RHEUMATOID ARTHRITIS
DR BIPUL BORTHAKUR
PROFFESOR AND HEAD
DEPARTMENT OF ORTHOPAEDICS ASSAM
MEDICAL COLLEGE
DIBRUGARH , ASSAM
INTRODUCTION
 Rheumatoid arthrits is an autoimmune
inflammatory disease but mainly involves synovial
joints
 Peak age of onset 40-60 years
 Females are more affected (3:1)
 Rheumatoid arthritis is most common cause of
inflammatory arthritis
 Distinctive features includes peripheral small joints
involvement ,symmetrical and morning stiffness
RISK FACTORS
 Familial and genetic risk factors –HLA DRB1 Alleles
 Demographic risk factors and lifestyle factors –
smoking
 Chronic inflammatory mucosal conditions and
infections
 Occupational exposures and inhalants-
silica,asbestos textile dust
PATHOPHYSIOLOGY
PANNUS
 Thick swollen synovial membrane with granulation tissue
made up of fibroblasts ,myofibroblasts and inflammatory cells,
 Immune system is responsible for pannus formation.
 Pannus damages
Cartilage
Erode bone
Surrounding sof tissues
CLINICAL FEATURES
 MC Inflammatory polyarthritis.
 Appendicular dominant
 Mostly involve small joints of the hands.
 Axial involvement is rare
 Symptoms >6 weeks duration
 Inflammatory synovitis
Palpable synovial swelling
 Symmetrical and polyarticular (>3 joints)
Typically involves wrists, MCP, and PIP joints
Typically spares :DIPs of the fingers and IPs of the
toes
CLINICAL FEATURES
 Subcutaneous or periosteal nodules at pressure
points.
 Ulnar deviation,
 Swan-neck
 Boutonniere deformities are common.
HAND DEFORMITIES
 FINGER DEFORMITIES
BOUTONNIERE DEFORMITY
Central slip distruption
Volar migration of lateral bands
Results in flexion at PIP& hyextension at PIP
SWANN NECK DEFORMITY
• Lateral band injury
• Results in DIP flexion and PIP Hyperextension
• Also seen in volar plate laxities and ehler danlos
syndrome
ULNAR DRIFT
 MCP Joint synovitis results loosening of the joint
weakness capsule and ligaments around the joint
results extensor tendon shifting to the web spaces
GAMEKEEPER THUMB ARTHRITIS MUTILANS
 Synovitic destruction of ulnar
collateral ligament of thumb
results in ligament laxity
 Shortening of fingers due to
destruction phalanges
 Excessive skin folds resembles
opera glass appearence
WRIST DEFORMITY
RA in wrist mainly affects
 Ulnar styloid
 Ulnar head
 Mid portion of scaphoid
synovitis of DRUJ causes stretching of ulnar carpal ligament complex
results in ulna subluxuates dorsally results in dorsal prominence of ulna.
 DRUJ Instability demonstrated by piano key sign.
 Z Deformity ( radial deviation of metacarpal and ulnar deviation of
phalanx)
TENOSYNOVITIS
EXTENSOR FLEXOR
 Can be 1st
presenting symptom of
RA.
 Painless soft tissue mass over dorum
of wrist.
 May be associated with DRUJ Injury.
 Rupture of extensor tendon results in
VAUGHAN JACKSON
SYNDROME
 Rare
 Painful soft tissue mass over
volar surface of wrist and
restrict flexion
 Rupture of FPL tendon resuts
in MANNERFELT NORMAN
SYNDROME
FOOT
 Earliest change seen in 4th
and 5th
metatarsal
phalangeal joints.
 The initial symptoms could be swelling and stiffness
including ankle joint.
 LANOIS DEFORMITY- Dorsal subluxuation of
metatarsal phalangeal joints with fibular deviation.
 Flattening and collapse of arch of foot are the
common deformities
ELBOW
 Effusion
 Ulnar neuropathy
 Subcutaneous nodules
EXTRA ARTICULAR MENIFESTATIONS
DIGNOSIS
1. LABORATORY:
HB – Normocytic normochromic anemia due to anemia of
chronic disease. Degree of anemia directly proportionate to
activity of the disease.
CRP increased
ESR increased
Platelet- Thrombocytosis
2. SEROLOGY:
RHEUMATOID FACTOR:
 Antibodies that recognize Fc portion of IgG
 Can be IgM,IgG,IgA.
 Clinical practice, IgM RF is usually measured
ANTI CCP
 Antibodies to cyclic citulinated peptide have a sensitivity of 78% and
specificity of 96% for RA.
