Oxford Handbook of Clinical Examination and Practical Skills (2 edn)
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Introduction
Joints
A joint is a connection or point of contact between bones, or between bone and cartilage. Joints are classified according to the type of material uniting the articulating surfaces, and the degree of movement they allow.
Fibrous joints (syndesmosis): held together by fibrous (collagenous) connective tissue, are ‘fixed’ or ‘immoveable’. They do not have a joint cavity. Examples include sutures between the bones of the skull.
Cartilagenous joints (synchondrosis): held together by cartilage, are slightly moveable, and again have no joint cavity. Examples include the symphysis pubis, and intervertebral discs.
Synovial joints (diarthrodial joint): covered by cartilage with a synovial membrane enclosing a joint cavity. These are freely moveable, and are the most common joint type, being typical of limb joints.
There are different types of synovial joints and some of the more important types are:
Hinge: movement occurs primarily in a single plane (e.g. elbow, knee, and interphalangeal joints)
Ball and socket: allows movement around three axes: flexion/extension, abduction/adduction, rotation (e.g. shoulder and hip)
Pivot: a ring of bone and ligament surrounds the surface of the other bone allowing rotation only (e.g. atlanto-axial joint between C1 and C2 vertebrae, and the connection between the radius and ulna)
Gliding: flat bone surfaces allow side to side and backwards and forwards movements (e.g. between carpals, tarsals, sternum and clavicle and the scapula and clavicle)
Saddle: similar to a hinge joint but with a degree of movement in a second plane (e.g. base of thumb).
Flexion: a decrease in the angle between the articulating bones (e.g. bending the elbow = elbow flexion)
Extension: an increase in the angle between the articulating bones (e.g. straightening the elbow = elbow extension)
Abduction: movement of a bone away from the midline (e.g. moving the arm out to the side = shoulder abduction)
Adduction: movement of a bone towards the midline (e.g. bring the arm in to the side of the body = shoulder adduction).
Movement of a bone about its longitudinal axis
Internal or medial rotation: rotating a bone towards the midline (e.g. turning the lower limb with extended knee such that the toes point inwards = internal rotation at the hip)
External or lateral rotation: rotating a bone away from the midline (e.g. turning the lower limb with extended knee such that the toes point outwards = external rotation at the hip).
These occur at specific joints only
Pronation: moving the forearm as if turning a dial anticlockwise
Supination: moving the forearm as if turning a dial clockwise
Dorsiflexion: moving the ankle to bring the dorsum of the foot towards the tibia (i.e. pointing the foot upwards)
Plantar flexion: moving the ankle to bring the plantar surface in line with the tibia (i.e. pointing the foot downward)
Inversion: tilting the soles of the feet inwards to face each other
Eversion: tilting the soles of the feet outwards away from each other
Protraction: moving the mandible forward
Retraction: moving the mandible backward.
Synovial joints
Cartilage
Hyaline articular cartilage covers the intra-articular surface of the bones, ? friction at the joint, and facilitates shock absorption. Not all intra-articular bone is covered by hyaline cartilage; the part not covered by hyaline articular cartilage is the bare area of the joint and is the target site for erosions in inflammatory arthritis (e.g. rheumatoid arthritis).
Some synovial joints have an additional fibrocartilaginous disc (e.g. meniscus at the knee), or a fibrocartilaginous labrum (e.g. hip, shoulder).
Capsule and synovial membrane
A sleeve-like bag (fibrous capsule lined with synovial membrane) surrounds the synovial joint.
The inner synovial membrane secretes synovial fluid which has a number of functions including lubrication, and supply of nutrients to the cartilage (which is avascular and lacks pain fibres). The fluid contains phagocytic cells that remove microbes and debris within the joint cavity.
Ligaments are thickened portions of joint capsule. However, some ligaments may be distinct from the capsule.
Entheses
The bony attachment of capsules, ligaments, or tendons is called the enthesis. Entheseal inflammation (enthesitis) is the hallmark of sero-negative inflammatory arthritis (e.g. psoriatic arthritis, ankylosing spondylitis).
Tendon sheaths
Tendons e.g. those of flexor digitorum superficialis and profundus, biceps etc, are also covered by synovial sheaths called tenosynovium. This may get inflamed (tenosynovitis) due to mechanical (e.g. some cases of de Quervain’s tenosynovitis), or autoimmune (e.g. lupus, rheumatoid arthritis) conditions. The Achilles tendon, one of the largest tendons in the body, does not have a tenosynovium, and is only covered by a thin layer of connective tissue: the paratenon.
Important locomotor symptoms
As with any system, a carefully and accurately compiled history can be very informative and may point to a diagnosis even before examination or laboratory tests.
Pain
Pain is the most common symptom in problems of the locomotor system, and should be approached in the same manner as any other type of pain.
Anterior (groin): hip arthropathy, avascular necrosis, ilio-psoas bursitis, disc prolapse pressing on L1–L2 nerve root, inguinal or femoral hernia
Medial: adductor enthesopathy, inguinal or femoral hernia
Lateral: trochanteric bursitis, abductor enthesopathy (greater trochanteric pain syndrome), meralgia paresthetica
Posterior: inflammatory back pain due to sacro-iliitis (frequently reported as buttock pain), ischial bursitis, spinal stenosis, and disc prolapse pressing on L3–L5, and sacral nerve roots.
Chondromalacia patellae: softening of the patellar articular cartilage and is felt as anterior knee pain after prolonged sitting. Usually seen in young people
Osteochondritis dissecans: usually associated with trauma resulting in an osteochondral fracture which forms a loose body in the joint with underlying necrosis
Osgood–Schlatter’s disease: arises as a result of a traction injury of the tibial epiphysis which is classically associated with a lump over the tibia
Other causes: osteoarthritis, trauma, bursitis, tendonitis, rheumatoid arthritis, infection, malignancy.
Rotator cuff disorders (e.g. tendonitis, rupture, adhesive capsulitis/frozen shoulder)
Referred pain: e.g. cervical, mediastinal, cardiac
Arthritis: glenohumeral, acromioclavicular.
Epicondylitis (lateral = tennis elbow; medial = golfer’s elbow)
Olecranon bursitis
Referred pain from neck/shoulder (e.g. cervical spondylosis)
Osteo- and rheumatoid arthritis.
Arthritis
Trauma
Infection
Ankylosing spondylitis
Spondylolisthesis
Disc prolapse, lumbar spinal/lateral recess stenosis
Spinal tumours
Metabolic bone disease.
Determine the character, onset, site, radiation, severity, periodicity, exacerbating and relieving factors (with particular reference to how it is influenced by rest and activity), and diurnal variation. Pain due to mechanical/degenerative arthropathies increases with joint use, whereas pain due to inflammatory arthropathy improves with joint use.
Pain in a joint is called arthralgia.
Pain in a muscle is called myalgia.
Character
Bone pain is typically experienced as boring, penetrating, and is often worse at night. Causes include Paget’s disease, tumour, chronic infection, avascular necrosis, and osteoid osteoma.
Pain associated with a fracture is usually sharp and stabbing in nature, and is often exacerbated by movement.
Shooting pain is suggestive of nerve entrapment (e.g. disc prolapse).
Onset
Acute-onset pain is often a manifestation of infections such as septic arthritis, or of crystal arthropathy (e.g. gout).
Osteoarthritis, ankylosing spondylitis, and rheumatoid arthritis usually cause a slower (insidious) onset of pain.
Site
Determine the exact site of maximal pain if possible, and of any associated lesser pains. Ask the patient to point to the site of maximal pain.
Remember that the site of pain is not necessarily the site of pathology; often the pain is referred. Referred pain is due to inability of the cerebral cortex to distinguish between sensory messages from embryologically related sites. For example, hip pain is frequently referred down the thigh, towards the knee; and pain from the cervical spine is referred to the shoulder region. Referred pain is usually poorly localized, and is worsened by movement of the affected joint (not of the joint to which it is referred).
Stiffness
This is a subjective inability or difficulty in moving a joint.
If stiffness predominates without significant joint pain, consider spasticity or tetany. Look for hypertonia and other upper motor neuron signs.
Ask the patient:
When is the stiffness worst?
‘Early morning stiffness’, improving as the day goes by, is characteristically associated with inflammatory joint disease (e.g. rheumatoid arthritis, ankylosing spondylitis). This often takes hours before maximal improvement with activity
Early morning stiffness may be present in non-inflammatory joint diseases (e.g. osteoarthritis). In these cases, patients report a shorter duration of stiffness before improvement (often <20 minutes).
Which joints are involved?
Stiffness predominates in hands and feet in rheumatoid arthritis; in shoulder and pelvic girdle in polymyalgia rheumatica; and in the buttocks and lower back in ankylosing spondylitis.
How long does it take to ‘get going’ in the morning?
How is the stiffness related to rest and activity?
Stiffness in inflammatory joint disease tends to worsen with rest, and improves with activity. However, in non-inflammatory joint disease, stiffness is exacerbated by activity and it is typically worse at the end of the day.
Swelling
Joint swelling can be due to a variety of factors including inflammation of the synovial lining, an ? in the volume of synovial fluid, hypertrophy of bone, or swelling of structures surrounding the joint.
This symptom is particularly significant in the presence of joint pain and stiffness. Establish:
Which joints are affected (small or large)?
Is the distribution symmetrical or not?
What was the nature of onset of the swelling?
Rapid onset: haematoma, acute crystal synovitis, haemarthrosis (trauma, anticoagulants, or any underlying bleeding disorder)
Slow onset (over days to weeks) suggests inflammatory arthritis.
