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Clinical features of rheumatoid arthritis

Authors PJW Venables, MA, MB BChir, MD, FRCP RN Maini, BA, MB BChir, FRCP, FMedSci, FRS Section Editor RN Maini, BA, MB BChir, FRCP, FMedSci, FRS Deputy Editor Paul L Romain, MD

Last literature review version 17.1: January 2009 | This topic last updated: January 5, 2009 (More) INTRODUCTION Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory disorder of unknown etiology that primarily involves joints. The arthritis is symmetrical, may be remitting, but if uncontrolled may lead to destruction of joints due to erosion of cartilage and bone which leads to deformity. The disease usually progresses from the periphery to more proximal joints, and in patients who do not fully respond to treatment, results in significant locomotor disability within 10 to 20 years. Many of the clinical features that are discussed in this topic review are used in the clinical diagnosis of RA and also serve as classification criteria for RA. The latter are used to define patient populations with RA for clinical or other research purposes ( show table 1 ). The diagnosis and classification of RA are presented separately. ( See "Diagnosis and differential diagnosis of rheumatoid arthritis" ). The following is a summary of clinical features that are useful for diagnostic and classification purposes. Morning stiffness for at least one hour and present for at least six weeks Swelling of three or more joints for at least six weeks Swelling of wrist, metacarpophalangeal, or proximal interphalangeal joints for at least six weeks Symmetric joint swelling Hand x-ray changes typical of RA that must include erosions or unequivocal bony decalcification Rheumatoid subcutaneous nodules Rheumatoid factors PDF created with pdfFactory Pro trial version www.pdffactory.com

Rheumatoid factors CLINICAL PRESENTATIONS Polyarticular disease with a gradual onset, intermittent or migratory joint involvement, and a monoarticular onset are different types of clinical presentations of RA. In addition, extraarticular manifestations may be present. Patients need to be questioned regarding how the arthritis has affected their capacity to perform the activities of daily living (eg walking, stairs, dressing, use of a toilet, getting up from a chair, opening jars, doors, typing), the type of job they have, and their ability to do their job. Typical "classic" RA The disease onset is usually insidious, with the predominant symptoms being pain, stiffness, and swelling of many joints [ 1] . Typically, the metacarpophalangeal and proximal interphalangeal joints of the fingers, interphalangeal joints of the thumbs, the wrists, and metatarsophalangeal joints of the toes are sites of arthritis early in the disease. Other joints of the upper and lower limbs, such as the elbows, shoulders, ankles, and knees are also commonly affected [ 2,3] . Morning stiffness is a common feature of those with active RA; it has been defined as the following: "slowness or difficulty moving the joints when getting out of bed or after staying in one position too long, which involves both sides of the body and gets better with movement [ 4] ." Morning stiffness, or stiffness after any prolonged period of inactivity, is also seen in virtually all inflammatory arthropathies and myopathies [ 5] . However, morning stiffness lasting more than one hour reflects a severity of joint inflammation which rarely occurs in diseases other than RA. Up to one-third of patients have the acute onset of polyarthritis associated with prominent myalgia, fatigue, low grade fever, weight loss, and depression. Occasionally, the syndrome of polymyalgia rheumatica may be present. When this occurs in the absence of clinically detectable synovitis, the distinctive clinical features of RA may not develop until months or even years later. ( See "Polymyalgia rheumatica" ) Palindromic rheumatism The onset of RA is episodic in a few patients, with one to several joint areas being affected sequentially for hours to days, with symptom free periods that may last from days to months; an episodic pattern referred to as "palindromic rheumatism." Patients with palindromic rheumatism have similar predisposing genetic risk factors and exhibit a dose effect of carriage of certain HLA alleles, as do patients with a more typical persistent presentation of RA [ 6] . (See "Epidemiology, risk factors for, and possible causes of rheumatoid arthritis" , section on Genetic susceptibility). In one study, a majority of those with palindromic rheumatism also had PDF created with pdfFactory Pro trial version www.pdffactory.com

