Dallas Kingsbury

David Bressler

25: Rheumatoid Arthritis

PATIENT CARE

GOALS

Evaluate and develop a rehabilitative plan of care that is compassionate, effective, and targeted at the individual patient with rheumatoid arthritis (RA).

OBJECTIVES

HISTORY AND PHYSICAL

The history and physical examination in patients with either suspected or confirmed RA should reflect the understanding that it is an autoimmune disease primarily of the joints, with an array of possible comorbid systemic conditions. Areas of the patient history that are notably important for diagnosing and characterizing RA include the number and site of involved joints, as well as the duration of symptoms, as these questions are directly part of the diagnostic criteria. Especially at the onset, RA may be difficult to differentiate from other immune-mediated diseases. It may coexist with other rheumatologic diseases, such as mixed connective tissue disease and overlap syndrome, or the symptoms may be fleeting as in palindromic rheumatism. RA classically affects joints symmetrically, and more than other rheumatic disorders, it has a preference for small joints of the hands and feet. Protracted morning stiffness is a hallmark of the disease. Extraarticular manifestations of RA are common, with cardiac, pulmonary, integumentary, and hematologic systems being most affected (1).

Rheumatoid nodules are painless, firm areas of swelling of subcutaneous tissue, typically found on the extensor surfaces of the limbs (i.e., olecranon, dorsal hand at metacarpophalangeal [MCP] joints). Histologically, the nodules are comprised of a center of fibrinoid necrosis surrounded by a fibrous tissue shell, the larger of which can be multiloculated and contain synovial fluid. The appearance of rheumatoid nodules portends a poor prognosis and a sign of heightened disease activity.

The physical examination must be organized to include articular and extraarticular manifestations. As the patient transitions through the natural history of the disease, joint pathology will change over time. Fortunately, due to earlier diagnosis and earlier initiation of disease-modifying antirheumatic drug (DMARD) and biologic therapy, many of the debilitating, latestage manifestations of RA are becoming less frequent. Initially, joint swelling and tenderness may appear similar to other forms of arthritis. Palpation can differentiate between the bogginess of synovial edema in RA from the bony osteophytes of osteoarthritis (OA). Periarticular edema is more common in gout, while the rheumatoid joint will have swelling confined to the capsule. As the disease progresses, abnormal synovium can proliferate and migrate across articular cartilage into the joint capsule or surrounding tendons. This boggy mass of synovium laden with inflammatory mediators is called a pannus.

The wrist is the most commonly affected joint in up to 75% of RA patients (2), with synovitis progressively weakening the ligaments between the radius, ulna, and carpal bones. One area to focus is the scapholunate ligament, assessing for laxity or subluxation, since compromise of this area leads to a cascade of events in which the radial support structures collapse, volar subluxation of the radius occurs, the metacarpals deviate radially, and the fingers deviate in an ulnar direction (3). Chronic synovitis of the MCP joints accentuates the ulnar drift of the fingers. Finger deformities are also very common in RA. One of the earliest physical findings is proximal interphalangeal joint edema, with tendon and ligament weakening or rupture occurring after many years of active disease. The two major late findings at the proximal interphalangeal (PIP) joint include the boutonnière deformity and swan-neck deformity. With a boutonnière deformity, the PIP is set into flexion, with reciprocal extension of the MCP and distal interphalangeal (DIP) joints. Synovial inflammation leads to a rupture of the extensor hood and causes the lateral bands to migrate downward, causing PIP flexion and DIP hyperextension. The swan-neck deformity is a hyperextension at the PIP joint, with MCP and DIP joint flexion. It can occur from multiple combinations of joint disruptions, which usually involve PIP volar support loss (e.g., volar plate rupture) and eventual contracture of the hand intrinsic muscles. In the upper extremity, elbow synovitis can lead to loss of extension and sometimes a compressive ulnar neuropathy. Shoulder and hip involvement is less common than the more distal joints, and typically occurs later in the disease process. Painful synovitis can lead to loss of range of motion (ROM) and joint contractures.

The spine is not frequently involved, with the notable exception of the atlantoaxial joint. Rupture of the transverse ligament between C1 and C2 can lead to myelopathy and possible death due to migration of the odontoid into the brainstem. It is important to obtain lateral, flexion/extension, and open mouth views, since an anterior subluxation of 9 mm or more between C1 and C2 increases the risk for cord compression (4). In advanced disease, atlantoaxial involvement becomes more of a concern, considering that up to 60% of RA patients who needed hip or knee arthroplasty were found to have cervical spine instability on radiographic screening (5) (Box 25.1).

