RA is commonly used as the prototype for inammatory arthritis. The incidence rate is approximately 3%, with a two to three times greater incidence in women (Ruddy et al., 2001). In RA, the autoimmune reaction (Fig. 54-3) primarily occurs in the synovial tissue. Phagocytosis produces enzymes within the joint. The enzymes break down collagen, causing edema, proliferation of the synovial membrane, and ultimately pannus formation. Pannus destroys cartilage and erodes the bone. The consequence is loss of articular surfaces and joint motion. Muscle bers undergo degenerative changes. Tendon and ligament elasticity and contractile power are lost.
Pathophysiology and associated physical signs of rheumatoid arthritis.

Clinical Manifestations

Clinical manifestations of RA vary, usually reecting the stage and severity of the disease. Joint pain, swelling, warmth, erythema, and lack of function are classic. Palpation of the joints reveals spongy or boggy tissue. Often uid can be aspirated from the inamed joint. Characteristically, the pattern of joint involvement begins with the small joints in the hands, wrists, and feet. As the disease progresses, the knees, shoulders, hips, elbows, ankles, cervical spine, and temporo mandibular joints are involved. The onset of symptoms is usually acute. Symptoms are usually bilateral and symmetric. In addition to joint pain and swelling, another classic sign of RA is joint stiffness, especially in the morning, lasting for more than 30 minutes (Klippel, 2001).

In the early stages of disease, even before bony changes occur, limitation in function can occur when there is active inammation in the joints. Joints that are hot, swollen, and painful are not easily moved. The patient tends to guard or protect these joints through immobilization. Immobilization for extended periods can lead to contractures, creating soft tissue deformity.

Deformities of the hands and feet are common in RA (Fig. 54-4). The deformity may be caused by misalignment resulting from swelling, progressive joint destruction, or the subluxation (partial dislocation) that occurs when a bone slips over another and eliminates the joint space.

RA is a systemic disease with multiple extra-articular features. Most common are fever, weight loss, fatigue, anemia, lymph node enlargement, and Raynaud’s phenomenon (cold- and stress-induced vasospasm causing episodes of digital blanching or cyanosis). Rheumatoid nodules may be noted in patients with more advanced RA and develop at some time in up to half of patients (Klippel, 2001). These nodules are usually nontender and movable in the subcutaneous tissue. They usually appear over bony prominences such as the elbow, are varied in size, and can disappear spontaneously. Nodules occur only in individuals who have rheumatoid factor. The nodules often are associated with rapidly progressive and destructive disease. Other extra-articular features include arteritis, neuropathy, scleritis, pericarditis, splenomegaly, and Sjögren’s syndrome (dry eyes and dry mucous membranes).
Rheumatoid arthritis. (A) Early
Rheumatoid arthritis. (A) Early
Rheumatoid arthritis. (B) Advanced.
Rheumatoid arthritis. (B) Advanced.

Assessment and Diagnostic Findings

Several factors can contribute to a diagnosis of RA: rheumatoid nodules, joint inammation detected on palpation, and certain laboratory ndings. The history and physical examination address manifestations such as bilateral and symmetric stiffness, tenderness, swelling, and temperature changes in the joints. The patient is also assessed for extra-articular changes; these often include weight loss, sensory changes, lymph node enlargement, and fatigue. Rheumatoid factor is present in more than 80% of patients with RA, but its presence alone is not diagnostic of RA. The erythrocyte sedimentation rate (ESR) is signicantly elevated with RA. The red blood cell count and C4 complement component are decreased. C-reactive protein and antinuclear antibody test results may also be positive. Arthrocentesis shows synovial uid that is cloudy, milky, or dark yellow and contains numerous inammatory components, such as leukocytes and complement.

X-ray studies, performed to help diagnose and monitor the progression of disease, show characteristic bony erosions and narrowed joint spaces occurring later in the disease.

Medical Management


In patients with early RA, treatment begins with education, a balance of rest and exercise, and referral to community agencies for support. Medical management begins with therapeutic doses of salicylates or NSAIDs. When used in full therapeutic dosages, these medications provide both anti-inammatory and analgesic effects. Taking medications as prescribed to maintain a consistent blood level is necessary to optimize the effectiveness of the anti inammatory medication.

Several COX-2 inhibitors, another class of NSAIDs, have been approved for treatment of RA. COX (cyclo-oxygenase) is an enzyme involved in the inammatory process. COX-2 inhibitors block the enzyme involved in inammation while leaving intact the enzyme involved in protecting the stomach lining. As a result, COX-2 inhibitors are less likely to cause gastric irritation and ulceration than other NSAIDs (Bombardier et al., 2000).

