Oxford Handbook of Clinical Medicine (9 edn)
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History and examination: Contents
Symptoms 26
Signs 28
Examination of the hands 30–32
Cardiovascular system:
History 34
Examination 36–38
The jvp 40
Pulses 40
Respiratory system:
History 48
Examination 50–52
Gastrointestinal system:
History 56
Genitourinary system:
History 64
The breast:
History 66
Examination 67
The thyroid:
Examination 68
Neurological system:
History 70
William Osler (1849-1919) was a great medical educationalist who loved practical jokes. He introduced many novelties to the classroom, including, on one occasion, a gaggle of geese. We can all identify with his geese, because these birds show exceptional learning ability and resilience.
Osler did not agree with gavage, a method whereby geese (and medical students) are forcibly stuffed by funnel to fatten them for the delight of gluttons. We are too familiar with the 3 Rs of medical education: Ram→Remember→Regurgitate, a sequence that turns once-bright medical students into tearful wrecks. Luckily in the realm of History & Examination we can flee the library and alight at the bedside, bearing in mind another of Osler's aphorisms: “He who studies medicine without books sails an uncharted sea, but he who studies medicine without patients does not go to sea at all.”
A number of images are taken from the Oxford Handbook of Clinical Examination and Practical Skills (ohceps), which gives an even more detailed account of this subject. Our thanks to Dr James Thomas and Dr Tanya Monaghan for their kind permission. We thank Junior Reader Shahzad Arain for his contribution.
History and examination: Overview
Other relevant pages:
In ohcs:
Vaginal examination (ohcs p242); abdominal examination in pregnancy (ohcs p40); the history and examination in children and neonates (ohcs p100–p102); examination of the eye (ohcs p412); visual acuity (ohcs p414); eye movements (ohcs p422); ear, nose, and throat examination (ohcs p536); skin examination (ohcs p584); examination of joints—see the contents page to Orthopaedics and trauma (ohcs p656).
The way to learn physical signs is at the bedside, with guidance from a senior doctor or an experienced colleague. This chapter is not a substitute for this process: it is simply an aide-mémoire both on the wards and when preparing for exams.
We ask questions to get information to help with differential diagnosis. But we also ask questions to find out about the lives our patients live so that we can respect them as individuals. The patient is likely to notice and reciprocate this respect, and the rapport that you build with your patient in this way is a key component to diagnosing and managing their disease.
Patients (and diseases) rarely read the textbook, so don't be surprised that some symptoms are ambiguous, and others are meaningless. Get good at recognizing patterns, but not so good that you create them when none is there. We all fall into this trap!
With increasing targets, shift patterns and the move towards more and more specialist services, patients can be bounced around from team to team many times during their admission. The Royal College of Physicians in the uk has recognized this and produced guidance on how best to approach handover.1
Both written and verbal communications are key to effective handover; although a written note explaining who is unwell, what the plan is, and who to call if things deteriorate is essential, nothing substitutes for face to face handover. Discussion of patients is important for safety as well as learning and good practice. Make a point of handing over weekend and evening plans, and patients you are worried about. Take advantage of the experience and knowledge of the person you are handing over to. Can they offer advice on what you could have done differently?
Make sure senior colleagues know who is unwell and who you would like help with. Senior doctors would far rather see someone before they deteriorate, putting together an action plan for what to do next, than be called to an acutely unwell patient who may need escalation to icu when a few early interventions could have prevented deterioration. There is no shame in asking for help, but remember you should do what you can first; never call without knowing your patient or having examined them. See p23 for key things to know before calling for advice. Ultimately we are all there for the patient, so if they are deteriorating despite your best efforts, call for advice.
Taking a history
Taking (or receiving) histories is what most of us spend most of our professional life doing, and it is worth doing well. A good history is the biggest step towards correct diagnosis. Try to put the patient at ease: a good rapport may relieve distress. Introduce yourself and check whether the patient is comfortable. Be conversational rather than interrogative in tone. Start with open questions, allow the patient to tell their story, but if they stray off topic, try to gently steer them back towards the important points.