antibodies to cyclic citrullinated peptides (CCP), a serologic finding that is common in RA [7] . In another study, anti-CCP antibodies were positive in 83 percent of patients who progressed to definite RA [ 8] . (See "Clinically useful biologic markers in the diagnosis and assessment of outcome in rheumatoid arthritis" , section on Anti-cyclic citrullinated peptide (CCP) antibodies). However, of all patients presenting with palindromic rheumatism, only a minority progress to develop RA or another well defined disease. As an example, among 147 such patients seen in a tertiary referral center, 41 were eventually diagnosed with RA (28 percent) and 4 with other disorders (3 with systemic lupus erythematosus and 1 with Behcet's disease) [ 6] . Use of antimalarial drugs may reduce the risk of progression to RA. One retrospective study of 113 such patients found that those who received antimalarials were 20 percent less likely to develop a chronic rheumatic disease [ 9] . Monoarthritis Persistent single joint arthritis (monoarthritis), frequently of a large joint such as the knee, shoulder, hip, wrist, or ankle, may be the sole manifestation, or may herald the onset of polyarticular disease. There may be a history of joint trauma as an apparent initiating event. The interval between monoarthritis and polyarthritis may extend from days to several weeks in patients whose disease progresses. Until polyarthritis develops the approach to such patients is that for any patient with monoarticular arthritis. ( See "Evaluation of the adult with monoarticular pain" ). Extraarticular involvement Extraarticular features of RA, including anemia, fatigue, subcutaneous ("rheumatoid") nodules, pleuropericarditis, neuropathy, episcleritis, scleritis, splenomegaly, Sjgren's syndrome, vasculitis, and renal disease may occur during the course of the disease These and other systemic and extraarticular manifestations are presented in more detail separately. (See "Overview of the systemic and nonarticular manifestations of rheumatoid arthritis" ). Most patients with extraarticular manifestations also have the classic joint symptoms of RA. Rarely, patients present with extraarticular disease in the absence of clinical arthritis. ( See "Overview of the systemic and nonarticular manifestations of rheumatoid arthritis" ). In addition, a proportion of patients complain of persistent nonarticular symptoms, such as generalized aching, stiffness, bilateral carpal tunnel syndrome, loss of weight, depression, and fatigue (the last simulating chronic fatigue syndrome). This constellation of symptoms may antedate the onset of polyarthritis by many months. DISTRIBUTION OF JOINT INVOLVEMENT RA eventually affects the peripheral joints in almost all patients. Involvement of axial and central joints, such as the interfacetal and atlantoaxial joints of the neck, acromioclavicular [10] , sternoclavicular, temporomandibular, cricoarytenoid joints, and PDF created with pdfFactory Pro trial version www.pdffactory.com

shoulders and hips is less common, occurring in 20 to 50 percent of patients. Symmetrical involvement of joints is a characteristic feature, although this may be less apparent early in the disease. The severity of joint disease and consequent deformity is sometimes notably asymmetrical, an observation that may be attributed to increased structural damage to joints related to unilateral overuse of a dominant limb, or joint protection of a limb resulting from neurologic disease. The pattern of joint involvement may also be diagnostically useful. As an example, involvement limited to the distal interphalangeal joints is usually due to osteoarthritis, whereas proximal interphalangeal involvement can reflect either RA or osteoarthritis. Squeeze tenderness at the MCP and MTP joints and palpable synovial thickening at these joints are characteristic of RA CLINICAL COURSE RA shows a marked variation of clinical expression in individual patients ( show figure 1 ). This difference may be apparent in the number and pattern of joint involvement. As an example, some patients may have mainly small joints or large joints affected. A given patient may also have only a few, or almost all joints involved. Finally, extraarticular disease may be prominent in a subset of patients. Patterns of progression Variation is also seen in the course of disease activity and the rapidity of structural damage to joints [ 11] . Most patients show fluctuation of disease activity over periods lasting weeks to months. This corresponds to an increase or decrease in symptoms of arthritis, a pattern which may recur throughout the course of the disease. Disease activity may not abate in about 10 to 20 percent of cases. Remission has been reported in a small proportion of patients with a well established diagnosis of RA [ 12] . In our experience, however, this is very rare without disease modifying antirheumatic drugs (DMARDs). As an example, among 191 patients treated with such drugs beginning within a year of disease onset, 48 (25 percent) met criteria for remission after three years of treatment, and 38 (20 percent) after five years of DMARD therapy [ 13] . Some clinical features that can be assessed early in the course of RA may be predictive of the likelihood of achieving a remission with DMARD treatment. Patients with less initial disease activity, less disability, lower levels of acute phase reactants, absence of RF and antibodies to citrullinated peptides (CCP), and less radiographic joint damage when initially evaluated, are more likely to achieve a remission when treated with DMARDs within the first year of disease [13] . PDF created with pdfFactory Pro trial version www.pdffactory.com