Are the joints always swollen or does the swelling come and go?
Is there any associated pain?
Do the joints feel hot to touch?
Is there erythema? (Common in infective, traumatic, and crystal arthropathies.)
Have the joints in question sustained any injuries?
Does the whole finger or toe swell up like a sausage? (Dactylitis.)
Crepitus
A crunching sound and feeling on moving the joint.
Distinguish crepitus from other articular/peri-articular noises like cracking, clonking, popping, and snapping which are usually not pathological.
Locking, triggering, and giving way
Locking
Locking is the sudden inability to complete a certain movement and suggests a mechanical block or obstruction usually caused by a loose body or torn cartilage within the joint. This frequently occurs at the knee.
Triggering
A similar phenomenon to locking. This may occur at the fingers, when there is an inability to actively extend the digit completely. This is usually due to thickening of the flexor tendon sheath but may occur in the context of trauma or other pathology to the extensor tendons. The triggering finger can be extended passively by the patient or the examiner.
Giving way
Patients with degenerative arthritis affecting the lower limb joints (typically the knee or ankle) often report a feeling of instability when weight-bearing. This is described as a sensation of ‘giving way’, a subjective sensation which may or may not be associated with falls.
Deformity
Acute deformity may arise with a fracture or dislocation. Chronic deformity is more typical of bone malalignment and may be partial/subluxed or complete/dislocated. (See Box 10.6.)
The bone or part of limb distal to the joint is deviated laterally.
For example, a valgus deformity at the knees would give ‘knock knees’ that tend to meet in the middle despite the feet being apart.
Here, the bone or part of limb distal to the joint is deviated medially.
For example, a varus deformity at the knees would give ‘bow legs’ with a gap between the knees even if the feet are together.
Establish:
The time frame over which the deformity has developed.
Any associated symptoms such as pain and swelling.
Any resultant loss of function? (What is the patient unable to do now, which he or she could do before?).
Weakness
Always enquire about the presence of localized weakness (peripheral nerve lesion) or generalized weakness (systemic cause).
In some patients, subjective weakness may result from pain. This is often seen in patients with polymyalgia rheumatica who report ‘weakness’ around their hips and shoulders.
Sensory disturbance
Ask about the exact distribution of any numbness or paraesthesia as well as documenting any exacerbating and relieving factors.
Loss of function
This is the inability to perform an action (disability) and is distinguished from the term ‘handicap’ which is the social/functional result or impact that disability has on the individual’s life.
Loss of function can be caused by a combination of muscle weakness, pain, mechanical factors, and damage to the nerve supply.
The questions you ask will depend partly on the patient’s occupation. It is also essential to gain some insight into the patient’s mobility (can they use stairs? How they cope with personal care such as feeding, washing, and dressing? Can they manage shopping and cooking?).
Affect and sleep
Patients with chronic musculoskeletal conditions may have, or develop, low mood. Therefore, targeted enquiries should be made about the patient’s mood.
Similarly, these patients may have reduced and/or poor quality of sleep. Chronic sleep deprivation results in increased pain sensitivity, increasing the perception of pain. If pronounced, this may result in chronic widespread pain (e.g. fibromyalgia).
You may enquire about sleep in the following ways:
How is your sleep?
Do you have problems falling asleep?
Do you frequently wake up at night? If so, why?
Is your sleep refreshing?
Extra-articular features
Several locomotor disorders (e.g. rheumatoid arthritis, SLE) cause extra-articular or multisystem features, some of which are outlined below:
Systemic symptoms: low-grade fever, weight loss, fatigue, lethargy.
Skin rash: vasculitic, photosensitive, nail-fold infarcts, alopecia (see 
Chapter 4).
Oral:
Dry mouth (Sjögren’s syndrome)
Ulcers (non-scarring: SLE; scarring: Behçet’s disease).
Raynaud’s phenomenon (primary, SLE, systemic sclerosis).
Urethritis (Reiter’s syndrome).
Scarring oro-genital ulcers (Behçet’s disease).
Eye symptoms:
Dry eyes (Sjögren’s syndrome)
Episcleritis, scleritis, scleromalacia perforans (rheumatoid arthritis)
Uveitis (sero-negative inflammatory arthirtis).
Cardiorespiratory: breathlessness (pulmonary fibrosis?), pericarditis, and pleurisy (rheumatoid arthritis); aortic regurgitation (ankylosing spondylitis).
Neurological:
Nerve entrapment (rheumatoid arthritis)
Migraine, depression, psychosis (SLE)
Stroke (anti-phospholipid antibody syndrome).
The rest of the history
Past medical history
Ask about all previous medical and surgical disorders and enquire specifically about any previous history of trauma or musculoskeletal disease. (See Box 10.7.)
If the locomotor system is not the main area of concern, you may wish to take a very short screening history in the form of three questions:
Do you have any pain or stiffness in your muscle, joints, or back?
Are you able to dress yourself completely without any difficulty?
Are you able to walk up and down stairs without any difficulty?
If any of these questions reveal a problem, the issue should be explored in more detail.
Family history
It is important to note any FHx of illness, especially those locomotor conditions with a heritable element:
Osteoarthritis.
Rheumatoid arthritis.
Osteoporosis.
Psoriasis.
SLE.
Sero-negative spondarthropathy.
Note that the seronegative spondyloarthropathies (e.g. ankylosing spondylosis) are more prevalent in patients with the HLA B27 haplotype.
Drug history
Take a full DHx including all prescribed and over-the-counter (including herbal) medications. Attempt to assess the efficacy of each treatment, including all those past and present.
Ask about any side effects of any drugs taken for locomotor disease including:
Gastric upset associated with non-steroidal anti-inflammatory drugs.
Long-term side effects of steroid therapy such as skin thinning, osteoporosis, myopathy, infections, and avascular necrosis.
Ask also about medication with known adverse musculoskeletal effects including:
Statins: myalgia, myositis, and myopathy.
ACE inhibitors: myalgia.
Anticonvulsants: osteomalacia.
Quinolone: tendinopathy.
Diuretics, aspirin, alcohol: gout.
Procainamide, hydralazine, isoniazid: drug-induced lupus.
It is also worth bearing in mind that illicit drugs may ? the risk of developing infectious diseases such as tuberculosis, HIV, and hepatitis, all of which can cause musculoskeletal symptoms.
Smoking and alcohol
As always, full smoking and alcohol histories should be taken.
Social history
This should form a natural extension of the functional enquiry and should include a record of the patient’s occupation if not already noted, as well as ethnicity.
Certain occupations predispose to specific locomotor problems.
Mechanically demanding occupations result in osteoarthritis in the mechanically loaded joints
Repetitive strain injury is seen in office workers
Vibrating power tools predispose to hand-vibration syndrome
Fatigue fractures may be seen in athletes.
Ethnicity is relevant as there is an overrepresentation of lupus and TB in the Asian population, both of which are linked to a variety of locomotor complaints.
Age: if the patient is an older person, make a note about the activities of daily living, how mobile the patient is, and if there are any home adaptations such as a chair lift or railings.
Remember to ask about home care or other supports.
Where appropriate, take a sexual history. This is important because reactive arthritis or Reiter’s syndrome may be caused by sexually transmitted diseases such as chlamydia and gonorrhoea. Where applicable, take a history of risk factors for HIV and hepatitis.
Outline locomotor history
As with other systems, organizing the clinical data (and your thoughts) into a structured framework can be crucial in clinching the diagnosis (see Box 10.8).
Presenting complaint(s)
How many joints are affected?
Establish their locations and timeline
What is the pattern of joint involvement?
Single episode
Episodic/intermittent
Progressive/additive
Extra-articular features
Past medical history
Family history
Allergies
Drug history
Smoking
Alcohol
Social history.
Formulations
At the end of a locomotor history, you should be able to identify:
Crystal arthropathy
Haemarthrosis
Infection
Degenerative
Post-traumatic
A mono-articular presentation of an oligo- or polyarthritis.
Inflammatory arthritis (rheumatoid, psoriatic, reactive, ankylosing spondylitis)
Infection (endocarditis, acute rheumatic fever)
Osteoarthritis.
Inflammatory (rheumatoid, psoriatic, SLE)
Osteoarthritis.
MCPJs, PIPJs, wrist, and MTPJs
Typically does not affect DIPJs & 1st CMCJ.
Typically affects DIPJs more commonly than other hand joints
May sometimes mimic RA.
Sacro-iliac joints, spine, shoulder, and hips
MCPJs and wrists
Knees, 1st CMCJ, DIPJ, PIPJ, spinal apophyseal joints, hips, and ankle
1st MTPJ, IPJs, knees, and ankles
Knees, wrist, MCPJs.
Reactive arthritis, first presentation of crystal or inflammatory arthritis, septic arthritis
Crystal synovitis (gout, acute CPP crystal synovitis), palindromic rheumatoid arthritis
Rheumatoid arthritis (typically symmetric), seronegative inflammatory arthritis (typically asymmetric)
Progression may be over months or years.
Sero-negative spondarthropathy
Peripheral large joint oligo-arthritis may also occur.
Osteoarthritis
Progressive involvement of several IPJs over a period of few months may occur at disease onset in ‘nodal’ OA. This typically occurs in post-menopausal women.
This allows you to formulate a clinical diagnosis in most instances.
Outline locomotor examination
A full examination of the entire locomotor system can be long and complicated.
In this chapter, we have broken the examination down into the following joints/regions: hand (including wrist), elbow, shoulder, spine, hip, knee, ankle, and foot. (See Box 10.12.)
The examination of each joint should follow the standard format:
Look
Feel
Move
Active
Passive.
