M.SK

Session Objectives:

By the end of the session the participant will be

able to :

 Identify musculo- skeletal disorders ( Collagen ,

metabolic).

Describe the clinical picture of musculo-

skeletal disorders .

Discuss D.D. (differential diagnosis).

Management skills.

Osteoarthritis (OA)

OA is the single most important cause of

locomotor disability.

OA used to be considered as ‘wear and tear’

of the bone and cartilage of synovial joints

but is now recognized as a metabolically

active process involving the whole joint i.e.

cartilage, bone, synovium, capsule and

muscle.

The main reason for patients seeking medical

help is pain.

The level of pain and disability are greatly

influenced by the patients’ personality, level

of anxiety, depression and activity and often

do not correlate well with the clinical signs.

Risk Factors:

↑age (uncommon <45y.).

F > M.

↑ in black and Asian populations.

Genetic predisposition

Obesity.

Risk Factors:

Abnormal mechanical loading of joint e.g. instability.

Poor muscle function.

Post-meniscectomy.

Certain occupations e.g. farming.

Symptoms and

Signs Joint pain ± stiffness, synovial thickening,

deformity, effusion, crepitus, muscle weakness

and wasting and ↓ function.

Most commonly affects hip, knee and base of

thumb.

Typically exacerbations occur that may last

weeks to months.

Nodal OA, with swelling of the distal

interphalangeal joints (Heberdens nodes) has a

familial tendency.

Investigations

X-rays may show ↓ joint space, cysts and

sclerosis in subchondral bone and

osteophytes.

Check FBC and ESR if inflammatory arthritis

is suspected (normal in OA).

Disc space containing:Disc space containing:-osteophytes (arrows)-osteophytes (arrows)-sclerosis of adjacent surfaces of vertebral -sclerosis of adjacent surfaces of vertebral bodiesbodies

Cervical spondylosis:Cervical spondylosis:-c5_c6 & c6_c7 disc spaces are -c5_c6 & c6_c7 disc spaces are narrowednarrowed-osteophytes (arrow)-osteophytes (arrow)

Cervical spondylosisCervical spondylosisOsteophytes (arrows) are narrowing Osteophytes (arrows) are narrowing

foraminaforamina

Management

Exclude other causes of pain:

sepsis, bursitis.

Gout.

Inflammatory arthritis and fibromyalgia.

OA may be a coincidental finding and not the

cause of the patients’ pain.

Aim of treatment :

Patient education.

↓ pain.

Optimisation of function and minimization of

progression.

Give information and advice and refer to

other members of the multidisciplinary

team as appropriate e.g. physiotherapist

for advice on exercises.

Strapping and splints.

OT for aids, chiropodist for foot care and

insoles.

Social worker for advice on disability

benefits and housing and orthopaedic

surgeon for assessment for joint

replacement.

↓ load on the joint: Weight reduction can ↓

symptoms and may ↓ progression in knee

OA.

Using a walking stick (opposite hand to

affected hip) and cushioned insoles or

shoes (e.g. trainers) can help.

Exercise and improving muscle strength ↓

pain and disability e.g. walking (for OA knee),

swimming (for OA back and hip but may make

neck worse), cycling (for OA knee but may

worsen patellofemoral OA).

Refer to physiotherapy for advice on

exercises especially isometric exercises

for the less mobile.

Pain control: Regular Paracetamol is

effective for many patients.

NSAIDs are overused and there is no

evidence of additional benefit over simple

analgesics except in acute exacerbations.

Topical NSAIDS have fewer side effects than

oral and may be helpful for superficial joints,

as may rubefacients and counter-irritants

(e.g. Capsaicin cream).

Some patients find local heat or cold

soothing.

Low dose antidepressants e.g.

Amitriptyline are a useful adjunct

especially for pain causing sleep

disturbance.

Aspiration of joint effusions and Steroid

injections can help in exacerbations.

There are ongoing trials of injections of

joint lubricants e.g. hyaline.

Psychological factors have a major impact on

the disability from OA.

Education about the disease and emphasis

that it is not progressive in most people is

important.

Seek and treat depression and anxiety.

Refer: To orthopaedics if diagnosis in

doubt (urgently if you suspect joint sepsis),

or if symptoms are severe for assessment

for joint washout, cartilage debridement or

joint replacement.

Gout Gout

Gout:

Intermittent attacks of acute joint pain due

to deposition of uric acid crystals.

Prevalence: 3—8/1000.

↑ with age.

M:F ≈ 5:1.

Predisposing factors: FH, obesity, excess

alcohol intake, high purine diet, diuretics,

acute infection, ketosis, surgery,

polycythemia, leukaemia, cytotoxics and renal

failure.

Associations:

Gout may be linked to ↑ risk of

hypertension and coronary heart

disease.

