Musculoskeletal System

Osteoarthritis

Osteoarthritis (OA) is the most common joint disorder in older patients causing 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)
Vascular congestion
New growth of cartilage and bone (osteophytes)
Capsular fibrosis

Inherited factors determine susceptibility but individual genes not identified. Increasing age is the strongest 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 avoidable 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

Pain—assess severity, disability and impact on life (handicap). Usually insidious in onset and variable over time, worse with activity and relieved by rest. Chronic pain may cause poor sleep and low mood
Only one or a few joints are affected with minimal morning stiffness and often worsening of symptoms during the day
Restricted movement—eg walking, dressing, rising from a chair
Severe OA can contribute to postural instability and falls

Investigations

▶OA is a clinical diagnosis. Symptoms correlate poorly with radiological findings. The main role of X-ray is in assessing severity of structural change prior to surgery. Features include joint space narrowing, osteophytes, sclerosis, cysts, and deformity. Blood tests are normal even when an osteoarthritic joint feels warm—reconsider your diagnosis if inflammatory markers are elevated.

Osteoarthritis: management

OA is the most common, chronic painful condition. Drug dependence and side effects are a big problem.

▶Always consider non-pharmacological treatments first.

Non-drug treatments

Exercise: stretching and strengthening. Swimming, yoga, and Tai Chi are particularly good. Encourage the patient to exercise despite the pain—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 fix but influences other health outcomes
Sensible footwear: soft soles with no heels. Trainers are ideal
Walking aids: eg stick (in contralateral hand)
Education and support: can improve pain and function
Osteopaths or chiropractors help some patients but are expensive

Drug treatments

▶▶No patient should be offered more dangerous medication unless they have tried and failed regular paracetamol in maximum dose (1g qds). Patients may need persuading to try a regular prophylactic dose, perceiving it as a ‘weak’ drug.

The next step is to add a low potency opiate—often combined with paracetamol, eg co-codamol (start with codeine 8mg/paracetamol 500mg ii qds). Beware constipation and sedation
A short course of oral NSAIDs can be useful in acute exacerbations but try to avoid long-term use. If NSAIDs are used for more than 2 weeks or in the presence of known dyspepsia or ulceration, reduce the gastrointestinal risk by co-prescribing, eg lansoprazole 15mg od. The COX-2 selective inhibitors have better gastrointestinal tolerability but have fallen from favour due to vascular adverse events
Intra-articular steroids (eg triamcinolone hexacetonide 20mg) can be rapidly effective particularly if the joint is hot/very painful. There is a substantial placebo effect, but symptoms tend to recur after 4-6 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
Counter-irritants, eg capsaicin cream are safe and have some effect
Oral chondroitin and glucosamine are available unlicensed over-thecounter and are very widely used. They may have a slow-onset mild analgesic action and may slow the progression of disease

Surgical treatment

Includes arthroscopic joint wash-outs and joint replacements. Indications include pain, deformity or joint instability where other treatments have failed. Outcomes can be excellent for fitter older people, but caution in the frail for whom it is rarely beneficial overall.

Further reading

NICE. The care and management of osteoarthritis in adults (2008) online:

www.nice.org.uk/cg59.

Harvey WF, Hunter DJ. (2010). Pharmacological intervention for osteoarthritis in older adults. Clin Geriatr Med 26(3): 503-15.

Osteoporosis

Osteoporosis is the reduction in bone mass and disruption of bone architecture, resulting in increased bone fragility and fracture risk. Results from prolonged imbalance in bone remodelling where resorption (osteoclastic activity) exceeds deposition (osteoblastic activity).

Osteoporosis is very common and very much under-recognized and under-treated. In combination with falls (see

‘Interventions to prevent falls’, p.106) osteoporosis contributes 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.

▶If you make the diagnosis do not delay initiating secondary prevention. Always think of osteoporosis when assessing postoperative orthopaedic patients.

Pathology

Total bone mass increases throughout childhood and adolescence, peaks in the third decade, and then declines at about 0.5% per year
Bone loss is accelerated after the menopause (up to 5% per year) and by smoking, alcohol, low body weight, hyperthyroidism, hyperparathyroidism, hypoandrogenism (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

Osteoporosis itself is asymptomatic—it is the fractures that cause problems
Often presents with an acute fragility (ie low energy) fracture—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:
- An incidental, asymptomatic finding (in around a third)
- Acute painful fracture
- A progressive kyphosis (‘Dowager’s hump’). The bent-over posture is not just unattractive, it causes loss of height, protuberant belly, abdominal compression, oesophageal reflux, and impaired balance with further predisposition to falls and fracture. Restricted rib movements lead to restrictive lung disease

Diagnosis

▶Blood tests are normal (except after a fracture). If calcium or ALP is elevated consider alternative diagnosis, eg metastases or Paget’s disease.

