Inflammatory Arthritides

Author(s): Mary Catherine Spires, MD

Originally published:11/10/2011

Last updated:12/27/2012

1. DISEASE/DISORDER:

Definition

Inflammatory arthritides are inflammatory diseases affecting the synovial joints and related structures. Presentation includes monoarticular, oligoarticular or polyarticular involvement; may be acute or chronic. Four groups are recognized:

  1. Inflammatory connective tissue diseases (rheumatoid arthritis, systemic lupus erythematosus)
  2. Crystal induced inflammatory arthritis (gout, pseudo-gout)
  3. Seronegative spondyloarthropathies (ankylosing spondylitis, psoriatic arthritis)
  4. Infectious arthritis (gonorrhea, tuberculosis, osteomyelitis)

Etiology

Unknown; however, inflammation and autoimmunity are key factors. The role of the immune system and genetics remain unclear.Bacteria, fungi and viruses cause infectious forms. Systemic autoimmune diseases may present as arthritis.

Epidemiology including risk factors and primary prevention

Affects all age groups. Certain populations are more susceptible to specific arthridites. Severity varies by specific disease, age and gender. In inflammatory connective tissue diseases, e.g., rheumatoid arthritis (RA), 75% are women; peak age is 25 to 50; more common in European descent. Systemic lupus erythematosus (SLE) is 3 times higher in African Americans; female: male ratio is 9:1. Psoriatic arthritis (PsA) and ankylosing spondylitis (AS) are more common in younger populations.

Patho-anatomy/physiology

Through autoimmune and inflammatory responses, inflammatory arthridites disrupt joint structure and function. A pre-articular phase, consistent with a breach in autoimmunity, occurs early. T-lymphocytes induce monocytes to produce pro-inflammatory cytokines and stimulate B-Lymphocytes and plasma cells.Neutrophils subsequently release proteases and elastase which degrade joint/ peri-articular components resulting in synovitis, cartilaginous and osseous damage. In gout and pseudogout, uric acid, calcium pyrophosphate, hydroxyapatite and cholesterol crystals precipitate inflammatory responses. Seronegative spondyloarthropathies appear to occur in genetically susceptible individuals (e.g., B-27 antigen positivity).

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Acute or insidious onset. An insidious onset occurs in > half of RA patients. Early presentation includes joint swelling and pain. Some report nonspecific musculoskeletal pain which evolves into joint/peri-articular disease.Seronegative arthritis typically presents asymmetrically while RA present with symmetrical small joint disease followed by large joint disruption. Distal interphalangeal joint disease suggests PsA. Inflammatory back pain suggests AS but sacroiliitis may not be present initially. The spine becomes progressively stiff; ankylosis of the spine and sacroiliac joints can occur.

Specific secondary or associated conditions and complications

Skin plaques suggest PsA. SLE and Lyme disease are associated with rashes. RA is associated with atlanto-axial subluxation, cardiopulmonary disease, vasculitis and renal impairment.

2. ESSENTIALS OF ASSESSMENT

History

Joint pain is the most common presenting complaint.Document symptom onset. Record location, symmetry, stiffness and joint swelling/pain. Onset and duration help differentiate acute inflammatory from non-inflammatory arthritis. Constitutional symptoms, (e.g., fatigue, weight loss, fever) suggest systemic disease, e.g. RA, SLE.

Physical examination

Examine all joints, peripheral and axial, for pain, joint effusion, synovitis, deformities, ROM and strength. Count/ list joint involvement or use an articular homunculus. Acute monoarticular inflammatory arthritis is infectious or crystal induced until proven otherwise. Oligoarthritis suggests seronegative arthridites. Weakness and muscle pain suggests polymyositis. Ophthalmic involvement suggests Reiter’s syndrome, RA or sarcoidosis. Oral ulcers are seen in Behçet disease. Finger/toe nail pitting suggests PsA. Dry eyes, parotid enlargement and lymphadenopathy suggest Sjögren syndrome. Cognitive deficits can occur in SLE.

