Rheumatological Conditions

What are the risk factors for osteoarthritis?

• >50 years

• Women, menopausal

• High BMI

• Family hx of joint replacement

• Comorbidities

What is the pathophysiology of osteoarthritis?

• Early:

  • Affects articular cartilage and subchindral bone

  • Bone marrow oedema may preced cartilage damage

• Established

  • Low-grade inflammation due to damaged cartilage

  • Synovitis

  • Bone marrow ‘oedema’ like lesions

  • Subchondral bone ‘cysts’

What is the clinical presentation of osteoarthritis?

• Early Stage:

  • Pain over weeks to months

  • Increases with load and overuse

  • Joint line tenderness

  • Crepitis

  • Mid joint effusion

• Estabilished:

  • Pain not eased by rest

  • Pain sensitisation

  • Knee effusion

  • Loss of ROM

  • Muscle wasting

What are the radiological featires of osteoarthritis

• Loss of joint space

• Deformity

• Osteophytes

• Subchondral scleosis (increased bone density)

• Subchondral bone cysts

Kellgren-Lawrence Scale for Osteoarthritis

0: No radiographic features

1 (Mild): Possible joint space narrowing and osteophyte formation

2: (Mild-Mod): Definite osteophyte formation with possible joint space narrowing

3 (Mod): Multiple osteophytes, definite joint space narrowing, sclerosis and possible bony deformity

4 (Severe): Large osteophytes, marked joint space narrowing, severe scleorsis and definite bony deformation

What is the management of osteoarthritis?

• Address modifiable risk factors/triggers

• Reduced function impairments

• Improve quality of life

• Manage pain

• Eduction

• Moderate Load Bearing Exercise

• Weight control

• Surgery

What is the pathophysiology behind rheumatoid arthritis?

• Inflammation begins in synovium

• Cells of synovial tissue proliferate causing synovium to form in pannus (erodes other tissue)

• Cytokines produced, destroying components of joint

• Pannus grows into hoing cavity→ erodes cartilage, bone & tendon→ deformity

• Fibrosis→ joint thickening and stiffness

What is the clinical presentation of rheumatoid arthritis?

• Pain & stiffness in morning >30 mins

• Heat, swelling and occassional redness

• Loss of function

• Fatigue, weakness, loss of appetite, fever

• Reduced muscle strength

• Muscle inflammation

• Decreased fitness

What are the hand deformities of rheumatoid arthritis?

• Swan neck: flexion DIP and hyper extension of PIP

• Boutonniere: flexion PIP, extension DIP

• Z deformity of thumb

What are the radiological findings for rheumatoid arthritis?

• Marginal erosions- areas not covered by articular cartilage

• Soft tissue swelling

• Osteopenia

• Joint space narrowing

• Deformity

What is the management for rheumatoid arthritis?

• Rheumatologist, physio & OT

• Careful assessment & monitoring

• Education

• Drug treatment- DMARDs or NSAIDs

• Joint protection

• Exercise: cycling, swimming, hydrotherapy (supervised and tailored exercise)

• Surgery

What is the pathophysiology behind gout?

• Metabolic disease

• Defect in uric acid metabolism→ urate crystal deposity in joint and soft tissue→ tissue damage and inflammation

• Chronic: develops synovitis and erosions

What are the risk factors for gout?

• Male

• >30 years, peak 40-60 years

• Overweight

• High cholesterol

• High BP

• Glucose intolerance

• Kidney disease

• Taking diuretics

What is the clinical presentation for gout?

• Severe pain, rapid onset

• Swelling

• Redness

• Tenderness

• Chronic: tophi and multiple joints

What is the management for gout?

• Drugs: NSAIDs to reduce inflammation or allopurinol to reduce urate levels

• Assisted aids: stick

• Surgery for symptomatic tophi

• Prevention of complications e.g. ROM, strength

What is the pathophysiology behind ankylosing spondylitis?

