Rheumatoid Arthritis

By: Kelly Marie Hale, SPT

I. Description [1], [2], [3]

Rheumatoid arthritis (RA) is defined as a chronic, autoimmune, inflammatory disease that affects multiple joints in the body that are lined with synovial fluid. It is distinct from other arthritis conditions such as osteoarthritis in that RA affects the synovial lining of the joints, follows a symmetrical pattern of joint presentation, and causes severe pain, redness, inflammation and fatigue. Rheumatoid Arthritis is a progressive disease that can lead to decreased function, joint destruction, and possible joint deformity, but can be managed with medications and therapeutic interventions.
17128.jpg

II. Anatomy [4]

Joints act to protect the body from the demands of walking and repetitive motions. Cartilage that lies at the end of bones is lined with a synovial tissue containing fluid that lubricates the joint, prevents bone erosion, and assists in joint mobility. The nature of rheumatoid arthritis is that it is an autoimmune condition, meaning that a person’s immune system attacks joint tissues for unknown reasons; white blood cells navigate to the synovium and cause an inflammatory cascade which then causes the symptoms of RA. With the progression of RA, cartilage is destroyed by the inflammation that exists in the synovium. This can disturb the surrounding structures and disrupt the integrity of muscles and ligaments.

Hands: [5], [6]
Rheumatoid arthritis in the hands is quite common, with approximately 2/3 of patients who are diagnosed with the disease exhibiting wrist and hand problems. Commonly, the metacarpophalangeal joint (MCP), proximal interphalangeal joint (PIP), carpometacarpal and radiocarpal joints, distal ulna and radial styloid are compromised. A patient who experiences RA in the hands will suffer pain, redness, and inflammation in the wrist and the knuckles, possible nodules along the fingers and a number of deformities to the hand, such as a boutonniere deformity in the thumb, deviation of the metacarpophalangeal joints, and swan-neck deformity of the fingers.

rheumatoidarthritishand.jpg

Knees: [1], [3], [6]
Rheumatoid arthritis in the knees can cause excessive swelling and pain, warmth and tenderness in the knee, and difficulty with motion. This inflammation of the synovium that spreads across the joint surfaces may lead to ligament laxity, breakdown of cartilage and other supporting structures in the knee, reduced space in the joint cavity and erosion of the femur and/or tibia.

Feet: [7], [8]
Almost all patients diagnosed with rheumatoid arthritis experience symptoms in the foot. Pain in the ball of the foot, edema, rheumatoid nodules, and stiffness in the feet or ankles is common. Metatarsophalangeal and interphalangeal joints of the foot can become deformed over time, causing the toes to contract in a “clawtoe” deformity. The forefoot tends to be the more prevalent problem area, because RA initiates a swelling of the synovial membrane (synovitis) that erodes the joint capsule, and causes ligament laxity over time. Typically in the forefoot, the longitudinal arch of the foot will flatten over time due to destruction of tissues. Hallux valgus occurs in the great toe which leads to changes in weight shifting and gait, and possibly pain in other areas of the lower extremity due to gait compensation. If there is hindfoot involvement, soft tissue structures of the foot can degrade, affecting the alignment of the subtalar joint. The change in angle of the subtalar joint can eventually cause the foot to become fixed.

rheumatoid2.jpg

Other areas affected by RA: [4]
Some cases of rheumatoid arthritis involve areas not associated with joints. Inflammation of the blood vessels, fluid collection in the lining of the lungs or the pericardial sac of the heart, anemia, and dry eyes and mouth can occur in a patient with rheumatoid arthritis. These areas aren’t as prevalent as the typical joint presentation of the disease.

rheumatoid_arthritis_s9_inflammation.jpg

III. Incidence/Prevalence [3], [9], [10]

Arthritis is a general term that is used to describe a large number of pathologies that greatly impact the overall quality of life for many individuals, and is the second most frequently reported chronic problem in the United States. Rheumatoid arthritis has a global distribution with a prevalence of 1-2%, and affects people of all races and ethnic groups. Rates for RA are high in people of Caucasian descent because of genetic predisposition and environmental factors, low in people of African descent, but affect about 5-6% of Native Americans. Prevalence for the disease in the United States is about 70 per 100,000 people, according to The Johns Hopkins Arthritis Center, can present at any age, and affects 2 to 3 times more women than men. In the United States, rheumatoid affects 1.3 million Americans with onset occurring mostly in middle-age, but can occur in the 20s or 30s or even present as early as childhood (juvenile rheumatoid arthritis – JRA).

