Chapter 11 Rheumatology and bone disease
Many common locomotor problems are short-lived and self-limiting or settle with a course of simple analgesia and/or physical treatment; e.g. physiotherapy or osteopathy. However, they represent 20–30% of the workload of the primary care physician, where non-inflammatory problems predominate. Recognition and appropriate early treatment of many painful rheumatic conditions may help reduce the incidence of chronic pain disorders. Early recognition and subsequent treatment of inflammatory arthritis by specialist multidisciplinary teams leads to better symptom control and prevents long-term joint damage and disability. The patient should always be included when decisions about treatment are being discussed. Pamphlets and websites offer helpful advice for patients, and their use should be encouraged.
They possess a cavity and permit the opposed cartilaginous articular surfaces to move painlessly over each other. Movement is restricted to a required range, and stability is maintained during use. The load is distributed across the surface, thus preventing damage by overloading or disuse.
Synovium and synovial fluid. The joint capsule, which is connected to the periosteum, is lined with synovium, which is a few cells thick and vascular. Its surface is smooth and non-adherent and is permeable to proteins and crystalloids. As there are no macroscopic gaps, it is able to retain normal joint fluid even under pressure. Macrophages and fibroblast-like synoviocytes form the synovial layer by cell-to-cell interactions mediated by cadherin-II. The synoviocytes release hyaluronan into the joint space, which helps to retain fluid in the joint. Synovial fluid is a highly viscous fluid secreted by the synovial cells and has a similar consistency to plasma. Glycoproteins ensure a low coefficient of friction between the cartilaginous surfaces. Tendon sheaths and bursae are also lined by synovium.
The bone which abuts a joint (epiphyseal bone) differs structurally from the shaft (metaphysis) (see Fig. 11.32). It is highly vascular and comprises a light framework of mineralized collagen enclosed in a thin coating of tougher, cortical bone. The ability of this structure to withstand pressure is low and it collapses and fractures when the normal intra-articular covering of hyaline cartilage is worn away as in osteoarthritis (OA; see p. 512). Loss of surface cartilage also leads to the abnormalities of bone growth and remodelling typical of OA (see p. 512).
Hyaline cartilage forms the articular surface and is avascular. It relies on diffusion from synovial fluid for its nutrition. It is rich in type II collagen that forms a meshwork enclosing giant macromolecular aggregates of proteoglycan. These heterogeneous macromolecules comprise protein chains with side-chains of the carbohydrates keratan and chondroitin sulphate (aggrecans). These molecules have a negative charge and retain water in the structure by producing a dynamic tension between the retaining force of the collagen matrix and the expansive effect of osmotic pressure. Intermittent pressure from ‘loading’ of the joint is essential to normal cartilage function and encourages movement of water, minerals and nutrients between cartilage and synovial fluid. Chondrocytes secrete collagen and proteoglycans and are embedded in the cartilage. They migrate towards the joint surface along with the matrix they produce.
These structures stabilize joints. Ligaments are variably elastic and this contributes to the stiffness or laxity of joints (see p. 559). Tendons are inelastic and transmit muscle power to bones. The joint capsule is formed by intermeshing tendons and ligaments. The point where a tendon or ligament joins a bone is called an enthesis and may be the site of inflammation.
All connective tissues contain an extracellular matrix of macromolecules: collagens, elastins, non-collagenous glycoproteins and proteoglycans, in addition to cells, e.g. synoviocytes. There are several different types of cell surface receptors that bind extracellular matrix proteins including the integrins, CD44 and the proteoglycan family of receptors, e.g. syndecans.
Collagens. Collagens consist of three polypeptide (α) chains wound into a triple helix. These alpha chains contain repeating sequences of Gly-x-y triplets, where x and y are often prolyl and hydroxypropyl residues. Collagen fibres show genetic heterogeneity, with genes on at least 12 chromosomes. Hyaline cartilage is 90% type II (COL2A1). There are several classes of collagen genes, based on their protein structures, and abnormalities of these may lead to specific diseases (see p. 560).
