The document discusses rheumatoid arthritis (RA), a chronic inflammatory disease that affects the joints and can damage heart tissue over time. It provides definitions of RA, discusses common symptoms like joint pain and stiffness, outlines diagnostic criteria and investigations used to diagnose the condition, such as checking for rheumatoid factor in the blood. The document also summarizes the pathological stages of RA and long term effects like joint deformity and disability.

1. The disease which hurts the
joints and kills the heart

3. Q: What do comedienne Lucille Ball, French
painter Pierre-Auguste Renoir, Hollywood
actress Kathleen Turner and heart transplant
surgeon Dr. Christiaan Barnard have in
common?

4. Rheumatoid
Arthritis [RA]

5. Definition
 RA is a non-suppurative, systemic inflammatory
disease of unknown cause characterized by a
symmetrical poly-arthritis affecting peripheral joints
& extra articular structures.
 It is a chronic inflammatory disease affecting the
synovium & leading to joint damage & absorption of
adjacent bone.
 The course of disease is variable but tend to be
chronic & characterized by exacerbations &
remissions.

6. INTRODUCTION
 Chronic systemic inflammatory disease of unknown
etiology
 Affects the synovial membranes of multiple joints
 Prevalence 1-2% of the population
 0.7% in rural area Indians
 Female : Male ratio 3:1
 Usual age of onset 20-40 years though individuals
of any age group may be affected

7. Hypothesized causes
1. Initiating factor therapy:
 An initiating factors causes joint inflammation
 It does not switch off after acute episode
2. Infectious theory:
 Infection from diphtheroids & mycoplasms or from the
viruses – rubella, harpes zoster
3. Genetic predisposition:
 Relative of people with RA are more prone to develop
the disease than rest of population.

9. Genetics of RA
 Genetic factors gives prevalence of 2%–12% in
first-degree relatives of RA sufferers – i.e. approx
ten times that of other population.
 The human leukocyte antigen (HLA) component
accounts for around 30% of the genetic risk.

10. 1987 AMERICAN COLLEGE OF
RHEUMATOLOGY CRITERIA FOR RA
 Patients must have 4 of the 7 criteria:
1. Morning stiffness lasting at least 1 hour*
2. Swelling in three or more joints*
3. Swelling in hand joints*
4. Symmetric joint swelling*
5. Erosions or decalcification on x-ray of hand
6. Rheumatoid nodules
7. Abnormal serum rheumatoid factor.
[*Must be present at least six weeks]

11. American Rheumatology Association
Remission Criteria for RA (Eberhardt a Fex 1998)
 4 or more of the following criteria must be fulfilled
for at least 2 consecutive months:
1. Duration of morning stiffness not exceeding 15 min
2. No fatigue
3. No joint pain (by history)
4. No joint tenderness or pain on motion
5. No soft tissue swelling in joints or tendonsheaths
6. ESR<30mm after 1 hour for a female or <20mm after 1
hour for a male

12. Pathology
 RA is generalized disorder of connective tissue
affecting –
 Articular structure &
 Extra articular structures

13. Progressive changes in joints
 Stage I:
 Inflammation of the synovial membrane spreads to articular
cartilage & other soft tissues.
 Limitation of joint movt with pain & muscle spasm

14. Stage II:
 Granulation tissue formation within synovial membrane
& spread to periarticular tissue.
 Cartilage disintegration & joint filled with granulation
 Thickening of joint capsule, tendon (with sheaths) &
impaired joint movt permanently.

15. Stage III:
 Granulation tissue converted into fibrous tissue with
adhesion formation between tendon, joint capsule &
articular surface.
 Articular surface cover partly by cartilage & partly by
fibrous tissue.

16. Stage IV:
 Permanent joint damage and deformity  disability

17. Extra articular changes
 Nodule formation:
 In the pressure area & may be
subcutaneous or intracutaneous.
 They may present in organs such as
lung & heart.
 Vascular changes:
 It constitute inflammation of all size
arteries.
 The lumen of small vessels can
become obliteration.

