466 CHAPTER 17 Musculoskeletal system Osteoarthritis Osteoarthritis (OA) is the most common joint disorder in older patients caus ing massive burden of morbidity and dependency. It is not inevitable with ageing. A disorder of the dynamic repair process of synovial joints causing: Loss of articular cartilage (joint space narrowing) \200 Vascular congestion \200 New g rowth of cartilage and bone (osteophytes) \200 Capsular \201 brosis Inherited factors d etermine susceptibility but individual genes not identi- \201 ed. Increasing age is the s trongest risk factor. Females and those with high bone density are at higher risk. Obesity, trauma, and repetitive adverse loading (eg miners or footballers) are potentially avoidabl e factors. Burnt out rheumatoid arthritis or neuropathic joints (eg in diabetes) as well as congenital factors (eg hip dysplasia) can result in secondary OA. Clinical features \200 Pain \200\224 assess severity, disability and impact on life (han dicap). Usually insidious in onset and variable over time, worse with activity and relieved by rest. Chronic pain may cause poor sleep and low mood \200 Only one or a few joints ar e affected with minimal morning stiffness and often worsening of symptoms during the day Restricted movement \200\224 eg walking, dressing, rising from a chair \200 Severe OA ca n contribute to postural instability and falls Examination \200 Heberden \200\231s nodes (asymptomatic bony swellings on distal \201 n gers) associated with inherited knee OA Limp with jerky \200\230antalgic \200\231 gait \200 Deformity including: \200 Muscle w asting \200 Knees may have valgus (knees apart, feet together), varus (knees together, foot outwards) or \202 exion deformity Hip shortening/ \202 exion (check on couch by \202 exing opposite hip to see if affected hip lifts off bed \200\224 Thomas \200\231 test) Restricted range of movement \200 Crepitus \200 Effusions Investigations 2OA is a clinical diagnosis. Symptoms correlate poorly with radiolog- ical \201 ndings. The main role of X-ray is in assessing severity of structural change prior to surgery. Features include joint space narrowing, osteo- phytes, sclerosis, cysts, and defo rmity. Blood tests are normal even when an osteoarthritic joint feels warm \200\224 recons ider your diagnosis if in \202 amma- tory markers are elevated. OSTEOARTHRITIS: MANAGEMENT 467 Osteoarthritis: management OA is the most common, chronic painful condition. Drug dependenc e and side effects are a big problem. 2Always consider non-pharmacological treatments \201 rst. Non-drug treatments \200 Exercise : stretching and strengthening. Swimming, yoga, and Tai Chi are particularly good. Encourage the patient to exercise despite the pain \200\224 no harm will be done Heat packs : but be very careful to avoid burns in patients who may have decreased temperature awareness Weight loss : not a quick \201 x but in \202 uences other health outcomes \200 Sensibl e footwear : soft soles with no heels. Trainers are ideal \200 Walking aids : eg stick (i n contralateral hand) \200 Education and support : can improve pain and function \200 O steopaths or chiropractors help some patients but are expensive Drug treatments 3No patient should be offered more dangerous medication unless they have tr ied and failed regular paracetamol in maximum dose (1g qds). Patients may need persuading t o try a regular prophylactic dose, perceiving it as a \200\230weak \200\231 drug. \200 T he next step is to add a low potency opiate \200\224 often combined with paracetamol, eg c o-codamol (start with codeine 8mg/paracetamol 500mg ii qds). Beware constipation and sedati on A short course of oral NSAIDs can be useful in acute exacerbations but try to avoid long-te rm use. If NSAIDs are used for more than 2 weeks or in the presence of known dyspepsia or u lceration, reduce the gastrointestinal risk by co-prescribing, eg lansoprazole 15mg od. The COX-2 selective inhibitors have better gastrointestinal tolerability but have fallen from favor due to vascular adverse events Intra-articular steroids (eg triamcinolone hexacetonide 20mg) can be rapidly effective part icularly if the joint is hot/very painful. There is a substantial placebo effect, but sympt oms tend to recur after 4 \200\2236 weeks. Side effects limit use to four injections/joint/ year. The cumulative systemic effect risks osteoporosis Topical NSAIDs can be helpful and are lower risk than oral \200 Counter-irritants, eg cap saicin cream are safe and have some effect \200 Oral chondroitin and glucosamine are avai lable unlicensed over-the- counter and are very widely used. They may have a slow-onset mil d analgesic action and may slow the progression of disease Surgical treatment Includes arthroscopic joint wash-outs and joint replacements. Indication s include pain, deformity or joint instability where other treatments have failed. Outcomes can be excellent for \201 tter older people, but caution in the frail for whom it is rar ely bene \201 cial overall. Further reading NICE . The care and management of osteoarthritis in adults ( 2008 ) online: M www.nice.org.uk/cg59 . Harvey WF , Hunter DJ . ( 2010 ). Pharmacological intervention fo r osteoarthritis in older adults . Clin Geriatr Med 26 ( 3 ): 503 \200\223 15 . 