Acute Gout

Presentation: Severely painful swollen joint (big toe most common site).

Red skin which may peel.

May have fever.

↑ WCC.

↑ ESR.

↑ blood urate (but may be normal)

Resolves in <2wk.—often after 2—

7d. if treated.

Exclude infection as cause of

symptoms.

Microscopy of synovial fluid reveals sodium

monourate crystals.

X-rays show soft tissue swelling only.

These investigations are not routinely

required.

Treatment

Rest joint.

NSAIDs (e.g. Diclofenac or Indomethacin

50mg tds—caution if GI problems)

Or Colchicine (1mg then 500mcg 2—3hrly

until pain is relieved or side effects e.g.

nausea, vomiting or diarrhoea, max 6mg. do

not repeat within 3d).

Prevention

Lose weight.

Avoid excess alcohol.

Avoid purine rich foods (e.g. offal,

red meat, yeast extracts, pulses and

alcohol).

Avoid Thiazide diuretics and Aspirin.

Prophylactic medication:

Allopurinol 100—300mg daily

wait until 1mo. after acute attack and co-

prescribe Colchicine (500mcg bd) or NSAID for

first l—3mo. to try and avoid precipitation of

another acute attack.

Side effect—rash.

Check serum urate level after 2mo.

Aim for 4—7mg/dl.

Alternatively try an uricosuric e.g.

Probenecid 250—500mcg bd.

Chronic Gout

Recurrent attacks, tophi (urate deposits)

in pinna, tendons and joints and joint

damage.

Refer to a rheumatologist for on-going

treatment.

Gout:Gout: well defined erosion (arrow)at well defined erosion (arrow)at metatarsophalangeal joint of big toe metatarsophalangeal joint of big toe

Gout:Gout:--tophi ; largetophi ; large soft tissue swellings e.g: around soft tissue swellings e.g: around proximal interphalangeal joint of the proximal interphalangeal joint of the indexindex-erosions (arrow)-erosions (arrow)

Pseudogout And Calcium Pyrophosphate

Deposition Inflammatory arthritis due to

deposition of Pyrophosphate crystals.

Chondrocalcinosis seen on X-ray

(calcification of articular cartilage).

Knee, wrist and shoulder are most

commonly affected.

Attacks are less severe than gout and

may be difficult to differentiate from OA.

Presence of joint crystals confirms

diagnosis.

Chronic form also occurs—non-

erosive.

Treat with analgesia and NSAIDs.

Osteoporosis

Osteoporosis Bone mineral density (BMD) >2.5 standard

deviations (SD) below the young adult mean.

There is an ↑ relative risk of fracture x2—3 for

each SD ↓ in BMD.

Prevalence: 5%. F:M ≈ 4:1. ↑ risk with ↑ age.

1:2 women and 1:6 men will have an

osteoporotic fracture by the age of 90y.

Other Risk Factors:

Menopause (particularly if <45y.) or

amenorrhoea during reproductive years.

Prolonged steroid use or Cushing’s

disease

Anorexia (and thin women generally)

Mlabsorption.

Other Risk Factors:

•Prolonged bed rest/immobility.

• Family history.

• Thyrotoxicosis.

• Smoking.

Common fractures:

Wrist (Colles’).

Spine and hip (associated with 15% ↑

mortality).

Diagnosis

Usually diagnosed after fracture occurs.

Osteoporotic vertebral collapse causes pain,

loss in height and kyphosis.

Pain can take 3—6mo. to settle and requires

strong analgesia.

Exclude other causes of pathological

fracture (e.g. malignancy).

Investigations:

Ca2+, P04 and Alk Phos are normal.

Osteopoenia cannot be reliably diagnosed on

X-ray—though vertebral fractures may be

seen.

BMD measurement by DEXA (dual energy X-

ray absorpiometry) scan can quantify

osteoporosis.

Follow local referral guidelines.

Senile osteoprosis:Senile osteoprosis: --decrease bone density decrease bone density -well demarcated edge of vertebral -well demarcated edge of vertebral bodiesbodies-partial collapse of vertebral bodies-partial collapse of vertebral bodies-widening of disc spaces-widening of disc spaces

BMDBMD

T-SCORE:T-SCORE:

Comparison of patient’s bone mass to Comparison of patient’s bone mass to that of young normal subjectthat of young normal subject

Z-SCORE:Z-SCORE:

Comparison of patient’s bone mass to Comparison of patient’s bone mass to that of age and sex matched subjectsthat of age and sex matched subjects

T-SCORE:T-SCORE:

T-SCORE > -1 normalT-SCORE > -1 normal

T-SCORE -1 : -2.5 osteopeniaT-SCORE -1 : -2.5 osteopenia

T-SCORE < -2.5 osteoprosisT-SCORE < -2.5 osteoprosis

Treatment Treat those at high-risk and/or with history

of osteoporotic fracture without

investigations.

