RHEUMATOID ARTHRITIS
Definitions
 Rheumatoid arthritis (RA) is a systemic autoimmuine inflammatory disease involving
primarily the synovial membranes.
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Diagnostic criteria - 4 of 7 (American College of Rheumatology). Symptoms must be present
for at least six weeks:
1. Morning stiffness lasting longer than 1 hour before improvement
2. Arthritis involving 3 or more joints
3. Bilateral joint involvement (ie, both wrists, symmetric PIP and MCP joints)
4. Arthritis of the hand, particularly involvement of the proximal interphalangeal (PIP)
joints, metacarpophalangeal (MCP) joints, or wrist joints
5. Positive serum rheumatoid factor (RF)
6. Rheumatoid nodules (50-80%)
7. Radiographic evidence of RA
 Joint space narrowing
 Periarticular osteopenia
 Juxtaarticular erosions
 Periarticular soft tissue swelling
 Subluxation and gross deformity
Epidemiology
 1% in US. Lower in Asia
 3:1 F:M
 incidence increases with advancing age. Peak incidence 40-60 years.
Prognosis
 clinical course of the disease is variable and ranges from mild, self-limited arthritis to a
progressive multisystem disease
 Daily living activities are impaired in most patients. Spontaneous clinical remission is
uncommon (approximately 5-10%). After 5 years of disease, approximately 33% of patients
will not be working; after 10 years, 50% will have substantial functional disability.
 Poor prognostic factors:
1. persistent synovitis
2. early erosive disease
3. extra-articular findings (including subcutaneous rheumatoid nodules),
4. positive serum RF findings
 although worse outcome than seronegative, response to surgery is more
predictable
5. elevated acute-phase markers (ESR/CRP)
6. family history of RA
7. female sex
8. advanced age.
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Life expectancy for patients with RA is shortened by 5-10 years, although those who respond
to therapy may have lower mortality rates
Mortality is increased by causes such as infections, cardiovascular disease, renal disease, GI
bleeding, and lymphoproliferative disorders; these events may be directly due to the disease
and its complications (eg, vasculitis, amyloidosis) or to therapy-induced adverse effects.
Aetiology
 RA is associated with a number of autoimmune responses, but whether autoimmunity is a
secondary or primary event is still unknown.
Genetics
 The so-called shared epitope of the HLA-DR4/DR1 cluster is present in up to 90% of
patients with RA, although it is also present in more than 40% of controls.
Environmental
 infectious agents have been suggested to induce RA. Among these are Mycoplasma
organisms, Epstein-Barr and rubella viruses, and others.
Hormonal
 Sex hormones may play a role, as evidenced by the disproportionate number of females
with RA, its amelioration during pregnancy, its recurrence in the early postpartum period,
and its reduced incidence in women using oral contraceptives.
Immunology
 Th-1 CD4 cells play a central role (produce IL-2 and interferon gamma.)
 They activate macrophages and other cell populations, including synovial fibroblasts.
The latter 2 populations are the main producers of the proinflammatory cytokines TNFalpha and IL-1 that appear to be the major driving forces of inflammation.
 Experimental models suggest that synovial macrophages and fibroblasts may become
autonomous and thus lose responsiveness to T-cell activities in the course of the disease.
 The hyperactive and hyperplastic synovial membrane is ultimately transformed into
pannus tissue and invades cartilage and bone, the latter being degraded by activated
osteoclasts.
 The major difference between RA and other forms of inflammatory arthritis, such as
psoriatic arthritis, does not lie in their cytokine patterns but rather in the highly
destructive potential of the RA synovial membrane and in the local and systemic
autoimmunity. Whether these 2 events are linked is unclear; however, the autoimmune
response conceivably leads to the formation of immune complexes activating the
inflammatory process to a much higher degree than is otherwise the case. This theory is
supported by the much worse prognosis of RA among patients positive for RF.
Pathophysiology
 RA is characterized by
1. destructive synovitis
2. digital vasculitis
3. rheumatoid nodules
4. carpal tunnel syndrome
Synovitis
Proliferative phase
 characterized by swelling and fibrin deposition that cause pain with motion, decreased
movement, and nerve compression.