Presenting complaint (pc)
Open questions: “Why have you come to see me today?” Record the patient's own words rather than medical terms.
History of presenting complaint (hpc)
When did it start? What was the first thing noticed? Progress since then. Ever had it before? ‘socrates’ questions: site; onset (gradual, sudden); character; radiation; associations (eg nausea, sweating); timing of pain/duration; exacerbating and alleviating factors; severity (eg scale of 1–10, compared with worst ever previous pain). Direct questioning (to narrow list of possible diagnoses). Specific or ‘closed’ questions about the differential diagnoses you have in mind (+risk factors, eg travel—p388) and a review of the relevant system.
Past medical history (pmh)
Ever in hospital? Illnesses? Operations? Ask specifically about mijthreads: MI, jaundice, tb, high bp, rheumatic fever, epilepsy, asthma, diabetes, stroke, anaesthetic problems.
Drug history (dh)
Any tablets, injections, ‘over-the-counter’ drugs, herbal remedies, oral contraceptives? Ask about allergies and what the patient experienced, eg may be an intolerance (nausea, diarrhoea), or may have been a minor reaction of sensitization (eg rash and wheeze) before full-blown anaphylaxis.
Social history (sh)
Probe without prying. “Who else is there at home?” Job. Marital status. Spouse's job and health. Housing—any stairs at home? Who visits—relatives, neighbours, gp, nurse? Are there any dependents at home? Mobility—any walking aids needed? Who does the cooking and shopping? What can the patient not do because of the illness?
The social history is all too often seen as a dispensable adjunct, eg while the patient is being rushed to theatre, but vital clues may be missed about the quality of life and it is too late to ask when the surgeon's hand is deep in the belly and they are wondering how radical a procedure to perform. It is worth asking a few searching questions of the gp if they are calling to arrange admission. They may have known the patient and/or family for decades. He or she may even hold a ‘living will’ or advance directive to reveal your patient's wishes if they cannot speak for themselves.
As part of the social history, tactfully ask about alcohol, tobacco & recreational drugs. How much? How long? When stopped? The cage questionnaire is useful as a screening test for alcoholism (p282). Quantify smoking in terms of pack-years: 20 cigarettes/day for 1 year equals 1 pack-year. We all like to present ourselves well, so be inclined to double stated quantities (Holt's ‘law’).
Family history (fh)
Areas of the family history may need detailed questioning, eg to determine if there is a significant family history of heart disease you need to ask about the health of the patient's grandfathers and male siblings, smoking, tendency to hypertension, hyperlipidaemia, and claudication before they were 60 years old, as well as ascertaining the cause of death. Ask about tb, diabetes, and other relevant diseases. Draw a family tree (see box). 
Be tactful when asking about a family history of malignancy.
Functional enquiry
(p22) helps uncover undeclared symptoms. Some of this may already have been incorporated into the history.
Always enquire if your patient has any ideas of what the problem might be, if he/she has any particular concerns or expectations, and give him/her an opportunity to ask you questions or tell you anything you may have missed.
Don't hesitate to review the history later: recollections change (as you will find, often on the post-take ward round when the Consultant is asking the questions!).
Advances in genetics are touching all branches of medicine. It is increasingly important for doctors to identify patients at high risk of genetic disease, and to make appropriate referrals. The key skill is drawing a family tree to help you structure a family history as follows:
Start with your patient. Draw a square for a male and a circle for a female. Add a small arrow (see below) to show that this person is the propositus (the person through whom the family tree is ascertained).
Add your patient's parents, brothers, and sisters. Record basic information only, eg age, and if alive and well (a&w). If dead, note age and cause of death, and pass an oblique stroke through that person's symbol.
Ask the key question “Has anybody else in your family had a similar problem as yourself?”, eg heart attack/angina/stroke/cancer. Ask only about the family of diseases that relate to your patient's main problem. Do not record a potted medical history for each family member: time is too short.
Extend the family tree upwards to include grandparents. If you haven't revealed a problem by now, go no further—you are unlikely to miss important familial disease. If your patient is elderly it may be impossible to obtain good information about grandparents. If so, fill out the family tree with your patient's uncles and aunts on both the mother's and father's sides.
