Chapter 23: Arthritis

The terms arthritis, rheumatism, and rheumatic disease are generic references to an array of more than 100 diseases that are divided into 10 classification categories. Two major forms of arthritis are considered in this chapter. Rheumatoid arthritis (RA), a systemic inflammatory disease, is considered in detail; osteoarthritis (OA), a more localized process that has been known previously as degenerative joint disease (DJD), is also discussed. Rheumatoid arthritis and osteoarthritis account for the majority of arthritis cases treated by physical therapists.

RA is a major subclassification within the category of diffuse inflammatory connective tissue diseases that also includes juvenile arthritis, systemic lupus erythematosus (SLE), progressive systemic sclerosis or scleroderma, polymyositis, and dermatomyositis. Rheumatoid arthritis is primarily a disease of the synovium. The first clinical description of RA is attributed to A. J. Landre-Beauvais in 1800, although analysis of pictorial art of the late Renaissance suggests the existence of RA in earlier times. Early descriptions of patient symptomatology were complicated by the lack of uniform agreement about the distinguishing disease characteristics, given its wide spectrum of clinical presentations. The term rheumatoid arthritis was first used by Garrod in 1858, but was not accepted by the American Rheumatism Association (ARA) as the official terminology until 1941.¹ Diagnostic criteria and terminology have been developed and, in some cases, revised based on current data.^2,3

Epidemiology

The estimated prevalence of RA among adults in the United States is approximately 1.3 million,⁴ and prevalence increases with age. Women are effected two to four times more often than men. Differences in prevalence exist among certain subpopulations, which suggest a possible role for genetic or environmental factors in the etiology of the disease. For example, African Americans may have a lower prevalence of RA than whites, whereas several Native American groups demonstrate higher prevalence rates. There also is a lower prevalence of RA in native Japanese and native Chinese peoples compared to whites.^4,5

Etiology

RA is an autoimmune disease of unknown complex etiology. RA is presently believed to have a genetic basis demonstrated by the increased disease risk and clustering in families.⁶ Briefly, an antigen is a substance, usually foreign to the host, that provokes the immune system into action. The immune system may respond to the antigen directly (cellular immunity) or by the production of antibodies that circulate in the serum (humoral immunity). These responses involve two general types of lymphocytes: T cells, which are responsible for cellular immunity, and B cells, which produce circulating antibodies specific to the antigen. Antibodies are immunoglobulins, a type of serum protein.¹

Given that individuals with RA produce antibodies to their own immunoglobulins, such as rheumatoid factor (RF) and anti–citrullinated protein antibody (ACPA), and these antibodies precede the clinical presentation of RA by years,^7,8 RA is considered an autoimmune disease.⁹ It is not clear, however, whether this antibody production is a primary event or results as a response to a specific antigen from an external stimulus. Current theory and research on the cellular basis of autoimmunity suggest that aberrant functioning of cell-mediated immunity and defective T lymphocytes may trigger the autoimmune response that underlies RA.⁹ A specific etiological agent for RA has not been identified, even though specific external agents may trigger disease expression.

The external agents that may initiate arthritis do so through various and differing mechanisms. For example, studies of smoking exposure suggest a strong association with tobacco smoke and manifestations of RA symptoms.¹⁰ Bacterial organisms, including streptococcus, clostridia, diphtheroids, and mycoplasmas, have been suggested as triggers but no connections have been definitively proven. There has also been discussion of a viral etiology for RA. As with other investigations seeking to identify an etiology for RA, research remains speculative.¹

Rheumatoid factors (RFs) are antibodies specific to immunoglobulin G (IgG) and are found in the sera of approximately 70% of all patients with RA. Current theory suggests that RFs arise as antibodies to "altered" autologous (the patient's own) IgG. Some modification of IgG changes its configuration and renders it an autoimmunogen, stimulating the production of RF. IgM is the first class of immunoglobulins formed after contact with an antigen and most RFs are of this class, although RFs may be of any immunoglobulin class.¹ The exact biological role of RF is unknown. Although RF has been implicated in the pathogenesis of RA, the disease occurs in the absence of RF in a substantial number of individuals.¹⁰ Research indicates that the presence of RF affects disease severity, because those who have RF, or seropositive disease, have increased frequency of subcutaneous nodules, vasculitis, and polyarticular involvement.¹

Ollier and Worthington⁶ examined the literature investigating a genetic predisposition to the development of RA.⁶ Human leukocyte antigens (HLAs) found on the surface of most human cells are capable of generating an immune response when genetically incompatible tissues are grafted to each other, for example, during organ transplants. Genes controlling these HLAs are found on the sixth chromosome. Four loci have been described: HLA-A, HLA-B, HLA-C, and HLA-D. RA has been associated with increased HLA-D and HLA-DR (D-related) antigens, suggesting that certain genes determine whether a host is more or less at risk for an immunological response that leads to RA.⁶ A "rheumatoid epitope" has been identified through DNA typing of HLA-DR4 as a particular sequence of amino acids common among patients with RA.¹¹ A recent national case-control study conducted in Sweden focused on citrulline-modified proteins, proteins not normally present in healthy adults but found in about two-thirds of patients with RA, to determine if smoking and the presence of shared epitope (SE) HLA genes triggered RA. The investigators concluded that the interaction of smoking and carrying two copies of the SE gene increases the risk of developing RA by 21-fold.¹² Further studies of genomic organization of the HLA-D region specifically implicate a short sequence on the HLA-DRB1 gene and suggest that HLA-DRB1 alleles (alternate forms of a gene) modify disease expression and progression.¹ Various studies of different ethnic groups have also shown that particular variations of the HLA-DRB1 allele are overrepresented in people with RA.¹

Pathophysiology

In early RA, synovial inflammation leads to pain, stiffness, and restricted range of motion (ROM). As the disease progresses, the joint capsule becomes inflamed and immune cells degrade the cartilage. With longstanding RA the synovium appears grossly edematous with slender villous or hair-like projections into the joint cavity (Fig. 23.1). Distinctive vascular changes, including venous distention, capillary obstruction, neutrophilic infiltration of the arterial walls, and areas of thrombosis and hemorrhage, may be evident. Synovial proliferation of vascular granulation tissue, known as pannus, dissolves collagen as it extends over the joint cartilage. Eventually, with disease progression, the granulation tissue leads to adhesions, fibrosis, or bony ankylosis of the joint. Chronic inflammation associated with RA weakens the joint capsule and its supporting ligamentous structures, altering joint structure and function. Tendon rupture and fraying tendon sheaths produce imbalanced muscle pull on pathologically altered joints resulting in the characteristic musculoskeletal deformities seen in advanced RA.¹³

Following alterations in blood flow, rapid changes in the cellular content and volume of the synovial fluid may result owing to low pressure in the joint space and the lack of a limiting membrane between the joint space and synovial blood vessels. High-molecular-weight substances such as macroglobulins and fibrinogens can pass through the synovial capillaries during periods of inflammation and are not easily cleared.¹ Antigen-antibody complexes may be isolated within the joint cavity and stimulate phagocytosis and further development of pannus. Although sustained synovitis requires the proliferation of new blood vessels, the exact mechanism of capillary growth is not understood. One hypothesis suggests that activated macrophages, responding to antigen-antibody complexes, may stimulate this development. With established synovitis, polymorphonuclear (PMN) leukocytes are drawn into the joint cavity and coupled with lysosomal enzyme activity contribute to destruction of synovial tissues.⁹

Laboratory Tests

Sensitivity and specificity are two concepts of testing that are useful in explaining the value of laboratory tests in the detection of RA. Test sensitivity is the proportion of truly diseased individuals who have tested positive. The clinical value of sensitive tests is particularly important when a misdiagnosis (informing the patient that he or she does not have the disease when in fact the patient does have RA) would be deleterious to the health of the patient. In research terms, sensitivity is equivalent to the laboratory test's ability to avoid a false-negative result. Specificity, on the other hand, refers to the proportion of truly nondiseased individuals who have a negative test. In other words, the specificity of a laboratory test is a measure of its ability to avoid false positives. A diagnostician usually uses a combination of sensitive and specific tests to confirm clinical impressions during the diagnostic process.

Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are acute phase reactants that indicate the presence of active inflammation. Although patients with RA characteristically have active inflammation, up to 40% may have normal values for these tests despite clinical evidence of inflammation. Normal ESR and CRP values are nonspecific and alone cannot confirm or refute a diagnosis of RA. RF is the result of the binding of two immunoglobulins. The presence or absence of RF alone neither confirms nor rules out a diagnosis of RA. Nearly 25% of people with RA do not have a positive RF (seronegative RA), whereas a positive RF is seen in a number of other immunologic conditions (e.g., leprosy, tuberculosis, chronic hepatitis) and occasionally in individuals with no disease. A positive RF in combination with clinical criteria may help to confirm a clinical impression.

A complete blood count (CBC) is routinely ordered because a number of findings are commonly associated with RA. Red blood cell counts are often decreased, indicating the anemia of chronic disease found in approximately 20% of individuals with RA. By comparison, the white blood cell count is generally normal. Thrombocytosis, a high platelet count, is not uncommon in active RA.

Synovial fluid analysis can greatly enhance the process of differential diagnosis. Normal synovial fluid is transparent, yellowish, viscous, and without clots. Synovial fluid from inflamed joints is cloudy, less viscous owing to a change in hyaluronate proteins, and will clot. Significant inflammation also increases the number of fluid proteins. A culture can be performed to identify potential bacterial agents as the cause of joint inflammation. If the joint is inflamed, white blood cells will elevated in the fluid. Crystals are not common. If present they may confirm the diagnosis of gout (urate crystals) or pseudogout (calcium pyrophosphate crystals). A mucin clot test (a measure of viscosity) of the synovial fluid can be used to discriminate between acute infectious arthritis and inflammatory arthritis, such as RA. Poor clotting accompanies acute infectious arthritis whereas RA produces fair mucin clotting.¹

Radiography

Radiographic study is essential in a diagnostic workup for RA. Physical therapists practicing in rheumatology should develop a basic proficiency in identifying abnormalities in joint structure and the surrounding soft tissues as these abnormalities influence the course and outcome of rehabilitation. To identify radiographic abnormalities, the therapist must be able to describe how a normal joint appears on a radiograph. Therapists can orient themselves to a radiograph by considering several parameters: alignment, bone density and surface, and cartilaginous spacing (Figs. 23.2 and 23.3). Normal alignment is present when the long axes of the proximal and distal bones of the joint are in their normal spatial relationships and the convex surface of one bone fits well with the concavity of the other. Bone density, in the absence of osteoporosis, should be somewhat opaque and milky and appear evenly distributed throughout. The cortices of each bone should be distinct, appropriately thick, and well defined. The joint soft tissues should conform to known anatomical shape. Soft tissue swelling and evidence of uneven spacing between joint surfaces on radiograph may suggest activity limitations. Uneven, reduced, or absent spacing suggests joint cartilage loss or joint surface erosion. A normal joint surface should be smooth and conform to known anatomical shape without osteophytes. RA progression can be characterized in four sequential stages using periodic radiographic examination (Box 23.1). Radiographic changes evident in early RA are nonspecific and usually limited to soft tissue swelling, joint effusion, and periarticular demineralization. Diagnostic confirmation is made when the disease process leads to bilateral joint space narrowing and erosions in the hands and feet.¹

Classification and Diagnostic Criteria

The differential diagnosis of RA is predicated on the history, clinical examination of signs and symptoms, and careful exclusion of other disorders. The American College of Rheumatology (ACR) classification criteria,² developed using data from patients in outpatient clinics, are commonly used to confirm whether an individual's clinical presentation should be confirmed as a case of RA. Originally these criteria had four classifications of RA: classical, definite, probable, and possible. Some of these classifications were judged to be problematic. The 1987 revised criteria are presented in Table 23.1. In 2010 the ACR and the European League Against Rheumatism (EULAR) revised the 1987 classification criteria for RA² to help identify early RA. These criteria are based on a combination of signs, symptoms, and laboratory findings that have persisted for a specified period of time.³ A diagnosis of definite RA is now established on the confirmed presence of synovitis in at least one joint, absence of an alternative diagnosis that better explains the synovitis, and a total score of 6 or greater (out of a possible 10) from four domains (Table 23.2). The domains are (1)Joint Involvement, designating the number and site of involved joints (score range 0–5); (2)Serology, indicating serologic abnormalities (score range 0–3); (3)Acute-Phase Reactants, describing elevated acute-phase response (score range 0–1); and (4)Duration of Symptom (2 levels; range 0–1).³ The inclusion of criteria for early RA may help rheumatologists to target treatment at earlier stages of the disease and decrease RA progression.

Patients with RA can also be classified based on global functional status criteria.¹⁴ There are four functional classifications based on a person's ability to complete functional and self-care activities ranging from independence to full dependence. In addition to their clinical relevance, these functional classifications enable clinicians and researchers to classify subjects in clinical trials and inform evidence-based clinical recommendations for therapies(Table 23.3).

Disease Onset and Course

RA is commonly characterized by an exacerbating and remitting disease course. Disease onset is accompanied by complaints of generalized joint pain and stiffness, usually in multiple small joints (polyarthritis) though it may be localized to a single joint. Symptoms may appear spontaneously or over a prolonged period of time. Disease progression is highly variable. High titers of RF indicate a more severe disease course. Spontaneous remissions can occur. Some patients experience an intermittent course, characterized by partial to complete remissions longer than the periods of exacerbations. A third group of patients experience the full unremitting destructive process of progressive RA.¹ Comparisons of elderly-onset RA with early-onset RA revealed that abrupt onset and large joint involvement, particularly of the shoulder girdle, were more common in the older adults. The elderly-onset group demonstrated clinical features more commonly associated with polymyalgia rheumatica, a separate and distinct disease affecting the shoulder and pelvic musculature leading to muscle inflammation.¹⁵

Clinical Presentation

Systemic

Systemic features of RA include weight loss, fever, and extreme fatigue. Fatigue greatly affects function and participation in daily life and is often underappreciated on physical examination.¹⁶ A hallmark clinical feature of RA is morning stiffness in and around the joints lasting at least 1 hour before maximal improvement.³ In contrast, OA-induced stiffness results from inactivity. Morning stiffness can be qualified in terms of its severity and duration, both of which are directly related to the degree of disease activity.