468 CHAPTER 17 Musculoskeletal system Osteoporosis Osteoporosis is the reduction in bone mass and disruption of bone archi- tectu re, resulting in increased bone fragility and fracture risk. Results from prolonged imbalan ce in bone remodeling where resorption (osteoclastic activity) exceeds deposition (osteobla stic activity). Osteoporosis is very common and very much under-recognized and under-treated. In combinatio n with falls (see b \200\230Interventions to prevent falls \200\231, p.106) osteoporosis c ontributes to the high incidence of fractures in older people. In the UK 30 % of women aged 70 have at least one vertebral fracture and 32 % aged 90 will have had a hip fracture. 2If you make the diagnosis do not delay initiating secondary prevention. Always think of osteo porosis when assessing postoperative orthopedic patients. Pathology \200 Total bone mass increases throughout childhood and adolescence, peaks in t he third decade, and then declines at about 0.5 % per year \200 Bone loss is accelerated after the menopause (up to 5 % per year) and by smoking, alcohol, low body weight, hyperthyroidism, hyperparathyroidism, hypoandroge nism (in men), kidney failure, and immobility Steroids, phenytoin, long-term heparin, and ciclosporin cause secondary osteoporosis High peak bone mass reduces later risk. Determined by genetics, nutrition (plenty of calcium/vitamin D especially in childhood and the heavier the better) and weight-bearing exercise There are changes in bone structure as well as bone mass. Both contribute to fragility Diagnosis is complicated by the common coexistence of asymptomatic osteomalacia (defective mineralization) in older people with low sunlight exposure Clinical features \200 Osteoporosis itself is asymptomatic \200\224 it is the fractures that cause problems Often presents with an acute fragility (ie low energy) fracture \200\224 wrist, femoral neck, or crush fracture of vertebral body Wedging of vertebrae is caused because there is higher load-bearing by the anterior part of the vertebral body. This can present as: \200 An incidental, asympto matic \201 nding (in around a third) \200 Acute painful fracture \200 A progressive k yphosis ( \200\230Dowager \200\231s hump \200\231). The bent-over posture is not just unatt ractive, it causes loss of height, protuberant belly, abdominal compression, oesophageal re \202 ux, and impaired balance with further predisposition to falls and fracture. Restrict ed rib movements lead to restrictive lung disease OSTEOPOROSIS 469 Diagnosis 2Blood tests are normal (except after a fracture). If calcium or ALP is elevated consider alternative diagnosis, eg metastases or Paget \200\231s disease. \200 X-rays may show fractures and give an idea of bone density \200 The gold standard is d ual X-ray ab sorpt i ometry (DEXA) scanning (rarely employed in the elderly population but useful in you nger women). Usually two scores are quoted at hip and spine. The T-score compares bone dens ity to peak bone mass while Z score compares it to age/sex/weight-matched sample. A T-score less than \200\2232.5 indicates osteoporosis, with scores \200\2231 to \200\2232.5 indi cating osteopenia Peripheral densitometry assessments can be done at the heel and ankle, the advantage being that the required machine is more portable. Results correlate wi th formal testing, but there are concerns about reliability Think of secondary causes: TSH in all \200 Testosterone levels in men In a woman aged > 65 years, a pragmatic approach is to assume that oste- oporosis exists wh ere there is a: \200 Low energy fracture of wrist, femoral neck, or vertebra \200 Progr essive kyphosis without features of malignancy Primary prevention of osteoporosis \200 Sensible public health measures (eg diet, exercis e, stop smoking, reduce alcohol) should be advised but generally affect peak bone mass, ie too late for older people Prophylaxis with a bisphosphonate should be started for those taking signi \201 cant steroid therapy ( > 7.5mg/day for more than a month) (see b \200\230Osteo porosis: management \200\231, p.470) HRT is not particularly effective \200\224 postmenopausal bone loss returns after it is st opped. Increased thromboembolic, cancer, and vascular risk argue strongly against its use 470 CHAPTER 17 Musculoskeletal system Osteoporosis: management \200 Oral calcium and vitamin D is cheap and effective, especial ly in frail institutionalized people (possibly due to