18. Clinical feature
Articular features
 Pain  Loss of function
 Tenderness  Stiffness
 Swelling  Deformity
 Warmth over the joint  Muscle wasting
 Erythema  Decreased ROM

19. Common Extra Articular Feature of RA
Nodules, Anaemia, Lymphadenopathy,
Systemic
Amyloidosis, Vasculitis, Felty’s Syndrome
Ocular Keratoconjunctivitis, Scleritis & Episcleritis
Bone Osteoporosis
Peripheral nerve entrapment, Peripheral
Neurology neuropathy, Cervical spine instability, Cervical
cord compression, nerve root compression
Pleuritis, Pleural effusion, Pulmonary alveolitis
Pulmonary
and fibrosis
Pericarditis & myocarditis, Pericardial effusion,
Cardiovascular
Conduction defect, Atherosclerosis

20. CLINICAL FEATURE
 Swelling is confined to the
area of the joint capsule
 Synovial thickening feels
like a firm sponge
 Prominent ulnar deviation in
the right hand
 MCP and PIP swelling in
both hands
 Synovitis of wrist

21. Commonly affected joints
Temporomandibular 20-30%
Cervical spine 40-50%
Shoulder 50-60%
Elbow 40-50%
Wrist 80-90%
MCP 90-95%
PIP 65-90%
Hip 40-50%
Knee 60-80%
Ankle 50-80%
MTP 50-90%

23. Common Deformities in RA
UPPER LIMB
Shoulder girdle Protraction
Shoulder Flexion, adduction, medial rotation
Elbow Flexion, increase carrying angle
Forearm Pronation
Wrist Volar subluxation, flexion, radial deviation
MCP Volar subluxation, flexion, ulnar deviation
Boutonniere (flexed PIP, hyper extended DIP)
PIP & DIP
Swan neck (hyper extended PIP, flexed DIP)
LOWER LIMB
Hips Flexion, adduction, lateral rotation
Knees Flexion, valgus
Ankle valgus
MTP Plantar subluxation, hyper extended
PIP & DIP flexion

25. Referral, Diagnosis And
Investigations

26. Referral for Specialist Treatment
 Refer for specialist opinion with any person
suspected persistent synovitis of undetermined
cause.
 Refer urgently if any of the following apply:
1. The small joints of the hands or feet are affected
2. More than one joint is affected
3. There has been a delay of 3 months or longer between
onset of symptoms and seeking medical advice.

27.  Do not avoid referring urgently any person with
suspected persistent synovitis of undetermined
cause whose blood tests show a normal acute-
phase response or negative Rh factor.

28. Elbow=48
Wrist=32
MCP=5
PIP=3
Knee=95
Ankle=32
MTP=3

29. Investigation
 There is no single diagnostic test for RA
 Investigations are used to support the clinical
diagnosis and negative results do not exclude
the diagnosis of RA
 No of test are available with rheumatologist
to rule out the different remarks of the disease
 Acute phase reactants, Autoantibodies, Synovial fluid
examination, radiography, newer markers of inflammation etc

30. Investigations helpful in Dx of RA
 Acute phase reactants (APRs)  Uric acid/ Synovial fluid
 Erythrocyte sedimentation analysis
rate (ESR)  Urinalysis
 C-reactive protein (CRP)  Bone marrow examination
 Full blood count (FBC)  Thyroid function
 Rheumatoid factor (RF) (TSH, T3,T4)
 Antinuclear antibody (ANA)  Hepatic enzymes
 Urea & electrolytes (U&E) (SGOT, SGPT, alkaline
phosphatase)
 Liver function tests (LFT)
 Muscle enzyme (CPK,)

31. Acute phase reactant
 These are the proteins produce by hepatocytes
 Synthesis is effected by the proinflammatory
cytokines IL-6, IL-1 &TNF-alfa
 The concentration of these protein may-
 Increase (+ve APRs)
 Decrease (-ve APRs)

32. Positive acute phase reactant
Ceruloplasmin
Mild elevation Complement C3
Complement C4
Alfa1-acid glycoprotein
Alfa1-proteinase inhibitor
Moderate elevation
Haptoglobin
Fibrinogen (causing elevate ESR)
C reactive protein
Marked elevation
Serum amyloid A protein
Negetive acute phase reactants
Albumin
Transferrin