Glycoproteins. Fibronectin is the major non-collagenous glycoprotein in the extracellular matrix. Its molecule contains a number of functional domains, or cell recognition sites that bind ligands and are involved in cellular adhesion. Fibronectin plays a major role in tissue remodelling. Its production is stimulated by interferon-gamma (IFN-γ) and by transforming growth factor-beta and inhibited by tumour necrosis factor and interleukin-1.
Proteoglycans. These proteins contain glycosaminoglycan (GAG) side-chains and are of variable form and size. Many different molecules have been identified at different sites in connective tissue. Their function is to bind extracellular matrix together, retain soluble molecules in the matrix and assist with cell binding. Abnormalities of any of these structures may lead to periarticular or articular symptoms and/or predispose to the development of arthritis.
The ligaments, periosteum, synovial tissue and capsule of the joint are richly supplied by blood vessels and nerves. Pain usually derives from inflammation of these sites because the synovial membrane is relatively insensitive.
Connective tissue constantly undergoes repair and re-modelling. Degradation is mediated by enzymes such as aggrecanase and matrix metalloproteinases (MMPs) which require zinc and act at a neutral pH. There are several MMPs which act on different collagens, e.g. the gelatinases (MMP-2 and -9), which degrade denatured collagen. MMPs also act on non-collagen proteins, e.g. the stromelysins (MMP-3, -10, -11), which degrade proteoglycans and fibronectin.
This consists of bundles of myocytes containing actin and myosin molecules. These molecules interdigitate and form myofibrils which cause muscle contraction in a similar way to myocardial muscle (p. 671). Bundles of myofibrils (fasciculi) are covered by connective tissue, the perimysium, which merges with the epimysium (covering the muscle) and forms the tendon which attaches to the bone surface (enthesis).
Are there any associated neurological features? Numbness, pins and needles and/or loss of power suggest ‘nerve’ involvement. The distribution of symptoms is a useful clue to the nerve or nerve root affected.
Is it of one joint, or of several? Look for symmetry or asymmetry, and/or a peripheral or proximal pattern. An acute monoarthritis may be due to trauma, gout (in a middle-aged male) or sepsis (fever or immunosuppression).
How old was the patient when the problem first started? Osteoarthritis (see p. 512) and polymyalgia rheumatica (p. 542) rarely affect the under-50s. Rheumatoid arthritis starts most commonly in women aged 30–50 years.
Are there other associated medical conditions that may be relevant? Psoriasis (see p. 1207) or inflammatory bowel disease is associated with spondyloarthritis (see p. 1004). Charcot’s joints (p. 547) are seen in diabetics.
Could a drug be a cause? Diuretics may precipitate gout in men and older women. Hormone replacement therapy or the oral contraceptive pill may precipitate systemic lupus erythematosus (SLE) (p. 535). Steroids can cause avascular necrosis. Some drugs cause a lupus-like syndrome (p. 535).
Have there been any similar episodes or is this the first? Are there any clues from previous medical conditions? Gout is recurrent; the episodes settle without treatment in 7–10 days. Acute episodes of palindromic rheumatism may predate the onset of rheumatoid arthritis (see p. 519).
What job does the patient do? This can be a factor in soft tissue problems and osteoarthritis (e.g. in heavy labourers and dancers). Work-related problems, particularly in those who use a keyboard, are becoming more common and are complained of more.
Has there been any recent major stress in family or working life? Could this be relevant? Stress rarely causes rheumatic disease but may precipitate a flare-up of inflammatory arthritis. It reduces a person’s ability to cope with pain or disability.