treatment of osteomalacia and associated myopathy as much as osteoporosis). Tablets are large and chalky \200\224 can be unpalatable. Effer vescent tablets or granules may be better tolerated. Take two combination tablets daily (eg CalciChew D3 Forte or Adcal D3). Probably not helpful as monotherapy in \201 t old er people Bisphosphonates are very effective, and used as \201 rst line. NICE recommends in any woman aged > 75 following a fragility fracture (without the need for DEXA scanning) \200 The weekly dose regimens (risedronate 35mg, alendronate 70mg once weekly) are easier to remember and to tolerate than daily dosing, but patients should still take d aily calcium and vitamin D. \200 Etidronate is also NICE recommended and comes in a prepa ration that includes calcium (Didronel PMO ) but must be taken daily \200 Upper gut ul ceration occurs rarely. Use bisphosphonates cautiously when there is dysphagia or a history of dyspepsia. Must be taken on an empty stomach 30min before breakfast or other medicines. Swallow the tablet whole with a full glass of water whilst sitting or standing. Remain sit ting or standing for 30min after swallowing \200 Up to 15 % of patients are \200\230non- responders \200\231 and continue to lose bone mass (measured by chemical bone turnover markers). This is unlikely to be detected in geriatric medicine because bone turnover is not monitored; consider change in treatment if fragility fractures continue Contraindicated in hypocalcaemia. Manufacturers advise avoiding in renal impairment, but it is often given if the indication is strong \200 Longer-acting iv preparations (eg zoledronic acid) are also available but cost/bene \201 t ratio is still under evaluation Osteonecrosis of the jaw is a rare, but serious side effect (increased risk with cancer, st eroid treatment, and poor dental hygiene). Stop the drug and refer to a maxillofacial surge on Strontium ranelate is recommended by NICE as second line if bisphosphonates are not tolerated. Side effects include diarrhea, vomiting, and thromboembo lism Teriparatide can also be used if bisphosphonates and strontium are not tolerated or ineffec tive. Recombinant fraction of parathyroid hormone, given by s/c injection. Expensive. Maxim um course 18 months Less common drugs, usually advised only by specialist teams include: raloxifene (an estroge n-like drug which decreases bone loss without measurable effects on the uterus, used if bis phosphonates are not tolerated or in non-responders) and calcitonin (available in nasal spr ay and improves pain after acute vertebral fracture) Vertebroplasty can be considered for severe pain after spinal wedge fracture where conservative measures are not effective Further reading NICE . Osteoporosis \200\224secondary prevention including strontium ranela te ( 2011 ) online: M www.nice.org.uk/ta161 . OSTEOPOROSIS: MANAGEMENT 471 HOW TO Manage non-operative fractures \200 Fractures that very rarely require opera tive intervention include pelvis, humerus, wrist, and vertebra Other fractures, often immobilized surgically in younger people, may be treated more conser vatively in older patients to avoid perioperative risks (eg fractured tibial plateaux may s imply be immobilized by plaster of Paris (POP) or splinting) Patients with these \200\230non-operative \200\231 fractures are often cared for by geriatricians having been transferred either: \200 From A&E, to medical, ortho-medical or ortho-geriatric units \200 From orthopedic wards for ongoing rehabilitation Minor fractures can result in signi \201 cant functional impairment, eg a Colles \200\231 fracture and POP may prevent an older person washing, dressing, and to ileting. Even walking may not be possible (if a frame can no longer be used) General principles of management These include: \200 Control of pain . This allows earlie r mobilization and reduces the risks of immobility (pressure sores, pneumonia, thromboembolism) \200 Consider novel trea tments such as heat, TENS, calcitonin, bisphosphonates, or vertebroplasty for vertebral fra cture A short course of NSAIDs is sometimes appropriate in low-risk patients, but remember to red uce analgesia as soon as possible \200 Encouraging mobility and independence as early as possible . Best achieved in a rehabilitation unit. Patient and family often expect \200\230bed rest \200\231 after a fracture and may need to be educated Consider the mechanism of the fall and injury (see b \200\230Assessment following a fall \200\231, p.104) \200\224 are there medical risks that could be reduced? Eg, sedating medication, excessive antihypertensive use, undiagnosed illnesses (eg urinary infection or uncontrolled AF), need for aids/adaptations Maintaining contact with orthopedic colleagues . They can advise on when to replace/remove plasters and how much exercise/ weight bearing is appropri ate. Ask