The trend in management is toward a more aggressive pharmacologic approach earlier in the disease. A window of opportunity for symptom control and improved disease management occurs within the rst 2 years of disease onset. Therefore, the disease modifying antirheumatic agents (antimalarials, gold, penicillamine, or sulfasalazine) are initiated early in treatment. If symptoms appear to be aggressive (ie, early bony erosions as seen on x-rays), methotrexate may be considered. Methotrexate is currently the gold standard in the treatment of RA because of its success in improving disease parameters (ie, pain, tender and swollen joints, quality of life). The goals are to control symptoms and prevent destruction of the joints (Koopman, 2001).

An alternative treatment approach for RA has emerged in the area of biologic therapies. Biologic response modiers are a group of agents that consist of molecules produced by cells of the immune system or by cells that participate in the inammatory reactions (Koopman, 2001). Recent studies (Moreland et al., 1999; Weinblatt et al., 1999) using tumor necrosis factor-alpha inhibitors, both alone and in combination with other medications, have shown that patients demonstrate signicant improvement based on American College of Rheumatology criteria (Felson et al., 1995). Two examples of biologic response modiers that are currently available are enatercept (Enbrel) and iniximab (Remicade). These agents inhibit the function of tumor necrosis factor-alpha, a key cytokine known to play a role in the disease process in RA (Miller, 2001). Research in this area is ongoing

Additional analgesia may be prescribed for periods of extreme pain. Opioid analgesics are avoided because of the potential for continuing need for pain relief. Nonpharmacologic pain management techniques (eg, relaxation techniques, heat and cold applications) are taught.


For moderate, erosive RA, a formal program with occupational and physical therapy is prescribed to educate the patient about principles of joint protection, pacing activities, work simplication, range of motion, and muscle-strengthening exercises. The patient is encouraged to participate actively in the management program. The medication program is reevaluated periodically, and appropriate changes are made if indicated. Cyclosporine, an immunomodulator, may be added to enhance the disease modifying effect of methotrexate.


For persistent, erosive RA, reconstructive surgery and corticosteroids are often used. Reconstructive surgery is indicated when pain cannot be relieved by conservative measures. Surgical procedures include synovectomy (excision of the synovial membrane), tenorrhaphy (suturing a tendon), arthrodesis (surgical fusion of the joint), and arthroplasty (surgical repair and replacement of the joint). Surgery is not performed during disease ares.

Systemic corticosteroids are used when the patient has unremitting inammation and pain or needs a “bridging” medication while waiting for the slower disease-modifying antirheumatic agent (eg, methotrexate) to begin working. Low-dose corticosteroid therapy is prescribed for the shortest time necessary to minimize side effects. Joints that are severely inamed and fail to respond promptly to the measures outlined previously may be treated by local injection of a corticosteroid (Ruddy et al., 2001)


For advanced, unremitting RA, immunosuppressive agents are prescribed because of their ability to affect the production of antibodies at the cellular level. These include high-dose methotrexate (Rheumatrex), cyclophosphamide (Cytoxan), and azathioprine (Imuran). These medications, however, are highly toxic and can produce bone marrow suppression, anemia, gastrointestinal disturbances, and rashes.

Through all stages of RA, depression and sleep deprivation may require the short-term use of low-dose antidepressant medications, such as amitriptyline (Elavil), paroxetine (Paxil), or sertraline (Zoloft), to reestablish an adequate sleep pattern and to manage chronic pain better.

The FDA has approved a medical device for use in treating patients with more severe and longstanding cases of RA who have failed to respond to or are intolerant of disease-modifying antirheumatic drugs. The device, a protein A Immunoadsorption column (Prosorba), is used in 12 weekly 2-hour apheresis treatments to bind IgG (ie, circulating immune complex). In this unique population of patients, a signicant improvement using the American College of Rheumatology Criteria for Improvement has been demonstrated in several studies using the Prosorba column (Felson et al., 1999; Gendreau, 2001).

Nutrition Therapy

Patients with RA frequently experience anorexia, weight loss, and anemia. A dietary history identies usual eating habits and food preferences. Food selection should include the daily requirements from the basic food groups, with emphasis on foods high in vitamins, protein, and iron for tissue building and repair. For the extremely anorexic patient, small, frequent feedings with increased protein supplements may be prescribed. Some medications (ie, oral corticosteroids) used in RA treatment stimulate the appetite and, when combined with decreased activity, may lead to weight gain. Therefore, patients may need to be counseled about eating a healthy, calorie-restricted diet.

