Rheumatoid Arthritis
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Transcript of Rheumatoid Arthritis
Dr.S.DineshPost graduate in M.S.Ortho
Prof . V. Thulasiraman unit IIInstitute of orthopaedics and Traumatology
MMC & GGHChennai
Rheumatoid Arthritis Pg cote 15/01/2010
INTRODUCTION
Chronic systemic inflammatory disease of unknown etiology
Affects the Synovial Membranes of multiple joints
Prevalence 1-2% Female : Male ratio 3:1 Usual age of onset 20-40 years though
individuals of any age group may be affected
HISTORY
1858 – Dr Alfred Baring Garrod, named the condition Rheumatoid Arthritis.
1895 – X-Ray was discovered. In the 1920’s, physicians suspected the
cause of RA was bacterial infection, they used gold and malaria drugs.
1940- Scientists discovered that RA was associated with a malfunction of the immune system
1949 – Dr. Phillip Hench treated arthritic patients successfully with Cortisone
PATHOPHYSIOLOGY
chronic synovitis with pannus formation. The pannus erodes cartilage, bone, ligament and tendons.
A membrane of granulation tissue covering the normal surface of the articular cartilage
RA IS CHARACTERISED BY SYNOVITIS AND JOINT DESTRUCTION
NORMAL RA
Synovial membrane
Cartilage
CapsuleSynovial fluid
Inflamed synovial
membrane
Pannus
Major cell types:
• T lymphocytes• macrophages
Minor cell types:
• fibroblasts• plasma cells• endothelium• dendritic cells
Major cell type:• neutrophils
Cartilage thinning
HISTOLOGY Nodular clusters lymphocytes and plasma cells near surface of synovial villi
ARTHROSCOPIC IMAGES- SYNOVIAL VILLI
CLINICAL FEATURES
usually presents insidiously; prodromal syndrome of malaise, weight loss and
vague periarticular pain and stiffness may be seen
less commonly, the onset is acute, triggered by a stressful situation such as infection, trauma, emotional strain or in the postpartum period.
the joint involvement is characteristically symmetric with associated stiffness, warmth tenderness and pain
DIAGNOSIS
Rheumatoid factor, an IgM antibody is seen in the sera of 75% of patients with rheumatoid arthritis. High titers of rheumatoid factor are associated with severe disease.
Rheumatoid factor is also found in other diseases like syphilis, sarcoidosis, infective endocarditis, TB, leprosy, parasitic infections; in advanced age and in asymptomatic relatives of patients with rheumatoid disease.
Antinuclear antibody are seen in 20% of patients with rheumatoid arthritis, though their titer is lower than in SLE
DIAGNOSIS
The ESR is elevated both in the acute and chronic phases of the disease
a moderate anemia is often present which is usually hypochromic normocytic
the white count is normal or slightly increased but leukopenia may occur, often in presence of splenomegaly (e.g., Felty’s syndrome)
the platelet count is often elevated in proportion to the degree of joint inflammation
ANTI-CCP
Anti-Cyclic Citrulline Peptide
IgG against synovial membrane peptides damaged via inflammation Value in IgM-RF negative
Sensitivity (65%) & Specificity (95%)
Predictive of Erosive Disease Disease severity Radiologic progression Poor functional outcomes
ARTHROCENTESIS
ACR CRITERIA, 1987
Morning stiffness: lasts at least 1 hour before improvement. Arthritis of 3 or more joint areas: The 14 possible areas include
the right and left proximal interphalangeal (PIP), metacarpophalangeal (MCP), wrist, elbow, knee, ankle, and metatarsophalangeal (MTP) joints.
Arthritis of hand joints: At least one area in a wrist, MCP, or PIP joint is swollen.