Disease activity versus structural damage The concept of disease activity is based upon the state of the underlying inflammatory response, and may be distinguished from the destructive process that leads to irreversible damage of the joint (show figure 2 ): Disease activity can (and does) vary. This variation in part reflects the endogenous rhythms of the disease process, but is mainly the result of therapeutic interventions. Thus, periods of spontaneous exacerbations and quiescence, characterized by an increase or decrease in symptoms, are modulated by both the beneficial effects of drug therapy, and withdrawal of therapy due to loss of efficacy or side effects. In contrast, structural damage is cumulative and irreversible. The degree of damage is closely linked to inflammation and hence to disease activity, but is also associated with degeneration and repair [14] . As structural damage progresses, the detection of variation in disease activity by clinical examination becomes increasingly difficult. At these later stages, symptoms and signs of inflammation, such as pain, stiffness, tenderness, swelling, and joint effusions, may be caused either by continuing rheumatoid disease or as a secondary result of mechanical and degenerative change. Remission Rarely, disease activity is absent; in this circumstance, the disease is said to be in remission. Attempts to define clinical remission, in order to understand better the natural history of RA and the effects of therapy, have resulted proposed diagnostic criteria by the America College of Rheumatology ( show figure 3 ) [12] . However, lack of joint pain, swelling, and tenderness may be impossible to achieve in patients who have developed structural damage of the joints, despite actual remission in the rheumatoid disease process. Achieving a clinical remission does not preclude the development of further erosive changes. This was illustrated in a retrospective study of 187 patients who were in remission for six months and whose clinical course and radiographic findings were subsequently followed [ 15] . A majority (52 percent) remained in remission during two years of follow-up. Despite inapparent clinically active disease, one new erosion in a previously unaffected joint appeared in 14 percent of these patients. Because the preliminary remission criteria of the American College of Rheumatology include measures of fatigue and require at least two months of sustained response, they have not been applied widely in clinical trials. Alternative criteria, proposed under the auspices of the European League Against Rheumatism (EULAR), use indices of disease activity (DAS<1.6 or DAS28<2.4 or 2.6) to determine remission [ 16,17] . When applied to the PDF created with pdfFactory Pro trial version www.pdffactory.com

results of at least one trial the DAS<1.6 and DAS28<2.4 remission criteria were more stringent than an ACR70 response [ 18] . PHYSICAL FINDINGS The key features of early rheumatoid inflammation are pain and swelling of the affected joints. Painful inflammation is demonstrated either by local tenderness from pressure applied on the joint, or by pain on moving the joint. Swelling may be due to synovial hypertrophy or effusion. Synovial thickening is detected by a "boggy" feel to a swollen joint, and effusion by demonstrating fluctuation. Heat and redness (the other signs of Celsus) are not prominent features of RA, although an involved joint is often perceptibly warmer on careful examination. The characteristic joint deformities are late manifestations of disease that result from the physical stresses and local anatomy of involved joints. The hands The main signs of disease can often be found in the hands early in the course of RA [ 19] . Symmetrical effusions and soft tissue swelling around the metacarpophalangeal joints and proximal interphalangeal joints typically occur, although distal interphalangeal involvement can be seen later in the disease [ 20] . These joints are tender to the touch and exhibit a restricted range of movement. Palmar erythema may be present (as with any peripheral arthritis). Occasionally, thickening of the flexor tendons can be detected by palpation of the palm; this finding is due to synovitis of the tendon sheaths ("tenosynovitis") ( show radiograph 1 ). Nodules may form along the palmar tendon sheaths, resulting in the tendon sheath catching (or triggering) and in an inability to fully extend the finger. The nodules may cause tendon rupture, especially of the extensor pollicis longus (extensor of the DIP joint of the thumb). Other physical signs include the following: Reduced grip strength can be a surprisingly sensitive indicator of early disease, as well as a useful parameter in the evaluation of disease activity and progression. However, the multiplicity of factors (joint pain, tendon involvement, nerve compression, and muscle wasting) that contribute to a weak grip makes this assessment rather nonspecific. The whole hand may be swollen in very acute RA, with pitting edema over the dorsum giving rise to the "boxing glove" appearance. The range of movement of involved joints is restricted, and loss of active flexion may be so severe that the patient is unable to oppose the finger tips to the palm. Between 1 and 5 percent of patients present with carpal tunnel syndrome. Affected patients develop dysesthesia and muscle weakness