FUNCTIONAL ASSESSMENT

A rehabilitation approach to RA should include an inventory of the patient’s daily activities. This will allow the physiatrist to tailor a patient-specific rehabilitation program, as opposed to relying on a generic template. Two patients with similar severities of ulnar deviations and boutonnière deformities may compensate differently for manual tasks, and therefore may require separate rehabilitation approaches. Questions to ask include the following: Can you dress yourself? Get in/out of bed? Walk outdoors on flat ground? Wash/dry your entire body? Bend down to pick up clothing from the floor? Turn faucets on/off? Get in/out of the car?

Based on American College of Rheumatology (ACR) guidelines (6), patients can be given a functional classification, from I to IV increasing in severity of disability (Boxes 25.2, 25.3).

REHABILITATION PROGRAM

Historically, any exercise for RA was controversial, but now therapeutic exercise is considered a basic component of any comprehensive rehabilitation program. Areas that have shown notable success include aerobic exercise, strengthening exercises, cognitive behavioral therapy, and self-efficacy training. Joint and energy conservation, adaptive equipment, and orthotic support are the basic tenets of a comprehensive occupational therapy program (7).

In RA patients, short-term (less than 3 months) land- or water-based dynamic exercise programs have a positive effect on aerobic capacity, muscle strength, and functional ability (8). Low-impact activities, such as swimming and biking, are preferred. One study directly compared land-based aerobic capacity training (walking) with water-based aerobic capacity training, and found no differences with regard to safety (9). Overall, studies have shown decreased inflammation, joint pain, and joint tenderness (10). Specifically for aerobic exercises (at 50%–90% maximum heart rate [HR]), a meta-analysis of 14 randomized controlled trials (RCTs) showed small, beneficial effects on cardiorespiratory function, functional ability, and disease activity (11).

For ROM therapy and stretching, it is recommended that each joint is moved through its complete ROM at least once daily. Joint movement is gently encouraged despite pain, and it needs to be emphasized that ROM therapy is not done to relieve pain, but to prevent contractures. All types of strengthening exercises may be employed, as long as they do not result in muscle soreness greater than 2 hours post exercise, or fatigue lasting more than 1 hour after exercise, or increased joint pain noted during exercise. Initially isometrics can be employed due to decreased dynamic/sheer forces on the joints compared to isotonic and isokinetic training.

Modalities can also assist in physical and occupational therapy programs. Cold therapy is ideal for acute flares, especially in joints with effusions. Deep heat is indicated for patients with chronic inflammation and contractures (Box 25.4).

HOW SHOULD THE REHABILITATION PROGRAM BE MODIFIED DURING A FLARE?

In a word, rest! Reevaluate and reduce all resistive exercises, especially those that stress the small joints of the hands and feet. In this case, splinting is helpful to ensure that joint stress is minimized. Limited passive ROM is performed to prevent contracture. Medically, flares often require steroid supplementation, in addition to considering a change in DMARD therapy (Box 25.5).

PAIN MANAGEMENT

Patients often come to the physiatrist, either directly or from another consulting physician, with the expectation of complete pain relief. The first step is explaining that complete pain relief is often unachievable. A reasonable goal is pain reduction sufficient enough to allow greater participation in activities of daily living (ADLs) (Box 25.6).

MEDICAL KNOWLEDGE

GOALS

Demonstrate knowledge of established evidence-based and evolving biomedical, clinical epidemiological, and sociobehavioral sciences pertaining to RA, as well as the application of this knowledge to guide holistic patient care.

OBJECTIVES

EPIDEMIOLOGY AND PATHOPHYSIOLOGY

RA is a symmetric, systemic, autoimmune, polyarthritis caused by abnormal growth of inflammatory synovial tissue, resulting in cartilage destruction and surrounding bone erosion. The worldwide prevalence is approximately 1%, annual incidence is about 3/10,000 adults, and it is two to three times more common in women (13). This incidence has remained stable over many years. New criteria for diagnosing early RA were published in 2010, and follow-up studies estimating incidence rates using the new criteria have yielded similar results (14). The etiology of RA remains unknown, but is considered to be multifactorial, resulting from an interaction between a genetic predisposition and environmental exposure, the exact contributions of which are still being elucidated. The important genetic contributors are major histocompatibility genes (mostly HLA-DRB1), in addition to minor immunomodulation genes. Environmental associations include alcohol, tobacco (increases susceptibility up to 20- to 40-fold), and even oral cavity flora (15).

