General aspects of examination

General principles of physical examination

The process of taking a history and conducting a physical examination is artificially separated in classical medical teaching, to encourage learners to develop a structured approach to information gathering. However, your physical assessment of patients undoubtedly begins as soon as you see them, and the astute clinician may notice signs of disease, such as subtle abnormalities of demeanour, gait or appearance, even before the formal consultation begins. The clinician can be likened to a detective, gathering clues, and the physical assessment of a patient can then be seen as the investigation itself!

Historically, great importance has been placed on the value of empirical observation of patients in the formulation of a differential diagnosis. Modern technological advances have increased the reliance on imaging and laboratory testing for diagnosis, sometimes even at the bedside (such as portable ultrasound or near-patient capillary blood ketone testing), and this has called into question the utility of systematic physical examination in modern practice. Nevertheless, the importance of performing a methodical and accurate physical examination cannot be overstated. The inconstancy of physical signs and the need to monitor patient progress by repeated bedside assessment, often conducted by different clinicians, mean that a standardised approach to physical examination resulting in reproducible findings is crucial. Additionally, the interpretation of many diagnostic investigations (such as detection of interstitial oedema on a chest x-ray in heart failure) is subject to variation between clinicians and is not always more sensitive than the detection of physical signs (such as audible crackles on auscultating the lungs). Furthermore, the utility of many diagnostic investigations relies heavily on the pre-test probability (the likelihood of the disease being present prior to the test being performed; p. 416), which depends on information gathered during the history and examination. Finally, there are a number of conditions, or syndromes, that can be diagnosed only by the detection of a characteristic pattern of physical signs. Thus, by mastering structured skills in physical examination, clinicians can improve the reliability and precision of their clinical assessment, which, together with the appropriate diagnostic investigations, lead to accurate diagnosis.

Preparing for physical examination

It is important to prepare both yourself and your patient for the physical examination. As a clinician, you must take reasonable steps to ensure that you can give the patient your undivided attention, in an environment free from interruption, noise or distraction. Always introduce yourself to the patient and seek permission to conduct the consultation. Make sure that you have the relevant equipment available ( Box 3.1 ) and that you have observed local hand hygiene policies ( Fig. 3.1 ). As discussed on page 4, privacy is essential when assessing a patient. At the very least, ensure that screens or curtains are fully closed around a ward bed; where possible, use a separate private room to avoid being overheard. Seek permission from the patient to proceed to examination, and offer a chaperone where appropriate to prevent misunderstandings and to provide support and encouragement for the patient. Regardless of whether the patient is the same gender as the doctor or not, chaperones are always appropriate for intimate (breast, genital or rectal) examination. Chaperones are also advised if the patient is especially anxious or vulnerable, if there have been misunderstandings in the past, or if religious or cultural factors require a different approach to physical examination. Record the chaperone’s name and presence. If patients decline the offer, respect their wishes and record this in the notes. Tactfully invite relatives to leave the room before physical examination unless the patient is very apprehensive and requests that they stay. A parent or guardian should always be present when you examine children (p. 343).

The room should be warm and well lit; subtle abnormalities of complexion, such as mild jaundice, are easier to detect in natural light. The height of the examination couch or bed should be adjustable, with a step to enable patients to get up easily. An adjustable backrest is essential, particularly for patients who feel breathless lying flat. It is usual practice to examine a recumbent patient from the right-hand side of the bed. Ensure that the patient is comfortably positioned before commencing the physical examination.

Seek permission and sensitively, but adequately, expose the areas to be examined; cover the rest of the patient with a blanket or sheet to ensure that they do not become cold. Avoid unnecessary exposure and embarrassment; a patient may appreciate the opportunity to replace their top after examination of the chest before exposing the abdomen. Remain gentle towards the patient at all times, and be vigilant during aspects of the examination that may cause distress or discomfort. Acknowledge any anxiety or concerns raised by the patient during the consultation.