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of the first three fingers and the radial side of the fourth finger. A positive Tinel's or Phalen's sign is usually present. ( See "Clinical manifestations and diagnosis of carpal tunnel syndrome" ). The characteristic joint deformities appear in more established chronic RA (show picture 1 ). These findings include ulnar deviation or "ulnar drift" ( show picture 2 ) swan neck or Boutonniere deformities of the fingers ( show picture 3), or the "bow string" sign (prominence of the tendons in the extensor compartment of the hand). Occasional patients present with extensor tendon rupture, most commonly affecting the thumb, little or ring fingers of either hand. The nails and fingertips should also be examined in every patient for evidence of digital infarcts. The upper limb All of the upper extremity joints may be involved in RA. The wrist is probably the most common to be involved. Early in the disease there is a loss of extension. Late changes due to erosive damage lead to volar subluxation and radial drift of the carpus, resulting in increasing prominence of the ulnar styloid and lateral deviation [ 21] . Tendon rupture can also occur at the wrist. The elbow is frequently affected, with loss of extension (fixed flexion) both in early and late disease ( show radiograph 2 ). An effusion or synovitis may be detected as a bulge between the head of the radius and the olecranon. A compressive neuropathy of the ulnar nerve, with dysesthesias of the 4th and 5th fingers, can result from elbow synovitis. Olecranon bursitis is also common. Destruction of the joint may occur due to erosion of cartilage and bone. The elbow is the most common site for subcutaneous rheumatoid nodules. These should always be looked and felt for in view of their diagnostic and prognostic importance. The shoulder, being more proximal, tends to be involved later in the disease. As an example, one prospective study assessed shoulder involvement over time in 74 patients with RA [ 22] . At 15 years, 55 percent had developed radiographic evidence of erosive glenohumeral joint disease [ 22] . The most common site for erosions was the superolateral aspect of the humerus. Disease in the glenohumeral joint leads to painful restriction of movement resembling a capsulitis, and can result in the development of a "frozen" shoulder. This will typically cause pain at night, when the patient lies on the affected shoulder. Rotator cuff injury is common. Effusions are relatively rare, but when they occur they may be detected in the anterior glenohumeral joint as a filling of the depression under the clavicle anterior to the head of the humerus. The lower limb Foot involvement is common in early disease, with a PDF created with pdfFactory Pro trial version www.pdffactory.com

pattern which mirrors that occurring in the hand. Tenderness of the metatarsophalangeal joints may be marked, resulting in the tendency to bear weight on the heels and hyperextend the toes. Erosive damage results in lateral drift of the toes, and plantar subluxation of the metatarsal heads, resulting in "cock-up" deformities. The latter may be palpable as bony lumps on the sole with associated callosities. Involvement of the tarsus and the associated tendon sheaths is also common, leading to pain on inversion or eversion of the foot and diffuse edema and erythema over the dorsum of the foot. Heel pain may be associated with retrocalcaneal bursitis tarsal tunnel syndrome, caused by impingement of the posterior tibial nerve. Tarsal tunnel syndrome is also associated with parasthesiae of the toes and is important because it is readily diagnosed by ultrasound and treated by local injection or surgical release. Two rare but easily missed causes of heel pain are Achilles tendon rupture or calcaneal stress fracture, [23,24] . Arthritis of the ankle can lead to a diffuse swelling around the tibiotalar joints which may be red and edematous. These findings may be wrongly attributed to fluid retention or an infective cellulitis of the skin. The knee manifests many changes in RA. Synovial thickening is easily detected at the knee, often extending around the patella. Effusion is a common feature of knee involvement and can be elicited by patellar tap. Restriction of movement, particularly flexion, is also a common physical finding. In addition, ligamentous laxity leading to deformities and quadriceps atrophy is frequently observed. The popliteal fossa should always be palpated for evidence of a popliteal (Baker's) cyst [25] . Ruptured Baker's cysts extending down the calf are of clinical importance because they can resemble a deep vein thrombosis or acute thrombophlebitis [ 26] . A history of arthritis, morning stiffness, lack of a palpable occluded venous cord, and edema below the posterior of the knee all suggest a Baker's cyst. Traditionally, a ruptured Baker's cyst is demonstrated by arthrography, though it can now be reliably demonstrated by ultrasonography or magnetic resonance imaging [ 27] (show radiograph 3 and show radiograph 4 ). Erosion of the femoral condyles and tibial plateau can result in either genu varus or genu valgus. Involvement of the hips typically occurs only in well established disease. Hip disease is most frequently manifested as pain in the groin, thigh, low back, or PDF created with pdfFactory Pro trial version www.pdffactory.com