Shade those in the family tree affected by the disease. • = an affected female; ▪ = an affected male. This helps to show any genetic problem and, if there is one, will help demonstrate the pattern of inheritance.
If you have identified a familial susceptibility, or your patient has a recognized genetic disease, extend the family tree down to include children, to identify others who may be at risk and who may benefit from screening. You should find out who is pregnant in the family, or may soon be, and arrange appropriate genetic counselling (ohcs p154). Refer for genetics opinion.
The family tree (fig 1) shows these ideas at work and indicates that there is evidence for genetic risk of colon cancer, meriting referral to a geneticist.
Genetic risk of colon cancer in a family tree.
Functional enquiry
Just as skilled acrobats are happy to work without safety nets, so experienced clinicians may operate without the functional enquiry. But to do this you must be experienced enough to understand all the nuances of the presenting complaint.
General questions
May be the most significant, eg in tb, endocrine problems, or cancer:
Weight loss
Night sweats
Any lumps
Fatigue/malaise/lethargy
Sleeping pattern3
Appetite
Fevers
Itch or rash
Recent trauma.
Cardiorespiratory symptoms
Chest pain (p88).
Exertional dyspnoea (=breathlessness): quantify exercise tolerance and how it has changed, eg stairs climbed, or distance walked, before onset of breathlessness.
Paroxysmal nocturnal dyspnoea (pnd). Orthopnoea, ie breathlessness on lying flat (a symptom of left ventricular failure): quantify in terms of number of pillows the patient must sleep on to prevent dyspnoea.
Oedema: ankles, legs, lower back (dependent areas).
Palpitations (awareness of heartbeats): can they tap out the rhythm?
Cough: sputum, haemoptysis (coughing up blood).
Wheeze.
Gastrointestinal symptoms
Abdominal pain (constant or colicky, sharp or dull; site; radiation; duration; onset; severity; relationship to eating and bowel action; alleviating or exacerbating, or associated features).
Tenesmus is the feeling of incomplete evacuation of the bowels (eg due to a tumour or irritable bowel syndrome).
Haematemesis is vomiting blood.
Melaena is altered (black) blood passed pr (p252), with a characteristic smell.
Genitourinary symptoms
Incontinence (stress or urge, p650).
Dysuria (painful micturition).
Urinary abnormalities: colour? Haematuria (streaks or pink urine?) Frothy?
Nocturia (needing to micturate at night).
Frequency (frequent micturition) or polyuria (the frequent passing of large volumes of urine).
Hesitancy (difficulty starting micturition).
Terminal dribbling.
Vaginal discharge (p418).
Menses: frequency, regularity, heavy or light, duration, painful? First day of last menstrual period (lmp). Number of pregnancies and births. Menarche. Menopause. Any chance of pregnancy now?
Neurological symptoms
Special senses: Sight, hearing, smell, and taste.
Seizures, faints, ‘funny turns’.
Headache.
‘Pins and needles’ (paraesthesiae) or numbness.
Limb weakness (“Are your arms and legs weaker than normal?”), poor balance.
Speech problems (p80).
Sphincter disturbance.
Musculoskeletal symptoms
Pain, stiffness, swelling of joints.
Diurnal variation in symptoms (ie worse mornings).
Functional deficit.
Signs of systemic disease: rashes, mouth ulcers, nasal stuffiness, malaise and constitutional symptoms.
Thyroid symptoms
Hyperthyroidism: Prefers cold weather, bad tempered, sweaty, diarrhoea, oligomenorrhoea, weight↓ (though often ↑appetite), tremor, palpitations, visual problems.
Hypothyroidism: Depressed, slow, tired, thin hair, croaky voice, heavy periods, constipation, dry skin, prefers warm weather.
History-taking may seem deceptively easy, as if the patient knew the hard facts and the only problem was extracting them; but what a patient says is a mixture of hearsay (“She said I looked very pale”), innuendo (“You know, doctor, down below”), legend (“I suppose I bit my tongue; it was a real fit, you know”), exaggeration (“I didn't sleep a wink”), and improbabilities (“The Pope put a transmitter in my brain”). The great skill (and pleasure) in taking a history lies not in ignoring these garbled messages, but in making sense of them.
