15 Musculoskeletal disorders
Disorders of the musculoskeletal (MSK) system are extremely common, accounting for up to a quarter of new consultations in general practice. They are the single most frequent cause of physical disability in the elderly. The principal manifestations are pain and impairment of locomotor function. Non-inflammatory conditions are far more prevalent than inflammatory disease. Osteoarthritis is the most common joint disorder, with knee involvement a major cause of disability. Osteoporosis is the most prevalent bone disorder, with 1 in 3 women sustaining an osteoporotic fracture at some point during their lifetime.
PRESENTING PROBLEMS
JOINT PAIN
ACUTE MONOARTHRITIS
Causes of acute inflammation in a single joint are listed in Box 15.1. The site affected rarely helps to identify the cause except in the case of gout, which typically affects the first metatarsophalangeal joint.
15.1 CAUSES OF ACUTE MONOARTHRITIS
Joint aspiration is normally required to exclude sepsis and to look for crystals.
OLIGOARTHRITIS
Oligoarthritis is arthritis affecting two, three or four joints. By far the most common cause is osteoarthritis (OA), which is a non-inflammatory condition characterised by degenerative joint change. Inflammatory oligoarthritis mainly targets lower limb joints and is usually asymmetrical; it is a common presentation of seronegative spondarthritis (e.g. reactive arthritis, psoriatic arthritis, ankylosing spondylitis, enteropathic arthritis). Sequential joint involvement ascending a limb suggests sepsis.
CLINICAL EXAMINATION OF THE MUSCULOSKELETAL SYSTEM
POLYARTHRITIS
Polyarthritis is inflammation affecting five or more joints. The symmetry and pattern of involved joints are important in determining the cause (Box 15.2). Accompanying periarticular or extra-articular features may aid diagnosis.
Cause | Characteristics |
---|---|
Non-inflammatory | |
Generalised osteoarthritis | Small and large joints, only a few joints symptomatic at any one time |
Inflammatory | |
Rheumatoid arthritis, juvenile idiopathic arthritis | Symmetrical, small and large joints, upper and lower limbs |
Seronegative spondarthritis (psoriasis, reactive, ankylosing spondylitis, enteropathic arthropathy) | Asymmetrical, large > small joints, lower > upper limbs, spondylitis |
Lupus | Symmetrical, small > large joints, joint damage uncommon |
Chronic gout | Distal > proximal joints preceded by acute attacks |
Viral arthritis | Very acute, self-limiting (<6 wks) |
Chronic sarcoidosis | Symmetrical, small and large joints |
Many viral infections can cause the rapid onset of an acute symmetrical inflammatory polyarthritis affecting small and large joints of the upper and lower limbs. The arthritis is usually self-limiting within 6 wks. Typical viruses include hepatitis B and C, mumps, rubella and infectious mononucleosis. The rapidity of onset, the presence of fever and the characteristic ‘viral’ rash suggest the diagnosis.
REGIONAL PERIARTICULAR PAIN
SINGLE REGIONAL PAIN
This usually results from over-usage strain or injury affecting a periarticular structure. Certain movements reproduce the pain. Examination reveals localised periarticular tenderness but minimal signs of inflammation. The pain may be reproduced by resisted active movement or by stressing the involved structure. Diagnosis is usually clinical. Management is aimed towards avoiding predisposing mechanical factors, pain relief and appropriate exercise to restore function.
Shoulder pain
Rotator cuff syndrome: In this common condition, tendinitis or bursitis around the glenohumeral joint causes pain which is reproduced by resisted movement. Treatment is by physiotherapy, analgesia and steroid injections.
Adhesive capsulitis (‘frozen shoulder’): This presents with upper arm pain that progresses over 4–10 wks before receding over a similar time course. Glenohumeral restriction is present from the outset, but progresses and reaches its maximum as the pain is receding. In the early phase there is marked anterior joint tenderness and pain at extremes of movement; later there is painless restriction, often affecting all movements. Treatment comprises analgesia, local corticosteroid injection and regular ‘pendulum’ exercises of the arm. The natural history is for slow but complete recovery.
Elbow pain
Lateral epicondylitis (‘tennis elbow’): The most common periarticular lesion (Box 15.3).