referred to the knee on standing or movement. Restriction of movement, leading to "log rolling the leg" or rotation of the hip, also may be seen. Pain in the lateral thigh suggests trochanteric bursitis. The axial skeleton Cervical spine joints are the most clinically important joints in the axial skeleton in RA. Long standing disease may lead to instability and cause symptoms such as neck pain, stiffness, radicular pain, related to subluxation. If the subluxation is causing spinal cord compression there may be signs of long tract involvement such as hyperreflexia or up going toes on Babinski testing. The clinical manifestations of cervical spine subluxation and the approach to diagnosis and management are discussed in detail separately. ( See "Cervical subluxation in rheumatoid arthritis" ). Cricoarytenoid joint Nearly 30 percent of patients with RA have involvement of the cricoarytenoid joint; symptoms may include hoarseness and an inspiratory stridor. INFORMATION FOR PATIENTS Educational materials on this topic are available for patients. ( See "Patient information: Rheumatoid arthritis symptoms and diagnosis" and see "Patient information: Rheumatoid arthritis treatment" and see "Patient information: Complementary therapies for rheumatoid arthritis" ). We encourage you to print or e-mail these topics, or to refer patients to our public web site, www.uptodate.com/patients , which includes these and other topics. Use of UpToDate is subject to the Subscription and License Agreement . REFERENCES 1. Lee, DM, Weinblatt, ME. Rheumatoid arthritis. Lancet 2001; 358:903. 2. Fleming, A, Crown, JM, Corbett, M. Early rheumatoid disease. I. Onset. II. Patterns of joint involvement. Ann Rheum Dis 1976; 35:357. 3. Jacoby, RK, Jayson, MIV, Cosh, JA. Onset, early stages and prognosis of rheumatoid arthritis: A clinical study of 100 patients with 11 year follow-up. Br Med J 1973; 2:96. 4. Lineker, S, Badley, E, Charles, C, et al. Defining morning stiffness in rheumatoid arthritis. J Rheumatol 1999; 26:1052. 5. Edworthy, SM. Morning stiffness: sharpening an old saw?. J Rheumatol 1999; 26:1015. 6. Maksymowych, WP, Suarez-Almazor, ME, Buenviaje, H, et al. HLA and cytokine gene polymorphisms in relation to occurrence of palindromic rheumatism and its progression to rheumatoid arthritis. J Rheumatol 2002; 29:2319. 7. Salvador, G, Gomez, A, Vinas, O, et al. Prevalence and clinical PDF created with pdfFactory Pro trial version www.pdffactory.com

