Rheumatoid arthritis #physicaltherapy #characteristic #management

2. Definition:
-an autoimmune disease in which the joint
lining and occasionally other tissues
become inflamed as a result of
overactivity of the body’s immune
system. RA is a chronic, systemic,
inflammatory disorder that primarily
involves the joints.

3. Epidemiology:
 10 cases per 1000 people, or ~ 2.1 million
adults in the United States
 Affects women two top four times more
often than men at all ages
 There is general increase in prevalence for
both sexes with increasing age
 There is lower prevalence of RA in native
Japanese and Chinese compared to whites

4. Etiology:
 like many other chronic diseases, the etiology of
RA is unknown
 Current research is based on a complex, but as yet
incomplete, appreciation of the functions of the
immune system
 Based on the fact that individuals with RA
produce antibodies to their own
immunoglobulins, there is some reason to believe
that RA is an autoimmune disorder. It is not clear,
however, whether this antibody production is a
primary event or results as a response to a specific
antigen from an external stimulus
 A specific etiological agent for RA has not been
identified

5. Etiology:
 Rheumatoid factors (RF) have received
considerable attention in the search for a
causative agent in RA because they are
found in the sera of approximately 70% of
all patients with RA
 Recent studies have also sought to establish
a genetic predisposition to the development
of RA. Human leukocyte antigens
(HLAs)are found on the cell surface of most
human cells and are capable of generating
an immune response when genetically
incompatible tissues are grafted to each
other for example, during organ transplants.

6. Pathophysiology:
 Long-standing RA is characterized by
the grossly edematous appearance of
the synovium with slender villous or
hair-like projections into the joint cavity
 There are distinctive vascular changes,
including venous distention, capillary
obstruction, neutrophilic infiltration of
the arterial walls, and areas of
thrombosis and hemorrhage

7.  Pannus – synovial proliferation of
vascular granulation tissue, dissolves
collagen as it extends over the joint
cartilage. Granulation tissue will
eventually result in adhesions, fibrosis or
bony ankylosis of the joint

8. Pathophysiology:
 Chronic inflammation can also weaken the
joint capsule and its supporting
ligamentous structures, altering structure
and function
 Tendon rupture and fraying tendon
sheaths may produce imbalance muscle
pull resulting in deformities seen in
advanced RA

9. Pathophysiology:
 Key features of a synovial joint that differentiates
it from other types of joints are the features that
make it susceptible to persistent inflammation
 High molecular weight substances such as
macroglobulins and fibrinogens can pass through
the synovial capillaries during periods of
inflammation and are not easily cleared. Because
the cartilage is avascular, antigen-antibody
complexes may be sequestered within the joint
cavity and may facilitate a process of phagocytosis
and further development of pannus.

10. Pathophysiology:
 In established synovitis,
polymorphonuclear (PMN) leukocytes
are chemotactically drawn into the joint
cavity and contribute to the inflammatory
destruction of the synovium. It is known
that the lysosomal enzymes, which are
released from these leukocytes, can
directly injure synovial tissues

11. Clinical Manifestations:
The 1987 Revised Criteria for the Classification of
Rheumatoid Arthritis
1. Morning stiffness
-Lasts at least an hour before maximal improvement
2. Arthritis of three or more joint areas
-at least three joint areas simultaneously have had soft
tissue swelling or fluid (not bony overgrowth alone)
3. Arthritis of hand joints
-at least one area is swollen (wrist, MCP, or PIP joints)
4. Symmetric arthritis
-simultaneous involvement of the same joint areas on
both sides of the body

12. 5. Rheumatoid nodules
-subcutaneous nodules over bony prominences or
extensor surfaces
6. Serum rheumatoid factor
-abnormal amount
7. Radiographic changes
-include erosions or unequivocal bony
decalcification localized in or most marked
adjacent to the involved joint
The joint signs and symptoms described in criteria
1-4 must have lasted for at least 6 weeks.

13. Signs and symptoms:
 Systemic manifestations
-morning stiffness, anorexia, weight loss, fatigue
 Joint involvement
-marked bilateral and symmetrical patterns
-arthralgia, crepitus
 Cervical spine
-50% takes place at the atlanto-axial joint
-ankylosing spondylitis
 Temporomandibular joints
-results in an inability to open the mouth fully with
normal side-to-side gliding
-normal approximation of the upper and lower teeth may
also be altered

14.  Shoulder
-involvement of GH, SC, and AC joints;
scapulothoracic articulation
-degeneration, pain, LOM
-capsule and ligaments become distended with
chronic inflammation
 Elbows
-capsular and ligamentous distention, and joint
surface erosion may lead to elbow instability
-Flexion contractures may result from
persistent spasm secondary to pain

15.  Wrists
-development of flexion contractures which
ultimately diminishes the ability to execute
power grasp
-volar subluxation resulting from chronic
inflammation of the proximal carpals
-Stenosing tenosynovitis (deQuervain’s
disease) may also occur

16.  Hand joints
MCP joint:
-soft-tissue swelling; volar subluxation; ulnar drift
PIP joint:
-swelling(sausage-like finger)
-Swan-neck deformity
-Boutonniere deformity
-Bouchard’s nodes
DIP joint:
-Heberden’s nodes
-mallet finger

20.  Thumb:
-Type I deformity – MCP flex; IP hypext; without
CMC involvement
- Type II deformity – CMC is subluxed; IP hypext
- Type III deformity – CMC subluxed; MCP hypext;
more commonly found in RA
 Mutilans Deformity (Open-Glass Hand):
-grossly unstable thumb and severely deformed
phalanges
-transverse folds of the skin resemble a folded
telescope

