Rheumatoid arthritis is a chronic inflammatory disease that commonly affects the joints, causing pain, swelling, and stiffness. It results from an autoimmune disorder where the immune system mistakenly attacks healthy joint tissue. Left untreated, it can cause permanent joint damage and deformity. The presentation involves symmetrical inflammation of small joints in hands and feet. While the cause is unclear, genetic and environmental factors are involved. Treatment involves medications to reduce inflammation like DMARDs and biologics, along with exercise and lifestyle changes. With proper aggressive treatment, outcomes have improved significantly in reducing joint damage and disability. However, uncontrolled disease can still lead to premature death from heart or lung complications.

1. RHEUMATOID ARTHRITIS
Dr Kishore .V
Assistant Professor Of Orthopaedics
Mapims

2. INTRODUCTION
• Most common chronic inflammatory disease(auto immune disease)
• Multisystem disorder- skeletal and systemic, internal viscera also invoved in
inflammatory process.
It can even cause death in young age due to myocardial infarction
• Prevalance of 1-2./. general population
• Urban communities
• Age- 30-50
• female; males= 3;1

3. ETIOPATHOGENESIS
• Unclear
• Genetic susceptibility- HLA DR4 +Ve In 70./.
• Environmental Factors
• Inflammatory reaction- type III hypersensitivity reaction autoantibodies (RF in
70-80./.)

5. STAGES OF DISEASE PROCESS…..
Preclinical stage
• Asymptomatic
• elevated ESR, CRP, RF in serum
• Many years before clinical
manifestations
Stage of synovitis
• acute swollen, painful,tender joints and
tendon sheaths.
• Proliferation of synovial cells and
syovial folds
• Vasular congestion
• Infiltration of cells
• Cll rich exudate into joints
• Reversible

6. STAGES OF DISEASE PROCESS…..
Stage of arthritis
• Cartilage damage and tendon destruction
• Proteolytic enzymes
• Increased osteoclastic activity and marginal
bone erosion
• Cytokines (IL1,IL6,TNF)
• Pannus
All causes cartilage and tendon destruction
Stage of deformity
• Deformity and instability of joints
• Articular destruction
• Capsular thicken
• Tendon rupture
• Often progressive……

7. CLINICAL FEATURES- SKELETAL
FEATURES
• Symmetrical polyarthralgia(pain & swelling) with morning stiffness >30minutes
• Proximal joints (MCP,PIP) of fingers
• Wrist > foot > knee > shoulder
• Rarely c1-c2 subluxation- pain and stiffness in cervical spine
• Tenosynovitis : extensors >> flexor sheath of fingers
(dequervains tenosynovitis)
Chronic stages:
Chronic aching pain
Progressive deformity and joint destruction
Instability of joints and tendon ruptures

8. RHEUMATOID DEFORMITIES
• Rheumatoid Hand:
• Ulnar Deviation Of Fingers
• Radial, Volar Deviation Of Wrist
• Boutennaire Deformity Of Thumb
• Swan Neck Deformity Of Fingers
• Valgus Foot, Clawed Toes
• Valgus Knees

9. EXRA SKELETAL MANIFESTATIONS
• Rheumatoid nodules:
• Granulomatous nodules with central necrosis surrounded by histiocytes.
• 25./. Of RA patients
• Most characteristic and pathognomic of RA
Locations:
• Commonly skin- subcutaneous (elbow commonly)
• synovium
• Tendons( nodules causes trigger finger)
• Eyes
• Viscera also

10. EXTRA SKELETAL RA…..CONTINUED
• Lymphadnopathy- local and distant nodes also can involve
Feltys syndrome: RA+ severe splenomegaly(increased
reticuloendothelial system)+ neutropenia
• Vasculitis: serious and lifethreatening
• Muscle weakness: common symptom (myopathy or neuropathy)
• Visceral organs: heart, kidney, lungs, git, brain also involved
• In RA , death in young age commonly due to ischemic heart disease

11. RADIOLOGY OF RA
• X RAY:
• EARLY- soft tissue shadow, periarticular osteoporosis
• late– marginal bony erosions, narrowing of joint space
• Advanced- deformity,subluxation

12. BLOOD INVESTIGATIONS
• Normal hypochromic anaemia
• Leukopenia(felty syndrome)
• Lymphocytosis
• Increased ESR, CRP – seen in acute stage
indicates prognosis
RHEUMATOID FACTOR(RF); IGG , 70-80./., prognostic marker
High levels indicate more disease activity and systemic activity
ANTI –CCP ( anti cyclic citrullinated peptide antibody) – more specific antibody for RA,
>95./. Of patients
Synovial biopsy: nonspecific

13. D/D
• Sero negative polyarthritis
(Reiters,Ankylosing spondylitis,Psoriatic,Enteropthy associated arthropathy)
• Gout
• Pseudogout
• Sarcoidosis
• Lyme disease
• Viral arthritis
• Polymyalgia rheumaticaa
• Osteoarthritis( dip is a territory of oa)

15. MANAGEMENT –( MEDICAL)
• Mulidisciplinary team required
• Medical management of RA is a revolution
• The main aim of medical management is Rapid and aggressive medication to
decrease inflammation to reduce morbidity and mortality of RA patients
• Principles:
• Identify early
• Start dmards immediately
• Consider combination therapy
• If not responds, start biological therapies

16. MEDICAL MANAGEMENT
• Corticosteroids and DMARDS(DISEASE MODIFYING ANTI RHEUMATOID DRUGS)
• CORTICOSTEROIDS: 30mg prednisolone oral
120mg im prednisolone with tapering over weeks
DMARDS:
Methotrexate(+ folic acid)
Hydoxychloroquine
Sulfasalazine
leflunamide
Penicillamine and gold- rarely used, high complications

17. BIOLOGICAL THERAPY INDICATED
WHEN PATIENT IS UNRESPONSIVE TO DMARDS
• TNF INHIBITORS:
• Infliximab
• Etanarcept
• Golimumab
• Certolizumab
• Adalimumab
• INHIBITORS OF T CELL CO STIMULATION: abatacept
• IL6 INHIBITORS: tocilizumab
• B CELL DEPLETING THERAPIES: rituximab

18. OTHER MEDICAL MANAGEMENT
• NSAIDS For Pain Relief
• Intraarticular Steroid Injection And Into Tendon Sheaths
• Balanced Exercise And Physiotherapyit Prolonged Rest And Immobility Likely To
Weaken The Muscles And Leads To Worse Prognosis .It Is Important To Encourage
Activity

19. SURGICAL MANAGEMENT
• Synovectomy and tendon repair in early stages
• Arthrodesis and arthroplasty in late cases of joint damage.

20. COMPLICATIONS
• Severe arthritis of joints
• Fixed deformities
• Infections
• Muscle weakness
• Spinal cord compression
• Systemic vasculitis
• amyloidosis

21. FACTORS OF POOR OUTCOME
• EARLY AGE ONSET
• FEMALE SEX
• HIGH BMI
• SMOKING
• MULTIPLE JOINT INVOLVEMENT
• SEVERE MUSCLE WASTING
• JOINT CONTRACTURES
• RHEMOTOID NODULES
• SYSTEMIC VASCULITIS
• HIGH ESR,CRP
• HIGH TITTRES RF,ANTI CCP
• SEVERE JOINT EROSIONS IN XRAYS

22. PROGNOSIS
• With out treatment
• 10./. – improve spontaneously
• 60./. – intermittent phases of activity and remission
• 20./. – severe joint erosion in 5 years
• 10./. – completely disabled
• a reduction of 5-10 years is common in these patients often due to premature
ischemic heart disease

23. •Thank you…..