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significance of anti-cyclic citrullinated peptide and antikeratin antibodies in palindromic rheumatism. An abortive form of rheumatoid arthritis?. Rheumatology (Oxford) 2003; 42:972. Russell, AS, Devani, A, Maksymowych, WP. The role of anti-cyclic citrullinated Peptide antibodies in predicting progression of palindromic rheumatism to rheumatoid arthritis. J Rheumatol 2006; 33:1240. Gonzalez-Lopez, L, Gamez-Nava, JI, Jhangri, G, et al. Decreased progression to rheumatoid arthritis or other connective tissue diseases in patients with palindromic rheumatism treated with antimalarials. J Rheumatol 2000; 27:41. Lehtinen, JT, Kaarela, K, Belt, EA, et al. Incidence of acromioclavicular joint involvement in rheumatoid arthritis: A 15 year endpoint study. J Rheumatol 1999; 26:1239. Masi, AT, Feigenbaum, SL, Kaplan, SB. Articular patterns in the early course of rheumatoid arthritis. Am J Med 1983; 75(Suppl 6A):26. Pinals, RS, Masi, AF, Larsen, RA, et al. Preliminary criteria for clinical remission in rheumatoid arthritis. Bull Rheum Dis 1982; 32:7. Gossec, L, Dougados, M, Goupille, P, et al. Prognostic factors for remission in early rheumatoid arthritis: a multiparameter prospective study. Ann Rheum Dis 2004; 63:675. Wolfe, F, Sharp, JT. Radiographic outcome of recent onset rheumatoid arthritis. Arthritis Rheum 1998; 41:1571. Molenaar, ET, Voskuyl, AE, Dinant, HJ, et al. Progression of radiologic damage in patients with rheumatoid arthritis in clinical remission. Arthritis Rheum 2004; 50:36. van Gestel, AM, Anderson, JJ, van Riel, PL, et al. ACR and EULAR improvement criteria have comparable validity in rheumatoid arthritis trials. American College of Rheumatology European League of Associations for Rheumatology. J Rheumatol 1999; 26:705. Aletaha, D, Ward, MM, Machold, KP, et al. Remission and active disease in rheumatoid arthritis: defining criteria for disease activity states. Arthritis Rheum 2005; 52:2625. van der, Heijde D, Klareskog, L, Boers, M, et al. Comparison of different definitions to classify remission and sustained remission: 1 year TEMPO results. Ann Rheum Dis 2005; 64:1582. Gordon, DA ed. Rheumatoid arthritis contemporary patient management series. 2d ed. Medical Examination Publishing, New York. 1985. Jacob, J, Sartorius, D, Kursunoglu, S, et al. Distal interphalangeal joint involvement in rheumatoid arthritis. Arthritis Rheum 1986; 29:10. Hastings, DE, Evans, JA. Rheumatoid wrist deformities and their relation to ulna drift. J Bone Joint Surg 1975; 57A:930.

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22. Lehtinen, JT, Kaarela, K, Belt, EA, et al. Incidence of glenohumeral joint involvement in seropositive rheumatoid arthritis. A 15 year endpoint study. J Rheumatol 2000; 27:347. 23. Rask, MR. Achilles tendon rupture owing to rheumatoid disease. JAMA 1978; 239:435. 24. Semba, CP, Mitchell, MJ, Sartoris, DJ, Resnick, D. Multiple stress fractures in the hindfoot in rheumatoid arthritis. J Rheumatol 1989; 16:671. 25. Gerber, NJ, Dixon, AS. Synovial cysts and juxta-articular bone cysts. Semin Arthritis Rheum 1974; 3:323. 26. Kraag, G, Thevathasan, EM, Gordon, DA, Walker, IH. The hemorrhagic crescent sign of acute synovial rupture. Ann Intern Med 1976; 85:477. 27. Torreggiani, WC, Al-Ismail, K, Munk, PL, et al. The imaging spectrum of Baker's (Popliteal) cysts. Clin Radiol 2002; 57:681.

GRAPHICS

American Rheumatism Association revised criteria for rheumatoid arthritis classification Criterion
Morning stiffness

Description
Morning stiffness in and around the joints, lasting at least one hour before maximal improvement. At least 3 joint areas (out of 14 possible areas; right or left PIP, MCP, wrist, elbow, knee, ankle, MTP joints) simultaneously have had soft- tissue swelling or fluid (not bony overgrowth alone) as observed by a physician. At least one area swollen (as defined above) in a wrist, MCP, or PIP joint. Simultaneous involvement of the same joint areas (as defined above) on both sides of the body (bilateral involvement of PIPs, MCPs, or MTPs, without absolute symmetry is acceptable). Subcutaneous nodules over bony prominences or extensor surfaces, or in juxta-articular regions as observed by a physician.

Arthritis of 3 or more joint areas

Arthritis of hand joints

Symmetric arthritis

Rheumatoid nodules

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Serum rheumatoid factor

Demonstration of abnormal amounts of serum rheumatoid factor by any method for which the result has been positive in less than 5% of normal control subjects. Radiographic changes typical of rheumatoid arthritis on posteroanterior hand or wrist radiographs, which must include erosions or unequivocal bony decalcification localised in, or most marked adjacent to, the involved joints (osteoarthritis changes alone do not qualify).

