PT 30 Arthritis and Fractures

Inflammatory arthritis

May involve single or multiple joints, periarticular structures, and other organ systems

May be an acute process that completely resolves (septic joint) or chronic process (RA)

May involve all joint structures: synovium, cartilage, tendons, capsule, bone, and surrounding muscles

Often part of a systemic RD (connective-tissue disease) such as RA, JIA, SLE, DM-PM, PSS, or MCTD

Clinical ft. of inflammatory arthritis

Acute, painful onset

Fever

Erythema of skin over joint/s involved

Warmth of joint/s

Tenderness that usually parallels degree of inflammation

Lab shows increased WBC with left shift, elevated erythrocyte sedimentation rate, and group II joint fluid

X-ray reveals soft tissue swelling, periostitis, bony erosions, or uniform cartilage loss

4 different groups of Inflammatory arthritis

Inflammatory connective-tissue disease

Inflammatory crystal-induced diseases

Inflammation induced by infectious agents

Seronegative Spondyloarthropathies

Inflammatory connective tissue disease

RA, JIA, SLE, PSS, DM-PM, MCTD, PSA

Inflammatory crystal-induced diseases

gout, pseudogout, basic calcium phosphate

Inflammation induced by infectious agents

bacterial, viral, spirochete, tuberculous, and fungal arthritis

Seronegative spondyloarthropathies

ankylosing spondylitis (AS), PSA, Reiter's syndrome (RS), inflammatory bowel disease

Noninflammatory arthritis can be classified as?

Degenerative, posttraumatic, or overuse

Inherited or metabolic

Degenerative, posttraumatic, or overuse

OA or posttraumatic aseptic necrosis

Inherited or metabolic

lipid storage disease, hemochromatosis, ochronosis, hypogammaglobulinemia, hemoglobinopathies

Rheumatoid arthritis

most common of the inflammatory arthropathies and often difficult to diagnose in early stages

Etiology of is Unknown and believed to be genetic

Age of onset RA

Usually begins between ages 15 and 50

Progression of RA

May develop suddenly within weeks or months

Manifestation of RA

Inflammatory synovitis and irreversible structural damage to cartilage and bone

Joint involvement of RA

-Usually bilateral symmetrical

MCP and PIP of hands, wrists, elbows and shoulders

Cervical spine

MTP, talonavicular and ankle

SCJ, ACJ

Joint signs and symptoms of RA

Redness, warmth, swelling and prolonged morning stiffness, increased joint pain with activity

Systemic signs and symptoms of RA

general feeling of sickness and fatigue, weight loss, and fever; may develop rheumatoid nodules; may have ocular, respiratory, hematological, and cardiac symptoms

Characteristics of RA

Symmetric (bilateral), erosive, synovitis with periods of exacerbation (flare) and remission

Insidious onset with pain, stiffness, and swelling of joints

Morning stiffness or stiffness after prolonged inactivity, often lasts more than an hour in the active inflammatory stage (hallmark feature)

⅓ of patients experience an acute onset of polyarthritis associated with systemic symptoms:

Fatigue

Myalgia

Depression

Low-grade fever

Weight loss

Most common joints involved in early stages of RA

MCP, PIP, IP of the thumb, wrists, MTP

GHJ, SCJ, or ACJ - leads to joint surface degeneration, pain, and loss of ROM

Shoulder pain is often referred to deltoid region

Chronic shoulder inflammation causes capsule & ligaments to become distended & thinned, leading to instability

Stage 1 Early stage of RA

No destructive changes on radiographic examination

Radiographic evidence of osteoporosis may be present

Stage II Moderate of RA

Radiographic evidence of osteoporosis with or without slight subchondral bone destruction: slight cartilage destruction may be present

No joint deformities although joint limitation may be present

Adjacent muscle atrophy

Extra articular soft tissue lesions such as nodules and tenosynovitis may be present