Sequence for performing a physical examination

The purpose of the physical examination is to look for the presence, or absence, of physical signs that confirm or refute the differential diagnoses you have obtained from the history. The extent of the examination will depend on the symptoms that you are investigating and the circumstances of the encounter. Often, in a brief, focused consultation (such as a patient presenting to a general practitioner with headache), a single system (the nervous system in this case) will be examined. In other circumstances, however, a full integrated physical examination will be required, and this is described in detail on page 424.

There is no single correct way to perform a physical examination, but standardised systematic approaches help to ensure that nothing is omitted. With experience, you will develop your own style and sequence of physical examination. Broadly speaking, any systematic examination involves looking at the patient (for skin changes, scars, abnormal patterns of breathing or pulsation, for example), laying hands on the patient to palpate (feel) and percuss (tapping on the body), and, finally, using a stethoscope, where appropriate, to listen to the relevant system (auscultate). This structured approach to the examination of the system can be summarised as:

• inspection

• palpation

• percussion

• auscultation.

Initial observations

The physical examination begins as soon as you see the patient. Start with a rapid assessment of how unwell the patient is, since the clinical assessment may have to be adjusted for a deteriorating or dying patient, and any abnormal physiology may need to be addressed urgently before the actual diagnosis is found (see Chapter 18 , p. 395). Early warning scoring systems (which include assessment of vital signs: pulse, blood pressure, respiratory rate and oxygen saturations, temperature, conscious level and pain score) are used routinely to assess unwell patients, and these clinical measurements aid decisions about illness severity and urgency of assessment (see Chapter 18 , p. 394). If your patient is distressed or in pain, giving effective analgesia may take priority before undertaking a more structured evaluation, although a concurrent evaluation for the cause of the pain is clearly important.

For the stable or generally well patient, a more measured assessment can begin. Observe the patient before the consultation begins. Do they look generally well or unwell? What is their demeanour? Are they sitting up comfortably reading or on the telephone to a relative, or do they seem withdrawn, distressed or confused?

Notice the patient’s attire. Are they dressed appropriately? Clothing gives clues about personality, state of mind and social circumstances, as well as a patient’s physical state. Patients with recent weight loss may be wearing clothes that look baggy and loose. Are there signs of self-neglect (which may be underpinned by other factors, such as cognitive impairment, immobility, or drug or alcohol dependence) or inappropriate attire? For example, a patient with thyrotoxicosis may come to see you dressed for summer in the depths of winter due to heat intolerance.

Often, there will be clues to the patient’s underlying medical condition given by the person’s effects (e.g. they may be wearing a subcutaneous insulin pump to treat their type 1 diabetes, or carrying a portable oxygen cylinder if they have pulmonary fibrosis). If they are in bed, look on the bedside table for a hearing aid, peak flow meter or inhaler device, and note any walking aid, commode and wheelchair, which provide clues to the patient’s functional status. Patients may be wearing a medical identity bracelet or other jewellery alerting you to an underlying medical condition or life-sustaining treatment. Note any tattoos or piercings; as well as alerting you to possible associated infections, these can provide important background information ( Fig. 3.2 ). Be sure to look for any venepuncture marks of intravenous drug use ( Fig .3.3 ) or linear (usually transverse) scars from recent or previous deliberate self-harm ( Fig. 3.4 ).

Hands

Some conditions are associated with pathognomonic signs. For example, the rare disease myotonic dystrophy (which is over-represented in candidate assessments) causes a patient to fail to release a handgrip (due to delayed muscle relaxation). A patient with neurological disease may be unable to move their hand or may have signs of muscle wasting or tremor. Detailed examination of the hands is described on page 303, but even a brief inspection and palpation may be very revealing.