for reassessment if progress is poor, eg ongoing severe pain, or apparent malunion \200\224 sometimes a diagnosis has been missed or an interval operation is needed \200 A pragmatic approach to weight-bearing may be needed, eg in dementia (where concordance with non-weight bearing is dif \201 cult), or where immobility causes an unacceptable rise in frailty Consider prophylactic heparin if there are multiple risk factors for thromboembolic disease or the patient is immobile Consider osteoporosis treatment (there is no evidence that bisphosphonates reduce callus fo rmation or delay bone union) \200 Start to plan discharge early . Many patients can be ma naged at home with a care package and outpatient rehabilitation. Others may need transitional care b eds (eg while they wait to be weight-bearing or for plasters to be removed) after which the y can return to an active rehabilitation program prior to going home 472 CHAPTER 17 Musculoskeletal system Polymyalgia rheumatica Polymyalgia rheumatica (PMR) is a common in \202 ammatory syndrome causing symmetrical proximal muscle aches and stiffness. It affects only older people (do n ot diagnose it under age 50). There is rapid (days) onset of shoulder and then thigh pain t hat is worse in mornings. Sometimes associated malaise, weight loss, depression, and fever. Often quite disabling with little to \201 nd on examination. Pathology Pathogenetically similar to giant cell arteritis (temporal arteritis); the two co nditions commonly coexist, and may represent a spectrum of disease. Pain in PMR is thought to be due to synovitis and bursitis. Diagnosis 2A dif \201 cult diagnosis to make reliably \200\224 a signi \201 cant number of patients are misdiagnosed. The following should be present for a \201 rm diagnosis: 1. Age > 50 2. Bilateral aching and morning stiffness (lasting 30min or more) persisting for at least 1 month. The stiffness should involve at least two of the following three areas: n eck or torso, shoulders or proximal regions of the arms, and hips or proximal aspects of th e thighs 3. ESR > 40 The following should also be considered: \200 Suggestive symptoms with raised in \202 am matory markers (ESR/CRP) and no other apparent cause may warrant treatment trial Often have anemia (usually normochromic normocytic) and mild abnormalities of liver (especially ALP) or renal function Clinical examination often normal \200\224 despite the name, muscle tenderness is absent and pain arises because of bursitis/synovitis. Rarely there may be pal pable synovitis in peripheral joints (eg knee, wrist) Muscle enzymes, and EMG are normal \200 Temporal artery biopsy is positive in less than 2 5 % and is rarely done. \200 Exclude other causes (eg connective tissue disease, tumor, c hronic infection, neurological diseases) particularly if a patient does not respond quickly to steroids Treatment \200 Prednisolone (doses more than 15mg are rarely required) usually produces a complete resolution of symptoms in a day or two Treat until symptom-free and ESR/CRP normalize then reduce dose quickly initially (eg 2.5mg /week), then more slowly below 10mg (1mg/ month) checking for relapse of symptoms or blood tests If symptoms recur with an associated rise in ESR/CRP then put the steroid dose up until bot h settle, then restart tailing more slowly \200 Some patients can be taken off steroids a fter 6 \200\2238 months but most need long-term steroids (mean duration 2 \200\2233 years) Always give bone protection (eg alendronate 70mg once weekly with calcium and vitamin D). I f a treatment trial, wait until diagnosis clear \200 Azathioprine or methotrexate may be used as steroid-sparing agents \200 Educate and involve the patient in monitoring disease POLYMYALGIA RHEUMATICA 473 Diagnostic dilemma and steroid \200\230dependency \200\231 Some older patients who were diagnosed with PMR years ago no longer exhibit or remember the ir symptoms, and will be having steroid side effects. They may resist steroid withdrawal or experience symp- toms as steroids are decreased or withdrawn, even if the characteristic s yndrome and in \202 ammatory responses are not displayed. Many other diseases (even simple osteoarthritis) respond to steroids (although usually less dramatically). Steroid withdrawal itself can cause general aches, which some have called \200\230pseudo-rheumatism \200\231. Avoid this dif \201 cult situation by: Comprehensive assessment at onset with good record-keeping, so that others can reappraise t he diagnosis if response to treatment is poor Ensuring that where the diagnosis is not clear, a treatment trial is reviewed early for imp act \200\224 if the response is not convincing, then stop the steroids. 