Chapter 9 The rheumatological system
The rheumatological history
Presenting symptoms (Table 9.1)
Peripheral joints
Pain and swelling
It is often useful to ask the patient to point to the painful place or area. For example, pain said to affect the knee may be in the popliteal fossa, the knee joint itself, or in the supra- or infra-patellar bursa. Remember also that pain in the knee or lower thigh may be referred from the hip (Figure 9.1).
Figure 9.1 Map of referral patterns for different joints
Adapted from Epstein O et al, Clinical Examination, 4th edn. Edinburgh: Mosby, 2008.
Find out if the symptoms are of an acute or chronic nature and whether they are getting better or worse. The effect of rest and exercise on the joint pain should be determined. Patients with rheumatoid arthritis have joint symptoms which are worse after rest, while those with osteoarthritis have pain which is worse after exercise. Ask about the sequence of onset of joint involvement. Precipitating factors such as trauma should be noted. The causes of monoarthritis (single joint) and polyarthritis (more than one joint), and the patterns of polyarthritis in various diseases, are presented in Tables 9.2, 9.3 and 9.4.
A single hot red swollen joint (acute monoarthritis) |
A single chronic inflamed joint (chronic monoarthritis) |
Fingers: distal (Heberden’s nodes) and proximal (Bouchard’s nodes) interphalangeal joints, and metacarpophalangeal joints of the thumbs |
Morning stiffness
Ask about the presence of early-morning stiffness and the length of time that this stiffness lasts. Morning stiffness classically occurs in rheumatoid arthritis and other inflammatory arthropathies, and the duration of stiffness is a guide to its severity. Stiffness after inactivity, such as sitting, is characteristic of osteoarthritis of the hip or knee.
Instability
Joint instability may be described by the patient as a ‘giving way’, or occasionally ‘coming out’, of the joint in certain conditions. This may be due to true dislocation (for example, with the shoulder or the patella) or alternatively to muscle weakness or ligamentous problems.
Back pain
This is a very common symptom. It is most often a consequence of local musculoskeletal disease.
Ask where the pain is situated, whether it began suddenly or gradually, whether it is localised or diffuse, whether it radiates to the limbs or elsewhere, and whether the pain is aggravated by movement, coughing or straining. Musculoskeletal pain is characteristically well localised and is aggravated by movement. If there is a spinal nerve root irritation there may be pain that occurs in a dermatomal distribution. This helps to localise the level of the lesion. Diseases such as osteoporosis (with crush fractures), infiltration of carcinoma, leukaemia or myeloma may cause progressive and unremitting back pain, which is often worse at night (Table 9.6). The pain may be of sudden onset but is usually self-limiting if it results from the crush fracture of a vertebral body. In ankylosing spondylitis the pain is usually situated over the sacroiliac joints and lumbar spine, it is also worse at night and is associated with morning stiffness. The pain of ankylosing spondylitis is typically better with activity which helps distinguish it from mechanical back pain.1,2 Pain from diseases of the abdomen and chest (e.g. dissecting abdominal or thoracic aortic aneurysm) can also be referred to the back.
Age > 50 years |
Cancer history |
Weight loss (unexplained) |
Pain on waking from sleep |
Pain for longer than one month and unresponsive to simple analgesics |
Fever |
History of drug use by injection |
Bowel or bladder dysfunction |
Limb pain
Musculoskeletal pain may be due to trauma or inflammation. Muscle disease such as polymyositis can present with an aching pain in the proximal muscles around the shoulders and hips, associated with weakness. Pain and stiffness in the shoulders and hips in patients over the age of 50 years may be due to polymyalgia rheumatica. The acute or subacute onset of symptoms in multiple locations suggests an inflammatory process. Bone disease
Class | Assessment |
Class 1 | Normal functional ability |
Class 2 | Ability to carry out normal activities, despite discomfort or limited mobility of one or more joints |
Class 3 | Ability to perform only a few of the tasks of the normal occupation or of self-care |
Class 4 | Complete or almost complete incapacity with the patient confined to wheelchair or to bed |
such as osteomyelitis, osteomalacia, osteoporosis or tumours can cause limb pain. Inflammation of tendons (tenosynovitis) can produce local pain over the affected area.
Spinal stenosis can cause pseudo-claudication—pain on walking but relieved by leaning forward.