Functional assessment

Assess pain, mobility, ADLs and social skills.The “Get Up and Go Test” and the 6- minute walk tests are useful. Health Assessment Questionnaire (HAQ) assesses mobility, self-care and pain and predicts later function and morbidity. The Arthritis Impact Measurement Scales (AIMS) assesses communication also.

Laboratory studies

CBC, sedimentation rate (ESR), rheumatoid factor (RF), antinuclear antibody and metabolic panels aid diagnosis.C-reactive protein, serum complement and ESR are useful for disease monitoring but requires clinical correlation. Specific auto-antibodies, e.g., antinuclear antibodies, often correlate with specific diseases.

Imaging

A normal X-ray does not exclude arthritis, including infectious arthritis. Early RA shows periarticular osteoporosis; marginal bony erosions appear later. X-Rays are useful to document severity and progression. Radiologic scoring systems, e.g., Modified Sharp Score, rate joint space abnormality and hand/ feet erosions. In gout, punched out lesions adjacent to bone occur. Fibrocartilage calcinosis àpseudogout.Symmetrical sacroiliac joint involvement à ankylosing spondylitis. Magnetic resonance imaging (MRI) with gadolinium assesses synovium, joint effusions muscles and soft tissue. Ultrasound (US) is useful for specific joints, e.g., shoulder joint motion.

Supplemental assessment tools

Joint fluid analysis differentiates inflammatory from non-inflammatory arthridites; aids in diagnosis crystal induced arthritis and infectious arthritis. Arthroscopy allows visualization of articular surfaces. In undefined arthritis, synovial biopsy can aid diagnosis.

Early predictions of outcomes

Formal educational level relates to outcomes: Pincas1 showed that mortality/ morbidity rates were inversely proportional to educational level. In severe baseline RA, RF positivity and elevated acute phase markers suggest poor outcome.Joint damage is predicted by ESR, baseline joint erosions and HLA-DR1 alleles.5-year disability correlates with HAQ scores and joint counts (Combe2).

Environmental

Assess home, work area and driving to identify and remove barriers. Consider mobility aids, orthoses/splints and assistive devices as indicated for support, rest or pain relief.

Social role and social support system

An individual’s role/ability to function at work, in the family and community is often disrupted.Periodically screen psycho-social well-being and evidence of the psychological complications, e.g., depression.

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

Though clinical care guidelines exist, clinical judgment is critical. The ACR web site3 publishes treatment guidelines for inflammatory arthritis, including recommendations/indications for non-biologic and biologic disease modifying antirheumatic drugs (DMARDs).The Rheumatic Disease Treatment Pyramid4 (revised) includes rehabilitation interventions. Individualized treatment plans are critical most effective when initiated early in the disease. Early engagement of the patient and his/her family improves compliance.

At different disease stages

Early treatment for inflammatory arthritides is critical. NSAIDs are the mainstay of pharmacological intervention; however, they do not alter the disease course. DMARDs, including methotrexate and hydroxychloroquine, are typically indicated early in RA and for vasculitic disease. Biologic agents are anti-cytokine therapies that block tumor necrosis factor (TNF); e.g., etanercept. Immunoregulatory drugs, e.g., cyclosporine, enhance disease control. Anti-hyperuricemic agents, e.g., allopurinol are used for crystal-induced arthritis. Combination pharmacotherapy is increasingly prescribed.

Early rehabilitation treatment includes orthoses/splints, joint protection, energy conservation, strengthening, stretching and local modalities. Rehabilitation interventions, including activity pacing, can reduce joint inflammation. During acute joint flares, avoid passive ROM. Prescribe exercise indicating specific goals for specific joints. Appropriate exercise can:

  1. Maintain strength, range of motion, bone mineralization
  2. Increase endurance, aerobic capacity, bone density
  3. Avoid atrophy associated with periods of inactivity

Isotonic exercise is suitable for joints without deformity or acute inflammation. Isometric exercise limits joint stress, maintains and restores strength and is preferred for mechanically disrupted joints. Stretching exercise is appropriate for restoring ROM, in the absence of acute inflammation.

Aquatic therapy provides pain control, decreases joint stress and enhances relaxation.