15.3 PERIARTICULAR LESIONS PRESENTING AS ELBOW PAIN
Lesion | Pain | Examination findings, tests |
---|---|---|
‘Tennis elbow’ | ||
‘Golfer’s elbow’ | ||
Olecranon bursitis | Olecranon | Fluctuant tender swelling over olecranon |
Olecranon bursitis: Can follow local repetitive trauma but may also be secondary to infection, gout or RA.
Disorders of the hand and wrist
Trigger finger: This tenosynovitis in the flexor tendon sheath causes intermittent locking of the finger in flexion. Local corticosteroid injection often relieves the problem and surgery is rarely required.
De Quervain’s tenosynovitis: Inflammation of the tendon sheaths of abductor pollicis longus and extensor pollicis brevis leads to pain over the radial aspect of the distal forearm and wrist. Examination reveals distal radial tenderness, sometimes with associated crepitus. The condition is usually caused by repetitive over-usage.
Dupuytren’s contracture: Results from fibrosis and contracture of the superficial palmar fascia. Inability to extend the fingers fully is associated with puckering of the skin. The ring and little fingers are generally the worst affected but the condition is usually painless. Dupuytren’s contracture is age-related, more common in men and often familial. It is also associated with alcohol misuse.
Lower limb pain
Causes of periarticular pain affecting the lower limb are listed in Box 15.4.
15.4 PERIARTICULAR LESIONS IN THE LOWER LIMB
BACK AND NECK PAIN
LOW BACK PAIN
Back pain is extremely common. In the UK, 7% of the adult population consult their GP each year with back pain, at a cost of 80 million lost working days.
Clinical assessment
The vast majority of cases are due to simple mechanical back pain and are managed conservatively. The aim of history and examination is to identify the small number of patients with serious spinal pathology who require specific investigation and treatment.
Mechanical pain: Accounts for >90% of back pain episodes, usually affecting patients aged 20–55 yrs. It is more common in heavy manual workers. The pain is often sudden in onset, and is associated with lifting or bending. Symptoms are worsened by activity and relieved by rest. Pain is typically asymmetrical and is confined to the lumbosacral region, buttock or thigh, but there is no clear-cut nerve root distribution (unlike radicular pain). Examination may reveal local paraspinal muscle spasm with painful restriction of movement. Mechanical pain has a good prognosis, with 90% recovery at 6 wks. Psychological factors (e.g. job dissatisfaction, depression) increase the risk of progression to chronic disability.
Non-mechanical pain: Causes of non-mechanical pain include bony destruction due to malignancy, fracture or infection. The pain is constant and progressive, and shows little variation with activity. ‘Red flag’ features suggesting serious spinal pathology include:
Examination may reveal painful spinal deformity with signs at multiple nerve root levels. In all cases it is important to exclude signs of cauda equina syndrome (see below).
Inflammatory pain: Pain due to spondylitis is gradual in onset and often occurs before the age of 30 yrs. It is usually axial, symmetrical and spread over many segments. Sacroiliitis causes maximal pain in the buttock, with radiation down the posterior thigh. Patients often experience morning stiffness which improves with activity.
Radicular (nerve root) pain: This is commonly caused by a prolapsed intervertebral disc in young adults, most commonly at L4 or L5. Patients experience severe, sharp pain radiating down the back of the leg beyond the knee (‘sciatica’). The unilateral leg pain is worse than the low back pain, and is aggravated by coughing and straining. Straight leg raising reproduces the pain, and examination may reveal motor weakness and/or sensory loss limited to one nerve root with loss of the corresponding reflex. Around 50% of patients recover by 6 wks with conservative management only. Compression of multiple nerve roots in the cauda equina constitutes a medical emergency (Box 15.5).
Investigations
NECK PAIN
Neck pain is less common than back pain but is a particular problem in elderly patients. It is usually due to mechanical or degenerative problems (Box 15.6). Nerve roots and/or the cervical cord may be compromised by osteophytes or disc prolapse (usually C6 disc compressing the C7 root). Surgery is occasionally required for severe radiculopathy or cervical myelopathy. The principles of investigation and management are similar to those for back pain.
BONE PAIN
Causes of bone pain are listed in Box 15.7.
