Rheumatoid Hands

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Different deformities seen in hands due to rheumatoid hands, Rheumatoid hands, Dr.Sushil vijay D.orth

Transcript of Rheumatoid Hands

RHEUMATOID HAND

DR.SUSHIL VIJAY PG STUDENT- D ORTH SANTOSH MEDICAL COLLEGE & HOSPITAL

Rheumatism Rheumatism is any painful disorder affecting the loco-motor system including joints, muscles, connective tissues, soft tissues around the joints, and bones. This also includes rheumatic fever affecting heart valves.

Origin The term ''rheumatology'' originates from the Greek word ''rheuma'', meaning something that which flows as a river or stream," and the suffix ''-ology'', meaning "the study of."

Rheumatoid arthritis is a chronic, systemic, inflammatory disease, most often involving the small joints of the hands and feet, although any synovial joint can be affected

Rheumatoid arthritis : overview It is most common* type of chronic inflammatory rheumatic disorder.

The term inflammatory rheumatic disorder covers a group of disorder that causes pain, stiffness, and swelling around joints and tendons.

Rheumatoid arthritis Basically , it is a systemic disease of young and middle aged adults characterised by proliferative and destructive changes in synovial membrane, periarticular structures, skeletal muscles and perineural sheaths. Eventually, joints are destroyed , fibrosed or ankylosed. It is a widespread vasculitis of the small arterioles.

Etiology Still incompletely worked out. Important factors in evolution are Genetic susceptibility An immunological reaction An inflammatory reaction The appearance of Rh factor in blood and synovium Articular cartilage destruction

Genetic susceptibility More common in first degree relatives HLA DR4 +ve in 70% of people with RA.

Inflammatory reaction In joints and tendon sheath. As the APC/T cell interaction is initiated, various local factors comes into play and leads to a progressive enhancement of immune response. There is a marked proliferation of cells in the synovium, with the appearances of new blood vessel formation. Cytokines activate inflammatory cells like macrophage and B cells. Some cytokines-chemokines attract other inflammatory cells to area. Importanat cytokines are :- TNF, IL-1 and IL-6. The resulting synovitis, both in joints and tendon sheath lining , is the hallmark of early RA.

Chronic synovitis and joint destruction Immune complexes are deposited in synovium and on the articular cartilage, where they appear to augment the inflammatory process. This leads to depletion of cartilage matrix and eventually damage to cartilage and underlying bone.Vascular proliferation and osteolytic activity most marked at the edges of the articular surface, may contribute further to the cartilage destruction and peri articular bone erosion.

Rheumatoid factor B cell activation in RA leads to the production of anti IgG autoantibodies which are detected in the blood as rheumatoid factor

High levels are likely inflammatory in origin. Low levels may normally be present in individuals. Other autoantibodies idenified are anti-CCP antibodies. Its presence is very specific for RA.

Pathology- Joints & tendons 4 stages: Stage 1- Pre-clinical(Only raised ESR, CRP and RF) Stage-II- Synovitis Stage III- Destruction Stage IV- Deformity

Pathology Due to synthesis of autoantibodies, against unknown antigenic antigens in the synovium, primary synovitis sets in. Primary synovitis Pannus formation forms villus. Villus migrates towards the joint causing its destruction and ankylosis, fibrous in early stage and bony in late stages. Pannus- medical term for an abnormal layer of fibrovascular tissue or granulation tissue Villus- any of the small, slender, vascular projections that increase the surface area of a membrane.

Rheumatoid arthritis = synovitis+vasculitis+granulomaSYNOVITIS

GRANULOMA FORMATION

VASCULITIS

Pathological process Vasculitis Necrosis Fibrosis

Tissue involved Joint structures

Results in Synovitis-effusion, articular cartilage destruction, Pericapsulitis, Ligamentous instability Arthritis

Deformities Swelling, stiffness, instability , subluxation or dislocation

Intrinsic plus deformity

Plasma cell proliferation

Tendon

Tenosynovitis, rupture Ulnar deviation of fingers, concertina collapse of fingers. Wasting, atrophy, fibrosis Osteoporosis-thin cortex loss of trabeculae, cyst formationsubchondral erosions, destruction Contracture, ankylosis

Granulation tissue and Muscle pannus formation Synovial hypertrophy : Bone in joint, in tendon

RA:- Clinical features Insideous onset Ocassionally acute Early stages:- polysynovitis, soft tissue swelling and stiffness. Female predominance Swelling and loss of mobility in PIP of fingers. Other joints involved-wrists, feet, knees and shoulders in order of frequency.