Nerve entrapment and neuropathy can both cause limb pain which is often associated with paraesthesiae or weakness. The usual cause is synovial thickening or joint subluxation—especially for patients with rheumatoid arthritis. The vasculitis associated with the inflammatory arthropathies can also cause neuropathy leading to diffuse peripheral neuropathy or mononeuritis multiplex. Patients with chronic rheumatoid arthritis often develop subluxation of the cervical spine at the atlanto-axial joint. This is caused by erosion of the transverse ligament around the posterior aspect of the odontoid process (dens). The patient may describe shooting paraesthesiae down the arms and an occipital headache. Neck flexion leads to indentation of the cord by the dens and can cause tetraplegia or sudden death. The abnormality may be obvious on lateral X-rays of the cervical spine (Figure 9.3). Injury to peripheral nerves can result in vasomotor changes and severe limb pain. This is called causalgia. Even following amputation of a limb, phantom limb pain may develop and persist as a chronic problem.
Raynaud’s phenomenon
Raynaud’s phenomenona is an abnormal response of the fingers and toes to cold. Classically, the fingers first turn white, then blue and finally red after exposure to cold. It is during the red phase that the pain may be most severe, but pain during the white stage may also be severe, as a result of ischaemia. Patients with Raynaud’s disease have Raynaud’s phenomenon without an obvious underlying cause. The disease tends to be familial and females are more likely to be affected. In connective tissue diseases, especially scleroderma, Raynaud’s phenomenon can occur and may lead to the formation of digital ulcers (Table 9.7).
Dry eyes and mouth
Dry eyes and dry mouth are characteristic of Sjögren’s syndrome (Table 9.8). This syndrome may occur in isolation (primary Sjögren’s) and is very common in association with rheumatoid arthritis and other connective tissue disease. Mucus-secreting glands become infiltrated with lymphocytes and plasma cells, which cause atrophy and fibrosis. The dry eyes can result in conjunctivitis, keratitis and corneal ulcers. Sjögren’s syndrome can also have an effect on other organs such as the lungs or kidneys.
In this syndrome mucus-secreting glands are infiltrated by lymphocytes and plasma cells, which cause atrophy and fibrosis of glandular tissue. |
1 Dry eyes: conjunctivitis, keratitis, corneal ulcers (rarely vascularisation of the cornea) |
2 Dry mouth |
3 Chest: infection secondary to reduced mucus secretion or interstitial pneumonitis |
4 Kidneys: renal tubular acidosis or nephrogenic diabetes insipidus |
5 Genital tract: atrophic vaginitis |
6 Pseudolymphoma: lymphadenopathy and splenomegaly, which may rarely progress to a true (usually non-Hodgkin’s) lymphoma |
Note: This syndrome occurs in rheumatoid arthritis and with the connective tissue diseases.
Red eyes
The seronegative spondyloarthropathies and Behçet’sb syndrome but not rheumatoid arthritis may be complicated by iritis (eye pain with central scleral injection—a ‘red eye’—radiating out from the pupil) (see Figure 9.51, page 279). In other diseases, such as Sjögren’s, red eyes may be due to dryness, episcleritis or scleritis.
Treatment history
Document current and previous anti-arthritic medications (e.g. aspirin, other non-steroidal anti-inflammatory drugs, gold, methotrexate, penicillamine, chloroquine, steroids, anti-tumour necrosis factor α therapy, or other biological agents). Any side-effects of these drugs (e.g. gastric ulceration or haemorrhage, from aspirin) also need to be identified. Ask about physiotherapy and joint or tendon surgery in the past.
Past history
It is important to inquire about any history of trauma or surgery in the past. Similarly, a history of recent infection, including hepatitis, streptococcal pharyngitis, rubella, dysentery, gonorrhoea and tuberculosis, may be relevant to the onset of arthralgia or arthritis. A history of tick bite may indicate that the patient has Lyme disease. Inflammatory bowel disease can be associated with arthritis, as described on page 191. A history of psoriasis may indicate that the arthritis is due to psoriatic arthropathy. It is also important to inquire about any history of arthritis in childhood. The smoking history is important: rheumatoid arthritis is more common in smokers, and smoking adds to their already increased risk of cardiovascular disease.
