assessment, MRI and ultrasonography are useful to gauge the extent of synovial hypertrophy and hyperemia, joint effusion, and articular cartilage change in the early phases of disease.⁴⁴ If arthroplasty is to be considered in this population, careful consideration must be given to intraoperative bleeding, transfusion requirements, and factor replacement.