IV. Clinical Presentation/Indications [1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11]

As discussed above, rheumatoid arthritis manifests in joints throughout the body and is accompanied by severe pain, stiffness, tenderness to palpation, formation of rheumatoid nodules, swelling and loss of motion. The joints that are most involved in rheumatoid arthritis included the proximal interphalangeal and metacarpophalangeal joints, carpometacarpal and radiocarpal joints, elbow, tibiofemoral joint, subtalar and metatarsophalangeal joints. Clinical presentation of the disease varies, but insidious onset with symptoms in the small joints is most common. Clinical signs also include malaise, fatigue, weight loss, and low-grade fever accompanying the above stated complaints. In 1987, The American College of Rheumatology developed classification criteria for rheumatoid arthritis that showed possible symptoms which would receive a diagnosis of rheumatoid arthritis. In 2010, a revised classification criterion from ACR-EULAR was published (see below).

1987 ACR Classification Criteria for Rheumatoid Arthritis
Patients must have four of the seven criteria:
• Morning stiffness lasting at least 1 hour*
• Swelling in three or more joints*
• Swelling in hand joints*
• Symmetric joint swelling*
• Erosions or decalcification on x-ray of hand
• Rheumatoid nodules
• Abnormal serum rheumatoid factor
*must be present at least six weeks
rheumato1.jpg

Once a diagnosis has been attained, the earlier the intervention, the better. Proactive approaches to managing rheumatoid arthritis can significantly benefit overall quality of life and disease progression.

V. Potential Etiologies [1], [12], [13]

While the cause of rheumatoid arthritis is not certain, there is strong correlation between environmental risk factors and genetic susceptibility to the development of the disease. It is well documented that genetic components contribute to the disease, with research on this topic dating back over 30 years. Throughout the late 1960s to mid 1970s, it was discovered that the HLA (human leukocyte antigen) locus indicates a contribution to the disease. In 2003, peptidylarginine deiminase type 4 (PADI4) became known as the second genetic risk factor to rheumatoid arthritis. Since 2004, over 20 genes have been found to contribute to the cause of rheumatoid arthritis, unique to anti-citrullinated protein (ACPA) specific antibodies. Expectantly, studies conducted suggest familial traits in first-degree relatives (parents, children, siblings) compared to the general population are evidence for occurrence of the condition. Sufficient evidence to date also shows that RA is possible to be heritable among twins.

VI. Diagnostic Tests [14], [15], [16], [17], [18]

Rheumatoid arthritis has proven to be an immune-complex disease and requires a combination of radiographic and diagnostic testing to aid in its detection. As far as serologic testing is concerned, RA involves a multitude of antibodies that are thought to be responsible for the disease. Rheumatoid factor (RF) is a diagnostic marker for testing for RA, as well as other autoimmune conditions; this autoantibody is linked to interfering with the normal function of joints. Along with RF, The American College of Rheumatology Subcommittee on Rheumatoid Arthritis (ACRSRA) recommends erythrocyte sedimentation rate (ESR), anti-CCP antibodies, and other laboratory tests should also be taken when a complete blood count is performed. The following table, adapted from the ACRSRA, is an example of typical findings associated with clinically diagnosing rheumatoid arthritis:

Laboratory and Imaging Findings Associated with Rheumatoid Arthritis:
Laboratory test Associated findings
C-reactive protein* Typically increased to >0.7 picograms per mL; may be used to monitor disease course
Erythrocyte sedimentation rate Often increased to >30 mm per hour; may be used to monitor disease course
Hemoglobin/hematocrit* Slightly decreased; hemoglobin averages around 10 g per dL (100 g per L); normochromic anemia, also may be normocytic or microcytic
Liver function* Normal or slightly elevated alkaline phosphatase
Platelets* Usually increased
Radiographic findings of involved joints* May be normal or show osteopenia or erosions near joint spaces in early disease; wrist and ankle films are useful as baselines for comparison with future studies
Rheumatoid factor* Negative in 30 percent of patients early in illness; if initially negative, can repeat six to 12 months after disease onset; can be positive in numerous other processes (e.g., lupus; scleroderma; Sjögren’s syndrome; neoplastic disease; sarcoidosis; various viral, parasitic, or bacterial infections); not an accurate measure of disease progression.
White blood count* May be increased
Anticyclic citrullinated peptide antibody Tends to correlate well with disease progression; increases sensitivity when used in combination with rheumatoid factor; more specific than rheumatoid factor (90 versus 80 percent); not readily available in many laboratories
Antinuclear antibody Limited value as a screening study for rheumatoid arthritis
Complement levels Normal or elevated
Immunoglobulins Elevated alpha-1 and alpha-2 globulins possible
Joint fluid evaluation Consider if an affected joint can be tapped and diagnosis is uncertain; straw-colored fluid with fibrin flecks often seen; fluid may clot at room temperature; 5,000 to 25,000 white blood cells per mm3 (5 to 25 × 109 per L) with 85 percent polymorphonuclear leukocytes a common finding; in rheumatoid arthritis, cultures are negative, there are no crystals, and fluid glucose level typically is low.
Urinalysis Microscopic hematuria or proteinuria may be present in many connective tissue diseases
h9991226.jpg
h9991227.jpg

Radiographic imaging is also used to mark progression of rheumatoid arthritis. X-rays of the hands and feet should be taken shortly after diagnosis and throughout time to investigate erosion of the joints. The Steering Committee, in a comprehensive literature review for a consensus in the treatment of rheumatoid arthritis in 2010, discussed that x-rays should be obtained annually and progression of the disease estimated. From this determination, attempts to progress treatment can be discussed.
Magnetic resonance (MR) imaging is also used to identify pathological factors of rheumatoid arthritis and can also aid in the diagnosing process. According to research from Narvaez et al. in 2010, MR imaging can be used to identify visible synovitis, a key abnormality present in rheumatoid, effusion, erosions in bone, and bone marrow edema (an early marker of inflammation).

VII. Evaluation/Special Orthopedic Tests

Rheumatoid arthritis is a clinical diagnosis made by a rheumatologist with the above mentioned radiographic and diagnostic testing. There are no special orthopedic tests to use for the diagnosis of rheumatoid arthritis. When a patient is referred to physical therapy for management of the disease, their evaluation will be dependent on the symptoms that the individual patient presents. Therapy will progress from hypotheses formed from the initial evaluation and will focus on pain relief, restoring motion, and return to/maintenance of daily activities.

VIII. Conservative Treatment [19], [20]

When a diagnosis of rheumatoid arthritis is made, a patient must understand that treatment of the disease must be a well-rounded process that involves both medical management and lifestyle changes. Patients should be educated on options to manage their condition, and must be in constant conversation with a rheumatologist on progression of the disease. Since there is currently no cure for rheumatoid arthritis, the main focus of treatment should be to control symptoms and prevent further progression of the disease in hopes of reaching a point of remission, which according to the Steering Committee, is an absence of symptoms of inflammatory disease activity. Conservative management of rheumatoid can be divided into categories of medications, lifestyle changes and physical/occupational therapies.

Physical Therapy Management of Rheumatoid Arthritis

Medications:
The Mayo Clinic summarizes the types of medications used to treat this disease with the following table below:

NSAIDs. Nonsteroidal anti-inflammatory drugs (NSAIDs) can relieve pain and reduce inflammation. Over-the-counter NSAIDs include ibuprofen (Advil, Motrin, others) and naproxen (Aleve). Stronger NSAIDs are available by prescription. Side effects may include ringing in your ears, stomach irritation, heart problems and liver and kidney damage.
Steroids. Corticosteroid medications, such as prednisone, reduce inflammation and pain and slow joint damage. Side effects may include thinning of bones, cataracts, weight gain and diabetes. Doctors often prescribe a corticosteroid to relieve acute symptoms, with the goal of gradually tapering off the medication.
Disease-modifying antirheumatic drugs (DMARDs). These drugs can slow the progression of rheumatoid arthritis and save the joints and other tissues from permanent damage. Common DMARDs include methotrexate (Trexall), leflunomide (Arava), hydroxychloroquine (Plaquenil), sulfasalazine (Azulfidine) and minocycline (Dynacin, Minocin, others). Side effects vary but may include liver damage, bone marrow suppression and severe lung infections.
Immunosuppressants. These medications act to tame your immune system, which is out of control in rheumatoid arthritis. Examples include azathioprine (Imuran, Azasan), cyclosporine (Neoral, Sandimmune, Gengraf) and cyclophosphamide (Cytoxan). These medications can increase your susceptibility to infection.
TNF-alpha inhibitors. Tumor necrosis factor-alpha (TNF-alpha) is an inflammatory substance produced by your body. TNF-alpha inhibitors can help reduce pain, morning stiffness, and tender or swollen joints. Examples include etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira), golimumab (Simponi) and certolizumab (Cimzia). Potential side effects include increased risk of serious infections, congestive heart failure and certain cancers.
Other drugs. Several other rheumatoid arthritis drugs target a variety of processes involved with inflammation in your body. These drugs include anakinra (Kineret), abatacept (Orencia), rituximab (Rituxan) and tocilizumab (Actemra). Side effects vary but may include itching, severe abdominal pain, headache, runny nose or sore throat.