Joint Impairments (Articular and Nonarticular)

RA is characterized by bilateral and symmetrical synovial joint involvement. Clinically, patients present with limited mobility and signs of inflammation including pain, redness, swelling, and warm joints. The most common joints involved are the hands, feet, and cervical spine with the hands generally affected early in the disease course.¹⁶ The term arthralgia refers to joint pain. The joint examination may reveal crepitus, an audible or palpable grating or crunching evident as the joint is moved through its ROM. Crepitus is the result of uneven degeneration of the joint surface.

Cervical Spine and Temporomandibular Joint

The cervical spine is often involved in RA and on examination ROM may be limited in all planes. The occipitoatlantal (occiput–C1) and atlantoaxial (C1–C2) joints are frequently affected due to their extensive synovial tissue. The midcervical region is also a common site of inflammation, leading to decreased ROM, particularly in rotation, accompanied by instability. Three patterns of cervical spine involvement are described: atlantoaxial subluxation (65%), atlantoaxial impaction (20% to 25%), and subaxial subluxation (10% to 15%).¹⁷ Involvement of the C1 and C2 vertebrae may produce life-threatening situations if the transverse ligament of the atlas should rupture or if the odontoid process should fracture or herniate through the foramen magnum, compressing the upper cervical cord. Patients presenting with cervical radiculopathy and neurological signs should be immediately referred to a physician. Magnetic resonance imaging (MRI) is the most effective tool to visualize both the spinal column and the cord.¹⁷ Ankylosing (i.e., fusion) of one or more vertebrae of the spine may accompany RA and can lead to loss of ROM and function of the involved joints.

The temporomandibular joint (TMJ) is usually among the last joints involved. Inflammation of the TMJ results in pain, swelling, and limited movement and eventually to ankylosis. With juvenile RA involvement of the TMJ can lead to destruction of the condyle and potential alterations in mandibular growth and facial deformity. With early disease, TMJ x-rays are usually negative but with time and chronic inflammation can demonstrate bone destruction, which may affect the child's ability to open the mouth fully (approximately 2 in [5.08 cm]) with normal side-to-side gliding and protrusion. In resting position, the normal approximation of the upper and lower teeth may be altered following persistent inflammation.¹⁸

Shoulders and Elbows

Shoulder involvement may be evident in the glenohumeral, sternoclavicular, or acromioclavicular joints leading to joint surface degeneration, pain, and loss of ROM. Shoulder pain is often referred to the deltoid region. The scapulothoracic articulation may secondarily exhibit a loss of ROM as well. Chronic shoulder inflammation causes the capsule and the ligaments to become distended and thinned. As joint surfaces erode, the shoulder eventually becomes unstable. In addition, tendinitis and bursitis may complicate management.¹⁸ Typical elbow joint findings include effusions between the lateral epicondyle and olecranon prominence, bilateral swelling of the olecranon bursa (more prevalent with severe disease), and rheumatoid nodules on the olecranon or extensor surface of the proximal ulna.¹⁷ Inflammation, capsular and ligamentous distention, and joint erosion may lead to instability and irregular or catching movements. Flexion contractures frequently develop, due to patient posturing to reduce pain and persistent spasm.

Wrists

Early synovitis among the carpal bones and the ulna leads to a fairly rapid development of a flexion contracture, which ultimately diminishes the individual's ability to grasp. Additionally, carpal tunnel syndrome may occur due to compression of the median nerve in the carpal tunnel. Chronic inflammation around the ulnar styloid coupled with laxity of the radioulnar ligament produces the piano key sign on examination. The piano key sign is defined as an up and down movement of the styloid in response to point pressure from the examiner. Over time ulnar deviation or drift may occur from chronic inflammation causing movement of the wrist toward the ulna (Fig. 23.4). Chronic inflammation of the proximal row of carpals can lead to a volar subluxation of the wrist and hand on the radius, accentuating the normal 10° to 15° of volar inclination of the carpus on the distal radius (Fig. 23.5). In addition, radial deviation of the distal carpals can occur due to loss of radial ligamentous support, destruction of the extensor carpi ulnaris and the fibrocartilage on the distal side of the ulna. This allows the proximal carpals to slide down the distal radius toward the ulna, contributing to radial deviation of the distal row of carpals relative to the two bones of the forearm, where normally there is 5° to 10° of ulnar deviation.¹⁹ Stenosing tenosynovitis of the first dorsal compartment of the wrist (deQuervain's disease) may also occur.

Hand Joints

Metacarpophalangeal Soft-tissue swelling around the metacarpophalangeal (MCP) joints, especially the index and long fingers, is common. The volar subluxation and ulnar drift of the MCPs frequently seen in RA results from exaggeration of the joints' normal structural shape that tilt the proximal phalanges in an ulnar direction. The anatomical placement and length of the collateral ligaments, which are most stretched during MCP flexion, and the insertions of the intrinsics, which also pull from an ulnar direction, contribute to ulnar drift at the MCPs during hand motion. Weakened ligaments cannot resist a pull toward volar subluxation during power pinch or grasp when flexor tendons bowstring across MCPs through frayed tendon sheaths damaged by long-term synovitis. The bowstring effect results from moving the fulcrum of the flexor tendons distally, placing an ulnar and volar pull on the proximal phalanges (Fig. 23.6). Radial deviation of the carpals further enhances MCP ulnar drift as the phalanges try to compensate for the loss of normal ulnar deviation at the wrist. This is known as the zigzag effect, where forces in the hand try to move the index finger back into its normal functional position in line with the radius. A trigger finger may be evident whereby a snapping sensation is felt when flexing or extending the finger due to flexor tenosynovitis and resultant slippage of the tendon, friction with movement, or presence of tendon nodules.^17,20

Proximal Interphalangeal Swelling of the proximal interphalangeal (PIP) joints is common and is easily appreciated with lateral joint palpation. There are two characteristic irreversible deformities (if not surgically repaired early) seen at the PIPs in individuals with severe RA. The first of these is known as swan neck deformity and consists of PIP hyperextension and distal interphalangeal (DIP) flexion (Fig. 23.7). Swan neck deformities arise in three distinct ways, depending on the site of initial involvement. Most commonly, swan neck deformity follows from initial synovitis of the MCP, where the pain of chronic synovitis leads to reflex muscle spasm of the intrinsics. The biomechanical force of the intrinsics then combines with the hypermobility found in the chronically inflamed and structurally changed PIP, resulting in volar subluxation and PIP hyperextension. Swan neck deformity may also result when the volar capsule of the PIP is stretched, the lateral bands move dorsally, and tension is placed on the flexor digitorum profundis by the PIP flexes the DIP. In these instances, a rupture of the flexor digitorum sublimus further predisposes an individual to swan neck deformity. A third mechanism for developing swan neck deformity involves a rupture of the extensor digitorum communis at its insertion on the DIP resulting in DIP flexion and PIP hyperextension owing to unrestrained pull by the flexor digitorum profundis.^17,19

The other characteristic deformity of the PIP is known as a boutonniere deformity and consists of DIP extension with PIP flexion (Fig. 23.8). As a result of chronic synovitis, the insertion of extensor digitorum communis into the middle phalanx (known as the central slip) lengthens, and the lateral bands slide volarly to force the PIP into flexion. Bony formation or outgrowths around the end of a joint are termed osteophytes. Those found at the PIP are known as Bouchard's nodes, and may be seen in OA. They are unrelated to RA, although an individual may have both kinds of arthritis at the same time.^17,20

Distal Interphalangeal The distal interphalangeal (DIP) joints are rarely affected in RA. Osteophytes are, however, common in OA and are called Heberden's nodes. Occasionally, a mallet finger deformity will result from rupture of the tendon of the extensor digitorum communis, pulling the DIP into flexion as force from the flexor digitorum profundis is unopposed.²⁰

Thumb A number of deformities can occur in the thumb due to synovitis. The most prevalent is a flail IP in which the patient loses the ability to flex the interphalangeal (IP) joint. The fibers of the dorsal hood mechanism over the MCP, the joint capsule and the collateral ligaments, and the tendons of extensor pollicis brevis and extensor pollicis longus are particularly affected. The exact mechanism of thumb deformities depends on the particular combination of affected structures. Similar to other hand deformities, the actual presentation depends on the site of initial synovitis, the direction of imbalanced muscle forces, and the integrity of the surrounding joint structures. A type I deformity, consisting of MCP flexion with IP hyperextension without involvement of the carpometacarpal (CMC) joint, is most commonly seen. Type II deformity is assigned when the CMC is subluxed and the IP is held in hyperextension. CMC subluxation and MCP hyperextension is classified as a type III deformity, and is more common in RA than a type II deformity.^17,18,19,20

Mutilans Deformity (Opera-Glass Hand) Grossly unstable thumbs and severely deformed phalanges are indicative of mutilans-type deformity. Also known as opera-glass hand, the transverse folds of the skin of the thumb and fingers resemble a folded telescope. Radiographic study of the bones of the hand reveal severe bone resorption, erosion, and shortening of the MCP, PIP, radiocarpal, and radioulnar joints especially. The negative impact of this deformity on hand function and activities of daily living (ADL) is significant.²⁰

Hips and Knees

Radiographic hip disease is evident in approximately half of all patients with RA. Patients may present with complaints of pain in the groin and medial thigh. Pain over the greater trochanter often is secondary to trochanteric bursitis. Severe inflammatory destruction of the femoral head and the acetabulum may push the acetabulum into the pelvic cavity, a condition known as protrusio acetabuli. With progressive hip disease, patients may require a total hip arthroplasty.¹⁷

The clinical presentation of the knee joint frequently includes synovitis, causing accumulation of relatively large amounts of fluid. The knee ballottement test is used to examine for excess fluid. The examiner presses on the patella with the index finger, resulting in a downward motion of the patella; a sensation of bogginess indicates effusion of the knee. Posterior accumulation of fluid in the knee produces a Baker's cyst. If a Baker's cyst ruptures it produces pain, swelling, and heat in the posterior calf similar to symptoms of a deep vein thrombosis. The bulge test is a simple procedure to examine for anterior synovitis. With this procedure the examiner strokes the medial aspect of the knee in an upward motion, then presses on the lateral aspect of the knee. A positive sign is a wavelike movement of fluid medially. Chronic synovitis results in distention of the joint capsule, attenuation of the collateral and cruciate ligaments, and destruction of the joint surfaces. Painful knees may be held in slightly flexed positions, ultimately resulting joint tightness or flexion contractures.¹⁷

Ankles and Feet

Early inflammation of the feet is often evident in the forefoot where patients note pain with compression of the forefoot on examination. Chronic synovitis accentuates the natural tendency of the talus to glide medially and plantarward, resulting in pressure on the calcaneus and leading to hindfoot pronation. The spring ligament is also stretched by these occurrences, flattening the medial longitudinal arch (Fig. 23.9). The calcaneus may erode or develop bony exostoses known as spurs. As synovitis weakens the transverse arch, the metatarsals spread and a splayed forefoot (splayfoot) may develop (Fig. 23.10). Instability of the talocalcaneal joint, if severe, can lead to the need for surgical fusion. Synovitis of the metatarsophalangeal (MTP) joints is extremely common and metatarsalgia (pain over the metatarsal heads) may develop. A hallux valgus and bunion (a painful bursitis over the medial aspect of the first MTP joint) may also be present. When volar subluxation of the MTP combines with flexion of the PIP and hyperextension of the DIP joints, this condition is commonly referred to as hammer toes (Fig. 23.11). The MTPs may also exhibit volar subluxation of the metatarsal head with flexion of the PIP and DIP joints, known as cock-up or claw toes (Fig. 23.12). As the capsule and intertarsal ligaments are weakened and stretched, the proximal phalanges move dorsally on the metatarsal head (Fig. 23.13). Similar to conditions observed in the hand, the long toe extensors "bowstring" over the PIP joints while the flexors are displaced into the intertarsal spaces.¹⁷

Muscle Involvement

Muscle atrophy around affected joints may be present early. It is not definitively known, however, whether this atrophy results from disuse or selective attrition of muscles owing to some unknown mechanism specifically related to the disease process. Atrophy in the hand intrinsics and the quadriceps is particularly evident in long-standing disease, although the mechanisms for these changes may not be the same. It appears that individuals with RA experience selective attrition of Type II (phasic) muscle fibers through some unknown mechanism.^21,22 There is also some evidence that Type I (tonic) muscle fibers of the quadriceps will undergo selective atrophy following anterior cruciate ligament damage.²³ Loss of muscle bulk may also be the result of a peripheral neuropathy, myositis, or steroid-induced myopathy. Muscle weakness may be due to either reflex inhibition secondary to pain or atrophy.^21,22,23

Tendon Involvement

Tenosynovitis, inflammation of the lining of the sheath that surrounds a tendon, may occur with active disease and interferes with the smooth gliding of the tendon through the sheath. Inflammation may directly damage the tendon, eventually leading to a tendon rupture. Common sites of tenosynovitis are wrist flexors, thumb flexors, patella, and Achilles tendons. Trigger finger and deQuervain's disease may occur. A patient with tendon damage or muscle weakness may exhibit a lag phenomenon, which refers to a substantial difference in passive versus active ROM. This is a nonspecific finding that therapists need to examine carefully to determine its cause and design appropriate treatment.²⁰

Deconditioning

Deconditioning is a significant clinical feature of RA. Research assessing physical fitness in persons with RA has demonstrated diminished cardiorespiratory status, muscular strength and endurance, flexibility, and altered body composition among these individuals when compared with healthy individuals of the same age and gender without arthritis. Deconditioning results from both direct and indirect impairments.^24,25 Direct impairments of RA include loss of Type II muscle fibers, systemic fatigue, cachexia (wasting of lean body mass),²⁵ and shortening of contractile tissues. Indirect impairments of RA include deconditioning secondary to inactivity and elevated resting energy expenditure (calories required by the body during a 24-hour period under resting conditions). Immune system activity and inflammation, even in individuals with well-controlled disease, create an increased metabolism with subsequent loss of lean body tissue.²⁵

Rheumatoid Nodules

Rheumatoid nodules occur in approximately 20% to 25% of patients and are associated with a positive serological test for RF. Nodules are generally tender and accompany severe disease. When nodules are present in early RA they are suggestive for a greater likelihood of severe extra-articular manifestations. Nodules are found in the subcutaneous or deeper connective tissues in areas subjected to repeated mechanical pressure such as the olecranon bursae, the extensor surfaces of the forearms, and the Achilles tendons. The presence of nodules on tendon mechanisms may lead to mechanical breakdown and tenosynovitis.^17,20

