Rheumatoid Arthritis

Original Editors - Florence Brachotte

Top Contributors - Vidya Acharya, Bruno Luca, Annelore Oyen, Rachael Lowe and Max Louis  

Definition/Description

Rheumatoid arthritis (RA) is a systematic autoimmune inflammatory disease and results in persistent inflammation of synovial tissue especially of the wrists, hands and feet. Individuals with RA are 8 times more likely to have the functional disability compared with adults in the general population from the same community. The structures around the joint can also be affected, like the tendon sheath, the bursa and tendons. This pathology causes pain, stiffness in the morning and after periods of inactivity, joint swelling, weakness, fatigue and restricted joint mobility leading to reduced function. Without treatment, RA can lead to irreversible damage, namely deformity and finally provoke considerable physical functional loss or even permanent disability. Thus, RA causes dramatic interference with quality of life if early diagnosis and appropriate treatment are not obtained.[1][2]

Clinically Relevant Anatomy

Diagram showing how Rheumatoid Arthritis affects a joint in the hand
Characterizing in rheumatoid arthritis is the inflammation of the synovium also characterized is the destructive erosion of bone and loss of joint integrity what frequently leads to disability. [2] The synovium is a thin layer of tissue which lines the joint space where there is no cartilage. It can also be found in tendon sheaths and bursae. Under normal circumstances, the synovium consists of 2 - 3 layers of cells. In patients with rheumatoid arthritis, the synovium is strongly thickened and inflamed. Due to the inflammation production of enzymes occurs, which breaks down the cartilage. This can cause local damage to the bone-tissue and cartilage. The cause of this inflammation in rheumatoid arthritis is unknown.[1]

Epidemiology /Etiology

The cause of Rheumatoid Arthritis remains unknown and can therefore not be prevented. A simple disorganisation of the immune system can be at the origin of the body attacking its own tissue. The evolution of the disease varies from person to person; sometimes the inflammation can become systemic, what means that it will expand and also affect multiple organs, systems or tissues. [1] When RA affects the pediatric population, it is called Junevile Idiopathic Arthritis (JIA) and usually begins before the age of 16.

Systemic inflammation and autoimmunity in RA begin long before the onset of detectable joint inflammation[3]. Emerging data suggest that RA-related autoimmunity may be initiated at a mucosal site years before the onset of joint symptoms. The candidate sites of origin include the oral, lung and gastrointestinal mucosa, as data consistent with this hypothesis have been generated for each location. Individual patients may undergo initiation events at unique sites but still converge on similar joint findings as the disease process evolves. RA is typically divided into two subtypes designated “seropositive” and “seronegative” disease, with seropositivity being defined as the presence of serum elevations of the autoantibodies rheumatoid factor (RF) and the more recently described antibodies to citrullinated protein/peptide antigens (ACPAs).

Multiple genetic and environmental factors[4] have been associated with an increased risk for rheumatoid arthritis (RA)

Genetic and familial risk factors for RA

There is a generally increased prevalence of RA within families, leading to estimations of familial risk contribution of ∼40–50% of seropositive RA, with strongest risks seen in first-degree relatives (FDRs). In addition, genetic factors in RA are suggested by an increased prevalence of disease within certain racial groups such as North American natives, who exhibit prevalence rates of RA of 5–7%. Although there may be non-genetic familial or cohort factors that play a role in the family or racial/ethnic group risk, multiple specific genetic loci have been identified that are associated with increased risk for RA and in some cases decreased risk.

The strongest of the genetic risk factors is a set of alleles within the major histocompatibility complex (MHC) that encode amino acid sequences that predict structural similarities in the human leukocyte antigen (HLA) peptide-binding groove and are termed in the aggregate “shared epitope,”(SE). SE alleles are believed to contribute up to ∼40% of the genetic risk for RA, although other studies suggest less contribution[4].

Environmental factors

Multiple environmental, dietary, and lifestyle factors have been associated with RA[4].