33. Erythrocyte sedimentation rate (ESR)
 ESR has been using as a reliable indicator of
inflammation & still clinically useful
 Rises >24 hours after inflammation onset and
symptoms
 Gradually returns to normal 4 weeks after resolution
 It is a measure of rouleaux formation which is
dependent on the concentration of –
 Fibrinogen, Immunoglobulin & Some other plasma protein
 Normal ESR is – 0–20mm in females, 0–15 in male

34.  In rheumatology -
 Elevated ESR increases the probability of
inflammatory arthritis, whereas a normal ESR
increases the probability of non-inflammatory
condition like mech. pain
 Moderately elevated ESR can help to asses the disease
activities in RA

35. C-reactive protein
 It raises 24 hr after the onset of inflammation.
Short half life of 5-7 hours
 Rapidly declines after condition resolves
 Can raises up to 1,000 fold
 It is a sensitive & early indicator of inflammation
 The normal concentration is less then 0.6 mg/dl
 In rheumatic conditions
 The level range between 1-10 mg/dl except in systemic
vascuities (500 mg/dl)

36. Rheumatoid Factor
 Rheumatoid factor (RF) is a term used to describe a
group of autoantibodies
 The RF test is considered the basic screen and
hallmark for the autoimmune disorder RA
 The three subclasses of RF include IgM, IgA and
IgG autoantibodies. Most tests for RF measure each
of these subtypes

37.  The simultaneous presence of all 3 types is usually
only seen in RA
 In patients with RA, IgM RF predominates & the
other subtypes are usually present in lower amounts
 It is found in the sera of 80% of pts with RA
 Extra-articular features of RA are common in pts
with high concentrations of rheumatoid factor
 But it is a poor guide to the severity of joint disease
& to the success or otherwise of Rx

38. Antinuclear antibody (ANA)
 The test is to exclude the systemic lupus erythromatus when
the test is negative
 Presence of ANA increases the likelihood of an autoimmune
disease
 It checks blood levels of antibodies that are often present in
connective tissue diseases or other autoimmune
disorders, such as lupus
 There are also tests for individual types of ANA’s that may
be more specific to people with certain autoimmune disorders
 ANA’s are also sometimes found in healthy people
 Therefore, having ANA’s in the blood does not necessarily
mean that a person has a disease

39. Urea & electrolytes (U&E)
 Mild elevation of alkaline phosphatase and
gamma-GT in rheumatic conditions

40. Uric acid/ Synovial fluid analysis
 It is a simple test & provides valuable information
specially in mono arthritis patient
 Joint aspiration is done to obtain a sample of
synovial fluid
 The test provides important diagnostic information
whether
 Crystals (found in pts with gout or other types of crystal-
induced arthritis)
 Bacteria or viruses (found in pts with infectious arthritis)
are present in the joint.

41. Classification of Synovial fluid finding
Non inflammatory Inflammatory
Normal Septic
(OA) (RA)
Colour Colourless Straw to yellow Yellow Variable
Clarity Transparent transparent Translution Opaque
Viscosity High High Low Variable
Mucin clot Firm Firm Friable Friable
Cell count/ul <200 200 - 2,000 2,000 - 75,000 > 10,000
Polymorphs < 25% < 25 % > 50 % > 75 %
Culture Sterile Sterile Sterile Positive

42. Urinalysis
 In this test, a urine sample is studied for
protein, RBC, WBC or casts
 These abnormalities indicate kidney
disease, which may be seen in several rheumatic
diseases such as lupus or vasculitis
 Some medications used in the Rx of arthritis can
also cause abnormal findings on urinalysis

43. Complete blood count (CBC)
 CBC determines the number of WBC, RBC &
platelets present in a sample of blood
 Some rheumatic conditions or drugs used to treat
arthritis are associated with a low WBC
(leukopenia), low RBC (anemia), or low platelet
count (thrombocytopenia)
 When doctors prescribe medications that affect
the CBC, they periodically test the patient’s blood

44. White blood cell count (WBC)
 This test determines the number of WBC present
in a sample of blood
 The number may increase as a result of infection
or decrease in response to certain medications, or
with certain diseases, such as lupus
 Low numbers of WBC increase a person’s risk of
infections

45. Hematocrit (PCV, packed cell volume)
 This test and the test for hemoglobin measure the
number of RBC present in a sample of blood
 A decrease in the number of RBC (anemia) is
common in people with inflammatory arthritis
and rheumatic diseases.