• Systemic autoimmune disease

• 2-3x more common in males

• Develops in yound adulthood (peak 20 years)

• Inflammation of the SIJ and vertebrae (fibrocartilage) and entheses of tendonss/ligaments

• Inflammatory cells infiltrate → structural damage to bone’

• Repair by fibroblasts → forms scar tissue

• Calcified over time → joints fuse

What is the clinical presentation of ankylosing spondylitis?

• Low back and buttock pain

  • Onset before age 40

  • Persistent for >3 months

  • Worse at night

• Morning stiffness >60 mins

• Improvement with exercise

• Response to NSAIDs

• Postural changes

  • Increases throacic kyphosis

  • Decreased lumbar lordosis

What are the radiological findings for ankylosing spondylitis?

• Changes in sacroiliac joints (erosions, fibrosis, fusion)

• Calcifocation of outer layer of vertebral discs

• Syndesmophytes (bone spurs adjacent vertebrae)

• Multi-level spinal fusion

• Bone remodelling (vertebral body become square shaped)

• Bamboo appearance in ligaments

What is the management for ankylosing spondylitis?

• Reduce pain, improve function and decrease complications

• NSAIDs (1st line of therapy)

• DMARDs

• Exercise to maintain spinal mobility and strength

• Smoking cessation

• Treat and monitor for osteoporosis

What is osteoporosis?

• Metabolic disease- loss of bone mineral density and skeletal fragility

• 2-3 fold increased risk of fracture

• Asymptomatic

• May present with vertebral compression, wedging and collapse, kyphosis

What is the pathophysiology for osteoporosis?

• Imbalance between bone resoprtion and formation causing loss of bone mineral density

• More serious progression of osteopenia

What is the risk factors for osteoporosis?

• Age, race, small vone structure, female, postmenopausal, family hx

• Sedentary, calcium deficiency, nutrition, alcohol, caffeine intake, smoking

• Heparin, diabetes, COPD, malignancy, hyperthyroidism, hyperparathyroidism, RA

• Antigravity

What is the management for osteoporosis?

• Exercise (skipping, weights, WB, resistance ect) and falls prevention

• Refer to dietition (calcium and vitamin D supplements)

• Anti-resorptive drugs

• Surgery- stable fracture fixation

• Balance and gait training

• Dual task training

• Muscle strengthening

What is Osgood-Schlatter Disease?

• Osteochondrosis of tibial tubercle where patella tendon inserts

• Boys during growth period more common

• Caused by repetitive strain, often jumping sports

• Chronic avulsion injury during process of ossification → abnormal bone formation at apophysisi of tibial tubercle

What is the presentation of Osgood-Schlatter disease?

• Inflammation and thickening of patella tendon

• Pain, swelling, tenderness, increased prominence of tibial tubercle

• Radiograogs show irregularity of apophysis with separation from tibial tuberosity and bony ossicles in later stages

What is the treatment of Osgood-Schlatter diease?

• Advice and education (Limitation/modification of activity)

• Taping or braces if severe

• Anti-inflammatory, application of cold modalities

• Release tension of quads (stretches)

• Resolution can take 1-2 years

What is Legg-Calve Perthes Disease?

• Idiopathic osteonecrotic disease of proximal femoral epiphyses

• Boys more trhan girls (4-10 years)

• Unkown cause

What are the stages of Legg-Calve-Perthes disease?

• Avascular necrosis (6-12 mths)

• Revascularisation (1-3 years)

• Repair/re-ossification

• Healing (flattening femoral head)

What is the presentation of Legg-Calve-Perthes disease?

• Painless limp

• Hip, knee or groin pain, exacerbated by hip/leg movement

• Reduced ROM at hip

• Atrophy of thigh muscles in severe cases

What is the treatment of Legg-Calve-Perthes disease?

• Reduce deformity and preserve integrity of femoral heald while necortic bone is resorbed

• Advice and education

• Exercises for ROM & strength

• Walking aids

• Preiods of rest/NWB

• Abduction braces

• Surgical intervention- if severe and >6 years old