BMD helps determine whether to start

preventative treatment in those with

borderline risk factors (treat if BMD >2.5 SD

below young adult mean).

Address risk factors.

Refer to start drug treatment with HRT or

Bisphosphonates—choice depends on

acceptability, tolerability and presence of

other indications or contraindications for

HRT.

Vitamin D (400—800 IU) combined with

Calcium supplements:

↓ fractures in the elderly.

Consider in housebound and institutionalized

patients.

Ca2+ supplements (≥l g elemental Ca2+/d.)

alone slow bone loss in postmenopausal

women but are less effective than

HRT/Bisphosphonates and there is no

evidence of ↓ fracture rate.

Calcitriol and Raloxifene

Role uncertain.

Use only on specialist advice.

Prevention:

Prevention is better than cure.

Aim to prevent fractures by targeting

high-risk patients.

Stop smoking:• Stopping before the menopause

↓ later fracture rate by 25%.

Adequate dietary calcium intake:

• >800mg calcium (=1 pint milk) + 400-800Iu Vitamin D/d.

Regular exercise:

Weight-bearing activity >30min./d. ↓

fractures even in those >70y.

Hip protector pads:

For elderly likely to fall can ↓ fractures

but are poorly tolerated.

HRT:

Was the mainstay of osteoporosis

prevention in post-menopausal women and

is especially beneficial for women with pre

mature menopause.

It postpones postmenopausal bone loss

and ↓ fractures.

Optimum duration of use is uncertain (>5

—7y.) but benefit is limited to current or

recent users (no effect >5y. after stopping).

Whether to start HRT straight after the

menopause or later is uncertain.

HRT use brings concerns regarding ↑ breast

cancer and venous thromboembolism.

Balance benefits and risks in each patient.

Long-term compliance with HRT is poor.

Prophylaxis for those on long term steroids:

>7.5mg Prednisolone/d. for >6mo. accelerates

bone loss and ↑ fracture risk.

Advise patients on risk, assess other risk

factors and ensure adequate calcium + vitamin

D intake.

Prescribe concurrent prophylaxis (e.g.

HRT or Bisphosphonates) if >65y., >l5mg/d.

or strong risk factors without further

investigation.

Otherwise assess BMD at baseline yearly

thereafter— treat if significant bone loss.

Rickets/Osteomalacia

Rickets/Osteomalacia

Vitamin D deficiency leads in children to

softening and deformity, particularly of the

long bones and in adults to fractures, bone

pain and proximal myopathy.

Characteristic features are: soft skull bones,

enlarged ends of ribs (rachitic rosary), bowed

legs or knock knees.

May also cause bone pain, pseudofractures

and short stature.

Dietary deficiency: Occurs particularly in

children with pigmented skin and in Northern

climates where there is less sunlight.

2ry rickets: Vitamin D deficiency is due to

other disease e.g. malabsorption, liver

disease, renal tubular disorders or chronic

renal failure.

Causes:

Vitamin D dependent rickets:

Rare autosomal recessive disorder resulting in

an enzyme deficit in the metabolism of vitamin

D.

Refer for specialist management.

Treatable with vitamin D and calcium.

Hyperphosphataemic rickets (vitamin D

resistant rickets):

X-linked dominant trait resulting in ↓

proximal renal tubular resorption of

phosphate.

Parathyroid hormone and vitamin D levels

are normal.

•Specialist management is needed.

OsteomalaciaOsteomalacia

AsymptomaticAsymptomatic

Diffuse skeletal painDiffuse skeletal pain

Proximal muscle weakness;waddling Proximal muscle weakness;waddling gait and difficulties in climbing stairsgait and difficulties in climbing stairs

PseudofracturePseudofracture

Treated by vit D and calciumTreated by vit D and calcium

Osteomalacia:Osteomalacia: - -looser’s zone (arrow)looser’s zone (arrow) --dec. bone densitydec. bone density -partial collapse of vertebral -partial collapse of vertebral bodiesbodies

Paget’s Disease Of BonePaget’s Disease Of Bone

Paget’s Disease Of Bone

Accelerated disorganized bone remodelling

due to abnormal osteoclast activity.

Affects up to 1:10 of the elderly but only 5%

are symptomatic.

M:F ≈ 3:1.

Signs and symptoms: Pain—dull ache

aggravated by weight bearing.

Deformity (bowing of weight bearing bones

especially tibia (sabre), femur and forearm

—usually asymmetrical), frontal bossing of

forehead.

Diagnosis:

Clinical X-ray (distinctive changes).

↑ bone specific Alkaline phosphatase

(normal Ca2+, PO4, PTH).

Management

↓ pain and long term complications with

Bisphosponates (e.g. Alendronate 40mg/d

for 6mo.) and analgesia.

Thank You