The patient’s own perception of limitation must be taken into account during assessment, as well as the impact of physical causes due to disease. Subjective and objective assessments must be made. Quality of life (QoL) involves physical and psychosocial factors. The aim of treatment is to reduce or cure physical and/or psychological disease and to reduce the impact of any impairment or disability on the individual. A variety of different standard questionnaires is used to assess pain, disease impact and outcome (e.g. Health Assessment Questionnaire, HAQ; Arthritis Impact Measurement Scale, AIMS).
Always observe a patient, looking for disabilities, as he or she walks into the room and sits down. General and neurological examinations are often necessary. Guidelines for rapid examinations of the limbs and spine are shown in Practical Box 11.1.
Practical Box 11.1
Rapid examinations of the limb and spine
Place the hands in the ‘prayer’ position with the elbows apart. Flexion deformities of the fingers may be due to arthritis, flexor tenosynovitis or skin disease. Painful restriction of the wrist limits the person’s ability to move the elbows out with the hands held together.
Ask the patient to (a) bend forwards to touch the toes with straight knees, (b) extend backwards, (c) flex sideways, and (d) look over each shoulder, flexing and extending and sideflexing the neck. Observe abnormal spinal curves – scoliosis (lateral curve), kyphosis (forward bending) or lordosis (backward bending). A cervical and lumbar lordosis and a thoracic kyphosis are normal. Muscle spasm is worse whilst standing and bending. Leg length inequality leads to a scoliosis which decreases on sitting or lying (the lengths are measured lying).
Examining an individual joint involves three stages: looking, feeling and moving (Table 11.1). A screening examination of the locomotor system, known by the acronym GALS (Global Assessment of the Locomotor System) has been devised. X-ray or ultrasound of the joint often forms an integral part of the examination.
LOOK at the appearance of the joint
Swelling – could be bony, fluid or synovial
Deformity – valgus, where the distal bone is deviated laterally (e.g. knock-knees or genu valgum)
Varus where the distal bone is deviated medially (bow-legs or genu varum)
Fixed flexion or hyperextension
Rash – especially psoriasis
Muscle wasting – easier to see in large muscles like the quadriceps
Scars – from surgery or trauma
Signs of inflammationSymmetry – are the right and left joints (e.g. hips, knees, any other paired joint) the same? If not which do you think is abnormal?
Swelling – fluid swelling (effusion) usually represents increased synovial fluid in inflammatory arthritis, but can be due to blood or pus
Synovial swelling is rubbery or boggy and usually occurs in inflammatory arthritis
Bony swelling, such as Heberden’s nodes in the fingers is usually seen in osteoarthritis
Warmth – a warm joint may be inflamed or infected
Tenderness – may represent joint inflammation, but many people have chronic tenderness all over the body (e.g. in fibromyalgia)
Active movement – is the range full and pain-free? Is the movement fluid? In the hands – can the patient perform fine movements? In the legs – can the patient walk properly?
Compare movements on the right and left side – are they symmetrical?
Is there crepitus when the joint is moved?
If active movement is limited try passive movement. In a joint problem both will usually be affected. If it is a muscle or nerve problem passive movement may remain full.
Investigations are unnecessary in many of the common musculoskeletal problems; the diagnosis is clear from the history and examination findings. Tests help to exclude another condition and to reassure the patient or their primary care physician.
Bone and liver biochemistry. A raised serum alkaline phosphatase may indicate liver or bone disease. A rise in liver enzymes is seen with drug-induced toxicity. For other investigations of bone, see page 550.
Rheumatoid factors (RFs) (see also p. 518). Rheumatoid factors are detected by enzyme linked immunoabsorbent assay (ELISA). RFs are antibodies (usually IgM, but also IgG or IgA) against the Fc portion of IgG. They are detected in 70% of people with rheumatoid arthritis (RA), but are not diagnostic. RFs are detected in many autoimmune rheumatic disorders (e.g. SLE), in chronic infections, and in asymptomatic older people (Table 11.2).
