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.
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 medicalhelp is pain.The level of pain and disability are greatlyinfluenced by the patients’ personality, levelof anxiety, depression and activity and oftendo 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 weaknessand wasting and ↓ function.Most commonly affects hip, knee and base ofthumb.
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 andsclerosis in subchondral bone andosteophytes.Check FBC and ESR if inflammatory arthritisis suspected (normal in OA).
Disc space containing:-osteophytes (arrows)-sclerosis of adjacent surfaces of vertebralbodies
Cervical spondylosisOsteophytes (arrows) are narrowing foramina
ManagementExclude 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 kneeOA. Using a walking stick (opposite hand toaffected hip) and cushioned insoles orshoes (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 makeneck worse), cycling (for OA knee but mayworsen patellofemoral OA).
Refer to physiotherapy for advice onexercises especially isometric exercisesfor 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 adjunctespecially for pain causing sleepdisturbance.
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 indoubt (urgently if you suspect joint sepsis),or if symptoms are severe for assessmentfor joint washout, cartilage debridement orjoint replacement.
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, excessalcohol intake, high purine diet, diuretics,acute infection, ketosis, surgery,polycythemia, leukaemia, cytotoxics and renalfailure.
Associations: Gout may be linked to ↑ risk of hypertension and coronary heart disease.
Acute GoutPresentation: 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: well defined erosion (arrow)atmetatarsophalangeal joint of big toe
Gout:-tophi ; large soft tissue swellings e.g: around proximal interphalangeal joint of theindex
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 Bone mineral density (BMD) >2.5 standarddeviations (SD) below the young adult mean.There is an ↑ relative risk of fracture x2—3 foreach SD ↓ in BMD.Prevalence: 5%. F:M ≈ 4:1. ↑ risk with ↑ age. 1:2 women and 1:6 men will have anosteoporotic 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:-decrease bone density -well demarcated edge ofvertebral bodies-partial collapse of vertebral bodies
BMDT-SCORE:Comparison of patient’s bone mass to that of young normal subjectZ-SCORE:Comparison of patient’s bone mass to that of age and sex matched subjects
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 withCalcium supplements:↓ fractures in the elderly.Consider in housebound and institutionalizedpatients. Ca2+ supplements (≥l g elemental Ca2+/d.)alone slow bone loss in postmenopausalwomen but are less effective thanHRT/Bisphosphonates and there is noevidence 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 osteoporosisprevention in post-menopausal women andis especially beneficial for women with pre-mature menopause. It postpones postmenopausal bone lossand ↓ 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 ↑ breastcancer 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. acceleratesbone loss and ↑ fracture risk. Advise patients on risk, assess other riskfactors and ensure adequate calcium + vitaminD 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 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), bowedlegs or knock knees. May also cause bone pain, pseudofracturesand short stature.
Causes: 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.
Vitamin D dependent rickets: Rare autosomal recessive disorder resulting inan enzyme deficit in the metabolism of vitaminD. Refer for specialist management. Treatable with vitamin D and calcium.
Hyperphosphataemic rickets (vitamin Dresistant rickets): X-linked dominant trait resulting in ↓proximal renal tubular resorption ofphosphate.Parathyroid hormone and vitamin D levelsare normal.
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.