X-rays may show fractures and give an idea of bone density
The gold standard is dual X-ray absorptiometry (DEXA) scanning (rarely employed in the elderly population but useful in younger women). Usually two scores are quoted at hip and spine. The T-score compares bone density to peak bone mass while Z score compares it to age/sex/weight-matched sample. A T-score less than -2.5 indicates osteoporosis, with scores -1 to -2.5 indicating osteopenia
Peripheral densitometry assessments can be done at the heel and ankle, the advantage being that the required machine is more portable. Results correlate with formal testing, but there are concerns about reliability
Think of secondary causes:
- TSH in all
- Testosterone levels in men

In a woman aged >65 years, a pragmatic approach is to assume that osteoporosis exists where there is a:

Low energy fracture of wrist, femoral neck, or vertebra
Progressive kyphosis without features of malignancy

Primary prevention of osteoporosis

Sensible public health measures (eg diet, exercise, 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 significant steroid therapy (>7.5mg/day for more than a month) (see ‘Osteoporosis: management’, p.470)
HRT is not particularly effective—postmenopausal bone loss returns after it is stopped. Increased thromboembolic, cancer, and vascular risk argue strongly against its use

Osteoporosis: management

Oral calcium and vitamin D is cheap and effective, especially in frail institutionalized people (possibly due to treatment of osteomalacia and associated myopathy as much as osteoporosis). Tablets are large and chalky—can be unpalatable. Effervescent 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 fit older people
Bisphosphonates are very effective, and used as first line. NICE recommends in any woman aged >75 following a fragility fracture (without the need for DEXA scanning)
- 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 daily calcium and vitamin D.
- Etidronate is also NICE recommended and comes in a preparation that includes calcium (Didronel PMO®) but must be taken daily
- Upper gut ulceration 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 sitting or standing for 30min after swallowing
- Up to 15% of patients are ‘non-responders’ 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
- Longer-acting iv preparations (eg zoledronic acid) are also available but cost/benefit ratio is still under evaluation
- Osteonecrosis of the jaw is a rare, but serious side effect (increased risk with cancer, steroid treatment, and poor dental hygiene). Stop the drug and refer to a maxillofacial surgeon
Strontium ranelate is recommended by NICE as second line if bisphosphonates are not tolerated. Side effects include diarrhoea, vomiting, and thromboembolism
Teriparatide can also be used if bisphosphonates and strontium are not tolerated or ineffective. Recombinant fraction of parathyroid hormone, given by s/c injection. Expensive. Maximum course 18 months
Less common drugs, usually advised only by specialist teams include: raloxifene (an oestrogen-like drug which decreases bone loss without measurable effects on the uterus, used if bisphosphonates are not tolerated or in non-responders) and calcitonin (available in nasal spray 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—secondary prevention including strontium ranelate (2011) online:

www.nice.org.uk/ta161.

HOW TO … Manage non-operative fractures

Fractures that very rarely require operative intervention include pelvis, humerus, wrist, and vertebra
Other fractures, often immobilized surgically in younger people, may be treated more conservatively in older patients to avoid perioperative risks (eg fractured tibial plateaux may simply be immobilized by plaster of Paris (POP) or splinting)
Patients with these ‘non-operative’ fractures are often cared for by geriatricians having been transferred either:
- From A&E, to medical, ortho-medical or ortho-geriatric units
- From orthopaedic wards for ongoing rehabilitation
Minor fractures can result in significant functional impairment, eg a Colles’ fracture and POP may prevent an older person washing, dressing, and toileting. Even walking may not be possible (if a frame can no longer be used)

General principles of management

These include:

Control of pain. This allows earlier mobilization and reduces the risks of immobility (pressure sores, pneumonia, thromboembolism)
- Consider novel treatments such as heat, TENS, calcitonin, bisphosphonates, or vertebroplasty for vertebral fracture
- A short course of NSAIDs is sometimes appropriate in low-risk patients, but remember to reduce analgesia as soon as possible
Encouraging mobility and independence as early as possible. Best achieved in a rehabilitation unit. Patient and family often expect ‘bed rest’ after a fracture and may need to be educated
Consider the mechanism of the fall and injury (see ‘Assessment following a fall’, p.104)—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 orthopaedic colleagues. They can advise on when to replace/remove plasters and how much exercise/weight bearing is appropriate. Ask for reassessment if progress is poor, eg ongoing severe pain, or apparent malunion—sometimes a diagnosis has been missed or an interval operation is needed
A pragmatic approach to weight-bearing may be needed, eg in dementia (where concordance with non-weight bearing is difficult), 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 formation or delay bone union)
Start to plan discharge early. Many patients can be managed at home with a care package and outpatient rehabilitation. Others may need transitional care beds (eg while they wait to be weight-bearing or for plasters to be removed) after which they can return to an active rehabilitation programme prior to going home

Polymyalgia rheumatica

Polymyalgia rheumatica (PMR) is a common inflammatory syndrome causing symmetrical proximal muscle aches and stiffness. It affects only older people (do not diagnose it under age 50). There is rapid (days) onset of shoulder and then thigh pain that is worse in mornings. Sometimes associated malaise, weight loss, depression, and fever. Often quite disabling with little to find on examination.