Smoking/Tobacco Exposure:

Many studies have found that exposure to smoking accounts for ∼20–30% of the environmental risk for RA. Primarily, smoking is most strongly associated with antibodies to citrullinated protein/peptide antigens (ACPA) - positive RA. It has been proposed that smoking may lead to increased citrullination and in presence of the right genetic background, it may lead to the presentation of citrullinated proteins and the generation of ACPA, along with other local and systemic effects of smoking tobacco influencing the immunity. Smoking has long been associated with the presence of RF even in the absence of RA. This suggests that there may be biologic interactions between these factors that drive the development of RA or at the very least RA-related autoimmunity.

Thus, a major unanswered question regarding the role of smoking in RA is where it acts in the natural history of RA. Specifically, does exposure to tobacco smoke act to trigger the initial autoimmunity or does it drive the propagation of autoimmunity to the point of classifiable disease? These issues need to be investigated thoroughly, especially given the potential for smoking to be a modifiable risk factor and therefore a potential preventive intervention in RA development.

Dietary factors:

Lower intake of vitamin D and antioxidants and higher intake of sugar, sodium, red meats, protein, iron and certain medications are associated with increased risk of RA.  

Environmental and other factors associated with rheumatoid arthritis risk[4].
Increased risk
Female sex
Exposure to tobacco smoke
Occupational dust (silica)
Air pollution
High sodium, red meat, and iron consumption
Obesity
Low vitamin D intake and levels
Decreased risk
Fish and omega-3 fatty acid consumption
Moderate alcohol intake
Healthy diet
Statin use
Oral contraceptive use/hormone replacement

Microbes and mucosal processes influencing RA development

Data suggest[3] that the initial inflammation and autoimmunity in RA begins outside of the joints. Several lines of evidence support that RA-related autoimmunity may originate at a mucosal site. The general model[4] underlying a hypothesis that mucosal surfaces (and potentially microbes) play a role in the pathogenesis of RA is as follows. At some point in preclinical RA, at a mucosal surface (e.g., the oral cavity, lung, gut) interactions between microbes potentially other environmental factors (e.g., tobacco smoke) and host factors lead to mucosal inflammation and initial breaks in RA-related immune tolerance.

This mucosal inflammation may then facilitate local, and then systemic, propagation of autoimmunity through mechanisms that may include molecular mimicry or facilitation of development of direct autoimmunity to self-antigens.

Few epidemiologic and other observational studies have linked inflammation in the oral cavity and specifically periodontitis to the preclinical period of RA. In addition, studies of RA-related autoantibody-positive individuals without IA have demonstrated the presence of airways inflammation and/or lung parenchymal abnormalities by imaging with a number of subjects later progressing to clinically apparent RA[4].

Certain studies have shown alteration of the oral or gut microbiota may affect mucosal immunity, inducing aberrant immune responses that affect joints in patients with RA[5]

Scher J U et al identified the presence of Prevotella copri[6] as strongly correlated with disease in new-onset untreated rheumatoid arthritis patients. Increases in Prevotella abundance correlated with a reduction in Bacteroides and a loss of reportedly beneficial microbes in new-onset untreated rheumatoid arthritis subjects.

Female sex and rheumatoid arthritis

A large number of epidemiologic studies point to sex-related factors in RA risk, it has long been considered that there are female-specific factors that influence risk for RA. However, many controversies still exist[7]. The post-menopause stage, an early age at menopause, the post-partum period and the use of anti-oestrogen agents are associated with RA onset. All these phenomena have in common an acute decline in ovarian function and/or in oestrogen bioavailability. However, there are controversies regarding other female hormonal factors. The influence of systemic hormonal treatments, including contraceptive and HRT, on RA onset, remains unclear. The effect of other factors related to diverse hormonal changes (such as parity, breastfeeding or PCO) is also controversial.

The timing of oestrogen exposure also plays a role in RA onset, with female hormonal factors having varying effects during premenopause and post-menopause. Overall, the effect of sex hormones on the immune system and their interaction with environmental and genetic factors could explain the higher prevalence of RA in women. As some female hormonal factors are potentially modifiable, understanding their precise role is key for future preventive interventions focusing on women at high risk[4].