Vascular and Neurologic Complications

Vasculitis, or inflammation of the blood vessels, has been found in 25% to 30% of individuals with RA on autopsy.²⁰ Most forms of vascular lesions associated with RA are silent and difficult to diagnose due to variability in the size of blood vessels affected. Skin vasculitis is the easiest to observe and can present as discoloration of the nail beds, purpura (red or purple discoloration), and petechiae (red or purple spots). The fulminant form of rheumatoid arteritis (arterial inflammation associated with a rheumatoid disorder) can be life threatening, and accompanied by malnutrition, infection, congestive heart failure (CHF), and gastrointestinal bleeding. Vasculitis of the vessels supplying nerves can lead to peripheral neuropathies such as foot or wrist drop.¹ Peripheral neuropathies may also occur secondary to mechanical compression of nerves such as carpal tunnel or tarsal tunnel syndrome. Spinal cord compression may result from inflammation in the cervical spine (see section on cervical spine and temporomandibular joint), and if clinical signs of cord compression are present, this requires immediate medical attention.¹

Cardiopulmonary Complications

Morbidity and mortality from cardiovascular disease is elevated in persons with RA due to a greater prevalence of ischemic heart disease, secondary to accelerated atherosclerosis. Although the exact etiology of accelerated atherosclerosis is unclear, it is hypothesized that metabolic and vascular effects of chronic inflammation may be the causative factor.²⁴ Subclinical pericarditis may be present and has been demonstrated at autopsy. Pulmonary involvement is frequent and more prevalent in men than women. Pleuritis and pulmonary nodules may be present. Pulmonary nodules are related to presence of nodules elsewhere and found among seropositive patients with profuse synovitis. Nodules may be .40 to 3 in (1 to 8 cm) in size and affect gas exchange.¹⁷

Ocular Complications

Episcleritis, a benign and self-limiting process, and scleritis, a serious condition that can lead to blindness, may be present. The difference between these two is difficult to detect with clinical symptoms. Therefore, patients with RA should undergo annual eye examinations, and, if symptoms of suspected eye disease are present, they should be referred to an ophthalmologist.²⁰

Activity Limitation and Participation Restriction

Patients with milder forms of RA may suffer from activity limitations and decreased participation in ADL due to joint destruction. Almost 50% of individuals with RA will eventually have marked restrictions in ADL.¹ Late-onset RA is generally associated with better functional outcomes and less activity limitations and participation restrictions, though the cause of these findings is unclear. Table 23.3 presents a broad classification of functional status in RA that characterizes the progressive impact of the disease.¹⁴ Loss of income is a major consequence of RA and is directly attributable to work disability. In a large international comparison study, work disability rates were high in persons with RA and disability was associated with disease factors as well as societal factors.²⁶

Prognosis

RA causes increased morbidity and reduces life span. The question of mortality associated with RA is controversial. Previously, it was believed that RA itself was not usually a cause of death, although conditions such as systemic vasculitis and atlantoaxial subluxation could be fatal. There is presently a growing body of evidence that individuals with RA have decreased survival compared to their siblings and may not live as long as their counterparts without disease, especially if the early years of RA were marked by aggressive disease and poor functional status. Causes of death occurring more frequently in patients with RA as compared to the general population are infections, ischemic heart disease, and renal, respiratory, and gastrointestinal disease.^17,20,27

Although numerous prognostic factors have been identified in the literature, there is no firm consensus regarding specific prognostic factors. Research demonstrates that individuals with a positive RF are more likely to progress to severe disease, as are those with high ESR and CRP at baseline. Baseline CRP is also associated with radiographic changes later in life.²⁸ Similarly, baseline radiographics are strongly associated with pattern of progression. Genetic research suggests that a shared epitope in the hypervariable region of the HLA-DR is associated with disease severity in a dose-dependent manner.²⁹

Remission Criteria

In 2011, in response to the increasing ability to achieve remission with appropriate medical management, the American College of Rheumatology (ACR), the European League Against Rheumatism (EULAR), and the ACR Outcomes Measures in Rheumatology Initiatives developed a rigorous set of remission criteria. Remission, described as little if any active disease, can be operationally confirmed based on one of two definitions: (a) when scores on the tender joint count, swollen joint count, CRP (in mg/dL), and the Patient Global Assessment (0–10 scale rating how patient feels overall) are all less than or equal to 1, or (b) when the score on the Simplified Disease Activity Index (numerical sum of all of the above plus the score on the Physician Global Assessment) is less than or equal to 3.3.³⁰

Osteoarthritis (OA) is primarily confined to one or more synovial joints and its surrounding soft tissues. Two predominant, pathological features once defined OA: the progressive destruction of articular cartilage and the formation of bone at the margins of the joint.¹ OA is now recognized as a disease involving the entire joint including the periarticular musculature³¹ (Fig. 23.14). Accordingly, the impairment, activity limitations, and participation restrictions related to OA extend far beyond the perimeters of the synovial joint. Data on the personal and societal impact of OA increasingly demonstrate its importance as an individual and public health issue.

Epidemiology

Osteoarthritis is the most common form of arthritis and extremely prevalent among individuals over 40 years of age. Based on data from several large population-based studies, it is estimated that approximately 12% of the U.S. population or 27 million adults age 25 and older have clinical OA of some joint.³² It is widespread in adults older than 65, and affects men more than women before age 50, but reverses after age 50.¹ Studies concerning racial predisposition to OA have yielded conflicting data, depending on the joint studied. Data from the third National Health and Nutrition Examination Survey (NHANES) reveal that the prevalence of radiographic knee OA was highest in non-Hispanic African Americans (52.4%) compared to non-Hispanic whites (36.2%) or Mexican Americans (37.6%).³²

Etiology

Similar to RA, no single factor that predisposes an individual to OA has been identified. Although aging is indeed strongly associated with OA, it must be emphasized that aging in itself does not cause OA, nor should OA be considered synonymous with the "normal" aging process.^1,33 In fact, many OA-related changes seen at both a cellular and tissue level are opposite those seen with normal aging.³⁴ Several factors related to aging may, however, contribute to its development. Genetic factors account for between 39% and 65% of radiographic OA of the hand, hip, and knee in women and as much as 70% of OA cases of the spine.³⁵ Trauma before adulthood may initiate a remodeling of bone that alters joint mechanics and nutrition in a way that becomes problematic only later in life. The role of repetitive microtrauma in the etiology of OA has also received attention.¹ Specifically, occupational tasks involving heavy lifting are associated with the development of hip OA,³⁶ and those involving kneeling and heavy lifting are related to the development of knee OA.^37,38 Malalignment, including varus and valgus deformities, and leg length discrepancy are associated with greater prevalence of knee and hip OA, respectively.^38,39 The strongest predictor of disease progression in the knee is varus malalignment.⁴⁰ At the hip, there is increasing recognition of the role of femoroacetabular impingement (FAI) (a mechanical mismatch between the femoral head and acetabulum) in development of OA.⁴¹ Finally, obesity has been shown to be a risk factor for the development of OA in later life; most evident in the knee joint and to a lesser extent in the hip and hands.^1,39 The relationship between obesity and incidence of OA is stronger in women than in men.³⁹ Risk factors for OA can be classified as either systemic or local (Box 23.2), and OA most likely results from the combined effect of multiple factors acting on a vulnerable joint that leads to disease.³⁹ It is imperative that physical therapists understand and are able to counsel patients on those factors that are modifiable and amenable to therapeutic interventions.

Pathophysiology

Animal models involving knee trauma have provided much of the basis for what we now know about the earliest changes associated with OA in humans. Thus, it is possible that subtle, crucial, and as yet undiscovered differences in humans may alter our understanding of OA in the future.

Normal Cartilage

Healthy articular cartilage is composed of an extracellular matrix and chondrocytes. Water makes up between 65% and 80% of the matrix by weight, mostly Type II collagen contributes approximately 10%, and proteoglycans (molecules found in articular cartilage), noncollagenous proteins, and glycoproteins the remainder.^38,42 It is the matrix that protects the chondrocytes from damage during normal joint use.⁴² Chondrocytes, the only cells in articular cartilage, secrete the matrix yet make up only 1% of the total volume of adult human articular cartilage.⁴² Chondrocytes are dispersed throughout the extracellular matrix but most concentrated in the deep layer. The superficial layer has the highest concentration of water and collagen fibers giving this zone the greatest tensile stiffness and strength and ability to resist shearing forces.⁴² Proteoglycans consist of a protein core and one or more glycosaminoglycans (GAGs), including hyaluronic acid and chondroitin sulfate. Proteoglycan concentration is highest in the middle and deep zones.⁴²

Articular cartilage contains no nerves, blood vessels, or lymphatic vessels. It receives its nutrition and eliminates waste via diffusion through synovial fluid and by facilitated imbibition (absorption of fluid by a solid body).³⁸ The multiple roles of articular cartilage include decreasing friction between articulating joint surfaces, distributing static and dynamic joint forces to the underlying bone and absorbing shock.^38,43 Cartilage's shock-absorbing function is minimal (1% to 3% of load forces), however, compared to that of subchondral bone (30%)³⁸ and periarticular muscles (which requires timely and coordinated muscle contraction). These joint structures together with ligaments, menisci, capsule, synovium, and synovial fluid serve to protect the joint from regular wear and tear and damaging forces. Regular forces acting on the articular cartilage include body weight, muscle contractions, and ground reaction forces that vary with the rate and duration of loading and the available load-bearing surface.^38,42 Extremes of joint loading in either direction can lead to detrimental morphological and metabolic changes in the cartilage whereas moderate, cyclic loading enhances proteoglycan synthesis and concentration.^38,42

Joint Pathology

The first osteoarthritic change in articular cartilage, which has been confirmed in humans, is an increase in water content. This increase suggests that the proteoglycans have become swollen with water far beyond normal. This process, together with disruption of other components of the extracellular matrix, decreases the stiffness of the matrix and leads to further mechanical damage.⁴² In later stages of disease progression, proteoglycans are lost, which diminishes the water content of cartilage. As proteoglycans are lost, articular cartilage loses its compressive stiffness and elasticity, which, in turn, results in the transmission of compressive forces to underlying bone. Collagen synthesis is increased initially, although there is a shift from type II collagen fibers to a larger proportion of type I collagen, the kind found in skin and fibrous tissue. Chondrocytes attempt to respond to this early tissue damage by synthesizing new matrix molecules and proliferating and forming clusters of cells.⁴² As the articular cartilage is destroyed, the joint space narrows.³¹ In summary, the early phases of cartilage degeneration are characterized by biosynthesis and repair as the chondrocytes attempt to restore the damaged matrix while the later phase is degradative in nature as catabolic enzyme activity digests the matrix and erodes the cartilage.

One of the first noticeable changes in cartilage is the mild fraying or "flaking" of superficial collagen fibers. Deeper fraying, or "fibrillation," of the upper third of the cartilage follows in areas of greater weight-bearing and may progress to full-thickness fissures (Fig. 23.15). As the cartilage degenerates, there are accompanying changes in the subchondral bone including increased bone density or subchondral sclerosis, creation of cyst-like bone cavities, and formation of marginal osteophytes.¹ The cartilage may degenerate to the point that the exposed subchondral bone becomes necrotic and eburnated (polished or ivory-like) (Fig. 23.16). The stiffer than normal subchondral bone further decreases the shock-absorbing properties of the joint and results in greater impact loading.³⁸ The traditional view of OA is that the disease process starts with an unrepaired injury to articular cartilage; however, there is also evidence that reduced compliance in subchondral bone and periarticular structures may initiate the degenerative processes.^38,42

Osteophytes may be fibrous, cartilaginous, or bony in composition and marginal prominences are palpable and often tender in more superficial joints.⁴² The process of osteophyte formation in OA is not well understood. Current hypotheses have implicated increased vascularity in the deepest layers of the degenerated cartilage, venous congestion from subchondral cysts and thickened subchondral trabeculae, and the continued sloughing of articular cartilage.⁴⁴ Each of these hypotheses may explain how this bony growth contributes to the pain and loss of motion that accompany OA. Subchondral cysts containing myxoid, fibrous or cartilaginous tissue along with bone marrow lesions identified through MRI, are associated with painful knee OA.³¹

Although traditionally viewed as a non-inflammatory disease, improved detection methods suggest that inflammation does play a role and that inflammatory pathways are up-regulated (increased responsiveness).^1,43 Further inflammatory reactions occur in response to cartilage fragments in the synovial cavity and resultant low-grade synovitis.³⁸

Radiography

It is widely recognized that radiographic findings are not strongly related to clinical symptoms and pain severity³⁹ and add little to the accuracy of the clinical diagnosis. In knee OA, muscle strength and pain are more explanatory of functional loss than radiographic findings.⁴⁵ Although the diagnosis of OA can be made through history and clinical assessment, radiographs are frequently used to confirm the extent of joint damage and disease progression and continue to be a component of the ACR diagnostic criteria.³¹ The Kellgren and Lawrence 5-point classification system remains the most widely used criteria for grading radiographic changes both clinically and for purposes of research.⁴⁶

• Grade 0: normal radiograph

• Grade 1: doubtful narrowing of the joint space and possible osteophytes

• Grade 2: definite osteophytes and absent or questionable narrowing of the joint space

• Grade 3: moderate osteophytes and joint space narrowing, some sclerosis, and possible deformity

• Grade 4: large osteophytes, marked narrowing of joint space, severe sclerosis, and definite deformity

In Figure 23.17, early OA changes of the right hip are depicted. Newer imaging techniques including high-resolution MRI are able to detect early structural changes and pathology in pain-sensitive structures well before changes are observable on radiographs.^31,47 Real-time ultrasound allows visualization of both bony and soft tissue structures and is more sensitive than clinical examination in detecting effusion, synovitis, and early osteophytes in OA.⁴⁷ Ultrasound imaging has greater potential for routine use in clinical practice than MRI.

Disease Onset and Course

OA typically starts in an insidious fashion and may progress undetected in some individuals when early, aneural articular cartilage is the only involved tissue. Pain is initially episodic and triggered by specific activity. In later disease, pain becomes a chronic, dull ache accentuated with episodic severe pain.³¹ It is pain that leads an individual to seek medical help. Unlike RA, there are no systemic features such as fatigue, fever, or malaise with the onset of OA.