Deformity

Deformity in the hands may indicate nerve palsies or arthritic changes (such as ulnar deviation at the metacarpophalangeal joints in longstanding rheumatoid arthritis; see Fig. 13.22 , p. 266). Arthritis frequently involves the small joints of the hands. Rheumatoid arthritis typically affects metacarpophalangeal and proximal interphalangeal joints ( Fig. 13.22 , p. 266), and osteoarthritis and psoriatic arthropathy affect the distal interphalangeal joints ( Fig. 13.8 , p. 295). Small-muscle wasting of the hands is common in rheumatoid arthritis, producing ‘dorsal guttering’ of the hands, and also occurs in cervical spondylosis with nerve root entrapment. In carpal tunnel syndrome, median nerve compression leads to wasting of the thenar muscles, also seen in damage affecting the T1 nerve root ( Fig. 13.23 , p. 305).

Dupuytren’s contracture is a thickening of the palmar fascia causing fixed flexion deformity, and it usually affects the little and ring fingers ( Fig. 3.5 ). Arachnodactyly (long, thin fingers) is typical of Marfan’s syndrome ( Fig. 3.21B ). Trauma is the most common cause of hand deformity.

Colour

Look for peripheral cyanosis in the nail bed and tobacco staining of the fingers (see Fig. 5.7 , p. 94). Examine the skin creases for pigmentation, although pigmentation is normal in many non-Caucasian races ( Fig. 3.6 ).

Temperature

The temperature of the patient’s hand is a good guide to peripheral perfusion. In chronic obstructive pulmonary disease, the hands may be cyanosed due to reduced arterial oxygen saturation but warm due to vasodilatation from elevated arterial carbon dioxide levels. In heart failure the hands are often cold and cyanosed because of vasoconstriction in response to a low cardiac output. If they are warm, heart failure may be due to a high-output state, such as hyperthyroidism.

Skin

Skin changes in the hands can indicate systemic disease, as in the coarse skin and broad hands of a patient with acromegaly (see Fig. 10.8 , p. 228), or the tight, contracted skin (scleroderma) and calcium deposits associated with systemic sclerosis ( Figs 3.30C and 13.6 , p. 294). Clues about lifestyle can also be seen in the hands: manual workers may have specific callosities due to pressure at characteristic sites, while disuse results in soft, smooth skin.

Nails

Nail changes occur in a wide variety of systemic diseases. Box 3.3 and Fig. 3.7 summarise nail changes seen on general examination that may indicate underlying systemic disease.

3.3

The nails in systemic disease

Nail changes	Description of nail	Differential diagnosis
Beau’s lines	Transverse grooves ( Fig. 3.7B )	Sequela of any severe systemic illness that affects growth of the nail matrix
Clubbing	Loss of angle between nail fold and nail plate ( Fig. 3.8 )	Serious cardiac, respiratory or gastrointestinal disease ( Box 3.4 )
Leuconychia	White spots, ridges or complete discoloration of nail ( Fig. 3.7C )	Trauma, infection, poisoning, chemotherapy, vitamin deficiency
Lindsay's nails	White/brown ‘half-and-half’ nails (see Fig. 12.7 , p. 278)	Chronic kidney disease
Koilonychia	Spoon-shaped depression of nail plate ( Fig. 3.7D )	Iron deficiency anaemia, lichen planus, repeated exposure to detergents
Muehrcke’s lines	Narrow, white transverse lines (see Fig. 12.6 , p. 278)	Decreased protein synthesis or protein loss
Nail-fold telangiectasia	Dilated capillaries and erythema at nail fold (see 14.17B , p. 335)	Connective tissue disorders, including systemic sclerosis, systemic lupus erythematosus, dermatomyositis
Onycholysis	Nail separates from nail bed ( Fig. 3.7A )	Psoriasis, fungal infection, trauma, thyrotoxicosis, tetracyclines (photo-onycholysis)
Onychomycosis	Thickening of nail plate with white, yellow or brown discoloration	Fungal infection
Pitting	Fine or coarse pits in nail ( Fig. 3.7A )	Psoriasis (onycholysis, thickening and ridging may also be present), eczema, alopecia areata, lichen planus
Splinter haemorrhages	Small red streaks that lie longitudinally in nail plate ( Fig. 4.5B , p. 51)	Trauma, infective endocarditis
Yellow nails	Yellow discoloration and thickening ( Fig. 14.18 , p. 336)	Yellow nail syndrome