Examination anatomy
Joint structures (Figure 9.4)
Joint pain may be well localised if there is inflammation close to the skin, but deeper joint abnormalities may cause pain to be referred. The areas where joint pain is felt correspond to the innervation of the muscle attached to that joint—the myotome. For example, the glenohumeral joint of the shoulder and the posterior scapular muscles are supplied from C5 and C6, so pain over the shoulder or scapula may arise from any structure supplied from these nerve roots—including the shoulder muscles and joints but also the C5 and C6 segments of the spine. Figure 9.1 shows a map of approximate referral patterns for important joints.
The extra-articular structures that surround a joint—the ligaments, tendons and nerves—may also be the source of joint pain. Disease of the joint itself tends to limit movement of the joint in all directions, both active movement (moved by the patient) and passive movement (moved by the examiner). Extra-articular disease causes variable limitation of movement in different directions, and tends to cause more limitation of active than of passive movement.
The rheumatological examination
There are certain established ways of examining the joints and related structures3 and it is important to be aware of the numerous systemic complications of rheumatological diseases. The actual system of examination depends on the patient’s history and sometimes on the examiner noticing an abnormality on general inspection. Formal examination of all the joints is rarely part of the routine physical examination, but students should learn how to handle each joint properly and a formal examination is an important part of the evaluation of patients who present with joint symptoms or who have an established diagnosis and active symptoms. Diseases of the extra-articular soft tissues are particularly common.
General inspection
This is important for two reasons: first, it gives an indication of the patient’s functional disability, which is essential in all rheumatological assessments; and second, certain conditions can be diagnosed by careful inspection. Look at the patient as he or she walks into the room. Does walking appear to be painful and difficult? What posture is taken? Does the patient require assistance such as a stick or walking frame? Is there obvious deformity, and what joints does it involve? Note the pattern of joint involvement, which gives a clue about the likely underlying disease (Tables 9.2 to 9.4).
Principles of joint examination
Look
The first principle is always to compare right with left. Remember that joints are three-dimensional structures and need to be inspected from the front, the back and the sides. The skin is inspected for erythema indicating underlying inflammation and suggesting active, intense arthritis or infection, atrophy suggesting chronic underlying disease, scars indicating previous operations such as tendon repairs or joint replacements, and rashes. For example, psoriasis is associated with a rash and polyarthritis (inflammation of more than one joint). The psoriatic rash consists of scaling erythematous plaques on extensor surfaces. The nails are often also affected (page 252). Also look for a vasculitic skin rash (inflammation of the blood vessels of the skin), which can range in appearance from palpable purpura or livedo reticularis (bluish-purple streaks in a net-like pattern) to skin necrosis.
A small, firm, painless swelling over the back (dorsal surface) of the wrist is usually a synovial cyst—a ganglion.c A larger, localised, soft area of swelling of the dorsum of the wrist generally indicates tenosynovitis.
Deformity is the sign of a chronic, usually destructive, arthritis, and ranges from mild ulnar deviation of the metacarpophalangeal joints in early rheumatoid arthritis to the gross destruction and disorganisation of a denervated (Charcot’sd) joint (Figure 10.20, page 319). Deviation of the part of the body away from the midline is called valgus deformity, and towards the midline, varus deformity. For example, genu valgum means knock-kneed and genu varum, bow-legged.
Muscle wasting results from a combination of disuse of the joint, inflammation of the surrounding tissues and sometimes nerve entrapment. It tends to affect muscle groups adjacent to the diseased joint (e.g. quadriceps wasting with active arthritis of the knee) and is a sign of chronicity.
Assessment of individual joints
The hands and wrists (Figures 9.5 to 9.9)
Examination anatomy
Figure 9.5 Examination of the hands and wrists
Sitting up (hands on a pillow)
Figure 9.6 (right) X-ray of normal hand
Courtesy M Thomson, National Capital Diagnostic Imaging, Canberra.
History
Pain may be present in some or all of the joints. It is more likely to be vague or diffuse if it has radiated from the shoulder or neck or is due to carpal tunnel syndrome, and to be localised if it is due to arthritis. Stiffness is typically worse in the mornings in rheumatoid arthritis. Swelling of the wrist may indicate arthritis or tendon sheath inflammation. Swelling of individual joints suggests arthritis. Deformity of the fingers and hand due to rheumatoid arthritis or of the fingers as a result of arthritis or gouty tophi may be the presenting complaint. The sudden onset of deformity suggests tendon rupture. Locking or snapping of a finger (trigger finger) is typical of inflammation of a flexor tendon sheath (tenovaginitis). Loss of function is a serious problem when it involves the numerous functions of the hand and wrist. The history should include an assessment of the difficulties the patient has in using the hands and wrists. Neurological symptoms as a result of nerve compression may cause paraesthesiae or limitation of strength or of complicated hand functions.