OA is typically a slowly progressive condition; however, most people with radiographic evidence of joint damage in their hips or knees stabilize and do not require joint replacement surgery.¹ The pathological process involved in OA appears to be cyclical with active periods of increased matrix protein turnover interspersed with inactive phases.⁴⁸ The prognosis is variable and not necessarily bad. However, in combination with normal aging, co-morbidities often present in older adults, and high levels of inactivity in this population, OA can contribute to increasing disability.¹

Classification and Diagnostic Criteria

Most researchers have used Kellgren and Lawrence's grade 2 definition (the presence of definite osteophytes) as the criterion for identifying disease, although a few others have required evidence of joint space narrowing (grade 3 corresponding to clinically identified disease) to designate OA.⁴⁶ Although radiographic evidence of joint space narrowing and osteophytes may help confirm the diagnosis and classify the stage of OA, the clinical criteria for hip,⁴⁹ knee,⁵⁰ and hand⁵¹ OA are described primarily in terms of pain and limitation of motion (Box 23.3).

OA is typically differentiated in two ways: primary (idiopathic) and secondary disease.¹ When the etiology of the disease is unknown with no known prior event, it is termed primary or idiopathic OA. This category can be further divided into localized (one or two joints affected) or generalized OA (affecting three or more joints).¹ Generalized OA typically involves the hands in a more symmetrical fashion not unlike inflammatory forms of arthritis and has a stronger genetic association.¹ OA is classified as secondary when the etiology (e.g., trauma, biomechanical factors, congenital malformation, or other musculoskeletal disease) can be identified. There is increasing evidence that many cases categorized as idiopathic are more appropriately recognized as secondary disease as our ability to detect subtle and early biochemical, histological, morphological, and biomechanical factors improves.

Clinical Presentation

Signs and Symptoms (Impairments)

As noted above, the clinical diagnosis is often made on the basis of signs and symptoms (e.g., pain and swelling, loss of ROM, and bony deformity). Not all joints are equally affected by OA. In the upper extremity (UE), the finger DIP and PIP joints and CMC of the thumb are commonly involved. The cervical and lumbar spine, hips, knees, and MTP of the great toe are also sites for OA. The MCP joints, wrists, elbows, and shoulders are usually spared in primary OA.¹ Unlike RA, OA does not have a bilateral, symmetrical presentation (with the exception of generalized OA).¹

A single joint or any combination of joints may be affected and of differing "etiological origins." OA is not a systemic disease, and is therefore not associated with systemic complaints such as fatigue, generalized morning stiffness, fever, or loss of appetite. Individuals with OA may experience some stiffness in particular joints on awakening that is similar to the stiffness felt when moving the same joints after inactivity during the day, but this stiffness (articular gelling) typically does not last more than 30 minutes, nor is it generalized to the entire body.^1,31 Crepitus is a common clinical finding in OA and may progress from a painless grating sensation to an extremely painful, high-pitched sound as a result of bone-on-bone articulation.

Although cartilage degeneration is the primary manifestation of OA, cartilage is aneural, and therefore not the cause of a person's pain. Pain in OA can arise from any innervated tissue and may be attributed to incongruent articulations of joint surfaces, periosteal elevation secondary to bone proliferation at the joint margin (osteophytes), vasocongestion in subchondral bone, trabecular microfractures, distention of the joint capsule, and muscle spasm or strain.^31,42 Many patients will also experience a secondary synovitis and effusion, especially when the knee is involved.^43,52

As noted earlier, symptoms do not always match the severity of the disease on radiographs. Further, some patients with OA may have an amplified pain experience and central pain sensitization at the spinal or cortical level.⁴³ Unlike individuals with RA who often report more pain and stiffness at rest, the pain associated with OA is likely to occur or worsen with motion, except in the later stages of the disease when it is present at rest and with activity.^1,31

Joints

Hands and Fingers Osteoarthritis may present differently and result in varied levels of impairment depending on the joints involved. In the hand, DIP and PIP involvement may result in reduced ROM, poor grip strength, bony nodes, and joint angulation as a result of stretched collateral ligaments or bone erosion. Bouchard's nodes at the PIP joints and Heberden's nodes at the DIP joints are often tender in the early stages and can lead to marked restrictions in finger ROM and fine motor skills later in the disease (Fig 23.18). Osteoarthritic damage in the first CMC joint results in pain or aching at the base of the thumb and can lead to decreased pinch strength and squaring of the thumb (thickening and prominence of CMC due to subluxation of first metacarpal) as a result of weakness and contracture of the thenar muscles.^53,54 This in turn affects abduction, extension, and opposition ROM of the thumb and greatly affects grip strength and hand function. In cases of generalized OA, the hands are always affected and in a more symmetrical pattern.¹ Painful inflammation with synovitis, erosive changes, cystic swellings, and osteophytes are present in this less common form of OA and may lead to ankylosis of the DIP and PIP joints.^1,54

Hips Symptoms of hip OA are usually insidious in onset and may include a limp and decreased ROM with a tendency for the hip to be held in a somewhat flexed, abducted, and externally rotated position. Internal rotation is usually restricted and painful.⁵⁵ Pain arising from the hip joint is commonly experienced in the groin, but can also be felt in the buttock, trochanteric, or knee region.⁵⁵ Decreased hip ROM is associated with decreased walking speed, decreased stride length, poor balance, and increased energy expenditure. Hip OA is also associated with increased risk of falls.⁵⁶

Knees Early presentation of knee OA includes pain with weight-bearing activities such as climbing stairs and squatting. In later stages, both pain and stiffness are reported after prolonged sitting such as with watching a movie. Symptoms of joint locking and buckling (giving way) may also occur with damage to stabilizing menisci and ligaments⁵⁵ and lead to increased risk of falls.³¹ Knee OA more commonly affects the medial joint due to the higher weight-bearing load placed on this compartment. As a result, medial joint space narrowing often results in pseudolaxity of the medial collateral ligament, stretching of the lateral collateral counterpart, and a genu varus deformity (Fig. 23.19). Genu valgus as a result of greater lateral compartment involvement is less common. A flexion deformity of several degrees can develop quickly in the painful knee and contribute to a functional leg length discrepancy, decreased step length, and quadriceps muscular fatigue or strain. Patellofemoral compartment OA, with its hallmark anterior knee pain, can occur in isolation as a result of patella malalignment, abnormal tracking and loading, and direct trauma to the patella.⁵⁵

Feet and Toes The first MTP joint is the most common site of OA affecting the foot and may result in hallux rigidus or hallux valgus deformities. Changes in the other MTP joints and toes as a result of OA and resultant shortening of the long extensors can lead to hammer toes. Forefoot involvement contributes to poor push-off in the terminal stance phase of gait and balance issues.⁵⁷

Spine The lower cervical and mid to lower lumbar regions of the spine are most susceptible to OA. All spinal articulations can experience degenerative changes; however, the facet (zygapophyseal) joints are the only true synovial joints in the spine.⁵⁸ Facet joint osteophytes can contribute to lateral and central lumbar stenosis and subsequent nerve root impingement⁵⁸ (Fig. 23.20). Pain from facet joint OA can originate from the joint itself and affected nerve roots (radicular pain) and in the lumbar area, and typically increases with spinal extension, rotary motions, and when standing or sitting.⁵⁸ Lying and spinal flexion lead to pain relief.

Activity Limitations and Participation Restrictions

Overall, OA of the knee can impose functional limitations to a degree equivalent to heart disease, CHF, and chronic obstructive pulmonary disease (COPD) and accounts for a substantial proportion of the burden of disability among community-living elders.⁵⁹

Patients with the most severe disease may not move their joints as often or in the ways that exacerbate their symptoms. Therefore, pain, disease severity, and functional disability in individuals with OA are interrelated.

Among elders, it has been shown that the functional loss associated with severe radiographic OA without pain is more likely than the loss associated with symptomatic but milder disease.⁶⁰ One explanation of this finding is that individuals with OA limit their functional activities to avoid movements that are painful. In the clinical examination it is important to determine functional status even in the absence of pain. Given that individuals with OA may reduce or eliminate their symptoms by avoiding certain activities, clinicians should explore activity limitations and physical inactivity–related symptoms in patients with OA separately from the evaluation of symptoms.

Greater self-reported disability in advanced knee OA was associated with pain, joint laxity, age, and body mass index (BMI) among Finnish adults ages 60 to 80 years while performance-based functioning was related to the self-report Western Ontario and McMasters Universities Arthritis Index (WOMAC) function score, pain, and obesity.⁶¹ Of interest, the authors found no association between radiographic severity of knee OA and self-reported and performance-based function.⁶¹ The comprehensive International Classification of Functioning, Disability, and Health (ICF) Core Set of impairments, activity limitations, and participation restrictions has been established through an international team of researchers, clinicians, and patients to identify those areas of functioning that are affected by OA, with the shorter Brief ICF Core Set created for clinical purposes.^62,63 OA is a leading cause of disability and major contributor to work-related disability, reduced productivity, and absenteeism.⁶⁴

Prognosis

OA is a slow progressing disease that can be self-limiting or progress to advanced joint and soft tissue damage leading to complete failure of that joint. In such a case, joint surgery including arthrodesis of some joints in the foot, or arthroplasty, for example, of the knee is the final treatment option to help the patient regain function. However, rapidly progressive joint damage is uncommon and in most cases patients stabilize.¹ Increasing disability may be more related to advancing years, co-morbidities, and inactivity.

Pharmacological Therapy in Rheumatoid Arthritis

Joint destruction and irreversible damage are most pronounced early in the disease course. Current medical management is based on the implementation of an early and aggressive approach to disease management to halt or decrease progression. Medical therapies also focus on decreasing pain and inflammation. Early aggressive pharmacological therapy is associated with diminished joint damage and long-term maintenance of function. The major classifications of drugs used in RA management include nonsteroidal anti-inflammatory drugs (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs), which include the biological response modifiers (BRMs) and corticosteroids.⁶⁵ Table 23.4 lists the most common drugs used in the management of RA.²⁰

Nonsteroidal Anti-inflammatory Drugs

NSAIDs provide both analgesic and anti-inflammatory effects depending on the dose prescribed; however, they do not alter disease progression. Discontinuance of NSAIDs quickly leads to exacerbation of symptoms. Thus, NSAIDs are generally given in combination with other disease-modifying agents. At lower doses, the NSAID effect is analgesic, through the peripheral inhibition of pro-inflammatory prostaglandin synthesis. At higher doses, the effect is anti-inflammatory, probably through both prostaglandin inhibition and alterations in macrophage and neutrophil function. Due to the mechanism of action of these medications, adverse effects include gastrointestinal (GI) complaints and renal effects. Mild GI adverse effects include distress and nausea. However, approximately 2% to 4% of patients experience serious adverse effects including gastrointestinal bleeding, ulcers, and perforation. Patients are encouraged to take these medications with food, to monitor GI signs, and/or are given prophylactic therapy to decrease gastrointestinal damage. Renal and other adverse effects associated with continued use and high doses of NSAIDs include dizziness, drowsiness, headache, tinnitus (ringing in the ears), kidney dysfunction, and elevation of liver enzymes. Complete blood counts (CBCs) and stool guaiac analyses for occult blood should be conducted every 3 to 4 months to monitor for potential adverse effects.⁶⁵

There are two primary categories of NSAIDs, based on whether they inhibit COX-1 and COX-2 enzymes or COX-2 enzymes alone. These enzymes are responsible for synthesis of prostaglandins. Traditional NSAIDs block both COX-1 and COX-2 enzymes. The main function of the COX-1 enzyme is synthesis of prostaglandins in the endothelium and gastric mucosa, tissues present in the stomach lining and kidneys. Caution should be taken when prescribing NSAIDs to specific groups of patients at risk for GI complications such as the elderly, smokers, those taking corticosteroids, and those with severe arthritis, co-morbidities, and history of GI symptoms. The selective COX-2 inhibitors were designed to decrease the risk of GI toxicity by inhibiting only the COX-2 enzyme, which is responsible for the pain and swelling associated with inflammation. Early studies of short duration exposure supported the reduced risk of GI side effects and increased tolerability of COX-2 inhibitors.⁶⁶ However, studies of longer selective COX-2 exposure and systematic evaluation of the data from numerous trials indicate that patients on selective COX-2 inhibitors are at greater risk of acute myocardial infarction and other cardiovascular events.^67,68,69

NSAIDs are an accessible and relatively inexpensive drug to manage inflammation; however, the decision to prescribe an NSAID must be based on risk factors, known toxicities, and dosing preferences. Individual response to an NSAID is extremely variable in terms of both effectiveness and tolerance. Therefore, it often requires several month-long trials to find the best product. Taking more than one NSAID increases the risk of toxicity with no increase in benefit. NSAIDs are prescribed for patients with RA at the onset of symptoms to provide rapid pain relief and control of inflammation while waiting for the slower-acting DMARD to become effective.

Disease-Modifying Antirheumatic Drugs

DMARDs are the primary class of drugs for managing disease progression in RA. An array of drugs with varying chemical structures, modes of actions, clinical indications, and toxicities are classified as DMARDs. Typical DMARDs used to manage RA include antimalarials, methotrexate, sulfasalazine, and leflumonide. Although DMARDs are effective in reducing disease progression, these medications do not provide an analgesic effect and are slow acting, taking from 3 weeks to 3 months to take effect. A drug that is classified as a DMARD must show evidence of affecting the course of RA for at least 1 year (improved function, reduced inflammation, and slowing or prevention of structural damage). DMARDs may be given alone or in combination for best effectiveness. Individuals taking DMARDs should be monitored regularly for the toxicities accompanying the specific drug. DMARDs are most often used to treat adult-onset RA; however, some are used to treat juvenile RA, ankylosing spondylitis, psoriatic arthritis, and systemic lupus erythematosus. The most commonly used DMARD to manage RA is methotrexate.²⁰

Biological Response Modifiers

Biological response modifiers (BRMs) are a class of disease-modifying agents in use since 1998 that are biologically engineered to mimic the activities of targeted immune cells to reduce or block the inflammatory process. These drugs are approved to treat moderate to severe RA that is nonresponsive to traditional therapy. The mechanism of action of BRMs varies and includes inhibition of cytokine activity, by blocking either tumor necrosis factor–alpha or interleukin-1. Evidence demonstrates both inhibition of the progression of structural damage and improvement of physical function in RA and represents a significant advance in the treatment of RA. Patients who begin BRMs usually continue with their NSAIDs or corticosteroids. Adverse effects of these medications can be quite serious and patients must be monitored for signs of infection, including colds and flus, which can rapidly progress during immunosuppression. Those with a history of tuberculosis (TB) are at risk for reactivation of TB and may be excluded from this form of therapy. The number of diseases in which these agents are useful continues to expand as do the number and types of agents available.