 40 % seronegative RA are Anti CCP positive.
 Level of CCP is directly correlated with the development of erosions
 Negative
 Low-moderate (35-200)
 High CCP (>200)
 Useful in monitoring prognosis of the disease
IMAGING
 X RAY
 EARLY STAGE(SYNOVITIS):
 Soft tissue swelling, periarticular
osteopenia
 LATER STAGE(DESTRUCTIVE):
 Juxta- erosions, narrowing of joint space
 ADVANCE STAGE(DEFORMITY):
 Articular destruction and joint deformity
MRI
1. JOINT EFFUSION
2. MARROW EDEMA
3. SYNOVIAL INFLAMMATION
USG
• Joint space widening
• Fluid collection
• Synovial hypertrophy
• Cartilage defects
• Bone erosions
• Tendon sheath widening and tears
2010ACR/EULAR CRITERIA
MANAGEMENT
 There is no cure for rheumatoid arthritis
 Aim to delay progression of the disease, alleviate
symptoms, reduce functional limitation
 Supportive and palliative
DRUGS
1. NSAIDs
 Ibuprofen, indomethacin, COX-2 inhibitors like
calecoxib and valdecoxib (reduce inflammation and
relieves pain)
2. Analgesics
 Morphine and acetaminophen (reduce pain)
3. Glucocorticoids or prednisolone
 Prescribed in a small dose to slow joint damage caused by
inflammation
DRUGS
4. DMARDS :
 Methotrexate, Hydroxychloroquine, azathioprine,
sulfasalazine
 New: Leflunomide, Etanercept
5. Biologic Response Modifiers
 Abatacept,Etanercept, Infliximab, Adalimumab, Anakinra,
Rituximab
METHOTREXATE
• 1ST
line of choice in RA
• MOST POTENT
• Adenosine efflux mechanism
• DOSE:10-25 mg/week
• Side effects:
 diarrhea, stomatitis
 hepatotoxic
 bone marrow suppression
 ILD
• Follow up: Baseline CBC,LFT every 3 month
• C/I in pregnancy
LEFLUNOMIDE
• Secreted in bile
• Loading dose 100mg/day for 3-5 days then
Maintenance dose 20 mg/day
• Severe hepatotoxicity.should not be considered with
methotrexate.
• Contraindicated in pregnancy and breast feeding.
SULFASALAZINE
• Safe in pregnancy
• 500 mg -2 gm/day oral
• Sulfa group of drugs causes granulocytopenia
and reduced sperm count
• C/I in G6PD deficiency anemia
HYDROXYCHLOROQUINE
• 1st
choice of drug in pregnancy
• Least effective among all 4 drugs,preferred in mild
cases
• 200-400 mg/day
• Side effects:
 bulls maculopathy
 phototoxicity
 torsades de pointes
• Follow up: fundoscopy annually and ECG
BIOLOGICS
 These are monoclonal antibodies derived from
live cell cultures
 They act on specific pathogic processes ,effect
faster disease control,are effective even when
DMARDs fail, and prevent or radiological
worsening of joints.
 Side effects:
 High cost
 Parentral admissions
 Risk of infections
 Unknown long term adverse effects
MECHANISM OF ACTION
TNF-α BLOCKERS:
•Infliximab
•Certolizumab
•Adalimumab
•Golimumab
•Etanarcept
IL-1 BLOCKERS:
Anakinra
3. IL-6 BLOCKERS:
Sarilumab
Tocilizumab
4. T Cell MODULATOR:
Abatacept
Anti CD20:
Rituximab
IMMUNOLOGICS
• TOFACITINIB - blocks JAK 1/3
• BARICITINIB – blocks JAK 1/2
• Tofacitinib was approved by the FDA in June 2012 at
a dose of up to 5 mg administered twice daily for the
treatment of moderate-to-severe RA with an
inadequate response to methotrexate
TREATMENT PROTOCOL
NON PHARMACOLOGICAL
 REST
 EXERCISE
 DIET/ WEIGHT CONTROL
 PHYSICAL THERAPY
 OCCUPATIONAL THERAPY
 USE OF ASSISTIVE DEVICE
 SURGICAL METHODS
SURGERY
 SYNOVECTOMY—Done if synovitis doesn’t respond
to medical treatment
 Common surgeries performed in cases of RA are---
 Decompression of entrapped nerves
 Reconstructive procedures including
arthroplasty
 Corrective arthrotomies of the metatarsals
 Arthrodesis,particularly of ankle joint
THANK YOU

RHEUMATOUD ARTHRITIS PRESENTATION_111926.pptx

  • 1.