Look
Go on to the metacarpophalangeal joints. Again note any skin abnormalities, swelling or deformity. Look especially for ulnar deviation and volar (palmar) subluxation of the fingers. Ulnar deviation is deviation of the phalanges at the metacarpophalangeal joints towards the medial (ulnar) side of the hand. It is usually associated with anterior (Volar) subluxation of the fingers (Figure 9.10). These deformities are characteristic but not pathognomonic of rheumatoid arthritis (Table 9.9).
Rheumatoid arthritis |
Seronegative spondyloarthropathy, particularly psoriatic arthritis, ankylosing spondylitis or Reiter’s disease |
Chronic tophaceous gout (rarely symmetrical) |
Primary generalised osteoarthritis |
Erosive or inflammatory osteoarthritis |
Next inspect the proximal interphalangeal and distal interphalangeal joints. Again note any skin changes and joint swelling. Look for the characteristic deformities of rheumatoid arthritis. These include swan neck and boutonnière deformity of the fingers and Z deformity of the thumb (Figure 9.10). They are due to joint destruction and tendon dysfunction. The swan neck deformity is hyperextension at the proximal interphalangeal joint and fixed flexion deformity at the distal interphalangeal joint. It is due to subluxation at the proximal interphalangeal joint and tendon shortening at the distal interphalangeal joint. The boutonnière (buttonhole) deformity consists of fixed flexion of the proximal interphalangeal joint and extension of the distal interphalangeal joints. This is due to protrusion of the proximal interphalangeal joint through its ruptured extensor tendon. The Z deformity of the thumb consists of hyperextension of the interphalangeal joint and fixed flexion and subluxation of the metacarpophalangeal joint.
Now look for the characteristic changes of osteoarthritis (Figure 9.11). Here the distal interphalangeal and first carpometacarpal joints are usually involved. Heberden’s nodese are a common deformity caused by marginal osteophytes that lie at the base of the distal phalanx. Less commonly, the proximal interphalangeal joints may be involved and osteophytes here are called Bouchard’sf nodes.
Now examine the nails. Characteristic psoriatic nail changes may be visible: these include pitting (small depressions in the nail), onycholysis (Figure 9.12) and, less commonly, hyperkeratosis (thickening of the nail), ridging and discoloration. The presence of vasculitic changes around the nailfolds implies active disease. These consist of black to brown 1–2 mm lesions due to skin infarction and occur typically in rheumatoid arthritis (Figure 9.13). Splinter haemorrhages may be present in patients with systemic lupus erythematosus (and infective endocarditis) and are due to vasculitis. Unlike nailfold infarcts they are located under the nails in the nail beds. Periungual telangiectasiae occur in systemic lupus erythematosus, scleroderma or dermatomyositis.
Figure 9.12 Psoriatic nails
Showing onycholysis and discoloration, with typical pitting and ridging.
Feel and move
Turn the hands back again to the palm-down position. Palpate the wrists with both thumbs placed on the dorsal surface by the wrists, supported underneath by the index fingers (Figure 9.14). Feel gently for synovitis (boggy swelling) and effusions. The wrist should be gently dorsiflexed (normally possible to 75 degrees) and palmar flexed (also possible to 75 degrees) with the examiner’s thumbs. Then radial and ulnar deviation (20 degrees) is tested (Figure 9.15). Note any tenderness or limitation of movement or joint crepitus. Palpate the ulnar styloid for tenderness, which can occur in rheumatoid arthritis.
Test for tenderness at the tip of the radial styloid. This suggests de Quervain’sg tenosynovitis.
Feel for tenderness in the anatomical snuff box if scaphoid injury is suspected (Figure 9.15). Test for tenderness distal to the head of the ulna for extensor carpi ulnaris tendinitis.
Go on now to the metacarpophalangeal joints, which are palpated in a similar way with the two thumbs. Again passive movement is tested. Volar subluxation can be demonstrated by flexing the metacarpophalangeal joint with the proximal phalanx held between the thumb and forefinger. The metacarpophalangeal joint is then rocked backwards and forwards (Figure 9.16). Very little movement occurs with this manoeuvre at a normal joint. Considerable movement may be present when ligamentous laxity or subluxation is present.
Palpate the proximal and distal interphalangeal joints for tenderness, swelling and osteophytes.