Special tests
Function.
Limitation of active movement alone reflects underlying pathology of the tendons and muscle surrounding the joint, but limitation of both active and passive movement suggests an intrinsic joint problem.
In a thorough locomotor examination, you should examine the joints ‘above’ and ‘below’ the symptomatic one. For example, for an elbow complaint, also examine the shoulder and wrist.
The GALS screen
The overall integrity of the locomotor system can be screened very quickly by using the ‘GALS’ method of assessment. (See Box 10.13.)
The GALS screen was devised as a quick screen for abnormality in the absence of symptoms.* With apologies to the original authors, below is a slightly modified version:
Watch the patient walk, turn, and then walk back
There should be symmetry and smoothness of movement and arm swing with no pelvic tilt and normal stride length. The patient should be able to start, stop, and turn quickly.
Inspection: look for muscle wasting and joint deformity at the shoulders, elbows, wrists, and fingers. Squeeze across the 2nd–5th metacarpals—there should be no tenderness
Shoulder abduction: ‘raise your arms out sideways, above your head’. Normal range 170–180°.
Shoulder external rotation: ‘touch your back between your shoulder blades’
Shoulder internal rotation: ‘touch the small of your back’. Should touch above T10
Elbow extension: ‘straighten your arms out’. Normal is 0°.
Wrist and finger extension: the prayer sign
Wrist flexion and finger extension: the reverse prayer sign
Power grip: ‘make a tight fist’—should hide fingernails
Precision grip: ‘put your fingertips on your thumb’.
Inspection: look for swelling or deformity at the knee, ankle, and foot as well as quadriceps muscle wasting. Squeeze across the metatarsals—there should be no tenderness
Hip and knee flexion: test passively and actively. Normal hip flexion is 120°, normal knee flexion is 135°.
Hip internal rotation: normal is 90° at 45° flexion
Knee: bulge test and patellar tap
Ankle: test dorsiflexion (normal 15°) and plantar flexion (normal 55°).
Inspection from behind: look for scoliosis, muscle bulk at the paraspinals, shoulders, and gluteals, level iliac crests
Inspection from the side: look for normal thoracic kyphosis and lumbar and cervical lordosis
Tenderness: feel over the mid-supraspinatus—there should be no tenderness
Lumbar flexion: ‘touch your toes’. Normal is finger–floor distance <15cm. Lumbar expansion (Schober’s test)
Cervical lateral flexion: ‘put your ear on your shoulder’.
You may also use the GALS screen to make a quick, ‘screening’ examination of the whole locomotor system in order to identify which joints or regions require to be examined in more detail.
The GALS screen consists of four components:
G = Gait.
A = Arms.
L = Legs.
S = Spine.
Hand
Patterns of joint involvement. (a) Rheumatoid arthritis. (b) Psoriatic arthritis. (c) Osteoarthritis. (d) Gout.
Inspection
Look around the room, or at the patient for any functional aids, or adaptations. Begin by exposing the forearms up to the elbows, and sit facing the patient. Inspect the dorsal surface first, asking the patient to place their hands flat, palms down on a pillow with fingers and thumbs resting on the pillow. Then, inspect the palms. Look for:
Skin and nails
Skin colour.
Erythema (acute gout, acute CPP crystal arthritis, infection)
Digital ischaemia: pallor or bluish discoloration.
Skin thickness.
Thin skin: corticosteroid use
Callosities: mechanically demanding occupation
Tight shiny skin, sclerodactyly: systemic sclerosis.
Discrete skin lesions.
Vasculitis
Psoriasis
Gottron’s papules (dermatomyositis)
Ulcers (systemic sclerosis—typically on fingertips).
Other soft-tissue lesions.
Rheumatoid nodules (along extensor tendons)
Gouty tophi (near interphalangeal joints on fingers).
Ganglion (near wrist).
Scars.
Wrist fusion: dorsal median longitudinal scar on wrist
MCPJ replacement: dorsal longitudinal scar on MCPJs
Tendon transfer: dorsal longitudinal scar.
Nails:
Clubbing: hypertrophic pulmonary osteo-arthropathy
Splinter haemorrhage: infective endocarditis, vasculitis, physical trauma (digital trauma in mechanically demanding occupations may also result in occasional splinters in the distal nail bed)
Onycholysis (psoriasis, hyperthyroidism)
Pitting of the nail plate (psoriasis)
Nail-fold capillary telangiectasia and peri-ungual erythema: dermatomyositis, SLE, systemic sclerosis.
Muscle wasting:
Look at the interossei and forearm muscles.
Attitude, deformity, and swelling
Inspect each of the following joint groups sequentially (see Box 10.14):
Distal interphalangeal (DIP)
Proximal interphalangeal (PIP)
Metacarpophalangeal (MCP)
Wrist.
You may also ask the patient to make a fist and look at the MCP heads.
Normally, there is a depression (‘valley’) between neighbouring MCP heads which become ‘filled in’ with MCPJ synovitis.
Ask the patient to hold their hand in front of their chest with elbow and shoulders flexed and wrist extended. In this position, look for:
Volar subluxation of the carpus in RA
Wrist drop in radial nerve palsy
Finger drop due to ruptured finger extensor tendons.
Swan neck: fixed flexion at the DIPJ and hyperextension at the PIPJs—associated with rheumatoid arthritis
Boutonni è re: hyperextension at the DIPJ and flexion at the PIPJs—associated with rheumatoid arthritis
Z-shaped thumb: flexion at the MCPJ of the thumb, hyperextension at the interphalangeal joint—associated with RA
Ulnar deviation at MCPJs: a feature of rheumatoid arthritis and other conditions, the fingers are deviated medially (toward the ulnar aspect of the forearm) at the MCPJs
Wrist subluxation: volar subluxation of carpus (RA)
Wrist deviation: radial deviation is frequently seen in RA
Heberden ’ s nodes: postero-lateral bony swelling (due to osteophytes) at the DIPJs—a feature of osteoarthritis
Bouchard ’ s nodes: similar to Heberden’s nodes, but at the PIPJs—a feature of osteoarthritis
Dorsal bar: merging of Heberden’s or Bouchard’s nodes at the IPJs
Telescopic fingers: advanced destruction of IPJs. The finger may be elongated when it is pulled out passively. There is concentric wrinkling of the skin. Seen in advanced psoriatic arthritis.
Palmar abnormalities
As well as the features noted on the dorsal aspect, look for:
Scar of carpal tunnel decompression: volar mid-line longitudinal scar.
Thenar or hypothenar wasting.
Palmar erythema (RA, liver disease, corticosteroid use).
Nodules near the distal palmar crease (Dupuytren’s contracture gives thickened palmar fascia).
Tendon nodules: usually occur at the level of MCPJ heads, associated with triggering.
Gouty tophi (fingertips).
Calcinosis cutis (fingertips; seen in limited cutaneous systemic sclerosis).
Digital pits (fingertips; seen in diffuse cutaneous systemic sclerosis).
Palpation
Ask the patient if there is any tenderness and palpate those areas last.
Using the dorsum of your hands, feel for temperature change over the wrists, thumb-base, MCPJs, and IPJs.
As a rule, skin in the peripheries gets cooler distally.
Palpate any abnormalities identified on inspection.
Perform an MCPJ squeeze (as in GALS) to screen for MCPJ synovitis.
Depress the ulnar styloid (piano key sign) to check for the integrity of the inferior radio-ulnar joint and its supporting ligaments.
Assess for skin thickening.
Gently pick the skin on the dorsum of the hand between your thumb and index finger to make a skin fold
If you are not able to make a skin fold, try to move the skin over the underlying soft-tissue structures.
Palpate finger flexor tendons on the palmar aspect for thickening.
Movement
Before assessing movement, ask the patient if they have any pain. Test active, and then passive movements.
Active movements
Wrist extension: test with the ‘prayer sign’ manoeuvre. Ask the patient to place their hands, palm to palm, in front of them with fingers extended as in Fig. 10.1.
Wrist flexion: test with the ‘reverse prayer’ position. Ask the patient to place their hands back to back in front of them with fingers extended as in Fig. 10.2.
Wrist abduction: with elbows flexed at 90°, palm facing up, and forearm fixed, ask the patient to point their fingers outwards.
Wrist adduction: with elbows flexed at 90°, palm facing up, and forearm fixed, ask the patient to point their fingers inwards.
Finger flexion: ask the patient to make a fist.
Also observe for range of movement. Normally a patient should be able to dig their finger nails into their palms
Detailed assessment of IPJ flexion may be carried out if necessary. Fix the proximal phalanx to assess PIPJ flexion (flexor digitorum superficialis) and the distal phalanx to assess DIPJ flexion.
Finger extension: ask the patient to straighten their fingers out. Also tested with the prayer and reverse prayer positions. Triggering of the finger may be revealed during extension.
Thumb movements: assess flexion, extension, abduction, adduction, opposition (see Chapter 8).
The prayer position.
The reverse prayer position.
Passive movements
Move each joint and assess the range of movement and watch for any pain.
Feel for crepitus, especially over the base of the thumb.
Function
Testing function is a vital part of any hand examination and should not be overlooked. Ask the patient to:
Write their name.
Pour a glass of water.
Fasten and unfasten a button. Pick a coin up from a flat surface.
Examine this patient’s hands.
