erative changes that include the collapse of the articular surface of the humeral head. These patients could also benefit from TSA surgery; however, functional outcomes vary because of etiology of the osteonecrosis. As previously discussed, TSA is also a rea - sonable treatment option for patients who have a nonunion or malunion of the proximal humerus because of fracture. Shoulder OA is not as common as other joint OA, but it is just as debilitating. The loss of shoulder function can lead to a variety of conditions, including depression, anxiety, activity limitations, and job-performance problems. The causes of shoulder OA can be classified into primary and sec- ondary causes. Primary OA does not have a specific cause but is more prevalent and is not isolated to only older individuals. Sec - ondary OA has a known cause or a predisposing factor, such as major shoulder trauma, chronic dislocations, infection, congenital malformation, or chronic rotator cuff tear (Millett et al., 2008). Secondary atraumatic osteonecrosis may be caused by exces- sive alcohol consumption, corticosteroid therapy, cytotoxic drugs, Gaucher’s disease, lipid metabolism disorders, obesity, radiation, or sickle cell disease. Postinflammatory secondary OA may be caused by crystal arthropathies, postinfection arthritis, rheumatoid arthritis, or rotator cuff arthropathy. Postsurgical causes of second- ary OA include capsulorrhaphy arthropathy, intra-articular hard- ware, and an overtightened anterior joint capsule. Post-traumatic causes include dislocation, malunion of the proximal humerus, post-traumatic avascular necrosis, and shoulder subluxation. ● Morning stiffness may more likely indicate rheumatoid arthri- tis. ● Joint effusion may indicate OA, rheumatoid arthritis, or septic arthritis. ● Pain at night may indicate rotator cuff disease. ● Pain or a “clunking” sound with overhead motion may indi- cate a labral disorder. ● Pain that radiates down the arm may be caused by cervical disc disease. ● Upon physical examination, if there is shoulder joint line ten- derness, this is more likely to indicate shoulder OA. ● Warmth and erythema of the joint is more likely to indicate septic or rheumatoid arthritis. ● Decreased ROM, specifically external rotation and abduction, indicates shoulder OA or a soft tissue injury or frozen shoulder. ● Crepitus can be a sign of shoulder OA or rheumatoid arthritis. ● Decreased cervical ROM usually provides information about a cervical disk disease. ● Radiographic imaging can also help in the differential diagno- sis of shoulder OA. ● Joint space narrowing can indicate cuff-tear arthropathy, OA, or rheumatoid arthritis. ● Marginal joint erosions generally point to rheumatoid arthritis. ● A normal joint on radiographic imaging is generally part of the diagnosis of either frozen shoulder or septic arthritis. ● An osteophyte or subchondral sclerosis generally indicates shoulder OA when seen on imaging.
Patients with severe rheumatoid arthritis also benefit greatly from TSA. But confounding factors, which include poor bone stock and soft tissue deficiencies, could complicate the surgical procedure. Patients with a rotator cuff deficiency or cuff tear arthropathy may also benefit from TSA but may require the reverse TSA procedure to maximize outcomes. Osteonecrosis can lead to painful degen- Shoulder OA epidemiology Shoulder osteoarthritis—also known as degenerative joint disease of the shoulder—is a gradual, progressive, mechanical, biochemi- cal breakdown of articular cartilage and other joint tissues, includ- ing bone and joint capsule (Millett, Gobezie, & Boykin, 2008). As the articular surface of the shoulder joint wears, friction within the joint increases, which can cause progressive loss of the normal load-bearing surfaces with pain and disability. Risk factors for shoulder OA include age, genetics, sex, weight, joint infection, history of shoulder dislocation, and previous injury. Certain oc- cupations, including those in heavy construction, and a history of participation in overhead sports are also risk factors for shoulder OA. As the population ages, the prevalence of shoulder OA in- creases. Musculoskeletal disorders have had a significant impact on the world’s population. Arthritis and chronic joint symptoms affect one of three adults, which is why it is the most widespread dis - ease in America. The prevalence of arthritis for all joints is higher in whites, men older than 45 years, women older than 55 years, overweight and inactive persons, and persons with less than eight years of education (Millett et al., 2008). Nearly 60% of those af- fected by osteoarthritis are older than 65 years, and the incidence is increasing (Millett et al.). Evaluation of shoulder OA A shoulder OA diagnosis involves a specific set of symptoms, physical examination findings, and changes to the bone, which are visible by imaging. The typical presenting symptoms are pro- gressive activity-related pain often described as being deep in the joint and often is localized to the posterior aspect of the shoul- der. As the disease progresses, the patient may complain of pain at rest and disruption of sleep because of pain. In the advanced cases, the stiffness creates functional limitations. In younger pa- tients, a history of prior trauma, dislocation, or previous surgery for shoulder instability may be reported and are all factors associ- ated with the development of osteoarthritis. Patients in the early stages of this disease may complain of mild pain and may have an unremarkable examination. Radiography may show only subtle changes to the bone until the disease pro- gresses and there is destruction that is more advanced. The only objective evidence of the disease is articular cartilage wear, which may be shown on a magnetic resonance image (MRI). Physical ex- amination of a patient with shoulder OA will reveal painful crepi- tus, joint enlargement, and swelling. In more severe cases, au- dible and palpable grinding may occur when a mechanical stress is placed on the shoulder. During the evaluation, it is important to exclude other shoulder pathologies that cause pain besides OA. ● Pain not induced by joint palpation or passive range of motion (PROM) is more suggestive of bursitis, rotator cuff disease, or biceps tendinitis. ● Loss of PROM and active range of motion (AROM) can also occur with calcific tendinitis or idiopathic adhesive capsulitis.
TREATMENT STRATEGIES FOR SHOULDER OA
Nonsurgical treatment No known interventions can alter the natural history of early os- teoarthritis, but there are treatments that can control pain and restore function. The initial approach to treatment of shoulder os - teoarthritis begins with activity modification, rest, and ice. Physical therapy interventions can help control pain and restore function, which include strength training and aerobic exercises to help al- leviate symptoms. Acetaminophen can be used to manage pain,
and nutritional supplements, such as glucosamine and chondroi- tin, can be used as alternatives to acetaminophen—although only anecdotal evidence supports their use for shoulder osteoarthritis. Other pharmacotherapy for degenerative joint disease includes nonselective and selective cyclooxygenase-2 (COX-2) inhibitors or nonsteriodal anti-inflammatory drugs (NSAIDS). Nonselective COX-2 inhibitors—including ibuprofen, diclofenac, naproxen,
EliteLearning.com/ Physical-Therapy
Book Code: PTCA2624
Page 193
Powered by FlippingBook