Anti-citrullinated peptide antibodies (ACPA). These antibodies are directed against citrullinated antigens, vimentin, fibrinogen, alpha enolase and type II collagen. They are measured by an ELISA technique and are present in up to 80% of people with RA. They have a high specificity for RA (90% with a sensitivity of 60%). They are helpful in early disease when the RF is negative to distinguish it from acute transient synovitis (see Box 11.6, p. 519). Positivity for RF and/or ACPA is associated with a worse prognosis and an increase in the likelihood of bony erosions in people with RA.
Antinuclear antibodies (ANAs). These are detected by indirect immunofluorescent staining of fresh-frozen sections of rat liver or kidney or Hep-2 cell lines. Different patterns reflect a variety of antigenic specificities that occur with different clinical pictures (see Box 11.16, p. 537). ANA is used as a screening test for systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) – a negative ANA makes either condition highly unlikely – but low titres occur in RA and chronic infections and in normal individuals, especially the elderly (Table 11.3).
Anti-double-stranded DNA (dsDNA) antibodies. These are usually detected by a precipitation test (Farr assay), by ELISA, or by an immunofluorescent test using Crithidia luciliae (which contains double-stranded DNA). Raised anti-dsDNA is highly specific for SLE and the levels usually rise and fall in parallel with disease activity so can be used to monitor the level of treatment required.
Anti-extractable nuclear antigen (ENA) antibodies (see Box 11.16, p. 537). These produce a speckled ANA fluorescent pattern, and can be identified by ELISA. The most commonly measured ENAs are:
Anti-neutrophil cytoplasmic antibodies (ANCAs) (see p. 544). These are predominantly IgG autoantibodies directed against the primary granules of neutrophil and macrophage lysosomes. They are strongly associated with small-vessel vasculitis. Two major clinically relevant ANCA patterns are recognized on immunofluorescence:
Immune complexes. Immune complexes are infrequently measured, largely because of variability between assays and difficulty in interpreting their meaning. Assays based on the polyethylene glycol precipitation method (PEG) or C1q binding are available commercially.
Autoimmune rheumatic diseases
RF (IgM) %
Systemic lupus erythematosus
Juvenile idiopathic arthritis
Chronic liver disease
Relatives of people with RA
Systemic lupus erythematosus
Polymyositis and dermatomyositis
Juvenile idiopathic arthritis
Idiopathic pulmonary fibrosis
Examination of joint (or bursa) fluid is used mainly to diagnose septic, reactive or crystal arthritis. The appearance of the fluid is an indicator of the level of inflammation. The procedure is often undertaken in combination with injection of a corticosteroid. Aspiration alone is therapeutic in crystal arthritis (see Practical Box 11.2, p. 508).
Aspiration and analysis of synovial fluid are always indicated when an infected or crystal induced arthritis is suspected, particularly a monoarthritis. Normal fluid is clear and straw coloured and contains <3000 WBC/mm3. Inflammatory fluid is cloudy and contains >3000 WBC/mm3. Septic fluid is opaque and less viscous and contains up to 75 000 WCC/mm3. There is much overlap.
X-rays can be diagnostic in certain conditions (e.g. established rheumatoid arthritis) and are the first investigation in many cases of trauma. X-rays can detect joint space narrowing, erosions in rheumatoid arthritis, calcification in soft tissue, new bone formation, e.g. osteophytes and decreased bone density (osteopenia) or increased bone density (osteosclerosis):
Ultrasound (US) is particularly useful for periarticular structures, soft tissue swellings and tendons and for detecting active synovitis in inflammatory arthritis. It is increasingly used to examine the shoulder and other structures during movement, e.g. shoulder impingement syndrome (see p. 500). Doppler US measures blood flow and hence inflammation. US is used to guide local injections.
Magnetic resonance imaging (MRI) shows bone changes and intra-articular structures in striking detail. Visualization of particular structures can be enhanced with different resonance sequences. T1-weighted is used for anatomical detail, T2-weighted for fluid detection and short tau inversion recovery (STIR) for the presence of bone marrow oedema. It is more sensitive than X-rays in the early detection of articular and periarticular disease. It is the investigation of choice for most spinal disorders but is inappropriate in uncomplicated mechanical low back pain. Gadolinium injection enhances inflamed tissue. MRI can also detect muscle changes, e.g. myositis.