Characteristics/Clinical Presentation

A major advance in understanding how these factors impact the development of RA has been the emergence of a model of RA development, and in particular seropositive RA development. There is typically a period of circulating autoantibody elevations that may last several years prior to the first appearance of inflammatory arthritis. This period can be termed “Preclinical RA,” and its presence has raised the issue that a subset of the genetic and environmental factors that drive RA , are likely acting years prior to the first appearance of arthritis. This process of disease progression is not universal, although some studies have identified a small percentage of patients where inflammatory arthritis presents prior to the appearance of circulating autoantibodies[4].

In rheumatoid arthritis, joint complaints are in the foreground.

Typically in a first stage, there is:

  • a chronic, symmetrical inflammation of the joints of the hands and the feet, especially the metatarsophalangeal joints (MTP), the wrists, the metacarpophalangeal joints (MCP) and the proximal interphalangeal joints (PIP).
  • Softening of the ligaments can lead to deformation of the fingers, like subluxations of the metacarpophalangeal joints.

Rheumatoid arthritis causes deformity, pain, weakness and restricted mobility and will result in loss of function.[8]

The three most important complaints are the pain, morning stiffness and fatigue.

Muscular strength, muscular endurance and aerobic endurance are typically reduced in patients with rheumatoid arthritis in comparison with healthy patients.

In 80-90% of the patients with rheumatoid arthritis the cervical spine is involved, which can lead to instability, caused by the ligamentous laxity. Usually, the instability occurs between the first and second cervical vertebrae. This instability can lead to pain and neurological symptoms, like a headache and tingling in the fingers. [1]

RA is a highly disabling disease associated with high morbidity. Consequently, RA results in considerable direct costs, such as health care expenses, and indirect costs, such as loss of productivity due to morbidity and decreased life expectancy.[9] The increased mortality in RA patients is mostly associated with cardiovascular disease. Accelerated atherosclerosis is of growing concern in these patients. There is increasing evidence that atherosclerotic disease is driven by inflammatory mechanisms similar to those in RA. Cardiovascular morbidity correlates with inflammatory activity in RA.

Differential Diagnosis

There is no unique test or feature that is pathognomonic for RA. The diagnosis is made by recognizing a pattern of signs and symptoms. The classification criteria are helpful in classifying patients for the purpose of clinical research studies, but they might not clearly establish the diagnosis in an individual patient.
A thorough history and examination are necessary for the differential diagnosis in the individual patient. There are lots of disorders that mimic RA. Rheumatoid arthritis can resemble any disorder causing acute or chronic polyarthritis.

Common disorders to consider as differential diagnoses with RA are:

  • Osteoarthritis: best differentiated from RA by a careful history and examination. Two factors to distinguish the two disorders: the absence of systemic inflammatory signs and symptoms, onset in later life, and the pattern of joint involvement.
  • Infectious arthropathies: the important consideration in the setting of fever and polyarthritis. If bacterial arthritis is suspected, joint aspiration and synovial fluid cultures and blood cultures are often helpful in establishing the diagnosis.
  • Lyme disease: also associated with negative synovial fluid cultures. When a patient has been in an endemic region where tick exposure was likely, it should be considered.
  • Seronegative spondyloarthropathies (reactive arthritis, ankylosing spondylitis, inflammatory bowel disease–associated arthropathy): muscle weakness and antibodies associated with these disorders most often readily distinguish these disorders from RA.
  • Fibromyalgia (FMS): diffuse symmetrical arthralgias and stiffness at rest, but an absence of synovitis, the lack of pain on motion, and normal laboratory and imaging studies. [10]

Diagnostic Procedures

The diagnose is made on anamnestic data en clinical examination. The American College of Rheumatology has defined 7 criteria, where a patient has to correspond with at least 4 of these 7 criteria for the diagnose of rheumatoid arthritis.

The first 4 of these criteria are only valid if they persist for at least 6 weeks. These 7 criteria are:

  1. Morning stiffness
  2. Arthritis in 3 or more joints
  3. Arthritis in the joints of the hands (wrist, MCP, PIP)
  4. Symmetrical arthritis
  5. Nodules
  6. Rheumafactors
  7. Radiological deviations

The Multi-Dimensional Health Assessment Questionnaire (MDHAQ) is a recognized quality-of-care indicator. Assesses pain and fatigue using visual analogue scales (VASs) and includes items to assess disability in these patients.
The Multi-Dimensional Health Assessment Questionnaire (MDHAQ) derived from the HAQ (=a disease-specific questionnaire), which includes an index of the three RA core data set measures (physical function, pain, and global estimate), also known as a routine assessment of patient index data 3 (RAPID 3). The MDHAQ is created for the clinical standard care to save time for the rheumatologist and to improve the quality of patient visits.