 It starts in the synovial membrane, with the initial processes of edema, neovascularization,
and hyperplasia of the synovial lining.
 proliferative tissue is composed of synoviocytes that resemble macrophages and fibroblasts.
Accompanying the synovial proliferation is angiogenesis to support the new growth and
allow leukocyte infiltration.
 The influx of leukocytes is composed of T cells, B cells, macrophages, and plasma cells
 thickening of the synovial lining forms the pannus.
Destructive Phase
 Pannus is a sheet of invasive cellular tissue that is continuous with the synovial lining
 Synovium or pannus invades both tendon sheath and synovial joints causing tendon
displacement and abnormal pull, tendon rupture and articular damage.
 Prominent villous formation occurs in the synovium, as does an inflammatory joint effusion.
The effusion causes capsule distension and stretching of the ligamentous tissues, resulting
in laxity of the capsule. With further progression of disease, the joint becomes unstable and
subluxate.
 high level of proinflammatory cytokines is also present along with matrix metalloproteinase
production.
 2 main cytokines are tumor necrosis factor-alpha and interleukin-1, which induce cellular
proliferation, matrix metalloproteinase expression, adhesion molecule expression, and
secretion of other cytokines and prostaglandins.
 Matrix metalloproteinase degrades extracellular matrix components and is implicated in the
cartilage and bone destruction that occurs in the later stages of RA.
 Increased adhesion molecule expression aids in recruiting leukocytes to the joint spaces
and may perpetuate the inflammatory reaction and allow pannus to attach to cartilage and
bone.
Reparative/Deformational Phase
 inflammatory reaction extinguishes and is replaced by fibrosis, which causes tendon
adhesions, fibrous ankylosis and fixed deformities
1. imbalance between flexor and extensor tendons, which produces the
characteristic hand deformities.
Classifications
FUNCTIONAL STAGING (ACR)
Class I - Completely able to perform all activities of daily living
Class II - Able to perform usual self-care and vocational activities but limited in avocational
activities (hobbies)
Class III - Able to perform usual self-care activities but limited in vocational and avocational
activities
Class IV - Limited in ability to perform usual self-care, vocational, and avocational activities
REMISSION OF RA
* Five or more of the following conditions present for at least 2 consecutive months
1. Duration of morning stiffness not exceeding 15 minutes
2. No fatigue
3. No joint pain
4. No joint tenderness or pain with motion
5. No soft tissue swelling in joints or tendon sheaths
6. ESR of less than 30 mm/h for a female or less than 20 mm/h for a male
STAGING HAND SURGERY
STAGE I
synovitis without deformity
STAGE II
synovitis with passively correctable deformity
STAGE III
fixed deformity without joint involvement
STAGE IV articular destruction
Clinical
History
Time and Onset of Disease
1. monocyclic – only 1 attack followed by permanent remission (10%)
2. polycyclic – intermittent attacks of differing severity (45%)
3. progressive – unremitting, inexorfable course (45%)
Major Problems
Other Problems
Previous Treatment
Functional Assessment
 Self care, work, hobbies
 Use of aids
Pain
Weakness/Stiffness
Numbness and Parasthesias
Medications
Examination
Deformity
 Posterior subluxation of elbow
 Palmar subluxation of wrist
 Ulnar translocation of carpus
 Radial deviation of metacarpus
 Ulnar drift of fingers
 Volar subluxation of MCPJ
 Swan neck and Boutonniere deformities of fingers
 Z deformity of thumb
 Lateral dislocation of IPJ
Swelling
Rheumatoid nodules
Benign pseudo-rheumatoid nodules
Identical histologically but without other stigmata of rheumatoid disease
Rheumatoid nodulosis
Similar nodules in Rh(+) patients but no joint destruction or deformity
Prominent ulnar head
Synovial swelling
Tenderness
Stiffness
Pain on motion
Limitation on motion
Extraarticular manifestations
Rheumatoid nodules
Investigations
Imaging
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Xrays
o
o
o
o
soft tissue swelling
juxta-articular demineralization
uniform joint-space narrowing
erosions (rarely) - often first evident at the ulnar styloid and at the juxta-articular
margins, where the bony surface is not protected by cartilage.