Bone scintigraphy utilizes radionuclides, usually 99mTc, and detects abnormal bone turnover and blood circulation and, although nonspecific, helps in detecting areas of inflammation, infection or malignancy. It is best used in combination with other anatomical imaging techniques.
Positron emission tomography (PET) scanning uses radionuclides, which decay by emission of positrons. 18F-Fluorodeoxyglucose uptake indicates areas of increased glucose metabolism. It is used to locate tumours and demonstrate large vessel vasculitis, e.g. Takayasu’s arteritis (see p. 789). PET scans are combined with CT to improve anatomical details.
Arthroscopy is a direct means of visualizing a joint, particularly the knee or shoulder. Biopsies can be taken, surgery performed in certain conditions (e.g. repair or trimming of meniscal tears), and loose bodies removed.
Unilateral or bilateral muscular-pattern neck pain is common and usually self-limiting. It can follow injury, falling asleep in an awkward position, or prolonged keyboard working. Chronic burning neck pain occurs because of muscle tension from anxiety and stress.
Spondylosis seen on X-ray increases after the age of 40 years, but it is not always causal. Spondylosis can, however, cause stiffness and increases the risk of mechanical or muscular neck pain. Muscle spasm is palpable and tender and may lead to abnormal neck posture (e.g. acute torticollis). Muscular-pattern neck pain is not localized but affects the trapezius muscle, the C7 spinous process and the paracervical musculature (shoulder girdle pain). Pain often radiates upwards to the occiput and is commonly associated with tension headaches. These features are also seen in chronic widespread pain (see p. 509).
Patients are given short courses of analgesic therapy along with reassurance and explanation. Physiotherapists can help to relieve spasm and pain, teach exercises and relaxation techniques, and improve posture. An occupational therapist can advise about the ergonomics of the workplace if the problem is work-related (see p. 510).
Acute cervical disc prolapse presents with unilateral pain in the neck, radiating to the interscapular and shoulder regions. This diffuse, aching dural pain is followed by sharp, electric shock-like pain down the arm, in a nerve root distribution, often with pins and needles, numbness, weakness and loss of reflexes (Table 11.5).
Cervical spondylosis occurs in the older patient with posterolateral osteophytes compressing the nerve root and causing root pain (see Fig. 22.58, p. 1148), commonly at C5/C6 or C6/C7; it is seen on oblique radiographs of the neck. An MRI scan clearly distinguishes facet joint OA, root canal narrowing and disc prolapse.
A support collar, rest, analgesia and sedation are used initially as necessary. Patients should be advised not to carry heavy items. It usually recovers in 6–12 weeks. MRI is the investigation of choice if surgery is being considered or the diagnosis is uncertain (Fig. 11.3). A cervical root block administered under direct vision by an experienced pain specialist may relieve pain while the disc recovers. Neurosurgical referral is essential if the pain persists or if the neurological signs of weakness or numbness are severe or bilateral. Bilateral root pain with or without long track symptoms or signs is a neurosurgical emergency because a central disc prolapse may compress the cervical spinal cord. Posterior osteophytes may cause spinal claudication and cervical myelopathy.
Whiplash injury results from acceleration–deceleration forces applied to the neck, usually in a road traffic accident when the car of a person wearing a seat belt is struck from behind. A simple decision plan based on clinical criteria helps to distinguish those most at risk and who warrant radiography. There is a low probability of serious bony injury if there is:
Whiplash injury is a common cause of chronic neck pain, although most people recover within a few weeks or months. Delayed recovery depends in part upon the severity of the initial injury. The pattern of chronic neck pain is often complex, involving pain in the neck, shoulder and arm. Subjective symptoms such as headache, dizziness, and poor concentration sometimes accompany this. The subjective nature of these symptoms has led to controversy about their cause. The problem is more commonly seen in industrialized countries where the conflictive nature of the compensation process may actually delay recovery. Non-conflictive means of compensation may lead to a better prognosis.