Clean your hands
Introduce yourself
Explain the purpose of examination, obtain informed consent
Ask for any painful areas you should avoid
Ask the patient to expose the distal upper limb including the forearm, wrist, and hand
Sit opposite and ask the patient to position their hands on a pillow, palms facing down
Inspect the dorsum of the hand, wrist, and forearm. Look at the elbow
Feel for temperature over the joint areas (proximal to distal) using the dorsum of your hands
Compare opposite sides simultaneously
Palate the wrist, MCPJs, and IPJs for swelling and tenderness
Ask the patient to turn their hands over
Inspect the palmar surfaces of the hand, wrist, and forearm
Assess active, then passive movements
Examine sensation (see Chapter 8)
Examine the median, ulnar, and radial nerves specifically
Examine power (see Chapter 8)
Test reflexes (see Chapter 8)
Check the radial and ulnar artery pulsations
Assess function
Ask the patient to write and do up some buttons
Thank the patient.
Elbow
Look
Look around the bed for any mobility aids or other clues. Ask the patient to stand, make sure both upper limbs are exposed, and look at the patient from top to toe.
Inspect the elbow from the front, side, and behind, with the patient’s arm hanging by side, the forearm supine, and note:
Skin change (e.g. psoriatic plaques).
Skin or subcutaneous nodules (e.g. rheumatoid nodules, gouty tophi).
Scars.
Deformities:
Varus (cubitus varus): can be caused by a supracondylar fracture
Valgus (cubitus valgus): can be caused by non-union of a lateral condylar fracture or Turner’s syndrome
Fixed flexion deformity (inability to straighten the elbow completely): can be caused by synovitis in inflammatory arthritis or by joint damage in inflammatory arthritis or osteoarthritis.
Muscle wasting.
Swelling.
Synovial swelling is seen on the lateral aspect of elbow, around the radial head, or around the posterior para-olecranon fossa (felt lateral and medial to the olecranon process)
Bursal swelling occurs at the olecranon bursa posteriorly.
Feel
Always ask about pain before getting started.
Palpate the joint posteriorly and laterally and feel for:
Temperature.
Subcutaneous nodules (rheumatoid nodules, gouty tophi).
Swelling.
Soft swelling may be due to olecranon bursitis (e.g. sepsis, gout)
Boggy swelling suggests synovial thickening (e.g. rheumatoid)
Hard swelling suggests a bony deformity
If fluid is present, attempt to displace it on either side of olecranon.
Tenderness.
Carefully palpate the joint margin and epicondyles. Note the exact location of any pain.
Crepitus.
Palpate posterolaterally during flexion/extension and pronation/supination.
Ulnar nerve.
Feel medially for ulnar nerve subluxation (occurs with a ‘snap’ during flexion/extension; palpate medially for this)
Palpate the ulnar nerve for any thickening.
Move
Check that there is good shoulder function before attempting to assess elbow movements.
Remember to test passive movements (you do the moving) and active movements (the patient does the moving) at each stage. Test active movements before passive movements.
Ask the patient to place their arms on the back of their head.
Next, assess elbow flexion and extension with the upper arm fixed.
Remember to compare with the opposite side.
With the elbows tucked into the sides and flexed to a right angle, test the radio-ulnar joints for pronation (palms towards floor) and supination (palms towards the ceiling).
This position fixes the upper arm, and prevents any trick movement of the upper arm across the abdomen.
Resisted active motion
With the elbow flexed at 90° and prone, hold the patient’s forearm still. Ask the patient to extend their wrist against resistance (Fig. 10.4).
This reproduces pain in lateral epicondylitis (tennis elbow).
In the same position, ask the patient to flex the wrist against resistance.
This reproduces pain in medial epicondylitis (golfer’s elbow).
With the elbow flexed at 90° ask the patient to supinate, or flex their elbow against resistance.
This causes pain in distal bicipital tendonitis.
Assessing resisted active motion. (a) Wrist extension; (b) wrist flexion.
Measure
Measure elbow flexion and extension in degrees from the neutral position (i.e. consider a straight elbow joint to be 0°).
The normal ranges of movements at the elbow are:
0–150° for flexion/extension
0–85° for pronation
0–90° for supination.
Function
Observe the patient pour a glass of water and then put on a jacket.
Shoulder
Look
Look around for any aids or adaptations. Ask the patient to remove any covering clothing and expose the upper limbs, neck, and chest. Scan the patient from top to toe. Inspect from the front, side, and behind.
Look especially for:
Scars.
Bruising or other skin/subcutaneous tissue changes.
Contours.
Look for winging of the scapula, prominence of the acromioclavicular joint and muscle wasting in the deltoid or short rotators which overlie the upper and lower segments of the scapula (rotator cuff pathology)
Generalized atrophy of shoulder muscle suggests painful shoulder arthropathy, or brachial neuritis.
Joint swelling.
This may be a clue to acute bleeds, effusions, pseudogout, or sepsis
Sub-deltoid/subacromial bursa swelling appears on the lateral aspect of the shoulder.
Attitude/deformity: Look at the position of both shoulders looking for evidence of dislocation.
Posterior dislocation: the arm is held in an internal rotation
Anterior dislocation: the arm is displaced antero-inferiorly
In advanced glenohumeral arthropathy, the attitude of shoulder is internal rotation, and adduction.
Remember to inspect the axillary regions.
Feel
Always ask about pain before getting started.
Make note of any temperature changes, tenderness, or crepitus. Standing in front of the patient:
Palpate the soft tissues and bony points in the following order: sternoclavicular joint, clavicle, acromioclavicular joint, acromial process, head of humerus, coracoid process, glenohumeral joint, spine of scapula, greater tuberosity of humerus.
Check the interscapular area for pain.
Palpate the supraclavicular area for lymphadenopathy.
Move
Remember to test active movements (the patient does the moving) before passive movements (you do the moving) at each stage.
Compound movements
These may be employed as screening tests to assess shoulder dysfunction. See Fig. 10.5.
Ask the patient to put both hands behind the head (flexion, external rotation, and abduction).
Ask the patient to reach up their back with the fingers to touch a spot between their shoulder blades (extension, internal rotation, and adduction).
Compound movements. (a) Flexion, external rotation, and abduction. (b) Extension, internal rotation, and adduction.
Glenohumeral movements
To test true glenohumeral movement, anchor the scapula by pressing firmly down on the top of the shoulder. After about 70° of abduction, the scapula rotates on the thorax—movement is scapulothoracic.
Quantify any movement in degrees (measure).
Flexion: ask the patient to raise their arms forwards above their head.
Extension: straighten the arms backwards as far as possible.
Abduction: move the arm away from the side of the body until the fingertips are pointing to the ceiling.
Adduction: ask the patient to move the arm inwards towards the opposite side, across the trunk.
External rotation: with the elbows held close to the body and flexed to 90°, ask the patient to move the forearms apart in an arc-like motion in order to separate the hands as widely as possible.
Internal rotation: ask the patient to bring the hands together again across the body (loss of external rotation suggests adhesive capsulitis).
Special tests
Testing for a rotator cuff lesion/tendonitis: ‘the painful arc’
Ask the patient to abduct the shoulder against light resistance.
Pain in early abduction suggests a rotator cuff lesion and usually occurs between 40–120°. This is due to a damaged and inflamed supraspinatus tendon being compressed against the acromial arch. Similar symptoms may also occur in subacromial bursitis.
Testing for acromioclavicular arthritis
If there is pain during a high arc of movement (starting around 90°) and the patient is unable to raise their arm straight up above their head to 180°, even passively, this is suggestive of acromioclavicular arthritis.
Function
Ask the patient to scratch the centre of their back or to put on a jacket.
Spine
Look
Scan around the room for any clues such as a wheelchair or walking aids. Watch how the patient walks into the room or moves around the bed area. Study their posture, paying particular attention to the neck.
Ask the patient to strip down to their underwear. Ask the patient to walk, turn around, and walk back. Inspect from in front, the side, and behind in both the standing and sitting positions.
Look especially for:
Scars.
Pigmentation.
Abnormal hair growth.
Unusual skin creases.
Muscle spasm.
Height of iliac crest on each side.
Asymmetry including abnormal spinal:
Kyphosis: convex curvature—normal in the T-spine
Lordosis: concave curvature—normal in the L- and C-spines
Scoliosis: side-to-side curvature away from the midline. This may be postural (corrects on anterior flexion) or structural (unchanged or worsened on flexion).
A ‘question mark’ spine with exaggerated thoracic kyphosis and a loss of lumbar lordosis is classic of ankylosing spondylitis.
Feel
Palpate each spinous process noting any prominence or step and feel the paraspinal muscles for tenderness and spasm. Apply firm pressure using your thumb to elicit tenderness arising from facet joint arthritis.
You should also make a point of palpating the sacro-iliac joints.
Move
C-spine
Assess active movements of the cervical spine first. These include flexion, extension, lateral flexion, and rotation. It is often helpful to demonstrate these movements yourself.
Flexion: ask the patient to put their chin on their chest (0–80°).
Extension: ask the patient to look up to the ceiling (0–50°).
Lateral flexion: ask the patient to lean their head sideways, placing an ear on their shoulder (0–45°).
Rotation: ask the patient to look over each shoulder (0–80°).
T- and L-spine
Flexion: ask the patient to touch their toes, keeping knees straight.
Extension: ask the patient to lean backwards (10–20°).
Lateral flexion: ask the patient to bend sideways, sliding each hand down their leg as far as possible.
Rotation: anchor the pelvis (put a hand on either side) and ask the patient to twist at the waist to each side in turn.
Measure
Schober’s test
This is useful measurement of lumbar flexion.
Ask the patient to stand erect with normal posture and identify the level of the posterior superior iliac spines on the vertebral column.
Make a small pen mark at the midline 5cm below and 10cm above this.