46. Liver function
 Tests for liver function may give abnormal results
in patients with RA
 Serum concentrations of transaminases & alkaline
phosphatase may be moderately elevated when
the disease is active

47. Thyroid function (TSH, T3, T4)
 It was found that the mean T4 levels in the RA
patients were significantly higher
 T3 levels were more than 2 SD above controls
 T4 levels were higher in 27 patients
 TSH levels were more than 2SD above
 Thyroid hormonal defects are related with the disease
duration & not with the disease activity

48. Bone marrow examination
 There is mounting evidence that osteoclasts are
involved in the pathogenesis of a component of
the focal bone erosions in RA

49. Muscle enzyme (CPK)
 Patients with RA usually have low Creatine
Kinase (CK) values
 Even mild rise in CK levels may suggest presence
of polymyositis, which may be confirmed on
muscle biopsy
 High incidence of vasculitis in biopsied muscle
suggests that it may be the primary event in the
pathogenesis of myositis in RA

50. Labs (ARA recommended, but
do not exclude diagnosis)
 Initial Labs
 Complete Blood Count with differential
 Rheumatoid Factor (Initially positive in 70%)
 Sedimentation Rate (ESR) or C-Reactive Protein (C-RP)
 Additional labs in preparation for rheumatic agents
 Liver Function Tests
 Renal Function tests
 Markers of disease course
 C-Reactive Protein (C-RP)
 Erythrocyte Sedimentation Rate
 Wrist X-Ray or Ankle X-Ray
 Anticyclic citrullinated peptide antibody

51. Laboratory findings in RA
 Anaemia: normochromic or hypochromic, normocytic (if
microcytic consider iron deficiency)
 Thrombocytosis
 Raised erythrocyte sedimentation rate
 Raised C reactive protein concentration
 Raised ferritin concentration as acute phase protein
 Low serum iron concentration
 Low total iron binding capacity
 Raised serum globulin concentrations
 Raised serum alkaline phosphatase activity
 Presence of rheumatoid factor

52. Other causes of positive test for
rheumatoid factor
 Other connective tissue diseases
 Viral infections
 Leprosy
 Leishmaniasis
 Subacute bacterial endocarditis
 Tuberculosis
 Liver diseases
 Sarcoidosis
 Mixed essential cryoglobulinaemia

53. Differential diagnosis of RA
 Psoriatic arthritis--always seronegative
 Primary nodal osteoarthritis
 Other connective tissue diseases – SLE
 Calcium pyrophosphate deposition disease
 Polyarticular gout
 Fibromyalgia
 Medical conditions presenting with arthropathy –
thyroid disease

54. Clinical problem Provisional diagnosis Test to order
Monoarthritis Septic arthritis Synovial fluid examination (SFE)
Gout SFE Serum uric acid
Osteoarthritis Radiography
Tuberculosis Radiography, SF Culture
None SFE
Chronic Rheumatoid arthritis Hb, ESR, RF, X-Rays, CRP
polyarthritis Systemic lupus CBC, ANA, Anti-dsDNA,C3,C4,
erythromatus Urine examination
Psoriasis CBC, X-Ray
CBC, ANA, RF, Anti-Ro & La,
Sjogren's syndrome salivary gland biopsy
Muscle enzyme, EMG,ANA,
Inflammatory myositis Muscle biopsy

55. Principles of Treatment
 Early initiation of treatment
 Multidisciplinary team approach
 Patient education
 Assessment of response to treatment
 Hospital admission
 Complication (cost) of untreated disease

56. Early initiation of Treatment
 Goals of early treatment
 Symptom control
 Reduction of joint damage & disability
 Maintenance or improvement of quality of life

57. Multidisciplinary team approach
 GP
 Rheumatologist
 Physical therapist
 Occupational therapist
 Nurse specialist
 Dietitian
 Podiatrist
 Pharmacist
 Social worker

58. Patient education
 Should be adopted by all members of
multidisciplinary team in both 1ry & 2ndry care.
 Should be provided with an information on
booklet & if possible one to one education.

59. Assessment of response to Rx
 Quantification of disease activity & outcome is
important in assessing, comparing &
standardizing treatment of RA.