Symmetric arthritis . Rheumatoid nodules Serum Rheumatoid factor Radiographic changes
. First four criteria must be present for 6 weeks or more
ARTICULAR MANIFESTATIONS
HAND DEFORMITIES
Ulnar deviation, MCP subluxation, intrinsic muscle atrophy
HAND DEFORMITIES
Radial deviation , pronation at wrist
Ulnar deviation at MCP
Synovitis articular erosion
Intrinsic flexor overpull
Ulnar, volar extensor tendon migration
DEFORMITIES IN HAND
SWAN NECK DEFORMITY BOUTONNIERE DEFORMITY
Flexion at MCP,DIP Hyperext. At PIP Volar plate weakening Dorsal displacement of
lateral bands
Flexion at PIP jt Hyperext. At DIP jt Volar prolapse of lateral
bands
THUMB DEFORMITY
90/90 deformity/ Z deformityFlexion mcp,hyper extension of ip jt
OPERA GLASS HAND / MAIN EN LORGNETTE
Long standing cases , Severe jt. Destruction Loss of bone
substance, Shortening Telescoping Hypermobility of jts
CARPAL TUNNEL SYNDROME TRIGGER FINGER
TENDON RUPTURE
Dorsum of wristextensor digiti minimiExtensor digitorum communis
VolarFlexor pollicis longus
Finger flexorFDP index
Dorsal thumbEPL
ROTATOR CUFF TEAR GEODE CYST
Invagination of synovium through cortical surface leading to large cyst like lesions
HIP AFFECTION
IRREGULAR NARROWING OF JOINT SURFACEOSTEOPHYTES
CONCENTRIC NARROWING OF JOINT SPACEPERI ARTICULAR CYSTS
•Severe joint space narrowing
•Erosive changes of bony margins
•Subchondral cysts
•osteopenia
OTTO PELVIS /PROTRUSIO
KNEE
osteopenia subchondral erosion uniform narrowing
of the joint space
WIND SWEPT DEFORMITY
Genu valgum is the commoner deformity
BAKERS CYST
FOOT DEFORMITY
Erosions , osteopenia,lateral deviation and subluxation of mtp jts. Hallux valgus present
ATLANTOAXIAL SUBLUXATION Lateral view c-spine
flexion Pre- odontoid space
<3mm
EXTRA ARTICULAR MANIFESTATIONS
RHEUMATOID NODULES
•Usually non tender•Elbow,feet, fingers, occiput,Heels buttock•20% of pat with rh disease•Ass. With high titres of rheumatoid factor•Also seen in SLE and mixed connective tissue disorders
CARDIAC MANIFESTATIONS
•Constrictive pericarditis•Does not respond to immunosuppression•Requires steroids / pericardectomy
Bloody pericardial fluid rich in cholesterol crystals
SYSTEMIC MANIFESTATIONS
RHEUMATOID PACHYMENINGITIS CAPLANS SYNDROME
OCULAR MANIFESTATIONS
EPISCLERITIS SCLEROMALACIA
TREATMENT
goal of treatment reduce inflammation and pain, preservation of function, and prevention of deformity.
NON-PHARMACOLOGICAL MANAGEMENT Rest Exercise
Flexibility/stretching Muscle conditioning Cardiovascular/aerobic
Diet/weight control Physical/occupational therapy
MEDICAL MANAGEMENT
NSAIDS
DMARDS - xenobiotics - Biological agents
Glucocorticoids
XENOBIOTICS
Methotrexate Sulphasalazine Gold salts Minocycline
BIOLOGICAL AGENTS
Tnf –alfa blockersetanercept, infliximab, and adalimumab
Interleukin receptor antagonistanakinra
Abatacept prevents t- cell co-stimulation
SURGICAL MANAGEMENT
SYNOVECTOMY Does not prevent
disease progression Relieves symptoms
delays joint destruction
Can prevent a impending tendon rupture
PROBLEMS RELATED TO THR
steroids; the risks of fracture during surgery and infection after surgery
dermatitis, vasculitis, fragile skin, osteopenia, and poor musculature
femoral head and neck may be partially absent, and the femoral head may have protruded into the pelvis
Limitation of movement in neck,other joints they are relatively inactive, they are not
physically demanding of the hip
not to fracture the femur or acetabulum or tear the skin of the leg while dislocating or reducing the hip.
Preparation of the femur usually is easy because the canal is wide
Severe osteopenia often makes cementless fixation difficult
Small components may be necessary, especially in patients with juvenile rheumatoid arthritis,
REPLACEMENT SURGERIES
JRA
Juvenile chronic arthritis is similar to rheumatoid arthritis but is seen in children. Synovitis persisting for 6 weeks is essential to making this diagnosis. Four forms are recognized: polyarticular form resembles adult RA oligoarticular form affects young girls during peak
ages of 2-4 systemic onset disease or Still’s disease is
characterized by fever and rash a juvenile form of ankylosing spondilitis
THANK YOU