Transcript Document

RHEUMATOID ARTHRITIS
AND REHABILITATION
Prof. Dr. Ülkü Akarırmak
Rheumatic Diseases
• Rheumatoid arthritis RA
• Ankylosing spondylitis AS
spondyloarthropathies
• Osteoarthritis OA
What is Rheumatoid Arthritis?
RA is a chronic, systemic, inflammatory condition
which:
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Affects 1-2% of the adult population
More common among women than men (2-3x)
Highest incidence between ages 40 and 60
Causes pain, disability and loss of function
Unwnown pathogenesis
RA Background
RA is a chronic autoimmune disorder
Results from the interplay between an individual's
genetic background and unknown
environmental triggers
Human leukocyte antigens (HLAs) account for
~30% of the heritable risk. Most of the genetic
components are largely unknown
RA – Etiology / Risk Factors
• Genetics
HLA – DR4
Sex
Infection
• Proteus, Mikoplazma
EBV, Parvo, HTLV–1
Smoking
Age
Pathology
• Synovial hyperplazia
• Inflammatory cells
• Increased joint fluid
• Pannus
• Invasive synovium
• Erosion in bone and
cartilage
RA – Clinic
• Morning stiffness
• Arthritis –
Sinovytis / Effusion
Swelling
• Structural changes
• Loss of cartilage
bone erosion
periarticular lesions
Joint Involvement in RA
• Peripheral synovial joints
• Hands and feet
• Symmetrical
• Especially hands
• Wrist
• MCP
• PIP (+)
• DIP (-)
RA Deformities
MTP Subluxation / Toe Deformities
Atlantoaxiell Subluxation
RA – X-Ray - Erosions
2010 ACR/EULAR
Classification Criteria for RA
JOINT DISTRIBUTION (0-5)
1 large joint
0
2-10 large joints
1
1-3 small joints (large joints not counted)
2
4-10 small joints (large joints not counted)
3
>10 joints (at least one small joint)
5
SEROLOGY (0-3)
≥6 = definite RA
What if the score is <6?
Patient might fulfill the criteria…
Negative RF AND negative ACPA
0
Low positive RF OR low positive ACPA
2
High positive RF OR high positive ACPA
3
 Prospectively over time
(cumulatively)
SYMPTOM DURATION (0-1)
<6 weeks
0
≥6 weeks
1
ACUTE PHASE REACTANTS (0-1)
Normal CRP AND normal ESR
0
Abnormal CRP OR abnormal ESR
1
 Retrospectively if data on all
four domains have been
adequately recorded in the past
The Consequences of RA
• Decline in functional status
• Work disability
• Co-morbidity
• Increased mortality
Rationale for Early Intervention
• Some patients have early progressive
disease
• Joint damage begins within 6 months 1 year of onset
• Disease modification thought to correlate
with control of inflammation
RA – Treatment
• Early agressive treatment!
• DMARD = “disease modifying anti–rheumatic
drugs”
• Combination therapy
• Biologics – TNF- inhibitors, IL–1 antagonists,
Anti–CD20, CTLA4 – Ig
• NSAIDs
• Glucocorticoid
+ Osteoporosis prevention
+ Pain medication
RHEUMATOID ARTHRITIS
MEDICATIONS
• Medications are the cornerstone of treatment for
active RA
• The goals are to control inflammation, achieve
remission, prevent further damage of the joints and
loss of function
• The type and intensity of RA treatment depends upon
individual factors and potential drug side effects –
follow-up
DMARDs
• DMARDs reduce inflammation of RA, reduce or
prevent joint damage, preserve joint structure and
function, and enable a person to continue ADL
• DMARDs include methotraxate, hydroxychloroquine,
sulfasalazine and leflunomide
• Improvement in symptoms may require 4 – 6 weeks of
treatment with methotraxate, 1 – 2 months with
sulfasalazine. Even longer durations of treatment may
be needed
Biologic Agents
• Biologics, are DMARDs
• Biologics target molecules on cells of the immune
system, joints, and the products that are secreted in the
joint
• There are several types of biologics
• Biologics that bind TNF (anti-TNF agents or TNF
inhibitors) include etanercept, adalimumab, infliximab,
ertolizumab, tosilizumab and golimumab
Biologic Agents
• Biologics tend to work rapidly, within 2 and 4 to
6 weeks
• Biologics may be used alone or in combination
with other DMARDs (methotraxate), NSAIDs,
and/or glucocorticoids or other biologics