60.  Clinical measures of response to Rx includes –
 Patient opinion
 Physician opinion
 Extend of synovitis (no of swollen or tender or both)
 Duration/ severity of stiffness after inactivity
 Functional ability
 Laboratory measures of response to Rx includes –
 Acute phase response (ESR, CRP)
 Anaemia
 Radiological progression

61. Hospital admission
 Multiple joint involved acute phase patient may
required hospitalization.
 Selective patient may benefit from more intensive
hospital based Rx from multidisciplinary team.
 It is essential to maintained specialist IP facilities
for selected RA patients.

62. Complication/ Cost of untreated
disease
 Personal costs –
 Lost work opportunities
 Decreased leisure activities
 Stress on relationships
 Costs to society –
 Loss of working skills of RA individuals
 Loss of contributions to the home
 The burden of economic cost for care

63. Management
 Pharmacological management
 Analgesics –
 Simple analgesics should be used in place of NSAIDs
 Paracetamol, Codeine Or Compound Analgesics
 DMARDs should be introduced to suppress
disease activity.
 Cyclo-oxygenase-2 (COX-2) Inhibitors.

64. Diet and complementary therapies
 Inform people with RA that there is no strong
evidence that their arthritis will benefit with diet.
 However, they could be encouraged for the
principles of a Mediterranean diet
 Mediterranean Diet:
 More Bread, Fruit, Vegetables & Fish
 Less Meat & Replace Butter & Cheese With Products
Based On Vegetable And Plant Oils.
 Fasting has shown to be benefit in some patient.

65. Diet and complementary therapies
 Complementary therapies that although some may
provide short-term symptomatic benefit, there is
little or no evidence for their long-term efficacy.
 If a person with RA decides to try complementary
therapies, advise them:
 These approaches should not replace conventional Rx
 This should not prejudice the attitudes of members of
the multidisciplinary team, or affect the care offered.

66. Approach to PT Assessment
 Note the time of day you make assessment; this
could be very important for reassessment as many
patients have variation in symptoms throughout
the day.
 For example, if you carried out your initial assessment
early in the morning, then reassessed at midday, you
could get very different responses because ........???
 By noon her morning stiffness would have eased.

67. assessment

68. Subjective Assessment
 Demographic details & history of present
condition
 General health and past medical history
 Present medication and drug history
 Splints
 Social history

69. Objective Assessment
 General observation
 Joints involved
 Extra-articular manifestations
 Functional assessment

70.  How long does her morning stiffness last?
 Does she have any systemic symptoms that might
impact upon your ideas for management?
 e.g. has the RA affected her heart or does she fatigue
easily?
 Has she had any physiotherapy before and how
has she responded?

71. Problem list
 Pain in all joints affected especially hips & knees
 Reduced range of movement in all affected joints
 Reduced muscle strength
 Reduced mobility both in bed & during
locomotion (no longer able to get around with
walking frame)
 Reduced function.

72. Aims of Physiotherapy Rx
 To reduce pain & stiffness
 To maintain or increase ROM in affected joints
 To maintain or increase muscle strength in
affected groups
 To prevent deformities
 To maximise function, independence and quality
of life

73. An Approach to Physiotherapy Rx
 Despite pharmacological advances in Rx of RA
many patients still present with functional deficits
who need physiotherapy.
 According to World Confederation of Physical
Therapists (WCPT)
 Physiotherapy is ‘concerned with identifying &
maximizing movement potential, within the spheres of
promotion, prevention, treatment and rehabilitation’.

74. WCPT components of
physiotherapy interventions
 Thermotherapy – hot/cold packs, paraffin/wax
baths and infrared.
 Ice application –
 It provides cooling to skin temp which is raise by
inflammation.
 Cooling will diminish the rate of swelling &
production of irritants.
 It also helps in alleviate some of pain.
 Ice can be applied regularly @ 2/day

75.  Heat application –
 Acute conditions – Heat application to the inflamed
joint is not recommended.
 Chronic conditions – Thermotherapy, especially
paraffin baths combined with ex, should included as an
intervention to improve ROM & decrease pain &
stiffness.

