Rheumatoid Arthritis of the Hand and Wrist

Definition

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by symmetrical polyarticular arthritis, typically affecting the wrist and small joints of the hands and feet. Inflammation progresses to joint destruction with pain, deformity, and disability.

Nonarticular manifestations include rheumatoid nodules, pulmonary fibrosis, renal amyloidosis, pericarditis, endocarditis, atherosclerosis, Felty’s syndrome, keratoconjunctivis sicca, hemolytic anemia and generalized systemic symptoms such as malaise, anorexia, anemia, and weight loss. The course of RA is variable and unpredictable; premature mortality is well recognized.

The incidence of RA is generally quoted across European and North American literature as affecting 1% of the population. RA is two to four times more common in females than males, with a peak age of incidence in the seventh decade. RA may have a significant social and economic impact on the people afflicted with this disease. The UK National Institute for Health and Care Excellence (NICE) has estimated that approximately one-third of people stop work within 2 years of diagnosis and the total cost to the UK economy is £3.8 billion to £4.75 billion per year.

Diagnostic Criteria

In 2010 the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR) revised the classification schema for RA ( Table 59.1 ). Diagnosis is confirmed by affecting one or more joints, not explained by another cause and a total score of 6 or greater (out of 10) in four domains: joint involvement, serology, acute phase reactants, and duration of symptoms. A key aim was to identify patients with RA early, especially those with persistent or erosive disease, in order to allow early medication.

Pathophysiology

The cause of RA is unknown and tremendously complex. Antigen presenting cells (APCs) bind and present an as yet unknown arthritogenic antigen to T-cells. The binding of co-stimulatory ligands, also on the APCs, such as CD80 and CD86, assists in activation of T-cells. T-cells, fibroblasts, and macrophages secrete numerous proinflammatory cytokines, such as IL-1, IL-6, and TNF-α. These recruit and activate neutrophils, lymphocytes, macrophages, synovial cells, fibroblasts, and B-cells. Inheritance of certain HLA-II loci may mediate antigen presentation, T-cell reactivity and other immune relationships.

B-cells differentiate into plasma cells that secrete antibodies and autoantibodies. This process is abetted by IL-6. Autoantibodies include those to IgG (rheumatoid factor, RF) and citrullinated peptides (anticitrullinated protein antibody, ACPA), amongst others. The autoantibodies form immune complexes that drive the secretion of proinflammatory cytokines, augmenting the inflammatory process. Activated B-cells also act as APCs. In conjunction with cells of the innate and acquired immune system there are numerous other chemokines that guide and control this intricate process.

The final stage in the pathogenesis is swollen synovium full of macrophages, T-cells, B-cells, plasma cells, and synovial fibroblasts. This synovial pannus then erodes cartilage, bone, and supporting soft tissues leading to joint destruction, deformity, and pain. Synovial proliferation around tendons (tenosynovitis) may cause tendon attrition and rupture. Joint destruction begins early and erosive changes may occur within months.

Rheumatoid nodules are typically cutaneous, demonstrating central fibrinoid necrosis surrounded by macrophages and fibroblasts and a cuff of connective tissue containing lymphocytes and plasma cells. Rheumatoid nodules typically occur at sites of repeated mechanical stress or over bony prominences such as the olecranon, the calcaneum, and the metacarpophalangeal joints; they are associated with more aggressive disease. Due to generalized dysfunction of the immune system RA patients have an increased susceptibility to infection.

Management Principles and Operative Options

Assessment and Evaluation

Referral to a rheumatologist should be made for any patient with persistent and unexplained synovitis. This includes patients with normal inflammatory markers and those who are RF-negative. Referral should be expedited if the synovitis affects multiple joints, or if the duration of symptoms has been longer than 3 months. There is an urgency to diagnose RA since prompt treatment has been shown to reduce permanent joint damage.

RA should be managed by a multidisciplinary team (MDT), which may include a rheumatologist, occupational therapist, hand surgeon, besides other allied health professionals.

General Assessment

Assessment includes examination for joint synovitis and extraarticular manifestations ( Box 59.1 ). Blood tests should include inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Serology should include RF and ACPA, the latter being more specific for RA. Baseline full blood count (FBC), liver, and renal biochemistry are useful for planning treatment.

BOX 59.1

Initial Assessment of Rheumatoid Arthritis

Abbreviations as Table 59.1 .

• Clinical evaluation

  • Joint synovitis and extraarticular manifestations

• Blood work

  • ESR, CRP, RF, ACPA, complete blood count, liver and renal biochemistry

• X-rays of hands and feet

Radiological Features

X-rays provide a record of the permanent damage of RA ( Fig. 59.1 and Box 59.2 ). Changes include: surface erosions, cystic changes, cortical thinning, osteoporosis, and progressive joint narrowing through to frank ankylosis, subluxation, and dislocation. In mutilans arthropathy there is bony destruction, which may progress rapidly.

BOX 59.2

Radiological Features of Rheumatoid Arthritis

• Joint narrowing and destruction progressing to ankylosis

• Erosions

• Cortical thinning

• Osteoporosis

• Subluxation/dislocation

• Bony destruction (mutilans)

The Sharp and Larsen scores are the most widely used radiological assessments for RA. Each scores X-rays of the hands, wrists, and feet; higher scores indicate greater bony destruction. The Sharp method scores bony erosions and joint space narrowing separately over 31 areas to give a score from 0 to 448. The Larsen score assesses 20 joints to give a score out of 100. Although the Larsen score is more widely used, the Sharp assessment is more sensitive for detecting changes over time. The Sharp and Larsen assessments have significant correlation with each other and with the extent of joint and cartilage destruction.

Magnetic resonance imaging (MRI) is increasingly used to detect pre-erosive synovitis, and early bone damage not seen on standard radiography. Fat-suppressed gadolinium-enhanced T1-weighted images will demonstrate pre-erosive synovitis, tenosynovitis, and bony erosions. The presence of bone marrow edema, seen on T2-weighted images, is also predictive of the development of bony erosions. Identification and treatment of subclinical synovitis and prevention of bony erosions are the aims of more aggressive medical management regimes.

Identifying Patients with Aggressive Disease

One of the key goals of initial assessment is to identify those patients with signs that suggest an aggressive disease process ( Box 59.3 ). Such patients are monitored closely; a poor response to first-line medical treatment may warrant early use of biologic therapies to gain early control of the disease.

BOX 59.3

Poor Prognostic Features on Diagnosis of Rheumatoid Arthritis

Abbreviations as Table 59.1 .

• Positive RF or ACPA

• Early functional limitations

• Multiple swollen or tender joints

• Early bony erosions on X-ray

• Extra-articular manifestations

• High ESR or CRP

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