2Beware continuing steroids because the patient feels \200\230a bit better \200\231 Considering the differential diagnosis carefully \200 Discussing diagnosis and treatment with the patient \200 Agreeing with the patient a clear plan for reviewing steroid therap y \200 Explaining that steroid withdrawal can cause muscle aches, but the blood tests hel p us distinguish between this and disease reactivation 474 CHAPTER 17 Musculoskeletal system Giant cell arteritis Giant cell arteritis (GCA) or temporal arteritis (TA) is a relatively common (18 per 100,000 over age 50) systemic vasculitis of medium to large vessels. Mean ag e of presentation 70 (does not occur age <50). More common in women and Scandinavia/norther n Europe. Pathogenesis \200 Chronic vasculitis, mainly involving cranial branches arising from the aortic arch. Similar pathology seen in PMR, but different distribution \200 Possibly an a utoimmune mechanism but no antibodies/antigen isolated Clinical picture \200 Systemic : fever, malaise, anorexia, and weight loss \200 Muscles : symmetrical proximal muscle pain and stiffness as in PMR \200 Arteritis : tenderness o ver temporal arteries \200\224 not so much a headache as scalp tenderness. Classically una ble to wear a hat or brush hair. If an artery occludes, distal ischaemia or infarction occu rs \200 Headache is present in 90 % (due to ischaemia or local tenderness of facial or scalp arteries) Jaw claudication (occlusion of maxillary artery) \200 Amaurosis fugax or blindness are du e to occlusion of the ciliary artery, which supplies the optic nerve \200\224 this causes a pale swollen optic nerve but not retinal damage (which is a feature of central retinal artery occlusion with carotid di sease) Stroke (carotid artery) \200 Any large artery including the aorta can be affected. 2Always suspect GCA if amaurosis fugax involves both eyes (atheroma is more commonly unilat eral). Investigations \200 ESR usually > 100 \200 CRP also very high and falls faster with tre atment than ESR \200 May have normochromic normocytic anemia and renal impairment. \200 Temporal artery biopsy (TAB) is highly speci \201 c, and therefore the gold standard test . Because the vasculitis may be patchy, TAB is not always positive, ie the sensitivity is m oderate. TAB becomes negative quickly (1 \200\2232 weeks) with treatment GIANT CELL ARTERITIS 475 Treatment \200 Amaurosis fugax due to GCA is an ophthalmological emergency. Give 80 \200 \223100mg oral prednisolone or high-dose methylprednisolone iv Never delay treatment while waiting for a biopsy \200 Even without visual symptoms, highe r doses and slower dose reduction are required than for PMR (start at 30 \200\22340mg) Between a third and a half of patients are able to come off steroids by 2 years After stopping steroids, continue to monitor as relapse is common \200 Osteoporosis proph ylaxis should be started at initiation of steroids (usually a bisphosphonate with calcium and vitamin D) Azathioprine and methotrexate are sometimes used as steroid-sparing agents once therapy is established. Consider them if: \200 Steroid side effects are promi nent \200 High steroid doses are required \200 There is slow tailing off \200 There i s recurrent relapse off treatment 476 CHAPTER 17 Musculoskeletal system HOW TO Manage steroid therapy in giant cell arteritis A suggested protocol for steroid treatment in temporal arteritis is shown in Fig. 17.1 . Diagnosis Prednisolone 80mg od with Biphosphonate Calcium and vitamin D Monitor for glycosuria/BMs in known diabetic patients Initial review (2 weeks) Clinical improvement \200\224usually rapid \200\224if not reassess diagnosis Repeat inflamm atory markers \200\224ESR/CRP If ESR/CRP still elevated continue at 80mg and recheck in 2 weeks If ESR/CRP normal/near normal decrease to 70mg and review 2 weeks continue to reduce by 10m g/fortnight while markers remain satisfactory When reach 20mg then slow reduction by 2.5mg/fortnight If still no improvement reconsider diagnosis When reach 10mg then slow reduction by 1mg/fortnight Fig. 17.1 A protocol for steroid treatment in temporal arteritis. If rebound of symptoms or in \202 ammatory markers occurs, then take 2 steps back on the reduction schedule. Wait 4 weeks before reducing again Beware a steroid-withdrawal syndrome, which can occur without arteritis recurrence. ESR and CRP are normal (see b \200\230Diagnostic dilemma and steroid \200\234dependancy \200\235 \200\231, p.473) Other blood parameters (anemia, impaired liver function) may help guide treatment This page intentionally left blank 478 CHAPTER 17 Musculoskeletal system Muscle symptoms Muscular symptoms are common in older people, and can arise from a range of conditions. It should be possible to distinguish between the following: True muscle weakness due to: UMN lesions (eg midline brain lesions such as tumors, subdural bleeds, degenerative brain disease, or cord pathology such as disks or vertebral collapse) Anterior horn cell lesions (eg MND, polio) \200 Motor