76. Therapeutic ultrasound
 Therapeutic US without additional therapeutic
interventions is effective for reducing joint
tenderness caused by RA.
 Continuous US is more effective for patients with
chronic RA.
 Mechanical effect of both pulsed & continuous US
increases skin permeability, thus decreasing
inflammatory response, reducing pain & facilitating the
soft tissue healing process.

77.  Both pulsed and continuous US reduce nerve
conduction velocity of pain nerve fibres.
 Continuous US, however, has thermal effects that
reduce muscle spasms and pain.
 The thermal effects also cause vasodilatation,
which enhances the excretion of chronic
inflammatory cells.

78. Pulse electromagnetic energy
 There is minimal literature of PEME in RA
 But in some studies it has shown to be effective

79. Interferential therapy
 Helps in minimizing pain in RA
 The electrodes needs to place carefully in pts with
high dose steroid
 Used of such modalities may addicted to the patient
& when experiencing multiple joint pain it would
be impractical.
 Dosage –
 90 – 100 Hz – reduce nerve accommodation
 50 – 100 Hz – improve healing, blood supply &
membrane permeability

80. TENS
 It has been proven to be effective in managing
chronic pain.
 Different dosage may be used with disease
activity levels
 Many patient tend to substitute medication with
TENS.

81. Hydrotherapy
 Hydrotherapy produces physiological, functional
and psychological benefits.
 Long-term hydrotherapy reduces the rate of
hospital admissions and does not increase joint
destruction.
 However, it is not suitable for all RA patients due
to contra-indications and the cost of hydrotherapy
reduces its widespread availability.

82. Joint Protection & Provision of
Walking & Disability Aids / Splinting
 Provision of sticks or crutches
 Reduce lower limb loading
 Helps in pain relieve & improving mobility in RA.
 However, redistribution of load to the small joints of
the upper limbs requires especially designed walking
aids, e.g. gutter frames
 Splinting
 It can reduce pain & improve function.
 Splinting is usually applied by occupational therapists
(OTs), but a trained Therapist may supply splints.

83. Characteristics of an ideal splint
 The splint should be –
 Inexpensive
 Easy & quick to make
 Comfortable
 Light & neat
 Strong
 Functionally accurate
 Fitting optimal
 Cosmetically accepted

84. Advantage of splinting
 Correct deformities
 Provide support & rest
 Easy application & removal
 Prevent dynamic instability
 Offer functional efficiency
 Reduce the impact of unwanted force on body
 Provide means of strengthening, re-educative &
assistive aids.

85. Disadvantage of splint
 Possibility of muscular weakness & wasting
 Loss of mobility
 Tendency to fixed in one position of splint
 Fabrication, trial & application are painful.

86. Splint for swan neck deformity

87. Splint for boutonniere deformity

88. Exercise therapy
 On land & Aquatic physiotherapy includes –
 Aerobic activities,
 Flexibility
 Strengthening ex,
 Core stability ex,
 Balance rehabilitation,
 Promotion of lifestyle physical activity.

89. Manual therapy
 Manual therapy– includes –
 Mobilisation
 Manipulation
 Myofascial release
 Trigger point therapy
 Acupuncture and
 Massage.

90. Course & Prognosis of RA
 The course of disease is variable & unpredictable
 Prognosis in term of function is reasonably good:
 25 % - Remains fit for all-round activities
 40 % - Moderate impairment of function
 25 % - Badly disable
 10 % - Wheelchair dependent

91.  Prognosis is poor if –
 RH-f is high
 Erosion of the joint surface appear early
 Nodules
 Systemic manifestations

92. Reducing the risk of RA
 Health promotion
 Smoking cessation

93. Reference
 PK Pispati. Manual of Rhrumatology
 Michael L Snaith. ABC of rheumatology; London; BMJ
publishing group; 1996
 Hillary chappel et al. management of early rheumatoid
arthritis. Scottish Intercollegiate Guideline; 2000; 13-14
 Elaine Moore. Rheumatoid factor diagnosing rheumatoid
arthritis and related disorders; Mar 19, 2006
 Vinita Agrawal et al. Muscle involvement in rheumatoid
arthritis: clinical & histological characteristics and review of
literature, J Indian Rheumatol Assoc, 2003 : 11 : 98 - 103