Corticosteroids

Corticosteroids are powerful anti-inflammatory drugs creating rapid and potent suppression of inflammation. Corticosteroids are generally not given alone and may be administered orally, intravenously, or via intra-articular or periarticular injection. Unfortunately, these potent inflammatory medications also produce serious adverse effects when used long-term or in high doses. Potential adverse effects include thinning of the skin, osteoporosis, muscle wasting, adrenal suppression, increased susceptibility to infections, impaired wound healing, cataracts, glaucoma, hyperlipidemia, and aseptic bone necrosis. These drugs are generally prescribed in the presence of unremitting disease and severe extra-articular inflammation and are given in combination with other RA medications (e.g., DMARDs). Corticosteroids are often prescribed in pulse doses (low tapering doses over a specific time period) to reduce the risk of side effects. Patients on corticosteroids should have their blood counts, serum potassium, and glucose levels monitored and be observed for potential side effects.²⁰

When inflammation is confined to a specific location, steroid injections into a joint, bursa, tendon, or tendon sheath may be administered. However, use of steroid injections is commonly limited to no more than two to four per year to reduce the risk of osteonecrosis and soft tissue damage.

Pharmacological Therapy in Osteoarthritis

To date, drug therapy in OA has no effect on disease progression and is ancillary to nonpharmacological approaches to pain management including patient education and self-management, weight loss, joint protection, and exercise.^40,70,71,72 The goals of drug therapy in patients with OA are to relieve pain and decrease inflammation when it is present. Oral analgesics, NSAIDs, and corticosteroid injections are the primary medications used in OA management (see Table 23.4).^1,70,71,72

Acetaminophen, an oral analgesic, is usually the drug of first choice.^{40,70,71,72,73} Acetaminophen-containing compounds (Tylenol, Panadol, Anacin-3) have been cited as having almost no toxicity in recommended doses (up to 4 g/day) and little or no GI side effects. However, there is no anti-inflammatory effect; acetaminophen cannot be substituted for NSAIDs in this regard. Earlier clinical studies in OA demonstrated symptom relief from acetaminophen (3 to 4 g/day) greater than that of a placebo and slightly less than that of NSAIDs.⁷⁴ However, newer evidence suggests that acetaminophen has minimal clinically important effects on pain and no significant effect on stiffness or physical function in patients with symptomatic knee OA.⁷³ Further, acetaminophen use can lead to liver and, less commonly, kidney toxicity, especially in individuals who drink excessive amounts of alcohol. As well, there is increasing evidence of an increased incidence of hospitalization due to GI perforation, peptic ulceration, and bleeding with acetaminophen use of more than 3 g/day compared to lower doses (less than 3g/day).⁷³

NSAIDs have a place in the management of persons with OA who do not respond to acetaminophen and nonpharmacological measures.⁷² NSAIDs may be used in combination with acetaminophen, and should be kept to the lowest effective dose to minimize GI toxicity. The COX-2 NSAIDs, described for RA management, had been prescribed for people who are at increased risk for GI problems until longer-term trials called their safety into question.

Intra-articular corticosteroid injections are often used for acute episodes with a moderate effect for pain relief, irrespective of the number of injections.⁷² The knee is the most common site; however, soft tissue injections for subacromial, anserine, and trochanteric bursitis also may be effective.

Viscosupplementation or intra-articular injections of the knee with a form of hyaluronic acid (HA) is sometimes used. A number of synthetic forms are available (Synvisc, Hyalgan, Artzal). Hyaluronic acid is a naturally occurring polysaccharide that contributes to the thickness and viscosity of joint fluid in the healthy joint. In the OA knee, the levels of HA are lower and the joint fluid is thinner and less dense, reducing the ability of the fluid to lubricate and attenuate shock. Viscosupplementation therapy consists of a series of weekly injections. The reported effects of treatment are reduced pain and stiffness and improved function in people with mild to moderate knee OA, which may last for several months.⁷² It is not clear if HA injections are more effective than corticosteroid injections, NSAIDs, or placebo injections. The injected HA does not replace normal joint fluid to achieve its effect as most is absorbed and cleared from the joint within a week. The risk of adverse effects is low. The most serious reported adverse event is an allergic reaction and less serious effects are injection site reactions and joint swelling. There is no evidence that supports increased efficacy of one product over another; however, high-molecular-weight hylan (Synvisc) may have greater efficacy.⁷²

Glucosamine sulphate (GS) and glucosamine hydrochloride (GH) have been examined in placebo-controlled trials and found to be moderately effective for pain relief; however, the size of the effect diminishes when only high-quality trials are considered.⁷³ In one long-term follow-up study, patients who had taken GS, 1,500 mg/day for at least 12 months, were half as likely to undergo total knee replacement (TKR) at 5 years.⁷³ The structural-modifying effects of glucosamine products in hip and knee OA remain uncertain.

Topical agents include analgesics and anti-inflammatory preparations. Topical analgesics may be either rubifacients, which contain methyl salicylate, chemical compounds that produce a counterirritant effect, or capsaicin compounds, which reduce pain through depletion of the neurotransmitter substance P in peripheral nerves. To date, the only topical analgesic to show consistent efficacy in controlled clinical trials is capsaicin. Capsaicin is an alkaloid derived from red chili peppers and is available in topical analgesic creams in varying concentrations (Zostrix, Capsaicin-P, Dolorac). It has been shown to decrease pain approximately 33% when applied to specific joints four times daily.⁷² The initial stinging or burning sensation disappears after several days of use; however, the need for frequent daily applications may limit the acceptability of this therapy for some patients.⁷² Topical NSAIDs (diclofenac) are recommended as alternative or adjunctive therapy in symptomatic knee OA. Topical preparations delivered through gel, liquid, or patch formulations are absorbed through the skin with the help of an absorption enhancer are slightly less effective than oral NSAIDs with fewer adverse events.^31,72

The chronic progressive nature of arthritis dictates a plan of care (POC) that includes patient education and self-management beyond the initial presentation. Although RA is systemic and OA is a more localized condition, both diseases can significantly affect health, function, participation, and quality of life. The rehabilitation of persons with arthritis requires comprehensive and coordinated efforts of a team of health professionals, including physical therapists, and ensures that the patient is first and foremost in treatment planning. The patient's ability to self-manage successfully is a major predictor of better health outcomes.⁷⁵ The physical therapist plays a pivotal role in helping the patient with minimal disability gain confidence and experience in using self-management skills to deal with the condition. The general goals and outcomes for persons with RA and OA are similar (see Box 23.4).

The remainder of this chapter will discuss physical therapist examination and interventions for people with RA and OA of the hip and knee. Although OA also presents at other joints, these two are the most common and disabling sites for OA and are most frequently seen by a physical therapist.

Physical Therapy Examination

A comprehensive and multisystem examination and history is an essential component of physical therapy management. Whether the patient is a direct access client or seen in a system-based clinical setting, collaboration and communication with other care providers working with the patient is imperative. As with all patient-centered care, the patient is the primary stakeholder and should be actively engaged in goal setting and in the development of the POC.

Careful observation of the patient during the initial meeting and history can help inform the process. For example, observation of the patient's gait, ability to remove outerwear, and transfer into a chair for the history will provide the therapist with a quick assessment of functional ability.

History

The medical and social history will direct and inform the examination and provide insight into the development of a POC and need for potential resources. Ascertaining the patient's understanding of the disease and the implications of the disease is an important component of the interview process. In particular, the therapist should be concerned with identifying "red flag" signs and symptoms that indicate the need for immediate medical follow up (Table 23.5).⁷⁶ Pain assessment questions should include location, duration, pattern, quality, and intensity. Specific details regarding joint inflammation such as joint heat, swelling, and erythema should be recorded and confirmed during the physical examination. A determination of joint stiffness (morning versus after prolonged static posture), previous activity level, pattern and degree of fatigue, presence of co-morbidities, and current medication is also essential. Use and effectiveness of previous therapeutic interventions and complementary approaches should be noted. Although many physical therapy tests and measures are used during the examination, specific adaptations may be made to tailor the examination to the person with RA or OA. Especially in RA, the tender and swollen joint count appears to be a sensitive measure of systemic disease activity and guides the exercise prescription.¹⁶

Range of Motion

Tenderness and subjective reports of pain on passive range of motion (PROM) are highly indicative of inflammation; thus, gentle pressure and appropriate hand position is paramount during examination. Goniometric measurement of PROM is indicated and necessary at all affected joints after a gross joint screening to assist in monitoring treatment effectiveness. Standardized procedures are essential for reliable and valid measures. Otherwise, potential variations in intrarater and inter-rater reliability will reduce the accuracy of data comparison throughout the disease course.⁷⁷ If joint pain or poor activity tolerance prohibits measurement of PROM, the therapist may consider substituting a functional ROM test by asking the patient to touch various body parts (e.g., the top of the head and small of the back) to determine the available ROM for performing self-care activities. The therapist should note any tenderness, crepitus, or pain during examination of ROM.

Regardless of whether the patient has OA and monoarticular involvement or RA with polyarticular involvement, the impact of an involved joint on the kinematic chain or on the contralateral side should not be overlooked.⁷⁸ When there is OA in a hip or knee, active motion in functional positions should be examined in all joints of both lower extremities (LEs). It is important to observe motion for symmetry and smoothness during gait, stair climbing, and rising from a chair. Ascending stairs requires the greatest amount and velocity of knee flexion and may be one of the best activities to determine knee function.⁷⁹ Decreased ROM at the hip and knee increases the risk for injury and falls. Approximately 50° hip flexion and 90° knee flexion are required to recover balance from a stumble during walking.⁸⁰

Strength

Pain and joint effusions impede muscle contraction, limiting examination of strength. A patient may be able to generate force in the pain-free range but unable to completely contract in the painful range secondary to reflex inhibition. Traditional strength tests (e.g., manual muscle tests) are not appropriate in the presence of severely deformed and/or deranged joints. Functional strength assessments are more appropriate and will provide sufficient data to formulate treatment goals. Individuals who demonstrate a lag phenomenon will have limited active range and will not be candidates for traditional grading systems, because these are not sensitive to changes in the quality and quantity of muscle contraction. When documenting strength, it is important to include information on required modifications made to preferred testing positions, grade of strength exhibited in that arc of motion, and the method of strength testing used (e.g., break test, isometric holding at the end of range, or resistance throughout the ROM). Modifying the test protocol to include an isometric break test at midrange or most comfortable joint position generally yields higher grades than would be received if full range testing were done. Any modifications to standardized test protocols must be carefully documented. It is also important to document the time of day the patient was tested, as well as the use and timing of medications that might alter performance or exercise tolerance.

The functional threshold for LE strength has yet to be determined. However, reports from studies that have examined knee strength as a percentage of body weight suggest that isokinetic strength measured at velocities between 60° and 180° per second should be 20% to 30% body weight for knee extension and 20% to 25% for knee flexion.^78,79 Isometric knee extension below 10 kg (22 lb) of force (measured with the hip at neutral and knee at 90°) corresponded to marked disability in a study of persons with OA of the knee.⁸¹ It is also important to perform strength testing of the muscle groups proximal to the affected joints to detect deficits that can affect function and contribute to abnormal biomechanics.

Joint Stability

Joint stability is essential for normal biomechanics, function, and independence. Inflammatory aspects of RA can lead to joint instability and eventual deformity. Intra-articular ligaments are highly susceptible to inflammatory and erosive changes in RA. Thus, ligamentous laxity of any affected joint should be fully investigated. Pseudolaxity, often detected in unicompartmental knee OA, should be differentiated from true ligamentous laxity.

Cardiovascular Status

Fatigue is one of the systemic manifestations of RA and frequently unappreciated. Individuals with OA also report fatigue. To best ascertain the impact of fatigue on patient functioning and independence, assessments should be made over the course of a single day and over several days. The increased incidence of asymptomatic cardiovascular disease, elevated risk for ischemic heart disease, and decreased cardiovascular fitness of individuals with RA demands specific attention.²⁴ Heart rate, respiratory rate, blood pressure and ratings of perceived exertion should all be measured during a functional activity that is reasonably stressful for the patient's current level of fitness. Excessive increases in perceived exertion may indicate the presence of inflammation or impairment of pulmonary and cardiac function that requires more extensive and formal evaluation. It is also important to determine cardiovascular fitness in individuals with OA, because cardiovascular deficits and increased risk for coronary artery disease are clearly associated with long-standing or severe disease.^24,82

Functional Examination

Functional examination measures provide a rich and patient-centered approach to assessment. Functional measures may include ADL, work, and leisure activities (see Chapter 8, Examination of Function). The selection of a functional measure is based on the demographic features of the patient (e.g., age, gender), the level and depth of information required, and the measure's sensitivity/responsiveness in gauging the efficacy of treatment.^83,84,85 As with goniometric measurement, the reliability and validity are important for individual and comparative purposes. The Functional Status Index (FSI), a valid and reliable measure, was designed for use in outpatient rheumatologic settings to assess an individual's function in a sample of typical ADL. FSI parameters include pain, level of difficulty, and dependence (Appendix 23.A).^86,87 The Health Assessment Questionnaire (HAQ) is a generic measure consisting of the following five domains or subscales: disability, discomfort, pain, drug side effects (toxicity), and costs of care (Appendix 23.B).⁸⁸ The HAQ is a component of the ACR core of measures for rheumatoid arthritis⁸⁹ and has been shown to correlate highly with measures of disease progression in RA (x-ray changes).¹⁷ The modified HAQ, an abbreviated version of the HAQ, is a quick, easy to complete and score instrument that assesses the impact of disease activity on function and disability. Both versions are available for free online. Another arthritis-specific instrument, the revised Arthritis Impact Measurement Scales 2 (AIMS2), expands the concept of function to include performance in psychological and social domains as well as physical function. The AIMS2 also measures the patient's satisfaction with current functional status and individual preferences for outcome.⁹⁰ The AIMS2 is not well suited for program evaluation or research purposes due to its complicated scoring algorithm and associated costs. The WOMAC is a widely used, valid, and reliable self-report instrument of 24 items in three categories specific to OA of the hip and/or knee (pain, stiffness, and function). The WOMAC takes about 10 minutes to administer and is easily scored by hand. It is available in either Likert form (0–4) or visual analogue scale.⁹¹ Both the AIMS2 and the WOMAC are sensitive to clinical intervention and provide excellent clinically feasible, standardized measures in the domains of function and disability to monitor change over time. The Knee Injury and Osteoarthritis Outcome (KOOS) measure was developed using the WOMAC as a base and includes sports, recreation, and leisure items. This measure is readily accessible, is relatively easy to score, and demonstrates strong validity, reliability, and responsiveness in adults.⁹² A modified version of the KOOS was developed for persons with hip osteoarthritis (HOOS).⁹³

Mobility, Gait, and Balance

A complete and detailed gait examination is one of the most important contributions of the physical therapist to the rehabilitation team's understanding of the individual's functional abilities and serves to identify additional areas for examination and intervention.^94,95 (See Chapter 7, Examination of Gait, for a complete discussion.) Substantial differences in fall risks,⁵⁶ knee ROM, and gait velocity between patients with either OA or RA and their peers without arthritis have been demonstrated.^95,96

Sensory Integrity

With RA, alternations in sensation may be evident with the presence of Raynaud's disease or with compression of nerves due to inflammation or joint derangement. Any indication of peripheral neuropathy or nerve involvement should be investigated using standard examination procedures (see Chapter 3, Examination of Sensory Function). Sensory changes resulting from other co-morbidities or from the normal aging process should be considered when appropriate.