nerve root problems (spinal stenosi s, malignant in \201 ltration) \200 Peripheral motor nerve problems (in \202 ammatory p olyneuritis, thyroid disease, toxins) Neuromuscular transmission problems (myasthenia gravis, malignancy related impairments, dru g induced problems) Muscle abnormalities (dermatomyositis, inclusion body myositis, drug damage \200\224 especially steroids or statins, thyroid disease, vitamin D de \201 c iency, electrolyte or pH imbalances) Joint disease with local pain and stiffness, reducing use with resulting weakness (eg osteoarthritis) Asthenia \200\224 feeling of weakness, low energy and apathy as a result of systemic disea se (eg cancer, heart disease, and chronic lung disease), con \201 nement to bed or psychol ogical factors (anxiety, depression). Commonly present as feeling too tired/weak to partici pate in therapy History and examination \200 Take a full history including drugs and comorbidities \200 Ask about muscle pain (rarely a feature of true myopathy \200\224 consider overexertion or \201 bromyalgia) and cramps Look for muscle wasting and abnormal movement (localized wasting indicates a problem with t he relevant motor nerve or muscle body, fasciculation may indicate MND) Is the weakness generalized (usually due to cachexia or myasthenia gravis) or limited to sp eci \201 c tasks (more common with localized muscle weakness) Grade muscle strength with standardized score (see b \200\230HOW TO Grade muscle strength \200\231, p.479) for later comparisons A lack of demonstrable muscle weakness, despite symptoms usually indicates asthenia Check for fatigability (may indicate myasthenia gravis) \200 Ask about CNS disease and ex amine neurologically (brisk re \202 exes with upgoing plantars point to the CNS, whereas absent re \202 exes may indicate periphera l nerve disease) Check the joints for degenerative disease; ask about pain and stiffness \200 Look for evi dence of systemic disease (eg thyroid, malignancy) \200 Assess mood MUSCLE SYMPTOMS 479 Investigations \200 Screening bloods should include: K, Ca, Mg, urea, creatinine, LFTs, T FTs, autoantibody screen, FBC, ESR, CRP, serum electrophoresis and haematinincs. CK is elevated after intense exercise or an intramuscular injection or with pathology of the muscle unit Plain X-rays can reveal joint disease \200 Ultrasound can be used to assess joints and mu scle \200 CT or MRI scans can demonstrate CNS pathology, cord problems, and degree of muscle atrophy Electrodiagnostic testing (nerve conduction studies and electromyography) is useful to demonstrate nerve pathology, problems with neuromuscular tra nsmission and intrinsic muscle disease. It can con \201 rm the diagnosis in a number of co nditions (eg chronic in \202 ammatory demyelinating polyneuropathy) Muscle biopsy can sometimes be useful HOW TO Grade muscle strength The widely used Medical Research Council grading system allows sequential assessments to be compared. It involves assessing muscle activity in isolation, against gravity and against resistance, and is scored as follows (Table 17.1 ). Table 17.1 Medical Research Council grading system 0 No muscle contraction 1 Flicker or trace of muscle contraction 2 Limb or joint movement possible only with gravity eliminated 3 Limb or joint movement against gravity, but not resistance 4 Power decreased but limb or joint movement possible against resistance 5 Normal power against resistance Scores can be augmented if the category is not quite reached ( \200\223) or slightly exceed ed ( + ) eg minor reduction in power against resistance may be described as 5 \200\223. 480 CHAPTER 17 Musculoskeletal system Paget \200\231s disease This is a very common bone disease of old age (up to 10 % prevalenc e, more common in men). It is usually clinically silent \200\224 only about 5 % are sympto matic. It is thought to be due to a slow viral infection of osteoclasts, which causes abnormal bon e remodeling. Most commonly affects pelvis, femur, spine, skull, and tibia. The resultant b one is expanded and disordered and can cause pain, pathological fracture, and predisposes t o osteosarcoma. Presentation \200 Most commonly as asymptomatic elevated ALP \200 Often an incidental \201 nding on a pelvis or skull X-ray \200 Less commonly as: Pathological fracture (especially hip and pelvis) \200 Bone pain : constant pain commonly in legs, especially at night. The diseased bone itself can be painful or deformity can lead to accelerated joint disease at eg hip, knee or spine. Fracture or osteosarcoma can cause suddenly increased pain Deformity : bowing of legs or upper arm is often asymmetrical. The skull can take on a char acteristic \200\230bossed \200\231 shape due to overgrowth of frontal bones Deafness : bone expansion in the skull compresses the eighth cranial nerve causing conduction deafness, which can be severe \200 