RA:-Clinical features Another classic feature generalised stiffness after period of inactivity and especially after rising from bed in the early morning, usually lasts longer than 30 minutes. Physical signs may be minimal, but usually there is symmetrically distributed swelling and tenderness of the MCP joints, the PIP and the wrists. Tenosynovitis is common in the extensor compartments of the wrist and flexor sheath of the fingers, diagnosed by feeling thickness , tenderness and crepitations over back of the wrist or the palm while passively moving the fingers.

RA:- Clinical features If larger joints are involved, local warmth, synovial hypertrophy and intraarticular effusion may be obvious. In late stages:- joint deformity increases and the acute pain of synovitis is replaced by the more constant ache of progressive joint destruction. The combination of the joint instability and the tendon rupture produces the typical rheumatoid deformities, ulnar deviation of the fingers, radial, and volar displacement of the wrists, valgus knees, valgus feet and clawed toes.

RA:- Clinical features Joint movements are restricted and often very painful. Cervical spine may be involved Daily activities hampered.

Extra articular manifestation

Extra articular manisfestations mercer

Investigations 1. CBC- Hb low, normochromic hypochromic anemia. WBCs or normal, lymphocytes and ESR . 2. Serological tests : Rheumatoid factor:- this in presence of gamma globulins agglutinates certain strains of streptococci sensitized by sheep cells and latex prticles.

Latex fixation test:- Unknown serum + 7globulin latex suspension.agglutination

+ve when serum has abundant RAF

If ve , do more sensitive test as there is less RA factor in the serum

Inhibition test :- This test uses the characterstics of Euglobulin from unknown serum. Euglobulin from normal serum neutralise the rheumatoid factor thereby inhibiting agglutination. Euglobulin from rheumatoid serum has no effect on the rheumatoid factor and agglutination occurs. This is most sensitive test , positive even with minute amounts of RA factor.

RA serum of known high agglutination activity

+Unknown euglobulin + Standard 7-globulin latex suspension Agglutination occurs Unknown serum -ve latex test +ve inhibition test RA SLE (Le cell phenomenon)

Others C reactive proteins (inc.) Alkaline phosphatase (Inc) Platelets( Inc) Serum albumin (Dec) Anti CCP ANA may be +nt.

Synovial fluid not for diagnosis but to rule out other causes of infection. Fluid in RA is typically yellow, turbid and watery due to high WBC and low sugar content. MRI :- Info about extent of soft tissue involvement and damage

Classification criteria Different classification systems have evolved for the diagnosis of rheumatoid arthritis with time.

1987 criteria

Treatment 1. General measures 2. Splints 3. Drugs 4. Surgical intervention

1. General measures Aims to improve G.C of the patient and to keep joints properly splinted in functional position to guard against the ensuing ankylosis. Rest in bed Good diet, rich in proteins and minerals Correct anemia- hematinics or transfusion Hormones to improve bone stock Removal of any infective foci.

2. Splints Splinting in functional position helps avoid ankylosis. Removed daily Hot packs given or Hubbard tanks used and joints are put into full range of motion With splints , muscle setting exercises advocated and after removal of splints resistance exercises begun.

Hubbard tanks

3. Drugs Three classes used:1. Analgesics 2. Anti inflammatory 3. Disease modifying drugs

No treatment is ideal and it is important to assess the patient's response so that the most effective regimen is adopted.

Commonly used methods of assessment include; duration of early morning stiffness, number of tender swollen joints. Functional assessment ESR, radiographs, etc.

First Line of Drugs: NSAIDs These are aspirin/ibuprofen/ketoprofen/diclofenac sodium/ naproxen/piroxicam, etc.

Second Line of Drugs Second line of drugs are used only if an adequate trial of first line drugs have failed to relieve symptoms satisfactorily or if there is radiological evidence of progressive disease. Second line drugs are alternatively known as disease-modifying antirheumatic drugs (DMARD) and are slow acting drugs. When second line therapy is introduced, symptomatic NSAIDs need to be continued in parallel

Commonly prescribed drugs include: Injectable gold and oral gold (sodium aurothiomalate). This is no longer preferred. Penicillamine Sulphasalazine Antimalarial drugs (e.g. chloroquine) Dapsone and levamisole.

The choice of the drug to be given first will depend on the experience of the doctor and on the facilities available for monitoring. There is little evidence to suggest which drug should be prescribed first. Methotrexate has now emerged as the drug of choice due to its higher efficacy. Early insti