21.  Hip
-less commonly involved in RA
-severe inflammatory destruction of the
femoral head and the acetabulum may push
the acetabulum into the pelvic cavity
(protrusio acetabuli)
 Knees
-distention of the joint capsule and
attenuation of ligaments
-painful knees may be held in slightly flexed
positions, ultimately resulting to flexion
contractures

22.  Ankles and feet
-hindfoot pronation
-flattening of the medial longitudinal arch
-calcaneal exostoses
-splayfoot
-metatarsalgia
-hallux valgus and bunion
-hammer toes
-cock-up or claw toes

24.  Muscle involvement
-muscle weakness – may be due to either
reflex inhibition secondary to pain or
atrophy
 Tendons
-tenosynovitis – may eventually lead to a
tendon rupture
-lag phenomenon – refers to a substantial
difference between passive and active ROM

25.  No single test is definitive in diagnosing RA.
 Typical laboratory findings in active disease include:
 – Rheumatoid factor (see further detail below)
 – Elevated acute phase reactants: ESR and C-
reactive protein (CRP)
 – CBC: thrombocytosis, hypochromic
microcytic anemia, eosinophilia
 – Synovial fluid analysis (see below)
 – Antibodies to cyclic citrullinated peptides
(CCP): specific for RA and correlated with
aggressive disease

26. Synovial Fluid in RA
 • Low viscosity
 • WBC: 1,000–75,000/mm3
 • > 70% PMNs
 • Transparent—cloudy
 • Hypergammaglobulinemia
 • Hypocomplementemia
Rheumatoid Factor (RF) in RA
 • 85% of the patients with RA are RF (+).
 • The other 15% of patients with RA are RF (–) A ACR
criteria are fulfilled with other positive findings (see
above).
 • Associated with increased severity of disease with
increased systemic manifestations.
 • Serial titers are of no value.
 • RF (+) can be seen in other diseases: rheumatic (SLE,
scleroderma, Sjogren’s), viral, parasitic, bacterial,
neoplasms, hyperglobulinemic.

27.  Increased ESR and CRP
 • Acute phase reactants
 • Markers for inflammation
 • Nonspecific and not used in diagnosis
 • Indicate inflammation/inflammatory
disorder: nonspecific for RA.

28. Impairments and Complications:
 Neurological Manifestations
-mild neuropathies which result from nerve
compression, such as carpal tunnel or tarsal tunnel
syndromes
 Cardiopulmonary Complications
-pericarditis (seen in 4% of the patients)
-pleuritis
 Ocular manifestations
-dry eyes, associated with Sjogren’s syndrome

29. Impairments and Complications:
 Deconditioning
-compounded by inadequate levels of regular physical
activity
-Marked degree of cachexia and elevated resting
energy expenditure
-it appears that immune e system activity and
inflammation creates increased metabolism
 Rheumatoid nodules
-usually asymptomatic, although they can be tender
and may cause skin breakdown or become infected
 Vascular complications
-foot and wrist drop may occur as a result of vasculitis
of the vasa arteriosum to the nerve supply of the radial
or superficial peroneal nerves

30. Classification of Progression of Rheumatoid Arthritis
Stage I, Early
1. No destructive changes on radiographic examination
2. Radiographic evidence of osteoporosis may be
present
Stage II, Moderate
1. Radiographic evidence of osteoporosis, with or
without slight subchondral bone destruction; slight
cartilage destruction may be present
2. No joint deformities, although limitation of joint
mobility may be present
3. Adjacent muscle atrophy
4. Extra-articular soft tissue lesions, such as nodules
and tenosynovitis may be present

31. Stage III, Severe
1. Radiographic evidence of cartilage and bone
destruction, in addition to osteoporosis
2. Joint deformity, such as subluxation, ulnar
deviation, or hyperextension, without fibrous or
bony ankylosis
3. Extensive muscle atrophy
4. Extra-articular soft tissue lesions, such as
nodules and tenosynovitis may be present
Stage IV, Terminal
1. Fibrous or bony ankylosis
2. Criteria of Stage III

32. Medical Management:
Treatment Options for Rheumatoid Arthritis
 Medication
 DMARDs (disease-modifying antirheumatic
drugs)
 BRMs (Biologic response modifier)
 Corticosteroids
 NSAIDs
 Surgery
 Synovectomy
 Arthrodesis
 Tendon reconstruction

33. PT Management:
Exercise, Equipment, and Education
Treatment Options in Rheumatoid Arthritis
 Passive treatments
 Cold/heat
 Compression and elevation
 Massage
 TENS
 Acupuncture
 Orthosis

34.  Exercises
 LE strengthening
 Walking
 Whole-body physical activity
 Jogging in water
 Combined LE strengthening, flexibility, and
mobility
 Aerobic exercises
 LE range of motion, mobility, or flexibility
 Manual therapy with exercises

35.  Equipment
 Adaptive for ADL
 Assistive for ambulation
 Appropriate footwear or insoles
 Education
 Self-management
 Weight loss (if obese)
 Activity management or joint protection
 Social support
 Stress management/relaxation

43. ACR Revised Criteria for Classification of
Functional Status in Rheumatoid Arthritis
Class I
 Completely able to perform usual ADLs (self-
care, vocational, and avocational)
Class II
 Able to perform usual self-care and vocational
activities, but limited in avocational activities
Class III
 Able to perform usual self-care activities, but
limited in vocational and avocational activities
Class IV
 Limited in ability to perform usual self-care,
vocational, and avocational activities

44. SOURCES:
 O’Sullivan, S., Schmitz, T. (2007). Physical
Rehabilitation (5th ed., pp. 1075-
1083).Philadelphia, PA: F.A. Davis Company.
 Braddom, R. (2011). Physical Medicine and
Rehabilitation (4th ed., pp. 1419). Singapore:
Saunders Elsevier