The difference between the HAQ and MDHAQ are:

  1. The MDHAQ has two activities more than the HAQ – “Are you able to walk 2 miles or 3 kms?” and “Are you able to participate in recreation and sports as you would like?”. These ADLs were added as scores for eight items on a modified HAQ (MHAQ) and were systematically lower than HAQ scores by 0.2 units to 0.3 units. Scores on the HAQ and MDHAQ are quite similar. Inclusion of two complex activities reflects higher expectations for patient status in rheumatology care at this time than in the 1970s when the HAQ was developed.
  2. All 10 activities are listed on one side of the first page, allowing the physician or other health professionals to scan the information rapidly.
  3. The MDHAQ does not include HAQ queries concerning aids, devices, or help from another person, which complicates scoring, may not add important information (particularly at this time), and possibly elevate scores artifactually with use of a device.
  4. The MDHAQ VAS for pain and patient global estimate are in a format of 21 numbered circles, rather than a 10-cm line and require no ruler to score.
  5. The MDHAQ includes a patient self-report RA disease activity index (RADAI) joint count.
  6. Boxes are available on the MDHAQ to record scores for physical function, pain, patient global estimate, and RADAI self-report joint count.
  7. Scoring templates are available on the MDHAQ to convert physical function scores from 0-30 to a 0-10 scale, and RADAI self-report joint counts scores from 0-48 to a 0-10 scale.
  8. Scoring templates are also available to record RAPID composite scores. RAPID 4 adds a RADAI self-report joint count and RAPID 5 adds a physician global estimate.
  9. The MDHAQ also includes three psychological items concerning sleep, anxiety, and depression (queried in the standard patient-friendly HAQ format), not scored formally, a review of systems, medical history, fatigue VAS, queries about change in status, morning stiffness and exercise, and demographic data—within two sides of one page.

Two prerequisites are essential for success in having patients complete questionnaires:

  1. The questionnaire must be reviewed by the rheumatologist prior to seeing the patient, so the staff and patients recognize that this is an important matter and not simply an exercise to meet abstract goals or requirements for a clinical study (as is the situation in completion of questionnaires in many research studies) or requirements to administer a certain therapy.
  2. The staff must project an attitude of enthusiasm, reflecting the interest of the clinician. For example,
    a comment such as “Would you mind completing a questionnaire?” is inappropriate. A better comment might be: “We need you to complete this questionnaire as part of your medical evaluation.”
    The MDHAQ is useful in all rheumatic diseases by documenting changes in status over long periods, and by improving rheumatology care and outcomes. .
    Goals of the MDHAQ:
    - to be scanned (“eyeballed”) by a clinician in 5 sec to 10 sec
    - using scoring templates on the questionnaire for individual measures in less than 10 sec or 10 sec
    - RAPID indices based on self-report data.
    All quantitative data require interpretation by a clinician, along with information from a history, physical examination, and other sources in formulating a clinical decision. Nonetheless, the availability of quantitative data can add considerably to the decision process and help focus the visit on the concerns of the patient. [10]

Examination

Symptoms of rheumatoid arthritis can progressively increase but can also fluctuate in time, therefore it is important that we search for any active symptoms during the physical examination. We need to examine the joints on swelling, pain due to palpation, pain due to movement, decreased range of motion, deformation and instability. Other symptoms of RA are fatigue, depression and hallmark symptoms such as symmetrical joint swelling and tenderness, morning stiffness, positive rheumatoid factor (RF), elevated acute phase reactants, and radiographic evidence of erosive bone loss. Significant predictors of functional decline among persons with RA are slow gait and a weak grip. [1][11]