Heat provides muscle relaxation, pain reduction and decreased stiffness. Cold decreases pain, muscle spasm and local tissue metabolism.

Orthoses/splints provide rest, unweight joints, improve joint stability and provide pain. In acute/sub-acute inflamed joints, splints/orthoses and also maintain alignment. Ring orthoses can decrease/control finger deformity.

Joint replacement surgery is indicated in select cases of severe structural damage, refractory pain or disability. Inpatient rehabilitation may be indicated.

Coordination of care

Multidisciplinary approach is the standard and includes nursing, physical/occupational therapists, social worker and rehabilitation psychologist. Group programs are often helpful. Group exercise is useful in those with stabilized disease.

Patient & family education

Patient education and self-management programs reduce pain, decrease physician visits and are cost-effective. ACR website has many patient information handouts. Counseling and stress management training is effective in providing improvements in helplessness, self-efficacy, coping, pain, and health status measures.

Emerging/unique Interventions

IMPAIRMENT-BASED MEASUREMENT

Distinguish between additive damage and current disease activity. The America College of Rheumatology (ACR) publishes criteria for functional status classification (Class 1 through Class 4).

MEASUREMENT OF PATIENT OUTCOMES

In RA, the Disease Activity Measure and Disease Activity Scale-28 are commonly used to assess disease activity and determine remission. However, many report these are impractical. These measures count involved joints, the physician’s assessment of disease activity, and patients’ reported pain functional level. Measures of Disease Activity in Rheumatoid Arthritis: A Clinician’s Guide is a helpful review.5)

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

The ACR web site3 provides clinical documentation and patient encounter forms. Multidisciplinary teamwork and structured patient management lead to better outcomes. Education improves compliance and patient-provider communication. Rheumatologic consult is indicated to:

  1. Confirm an unclear diagnosis, e.g., undiagnosed multi-system or systemic disease
  2. Assess disease severity and activity
  3. Manage multi-organ and extra-articular involvement
  4. Treat uncontrolled disease and potentially life-threatening complications
  5. Special circumstances, e.g., pregnancy.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

The primary treatment goal is clinical remission, i.e., absence of signs and symptoms of significant inflammatory activity. New medications markedly improve outcomes; however, in cases of long-standing disease, achievement of low disease activity is often the practical goal. Current research is focused on cellular and genetic factors.

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

Knowledge about the immunology, genetics and pathophysiology of arthritis is growing rapidly. The current challenge is to capitalize on the emerging science and understand how to target the underlying mechanisms that will lead to cure.

REFERENCES

  1. Pincus T, Callahan LF: Formal education as a marker for increased mortality and morbidity in rheumatoid arthritis. J Chron Dis. 1984;311:552.)
  2. Combe B, Cantagrel A, Goupille P, et al Predictive factors of 5-year health assessment questionnaire disability in early rheumatoid arthritis. J Rheumatol. 2003;30(11):2344-2349.
  3. American College of Rheumatology (ACR). Web site. http://www.americancollegeofrheumatology.org. Site under construction June 5, 2011. See also American College of Rheumatology.org. Accessed June 5, 2011.
  4. Escalante A, Haas RW, Rincon I, et al. Measurement of global functional performance in patients with rheumatoid arthritis using rheumatology function tests. Arthritis Res Ther. 2004 6(4):R 315-R325.
  5. Ringold S, Singer NG. Measures of disease activity in rheumatoid arthritis: a clinician’s guide. Curt Rheumatol Rev. 2008;4:259-265, 259.

Other Resources

Dagfinrud H, Kvien TK, Hagen KB: Physiotherapy interventions for ankylosing spondylitis. Cochrane Database SystRev 2004;4(2):CD002822. doi: 10.1002/14651858. pub 2. ( reprinted 2007, issue 3).

Wolfe F, Rehman V, Lane NE, et al. Starting a disease modifying anti-rheumatic drug or biologic agent in rheumatoid arthritis: standards of practice for RA treatment. J Rheumatol. 2001; 28:1704-1711.

Author Disclosure

Mary Catherine Spires, MD
Nothing to Disclose

Related Articles