Treatment is with reassurance (the patient is often distressed and anxious), analgesia, a short-term support collar and physiotherapy. Pain may take a few weeks or months to settle and the patient should be warned of this.
The shoulder is a shallow joint with a large range of movement. The humeral head is held in place by the rotator cuff (Fig. 11.4) which is part of the joint capsule. It comprises the tendons of infraspinatus and teres minor posteriorly, supraspinatus superiorly and teres major and subscapularis anteriorly. The rotator cuff (particularly supraspinatus) prevents the humeral head blocking against the acromion during abduction; the deltoid pulls up and the supraspinatus pulls in to produce a turning movement and the greater tuberosity glides under the acromion without impingement. Shoulder pathology restricts or is made worse by shoulder movement. Specific diagnoses are difficult to make clinically but this may not matter for pain management.
Pain in the shoulder can sometimes be due to problems in the neck. The differential diagnosis of this is shown in Box 11.1. Adhesive capsulitis (true frozen shoulder) is uncommon (see below). Early inflammatory arthritis and polymyalgia rheumatica in the elderly may present with shoulder pain. Shoulder pain is more common in diabetic patients than in the general population.
Differential diagnosis of ‘shoulder’ pain
This is a common cause of shoulder pain at all ages. It follows trauma in 30% of cases and is bilateral in under 5%. The pain radiates to the upper arm and is made worse by arm abduction and elevation, which are often limited. The pain is often worse during the middle of the range of abduction, reducing as the arm is raised fully; a so-called ‘painful arc syndrome’. When examined from behind, the scapula rotates earlier than usual during elevation. Passive elevation reduces impingement and is less painful. Severe pain virtually immobilizes the joint, although some rotation is retained (cf. adhesive capsulitis, see below). There is also painful spasm of the trapezius. There may be an associated subacromial bursitis. Isolated subacromial bursitis occurs after direct trauma, falling on to the outstretched arm or elbow. Acromioclavicular osteophytes increase the risk of impingement and may need to be removed surgically.
Analgesics, NSAIDs and/or physiotherapy may suffice, but severe pain responds to an injection of corticosteroid into the subacromial bursa (Fig. 11.4). Patients should be warned that 10% will develop worse pain for 24–48 hours after injection. Some 70% improve over 5–20 days and mobilize the joint themselves. Physiotherapy helps persistent stiffness. Further ultrasound-guided corticosteroid injections may be needed but the long-term benefit is unclear.
This is caused by trauma but also occurs spontaneously in the elderly and in rheumatoid arthritis (RA). It prevents active abduction of the arm, but patients learn to initiate elevation using the unaffected arm. Once elevated, the arm can be held in place by the deltoid muscle. In younger people, the tear is repaired surgically but this is rarely possible in the elderly or in RA. Some patients require arthroscopic surgery.
Calcium pyrophosphate deposits in the tendon are visible on X-ray, but they are not always symptomatic. The pathogenesis is unclear, although ischaemia may play a part. The deposit is usually just proximal to the greater tuberosity. It may lead to acute or chronic recurrent shoulder pain and restriction of movement. A local corticosteroid injection may relieve the pain. The calcification may persist or resolve. Aspiration or breaking up of the deposit under ultrasound control may be required for persistent pain. Rarely, arthroscopic removal is necessary.
Shedding of crystals into the subacromial bursa causes a bursitis with severe pain and shoulder restriction. The shoulder feels hot and is swollen, and an X-ray shows a diffuse opacity in the bursa. The differential diagnosis of calcific bursitis is gout, pseudogout or septic arthritis. Aspiration and injection with corticosteroid can help.