If the carpal tunnel syndrome is suspected, ask the patient to flex both wrists for 30 seconds—paraesthesiae will often be precipitated in the affected hand if the syndrome is present (Phalen’sh wrist flexion test). The paraesthesiae (pins and needles) are in the distribution of the median nerve (page 363), when thickening of the flexor retinaculum has entrapped the nerve in the carpal tunnel (Table 9.10). This test is more reliable than Tinel’s sign,i in which tapping over the flexor retinaculum (which lies at the proximal part of the palm) may cause similar paraesthesiae.4
Now test active movements. First assess wrist flexion and extension as shown in Figure 9.17. Compare the two sides. Now go on to thumb movements (Figure 9.18). The patient holds the hand flat, palm upwards, and the examiner’s hand holds the patient’s fingers. Test extension by asking the patient to stretch the thumb outwards, abduction by asking for the thumb to be pointed straight upwards, adduction by asking him or her to squeeze the examiner’s finger, and opposition by getting the patient to touch the little finger with the thumb. Look for limitation of these movements and discomfort caused by them. Next test metacarpophalangeal and interphalangeal movements. As a screening test, ask the patient to make a fist then to straighten out the fingers (Figure 9.19). Then test the fingers individually. If active flexion of one or more fingers is reduced, test the superficial and profundus flexor tendons (Figure 9.20). Hold the proximal finger joint extended and instruct the patient to bend it; the distal fingertip will flex if the flexor profundus is intact. Then hold the other fingers extended (to inactivate the profundus) and check finger flexion (inability indicates the superficialis is unable to work). The most common tendon ruptures are of the extensors of the fourth and fifth fingers.
Function
It is important to test the function of the hand. Grip strength is tested by getting the patient to squeeze two of the examiner’s fingers. Even an angry patient will rarely cause pain if given only two fingers. Serial measurements of grip strength can be made by asking the patient to squeeze a partly inflated sphygmomanometer cuff and noting the pressure reached. Key grip (Figure 9.21) is the grip with which a key is held between the pulps of the thumb and forefinger. Ask the patient to hold this grip tightly and try to open up his or her fingers. Opposition strength (Figure 9.22) is where the patient opposes the thumb and individual fingers. The difficulty with which these can be forced apart is assessed. Finally, a practical test, such as asking the patient to undo a button or write with a pen, should be performed.
Tests of hand function should be completed by formally assessing for neurological changes (page 362).
Examination of the hands is not complete without feeling for the subcutaneous nodules of rheumatoid arthritis near the elbows (Figure 9.23). These are 0.5–3 cm firm, shotty, non-tender lumps which occur typically over the olecranon. They may be attached to bone. They are found in rheumatoid-factor-positive rheumatoid arthritis. Rheumatoid nodules are areas of fibrinoid necrosis with a characteristic histological appearance and are probably initiated by a small vessel vasculitis. They are localised by trauma but can occur elsewhere, especially attached to tendons, over pressure areas in the hands or feet, in the lung, pleura, myocardium or vocal cords. The combination of arthritis and nodules suggests the diagnostic possibilities listed in Table 9.11.
Rheumatoid arthritis |
Systemic lupus erythematosus (rare) |
Rheumatic fever (Jaccoud’s† arthritis) (very rare) |
Granulomas—e.g. sarcoidosis (very rare) |
* Gouty tophi and xanthomata from hyperlipidaemia may cause confusion.
† François Jaccoud (1830–1913), professor of medicine, Geneva.
The elbows
Examination
Look for a joint effusion, which appears as a swelling on either side of the olecranon. Discrete swellings over the olecranon or over the proximal subcutaneous border of the ulna may be due to rheumatoid nodules, gouty tophi, an enlarged olecranon bursa or, rarely, to other types of nodules (Table 9.11).
Small amounts of fluid or synovitis of the elbow joint may be detected by the examiner, facing the patient, placing the thumb of the opposite hand along the edge of the ulnar shaft just distal to the olecranon where the synovium is closest to the surface. Full extension of the elbow joint will cause a palpable bulge in this area if fluid is present.
If lateral epicondylitis is suspected, ask the patient to extend the wrist actively against resistance (see Figure 9.70, page 291). Test the range of active movements by standing in front of the patient and demonstrating. If there is any deformity or complaint of numbness, a neurological examination of the hand and arm are indicated for ulnar nerve entrapment.