    RHEUMATOID ARTHRITIS DR BIPULBORTHAKUR PROFFESOR AND HEAD DEPARTMENT OF ORTHOPAEDICS ASSAM MEDICAL COLLEGE DIBRUGARH , ASSAM
  • 2.
    INTRODUCTION  Rheumatoid arthritsis an autoimmune inflammatory disease but mainly involves synovial joints  Peak age of onset 40-60 years  Females are more affected (3:1)  Rheumatoid arthritis is most common cause of inflammatory arthritis  Distinctive features includes peripheral small joints involvement ,symmetrical and morning stiffness
  • 3.
    RISK FACTORS  Familialand genetic risk factors –HLA DRB1 Alleles  Demographic risk factors and lifestyle factors – smoking  Chronic inflammatory mucosal conditions and infections  Occupational exposures and inhalants- silica,asbestos textile dust
  • 4.
  • 5.
    PANNUS  Thick swollensynovial membrane with granulation tissue made up of fibroblasts ,myofibroblasts and inflammatory cells,  Immune system is responsible for pannus formation.  Pannus damages Cartilage Erode bone Surrounding sof tissues
  • 6.
    CLINICAL FEATURES  MCInflammatory polyarthritis.  Appendicular dominant  Mostly involve small joints of the hands.  Axial involvement is rare  Symptoms >6 weeks duration  Inflammatory synovitis Palpable synovial swelling  Symmetrical and polyarticular (>3 joints) Typically involves wrists, MCP, and PIP joints Typically spares :DIPs of the fingers and IPs of the toes
  • 7.
    CLINICAL FEATURES  Subcutaneousor periosteal nodules at pressure points.  Ulnar deviation,  Swan-neck  Boutonniere deformities are common.
  • 8.
  • 9.
    BOUTONNIERE DEFORMITY Central slipdistruption Volar migration of lateral bands Results in flexion at PIP& hyextension at PIP
  • 10.
    SWANN NECK DEFORMITY •Lateral band injury • Results in DIP flexion and PIP Hyperextension • Also seen in volar plate laxities and ehler danlos syndrome
  • 11.
    ULNAR DRIFT  MCPJoint synovitis results loosening of the joint weakness capsule and ligaments around the joint results extensor tendon shifting to the web spaces
  • 12.
    GAMEKEEPER THUMB ARTHRITISMUTILANS  Synovitic destruction of ulnar collateral ligament of thumb results in ligament laxity  Shortening of fingers due to destruction phalanges  Excessive skin folds resembles opera glass appearence
  • 13.
    WRIST DEFORMITY RA inwrist mainly affects  Ulnar styloid  Ulnar head  Mid portion of scaphoid synovitis of DRUJ causes stretching of ulnar carpal ligament complex results in ulna subluxuates dorsally results in dorsal prominence of ulna.  DRUJ Instability demonstrated by piano key sign.  Z Deformity ( radial deviation of metacarpal and ulnar deviation of phalanx)
  • 14.
    TENOSYNOVITIS EXTENSOR FLEXOR  Canbe 1st presenting symptom of RA.  Painless soft tissue mass over dorum of wrist.  May be associated with DRUJ Injury.  Rupture of extensor tendon results in VAUGHAN JACKSON SYNDROME  Rare  Painful soft tissue mass over volar surface of wrist and restrict flexion  Rupture of FPL tendon resuts in MANNERFELT NORMAN SYNDROME
  • 15.
    FOOT  Earliest changeseen in 4th and 5th metatarsal phalangeal joints.  The initial symptoms could be swelling and stiffness including ankle joint.  LANOIS DEFORMITY- Dorsal subluxuation of metatarsal phalangeal joints with fibular deviation.  Flattening and collapse of arch of foot are the common deformities
  • 16.
    ELBOW  Effusion  Ulnarneuropathy  Subcutaneous nodules
  • 17.
  • 18.
    DIGNOSIS 1. LABORATORY: HB –Normocytic normochromic anemia due to anemia of chronic disease. Degree of anemia directly proportionate to activity of the disease. CRP increased ESR increased Platelet- Thrombocytosis 2. SEROLOGY: RHEUMATOID FACTOR:  Antibodies that recognize Fc portion of IgG  Can be IgM,IgG,IgA.  Clinical practice, IgM RF is usually measured
  • 19.
