2. INTRODUCTION
• Rheumatoid Arthritis ( RA) is a systemic autoimmune disease characterized by
inflammatory polyarthritis which affects peripheral joints , especially the small joints of
hands and feet.
• It is a chronic , progressive disease in which untreated inflammation may lead to
cartilage and bone erosion and joint destruction resulting in functional impairment.
• Non – suppurative inflammation of synovial joints.
3. PREVALENCE
• 1% Worldwide
• Female: Male ratio = 3:1
• Age wise: Usually 4th and 5th decade . Steadily increases with age until the mid
70s.
4. ETIOLOGY
• Exact etiology is unknown.
• But…
• A genetic predisposition is strongly suspected; HLA-drw4/ HLA-DR1
• Agents such as mycoplasma, clostridium and some viruses i.e. EB virus have
been implicated in its etiology.
• Likely that a combination of genetic, hormonal and environmental factors.
5. PATHOPHYSIOLOGY
• Initially the synovium becomes edematous , filled with fibrin exudates and cellular
infiltrates.
• There is an increase in synovial fluid. As the inflammation persists , the synovium gets
hypertrophied and surrounds the periphery of the articular cartilage to form a pannus.
• The articular cartilage losses its smooth shiny appearance.
6. PATHOPHYSIOLOGY …
• The Pannus Extends Over The Cartilage From The Periphery And Burrows Into
Subchondral Bone.
• With further progress of disease , the cartilage becomes worn off and the bone
surfaces become raw.
7. PATHOPHYSIOLOGY…
Stages Of RA:
• Potentially reversible soft tissue proliferation: The disease is limited to the
synovium. There occurs synovial hypertrophy and effusion. No destructive
changes can be seen on X- ray.
• Controllable but irreversible soft tissue destruction and early cartilage erosion:
X- ray shows a reduction in joint space, but outline of the articular surface is
maintained.
• Irreversible soft tissue and bony changes: The pannus ultimately destroys the
articular cartilage and erodes the subchondral bone. The joint becomes
ankylosed usually in a deformed position ( fibrous ankyloses) . It may be
subluxated or dislocated.
9. CLINICAL MANIFESTATIONS
• Pain, Swelling and warmth I one or more peripheral joints.
• Morning stiffness > 30 minutes.
• Fatigue, Malaise, low grade fever and weight loss over a period of weeks to
months.
• Sometimes occur acute onset polyarthritis instead of insidious symptoms.
• Most common joint involved include metacarpophalangeal (MCP), Proximal
interphalangeal ( PIP) and Metatarsophalangeal (MTP) joints as well as wrist.
10. CLINICAL MANIFESTATIONS…
• Other Joints Affected involved include Elbows, Shoulders, Hips, Knees, and
Ankles.
BUT
Distal Interphalangeal Joints are SPARED.
• Sacroiliac and vertebral joints are SPARED except for the C1 and C2 articulation.
11. CLINICAL MANIFESTATIONS…
• Chronic Longstanding Disease:
i. Swan Neck Deformity
ii. Boutonniere Deformity
iii. Z-Thumb Deformity
iv. Ulnar Deviation and subluxation of MCP joints.
v. Radial deviation of wrist
vi. C1 to C2 inflammation can lead to odontoid erosion and transverse ligament rupture,
resulting in atlantoaxial subluxation and cord compression.
vii. Joint damage of wrists, elbows, shoulders, hips and knees can lead to severe
osteoarthritis, necessitating joint replacement surgery.
13. CLINICAL MANIFESTATIONS…
• Extra Articular Manifestations:
• Secondary Sjogren’s Syndrome
• Rheumatoid Nodules (25%) – Nontender, firm nodules on extensor surfaces and pressure
points, usually in RF positive cases. Most common site is Olecranon.
• Felty’s Syndrome: RA with splenomegaly. Most patients are positive for HLA-DR4 and RF.
• Pulmonary Diseases :
• Pleuritis,
• Interstitial lung disease,
• Bronchiolitis Obliterans,
• Pneumonia,
• Pulmonary nodules- A combination of RA and Pneumoconiosis is called Caplan Syndrome.
14. CLINICAL MANIFESTATIONS…
• Neuromuscular:
• Carpal Tunnel,
• Tarsal Tunnel,
• Cubital Tunnel syndromes are most commonly involved.
• Peripheral Neuropathy,
• Cervical myelopathy and cord compression in atlantoaxial subluxation.,
• Pachymeningitis (rare).