Stage III severe RA

radiographic evidence of osteoporosis; cartilage and bone destruction

joint deformity, such as subluxation. ulnar deviation or hyperextension without fibrous or bony ankyloses

extensive muscle atrophy

possible presence of extra-articular soft-tissue lesions

Stage 4 Terminal stage of RA

fibrous or bony ankylosis

the same criteria of stage III

Impairment, activity limitations and participation restrictions of RA

Tenderness and warmth over involved joints with swelling

Muscle guarding and pain on motion

Muscle weakness and atrophy

Joint stiffness and limited motion

Potential deformity and ankylosis from degenerative process and asymmetric muscle pull

Fatigue, Malaise and sleep disorders

Restricted ADLs and IADLs

POC of RA

educate pt

Relieve pain and muscle guarding

Minimize joint stiffness and maintain available motion

Minimize muscle atrophy

Prevent deformity and protect joint structures

Precautions of RA

Respect fatigue and increased pain

do not overstress osteoporotic bone or lax ligament

Contraindications of RA

Do not stretch swollen joints or apply heavy resistance exercise that cause joint stress or place deforming forces on the joint

OA etiology/ pathophysiology

Unknown etiology (idiopathic); may have mechanical, structural, genetic, and environmental factors

Associated with aging and wear-and-tear of joints

Also genetically related, especially in hands and hips and to some degree in the knees

Characteristics of OA

A chronic degenerative disorder primarily affecting the articular cartilage of synovial joints, with eventual bony remodeling and overgrowth at joint margins (spurs and lipping)

Progression of synovial & capsular thickening and joint effusion

Cartilage splits and thins out, losing ability to withstand stress leading to crepitation and loose bodies; subchondral bone becomes exposed

Affected joints become enlarged

Most commonly involved in weight-bearing joints, cervical and lumbar spine, and distal IP joints of fingers and CMC joints of thumbs

Heberden's Nodes

enlargement of DIP joints

Bouchard's Nodes

enlargement of PIP joints

Age of Onset OA

40+yrs old

Progression of OA

usually develops slowly over many years in response to mechanical stress

Manifestations of OA

cartilage degradation, altered joint architecture, osteophyte formation

Joint involvement of OA

usually asymmetrical

DIP, PIP and 1st CMC

Cervical and lumbar spine

Hips and knees and 1st MTP

Joint signs and symptoms of OA

Morning stiffness usually<30min

Increased joint pain with weight bearing and strenuous activity

Crepitus and loss of ROM

Grade 0 of OA

No radiographic findings

Grade 1 of OA

Doubtful narrowing of joint space and possible osteophytic lipping

Grade 2 of OA

Definite osteophytes with possible narrowed joint space

Grade 3 of OA

Definite osteophytes with moderate joint space narrowing with some sclerosis

Grade 4 of OA

Definite osteophytes with severe joint space narrowing, subchondral sclerosis and definite deformity of bone contour

Impairments, activity limitations and participation restrictions of OA

Pain with mechanical stress or excessive activity

Pain at rest in the advanced stages

Stiffness after inactivity

Muscle weakness

Limitation of motion

Decreased proprioception and balance

Functional limitations in ADLs and IADLs

POC of OA

Educate pt

Decrease effects of Stiffness

Decrease pain from mechanical stress and prevent deforming forces

Increase ROM

Improve balance

Improve Neuromuscular control, strength and muscle endurance

Improve physical conditioning

Acetaminophen and NSAIDs

used for analgesic properties, but conservative dosing & treatment duration is recommended due to many side effects

Viscosupplementation

intra-articular corticosteroid injection can reduce inflammation (compression) & angiogenesis within the synovium; effective for knee & hip OA but not long-lasting

Hyaluronic acid (HA)

intra-articular injection - believed to increase the viscosity and elasticity of the OA joint, and previous studies have shown that it exerts antinflammatory and antinociceptive effect; has been approved for treating knee OA

Glucosamine and Chondroitin sulfate

initially thought to help protect articular cartilage and halt/reverse joint degeneration, but recent evidence suggests negative effects

systemic lupus erythematosus etiology and pathophysiology

Obscure etiology, but viral inclusion bodies have been implicated because of electron microscopic observations made in lymphocytes and vessel walls

High risk population of SLE

Family members with SLE

Women in child-bearing years

Women taking progestation-based oral contraceptives

Characteristics of SLE

Multisystemic disease associated with abnormalities of immune regulation and immune complex-mediated tissue injury; has been called a classic autoimmune disease