Cause | Characteristics |
---|---|
Fracture (high-energy fractures, osteoporotic fractures, pathological fractures, e.g. secondary to bony metastases) | Acute pain, tenderness and deformity |
Metastatic bone disease or primary bone tumour | Progressive, localised, associated weight loss and fatigue |
Paget’s disease | Localised to affected sites +/− deformity |
Osteomalacia | Bone tenderness and associated limb girdle weakness |
Chronic infection (osteomyelitis) | |
Renal bone disease |
MUSCLE PAIN AND WEAKNESS
It is important to distinguish between a subjective feeling of generalised weakness or fatigue, and ‘true’ weakness with objective loss of muscle power. The former is a non-specific manifestation of many organic diseases and also of psychological distress. The latter, however, may indicate intrinsic muscle disease. Proximal muscle weakness causes difficulty in standing from a seated position, squatting and lifting overhead. Distal power (e.g. grip) is usually preserved. Causes of proximal myopathy are listed in Box 15.8. Distal muscle weakness normally has a neurological cause.
15.8 CAUSES OF PROXIMAL MUSCLE PAIN AND WEAKNESS
Inflammatory | e.g. Polymyositis, dermatomyositis |
Endocrine | e.g. Hypothyroidism, hyperthyroidism, Cushing’s syndrome, Addison’s disease |
Metabolic | e.g. Glycogen storage disorders, hypokalaemia, osteomalacia |
Drugs/toxins | e.g. Alcohol, fibrates, statins |
Infections | e.g. HIV, cytomegalovirus, Epstein–Barr, schistosomiasis |
Genetic | e.g. Muscular dystrophies |
The most sensitive biochemical test of muscle injury is creatine kinase (CK). However, although a raised level confirms the suspicion of muscle inflammation or necrosis, it does not establish the cause. Muscle biopsy and electromyography (EMG) may therefore be required to reach a precise diagnosis.
PRINCIPLES OF MANAGEMENT OF MUSCULOSKELETAL DISORDERS
Key aims of management of MSK conditions are:
These therapeutic objectives are achieved most effectively via a multidisciplinary team approach.
NON-PHARMACOLOGICAL INTERVENTIONS
Patient education has been shown to reduce pain and disability. Regular exercise helps strengthen muscles acting over compromised joints and improves function. Adverse mechanical factors should be addressed; examples include shock-absorbing footwear, walking aids, and weight loss in obese patients. Physical treatments such as local heat and ice packs can help induce muscle relaxation and symptom relief. Splints and orthoses help provide rest and support, and reduce joint instability. For those with severe disabilities, a variety of aids and appliances can be used to modify the environment and promote independence. Examples include raised toilet seats, high chairs, extended tap handles and devices to help pull on socks. Occupational therapy input is crucial for these individuals. Tuition in coping strategies (e.g. yoga, relaxation, avoiding maladaptive pain behaviour) can assist patients with incurable disease to deal with their chronic pain and disability.
PHARMACOLOGICAL OPTIONS FOR DIRECT SYMPTOM CONTROL
SIMPLE ANALGESIA
Paracetamol is effective for the treatment of mild to moderate pain. It acts by inhibiting central prostaglandin synthesis but has little effect on peripheral prostaglandin production. It is safe, has few contraindications and drug interactions, and is low in cost. It is therefore an appropriate first-line analgesic in most patients.
NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS)
NSAIDs (e.g. ibuprofen, diclofenac) are effective in combating pain and stiffness associated with inflammatory disease. They also help reduce bone pain due to metastatic deposits. They act by inhibiting cyclo-oxygenase (COX) and thereby reducing prostaglandin synthesis (Fig. 15.1). There are two isoforms of COX, encoded by distinct genes.
Details of the usage, dose and side-effects of NSAIDs are given on page 776.
NUTRIPHARMACEUTICALS
A wide variety of nutritional supplements are available for the relief of MSK symptoms. There are some data that glucosamine and chondroitin may provide modest pain relief in knee OA.
TOPICAL AGENTS
NSAID and capsaicin (chilli extract) creams provide safe and effective pain relief from arthritis (especially OA) and periarticular lesions. They may be used as monotherapy or as an adjunct to oral analgesics. Topical capsaicin causes pain fibres to discharge substance P. Initial application results in a burning sensation, but continued use reduces substance P activity with consequent pain reduction.