Psychological Status

Individuals with chronic arthritis experience years of functional and social loss that would stress any person's ability to cope and adapt.⁹⁷ Although pain is significantly correlated with self-reports of depression, no firm association with function has been identified.⁹⁸ The overall psychological status of the individual with RA is generally similar to those individuals with other chronic diseases that threaten a severe change in body image and disruption of social integration (see Chapter 26, Psychosocial Disorders). Individuals respond to these threats with various coping strategies to maintain psychological well-being. No single strategy can be deemed definitely better than another, although for individual patients some strategies will lead to better coping and more positive outcomes than others. Exploration of the patient's attitude toward rehabilitation and readiness to make health behavior changes, as well the availability of social support, can assist the therapist in shared goal setting and identifying realistic expectations of future functional ability. Persons with RA face the additional challenges of living with a chronic disease that is characterized by a fluctuating disease course and must learn to adapt their lifestyle, activity level and medication and sleep schedule according to their disease activity. Thus, it is paramount that the therapist works with the patient to set realistic, achievable goals and educate the patient about warning signs of flares to help the patient self-manage.

Anxiety and depression are also common in patients with OA and may alter the pain experience, function, and response to treatment interventions.⁹⁹ Chronic pain, fatigue, loss of function, and reduced activity levels can all contribute to emotional distress. It is therefore important to recognize the signs of anxiety and depression and, if indicated, refer to appropriate screening services and resources to help individuals manage their psychological symptoms through improved coping skills.¹⁰⁰ Participation in the Arthritis Self-Management Program has been shown to improve coping.

Environmental Factors

Therapists should be aware of environmental factors in the home, work, and leisure environments that might serve as facilitators or barriers to functioning and warrant specific identification, examination, and recommendations to address (see Chapter 9, Examination of Environment.) A discussion about the home and work environments may reveal conditions that threaten independence that can be addressed through ergonomic and environmental modifications and school or workplace accommodations. The costs of such changes may be a limiting factor for implementing these recommendations. The work environment affects employment and disability in more ways than the physical setting and task requirements. Acceptance and understanding by supervisors and co-workers of the disease and self-management requirements of the worker with arthritis are important determinants of maintaining employment and income. Other environmental factors common to both the RA and OA ICF Core Sets include technology and assistive devices for ADL, mobility, transportation, and employment; design and access to buildings; climate; and attitudes of family, friends, and health professionals.^{62,63,101,102}

Physical Therapy Intervention

The development of specific goals and expected outcomes for the individual with arthritis is based on the following general goals and expected outcomes developed in conjunction with the patient (Box 23.4).

The specific goals and outcomes identified for each patient will depend on the type of arthritis, disease activity level, the clinical presentation, and patient preferences in line with patient-centered care. Mutual goal setting promotes patient participation in treatment. It is the physical therapist's responsibility to document the POC, implement that plan safely and effectively, and delegate responsibility appropriately to ensure that the patient's goals can be reached. The therapist should ensure that treatment goals and objectives are measurable, attainable, and documented, with specific timeframes included (e.g., increase left shoulder flexion ROM by 10° in 2 weeks, and independent ambulation with platform crutches on level surfaces for at least 250 feet without fatigue within 1 month). Failure to achieve goals within the stated timeframe indicates the need for reevaluation and reformulation of the goals. Goals and outcomes should be revised to reflect changes owing to both personal and environmental factors that may affect progress or alter the proposed time frames (see Chapter 1, Clinical Decision Making).

Modalities for Pain Relief

A variety of physical agents are available to relieve pain and prepare the patient for passive and dynamic stretching and other exercise interventions. The most common form is thermotherapy.

Heat

Superficial heat, heat that penetrates only a few millimeters, produces localized analgesia and increases circulation in the vicinity where it is applied. Types of superficial heat include moist hot packs; dry heating pads; and lamps, paraffin, and hydrotherapy. The evidence supporting the effectiveness of these modalities is weak, but patients often report that they gain comfort from moist heat. Paraffin is particularly useful in delivering superficial heat to irregularly shaped joints or to individuals who cannot tolerate the weight of a moist hot pack. Hydrotherapy allows the therapist to combine heating of tissues with exercise, and provides the patient the experience of aquatic therapy, although it is expensive. Systematic reviews of heat and cold therapy in arthritis suggest small to modest effects.^103,104

Deep heating modalities, such as ultrasound, may affect the viscoelastic properties of collagen and increase the plastic stretch of ligaments, providing modest improvements in pain and function in individuals with knee OA.¹⁰⁵ However, their efficacy in RA is not demonstrated.¹⁰⁶ Their use in treating individuals with RA during the acute stage of inflammation is contraindicated because they may stimulate collagenase activity within the joint, furthering its destruction.^107,108 Furthermore, modalities that do not readily translate to home use foster a dependency on clinical care and do not promote self-management.

Cold

Local applications of cold will also produce local analgesia, increase superficial circulation at the site of application following an initial period of vasoconstriction, and decrease intra-articular temperature.¹⁰⁹ Cold is particularly useful around joints that are inflamed and swollen, a condition that usually worsens with the application of superficial heat modalities. Therapists may use either wet or dry application techniques. Superficial cold is contradicted in patients with Raynaud's phenomenon or cryoglobulinemia, linked to an abnormal protein (cryoglobulins) in the blood that gels at low temperatures. Both may be associated with RA.

Electrical Agents

Therapists may also wish to consider using other modalities for pain relief in treating the individual with RA, including transcutaneous electrical nerve stimulation (TENS), although the value of TENS as reported in the literature is inconsistent.^110,111 A meta-analysis of studies investigating TENS for knee OA pain concluded that the mode of TENS applied did affect results, repeated use was more effective than a single application, and use for at least 4 weeks was the most effective.¹¹¹

Orthoses, Splints, and Braces

In RA, hand and wrist orthoses may be used to immobilize specific joints and help reduce pain and swelling by providing local rest and support. There are three primary types of splints: functional (used to restore or improve function), corrective (used to improve alignment), and resting (used to maintain joint alignment and reduce pain). Resting splints are worn at night or periodically during the day. There is evidence of small benefits for pain reduction and increased function with the use of functional splints. Hand splints may improve grip and pincher strength.¹¹² There is evidence that wearing functional wrist splints decreases grip strength and does not affect pain, morning stiffness, pinch grip, or quality of life with regular wear.¹¹³ A study that investigated the effect of functional wrist splint wear on task performance reported that wearing a commercially available elastic wrist orthosis resulted in some decrement in performance speed on a number of common tasks, though pain was significantly reduced for all tasks.¹¹⁴ There is consistent evidence supporting the use of splints for short- and long-term pain relief in hand OA.¹¹⁵

Foot orthoses also may be used to alleviate pain through biomechanical support or correction for individuals with knee OA. A lateral wedge insole designed to reduce medial compartment stress appears to reduce pain and NSAID use in some individuals with knee OA.¹¹⁶ Other methods that show promise in treating knee OA pain are patellofemoral taping,¹¹⁷ and load shifting or unloader knee braces (stress shifted away from most involved area).¹¹⁶ All orthotic interventions require professional evaluation, selection, education, and monitoring of use.

Rest

Complete bed rest is rarely recommended. Adequate quality and quantity of sleep at night and short rests during the day are preferred. General recommendations include 8 to 10 hours of sleep per night and brief 30-minute rest periods during the day. Inactivity is a common problem for people with arthritis and may lead to deconditioning, depression, lower pain thresholds, diminished bone and soft tissue health, and increased risk for other serious health conditions. Thus, a major goal of therapy is to assist the person to maintain or regain adequate levels of physical activity and avoid the unnecessary consequences of inactivity.¹⁶

Range of Motion and Flexibility Exercise

A major factor affecting joint mobility in individuals with RA is the level of inflammation and resting position in which specific joints are maintained. For example, intra-articular pressure is reduced when the knee is slightly bent. Although helpful in reducing joint pain, this flexed position may lead to capsular and musculotendonous shortening and eventual contracture. Patients should be taught proper positioning when resting and should be encouraged to perform daily, active ROM as tolerated to maintain motion. Active-assisted, passive, and proprioceptive neuromuscular facilitation (PNF) techniques may also be applied to shortened muscles.¹¹⁸ Pain should be respected at all times and should be minimal during and after exercise. Evoking a pain response during stretching may lead to a reflex contraction of the agonist muscle as opposed to creating a relaxation response. Stretching exercises to lengthen shortened muscles should be performed slowly, held for 20 to 30 seconds two to three days a week or more often if indicated. It is important to educate the patient not to do stretching exercises that involve inflamed, swollen joints because they are at risk for capsular stretching and rupture.¹¹⁹ Common wisdom recommends that exercise-induced pain should subside within 1 hour. If the patient reports discomfort lasting longer than 1 hour, it may indicate that either the technique, intensity, or duration of the exercise was too great and should be reduced or modified at the next exercise session. Patients should be encouraged to exercise on their own during those times of the day when they feel best. Local pain relieving modalities before or immediately after exercise may be useful and increase exercise adherence.

In hip and knee OA, manual therapy may offer some additional benefit within a comprehensive treatment program that includes exercise.¹¹⁸ Manual therapy is not generally recommended for individuals with RA who have joint inflammation or resultant laxity.

Strengthening Exercise

Decreased muscle function (strength, endurance, power) in persons with arthritis arises from both direct and indirect effects of the disease. These include intra-articular and extra-articular inflammatory disease elements, side effects of medication, disuse, reflex inhibition in response to pain and joint effusion, impaired proprioception, and loss of mechanical integrity around the joint. A variety of conditioning programs can be effective for improving strength, endurance, and function without exacerbation of pain or disease activity.

Initially, isometric exercise may be indicated to improve muscle tone, strength, and static endurance; to recruit or activate specific muscles; and to prepare joints for more vigorous activity. Although isometric exercise does avoid dynamic joint stress and mechanical irritation, it can produce other unwanted effects. Isometric exercise performed at more than 50% of maximal voluntary contraction constricts blood flow through the exercising muscle, leading to post-exercise muscle soreness, and the increased peripheral vascular resistance produces increased blood pressure.¹¹⁹ In the knee and hip, high-intensity isometric contractions are associated with significant increases in intra-articular pressure and reduce synovial circulation.^120,121,122 Patients with cardiovascular disease should perform these exercises with caution and be sure to breathe during the contraction because holding one's breath can increase intra-abdominal pressure (Valsalva maneuver). Patient instructions for isometric exercise should include the cautions to (1) maintain the contraction for no more than 6 seconds; (2) avoid maximal effort because it is neither necessary nor desirable; (3) exhale during the contraction and inhale during a similar time period of relaxation; and (4) not contract more than two muscle groups at a time.

Dynamic exercise includes both shortening (concentric) and lengthening (eccentric) contractions. Strength and endurance may be improved through resistance (physiological overload) supplied by weight of the body part or external resistance in the form of free weights, elastic bands, or a variety of resistive exercise equipment. A cautious approach to resistance training is recommended to protect unstable or inflamed joints from damage.^16,119 Strengthening exercise should be performed within the pain-free range. Maximum benefit and maintenance can be achieved by incorporating functional movements and body positions in the recommended exercise routine. The use of well-controlled smooth movement toward the end part of the range is advised, and modifications to resistance, repetitions, or frequency are recommended as needed. Gradual progression of resistance and repetition is recommended. Reduce exercise intensity, frequency, or motion if increased joint swelling or pain occurs (local inflammatory response).