Now instruct the patient to bend at the waist to full forward flexion.
Measure the distance between the two marks using a tape measure.
The distance should have increased to >20cm (an increase of >5cm).
Modified Schober’s test
As above but only the 10cm segment above the level of posterior superior iliac spines is measured. Increase >3.5cm on flexion is normal.
Chest expansion
See Chapter 6. Expiration to peak inspiration should be ?5cm.
Occiput to wall distance
Ask the patient to stand upright with their heels and back touching the wall, looking straight forward with the chin at the usual carrying level.
Ask them to try to touch the wall with the back of their head.
Measure the distance between the occiput and the wall.
Any gap suggests thoracic kyphosis or fixed cervical flexion.
Other measurements
Students will not be expected to perform the following, but should be aware that they are used in patients with spondyloarthropathies.
Tragus to wall distance.
Cervical rotation (in degrees).
Lateral flexion (measure of lumbar spine mobility).
Special tests
Sciatic nerve stretch test
This test is used to look for evidence of nerve root irritation (Fig. 10.6).
With the patient lying supine, hold the ankle and lift the leg, straight, to 70–80°. Once at 70–80°, or at an angle at which pain is felt, dorsiflex the foot (Bragard test). If positive, pain will be felt at the back of the thigh, radiating to below the knee.
The pain may be relieved by knee flexion, returning the foot to a neutral position, or by reducing the degree of flexion at the hip.
A positive stretch test suggests tension of the nerve roots supplying the sciatic nerve, commonly over a prolapsed disc (L4/5 or L5/S1).
Sciatic nerve stretch test. (a) With the patient supine, hold the ankle and lift the leg, straight, to 70–80° or until pain is felt. (b) Dorsiflex the foot (Bragard test). If positive, pain will be felt at the back of the thigh, radiating to below the knee.
Femoral nerve stretch test
With the patient lying prone, extend the hip, flex the knee, and plantar-flex the foot. The stretch test is positive if pain is felt in the thigh/inguinal region.
Sacro-iliac joint distraction test
With the patient lying supine, apply firm outward pressure to both iliac crests at the anterior superior iliac spines.
Pain in the buttocks suggests sacro-iliac joint arthropathy.
Examine this patient’s spine.
Clean your hands
Introduce yourself
Explain the purpose of examination, obtain informed consent
Ask for any painful areas you should avoid
Ask the patient to undress to underwear
Ask the patient to walk. Watch the gait
With the patient standing, inspect from back and side
Palpate the spinous processes individually
Test active movements
Perform Schober’s test
If positive, perform other tests to assess restriction in spinal movements
Ask the patient to lie on the examination couch
Perform the straight leg raise test
Examine sensation and reflexes in the lower limbs
Assess function
Ask the patient to pick something up from the floor
Ask about how they manage to turn in bed
Thank the patient.
Hip
Look
Expose the whole lower limb. Look around the room for any aids or devices such as orthopaedic shoes or walking aids. If they have not done so already, ask the patient to walk and note the gait. Note if there is evidence of a limp or obvious pain.
Pay attention to the position of the limbs (e.g. external rotation, pelvic tilting, standing with one knee bent, or foot held plantar-flexed/in equinus).
With the patient in the standing position, inspect from the front, side, and behind. Look for:
Scars.
Sinuses.
Asymmetry of skin creases.
Swelling.
Muscle wasting.
Deformities/attitude.
Patients with structural hip arthropathy (e.g. advanced osteoarthritis) tend to hold the hip joint in flexion, external rotation, and abduction. A similar posture is adopted in hip synovitis.
Feel
Feel for bony prominences such as the anterior superior iliac spines and greater trochanters. Check that they are in the expected position.
Palpate the soft tissue contours and feel for any tenderness in and around the joint (usually elicited lateral to the femoral pulse) and over the greater trochanter.
Move
Ask the patient if they have any pain before examining.
Fix the pelvis by using your left hand to stabilize the contralateral anterior superior iliac spine since any limitation of hip movement can easily be hidden by movement of the pelvis.
Active movements
With the patient supine:
Flexion: ask the patient to flex the hip until the knee meets the abdomen, normal is around ~100–135°.
Abduction: with the patient’s leg held straight, ask them to move it away from the midline, normal is 30–40°.
Adduction: with the patient’s leg held straight, ask them to move it across the midline, normal is ~30°.
Internal rotation: ask the patient to keep the knees together and point the feet towards each other, normal is 30°.
External rotation: ask the patient to keep the knees together and point the feet as far apart as possible, normal is 15–30°.
With the patient prone:
Extension: ask the patient to raise each leg off the bed, normal is 15–30°. (This movement is not routinely measured in clinical practice.)
Passive movements
Most should be assessed by the examiner as for active movements whilst the patient is in a relaxed state. With the patient supine:
Passive flexion: flex the hip and knee simultaneously. (This relaxes the hamstrings and avoids performing a ‘straight leg raising test’.)
Passive external and internal rotation: flex the knee and hip to 90°, hold the knee with one hand, and move the ankle away or towards the midline with the other.
In hip arthropathy, internal rotation of the hip is the first movement to be restricted.
Passive abduction and adduction: examine with the limb in neutral.
Measure (limb length)
True shortening, in which there is loss of bone length, must not be confused with apparent shortening due to a deformity at the hip.
Technique
With the patient supine, place the pelvis square and the lower limbs in comparable positions in relation to the pelvis.
Measure the distance from the anterior superior iliac spine to the medial malleolus on each side (true length).
Apparent length is measured from a midline structure such as the xiphisternum (or the umbilicus) to the medial malleolus.
A difference of 1cm is considered abnormal.
Special tests
Trendelenberg test
This is useful as an overall assessment of the function of the hip and will expose dislocations or subluxations, weakness of the abductors, shortening of the femoral neck, or any painful disorder of the hip.
Ask the patient to stand up straight without any support.
Ask them to raise their left leg by bending the knee.
Watch the pelvis (should normally rise on the side of the lifted leg).
Repeat the test with the patient standing on the left leg.
A positive test is when the pelvis falls on the side of the lifted leg indicating hip instability on the supporting side (i.e. the pelvis falls to the left = right hip weakness).
Thomas’s test
A fixed flexion deformity of the hip (often seen in osteoarthritis) can be hidden when the patient lies supine by tilting the pelvis and arching the back. Thomas’s test will expose any flexion deformity.
With the patient supine, feel for a lumbar lordosis (palm upwards).
With the other hand, flex the opposite hip and knee fully to ensure that the lumbar spine becomes flattened.
If a fixed flexion deformity is present, the affected leg flexes too (measure the angle relative to the bed).
Remember to repeat the test on the other hip.
Function
Assess gait. See Chapter 8.
Knee
Look
Scan the room for any walking aids or other clues and inspect the patient standing. The lower limbs should be completely exposed except for underwear so that comparisons can be made.
Compare one side to the other and look for:
Deformity (e.g. genu valgus, genu varus, fixed flexion, or hyperextension ‘genu recurvatum’).
Scars or wounds to suggest infection past or present?
Muscle wasting (quadriceps).
Swelling (including posteriorly).
Erythema.
Look for loss of the medial and lateral dimples around the knees which suggest the presence of an effusion.
Feel
Always ask about pain before getting started. Always compare sides.
With the patient lying supine:
Palpate for temperature using the back of the hand.
Ask if the knee is tender on palpation.
Feel around the joint line while asking the patient to bend the knee slightly.
Palpate the collateral ligaments (either side of the joint).
Feel the patellofemoral joint (by tilting the patella).
Examining for a small effusion—the ‘bulge sign’
With the knee extended and the quadriceps relaxed, gently milk any synovial fluid from suprapatellar pouch downwards into the retropatellar space (Fig. 10.7).
Now, holding the patella still, empty the medial joint recess using a wiping motion of your palm.
This will milk any fluid into the lateral joint recess.
Now apply a similar wiping motion to the lateral recess and...
Watch the medial recess.
If there is fluid present, a distinct bulge should appear on the flattened, medial surface as it is milked out of the lateral side.
Examining for the ‘bulge sign’. (a) Wipe any fluid from the medial joint recess. (b) Wipe the fluid back out of the lateral joint recess and watch the medial side.
Examining for a large effusion—the ‘patellar tap’
If the effusion is tense or large, the bulge sign is absent as you will be unable to empty either recess of fluid—use the patellar tap instead.
Move any fluid from the medial and lateral compartments into the retropatellar space (Fig. 10.8).
Apply firm pressure over the suprapatellar pouch with the flat of the hand and use your thumb and index finger placed either side of the patella to push any fluid centrally.
With the first one or two fingers of the other hand, push the patella down firmly.
If fluid is present, the patella will bounce off the lateral femoral condyle behind. You will feel it being pushed down and then ‘tap’ against the femur.
Testing for ‘patellar tap’. (a) Use the palmar surface, thumb, and index finger of one hand to move any fluid into the retropatellar space. (b) Attempt to ‘tap’ the patella on the femur using the other hand.
Move
Remember to test active movements (the patient does the moving) before passive movements (you do the moving) at each stage. Quantify any movement in degrees (measure).
Flexion: ask the patient to maximally flex the knee, normal ~135°.
Extension: ask the patient to straighten the leg at the knee.
Hyperextension: assess by watching the patient lift the leg off the bed and then, holding the feet stable in both hands above the bed/couch, ask the patient to relax. Ensure that you are not causing the patient any discomfort.
Passive movements: Feel over the knee with one hand for any crepitus.
Measure
The visual impression of wasting of the quadriceps can be confirmed by measuring the circumference of the thighs at the same level using a fixed bony point of reference e.g. 25cm above the tibial tubercle.
