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

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.

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.

15.2 CAUSES OF POLYARTHRITIS

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

Lesion	Pain	Examination findings, tests
‘Tennis elbow’	Lateral epicondyle Radiation to extensor forearm	Tender over epicondyle Pain reproduced by resisted active wrist extension
‘Golfer’s elbow’	Medial epicondyle Radiation to flexor forearm	Tender over epicondyle Pain reproduced by resisted active wrist flexion
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

Lesion	Pain	Examination findings, tests
Trochanteric bursitis	Upper lateral thigh, worse on lying on that side at night	Tender over greater trochanter
Pre-patellar bursitis	Anterior patella	Tender fluctuant swelling in front of patella
Popliteal cyst (‘Baker’s cyst’)	Popliteal fossa	Tender swelling of popliteal fossa, usually reducible by massage with knee in mid-flexion
Plantar fasciitis	Under heel, worse on standing and walking	Tender under distal calcaneus/plantar fascia insertion site
Achilles tendinitis	Localised to tendon	Tender on squeezing tendon Pain reproduced by standing on toes or resisted plantar flexion

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:

• Age <20 or >50 yrs.

• Constant, progressive pain unrelieved by rest.

• Thoracic pain.

• Past medical history or symptoms of malignancy or TB.

• Systemic corticosteroid use.

• Constitutional symptoms: sweats, malaise, weight loss.

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).

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.

15.6 CAUSES OF NECK PAIN

Mechanical	e.g. Postural, ‘whiplash’, disc prolapse, cervical spondylosis
Inflammatory	e.g. Infection, spondylitis, RA, polymyalgia rheumatica
Neoplasia	e.g. Bony metastases, myeloma
Fibromyalgia
Referred pain	e.g. Pharynx, teeth, angina, Pancoast tumour

BONE PAIN

Causes of bone pain are listed in Box 15.7.

15.7 CAUSES OF BONE PAIN

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:

• Patient education.

• Pain control.

• Optimising function.

• Beneficially modifying the disease process.

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.

Fig. 15.1 COX-1 and COX-2 pathways.

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.

15.9 EXAMPLES OF SLOW-ACTING ANTIRHEUMATIC DRUGS^*

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.