Medical Management

Biological DMARDs (drug treatment), optimal outcome of treatment in rheumatoid arthritis (RA) is early clinical remission to delay joint damage. Therefore, severe RA patients with inadequate response to conventional disease modifying anti-rheumatic drugs (cDMARDs) need high-potency drug as biological DMARDs (bDMARDs). [12]

HMG-CoA reductase inhibitors (also known as statins) are widely used as lipid-lowering agents in patients with rheumatoid arthritis (RA) to reduce their cardiovascular risk. The Statin therapy also significantly reduced tender joint counts, swollen joint counts, erythrocyte sedimentation rate (ESR), compared with placebo groups.[13] However, statins influences immune regulation, which may potentially facilitate autoimmunity, eventually resulting in autoimmune diseases such as rheumatoid arthritis (RA)[14]. A matched cohort study[15] with prospectively collected data suggested the risk of RA is substantially increased in the first year after initiation of statins and then diminishes to baseline, suggesting an association between statin use and an increased risk of RA in the first year after initiating statin treatment.

Radiosynovectomy is a well-established therapy in arthritis and involves an intra-articular injection of small radioactive particles to treat a synovitis. The treatment can be repeated 3-time in an interval of 3 months if the first treatment showed an insufficient effect. Repeated treatments are more effective than single treatments with higher activity. The therapy is well-tolerated with a low rate of side effects. In respect of the specific uptake of particles in the synovia and short range of beta radiation, the radiation exposure outside the joint is very low.[16] Their findings may suggest that statins can accelerate disease onset in patients susceptible to develop RA, but in other patients, statins are probably safe and well tolerated, even after prolonged use.

Surgical treatment, operative treatment was aimed at the inflammatory focus elimination, reduction of the pain syndrome severity, the function loss, and the joint deformity correction. The most used operative interventions are tenonectomy, synovectomy, arthrodesis, total endoprosthesis.[17]

Nutritional Guidelines

Dietary interventions necessitate a widespread appeal for both patients as well as clinicians due to factors including affordability, accessibility, and presence of scientific evidences that demonstrate substantial benefits in reducing disease symptoms such as pain, joint stiffness, swelling, tenderness and associated disability with disease progression. However, there is still an uncertainty among the community about the therapeutic benefits of dietary manipulations for RA[18]. Dietary modification helps in staying in the remission phase of the inflammatory condition.

Eating certain foods can help you manage its symptoms. Dietary supplements[18] like vitamin D, cod liver oil, and multivitamins can also help in managing RA.

Avoiding food which causes inflammation like processed food, high salt, oils, butter, sugar, and animal products.

Physical Therapy Management

At the present, there is no therapy that can completely heal RA. But there are treatments that achieve pain relief and the slowdown of the activity of RA to prevent disability and increase functional capacity. RA patients are unfortunately committed to a treatment for life.[19] The benefits of physical therapy interventions have been well documented. 

Physical therapists play an integral role in the nonpharmacologic management of RA. They help patients with RA cope with chronic pain and disability through the design of programs that address flexibility, endurance, aerobic condition, a range of motion (ROM), strength, bone integrity, coordination, balance and risk of falls. All current UK clinical guidelines for the management of RA recommend the use of physiotherapy (PT) and occupational therapy (OT) as an adjunct to drug treatment. The three most common components of PT/OT for RA hands are exercise therapy, joint protection advice and provision of functional splinting and assistive devices, massage therapy, exercise therapy and patient education. Dynamic exercise (aerobic capacity and/or muscle strength training) was effective in improving muscular endurance and strength, without detrimental effects on disease activity or pain.

The therapy goals in most cases are: [20] 

  • Improvement in disease management knowledge
  • Pain control
  • Improvement in activities of daily living
  • Improvement in Joint stiffness (~ Range of motion)
  • Prevent or control joint damage
  • Improve strength
  • Improve fatigue levels
  • Improve the quality of life 
  • Improve aerobic condition
  • Improve stability and coordination


Patient questionnaires – not joint counts, radiographic scores, or laboratory tests – provide the most significant predictors of severe 5-year outcomes in patients with RA, including functional status, work disability, costs, joint replacement surgery and premature death. 