Physical examination
The physical examination is not so much an extension of the history, but more of the first investigation, to confirm, exclude, define, or show the progress of the provisional diagnosis as revealed in the history. Even in the emergency department where the history may be brief, eg “trauma”, the examination is to confirm a fracture, or to decide that a fracture is less likely. The examination sheds further light on the history. As you get better, your physical examination gets briefer. Establish your own routine—practice is the key.
End of the bed
Look at the patient—are they well or in extremis? What makes you think this? Are they in pain? If so, does it make them lie still (eg peritonitis) or writhe about (eg colic). What is the pattern of breathing: laboured; rapid; shallow; irregular; distressed? Are they obese or cachectic? Is their behaviour appropriate? Can you detect any unusual smell, eg hepatic fetor (p258), cigarettes, alcohol?
Also take a moment to look around the bed for other clues, eg inhalers, insulin administration kit, walking aids, etc.
Face and body habitus
Does the patient's appearance suggest any particular diseases, eg acromegaly, thyrotoxicosis, myxoedema, Cushing's syndrome, or hypopituitarism? See p196.
Is there an abnormal distribution of body hair (eg bearded ♀, or hairless ♂) suggestive of endocrine disease?
Is there anything about the patient to trigger thoughts about Paget's disease, Marfan's, myotonia, or Parkinson's syndrome? Look for rashes, eg the malar flush of mitral disease and the butterfly rash of sle.
Peripheral stigmata of disease
Specific signs are associated with different diseases: consider the nails (koilonychia = iron deficiency), subcutaneous nodules (rheumatoid, neurofibroma?), and look for lymph nodes (cervical, axillary, inguinal). See specific systems for features to assess for, but for all systems consider:
Skin colour:
Blue/purple = cyanosis (can also be central only, p28).
Yellow = jaundice (yellow skin can also be caused by uraemia, pernicious anaemia, carotenaemia—check the sclera: if they are also yellow it is jaundice).
Hyperpigmentation: Addison's, haemochromatosis (slate-grey) and amiodarone, gold, silver, and minocycline therapy.
Charts:
Blood pressure and pulse—trends are more important than one-off values; repeat if concerned.
Urine: check urinalysis and input/output charts if available.
Fluid status
When admitting an unwell patient, don't forget to assess their degree of hydration, check skin turgor and mucous membranes, look for sunken eyes, and check capillary refill (if well perfused <2s) and jvp.
When you don't know: ask. If you are wondering if you should ask: ask .
Frequently, the skills needed for diagnosis or treatment will lie beyond the team you are working for, so, during ward rounds, agree who should be asked for an opinion. You will be left with the job of making the arrangements, so check before your senior leaves exactly what their question is. Don't be intimidated: but follow these simple rules:
Know the history and examination findings (ideally your own), and have the patient's notes, observations, recent test results and drug charts to hand.
At the outset, state if you are just looking for advice or if you are asking if the patient could be seen. Make it clear exactly what the question is that you want addressed, allowing the listener to focus their thoughts and ask relevant questions.
Give the patient's age and run through a brief history including relevant past medical history. If you would like the patient to be seen, give warning if they will be leaving the ward for a test at a particular time.
The visiting doctor may be unfamiliar with your ward. When he or she arrives introduce yourself, get the notes and charts, and give your contact details in case they have further questions.