Pathology

Pathogenetically similar to giant cell arteritis (temporal arteritis); the two conditions commonly coexist, and may represent a spectrum of disease. Pain in PMR is thought to be due to synovitis and bursitis.

Diagnosis

▶A difficult diagnosis to make reliably—a significant number of patients are misdiagnosed. The following should be present for a firm diagnosis:

Age >50
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: neck or torso, shoulders or proximal regions of the arms, and hips or proximal aspects of the thighs
ESR >40

The following should also be considered:

Suggestive symptoms with raised inflammatory markers (ESR/CRP) and no other apparent cause may warrant treatment trial
Often have anaemia (usually normochromic normocytic) and mild abnormalities of liver (especially ALP) or renal function
Clinical examination often normal—despite the name, muscle tenderness is absent and pain arises because of bursitis/synovitis. Rarely there may be palpable synovitis in peripheral joints (eg knee, wrist)
Muscle enzymes, and EMG are normal
Temporal artery biopsy is positive in less than 25% and is rarely done.
Exclude other causes (eg connective tissue disease, tumour, chronic infection, neurological diseases) particularly if a patient does not respond quickly to steroids

Treatment

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 both settle, then restart tailing more slowly
Some patients can be taken off steroids after 6-8 months but most need long-term steroids (mean duration 2-3 years)
Always give bone protection (eg alendronate 70mg once weekly with calcium and vitamin D). If a treatment trial, wait until diagnosis clear
Azathioprine or methotrexate may be used as steroid-sparing agents
Educate and involve the patient in monitoring disease

Diagnostic dilemma and steroid ‘dependency’

Some older patients who were diagnosed with PMR years ago no longer exhibit or remember their symptoms, and will be having steroid side effects. They may resist steroid withdrawal or experience symptoms as steroids are decreased or withdrawn, even if the characteristic syndrome and inflammatory 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 ‘pseudo-rheumatism’.

Avoid this difficult situation by:

Comprehensive assessment at onset with good record-keeping, so that others can reappraise the diagnosis if response to treatment is poor
Ensuring that where the diagnosis is not clear, a treatment trial is reviewed early for impact—if the response is not convincing, then stop the steroids. ▶Beware continuing steroids because the patient feels ‘a bit better’
Considering the differential diagnosis carefully
Discussing diagnosis and treatment with the patient
Agreeing with the patient a clear plan for reviewing steroid therapy
Explaining that steroid withdrawal can cause muscle aches, but the blood tests help us distinguish between this and disease reactivation

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 age of presentation 70 (does not occur age <50). More common in women and Scandinavia/northern Europe.

Pathogenesis

Chronic vasculitis, mainly involving cranial branches arising from the aortic arch. Similar pathology seen in PMR, but different distribution
Possibly an autoimmune mechanism but no antibodies/antigen isolated

Clinical picture

Systemic: fever, malaise, anorexia, and weight loss
Muscles: symmetrical proximal muscle pain and stiffness as in PMR
Arteritis: tenderness over temporal arteries—not so much a headache as scalp tenderness. Classically unable to wear a hat or brush hair. If an artery occludes, distal ischaemia or infarction occurs
- Headache is present in 90% (due to ischaemia or local tenderness of facial or scalp arteries)
- Jaw claudication (occlusion of maxillary artery)
- Amaurosis fugax or blindness are due to occlusion of the ciliary artery, which supplies the optic nerve—this causes a pale swollen optic nerve but not retinal damage (which is a feature of central retinal artery occlusion with carotid disease)
- Stroke (carotid artery)
- Any large artery including the aorta can be affected.

▶Always suspect GCA if amaurosis fugax involves both eyes (atheroma is more commonly unilateral).

Investigations

ESR usually >100
CRP also very high and falls faster with treatment than ESR
May have normochromic normocytic anaemia and renal impairment.
Temporal artery biopsy (TAB) is highly specific, and therefore the gold standard test. Because the vasculitis may be patchy, TAB is not always positive, ie the sensitivity is moderate. TAB becomes negative quickly (1-2 weeks) with treatment