Other neurological compressio n syndromes , eg spinal cord (paraplegia), optic nerve (blindness), brainstem compression (dysphagia and hydrocephalus) Investigations \200 ALP is constantly elevated The bone isoenzyme is more speci \201 c and useful when liver function is abnormal Rarely (eg if only one bone is involved), total ALP can be normal but the bone isoenzyme is always raised Other markers of bone turnover, eg urinary hydroxyproline are raised \200 X-rays show mix ed lysis and sclerosis, disordered bone texture, and expansion (a diagnostic feature) Radioisotope bone scans show hot spots \200 Immobile patients with very active disease ca n become hypercalcaemic although this is rare. If calcium and ALP are raised, there is more likely to be another diagnosis (eg carcinomatosis, hyperparathyroidism) PAGET \200\231S DISEASE 481 Management As most cases are asymptomatic, often no treatment is required. Symptomatic case s may warrant referral to a rheumatologist \200 Analgesia and joint replacement may be ne eded \200 Fractures often require internal \201 xation to correct deformity and because they heal poorly Bisphosphonates (usually by iv infusion) are very useful. They have several effects: \200 Reduce pain \200 Reduce vascularity before elective surgery \200 Improve healing after fracture \200 Improve neurological compression syndromes \200 R educe serum calcium in hypercalcaemia Calcitonin is now rarely used \200 ALP, other bone turnover biochemical markers, and occa sionally nuclear bone scans can be used to monitor the effectiveness of treatment 482 CHAPTER 17 Musculoskeletal system Gout Uric acid crystals deposit in and around joints and intermittently produce in \202 am mation. Serum urate levels equate poorly with the disease manifestations. Increased incidence with age due to: Worsening renal function and impaired uric acid excretion \200 Increased hyperuricaemic d rug use, eg thiazides, aspirin, cytotoxics \200 Common acute precipitants, eg sepsis, sur gery Presentation \200 Acute monoarthritis in feet or hands is most common, but can also occur in large joints such as knee or shoulder. The joint is very painful, hot and red. Pat ients often refuse to bear weight or move the joint. The patient can look unwell and someti mes has a fever Chronic tophi (usually painless) over \201 nger joints and in ears can occur, associated with a chronic arthritis. Sometimes mistaken for other more common arthritides Olecranon bursitis \200 Uric acid kidney stones Investigations \200 During an acute attack serum uric acid may be normal or high \200 W BC , ESR , and CRP are usually high or very high \200 Joint \202 uid : May be cloudy or frankly purulent on visual inspection \200 Microscopy shows many in \202 ammatory cells \200 Under polarized light, negatively birefringent uric acid crystal s are seen in joint \202 uid or in phagocytes X-rays are usually normal (rarely see small punched-out erosions in \201 ngers in chronic tophaceous cases) The main aim is to exclude an infective arthritis. 2If in doubt, consider using iv antibiot ics until cultures are negative. Treatment \200 For acute gout : \200 Use paracetamol with a course of NSAIDs (consider gastric protection) \200 If you have ruled out infection, local steroid injections are of ten effective (eg methylprednisolone 40mg intra-articular) If NSAIDs are contraindicated (eg renal impairment) use a short course of oral steroids (eg prednisolone 40mg od for 7 days) or colchicine 0.5mg stat then 0.5mg every 6 \200\2238hr u ntil pain is controlled or diarrhea/vomiting side effects prohibit further use. Colchicine is an effective drug but dif \201 cult to use correctly \200\224 you will need to explain this protocol carefully to patient/carers For chronic arthritis with or without tophi: treat with allopurinol or uricosuric drugs (probenecid and sul \201 npyrazone). Uricosuric drugs are contraindicated in renal stones GOUT 483 Prevention One or two attacks of gout probably do not warrant prophylaxis (espe- cially as such drugs can precipitate further attacks). Instead, try: \200 Changing drugs (stop thia zides and aspirin) \200 Lifestyle advice: Reduce alcohol (beer is preferable to lager or wine) \200 Reduce dietary purines (meat) \200 Lose weight Do not leave patients on long-term NSAIDs. Very early use of NSAIDs or colchicine can abort a severe attack of gout Several attacks of gout merit slow introduction of allopurinol or urico- suric agents. This may cause a \202 are of acute gout \200\224 cover the introduction of therapy with NSAI Ds or low-dose colchicine. 