Finger clubbing describes painless soft tissue swelling of the terminal phalanges and increased convexity of the nail ( Fig. 3.8 ). Clubbing usually affects the fingers symmetrically. It may also involve the toes and can be unilateral if caused by a proximal vascular condition, such as arteriovenous shunts for dialysis. It is sometimes congenital, but, in over 90% of patients it accompanies a serious underlying disorder ( Box 3.4 ). Clubbing may recede if the underlying condition resolves.

Examination sequence

• Look across the nail bed from the side of each finger. Observe the distal phalanges, nail and nail bed:

  • Estimate the interphalangeal depth at the level of the distal interphalangeal joint (this is the anteroposterior thickness of the digit rather than the width). Repeat at the level of the nail bed.

  • Assess the nail bed (hyponychial) angle ( Fig. 3.9A ).

    

• Ask the patient to place the nails of corresponding (ring) fingers back-to-back and look for the normal ‘diamond-shaped’ gap between the nail beds (Schamroth’s window sign; Fig. 3.9B ).

• Place your thumbs under the pulp of the distal phalanx and use your index fingers alternately to see if there is fluctuant movement of the nail on the nail bed ( Fig. 3.9C ).

Finger clubbing is likely if:

• the interphalangeal depth ratio is >1 (that is, the digit is thicker at the level of the nail bed than the level of the distal interphalangeal joint; Fig. 3.9A ),

• the nail fold angle is >190 degrees ( Fig. 3.9A ), or

• Schamroth’s window sign is absent ( Fig. 3.9B ).

Increased nail-bed fluctuation may be present and may support the finding of clubbing, but its presence is subjective and less discriminatory than the above features.

3.4

Causes of clubbing

Congenital or familial (5%–10%)

Acquired

• Thoracic (∼70%):

  • Lung cancer

  • Pulmonary fibrosis, including asbestosis

  • Chronic suppurative conditions: pulmonary tuberculosis, bronchiectasis, cystic fibrosis, lung abscess, empyema

  • Mesothelioma

• Cardiovascular:

  • Cyanotic congenital heart disease

  • Infective endocarditis

  • Arteriovenous shunts and aneurysms

• Gastrointestinal:

  • Cirrhosis

  • Inflammatory bowel disease

  • Coeliac disease

• Others:

  • Thyrotoxicosis (thyroid acropachy)

  • Primary hypertrophic osteoarthropathy

Skin

A detailed approach to examination of the skin is described in Chapter 14 . In everyday practice, the skin can provide insights into present and past medical disorders, as well as information about the patient’s social or mental status.

The skin should be exposed where appropriate and inspected carefully for any abnormalities of pigmentation. Skin colour is determined by pigments – melanin, an endogenous brown pigment, and carotene, an exogenous yellow pigment (derived mainly from ingestion of carrots and other vegetables) – as well as by the amount of oxyhaemoglobin (red) and deoxyhaemoglobin (dusky blue) circulating in the dermis.

The autoimmune condition vitiligo causes irregular pale patches of skin depigmentation ( Fig. 3.10 ), commonly on the face, neck, hands and extensor aspects of the limbs. It can be symmetrical, but often is not. It is associated with other autoimmune diseases, such as diabetes mellitus, thyroid and adrenal disorders and pernicious anaemia. Hypopituitarism also results in pale skin due to reduced production of melanotrophic peptides. Albinism is an inherited disorder in which patients have little or no melanin in their skin or hair. The amount of pigment in the iris varies; some individuals have reddish eyes, but most have blue.