• All biologic agents must be injected (SC, IV) and
patients have to be followed closely
NSAIDs
• NSAIDs are used to relieve pain and reduce minor
inflammation. However, NSAIDs do not reduce the
long-term damaging effects of RA on the joints
• NSAIDs have significant side effects;
GIS bleeding, fluid retention, increased risk of heart
disease
• The risks need to weighed carefully against the benefit
Therapeutic Goals
• Control of pain
• Suppression of inflammation, CRP and the
absence of swollen joints
• Control of joint damage
• Maintenance of normal ADL
• Maximization of QOL
Optimal Management Strategies
• Early diagnosis
• Early use of effective second-line agents,
including, when required, the use of agents that act at
different levels
• Rest when joints are actively inflamed
• Physiotherapy when inflammation is suppressed
(multidisciplinary approach)
Multidisciplinary Approach
• Appropriate medical treatment
• Bed rest during active disease
• Splinting of actively inflamed joints
• Pain control
• Bone-sparing agents (for osteoporosis)
The Rehab Team
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Physiatrist
Physiotherapist
Occupational therapist
Social worker
Orthopedist
Internalist
Podiatrist
Ophtalmolog
Psychiatrist etc.
Flare-up Periods
• Resting
• Splints
• Positioning
• Bed rest
Deformities in RA
Joint
Deformity
Position of Splinting
Head and neck
.Flexion, rotation .
Full extension, cervical spine,
chin forward
Wrist
Palmar flexion
30 degreees dorsiflexion
Thumb
Finger
Hips
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Knee
Flexion
Extension, apposition
. Flexion, ulnar deviation
Extension, no lateral deviation
. Flexion,adduction,
Extension, in line with body;
external rotation .
foot pointing upward
Flexion
Extension
Splinting
• Relieve pain
• Relieve muscle spasm
• Prevent deformity
Involvement of the
Lower Exremity
Nonpharmacologic Therapy
• Education program
• Physiotherapy
• Occupational therapy
• Support from social workers
Physical Therapy and Rehab
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Effective in maintaining the ROM
Strengthening of muscles
Prevent contractures
Prevent deformities
Maintain ADL
Physical and Occupational Therapy
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Preserve joint structure and function in RA
The application of heat or cold can relieve pain or
stiffness
Ultrasound may reduce inflammation in tenosynovitis
Passive and active exercises can improve and maintain
ROM
Rest and rest splinting can reduce joint pain and
improve joint function
Physical Therapy
• Finger splinting and other assistive devices can
prevent deformities and improve hand function
• Podiatrist can make foot orthotics (devices for
correct position of foot) and supportive footwear
• Occupational therapists for active participation in
work and recreational activity
Physiotherapy
Methods
I - Exercises
II- Cold treatment: During stages of acute
inflammation
III- Heating modalities: During subacute and
chronic stages of the disease
IV- TENS: Pain control
V- Hydrotherapy
Exercises
I. Acute stage
Aim: Preservation of ROM
ROM and isometric
exercises
Subacute stage
III. Chronic stage
II.
Cold
TENS
US
Exercises
II. Subacute stage
III. Chronic stage
Aim: Increasing strength and endurance
Strengthening and endurance
ROM exercises
Stretching
ROM Exercises/ Hydrotherapy
Occupational Therapy
• Education of patients in the use of ADL
• Prevention of joint contractures and
deformities
Devices for ADL
Management of Ankylosing
Spondylitis
• Rehabilitation
• Exercises
• Hydrotherapy
Exercises in the Management of AS
Posture
ROM exercises
Flexibility exercises & stretching
Hip – Knee - Spine
Respitatory
Strengthening: Extensor / Core muscles
Education
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Life style modification
Exercises on a regular basis
Posture awareness
Swimming
Spa
Quit smoking
Patient schools
Secondary osteoporosis evaluation
Q&A
• Comments?