Special tests
Testing for medial and lateral collateral ligament instability
Normally, the joint should move no more than a few degrees laterally, excessive movement suggests a torn or stretched collateral ligament.
With the patient’s legs extended, take the foot in your right hand.
Hold the patient’s extended knee firmly with the other hand.
Attempt to bend the knee medially (varus) whilst feeling the lateral knee joint line.
This tests the lateral collateral ligament.
Attempt to bend the knee laterally (valgus), feeling the medial joint line.
This tests the medial collateral ligament.
Repeat the above with the knee at 30° flexion.
In this position, only the lateral and medial collateral ligaments (and not the cruciates) contribute to varus–valgus stability at the knee.
Anterior and posterior drawer tests
These test the anterior and posterior cruciate ligaments. These ligaments prevent the distal part of the knee moving anteriorly and posteriorly.
Ensure the patient is lying in a relaxed supine position.
Ask the patient to flex the knee to 90°.
In an anterior cruciate ligament tear, the tibia sags posteriorly in this position (‘sag sign’).
You may wish to position yourself perched on the patient’s foot to stabilize the leg. Warn the patient about this first!.
Wrap your fingers around the back of the knee using both hands, positioning the thumbs over the patella pointing towards the ceiling.
Push up with your index fingers to ensure the hamstrings are relaxed.
The upper end of the tibia is then pulled forwards and pushed backwards in a rocking motion.
Normally, there should be very little or no movement seen
Excessive anterior movement reflects anterior cruciate laxity
Excessive posterior movement denotes posterior cruciate laxity.
McMurray’s test
A test for meniscal tears (Fig. 10.9a).
With the patient lying supine, bend the hip and knee to 90°.
Grip the heel with your right hand and press on the medial and lateral cartilage with your left hand.
Internally rotate the tibia on the femur and slowly extend the knee.
Repeat but externally rotate the distal leg whilst extending the knee.
Repeated with varying degrees of knee flexion.
If a meniscus is torn, a tag of cartilage may become trapped and cause pain and an audible (and palpable) ‘click’.
Testing for meniscal tears. (a) McMurray’s test. (b) Apley’s grinding test.
Apley’s test
Another test for meniscal tears. If ‘positive’, the test will produce pain.
Position the patient prone with the knee flexed to 90° (Fig. 10.9b).
Stabilize the thigh with your left hand.
With the right hand, grip the foot and rotate or twist it whilst pressing downwards in a ‘grinding motion’.
Examine this patient’s knees.
Clean your hands
Introduce yourself
Explain the purpose of examination, obtain informed consent
Ask for any painful areas you should avoid
Ask the patient to expose their lower limbs including the ankles and feet, and stand up
Look for knee alignment and swellings
Ask the patient to walk. Watch the gait
Ask the patient to lie on the couch. Inspect the knees again
Palpate the knees for warmth
Examine for effusions
Feel for localized tenderness
Test active and passive movements
Test for integrity of the cruciate and collateral ligaments
To assess function, ask the patient to stand from sitting and ask how they find climbing stairs.
Ankle and foot
Look
Expose the lower limbs and make note of any walking or other aids. Take a moment to also examine the footwear for any adaptations, abnormal wear, or stretching.
Examine the feet and ankles with the patient lying on a couch or bed. Look from front, sides, back, and inspect the plantar surface.
Also examine the feet and ankle when the patient is standing up. Look from front, sides, and back. If you think the patient can, ask them to stand on tip-toes and then on their heels while you watch the foot from behind and from the sides.
Finally, watch the patient walk.
Look for:
Skin or soft-tissue lesions including calluses, swellings, ulcers and scars.
Muscle wasting at the calf and lower leg.
Swellings.
Deformities.
Examine the nails carefully for any abnormalities such as fungal infections or in-growing toenails. 
Don’t forget to look between the toes.
You may also wish to inspect for evidence of other abnormalities such as clubbing of the feet (talipes equinovarus).
Swellings
Ankle synovitis: diffuse anterior swelling ± lateral or medial extension.
Tenosynovitis: tubular swelling oriented longitudinally along a tendon.
Anterior: tibialis anterior, extensor hallucis, or extensor digitorum
Posterior to medial malleolus: tibialis posterior, flexor digitorum, or flexor hallucis
Posterior to lateral malleolus: peroneal tendons.
Achilles tendinopathy/tear, retrocalcaneal and retroachilles bursitis: posterior to calcaneum.
Deformities
Deformities involving the arch and hindfoot are better appreciated with the patient standing. Look for:
Hallux valgus: ‘bunion’. Medial deviation of the 1st metatarsal and lateral deviation and/or rotation of the great toe. Commonly bilateral.
Hammer toes: flexion deformity at the PIPJ of the affected toe(s) (commonly the 2nd toe), hyperextension of the MTPJ and DIPJ. Caused by an overpull of the extensor digitorum longus tendon.
Claw toes: Extension contracture with dorsal subluxation of the MTPJ, flexion deformities of the PIPJ and DIPJ.
Often idiopathic. Often elderly females with diabetes or RA.
Mallet toes: A flexed DIPJ (commonly the 2nd toe). May exist in conjunction with a claw-toe deformity.
Pes planus (flat foot): a lack of the normal plantar arches.
Physiologic pes planus (but not pathologic) may correct when standing on tip-toes.
Pes cavus (high-arched foot): exaggeration of the plantar arches.
Feel
Always ask about pain before getting started.
Assess the skin temperature and compare over both the feet.
Look for areas of tenderness, particularly over the ankle bony prominences (lateral and medial malleoli, MTPJs, interphalangeal joints, and heel) as well as the metatarsal heads.
Squeeze across the MTPJs, and assess pain and movement.
Remember to palpate any swelling, oedema, or lumps.
Move
The ankle and foot is a series of joints which function as a unit.
Remember to test passive movements (you do the moving) and active movements (the patient does the moving) at each stage.
Active movements should be performed with the patient’s legs hanging over the edge of the bed.
Ankle dorsiflexion: ask the patient to point their toes to their head (normal ~20°).
Ankle plantar flexion: ask the patient to push the toes down towards the floor ‘like pushing on a pedal’ (normal ~45°).
Inversion: (subtalar joint between the talus and calcaneum). Ask the patient to turn their sole inward (you may have to demonstrate this (normal ~20°).
Eversion: as inversion but turn the sole outwards, away from the midline (normal ~10°).
Toe flexion: ask the patient to curl their toes.
Toe extension: ask the patient to straighten the toes.
Toe abduction: ask the patient to fan out their toes as far as possible.
Toe adduction: ask the patient to hold a piece of paper between their toes.
Passive movements
Palpate for crepitus. Whilst checking inversion and eversion passively, grasp the ankle with one hand and with the other, grasp the heel, and turn the sole inwards towards the midline and then outwards.
Measure
Calf circumference can be measured bilaterally to check for any discrepancies which may highlight muscle wasting/hypertrophy (e.g. 10cm below the tibial tuberosities).
Special tests
Simmond’s test
This test is used to assess for a ruptured Achilles tendon.
Ask the patient to kneel on a chair with their feet hanging over the edge. Squeezes both calves.
Normally the feet should plantar-flex. If the Achilles tendon is ruptured, there will be no movement on the affected side.
Function
It is also helpful to observe the patient’s gait with and without shoes. Be sure to ask the patient if they are able to do this first.
Important presentations
Rheumatoid arthritis (RA)
RA is a chronic inflammatory multisystem autoimmune disease mediated by pro-inflammatory cytokines such as tumour necrosis factor alpha (TNF-?) and may associate with antibodies such as rheumatoid factor and anti-CCP. However, it is worth remembering that between 30–40% of patients with rheumatoid arthritis are not positive for rheumatoid factor. A smaller proportion of patients (10–20%) does not develop anti-CCP antibodies.
Usually the onset of symptoms in RA is over a few days to a few weeks, and the progression is slow. Additional joints are involved over weeks and months. It can rarely have an acute onset (over a day or two). The course can be episodic with complete resolution between attacks (palindromic). The clinical features of RA can be divided into articular and extra-articular features summarized below.
Demographics
Affects around 1–3% of the population.
Occurs in all races.
Peak age of onset in the 4th and 5th decades.
Female:male ratio ~3:1.
Articular features
RA usually presents as a symmetrical polyarthritis affecting the wrists and small joints of the hands and feet. Occasionally, a patient presents with a mono- or oligo-arthritis of larger joints such as the knees, wrists, shoulders, or elbows. Common symptoms are joint pain, stiffness, and swelling which are typically worse in the morning and improve as the day progresses.
Signs of RA
Synovitis involving the wrists (dorsal swelling), metacarpo-phalangeal (filling in of gaps between the MCP heads) and proximal interphalangeal joints (lateral expansion of IPJs), with sparing of the distal interphalangeal and 1st carpometacarpal joints.
With modern and aggressive treatment of synovitis, joint destruction and resulting deformities are not common in patients developing RA in the last decade. However, these deformities may be present in the patients who have had the disease for some years or in some with aggressive uncontrolled RA.
Inspection:
Symmetric swelling of proximal interphalangeal (PIP) joints.
Symmetric swelling of metacarpo-phalangeal (MCP) joints.
Ask the patient to make a fist; subtle swelling of MCP joints is seen as filling in of the ‘valleys’ between metacarpal heads.
Ulnar deviation at MCP joints.
Thin skin with scars. (Long-term corticosteroid use.)
Wasting of intrinsic muscles.