U/S – easily reveal soft tissue swelling and shows up erosions in 80% of patients at first
presentation
MRI – may reveal synovial hypertrophy as early as 4 months after the onset of synovitis
Blood tests
 FBC, ESR/CRP, Rh, ANA
Systemic Review
 Cervical spine instability
o Nearly one third of patients have unstable cervical joints, with atlantoaxial (C1-C2)
subluxation being the most common instability.
o Myelopathy secondary to rupture of the transverse ligament may lead to neurologic
deficits.
o Radiculopathy is most common at the C2 root, though symptomatic subluxations may
occur at any level.
o Pain frequently radiates over the occiput region in the distribution of the C1-3 nerve
roots.
o The Lhermitte sign, in which tingling paresthesias that descends through the
thoracolumbar spine into the limbs, occurs as the neck is flexed, is typically observed.
 TMJ involvement
 Pulmonary involvement
 Felty's syndrome (splenomegaly and neutropaenia)
 Anemia of chronic disease
 Sjogren’s syndrome – dry eyes
Medical Management
 Medications
1. NSAIDS
2. Gold compounds
o For patients who fail to improve on or who cannot tolerate methotrexate
o Gold is taken by macrophages, which in turn inhibit phagocytosis and lysosomal
membrane stabilization.
3. Immunosuppressants
o Methotrexate
o Cyclophosphamide
4. Antimalarials
o Hydroxychloroquine - inhibits chemotaxis of eosinophils, inhibits locomotion of
neutrophils, and impairs complement-dependent antigen-antibody reactions
5. Antiinflammatories
o Sulfasalazine - decreases inflammatory reactions and systemically inhibits
prostaglandin synthesis.
6. Steroids
7. Penicillamine
o depresses circulating IgM rheumatoid factor and T-cell activity but does not affect Bcell activity
8. Anti-TNF
o Adalimumab
 Recombinant human IgG1 monoclonal antibody specific for human TNF
o Etanercept
 recombinant human TNFa-receptor fusion protein.
 interferes with the inflammatory cascade by binding to TNFa, thereby
blocking its interaction with cell-surface receptors.
o Infliximab
 chimeric monoclonal antibody that binds with high affinity to TNFa, thereby
neutralising its activity.
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early intervention offers RA patients the most promise for preventing irreversible joint
damage and avoiding severe disability.
combination treatment, with DMARDs as well as with biologic agents, has been shown to
yield more favorable outcomes than a single treatment.
Continuation of DMARDs during surgery
o Continuation of methotrexate treatment does not increase the risk of either
infections or of surgical complications occurring in patients with RA within one year
of elective orthopaedic surgery. Thus methotrexate treatment should not be stopped in
patients whose disease is controlled by the drug before elective orthopaedic surgery.
(Ann Rheum Dis. 2001)
o in patients with RA undergoing elective foot and ankle surgery, the use of TNFalpha inhibition agents may be safely undertaken in the perioperative period without
increasing the risk of healing or infectious complications. (Foot Ankle Int. 2004)
o no statistically significant risk of wound infection or breakdown in patients taking
methotrexate or steroids or both having surgical procedures on the hand and wrist (J
Hand Surg [Am]. 2002)
AIMS and SURGICAL GOALS
1. Pain relief
2. Improvement of function
3. Retardation of disease progression
4. Improvement of cosmesis
SURGICAL SEQUENCE
 Painful before painless
 Function before cosmetic
 High priority to tendon ruptures and significant nerve compressions
 lower extremity recon. to be completed before hand and wrist in most cases
 proximal before distal, alternating fusion with motion-sparing procedures
 stabilizing operations before mobilizing operations
 procedures that are predictable and have a high patient acceptance
 procedures that are complimentary
 tendon reconstruction before MP arthroplasty
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thumb alignment to follow digital reconstruction so as to place the thumb in the most
useful position
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Indications for surgery
1. nodules
2. triggering
3. rupture
4. compression
5. prevention of progression
6. instability (pain)
7. mobility (function)
8. deformity (aesthetics)
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Five basic surgical procedures
1. synovectomy
2. tenosynovectomy
3. tendon surgery
4. arthroplasty
5. arthrodesis