15. CLINICAL MANIFESTATIONS…
• Vasculitis: Cardiac Diseases-
• Pericarditis ( Most Common)
• Myocarditis
• Valvular Nodules
• Ocular Diseases:
• Keratoconjunctivitis sicca ( Dry eyes without dry mouth; 10%)
• Episcleritis, Scleritis, Scleral thinning, Ulcerative Keratitis
• Amyloidosis: occurs in longstanding, poorly controlled RA. Usually
presents as Nephrotic Syndrome
17. DIFFERENTIAL DIAGNOSIS
• Systemic Lupus Erythematosus (SLE) : In SLE joint involvement is not
symmetrical; nor are ankyloses and erosions common. Absence of Anti- Nuclear
Antibody Factor (ANA) is in favour of RA, although its presence doesn’t confirm
SLE.
• Osteoarthritis: DIP joints are involved. Duration of morning stiffness, joint
swelling and ESR are less compared to RA.
• Psoriatic Arthritis: Characteristic skin and nail lesions may be present.DIP joints
are usually involved. RF is negative.
• Polyarticular Gout
18. DIFFERENTIAL DIAGNOSIS
• Pseudo RA or Calcium Pyrophosphate Deposition (CPPD)
• Polymyalgia Rheumatica
• Paraneoplastic Syndrome
• Seronegative Spondyloarthropathies
• Seronegative RA
• Septic Arthritis
• Infectious causes: Parvovirus B19, Hepatitis B/C, Post streptococcal reactive
arthritis, Acute rheumatic fever
21. DIAGNOSIS
• Laboratory:
• RF ( Sensitivity ~ 60% , Specificity ~ 80%) False positive are seen in – Hepatitis C,
SABE, Primary Biliary cirrhosis, Sarcoidosis, Malignancy, Sjogren’s Syndrome, SLE
and increasing age.
• Anti – CCP antibody: Sensitivity is similar to RF but it is more specific for RA than RF
( up to 95% to 98%)
• Elevated ESR and /Or CRP
• CBC : Possible anemia of chronic disease.
• Hypoalbuminemia and hypergammaglobulinemia
• ANA ( present in 20% to 30%)
22. DIAGNOSIS
• Inflammatory synovial fluid with >2000 Polymorphonuclear Leucocytes , patient with
RA have an increased risk of developing septic arthritis. Hence synovial fluid with white
blood cells > 50,000 cells/ mm3 is concerning for an infectious process and must always
be ruled out.
• LATEX FIXATION TEST: Sensitivity ~ 80%
• ROSE-WAALER TEST: Sensitivity ~ 60%
• Imaging Studies: X-Ray of affected joints – Reduced joint space, Erosion of articular
margins, Subchondral Cysts, Soft tissue shadow at the level of joint because of joint
effusion or synovial hypertrophy, Deformities.
• Synovial fluid examination
• Synovial Biopsy
23. TREATMENT AND GUIDELINE
• Aims Of Treatment Are:
a. Induction of remission and its maintenance: Disease activity is brought under
control by drugs.
b. Preservation of joint functions and prevention of deformities
c. Repair of joint damages which already exists.
24. TREATMENT AND GUIDELINE …
• Early identification and treatment of RA with DMARDs is crucial. More than half
of patients have radiographic joint damage within 2 years of disease onset, BUT
early aggressive treatment with DMARDs and/or biologic agents is associated
with decreased progression of synovitis and bone erosion, and with decreased
disability.
• Immunization, Cardiovascular disease prevention ( smoking cessation, blood
pressure control, cholesterol control) and osteoporosis prevention ( with
calcium and vitamin D supplementation and bisphosphonate therapy).
25. TREATMENT AND GUIDELINE …
• Treatments Are:
a. Medical Treatment: Consists of anti rheumatic drugs.
i. NSAIDs
ii. DMARDs
a. Synthetic – Methotrexate, Sulfasalazine, Hydroxychloroquine, Tofacitinib, Leflunomide
b. Biological – TNF inhibitors, Abatacept, Rituximab, Tocilizumab
c. Combination -- Methotrexate, Sulfasalazine, Hydroxychloroquine in combination
or Methotrexate with one TNF inhibitors
iii. Steroids – Low dose oral steroid ( Prednisolone 5 to 10 mg per day) produce prompt
anti inflammatory effect and slow the rate of articular erosion.
Folic Acid 1mg per day is
given with Methotrexate to
reduce the side effects.
26. TREATMENT AND GUIDELINE …
• Treatments Are: …
Orthopedic treatment:
a. Non Operative
i. Physiotherapy
ii. Occupational Therapy
iii. Rehabilitative
b. Operative
i. Preventive surgery
ii. Palliative surgery
iii. Reconstructive surgery
iv. Salvage surgery