Hallmark: immunoglobulin antibody generation to double stranded DNA

Progressive systemic sclerosis

Pathogenesis of organ involvement is most likely due to injury to endothelial cell lining of vessels

Disturbing the lining activates the clotting system

Stimulate smooth muscle cells to migrate in, proliferate, and deposit connective tissue

Results in the proliferative vascular lesions

Characteristics of PSS

Progressive disorder; microvascular obliterative lesions in multiple organs terminate in fibrosis and atrophy

Hallmark: induration of skin

Capillary abnormalities and small artery lesions that appear late with organ involvement

Idiopathic inflammatory myopathies Etiology and pathophysiology

Two leading hypothesis: viral infection and abnormal recognition of self

Types of IIM

Group 1: Primary idiopathic PM

Group 2: Primary idiopathic DM

Group 3: DM-PM associated with neoplasia

Group 4: DM-PM associated with vasculitis (juvenile dermatomyositis [JDM])

Group 5: DM-PM associated with collagen vascular disease

Group 6: IBM

Group 1: IIM

Primary idiopathic PM

Group 2: IIM

Primary idiopathic DM

Group 3: IIM

DM-PM associated with neoplasia

Group 4: IIM

DM-PM associated with vasculitis (juvenile dermatomyositis [JDM])

Group 5: IIM

DM-PM associated with collagen vascular disease

Group 6: IIM

IBM

Characteristics of IIM

Inflammation of muscle & skin

Often associated with profound weakness of striated muscle including the heart

Elevated levels of skeletal muscle enzymes

Crystal induced synovitis

Caused by uric acid, Ca2+, pyrophosphate, hydroxyapatite, and cholesterol crystals

Characteristics of CIS

Gout

Pseudogout

Gout

familial disorder in which deficiency of hypoxanthine-guanine phosphotransferase is present, resulting in overproduction of uric acid

Hyperuricemia results which ultimately results in monosodium urate crystals precipitating in the tissue

Injecting urate crystals subcutaneously will cause tophus formation → gouty attacks ensue in joints

Pseudogout

hereditary or sporadic; calcium pyrophosphate dihydrate deposition

Spondyloarthropathies Etiology and Pathophysiology

B27 Antigen

Antecedent urethritis

Pathology occurs at the entheses(insertion of tendon to bone)

Salmonella, shigella, and yersinia

In summary, etiology is likely infective agent; gram-negative bacteria interacting with susceptible gene host

B27

appears to be crucial link in the expression of disease

anteccedent urethritis

associated with acute arthritis, with chlamydia as primary organism identified

Salmonella, shigella, and yersinia

causes antecedent GI infection, probably due to gram-negative organisms

Characteristics of spondyloarthropathies

Polyarticular disorders that primarily involve the sacroiliac joints, vertebral column, and the larger peripheral joints such as shoulder & hip (lesser extent)

May also be associated with a variety of extraspinal lesions including the eyes, GI tract, cardiovascular system, lungs, kidneys, and skin

Mucocutaneous lesions, sacroiliitis, heel pain, and the B27 antigen

Infection arthritis

Wide variety of infectious agents can cause arthritis secondary to infection itself or as a consequence of host's immunologic response

Viral - hepatitis, rubella, mumps, herpes

Bacterial (Gram-positive Staphylococcus, Streptococcus, and Pneumococcus; Gram-negative Neisseria and Hemophilus influenzae; Pseudomonas, mycobacterium tuberculosis)

Spirochete (Lyme disease)

Fungal

Juvenile idiopathic arthritis

Umbrella term for a heterogenous group of arthritides of unknown cause that begin before 16 years old and occurs in all races

Types of JIA

Pauciarticular JIA

Polyarticular JIA

Systemic-onset JIA

Pauciarticular JIA

Also called oligoarthritis or oligoarticular JIA; means "few joints"

Most common of the JIA subtypes, affecting 50-60% of children with JIA

Presents in two ways:

Persistent oligoarthritis affecting 1-4 joints during first 6 months of disease

Extended oligoarticular arthritis affecting >4 joints in the first 6 months

Asymmetric pattern; benign course

Most commonly involves the knees, elbows, wrists, and ankles; females more affected than males

Swollen joint and limping/abnormal gait, usually early after child wakes up in morning

Leg length discrepancy is common

Polyarticular JIA 2 subgroups

JIA RF positive

JIA RF negative

JIA RF positive

Presence of positive immunoglobulin-M RF on at least 2 occasions, 3 months apart; aggressive & predominant in females

Symmetrically affects small joints of hands & wrists, along with large joints similar to adult RA

10% of those affected have rheumatoid nodules

Potential for severe, destructive arthropathy

JIA RF negative

Greatest risk for chronic, severe arthritis; predominant in females

Can be symmetric or asymmetric

Affects 5 or more joints, most commonly including small and large joints

Systemic Onset JIA

Also called Still's Disease

Affects adults but rare

Involves any number of joints; defined as arthritis in one or more joints with or preceded by fever of at least 2-week duration & at least 3 days of daily temperatures greater than 39°C, evanescent rash, generalized lymphadenopathy, hepatosplenomegaly or splenomegaly, or both, and serositis

Has the most severe extraarticular manifestations, affecting many body systems

Growth delays, osteopenia, anemia, leukocytosis, thrombocytosis, and elevated acute phase reactants

Psoriatic JIA

Combination of arthritis & psoriasis; female predominance

Diagnostic criteria:

Dactylitis

Nail pitting & onycholysis

Psoriasis in a first degree relative

Typically involved peripheral, asymmetric joints of hands, feet, knees, and ankles

Enthesopatic JIA

Characterized by arthritis, enthesitis, or both; additional symptoms may be at least two of the following:

SI joint tenderness and/or inflammatory lumbosacral pain

Positive HLA-B27 antigen

Acute symptomatic anterior uveitis

Onset of arthritis or enthesitis in a male greater than 6 years old

Physician-diagnosed HLA-B27-associated diseases in first- or second-degree relative

Other clinical Manifestations of JIA

Systemic

MSK

Systemic manifestation JIA

fever, rash, lymphadenopathy, polyarthritis, pericarditis, pleuritis, peptic ulcer disease, hepatitis, anemia, anorexia, and weight loss

MSK manifestation of JIA

polyarthritis, polyarthralgias, myalgia myositis, tenosynovitis, and skeletal growth disturbances (short stature & failure to thrive)

PT management

Aquatic PT

Strengthening program

Active exercise

Passive stretching and modified aquatic PT

Parent and pt education

WB exercise programs

Aquatic PT

buoyancy, joint protection, and engagement for children

Strengthening Program

can be part of exercise program, even as young as 6 years old; twice-daily sessions of 15-20 minutes advised

Active exercise

not advised during flare-ups; children may self-limit according to symptoms

Passive stretching and modified Aquatic PT

better choices during exacerbations

Parent and Pt education

educate on importance of avoiding forced or deep flexion of inflamed joints as this could lead to more joint compression

WB exercise programs

overload principle; reduces risk of low bone mineral density; effective for healthy children with JIA

Pain

most likely presenting symptom; character & severity should be included (numeric or Faces)

Stiffness

timing, duration, and location

Gelling phenomenon

RA morning stiffness noted after sitting or maintaining a fixed position for some period of time

Limitation of motion (LOM)

may accompany complaints of stiffness; check if acute or chronic through PROM & AROM testing

Joint swelling

documents by onset, persistence, location, and quantity

Pain with swelling

may be a sign of synovitis or bursitis

Weakness

differentiate from fatigue; proximal muscle weakness may indicated inflammatory myopathy such as PM, while persistent weakness may be neuromuscular disease (like Guillain-Barré's syndrome)

Fatigue

earliest symptom; patient may complain despite pain & swelling being controlled

Fracture

Structural break in the continuity of a bone, an epiphyseal plate, or a cartilaginous joint surface

Some degree of injury occurs to soft tissues surrounding the bone; could be serious if major artery or peripheral nerve is also involved

Most commonly injured region is the finger

Home is the most common setting