    ANTI CCP  Antibodiesto cyclic citulinated peptide have a sensitivity of 78% and specificity of 96% for RA.  40 % seronegative RA are Anti CCP positive.  Level of CCP is directly correlated with the development of erosions  Negative  Low-moderate (35-200)  High CCP (>200)  Useful in monitoring prognosis of the disease
  • 20.
    IMAGING  X RAY EARLY STAGE(SYNOVITIS):  Soft tissue swelling, periarticular osteopenia  LATER STAGE(DESTRUCTIVE):  Juxta- erosions, narrowing of joint space  ADVANCE STAGE(DEFORMITY):  Articular destruction and joint deformity
  • 22.
    MRI 1. JOINT EFFUSION 2.MARROW EDEMA 3. SYNOVIAL INFLAMMATION
  • 23.
    USG • Joint spacewidening • Fluid collection • Synovial hypertrophy • Cartilage defects • Bone erosions • Tendon sheath widening and tears
  • 24.
  • 25.
    MANAGEMENT  There isno cure for rheumatoid arthritis  Aim to delay progression of the disease, alleviate symptoms, reduce functional limitation  Supportive and palliative
  • 26.
    DRUGS 1. NSAIDs  Ibuprofen,indomethacin, COX-2 inhibitors like calecoxib and valdecoxib (reduce inflammation and relieves pain) 2. Analgesics  Morphine and acetaminophen (reduce pain) 3. Glucocorticoids or prednisolone  Prescribed in a small dose to slow joint damage caused by inflammation
  • 27.
    DRUGS 4. DMARDS : Methotrexate, Hydroxychloroquine, azathioprine, sulfasalazine  New: Leflunomide, Etanercept 5. Biologic Response Modifiers  Abatacept,Etanercept, Infliximab, Adalimumab, Anakinra, Rituximab
  • 29.
    METHOTREXATE • 1ST line ofchoice in RA • MOST POTENT • Adenosine efflux mechanism • DOSE:10-25 mg/week • Side effects:  diarrhea, stomatitis  hepatotoxic  bone marrow suppression  ILD • Follow up: Baseline CBC,LFT every 3 month • C/I in pregnancy
  • 30.
    LEFLUNOMIDE • Secreted inbile • Loading dose 100mg/day for 3-5 days then Maintenance dose 20 mg/day • Severe hepatotoxicity.should not be considered with methotrexate. • Contraindicated in pregnancy and breast feeding.
  • 31.
    SULFASALAZINE • Safe inpregnancy • 500 mg -2 gm/day oral • Sulfa group of drugs causes granulocytopenia and reduced sperm count • C/I in G6PD deficiency anemia
  • 32.
    HYDROXYCHLOROQUINE • 1st choice ofdrug in pregnancy • Least effective among all 4 drugs,preferred in mild cases • 200-400 mg/day • Side effects:  bulls maculopathy  phototoxicity  torsades de pointes • Follow up: fundoscopy annually and ECG
  • 33.
    BIOLOGICS  These aremonoclonal antibodies derived from live cell cultures  They act on specific pathogic processes ,effect faster disease control,are effective even when DMARDs fail, and prevent or radiological worsening of joints.  Side effects:  High cost  Parentral admissions  Risk of infections  Unknown long term adverse effects
  • 34.
    MECHANISM OF ACTION TNF-αBLOCKERS: •Infliximab •Certolizumab •Adalimumab •Golimumab •Etanarcept IL-1 BLOCKERS: Anakinra 3. IL-6 BLOCKERS: Sarilumab Tocilizumab 4. T Cell MODULATOR: Abatacept Anti CD20: Rituximab
  • 35.
    IMMUNOLOGICS • TOFACITINIB -blocks JAK 1/3 • BARICITINIB – blocks JAK 1/2 • Tofacitinib was approved by the FDA in June 2012 at a dose of up to 5 mg administered twice daily for the treatment of moderate-to-severe RA with an inadequate response to methotrexate
  • 36.
  • 37.
    NON PHARMACOLOGICAL  REST EXERCISE  DIET/ WEIGHT CONTROL  PHYSICAL THERAPY  OCCUPATIONAL THERAPY  USE OF ASSISTIVE DEVICE  SURGICAL METHODS
  • 38.
    SURGERY  SYNOVECTOMY—Done ifsynovitis doesn’t respond to medical treatment  Common surgeries performed in cases of RA are---  Decompression of entrapped nerves  Reconstructive procedures including arthroplasty  Corrective arthrotomies of the metatarsals  Arthrodesis,particularly of ankle joint
  • 39.