Lifestyle Changes: [21]
Patients can manage RA by changing daily lifestyle. While there is little scientific evidence to support this approach, diet is important to some patients in managing their rheumatoid arthritis. By eliminating foods that contribute to RA symptoms, and by adding omega-3 fatty acids for their anti-inflammatory properties, patients may report feeling less sluggish, fatigued, or report less pain. Over the counter ointments and patches like BenGay, Tigerbalm, etc. may be used for topical pain relief. Alternative therapies such as stress management techniques, herbal remedies, acupuncture, and hypnosis may also be potential choices for patients to control their RA symptoms

IX. Surgeries [22]

Surgical options for rheumatoid are preventative, in that efforts are taken to preserve the joint and repair any damage of the affected limb. In advanced rheumatoid, joint replacing surgery is also a possibility.

Synovectomy:
Surgeons will perform a synovectomy if pain, swelling and radiologic changes are so severe that conservative methods will not work. Tendons of the wrist and the ankle are the most common spots for a synovectomy, causing loss of function. A synovectomy is a procedure that involves excising inflammatory synovium, and is demonstrated in the video below:

Osteotomy:

473-0550x0475.jpg


Osteotomy involves correcting deviation of the lower extremity due to deformities from rheumatoid arthritis. The surgery involves the removal or addition of bone to change the alignment. It can be performed in the rheumatoid foot as well, by resecting the metatarsal heads.

Joint Replacement:
If the damage to a joint has destroyed its inner workings and preserving the joint is not an option, joint replacements can be performed on the rheumatoid patient. There are many types of joint replacement surgeries, including resection-arthroplasty or an allo-arthroplasty. It involves removing the affected joint and putting prosthesis in its place. The effort in replacing a joint is to provide a stable source for the limb to bear weight without pain or inflammation.

kneetransplant.jpg
finger_arthroplasty_surg04.jpg

X. Additional Web Based Resources

Arthritis Foundation: http://www.arthritis.org/

Journal of American Medical Association Patient Page for Rheumatoid Arthritis:
http://jama.ama-assn.org/content/305/17/1824.full.pdf

National Institute of Arthritis and Musculoskeletal and Skin Diseases: Rheumatoid Arthritis: http://www.niams.nih.gov/Health_Info/Rheumatic_Disease/default.asp

U.S. Department of Health & Human Services Agency for Healthcare Research and Quality – Rheumatoid Arthritis: A Guide for Adults: http://effectivehealthcare.ahrq.gov/ehc/products/14/86/RheumArthritisConsumerGuide_Singlepage.pdf

Mayo Clinic – Rheumatoid arthritis pain: Tips for protecting your joints: http://www.mayoclinic.com/health/arthritis/AR00015/METHOD=print