Physiotherapy Modalities:

Cold/Hot Applications: cold = for acute phase; heat = for chronic phase and used before exercise. Dose and/or withdraw thermal energy by means of hot/cold application. [21]

Electrical Stimulation: Aperitif administering of electric energy by means of an alternating current. Transcutaneous electrical nerve stimulation (TENS) is used to relieve pain. [22]

Hydrotherapy-Balneotherapy: allows exercise with minimal load on the joints.
Simply being in another environment, where the patient can relax has a positive effect on the disease's progression (physically as well as on mentally)[23]

This therapy is not recommended. [24]

Rehabilitative Treatment:

Joint Protection Strategies:
  • Rest & Splinting: Orthosis and splinting prevent the development of deformities and support joints
  • Therapy Gloves: to control and manage hand pain, to maintain or restore the patient’s hand function, or to psychologically help to relax or calm the wearer. Wearing therapy gloves led to the improvement in hand grip strength. The glove can be worn during the day or at night. They are made of various materials: nylon, wool and elastane fibres. [25]
  • Compression Gloves: moderate joint swelling and consequently reduce the pain
Assistive Devices and Adaptive Equipment:

Arrangements (like elevated toilet seats,...) to facilitate activities of daily living

Massage Therapy:

Massage and the manual trigger of an articular movement focused on the improvement of function, pain reduction, reduction of disease activity improve flexibility and welfare (dimension of depression, anxiety, mood and pain) [26]

Therapeutic Exercise:

Physical exercise helps to increase the physical capacity of the patient but it does not reduce the activity of the disease[19]. There is evidence suggesting that exercise improves general muscular endurance and strength without detrimental effects on disease activity or pain in rheumatoid arthritis. However, few studies have investigated the effect of exercises for the rheumatoid hand. Some improvement in strength, mobility and/or function with no negative effects have been reported, although the long-term effectiveness has not been established due to various weaknesses in trial design.[27] The duration and the frequency of the treatment depend on the perceived limitations in activities and participation, and the impairments in functions and structures.[28][29] 

Before beginning an exercise program, it is important to have a global evaluation of the situation: joint-inflammation local or systemic, state of the disease, age of the patient and grade of collaboration.[19]
Exercise therapy is used by patients with RA with the aim of improving daily functioning and the social participation by means of improvement of the strength, aerobic condition, the range of motion, stabilization and coordination.


In general, we can say that patients with RA need a high-intensive exercise program which is aimed at improving aerobic capacity, strength and endurance. This program can be completed with ROM-exercises and stabilization/coordination exercises. Sometimes the therapist chooses to start with a moderate-intensive exercise program and built this up. This is often the case in patients with joint prostheses, severe physical disabilities and/or kinesiophobia. [30][31] The duration and intensity of the exercises should be based on the individual patient and their assessment[19].

Precautions:[19]

  • When the patient experiences an exacerbation and the joints are acutely inflamed then isometric exercises should be done
  • Avoid stretching in acute cases.
  • Revise the exercise program if pain persists 2 hours after the activity or there is an increase in joint swelling
  • Patients with active RA in their knees should avoid climbing stairs or weight lifting as it could lead to intra-articular pressure in the knee joint
  • Avoid excessive stress over the tendons with stretches and avoid ballistic movements

Exercises:

  1. ROM exercises: In acute phase: isometric/static exercises -> be held for 6 seconds and repeated 5–10 times each day ; load = 40% 1RM. in chronic phase: isotonic exercises (= active exercises with constantly the same tension) for example: swimming, walking, cycling -> minimum 4 repetitions for each joint in 2 to 3 days These exercises increase the mobility of the joint, but the concerned joint will not be loaded during this exercises.[32] Contractures can be held for 6seconds and repeated 5-10 times daily[19].
  2. Stretching: Has to be avoided in acute cases.
  3. Strengthening: Moderate-intensive exercise therapy where a minimum of 8-10 exercises is necessary for the major muscle groups. Each exercise has to be repeated 8-10 times and a minimal start intensity of 30-50 percent of 1 repetition maximum (RM). [31] [32] Use light weights important for stabilization of the joint and prevention of traumatic injuries.
  4. Aerobic condition exercises: There are two types of exercises to improve the aerobic condition: Intensive exercises and moderate-intensive exercises. The intensive exercise therapy has a minimum duration of 20 minutes per session and this 3 times a week with an intensity of 65 to 90 percent of the maximal heart rate. The moderate-intensive exercise therapy has a minimum duration of 30 minutes per session and this 5 times a week with an intensity of 55 to 64 percent of the maximal heart rate. The aim of this exercises is to improve the muscle endurance and aerobic capacity.
  5. Stabilizing and coordinating exercises: The improvement of stabilization and coordination of a certain joint will be achieved by doing exercises that stimulate the sensorimotor system. For example, standing on a balance board. Important aspects during this exercises are motion control, balance and coordination.
  6. Routine daily activities: SARAH (Strengthening and stretching for rheumatoid arthritis of the hand) exercise program: The SARAH trial tests an intervention against the usual hand care. The main aim of the exercise program is increased hand function, which is suggested to be mediated by increases in strength, dexterity and range-of-movement. The exercise program consists of the usual care plus a hand and wrist exercise program which includes seven mobility exercises and four strength exercises against resistance (i.e. therapy putty, theraband or hand exerciser balls).[8]
  7. Conditioning exercises in people with chronic inactive RA: swimming walking, cycling (include adequate rest periods)[19].

Exercises Frequency Sets Repetitions Initial Hold Initial Load Progression
Mobility • MCP flexion
• Tendon gliding
• Finger radial walking
• Wrist circumduction
• Finger adduction
• Hand-behind-head
• Hand-behind-back
Daily 1 x 5 5 seconds (where required) Step 1: increase up to 10 repetitions
Step 2: Increase up to 10 seconds hold
Strength • Eccentric wrist extension
• Gross grip Finger adduction
• Pinch grip
Daily 1 X 8 (min. 8 repetitions, max. 12 repetitions) Between 3 and 4 on modified 10 pt Borg Scale Step 1: 2x 10 repetitions
Step 2: 4-5 on Borg scale
Step 3: 5-6 on Borg scale
Step 4: 3x 10 repetitions


A modified Borg scale is used to set the load (resistance) for the strength exercises based on self-perception of effort. The level of resistance is determined by the patients’ rating of perceived effort using the weaker hand for each strength exercise. Exercise therapy in patients with RA is used to improve the daily functioning and social participation through improving muscle strength, aerobic endurance, joint mobility (range of motion, ROM) and stability and/or coordination. Therefore, preference is given to an active policy, especially where the physiotherapist has a supporting role. However, in individual cases, passive treatments, such as manual operations, can be part of the treatment.

5. Patient Education: information about their condition and the different therapies disposed to improve their quality of life. In addition, patients are taught how to protect the joints during routine daily life. To let patients become more active, you have to adjust their movement-behaviour. Different manners to achieve a behavioural change by your patient:
• A behavioural change is a process with 3 phases: the motivation-phase, the initial-behavioural change phase and the phase where the intended behaviour is continued. It’s important to know in which phase your patient is located. In the 1st phase is education and motivation important. In the 2nd phase is structure and accompaniment important and in the 3rd phase is the patient capable to keep moving with the help of his natural environment.

• The therapist has to formulate achievable goals with the patient.

• The therapist should give proper instructions and be sure that the patient understands him.

• Enough variation in the exercises is important. Otherwise, the patient can become bored which is not positive for your therapy.

• The therapist needs to avoid that the patient gets again in his old movement-pattern. You must warn the patient for this.

• The therapist has to involve the partner and other important people in the process because they have an important motivation-role. Also, the therapist himself has to motivate the patient.
• Keep in touch with the patient to be sure that the treatment was effective. [33]

Resources

https://www.arthritis.org/

Clinical Bottom Line

Rheumatoid arthritis (RA) is a systematic autoimmune inflammatory disease and results in persistent inflammation of synovial tissue especially of the wrists, hands and feet. There is no therapy that can completely heal RA. But there are treatments that achieve pain relief and the slowdown of the activity of RA to prevent disability and increase functional capacity. Physical therapists play an integral role in the nonpharmacologic management of RA. They help patients with RA cope with chronic pain and disability through the design of programs that address flexibility, endurance, strength, bone integrity, coordination, balance and risk of falls.


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