Radiographic changes

Note: For classification purposes, a patient has RA if at least four of these criteria are satisfied (the first four must have been present for at least six weeks).

Natural history and prognosis of RA

70 percent of joint erosions detectable by x-ray of hands and feet occur in the first two years of disease At 20 years, over 60 percent of RA patients belong to functional class III (significantly impaired, self-caring, using aids, requiring joint replacements) or class IV (loss of independence, requiring daily care) Increased evidence of:
Infections Cardiovascular disease Lymphomas

Life-expectancy of RA less than age-sex matched control populations, especially in patients with:
Polyarticular disease Systemic extra-articular disease Persistent disease activity (high ESR, CRP) Rheumatoid factor and circulatory immune complex positivity HLA-DR & chain 'shared epitope' (especially bialleic)

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Assessment of disease activity in rheumatoid arthritis Symptoms

Duration of morning stiffness Pain score (visual analogue scale) Fatigue - severity (visual analogue scale) Patient's global score of disease activity (visual analogue scale)

Physical examination
Number of swollen joints Number of tender joints Degree of swelling and/or tenderness Extra-articular disease:
Minor nodules, episclertis, pure sensory neuropathy, pleruropericardial disease Major vasculitis, Felty's syndrome, motor neuropathy, interstitial lung disease

Laboratory
Elevated erythrocyte sedimentation rate Increased C-reactive protein Anemia (in the absence of chronic blood loss or hematuria) Leukocytosis Thrombocytosis Abnormal liver function tests (low albumin, raised alkaline phosphate) in the absence of drug toxicity or liver disease Inflammatory joint fluid (high polymorph count, low complement, fibrin)

Imaging
Low bone mineral density (juxta-articular, vertebrae, pelvis) in absence of glucocorticoid therapy or known cause

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ACR criteria for clinical remission of rheumatoid arthritis A minimum of five of the following for at least 2 consecutive months
Morning stiffness not to exceed 15 minutes No fatigue No joint pain No joint tenderness or pain on motion No soft tissue swelling in joints or tendon sheaths ESR (Westergren's method) less than 30mm/hour (females) or 20mm/hour (males)

Exclusions prohibiting a designation of complete clinical remission

Clinical manifestations of one or more of the following:
Active vasculitis Pericarditis Pleuritis Myositis Unexplained recent weight loss or fever secondary to RA

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Tenosynovitis in rheumatoid arthritis

Ultrasonography of the fingers of a patient with rheumatoid arthritis showing tenosynovitis of the extensor tendons. An inflamed common tendon sheath of the wrist may also be observed. Courtesy of Peter H Schur, MD.

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Synovial thickening of the metacarpophalangeal joint

Bilateral swelling of the MCP joints is evident in this patient with rheumatoid arthritis. Note also the mild swan neck deformities present in several fingers, particularly the left middle and fifth fingers. Courtesy of Patrick J Venables, MD.

Joint deformity in MCTD

Deforming arthritis in mixed connective tissue disease characterized by ulnar deviation and swan neck deformities.
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These abnormalities are also seen in rheumatoid arthritis. Courtesy of Robert M Bennett, MD.

Swelling of the metacarpophalangeal joints of the right hand

Swelling of the MCP joints, moderate MCP flexion, and swan neck deformities are evident in this patient with rheumatoid arthritis. Courtesy of Patrick J Venables, MD.

RA of the elbow

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Lateral view of the elbow in a patient with rheumatoid arthritis (RA) reveals soft tissue swelling and osteopenia with destruction of the elbow joint (arrows). There are also secondary proliferative bony changes, which have arisen due to joint space destruction. Courtesy of Jonathan Kruskal, MD.

Baker's cyst

Ultrasonography of the knee showing a Baker's cyst in a patient with rheumatoid arthritis. The cyst is compressing the popliteal artery (arrow). Courtesy of Peter H Schur, MD.

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Baker's cyst

Ultrasonography of the knee showing a Baker's cyst in a patient with rheumatoid arthritis. Calcifications (arrows) may be observed within the cyst. Courtesy of Peter H Schur, MD.

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