Because of repeated contact with the patient, the nurse has the opportunity to assess and intervene in patient concerns and issues that occur with the diagnosis of a chronic illness such as RA. Because the disease commonly affects young women, major concerns may be related to the effects of the disease on childbearing potential, caring for family, or work responsibilities. The patient with a chronic illness may seek a “cure” or have questions about alternative therapies. Frequently, however, patients are hesitant to share their concerns with health care professionals (American College of Rheumatology, 1998).



Belza, B. (2001). Fatigue. In L. Robbins, C. S. Burckhardt, M. T. Hannan, & R. J. DeHoratius (Eds.), Clinical care in the rheumatic diseases (pp. 251–254). Atlanta: Association of Rheumatology Health Professionals.
Burckhardt, C. (2001a). Pain management. In L. Robbins, C. S. Burckhardt, M. T. Hannan, & R. J. DeHoratius (Eds.), Clinical care in the rheumatic diseases (pp. 245–249). Atlanta: Association of Rheumatology Health Professionals.
Burckhardt, C. S. (2001b). Fibromyalgia. In L. Robbins, C. S. Burckhardt, M. T. Hannan, & R. J. DeHoratius (Eds.), Clinical care in the rheumatic diseases (pp. 135–139). Atlanta: Association of Rheumatology Health Professionals.
Klippel, J. H. (Ed.) (2001). Primer on the rheumatic diseases (12th ed.). Atlanta: Arthritis Foundation.
Lozada, C. J., & Altman, R. D. (2001). Osteoarthritis. In L. Robbins, C. S. Burckhardt, M. T. Hannan, & R. J. DeHoratius (Eds.), Clinical care in the rheumatic diseases (pp. 97–103). Atlanta: Association of Rheumatology Health Professionals.
Luck, J. N. (2001). Enhancing functional ability. In L. Robbins, C. S. Burckhardt, M. T. Hannan, & R. J. DeHoratius (Eds.), Clinical care in the rheumatic diseases (pp. 197–202). Atlanta: Association of Rheumatology Health Professionals
Michocki, R. J. (2001). Polypharmacy and principles of drug therapy. In A. M. Adelman & M. P. Daly (Eds.), 20 common problems in geriatrics. New York: McGraw-Hill.
Miller, D. R. (2001). Pharmacologic interventions in the 21st century. In L. Robbins, C. S. Burckhardt, M. T. Hannan, & R. J. DeHoratius (Eds.), Clinical care in the rheumatic diseases (pp. 169–177). Atlanta: Association of Rheumatology Health Professionals.
Minor, M. A., & Westby, M. D. (2001). Rest and exercise. In L. Robbins, C. S. Burckhardt, M. T. Hannan, & R. J. DeHoratius (Eds.). Clinical care in the rheumatic diseases (pp. 179–184). Atlanta: Association of Rheumatology Health Professionals.
Nadler, S. (1997). Arthritis and other connective tissue diseases. In M. L. Sipski & C. J. Alexander (Eds.), Sexual function in people with disability and chronic illness. Gaithersburg, MD: Aspen.
Paget, S. A. (2001). Polymyalgia rheumatica. In L. Robbins, C. S. Burckhardt, M. T. Hannan, & R. J. DeHoratius (Eds.), Clinical care in the rheumatic diseases (pp. 151–153). Atlanta: Association of Rheumatology Health Professionals.
Parker, J. C., Wright, G. E., & Smarr, K. L. (2001). Psychological assessment. In L. Robbins, C. S. Burckhardt, M. T. Hannan, & R. J. DeHoratius (Eds.), Clinical care in the rheumatic diseases (pp. 69–73). Atlanta: Association of Rheumatology Health Professionals.
Ramsey-Goldman, R. (2001). Connective tissue diseases. In L. Robbins, C. S. Burckhardt, M. T. Hannan, & R. J. DeHoratius (Eds.), Clinical care in the rheumatic diseases (pp. 97–103). Atlanta: Association of Rheumatology Health Professionals.
Ruddy, S., Harris, E. D., & Sledge, C. B. (Eds.) (2001). Kelley’s textbook of rheumatology. Philadelphia: W. B. Saunders.
U.S. Department of Health and Human Services. (2001). The Surgeon General’s call to action to prevent and decrease overweight and obesity. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service.
Wegner, S. T. (2001). Sleep problems. In L. Robbins, C. S. Burckhardt, M. T. Hannan, & R. J. DeHoratius (Eds.), Clinical care in the rheumatic diseases (pp. 255–259). Atlanta: Association of Rheumatology Health Professionals.