Tuck sign: tubular swelling due to extensor tenosynovitis, seen on the dorsal aspect of wrist and on finger extension.
Swan-neck deformity.
Hyperextension of PIPJ and flexion of DIPJ.
Boutonnière deformity.
Flexion at PIPJ, extension at DIPJ.
Volar subluxation at MCP and wrist joints.
Rheumatoid nodules on extensor tendons, joints, sites of mechanical irritation (elbow, toe, and heel).
Palpation:
Warmth and tenderness at DIP, PIP, MCP, and wrist joints (if active).
‘Doughy’ feeling of synovial proliferation at joints.
Piano key sign: up and down movement of the ulnar styloid in response to pressure from examiners’ fingers.
Extra-articular features of RA
Extra-articular features are the systemic manifestations of RA which are unique to, and caused by, the immune-pathological process of RA.
Common:
Rheumatoid nodules: common at sites of pressure (elbows and wrists). Associated with more severe disease and rheumatoid factor positivity.
Sjögren’s syndrome (keratoconjunctivitis sicca).
Raynaud’s phenomenon.
Interstitial lung disease (pulmonary fibrosis, pulmonary nodules).
Pleurisy/pleural effusions.
Episcleritis/scleritis.
Uncommon:
Neurological features:
Mononeuritis multiplex
Peripheral neuropathy.
Cardiac features:
Pericarditis/pericardial effusions.
Systemic features (fever, malaise, weight loss, and lymphadenopathy).
Rare:
Vasculitis:
Nail-fold infarcts
Cutaneous ulceration
Digital gangrene.
Skin lesions:
Pyoderma gangrenosum.
Lung features:
Caplan’s syndrome (massive lung fibrosis in RA patients with pneumoconiosis)
Obliterative bronchiolitis
Felty’s syndrome (RA, splenomegaly, and neutropenia).
Amyloidosis (proteinuria, hepatosplenomegaly).
Complications of RA
Extra-articular features of RA should be distinguished from ‘complications’. These are consequences of joint inflammation, systemic inflammation, or drug treatment and include:
Anaemia (Box 10.15).
Cataracts (chloroquine, steroids).
Peripheral nerve entrapment (e.g. carpal tunnel syndrome).
Cervical myelopathy (atlanto-axial subluxation).
Palmar erythema, skin thinning, and muscle wasting (synovitis in nearby joints).
Anaemia of chronic disease
GI bleeding
Non-steroidal anti-inflammatory drugs (NSAIDs) or corticosteroid use.
Bone marrow suppression
Disease-modifying anti-rheumatic drugs (e.g. methotrexate).
Megaloblastic anaemia
Due to folic acid deficiency or pernicious anaemia.
Macrocytic anaemia.
Methotrexate, azathioprine.
Recently, non-Hodgkin’s lymphoma (systemic inflammation), ischaemic heart disease (systemic inflammation), osteoporosis, and a propensity to lower respiratory tract infections have been recognized as complications of RA.
Osteoarthritis
Osteoarthritis is a chronic disorder of synovial joints characterized by focal cartilage loss and an accompanying reparative bone response.
It represents the single most important cause of locomotor disability with a prevalence which ? with age, and has a female preponderance.
Secondary causes of OA include:
Trauma (fracture, meniscal, or cruciate injury).
Inflammatory arthritis (e.g. RA).
Abnormalities in articular contour (hip and acetabular dysplasias) or alignment (varus or valgus knee malalignment).
Generalized or localized hypermobility (Ehlers–Danlos syndrome, Marfan’s syndrome, benign hypermobility syndrome).
Previous septic arthritis.
Avascular necrosis.
Symptoms
Common symptoms include swelling, deformity, stiffness, weakness, and pain which is normally worse after activity and relieved by rest.
Inspection
Posterolateral swelling at the distal interphalangeal (DIP) (Heberden’s nodes) and proximal interphalangeal (PIP) (Bouchard’s nodes) with characteristic radial or ulnar deviation of the phalanx.
Squaring of thumb base, wasting of thenar eminence observed on the volar aspect (1st carpometacarpal joint).
Inspection (knee)
Patient standing, examine from front. Look for:
Varus and valgus deformity.
Suprapatellar and infrapatellar effusion.
Quadriceps wasting.
Fixed flexion at knee with the patient lying supine.
Palpation (hands)
Cool bony swelling at IPJs.
Joint line tenderness at IPJ and 1st CMCJ.
Paget’s disease (osteitis deformans)
A disorder of bone remodelling characterized by ? osteoclast and osteoblast activity, leading to accelerated bone resorption and disorganized bone formation.
Paget’s disease is more common in males and affects around 1–2% of the Caucasian adults >55 years. It occurs more commonly in the UK than anywhere else in the world. The exact aetiology remains unknown, however a number of factors have been implicated, including a slow viral infection such as paromyxovirus. The axial skeleton is preferentially affected; common sites of involvement include the pelvis, femur, lumbar spine, skull, and tibia in a descending order of frequency.
Important clinical features and complications
Common
Pain: bone pain, not joint pain. Pain is present day and night and is not made worse by joint movements.
Deformity.
Enlargement of the skull
Exaggerated thoracic kyphosis
Anterior bowing of the tibia
Lateral bowing of the femur.
Fractures.
Hearing loss (ossicle involvement, or VIII nerve compression).
Less common
Spinal stenosis.
Nerve compression syndromes.
Rare
Hypercalcaemia during immobilization.
Cardiac failure.
Sarcomatous change.
Hydrocephalus.
Cord compression.
Crystal arthropathies
Gout
A disorder of purine metabolism. Characterized by hyperuricaemia due to either overproduction or underexcretion of uric acid. Prolonged hyperuricaemia (Box 10.16) leads to the deposition of urate crystals in synovium, connective tissues, and the kidney. These crystals are then shed leading to acute gout.
More common in the summer months due to reduced fluid intake and increased fluid loss.
Drugs: diuretics, ethanol, salicylates, pyrazinamide, ethambutol, nicotinic acid, and ciclosporin
Chronic renal failure
Myeloproliferative and lymphoproliferative disorders (? purine metabolism)
Obesity
Hypertension
Hypothyroidism
Hyperthyroidism
Familial
Excessive dietary purines.
Gout is associated with metabolic syndrome (central obesity, insulin resistance, hypertension, and ischaemic heart disease).
Most patients are middle aged or older with risk factors for gout such as renal failure, excess alcohol intake, and diuretic usage. Causes of premature gout include renal failure, solid organ transplant with immunosuppression with calcineurin inhibitors, haematological malignancy, and inherited errors of metabolism.
Clinical features of acute gout
Sudden onset (hours) of severe pain and swelling classically in the great toe MTPJ, worse at night, and associated with redness.
Occasionally multiple joints are involved e.g. knees, ankles ± systemic symptoms.
Some patients (frequently elderly and those on diuretics) present with large-joint (knee, ankle, shoulder, or wrist) involvement or with polyarticular gout.
Clinical features of chronic (tophaceous) gout
Tophi (deposits of urate crystal) occur in:
The digits (at IPJs, finger pulp). In the presence of osteoarthritis, gouty tophi preferentially occur at the IPJs affected by Heberden’s or Bouchard’s nodes.
Near the 1st metatarsophalangeal joint
In bursae (e.g. olecranon bursa)
Near the Achilles tendon
In tendon sheaths
On the helix (ear). In hands, gouty tophi preferentially occur at the IPJs affected by Heberden’s or Bouchard’s nodes.
Calcium pyrophosphate deposition (CPPD)
CPPD may occur in the cartilage (chondrocalcinosis), joint capsule, and tendons. Established risk factors include ? age (>60 years) and osteoarthritis. If CPPD is present in those <55 years or is florid and polyarticular, the patient should be screened for haemochromatosis, hypophosphataemia, hypomagnesaemia, and hyperthyroidism.
Knees, wrists, MCPJs, and hips are the most commonly involved joints.
CPPD may present as:
Asymptomatic: chondrocalcinosis.
Acute CPP crystal arthritis (formerly ‘pseudogout’): the commonest cause of acute mono-arthritis in the elderly.
CPPD and OA: symptoms of OA with or without superimposed episodes of acute synovitis.
Chronic CPP crystal inflammatory arthritis: uncommon.
Spondyloarthropathies
These include ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and enteropathic arthritis. This is a group of related and overlapping forms of inflammatory arthritis which characteristically lack rheumatoid factor and are associated with HLA B27. They present at any age, though young males are primarily affected.
They also share a number of key clinical features:
Enthesitis (an enthesis is the insertion of a tendon, ligament, or joint capsule onto a bone).
Sacroiliitis.
Dactylitis.
Peripheral arthritis predominantly affecting the large joints.
Ankylosing spondylitis
Ankylosing spondylitis usually develops in early adulthood with a peak age of onset in the mid-20s, and is 3 times more common in males.
Common symptoms
Back pain (which may be localized to the buttocks) and stiffness which are typically worse in early hours of the night (2am–5am) and on waking up in the morning.
Pain recurs after long periods of rest and is relieved by activity. Patients report a dramatic response to NSAIDs, which remains the first line of treatment.
Chest pain may be present as a result of T-spine involvement as well as enthesitis at the costochondral joints.
Pain, swelling, and stiffness may be present in peripheral joints affected by inflammatory arthritis e.g. shoulders, hips, knees, and ankles.
Musculoskeletal features/signs
‘Question mark’ posture (loss of lumbar lordosis, fixed kyphosis of the T-spine, compensatory hyperextension of the C-spine).
Protuberant abdomen.
Schober’s test positive.
Sacroiliac joint tenderness. (SIJ distraction test may be positive.)