Bibliography
1. Smith HS, Smith AR, Seidner P. Painful rheumatoid arthritis. Pain Physician. 2011;14(5):427-458.
2. National Collaborating Centre for Chronic Conditions. Rheumatoid arthritis: national clinical guideline for management and treatment in adults. London: Royal College of Physicians, February 2009.
3. Matsumoto AK. Rheumatoid arthritis clinical presentation. The Johns Hopkins Arthritis Center. http://www.hopkins-arthritis.org/arthritis-info/rheumatoid-arthritis/rheum_clin_pres.html
4. National Institute of arthritis and musculoskeletal and skin diseases. Rheumatoid arthritis. http://www.niams.nih.gov/Health_Info/Rheumatic_Disease/default.asp. April 2009.
5. American Society for Surgery of the hand. Arthritis: Rheumatoid Arthritis. http://www.assh.org/Public/HandConditions/Pages/ArthritisRheumatoidArthritis.aspx. 2011.
6. Rindfleisch JA, Muller D. Diagnosis and management of rheumatoid arthritis. Am Fam Physician 2005;72(6):1037-1047. http://www.aafp.org/afp/2005/0915/p1037.html
7. American Academy of Orthopaedic Surgeons. Rheumatoid arthritis of the foot and ankle. http://orthoinfo.aaos.org/topic.cfm?topic=A00163 2001.
8. Abdo RV, Iorio LJ. Rheumatoid arthritis of the foot and ankle. J Am Acad Orthop Surg. 1994;2:326-332
9. Helmick, CG, Felson DT, Lawrence RC, Gabriel S, Hirsch R, Kwoh CK, Liang MH, Kremer HM, Mayes MD, Merkel PA, Pillemer SR, Reveille JD, Stone, JH. Estimates of the prevalence of arthritis and other rheumatic conditions in the united states. Arthritis Rheum. 2008;58:15-25.
10. Lee HS, Korman BD, Le JM, Kastner DL, Remmers EF, Gregersen PK, Bae S. Lack of association of Caucasian rheumatoid arthritis susceptibility loci in a Korean population. Arthritis Rheum. 2009;60(2):364-371.
11. Aletaha D, Neogi T, Silman AJ, Funovits J, Felson DT, Bingham CO, Birnbaum NS, Burmester GR, Bykerk VP, Cohen MD, Combe B, Costenbader KH, Hobbs K, Huizinga TWJ, Kavanaugh A, Kay J, Kvien TK, Laing T, Mease P, Menard HA, Moreland LW, Naden Rl, Pincus T, Smolen JS, Stanislawska-Biernat E, Symmons D, Tak PP, Upchurch KS, Vencovsky J, Wolfe F, Hawker G. 2010 rheumatoid arthritis classification criteria. Arthritis Rheum. 2010;62(9):2569-2581.
12. Bax M, van Heemst J, Huizinga TWJ, Toes REM. Genetics of rheumatoid arthritis: what have we learned? Immunogenetics. 2011;63:459-466.
13. Raychaudhuri S. Recent advances in the genetics of rheumatoid arthritis. Curr Opin Rheumatol. 2010;22(2):109-118.
15. Tedesco A, D’Agostino D, Soriente I, Amato P, Piccoli R, Sabatini P. A new strategy for the early diagnosis of rheumatoid arthritis: a combined approach. Autoimmun Rev. 2009;8(3):233-237.
16. Farng E, Friedrich JB. Laboratory diagnosis of rheumatoid arthritis. J Hand Surg Am. 2011;36(5):926-927.
17. American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines. Guidelines for the management of rheumatoid arthritis: 2002 update. Arthritis Rheum. 2002;46:328–46.
18. Narvaez JA, Narvaez J, De Lama E, De Albert M. MR imaging of early rheumatoid arthritis. Radiographics. 2010;30:143-165.
19. Breedveld FC, Combe B. Understanding emerging treatment paradigms in rheumatoid arthritis. Arthritis Research & Therapy. 2011;13:1-10.
20. Smolen JS, Aletaha D, Bijlasma J, Breedveld FC, Boumpas D, Burmester G, Combe B, Cutolo M, de Wit M, Dougados M, Emery P, Gibofsky A, Gomez-Reino JJ, Haraou B, Kalden J, Keystone EC, Kvien TK, McInnes I, Martin-Mola E, Montecucco C, Schoels M, van der Heijde D. Treating rheumatoid arthritis to target: recommendations of an international task force. Ann Rheum Dis. 2010;69:631-637.
21. Simon H. University of Maryland Medical Center. Rheumatoid arthritis – lifestyle changes. http://www.umm.edu/patiented/articles/what_lifestyle_changes_can_help_manage_rheumatoid_arthritis_000048_10.htm 2009.
22. Trieb K, Hofstaetter SG. Treatment strategies in surgery for rheumatoid arthritis. Eur J Radiol. 2009;71:204-210.
Unless otherwise stated, the content of this page is licensed under Creative Commons Attribution-ShareAlike 3.0 License