Asterisks indicate nursing research articles.


American College of Rheumatology. (1998). Position statement: “Complementary” and “alternative” therapies for rheumatic diseases: http://www.rheumatology.org/position/alternative.html .
*Aaronson, L. S., Teel, C. S., Cassmeyer, V., et al. (1999). Dening and measuring fatigue. Image: Journal of Nursing Scholarship, 31(1), 45–50.
*Anderson, K. L., & Burckhardt, C. S. (1999). Conceptualization and measurement of quality of life as an outcome variable for health care intervention and research. Journal of Advanced Nursing, 29(2), 298–306.
Beehrle, D. M., & Evans, D. (1999). A review of NSAID complications: Gastrointestinal and more. Lippincott’s Primary Care Practice, 3(3), 305–315.
Bello, C. E., & Garrett, S. D. (1999). Therapeutic issues in oral glucocorticoid use. Lippincott’s Primary Care Practice, 3(3), 333–341.
*Belza, B., Topolski, T., Kinne S., et al. (2002). Does adherence make a difference? Results from a community-based aquatic exercise program. Nursing Research, 51(5), 285–291.
Buckley, L., Greenwald, M., Hochberg, M., et al. (2001). Recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis. Arthritis & Rheumatism, 44(7), 1496–1503.
Capriotti, T. (2000). The new NSAIDs: COX-2 inhibitors. MedSurg Nursing, 9(6), 313–317.
Davidson, A., & Diamond, B. (2002). Advances in immunology. Autoimmune diseases. New England Journal of Medicine, 345(5), 340–350.
*Jakobsson, U., & Hallberg, I. R. (2002). Pain and quality of life among older people with rheumatoid arthritis and/or osteoarthritis: A literature review. Journal of Clinical Nursing, 11(4), 430–443.

Rheumatoid Arthritis 

*Ailinger, R. L., & Dear, M. R. (1997). An examination of the self-care needs of clients with rheumatoid arthritis. Rehabilitation Nursing, 22(3), 135–140.
*Allaire, S. H., Anderson, J. J., & Meenan, R. F. (1996). Reducing work disability associated with rheumatoid arthritis: Identication of additional risk factors and persons likely to benet from intervention. Arthritis Care Research, 9(5), 349–357.
Bombardier, C., Laine, L., Reicin, A., et al. (2000). Comparison of upper gastrointestinal toxicity of Rofecoxib and Naproxen in patients with rheumatoid arthritis. New England Journal of Medicine, 343(21), 1520–1528.
Felson, D. T., LaValley, M. P., Baldassare, A. R., et al. (1999). The Prosorba column for treatment of refractory rheumatoid arthritis: a randomized, double-blind, sham-controlled trial. Arthritis & Rheumatism, 42(10), 2153–2159.
Felson, D. T., Anderson, J. J., Boers, M., et al. (1995). American College of Rheumatology preliminary denition of improvement in rheumatoid arthritis. Arthritis & Rheumatism, 38(6), 727–735.
Gendreau, R. M. (2001). A randomized double-blind sham-controlled trial of the Prosorba column for treatment of refractory rheumatoid arthritis. Therapeutic Apheresis, 5(2), 79–83.
Kellick, K. A., Martins-Richards, J., & Chow, C. (1998). Management of arthritis. Lippincott’s Primary Care Practice, 2(1), 66–80.
Koopman, W. J. (2001). Prospects for autoimmune disease: Research advances in rheumatoid arthritis. Journal of the American Medical Association, 285(5), 648–650.
MacLean, C. H., Rachel, L., et al. (2000). Quality of care for patients with rheumatoid arthritis. Journal of the American Medical Association, 284(8), 984–992.
Moreland, L. W., Schiff, M. H., Baumgartner, S. W., et al. (1999). Etanercept therapy in rheumatoid arthritis. Annals of Internal Medicine, 130(6), 476–486.
Multon, K. D., Parker, J. C., Smarr, K. L., et al. (2001). Effects of stress management on pain behavior in rheumatoid arthritis. Arthritis Care & Research, 45(2), 122–128.
Ramsburg, K. K. (2000). Rheumatoid arthritis. American Journal of Nursing, 100(11), 40–43.
Weinblatt, M. E., Kremer, J. M, Bankhurst, A. D., et al. (1999). A trial of etanercept, a recombinant tumor necrosis factor receptor: Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate. New England Journal of Medicine, 340(4), 253–259.