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: 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 large joints small joints (large joints not counted) small joints (large joints not counted) 3 >10 joints (at least one small joint) 5 SEROLOGY (0-3) Negative RF AND negative ACPA0 Low positive RF OR low positive ACPA2 High positive RF OR high positive ACPA3 SYMPTOM DURATION (0-1) <6 weeks0 ≥6 weeks1 ACUTE PHASE REACTANTS (0-1) Normal CRP AND normal ESR0 Abnormal CRP OR abnormal ESR1 ≥6 = definite RA What if the score is <6? Patient might fulfill the criteria…  Prospectively over time (cumulatively)  Retrospectively if data on all four domains have been adequately recorded in the past

ACPA Antibodies to citrullinated protein antigens

RA Classification Criteria 4 or >4 criteria, >6 weeks Morning stiffness > 1 hour Arthritis in 3 or >3 joints (PIP, MCP, wrist, elbow, knee, ankle and MTP) Arthritis of hand joints (wrist, MCP, PIP) Symmetrical arthritis Rheumatoid nodules RF (+) Radiologic findings Erosion Periarticular osteopenia

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 Physiatrist Physiotherapist Occupational therapist Social worker Orthopedist Internalist Podiatrist Ophtalmolog Psychiatrist etc.

Flare-up Periods Resting Splints Positioning Bed rest

Deformities in RA Joint Head and neck. Wrist Thumb Finger. Hips.. Knee Deformity Flexion, rotation. Palmar flexion Flexion Flexion, ulnar deviation Flexion,adduction, external rotation. Flexion Position of Splinting Full extension, cervical spine, chin forward 30 degreees dorsiflexion Extension, apposition Extension, no lateral deviation Extension, in line with body; foot pointing upward 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 Effective in maintaining the ROM Strengthening of muscles Prevent contractures Prevent deformities Maintain ADL

Physical and Occupational Therapy 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 II. Subacute stage III. Chronic stage

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 Life style modification Exercises on a regular basis Posture awareness Swimming Spa Quit smoking Patient schools Secondary osteoporosis evaluation

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