Hyperpigmentation can be due to excess of the pituitary hormone adrenocorticotrophic hormone (ACTH), as in adrenal insufficiency (or the very rare condition Nelson’s syndrome, in which there is ACTH overproduction following bilateral adrenalectomy for pituitary Cushing’s disease). Excess ACTH produces brown pigmentation, particularly in skin creases, recent scars, sites overlying bony prominences, areas exposed to pressure, such as belts and bra straps, and the mucous membranes of the lips and mouth, where it results in muddy brown patches (see Fig 10.9B , p. 229). Pregnancy and oral contraceptives may also cause blotchy hyperpigmentation on the face, known as chloasma, and pregnancy may increase pigmentation of the areolae, axillae, genital skin and linea alba (producing a dark line in the midline of the lower abdomen, called a ‘linea nigra’).

Haemochromatosis

This inherited condition of excessive iron absorption results in skin hyperpigmentation due to iron deposition and increased melanin production ( Fig. 3.11 ). When iron deposition in the pancreas also causes diabetes mellitus, this is called ‘bronze diabetes’.

Haemosiderin

This product of haemoglobin breakdown is deposited in the skin of the lower legs following subcutaneous extravasation of blood due to venous insufficiency. Local deposition of haemosiderin (erythema ab igne or ‘granny’s tartan’) occurs with heat damage to the skin from sitting too close to a fire or from applying local heat, such as a hot water bottle, to a site of pain ( Fig. 3.12 ).

Easy bruising

Easy bruising can be a reflection of skin and connective tissue fragility due to advancing age or glucocorticoid usage, or a more serious coagulopathy.

Hypercarotenaemia

Hypercarotenaemia occurs due to excessive ingestion of carotene-containing vegetables or in situations of impaired metabolism, such as hypothyroidism or anorexia nervosa. A yellowish discolouration is seen on the face, palms and soles but not the sclera or conjunctiva, and this distinguishes it from jaundice ( Fig. 3.13 ).

Discolouration

Skin discolouration can also occur due to abnormal pigments, such as the sallow yellow-brownish tinge in chronic kidney disease. A bluish tinge is produced by abnormal haemoglobins, such as sulphaemoglobin or methaemoglobin (see the section on cyanosis later), or by drugs, such as dapsone. Some drug metabolites cause strikingly abnormal colouration of the skin, particularly in areas exposed to light: for example, mepacrine (yellow), amiodarone (bluish-grey), clofazimine (brownish-black) and phenothiazines (slate-grey; Fig. 3.14 ).

Jaundice

Jaundice is an abnormal yellow discoloration of the skin, sclera and mucous membranes. It is usually detectable when serum bilirubin concentration rises above 50 μmol/L (3 mg/dL) as a result of parenchymal liver disease, biliary obstruction or haemolysis (see Fig. 6.8 , p. 115).

Pallor

Pallor can result from anaemia, in which there is a reduction in circulating oxyhaemoglobin in the dermal and subconjunctival capillaries, or from vasoconstriction due to cold exposure or sympathetic activation. The best sites to assess for the pallor of anaemia are the conjunctiva (specifically the anterior rim; Fig. 3.15 ), the palmar skin creases and the face, in general, although absence of pallor does not exclude anaemia. Nail-bed pallor lacks diagnostic value for predicting anaemia. In significant iron deficiency anaemia, there may be additional findings of angular stomatitis, glossitis ( Fig. 3.16 ), koilonychia (spoon-shaped nails) and blue sclerae.

Conversely, vasodilatation, or flushing, may produce a pink complexion, even in anaemia, and may be due to fever, heat, exercise, food, drugs and other neurological or hormonal disturbances ( Fig. 3.17 and Box 3.5 ). Facial plethora is caused by raised haemoglobin concentration with elevated haematocrit (polycythaemia). Polycythaemia may be primary or may indicate an underlying disease causing chronic hypoxia or excess erythropoietin production. Plethora of the head and neck only may indicate superior vena cava obstruction (see Fig. 5.9 , p. 96).

3.5

Conditions associated with facial flushing

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