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