Individuals with RA benefit from maintaining or restoring muscular fitness. A number of well-controlled studies have reported on strengthening programs that provide overload with results indicating positive adaptations in muscle and functional performance with no exacerbation of disease symptoms. Data from selected RA exercise studies are presented in Box 23.5 Evidence Summary.^123-135 Loads of up to 70% one repetition maximum (1RM) used in a circuit training resistance program for persons with controlled RA demonstrated no exacerbation in joint symptoms and significant improvements in strength and function.^{123,124,126,128}

Designing exercise interventions for individuals with RA requires careful consideration of the patient's disease activity, disease severity, and systemic disease features. Persons with RA in an active flare-up should limit their exercise to daily ROM exercises incorporated into ADLs to promote adherence to active joint movement and isometric exercises to promote strength. Walking as tolerated is encouraged together with daily periods of rest and a full night of sleep to manage fatigue. When the disease activity subsides, the exercise program can be progressed by adding dynamic strengthening exercises, with caution to avoid stress on deranged joints or cysts, and greater repetitions of isometric exercises as well as greater engagement in physical activity. When the disease is in remission, aerobic exercises and dynamic exercises with resistance should be considered to promote cardiovascular health and improve strength and conditioning.¹⁶

In persons with knee OA, the evidence is strong and consistent that LE exercise that includes neuromuscular and functional training reduces pain and improves function. Interventions have included isometric, isotonic, and functional exercise, as well as proprioceptive and balance training. Interventions have been tested in both clinically supervised and self-directed settings with positive results and acceptable adherence.^97,136 Evidence supporting the use of exercise in the management of knee and hip OA is presented in Box 23.6 Evidence Summary.^{137,138,139,140,141,142} Physical therapists should routinely incorporate strategies to enhance patient motivation and adherence to the therapeutic exercise and home exercise programs (HEPs) including exercise booster sessions (periodic follow-up appointments), goal setting, and other self-efficacy enhancing practices.¹¹⁹

Cardiovascular Training

Individuals with RA or OA are usually deconditioned compared to their age-matched peers. A number of systematic reviews and well-controlled trials have reported improvements in aerobic capacity and activity levels through regular cardiovascular conditioning without aggravating joints and other disease symptoms.^{16,24,125,130} Programs and guidelines appropriate for healthy adults or older individuals can be instituted following the Centers for Disease Control and Prevention (CDC) recommendations for exercise, which suggest 30 minutes of moderate-intensity exercise five times per week¹⁴³ or the more recent guidelines to accumulate 150 minutes each week.¹⁴⁴ If weight-bearing is a barrier to exercise, low– or non–weight-bearing activities such as stationary cycling, pool-based aerobics, or deep water running may be options.^16,127,145 For most people, walking and stationary bicycles are a safe and effective means of aerobic exercise.^16,145 Furthermore, patients who have engaged in such a program often report an increase in self-esteem and improved emotional status.¹⁶ Medical screening as appropriate for age and medical condition (e.g., Revised Physical Activity Readiness Questionnaire [PAR-Q]) should be performed before beginning an aerobic exercise program.

Functional Training

Functional training for the individual with arthritis proceeds in the same fashion as for other individuals with similar deficits. Therapists may choose to reduce the functional demands of an activity either temporarily, such as under conditions of acute inflammation, or permanently by incorporating a variety of adaptive equipment into ADL that substitute for lost ROM and strength. These modifications can include long-handled appliances and devices with built-up handles for easier grasp. There are aids for dressing and grooming, as well as personal hygiene. By breaking down functional tasks, such as rising from a chair or climbing stairs, into smaller movements, the therapist can help the patient identify faulty movement patterns and address specific components of the movement that are causing difficulty.

UE involvement in RA, particularly of the wrist and hands, may complicate the choice of an ambulatory assistive device by precluding any weight-bearing on these affected joints. In these instances, platform attachments can be used to transform the forearm into a weight-bearing surface. Rearranging the home or work environment also can improve a person's functional abilities. Raising beds or chairs can reduce the effort needed to stand up. Railings placed around the bed, bath, and along stairways also can help increase an individual's independence.

Gait and Balance Training

Specific deviations will be evident throughout the gait cycle. These may include gait asymmetries, decreased velocity, cadence and stride length, prolonged period of double support, inadequate initial contact and push-off, and diminished joint excursion through both swing and stance. Gait deviations in the patient with RA, specifically owing to foot pain or deformities, may also be evident (Table 23.6).^146,147 Therapists should address the underlying joint and muscle impairments that contribute to these deviations in the gait training program with persons with any type of arthritis.

The degree to which the gait of an individual with arthritis should, or can, approximate normal is one of the most difficult questions in designing a therapeutic program. Some "abnormalities" such as antalgic limping may in fact reduce joint loading. Joint destruction may necessitate the introduction of assistive devices as simple as a standard cane or as cumbersome as platform crutches or rolling walkers with platform attachments. The gait of the individual with RA or OA should be safe, functional, and cosmetically acceptable to the patient rather than an unattainable idealized version of the norm. Use of a properly fitted, standard cane in the contralateral hand is associated with decreased joint loading and pain in individuals with both hip and knee OA.

Decreased walking speed in arthritis is common, and there is general agreement that increased speed is a meaningful measure of functional improvement. For example, a person's ability to walk fast enough to cross the street with the timing of the traffic light is important for functional and safe community locomotion. However, increased walking speed without attention to joint biomechanics may be undesirable. In a clinical trial of a nonsteroidal drug for persons with knee OA, all with a varus deformity, gait variables were included as outcome measures. The researchers found that self-reported pain diminished and walking speed increased in the active therapy group. At the same time, kinetic analysis of joint forces showed the increased speed was accompanied by increased adductor moment at the knee and greater loading of the medial compartment.¹⁴⁸ This additional loading of the joint and increased stress on lateral supporting tissue may not be worth the gains of increased speed. Attention to biomechanical factors thus should be considered in comprehensive management, even when drug therapy decreases pain and improves gait speed.

Decreased proprioceptive input, impaired neuromuscular reflexes, altered joint biomechanics, pain, and muscle weakness contribute to static and dynamic balance problems in the individual with LE arthritis. Balance training may include progression from static postures moving from double- to single-limb support, stable to unstable surfaces, and adding perturbations where safe. Dynamic balance activities include maintaining postural alignment while shifting weight from one limb to the other in various directions and walking on different surfaces to challenge the vestibular and proprioceptive systems (see Chapter 10, Strategies to Improve Motor Function). Table 23.7 provides a summary of outcome measures for RA and OA organized by ICF Categories.

Joint Protection

Joint protection is a key component of arthritis management, due to the impact of the disease on the joint and supportive structures. A randomized controlled trial for persons with hand OA compared the effects of a 3-month education-behavioral joint protection program to standard education (each consisting of a 20-minute session and provision of a piece of Dycem [nonslip matting] to use when opening jars). This single-blinded study demonstrated that patients in the joint protection and exercise group increased grip strength by 25% and both groups reported better hand function with the joint protection information.^16,149 Patients should be encouraged to incorporate joint care into all ADL to minimize pain and conserve energy (see Appendix 23.C, Joint Protection, Rest, and Energy Conservation).

In addition to reducing pain and improving function, orthoses also may provide support and protection for vulnerable and painful joints. Foot orthotics or specially designed shoes can serve the dual purpose of relieving biomechanical stresses and enhancing function for the person with RA foot involvement.^150,151 The cost of special shoes may not be reimbursable under many insurance programs. A good shoe will provide support and eliminate unnecessary joint motion in the talocalcaneal joint with a firm and wide heel counter. It should also help to maintain normal bony alignment and accommodate all existing foot deformities within a toe box of adequate dimensions. Pressure should be evenly distributed along the plantar surface of the foot during weight-bearing. Commercially available gel inserts may be helpful and are inexpensive; however, with more advanced biomechanical changes in the foot, the fabrication of orthoses may be required. A rocker sole (shoe sole that is curved at the toe) can be used to facilitate push-off with limited ankle motion. A controlled trial was conducted of the effect of off-the-shelf extra-depth orthopedic footwear for people with RA and at least 1 year of foot pain. Outcomes were measures of pain, gait, and physical function after 2 months of wearing the extra-depth shoes. The footwear group improved significantly on self-reported disability, weight-bearing and non–weight-bearing pain, and gait. In addition to extra depth in the shoe toe box, the shoes provided greater rear foot stability, an arch support, a stiff shank, and a padded heel collar above the counter for improved fit. This study reported that walking pain accounted for 75% of the variability in physical function level of the subjects.¹⁵²

Education and Self-Management

Patient education in the rheumatic diseases has been shown to result in positive changes in knowledge, health behaviors, beliefs, and attitudes that affect health status, quality of life, and health care utilization. A recent review of the literature documented the well-established benefits of self-management programs on mental health.⁷⁵ As in any chronic illness, education should include information needed to deal with the condition (taking medications, exercise), self-management skills necessary to carry out important social and vocational roles, and resources needed to deal with the emotional consequences of chronic illness such as depression, fear, and frustration. The evidence is overwhelming that education designed to teach self-management skills and increase client self-efficacy for these tasks is the most effective.^75,153 The Arthritis Foundation (1330 West Peachtree Street, Atlanta, GA 30309, www.arthritis.org) can supply the clinician or the individual with a variety of educational materials, pamphlets, and self-help courses that will increase cognitive understanding of the disease process and self-management skills. Many local chapters of the Arthritis Foundation hold individual and family support groups to increase psychosocial adaptation, as well as conduct aquatic and land exercise programs in public facilities. The Association of Rheumatology Health Professionals, a division of the American College of Rheumatology (www.rheumatology.org), can provide the therapist with scientific and clinical resources for enhanced practice, as well as a network of professional colleagues who work in rheumatology. See Appendix 23.D for additional Web-based resources.

Surgery represents one of the greatest advances in the management of arthritis in the last 50 years. Surgery is not appropriate, however, for every individual with either RA or OA, and the careful selection of the patient and the timing of the procedure are critical. The primary indications for surgery are pain, loss of function, and progression of deformity, although the last two are not always correlated. Surgical outcomes are greatly affected by personal characteristics of the individual patient, such as anxiety, depression, expectations, and motivation,¹⁵⁴ and external factors, such as access to quality postoperative rehabilitation. General postoperative rehabilitation goals are to restore ROM to the affected joint, promote stability within the joint, regain neuromuscular control of joint motion, restore gait and balance, and improve quality of life.

In general, there are three procedures that may be performed on soft tissues: synovectomy, soft tissue release, and tendon transfers. Similarly, there are three general bone and joint procedures: osteotomy, prosthetic arthroplasty, and, less frequently, arthrodesis. The choice of specific postoperative physical therapy procedures will depend on the particular surgical intervention, the extent of joint involvement before surgery, individual characteristics of the patient (including co-morbid health conditions and physical activity level), and other manifestations of the disease. It is particularly important to remember that a patient with RA, compared to a peer with OA, will have multiple joint involvement, which will ultimately affect the functional outcome of the procedure. A patient with RA is also likely to be a surgical candidate at a much younger age than a patient with OA and is at greater risk for infection following surgery due to the systemic disease process and greater use of immunosuppressive drugs.¹

More than 800,000 total joint arthroplasty (TJA) surgeries of the hip or knee are performed in the United States annually, the majority of which are for patients with OA.¹⁵⁵ These highly successful procedures have revolutionized the management of disabling arthritis in the LE with significant long-term benefits,^156,157 including recovery of physical functioning.¹⁵⁸ The primary goals following TJA are to restore function, decrease pain, and gain muscle control to enable the individual to return to previous, or improved, levels of functioning. Immediate postoperative and rehabilitation management is shaped by a variety of factors, including the occurrence of perioperative complications, as well as surgical factors (type of prosthesis, surgical technique, and approach). Initial treatment includes therapeutic exercise, transfer and gait training, and instruction in ADL.^159,160 Once the individual has achieved an adequate level of function and is released from surgical precautions, instruction in establishing a routine of regular exercise and physical activity to support musculoskeletal and cardiovascular fitness is crucial to long-term outcomes and quality of life. A meta-analysis reviewing recovery of short- and long-term physical functioning after total hip arthroplasty (THA) found that patients had recovered between 46% and 81% of self-reported functioning compared to age-matched controls 6 to 8 months after surgery. Walking speed, daily activity in the home, and other measures of functional capacity all recovered to about 80% of that of controls 6 to 8 months after THA.^{158, 161} Recovery of physical functioning and quality of life after total knee arthroplasty (TKA) is more protracted and frequently less optimal than that of THA.¹⁵⁶ TKA and THA improve clinical outcomes in knees and hips damaged by RA and have a positive secondary systemic effect on RA disease activity; however, there are inconsistent benefits on long-term health-related quality of life.¹⁶²

RA and OA are the two kinds of arthritis that a physical therapist is likely to see in clinical practice. The primary activity limitations and participation restrictions in the individual with RA or OA result from disease activity, musculoskeletal impairments, and cardiovascular deconditioning. Joint surface irregularities, loss of joint space and ROM, muscle weakness, and atrophy contribute directly to limitations in ADL and the ability to work. Pain secondary to changes in normal joint structure and function often limits functioning as well. Musculoskeletal impairments related to arthritis may also lead to impairments of other systems, such as decreased cardiovascular endurance for functional activities. The physical therapist is well suited to evaluate and treat these impairments, remediate the activity limitations, and educate the patient in self-management skills to avoid unnecessary participation restrictions. Rehabilitation of the individual with arthritis is most often directed toward restoring or maintaining joint mobility and strength and emphasizes functional retraining and prevention of secondary health conditions.

Questions for Review

1. What epidemiological factors are related to RA?

2. What are the major pathological changes seen in RA?

3. State two hypotheses concerning the pathogenesis of RA.

4. Describe four modifiable risk factors that may predispose an individual to OA.

5. Describe two changes in articular cartilage associated with OA.

6. Name at least two laboratory tests used in the diagnosis of RA and state their purposes.

7. Describe the parameters used in examining radiographs of arthritic joints.

8. Describe the typical joint changes seen with RA for the following joints: occipitoatlantal, atlantoaxial, temporomandibular, carpals, knees, and talocalcaneal.

9. Define the following deformities: ulnar drift, swan neck, boutonniere, hammer toes, claw toes, and hallux valgus.

10. Describe the overall goals of medical management for RA and OA.

11. What are the primary indications for surgery in RA?

12. Describe the key points in taking a history for the individual with arthritis.

13. What adaptations of standard tests and measures might be required in examining the individual with RA?

14. What are the general physical therapy goals for individuals with RA or OA?

15. Explain the goals, modifications, and progression of a typical strengthening program.

16. Discuss treatment strategies for increasing ROM.

17. Design a cardiovascular conditioning program for an individual with LE arthritic joint involvement.

18. Describe strategies to enhance patients' adherence to therapeutic exercise programs.

19. State at least four principles of joint protection and give a practical application of each.

20. What criteria guide the selection of shoes for the individual with RA?

21. What are the purposes of splints?

22. What changes in gait are commonly associated with RA? What impairments contribute to static and dynamic balance problems in the individual with LE arthritis?

Two case studies are presented: Case 1 presents a patient with rheumatoid arthritis and Case 2 considers a patient with osteoarthritis.