OTHER ANALGESICS
Stronger analgesics are sometimes required for moderate to severe pain. The weak opioids codeine and dihydrocodeine are relatively mild analgesics, but may be effective when combined with paracetamol. Their use is often limited by side-effects such as constipation and confusion, particularly in the elderly. Continuous opioid use can give rise to dependence and tolerance. The centrally acting analgesic tramadol can also be useful for severe pain, but can cause nausea, constipation, dizziness, somnolence and confusion. Patients with refractory symptoms may merit referral to a specialist pain team.
SLOW-ACTING ANTIRHEUMATIC DRUGS
These drugs suppress chronic inflammatory disease, but can take several months to exert a beneficial effect. They may reduce target tissue damage and are therefore also called ‘disease-modifying antirheumatic drugs’ (DMARDs). They are used in the management of RA, seronegative spondarthritis and connective tissue diseases. All DMARDs carry potentially toxic side-effects, and regular monitoring is therefore required. Some of these drugs increase the risk of infection due to their immunosuppressant effect, and patients should therefore receive annual influenza vaccination, and pneumococcal vaccination every 5–10 yrs. The drugs may also compromise immunosurveillance, increasing the risk of solid tumours and lymphomas. Further details of individual DMARDs are given in Box 15.9.
OTHER TREATMENTS
ANTICYTOKINES
The pro-inflammatory cytokine tumour necrosis factor alpha (TNF-α) plays an important role in the pathogenesis of RA and is therefore a prime therapeutic target. Infliximab is an anti-TNF-α monoclonal antibody which is administered by i.v. infusion. Etanercept is a synthetic anti-TNF biological agent. Although these drugs are more effective than standard DMARDs, they are costly. They also have potential side-effects including the risk of serious infection and of immunosuppression-related malignancy, particularly lymphoma. They are therefore recommended in the UK for active RA when treatment with at least two other DMARDs has failed. Rituximab may be used with methotrexate in patients who have not responded to anti-TNF therapy.
CORTICOSTEROIDS
Glucocorticoids have a rapid and dramatic anti-inflammatory action. However, prolonged use is accompanied by an unacceptable level of side-effects, including the risk of iatrogenic Cushing’s syndrome, steroid-induced diabetes and osteoporosis. Their use in MSK disorders is therefore generally reserved for rapid and short-term control of severe synovitis or systemic inflammation. They are also useful for control of inflammatory disease during pregnancy (when DMARDs are contraindicated) and for the treatment of polymyalgia rheumatica. Prednisolone is the oral steroid of choice. The aim is to use the lowest effective dose for the shortest possible time to avoid unnecessary side-effects.
LOCAL INJECTIONS
Intra-articular injection of a long-acting corticosteroid (e.g. triamcinolone) can be a useful adjunctive therapy for controlling synovitis affecting one or a few joints. Symptom relief typically lasts for 2–8 wks. Iatrogenic infection is the most important adverse effect, which can be avoided by proper aseptic technique. Other side-effects include local skin atrophy and temporary symptom exacerbation. Periarticular steroid injections can be used to provide rapid, effective pain relief for conditions such as bursitis, tenosynovitis and lateral epicondylitis. The steroid is sometimes combined with local anaesthetic to provide more rapid analgesia.
SURGERY
A variety of surgical interventions may help relieve pain and improve function in patients with MSK disorders. Knee and hip replacement are commonly done and highly successful. Other examples include carpal tunnel release for median nerve compression, tendon repairs and synovectomy. In some cases, joint fusion (arthrodesis) may be appropriate. Each operation should be considered as part of an integrated programme of management, and this is often best achieved via a multidisciplinary team approach.
OSTEOARTHRITIS (OA)
OA is by far the most common form of arthritis. It is strongly associated with ageing, with 80% of people over the age of 65 showing radiographic evidence of OA, although only 25–30% are symptomatic. It is characterised by focal loss of articular cartilage with new bone proliferation and remodelling of the joint contour. Inflammation is not a prominent feature. OA preferentially targets certain small and large joints (Fig. 15.2); the knee and hip are the principal large joints involved.

Fig. 15.2 The distribution of osteoarthritis. Although OA can affect any synovial joint, those shown in red are the most commonly targeted.