This is uncommon but can develop with rotator cuff lesions, or following hemiplegia, chest or breast surgery or myocardial infarction. It causes severe shoulder pain and complete loss of all shoulder movements, including rotation. High doses of NSAIDs and intra-articular injections of local anaesthetic and corticosteroids are helpful. Once the pain settles, arthroscopic release speeds functional recovery.
Two common sites where the insertions of tendons into bone become inflamed (enthesitis) are the insertions of the wrist extensor tendon into the lateral epicondyle (‘tennis elbow’) and the wrist flexor tendon into the medial epicondyle (‘golfer’s elbow’). Both are usually unrelated to either sporting activity.
There is local tenderness. Pain radiates into the forearm on using the affected muscles – typically, gripping or holding a heavy bag in tennis elbow or carrying a tray in golfer’s elbow. Pain at rest also occurs.
Advise rest and arrange review by a physiotherapist. A local injection of corticosteroid at the point of maximum tenderness is helpful when the pain is severe but needs physiotherapy follow-up to prevent recurrences (Fig. 11.5). Avoid the ulnar nerve when injecting golfer’s elbow. Both conditions settle spontaneously eventually, but occasionally persist and require surgical release.
Hand pain is commonly caused by injury or repetitive work-related activities. When associated with pins and needles or numbness it suggests a neurological cause arising at the wrist, elbow or neck. Pain and stiffness that are worse in the morning are due to tenosynovitis or inflammatory arthritis. The distribution of hand pain often indicates the diagnosis.
|All ages||Older patients|
DIPs (Heberden’s nodes)
Flexor with/without triggering
PIPs (Bouchard’s nodes)
Trauma – scaphoid fracture
DIPs, PIPs, distal and proximal interphalangeal joints.
The finger flexor tendons run through synovial sheaths and under loops which hold them in place. Inflammation occurs with repeated or unaccustomed use, or in inflammatory arthritis. The thickened sheaths are often palpable.
Flexor tenosynovitis causes finger pain when gripping and stiffness of the fingers in the morning. Occasionally a tendon causes a trigger finger, when the finger remains flexed in the morning or after gripping and has to be pulled straight. A tender tendon nodule is palpable, usually in the distal palm. Trigger finger or thumb is commoner in diabetic patients.
De Quervain’s tenosynovitis causes pain and swelling around the radial styloid where the abductor pollicis longus tendon is held in place by a retaining band. There is local tenderness, and the pain at the styloid is worsened by flexing the thumb into the palm.
This is due to median nerve compression in the limited space of the carpal tunnel. Thickened ligaments, tendon sheaths or bone enlargement can cause it, but it is usually idiopathic. (Causes are discussed on p. 1144.) The history is usually typical and diagnostic with the patient waking with numbness, tingling and pain in a median nerve distribution. The pain radiates to the forearm. The fingers feel swollen but usually are not. Wasting of the abductor pollicis brevis develops with sensory loss in the radial three and a half fingers. The pain may be produced by tapping the nerve in the carpal tunnel (Tinel’s sign) or by holding the wrist in flexion (Phalen’s test).
Treatment is with a splint to hold the wrist in dorsiflexion overnight. This relieves the symptoms and is diagnostic; used nightly for several weeks it may produce full recovery. If it does not, a corticosteroid injection into the carpal tunnel (avoid the nerve!) helps in about 70% of cases, although it may recur. Persistent symptoms or nerve damage produce prolonged latency across the carpal tunnel on nerve conduction studies and require surgical decompression.
Inflammatory arthritis. This may present with pain, swelling and stiffness of the hands. In RA the wrists, proximal interphalangeal (PIP) joints and metacarpophalangeal (MCP) joints are affected symmetrically. In psoriatic arthritis and reactive arthritis a finger may be swollen (dactylitis) or the distal interphalangeal (DIP) joints and nails are affected asymmetrically.