Achilles tendonitis.
Plantar fasciitis.
Some extra-skeletal features
Anterior uveitis.
Aortic regurgitation.
Apical lung fibrosis.
AV block.
Amyloidosis (secondary).
Weight loss.
In some cases, a fracture may occur through the rigid spine and involve the intervertebral discs. A similar lesion may be produced by inflammatory granulation tissue. These are known as disco-vertebral or ‘Andersson’ lesions.
Psoriatic arthritis
Psoriatic arthropathy affects up to 10% of patients with psoriasis and may precede or follow the skin disease. Importantly the arthropathy does not correlate with the severity of the skin lesions.
There are five main subtypes of psoriatic arthropathy:
Asymmetrical distal interphalangeal joint arthropathy.
Asymmetrical large joint mono- or oligo-arthropathy.
Spondyloarthropathy and sacroiliitis (usually asymmetric).
Rheumatoid-like hands (clinically identical to RA but seronegative).
Arthritis mutilans (a destructive form with telescoping of the fingers).
Associated clinical features
Psoriatic plaques (extensor surfaces, scalp, behind the ears, navel and natal clefts).
Nail involvement (pitting, onycholysis, discoloration, and thickening).
Dactylitis (sausage-shaped swelling of the digits due to tenosynovitis).
Enthesitis.
Reactive arthritis
An aseptic arthritis, strongly linked to a recognized episode of infection. Common causes are gut and genitourinary pathogens.
It mainly affects young adult males and usually presents with an asymmetric oligoarthritis. Symptoms start a few days to a few weeks after the infection.
Enthesitis and dactylitis are other common features.
Extra-articular features include urethritis, conjunctivitis, and skin lesions.
Reiter’s syndrome
A form of reactive arthritis associated with the classic triad of:
Arthritis.
Urethritis.
Conjunctivitis.
It often follows dysenteric infections such as shigella, salmonella, campylobacter, and yersinia or infections of the genital tract. Other findings which may be encountered are mouth ulceration, circinate balanitis, keratoderma blennorrhagica (pustular-like lesions found on the palms or soles) and plantar fasciitis.
Enteropathic arthritis
Enteropathic arthritis is a peripheral or axial arthritis and is the commonest extra-intestinal manifestation of inflammatory bowel disease. Patients are usually young adults and there is no gender predisposition. The musculoskeletal manifestations include:
Sacroiliitis (symmetric usually).
Peripheral arthritis.
Dactylitis.
Enthesopathy (Achilles, plantar fascia, costovertebral, costosternal).
Only a minority of patients (7%) are HLA B27 positive. Enteropathic spondyloarthropathy does not typically correlate with the severity of bowel disease. However, in some cases, the peripheral arthritis has been shown to improve if the affected bowel is resected.
Osteoporosis
Osteoporosis is a systemic skeletal disorder involving ? bone mass (osteopenia) and micro-architectural deterioration, resulting in an ? risk of fracture (Box 10.17). Classification (and treatment) is based on measurement of the bone mineral density (BMD), with comparison to that of a young healthy adult.
Prolonged immobilization/weightlessness
Malignancy
GI diseases: malabsorption syndrome, IBD, liver disease, anorexia nervosa
Rheumatologic diseases: RA, SLE, AS
COPD
Genetic diseases: cystic fibrosis, Ehlers–Danlos syndrome
Endocrine diseases: diabetes type 1, hyperparathyroid, hyperthyroid, hyperprolactinaemia, Cushing’s syndrome, hypogonadism
Drugs: corticosteroids, phenytoin, long-term heparin
Alcohol (>recommended daily allowance) and smoking.
The underlying pathology is related to an imbalance between the osteoblasts producing bone and the osteoclasts removing bone which ultimately produces net bone loss. By the World Health Organization definition, patients with a BMD of <2.5 standard deviations below the mean of young adult BMD of the same gender have osteoporosis.
Primary osteoporosis
95% of osteoporosis in women, 70–80% osteoporosis in men.
Seen in postmenopausal women and elderly men.
No single underlying cause of osteoporosis. However, patients may have several risk factors including:
Older age (>50 years)
Female gender
Low dietary calcium and vitamin D intake
FHx of osteoporosis
Parental history of hip fracture
BMI <19 kg/m2
Delayed menarche
Premature menopause
Sedentary lifestyle
Excess caffeine intake.
Secondary osteoporosis
Has an identifiable underlying cause of osteoporosis (see Box 10.17).
In addition, patients may have other identifiable risk factors as for primary osteoporosis.
Clinical features
The process leading to osteoporosis is asymptomatic.
The condition is diagnosed usually after the patient has a fragility fracture.
A fragility fracture is a fracture caused by falling from a standing height or less
Common sites of osteoporotic fracture include femoral neck, wrist, and vertebrae
Vertebral fracture may be asymptomatic sometimes, being diagnosed only when the patient has a spinal radiograph for kyphosis, loss of height, or for unrelated reasons.
More information regarding the presentation and clinical signs of locomotor diseases to aid preparation for OSCE-type examinations and ward rounds can be found in the Oxford Handbooks Clinical Tutor Study Cards.
Rheumatoid arthritis
Osteoarthritis
Psoriatic arthritis
Ankylosing spondylitis
Paget’s disease
Tophaceous gout
Marfan’s syndrome
Systemic sclerosis
Vasculitides
Systemic lupus erythematosus
Rickets.
Dupuytren’s contracture
Hammer toe
Claw toes
Mallet toe
Mallet finger
Trigger finger
Olecranon bursitis
Swellings around the knee
Osteochondroma
Pes cavus
Charcot’s joint
Hallux valgus.
The elderly patient
Rheumatological diseases represent a huge spectrum of illness in older people, often complicating and concurrent with other diseases—e.g. the impact of severe arthritis on COPD; or heart failure, or the effect of hip or knee arthritis on recovery after acute stroke. Arthritis and osteoporosis are two major factors in the ‘geriatric giants’ of immobility and instability—pertinent reminders of the widespread effect of locomotor illness with advancing age.
History
Method of presentation: can vary, ranging from the fall that leads to a femoral neck fracture or a referral ‘off legs’ or with declining mobility. Older people will often have an existing diagnosis of some form of arthritis—the difficulty is not in the diagnosis, but understanding the impact on everyday life. Locomotor illnesses are a key part of such presentations, and attention to these illnesses is vital. However, it is important to remember that presentations such as falls are multifactorial—try to work out how locomotor illness contributes to mobility or falls risk.
Intercurrent illness: may often precipitate gout or particularly pseudogout. Equally important are those illnesses that disturb carefully balanced homeostasis, leading to a fall and fracture. Your task is not just to treat the consequence of the fall, but also to look at why it happened in the first place.
Septic joints: can be notoriously difficult to diagnose at times. Unilateral large joint swelling/acute arthritis should ring alarm bells instantly, especially if the patient is unwell. Myriad causes contribute to back pain, but never forget deep-seated infection such as discitis or osteomyelitis which may be a consequence of something as innocuous as a urinary infection.
DHx: as ever, a keystone of any assessment. Consider the side-effect profile of NSAIDs, or whether gout has been precipitated by the effects of diuretics or low-dose aspirin. If your patient has sustained a fragility fracture due to osteoporosis, are they on appropriate treatment? Never forget the number of older people whose arthritis is successfully treated with disease-modifying drugs—and understand the effects of such drugs (and the need to prescribe concurrent folic acid with methotrexate—don’t forget!).
Activities, occupation, and interests: overlaps with the functional history, a key message of these sections. Multi-disciplinary assessment is vital in terms of tailoring rehabilitation, aids, and future care where appropriate. Ask too about hobbies and interests—improving balance, minimizing pain, and maximizing function may allow patients to carry on with activities that are a key part of their lives (and might represent an opportunity for continued exercise or rehabilitation).
Examination
General: the signs are often very clear, but despite this, easily overlooked. The need here is for a careful and thoughtful assessment of function as well as disease activity. Always be solicitous of your patient’s comfort—and examine carefully, explaining what you wish to do to avoid misunderstanding and pain.
Pattern of disease: look out for typical patterns of disease, and also single joint pathology. Look at ankles, feet, and back—it takes only a little more time to undertake a good examination, but is depressingly common to see patients with poor balance and falls with a clerking that details no locomotor assessment.
Disease activity: be careful when palpating—but look to see if an acute exacerbation of joint disease may well have contributed to the current presentation.
Gait and balance: often overlooked, but a vital part of the examination. Learn (e.g. from the ward physiotherapist) how to undertake the ‘get up and go test’ (Box 10.18), a well-validated test of gait and balance. This assessment should overlap with neurological assessment when appropriate. (See Box 10.19.)
An easy test to do, and one which gives a wealth of information. Ask the patient to perform the following 3-part task:
Rise to standing from a chair
Walk 3 metres
Turn and return to the chair.
This is not a pure observer role for the clinician—you must make an assessment of safety and be on hand to support the patient if needed.
It is a sad fact that we still see patients labelled with awful terms such as ‘acopia’ or ‘social admission’ after failing and/or falling at home. They are not to be used as they reflect:
Your (and your seniors’) limited thinking
Missed diagnoses
Such as infections, overmedication, pain, fractures.
A lack of respect.
Older people would almost certainly prefer not to be in hospital and it is extremely rare that the reason for admission is their ‘fault’.
Do your best for them with as thorough and detailed an assessment as you would do for any other patient presentation.
Consider using your own ‘family and friends test’. Would you be satisfied if these labels were attached to an older person you knew who had been admitted acutely to hospital?