Family history is a major risk factor for OA. The condition is more common in Caucasians, and women are more commonly symptomatic. Most cases of OA are ‘primary’, meaning the cause of joint damage remains unclear; ‘secondary’ OA affects joints which have been subject to trauma or adverse loading over prolonged periods (e.g. knee OA in miners and footballers).
The pathogenesis of OA involves enzymatic degradation of aggrecan and collagen within the articular cartilage, with fissuring and thinning of the cartilage surface (Fig. 15.3). Cysts develop within the subchondral bone, possibly due to osteonecrosis resulting from increased pressure on the bone as the cartilage fails. At the joint margins there is new fibrocartilage production which then ossifies, forming osteophytes. Bone remodelling and cartilage thinning gradually alter the shape of the OA joint. This is commonly accompanied by wasting of the muscles acting across the joint, synovial hyperplasia and thickening of the joint capsule.
Clinical features
Nodal generalised OA: This common form of OA has a strong genetic predisposition and is more common in middle-aged women. Patients develop pain, stiffness and swelling affecting the finger interphalangeal joints (IPJs) (distal > proximal). Affected joints develop swellings which harden to become Heberden’s (distal IPJ) and Bouchard’s (proximal IPJ) nodes (Fig. 15.4). Involvement of the first carpometacarpal joint is also common. The condition is associated with a good functional prognosis. There is, however, an increased risk of OA at other sites (‘generalised OA’), especially the knee.

Fig. 15.4 Nodal osteoarthritis. Heberden’s nodes and lateral deviation of distal interphalangeal joints, with mild Bouchard’s nodes at the proximal interphalangeal joints.
Knee OA: May be primary or may be secondary to trauma; the latter is more common in men and is typically unilateral. Pain is usually localised to the anterior and medial aspects of the knee. Functional difficulties include prolonged walking, rising from a chair and bending to put on shoes. Examination findings may include:
Hip OA: Pain due to hip OA is usually maximal deep in the anterior groin, with variable radiation to the buttock, thigh or knee. Lateral hip pain, worse on lying on that side with tenderness over the greater trochanter, suggests secondary trochanteric bursitis. Functional difficulties are similar to those for knee OA. Examination may reveal:
Investigations
Management
Treatment follows the principles set out on page 577 and includes:
INFLAMMATORY JOINT DISEASE
RHEUMATOID ARTHRITIS (RA)
RA is the most common form of inflammatory arthritis in women. The typical clinical phenotype of RA is a symmetrical, deforming, small and large joint polyarthritis, often associated with systemic disturbance and extra-articular disease. The clinical course is usually life-long, with intermittent exacerbations and remissions and highly variable severity. RA occurs throughout the world and in all ethnic groups. The prevalence is lowest in black Africans and Chinese; in Caucasians it is around 1.0–1.5% with a female : male ratio of 3 : 1. Prevalence increases with age, with 5% of women and 2% of men >55 yrs being affected. Concordance rates are higher in monozygotic twins (12–15%) than in dizygotic twins (3%). Up to 50% of the genetic contribution to susceptibility is due to genes in the HLA region, particularly HLA-DR4.
RA is an autoimmune condition characterised by chronic inflammation, granuloma formation and joint destruction. The earliest change is swelling and congestion of the synovial membrane and the underlying connective tissues, which become infiltrated with lymphocytes, plasma cells and macrophages. Effusion of synovial fluid into the joint space takes place during active phases of the disease. Hypertrophy of the synovial membrane occurs, and inflammatory granulation tissue (pannus) spreads over the articular cartilage, causing progressive cartilage destruction. Muscles adjacent to inflamed joints atrophy and there may be focal infiltration with lymphocytes. Subcutaneous rheumatoid nodules are granulomatous lesions consisting of a central area of fibrinoid material surrounded by proliferating mononuclear cells. Similar nodules may occur in the pleura, lung and pericardium.
Clinical features
The diagnosis of RA is made clinically, and is supported by a raised ESR or CRP and, in the majority, a positive rheumatoid factor. The clinical hallmark of inflammatory joint disease is persistent synovitis. Diagnostic criteria for RA are listed in Box 15.10.
15.10 CRITERIA FOR DIAGNOSIS OF RHEUMATOID ARTHRITIS*
Diagnosis of RA is made with four or more of the following:
Other patterns of presentation also exist:

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