484 CHAPTER 17 Musculoskeletal system Pseudogout Features This is an acute, episodic synovitis closely resembling gout except tha t: \200 Calcium pyrophosphate rather than uric acid crystals (with positive rather than negative birefringence) are found Large joints are more commonly affected (especially knees but also shoulder, hips, wrists and elbows) It is not associated with tophi, bursitis, or stones \200 X-rays often show calci \201 c ation of articular cartilage \200\230chondrocalcinosis \200\231 in the affected joint It doesn \200\231t respond to allopurinol or uricosuric agents \200\224 so consider this diagnosis where recurrent attacks persist despite allopurinol As with gout the patient has an acutely in \202 amed joint which is very painful to move. They may be systemically unwell with a fever and highly elevated in \202 ammatory markers. Serum calcium is normal. 2Consider this diagnosis in the post-acute patient with a hot swo llen wrist. Management Make a con \201 dent diagnosis. This usually involves immediate synovial \202 uid sampling and urgent microscopy to exclude infection and gout. Effective treatments for acute pseudogout include: Intra-articular steroid injections \200 Oral NSAIDs \200 Oral corticosteroids \200 Co lchicine Long-term preventative treatment is very rarely needed. CONTRACTURES 485 Contractures Contractures are joint deformities caused by damaged connective tissue. Where a joint is immobilized (through depressed conscious level, loss of neural input, or local t issue damage) the muscle, ligaments, tendons, and skin can become inelastic and shortened c ausing joints to be \202 exed. Common causes worldwide include polio, cerebral palsy, and leprosy; in geriatric medicine c ommon causes include stroke, dementia, and musculoskeletal conditions, eg fracture. Contrac tures are an under- recognized cause of disability \200\224 they occur to some degree in a bout a third of nursing home residents and it is still not uncommon to \201 nd patients w ho are bedbound and permanently curled into the fetal position. Problems \200 Pain : especially on moving joint but can occur at rest \200 Hygiene : sk in surfaces may oppose (eg the hand after stroke or groins in abduction/ \202 exion contra ctures) making it dif \201 cult for carers and painful for the patient to keep clean and o dorless Pressure areas : abnormal posture increases risk \200 Esthetics : although the lack of mo vement causes most disability the abnormal posture/appearance can be more noticeable Function : chronic bedbound patients may become so \202 exed that they are unable to sit out in a chair Prevention \200 Where immobilization is short term, eg after a fracture, passive stretching followed by exercise regimens should be initiated promptly \200 All healthcare staff should understand the importance of maintaining mobility (including sitting out of bed for short periods) and positioning of immobile patie nts Preventative measures are rarely successful at preventing contractures in joints with long- term immobility, eg in residual hemiparesis after stroke. Splinting might help mold the pos ition Treatment \200 Periodic injection of botulinum toxin may be helpful where muscle spasticity is the major problem. There are no real adverse effects but some patients develo p an antibody response after repeated treatment, which renders therapy less effective. Newe r preparations are less immunogenic There is little point using muscle relaxants except to help with pain. Even then drugs such as baclofen, dantrolene, tizanidine, and diazepam usually cause side e ffects of drowsiness before they reach therapeutic levels. Occasionally assist with physiot herapy stretches Surgery eg tendon division has a place in severe cases \200 Physiotherapy can to some ext ent reverse established changes, especially if not severe and of relatively recent onset Repositioning with serial plaster casts takes a long time and is really only used in younger patients 486 CHAPTER 17 Musculoskeletal system Cervical spondylosis and myelopathy Degeneration in the cervical spine causes neurological dysfunction with both radiculopathy (compression of nerve roots leaving spinal foramina) an d myelopathy (cord compression). The resulting mixture of lower (nerve root) and upper (cor d) nerve damage causes pain, weakness and numbness. Progress is usually gradual but can be sudden (especially fol- lowing trauma). The disease is unusual before the age of 50. Mild f orms are very common in the elderly population. History \200 Neck pain and restricted movement may be present but are neither speci \201 c nor sensitive markers of nerve damage. Pain may radiate to shoulder, chest or arm in a d ermatomal distribution (see b Appendix, \200\230Dermatomes \200\231, p.686) Arms and hands become clumsy especially for \201 ne movements (eg doing up buttons). Weak ness, numbness and paraesthesia can occur \200 Leg symptoms usually occur later, with a U MN spastic weakness and a wide-based and/or ataxic gait, often with falls Urinary dysfunction is unusual and late \200 Rarely can cause vertebrobasilar insuf \201 ciency symptoms