Scaphoid fractures. These cause pain in the anatomical snuffbox. They are not seen immediately on X-ray. A cast is necessary. Untreated scaphoid fractures can eventually cause pain because of failed union.
Ganglion. A ganglion is a jelly-filled, often painless swelling caused by a partial tear of the joint capsule or tendon sheath. The wrist is a common site. Treatment is not essential as many resolve or cause little trouble, otherwise surgical excision is the best option.
This is a painless, palpable fibrosis of the palmar aponeurosis, with fibroblasts invading the dermis due to abnormal signalling in the Wnt pathway. It causes puckering of the skin and gradual flexion, usually of the ring and little fingers. It is more common in males, Caucasians, in diabetes mellitus and in those who overuse alcohol. A similar fibrosis occurs in the feet and is often more aggressive. It is also associated with Peyronie’s disease of the penis – a painful inflammatory disorder of the corpora cavernosa, leading eventually to painless fibrosis and angulation of the penis during erection. Intralesional steroid injections may help in early disease and some advocate transcutaneous needle aponeurotomy. Collagenase injection into the collagen contracted cord improved the amount of movement in one randomized study. Plastic surgical release of the contracture is restricted to those with severe deformity of the fingers.
Low back pain is a common symptom. It is often traumatic and work-related, although lifting apparatus and other mechanical devices and improved office seating help to avoid it. Episodes are generally short-lived and self-limiting, and patients attend a physiotherapist or osteopath more often than a doctor. Chronic back pain is the cause of 14% of long-term disability in the UK. The causes are listed in Table 11.7, and the management of back pain is summarized in Box 11.2.
Neoplastic (see p. 589)
Management of back pain
MRI is preferable to CT scanning when neurological signs and symptoms are present. CT scans demonstrate bony pathology better. Interpretation of the relevance of the findings may require a specialist opinion.
Full blood count, ESR and biochemical tests are required only when the pain is likely to be due to malignancy, infection or a metabolic cause. Normal ESR and CRP distinguish mechanical back pain from polymyalgia rheumatica, a likely differential in the elderly.
The back is stiff and a scoliosis may be present when the patient is standing. Muscular spasm is visible and palpable and causes local pain and tenderness. It lessens when sitting or lying. Pain relief and physiotherapy are helpful. Acupuncture helps some. Excessive rest should be avoided. Re-education in lifting and exercises help to prevent recurrent attacks of pain. Once a patient develops low back pain, although the episode itself is usually self-limiting, there is a significantly increased risk of further back pain episodes. Risk factors for recurrent back pain include:
Spinal movement occurs at the disc and the posterior facet joints, and stability is normally achieved by a complex mechanism of spinal ligaments and muscles. Any of these structures may be a source of pain. An exact anatomical diagnosis is difficult, but some typical syndromes are recognized (see below). They are often associated with but not necessarily caused by radiological spondylosis (see p.1148).
Lumbar spondylosis. The fundamental lesion in spondylosis occurs in an intervertebral disc, a fibrous joint whose tough capsule inserts into the rim of the adjacent vertebrae. This capsule encloses a fibrous outer zone and a gel-like inner zone. The disc allows rotation and bending.
Changes in the discs occasionally start in teenage years or early 20s and often increase with age. The gel changes chemically, breaks up, shrinks and loses its compliance. The surrounding fibrous zones develop circumferential or radial fissures. In the majority this is initially asymptomatic but visible on MRI as decreased hydration. Later the discs become thinner and less compliant. These changes cause circumferential bulging of the intervertebral ligaments.
Reactive changes develop in adjacent vertebrae; the bone becomes sclerotic and osteophytes form around the rim of the vertebra (Fig. 11.6). The most common sites of lumbar spondylosis are L5/S1 and L4/L5.
Figure 11.6 MRI of lumbar spine, showing a central disc prolapse at the L4/L5 level (arrow). The signal from the L4/L5 and L5/S1 discs indicates dehydration, while the L3/L4 signal appearance is normal.