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?
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.
8.
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.
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
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.
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.
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
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.
68. Subjective Assessment
Demographic details & history of present
condition
General health and past medical history
Present medication and drug history
Splints
Social history
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.
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