Four laboratory tests are incorporated into the 2010 ACR criteria. RF with titer and ACPAs contribute to the “serological abnormality” section. For either RF or ACPA, a “low positive” (above the upper limit of normal [ULN]) is worth 2 points, whereas a “high positive” (greater than three times the ULN) contributes three points. Either erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) levels above the ULN contribute 1 point to the “elevated acute phase” section of the criteria.

Other laboratory tests that do not directly contribute to the diagnosis are often ordered for the purposes of ruling out other diseases or in preparation for starting pharmacologic therapy. For example, a negative ANA helps exclude systemic lupus erythematosus (SLE). Arthrocentesis is helpful for ruling out crystal arthropathies and pyogenic infection. A complete blood count and liver function tests are required prior to treatment with methotrexate. A purified protein derivative (PPD) test is required prior to initiation of biologic agents due to the risk of reactivation of tuberculosis (Box 25.7).

RADIOLOGY

During the initial evaluation, plain radiographs of affected joints should be obtained. It is important to note that small joints in the hand may have commensurate changes in the foot and ankle. As previously described, osteopenia is seen in stage 2 and bony erosions in stage 3. Pathologically, erosions on x-ray represent sections of joint margins where the outer cortex has been destroyed by synovial proliferation. Erosions are seen in affected joints in up to 90% of patients not responding to treatment (21). MRI is more sensitive than plain radiography in early detection of erosions (22), but hasn’t yet been incorporated into any official clinical decision-making criteria. A normal chest x-ray is important prior to initiation of methotrexate due to hepatotoxic side effects and interstitial pulmonary fibrosis (Box 25.8).

DIFFERENCE BETWEEN RHEUMATOID ARTHRITIS AND OSTEOARTHRITIS

Many patients do not understand the difference between RA and osteoarthritis (OA). Of paramount importance is an understanding that RA is a systemic disease with potential multiorgan involvement.

Radiological differences between RA and OA are described below.

Overall, joints affected by RA are warm and tender, reflecting an inflamed synovium. Areas of synovial proliferation may be palpably soft, whereas joints in OA are hard and bony due to osteophyte formation. RA predominates in joints with robust synovium, which in the hand include the MCP and PIP joints. In contrast, OA affects the distal interphalangeal joints and carpometacarpal joint of the thumb. Typically, patients with RA will notice the worst joint stiffness in the morning for a prolonged period of time, as compared to the brief stiffness or “gelling” which is typical for the OA patient. As opposed to RA, there are no specific serologic markers for OA (Table 25.1).

MEDICAL TREATMENT

Pharmacologic therapy for RA has changed drastically since the early 20th century, starting with aspirin and gold salts through the 1940s.

The discovery of steroids in the 1950s was initially greeted with great fanfare by the medical community; however, over time further use revealed their limitations and shortcomings. Nonetheless, they remain an important part of medical management of RA. Further advances were seen with the discovery of DMARDs in the 1970s, but significant systemic side effects also frequently interfered with long-term use. The turn of the 21st century brought advancements with the advent of the “biologic” class of medications, which targets specific immunologic cytokines or receptor sites.

In 2012, the ACR revised their 2008 guidelines for the use of DMARD and biologic agents for RA (24). Examples of currently utilized DMARDs include hydroxychloroquine, leflunomide, and methotrexate. Biologic agents include the nontumor necrosis factor (TNF) abatacept, rituximab, and tocilizumab; and the anti-TNF: adalimumab, etanercept, and infliximab. New biologic agents are constantly being introduced in the market (Figure 25.1).

Prior to initiation of pharmacologic therapy patients should meet the proper diagnostic criteria (see above). ACR recommendations diverge between patients with early and established RA. In early RA, suggestions for therapy depend on disease activity (scored as low, moderate, or high) and on presence or absence of “features of a poor prognosis.” For early RA, low disease activity, and no poor prognostic factors, the recommendation is to start with DMARD monotherapy (which is most often methotrexate). In early RA, as disease activity and prognostic factors worsen, the ACR recommends adding an additional DMARD. Anti-TNF agents for early RA are reserved for patients with both high disease activity and poor prognostic factors.

TABLE 25.1 Radiological Differences (24)

FLARES

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