HISTORY

The patient is a 52-year-old married woman who has two children in high school. She is a nurse and works about 40 hours a week. She has had symptoms of joint swelling and pain, fatigue, and increasing weakness for 2 years. During initial onset of symptoms, a primary care physician diagnosed her with carpal tunnel syndrome, knee osteoarthritis, fibromyalgia, and Lyme disease. However, her symptoms continued to worsen on NSAIDs. She was also prescribed antidepressants, and she was referred to the rheumatologist 3 months ago. Based on her history, physical examination, laboratory values (Disease Activity Score [DAS] = 3.2; RF= 12.30; ESR = 26), and radiographic evidence the rheumatologist confirmed a diagnosis of seropositive RA. She began a course of methotrexate and has been referred to physical therapy.

PHYSICAL THERAPY EXAMINATION

At the initial physical therapy examination, she reports that her morning stiffness is now less than 30 minutes (previous high of 3 hours). The pain and swelling in her hands, feet, and elbows is markedly decreased, and she is feeling more energetic. Systems review of the integumentary system is unremarkable except for a slight edema and redness of the distal finger joints and wrist R > L. Her blood pressure and respiratory rate are within normal limits. Her resting heart rate is 72 but increases to 96 with modest exertion.

ROM is limited at the shoulder, elbows, wrists, and MCPs. She lacks 10° of knee extension and has no ankle dorsiflexion or hip extension beyond neutral. Bilateral strength is good minus. She exhibits a forward head, rounded shoulder posture, with the beginning of a marked kyphosis. Her pain is most prominent in her wrists, elbows, and ankles (4/10 visual analogue scale [VAS]) and indicates general fatigue. She has flat feet and moderate swelling of the metatarsal heads. She is relieved that at last she has been diagnosed with a condition for which there is effective treatment and she trusts her rheumatologist. Her immediate goals are to regain comfortable motion, strength, and stamina and to avoid deformity.

QUESTIONS

1. Identify the general anticipated goals and expected outcomes of physical therapy for this patient.

2. What self-management strategies would you recommend and/or instruct the patient to use?

3. Describe the types of community resources you would recommend the patient explore.

4. What supportive devices might be used to decrease symptoms and increase function?

5. How would her physical therapist optimally schedule her return visits to clinic?

HISTORY

The patient is a 64-year-old Caucasian woman whose low back and bilateral knee pain have increased over the past year. She is 5 ft 7 in tall and weighs 195 lb. She has hypertension and chronic renal insufficiency for which she takes prescribed medication. She works part-time as a teacher's assistant in a local elementary school and lives alone in a 3rd floor walk-up apartment. On weekends she serves as the assistant building manager, which includes both cleaning and minimal maintenance duties. She has difficulty using stairs, getting up and down from sitting, getting on and off the bus, and walking for more than 15 minutes at a time. She has had progressively greater knee pain and stiffness for the past 3 years and has recently experienced episodes of "giving way" in the right knee. Her low back pain is worse after prolonged sitting, vacuuming, and at the end of the day. She avoids over-the-counter medications due to her underlying kidney disease but reports moderate pain relief with topical diclofenac applied to both knees. The patient recently joined a local seniors' fitness club but admits to rarely attending classes.

On a recent visit to her primary care physician, she underwent radiographs of both knees, which revealed bilateral joint space narrowing, with the right knee more affected than left and greater lateral compartment involvement than medial. There is evidence of bony sclerosis, osteophytes, and mild malalignment (genu valgum) greater on the right. Her physician has suggested continued use of the topical NSAID, use of a cane, and referred her to a physical therapist for evaluation and exercise advice. The patient and her doctor have agreed to discuss surgical options for the knee if she is not satisfied with her condition in 3 to 6 months.

PHYSICAL THERAPY EXAMINATION

During the initial history and systems review, the patient reports that she is finding both of her part-time jobs difficult, and in particular her cleaning responsibilities in the apartment building. She is frequently tired and lacks the energy to go to the fitness classes despite enjoying the session she last attended about 2 months ago. She admits to not sleeping well and having to take occasional sick days from her school-based job. She is concerned about finances and feels that she needs to continue working for at least another 3 years. Her pain is intermittent during the day but wakes her up frequently during the night. Her heart rate is 82, her blood pressure is 140/85, and her respiratory rate is 16. Her skin and circulation in the lower extremities are unremarkable and sensory integrity and reflexes are intact. Her concerns are being able to keep working and to avoid knee surgery.

Selected tests and measures reveal weakness and loss of motion in hips and knees bilaterally, and an antalgic and slow gait. Her spinal ROM is restricted in extension and rotation. Anterior-posterior knee stability is good, but there is moderate pseudolaxity of the lateral collateral ligaments bilaterally. Using a numeric pain rating scale (NPRS), she rates her left knee pain as 7 out of 10 while walking and 8 out of 10 while climbing stairs, and right knee pain at 6 out of 10 for all activities. She is wearing unsupportive slip-on shoes and shows marked ankle pronation on the right and bilateral hallux valgus.

QUESTIONS

1. What anticipated goals should the physical therapist discuss with the patient for the episode of care?

2. Formulate a home exercise program for this patient and determine an optimal schedule for follow-up by the physical therapist.

3. What kind of orthotic device(s) would reduce this patient's symptoms and increase her function?

4. What should be included in patient-related instruction to maximize this patient's function?

5. What strategies would maximize this patient's adherence to a home exercise program and regular physical activity?

6. What other health professional(s) and/or community resources would you recommend for this patient?

© Stanford University School of Medicine

Division of Immunology and Rheumatology

Name _____________________________Date _____________________________

In this section we are interested in learning how your illness affects your ability to function in daily life. Please feel free to add any comments on the back of this page.

Please check the response which best describes your usual abilities OVER THE PAST WEEK:

Please check any AIDS or DEVICES that you usually use for any of these activities:

__Cane     __Devices used for dressing (button hook, zipper, long-handled shoehorn)

__Walker    __Built-up or special utensils

__Crutches    __Special or built-up chair

__Wheelchair     __Other (specify) ________________

Please check any categories that you usually need HELP FROM ANOTHER PERSON:

__Dressing and Grooming    __ Eating

__Arising    __ Walking

Please check the response which best describes your abilities OVER THE PAST WEEK:

Please check any AIDS or DEVICES that you usually use for any of these activities:

__Raised toilet seat    __Bathtub bar

__Bathtub seat    __Long-handled appliances for reach

__Jar opener (for previously opened jars)    __Other (specify)___________________

Please check any categories that you usually need HELP FROM ANOTHER PERSON:

__Hygiene    __Gripping and opening things

__Reach    __Errands and chores

We are also interested in whether or not you are affected by pain because of your illness.

How much pain have you had because of your illness IN THE PAST WEEK:

PLACE A VERTICAL (|) MARK ON THE LINE TO INDICATE THE SEVERITY OF PAIN

No Pain    Severe Pain

0                100

JOINT PROTECTION

Why Is Joint Protection Important?

Overuse and abuse of arthritic joints may lead to progressive deterioration of the joint and its surrounding tissues. Positive action is necessary to protect joints, conserve energy, and preserve function.

During activity, a normal joint is protected by the muscles around it that absorb the forces on the joint, preventing undue strain on the tendons, ligaments, and cartilage. A diseased joint is mechanically weak and poorly stabilized, which can contribute to the overstretching of the tendons and ligaments and damage to the cartilage. This increased stress can increase the destruction of the joint and cause increased pain.

How Can Joints Be Protected?

The main idea in joint protection is to minimize the strain on joints in daily activities. Joint protection techniques try to reduce the force on the joint, to slow down the joint damage. Good posture and positioning, changing the method of an activity, and pacing all help to protect the joint.

Which Joints Need Protection?

People with a local type of arthritis, such as osteoarthritis, need to pay close attention to the joints that are involved with the arthritis. People with a systemic or whole-body type of arthritis, such as rheumatoid arthritis, need to reduce the stress on all their joints. In addition to the joint protection principles and examples listed below, people with rheumatoid arthritis should look at the section below titled Additional Reminders for Protection of the Rheumatoid Hand.

In planning your joint protection, start by concentrating on the joints that are currently giving you the most trouble. Check off the principles that apply most strongly to you, and list several examples of how you can apply that principle to your problem joints.

Additional Reminders for the Protection of the Rheumatoid Hand

1. Through exercise, maintain wrist extension (ability to pick hand up off table) to ensure power grip.

2. Through exercise, maintain supination (ability to turn palm up) to ensure ability to hold and to carry objects.

3. Avoid positions of deformity.

   1. Finger flexion

1. Avoid making fist or tight grip—use built-up handles.

2. Work with hand flat—use dust mitts, sponges.

3. Avoid prolonged holding of objects: pen, book, pan, needle.

4. Avoid putting any pressure on bent knuckles.

   • b. Ulnar deviation (tendency of fingers to slide to little finger side)

1. Avoid pressure toward little finger side of hand.

2. Any twisting of hand, open door knobs, jars, and so forth should be turned toward thumb.

3. Grip objects parallel across palm, not diagonal; for example, hold utensil like dagger to cut food, stir with wooden spoon.

4. Avoid stress on small joints of hand.

   1. Use two hands whenever possible.

   2. Substitute larger stronger joints: for example, lift or carry with palms or forearm, not small finger joints; carry bag over elbow or shoulder, not in fingertips.

   3. Avoid activities involving pinching motions.

   4. Avoid twisting and squeezing motions with hands.

GETTING ADDITIONAL REST

Rest is important because it reduces the pain and fatigue that accompany arthritis. In addition, it aids the body's healing process and helps control the inflammation. Rest also may reduce the stress on joints and protect them from further damage. All of these benefits are important in managing arthritis.

Each day you need to make sure you get enough whole body rest, local joint rest, and emotional rest. There are many options: Mark off the options that may be possible for you.

• □ 1. Plenty of Nightly Rest

  Get the usual 8 to 10 hours of nightly rest. It is not as important that you sleep for that length of time, but make sure you stretch out with your joints supported, so that your body can rest.

• □ 2. Daily Rest Periods

  Ideally, several times a day you can stretch out for 15 to 60 minutes with your joints supported. Again, it is the body rest, not sleep, that is most important.

• □ 3. Five-Minute "Breathers"

  Partway through a task, sit back and take it easy for a few minutes. This will allow you to finish the task almost as quickly but more comfortably and with less fatigue.

• □ 4. Local Joint Rest

  When a joint hurts, stop and rest. If your hip or knee hurts while walking, sit down for a few minutes with your legs supported; if your hand hurts while writing, stop and lay it flat for a few minutes. Splints can be used to rest painful wrists or fingers. If your neck hurts, lay down with just a small pillow supporting the curve of your neck. Any painful joint can be given extra rest.

• □ 5. Take Time for Relaxing Activities

  Listening to music, reading, playing cards, or other light leisure activities all can be a pleasant change of pace and can be restful and refreshing for you. There are unlimited options for getting additional rest. It takes creativity to find ways to fit extra rest into your schedule; then it takes self-discipline to make sure you follow through, incorporating the additional rest in your activities. Making the effort to get more rest can pay off in a reduction of pain and fatigue.

  Ways to get more rest: ____

  Systemic, whole body rest

  Local joint rest _________

  Emotional rest _________

ENERGY CONSERVATION TO REDUCE FATIGUE

Why Is Energy Conservation Important?

One of the major symptoms of arthritis may be fatigue—getting tired very easily. In the inflammatory types of arthritis, fatigue may be part of the disease process. In all types of arthritis, pain and difficult movement may use up energy, so you tire more easily.

It is important to avoid getting overtired. Fatigue may increase the possibility of a flare-up in inflammatory types of arthritis such as rheumatoid arthritis. In all types of arthritis, fatigue may make the pain and stiffness seem worse, and it will make activities more difficult. We hope to reduce this fatigue by conserving energy and using it carefully.

How Can You Reduce Fatigue?

Some people try to conserve energy and reduce fatigue by staying in bed all day. Others stop doing anything that is not absolutely necessary each day. Unfortunately, the activities that are usually cut out are the leisure activities—the enjoyable things people do for themselves or for fun. These are not good ideas.

You can conserve energy and reduce fatigue by modifying and simplifying your activities, pacing yourself, getting additional rest, and using adapted equipment.

Energy Conservation

By conserving your energy, you may be able to do as much or more activity with less pain and fatigue. We are trying to avoid both overactivity and underactivity. Conserving your energy and simplifying your work is not being lazy. It is not sensible to overtire yourself. Overwork will not keep your joints mobile, but it may damage your joints further.

It is not so much what you do, but how you do it that can help control your fatigue. An attempt should be made to modify any activities that leave you overly tired or cause pain that continues for more than 1 to 2 hours.

You will need to identify ways that your own daily activities can be simplified. As you read through the energy conservation strategies, check off strategies that may work for you, and list several of your own examples.

• □ 1. Plan the Task.

  Your Examples

  1. Think the task through.  ____

  2. Decide when and where the job is best done.  ____

  3. Plan out the simplest approach to the job.  ____

  4. Gather all supplies before you begin.   ____

  5. Arrange step sequence so that it moves in one direction (usually left to right).  ____

  6. Use fewer, more efficient movements to complete task.  ____

• □ 2.Eliminate Extra Trips.

  1. Organize your shopping list according to how the store is laid out.  ____

  2. Stay in the laundry room until your laundry is finished.  ____

  3. Clean one area at a time.  ____

• □ 3. Use Good Posture and Body Mechanics.

  1. Sit to work; you will be more stable and use your strength more efficiently.  ____

  2. Use large strong muscle groups, rather than straining individual muscles and joints.  ____

  3. Lift with your knees bent, your back straight.  ____

  4. Carry objects close to your body.  ____

  5. Push objects, with body weight behind it, rather than pulling or carrying.  ____

  6. Avoid awkward bending, reaching, and twisting.  ____

• □ 4. Don't Fight Gravity.

  1. Slide rather than lift objects.  ____

  2. Use wheeled cart.  ____

  3. Use lightweight equipment.  ____

  4. Stabilize pitcher on surface and tilt to pour, rather than picking it up.  ____

• □ 5. Pace Yourself.

  1. Get plenty of nightly rest.  ____

  2. Plan several rest periods during the day.  _____

  3. Rest before you get tired.  ____

  4. Avoid a rush.  _____

  5. Work at a steady rate with rest period.  ____

  6. Develop a rhythm to your movements.  ____

• □ 6. Use Energy-Saving Devices.

  1. Convenience foods.  ____

  2. Adapted equipment.  ____

Strategies to be tried:    Activities to be modified: ___

_____________        _____________

_____________        _____________

_____________        _____________