The following table may be useful to bear in mind, as you will be asked!
| Team | Key questions |
|---|---|
Anaesthetics | Previous anaesthetic? Reaction? Last ate/drank? |
Cardiology | Known ihd? bp? ecg findings? Echo findings? Murmurs? Troponin? Temperature/possibility of endocarditis? (esr, microscopic haematuria etc. p144) |
Dermatology | Site, onset and appearance of rash? Drugs? Systemic disease? History of atopy? |
Endocrinology | Diabetes: blood glucose, usual insulin regimen, complications. Other: blood results? Stable/unstable—eg Addisonian crisis. Usual steroid dose? |
Gastroenterology/Hepatology | Bleeding: Rockall score (p253)? Shock? Diarrhoea: Blood? Foreign travel? Frequency per day? Liver disease: signs of decompensation (p258)? Ascites? Encephalopathy grade? |
Gynaecology/ Obstetrics | lmp? Possibility of pregnancy? Previous pregnancies? Vaginal discharge? Hormonal contraceptives? stis? |
Haematology | Blood results? Splenomegaly? Fever? Lymphadenopathy? Bleeding: Anticoagulants? Clotting results? |
Infectious diseases/Microbiology | Possible source? Antibiotics (current/recent/previous)? Foreign travel? Risk factors for hiv? |
Nephrology | Creatinine (current, old)? Clotting? Urine output? Potassium? bp? Fluid status? Drugs? Known renal disease? |
Neurology/Stroke | Neurological examination?1 ct/mri scan findings? |
Radiology | See p734. Contrast or not? Creatinine? Clotting? Cannula in situ? Metallic implants? |
Respiratory | O2 sats? Respiratory rate? abg? cxr? Inhalers/nebs? Home O2? Respiratory support, eg niv/cpap? |
Surgery (general) | Pain? Scan findings? Acutely unwell? Clotting? |
Urology | History of luts (lower urinary tract symptoms) p644? Catheter? Haematuria? History of stones? Scan findings (ultrasound, ct)? |
| Team | Key questions |
|---|---|
Anaesthetics | Previous anaesthetic? Reaction? Last ate/drank? |
Cardiology | Known ihd? bp? ecg findings? Echo findings? Murmurs? Troponin? Temperature/possibility of endocarditis? (esr, microscopic haematuria etc. p144) |
Dermatology | Site, onset and appearance of rash? Drugs? Systemic disease? History of atopy? |
Endocrinology | Diabetes: blood glucose, usual insulin regimen, complications. Other: blood results? Stable/unstable—eg Addisonian crisis. Usual steroid dose? |
Gastroenterology/Hepatology | Bleeding: Rockall score (p253)? Shock? Diarrhoea: Blood? Foreign travel? Frequency per day? Liver disease: signs of decompensation (p258)? Ascites? Encephalopathy grade? |
Gynaecology/ Obstetrics | lmp? Possibility of pregnancy? Previous pregnancies? Vaginal discharge? Hormonal contraceptives? stis? |
Haematology | Blood results? Splenomegaly? Fever? Lymphadenopathy? Bleeding: Anticoagulants? Clotting results? |
Infectious diseases/Microbiology | Possible source? Antibiotics (current/recent/previous)? Foreign travel? Risk factors for hiv? |
Nephrology | Creatinine (current, old)? Clotting? Urine output? Potassium? bp? Fluid status? Drugs? Known renal disease? |
Neurology/Stroke | Neurological examination?1 ct/mri scan findings? |
Radiology | See p734. Contrast or not? Creatinine? Clotting? Cannula in situ? Metallic implants? |
Respiratory | O2 sats? Respiratory rate? abg? cxr? Inhalers/nebs? Home O2? Respiratory support, eg niv/cpap? |
Surgery (general) | Pain? Scan findings? Acutely unwell? Clotting? |
Urology | History of luts (lower urinary tract symptoms) p644? Catheter? Haematuria? History of stones? Scan findings (ultrasound, ct)? |
You would be amazed at how many people refer to neurology/stroke without having done a neurological examination! Don't be one of them…
Symptoms
Symptoms are features which patients report. Physical signs are elicited at the bedside. Together, they constitute the features of the condition in that patient. Their evolution over time and interaction with the physical, psychological, and social spheres comprise the natural history of any disease. Throughout this chapter, we discuss symptoms in isolation and attempt to classify them into a ‘system’ or present them below as ‘non-specific’. This is unnatural but a good first step in learning how to diagnose. All doctors have to know about symptoms and their relief: this is what doctors are for. Part of becoming a good doctor is learning to link symptoms together, to identify those that may be normal, and those that are worrying. There are many online tools and books that can help with this, but there is no substitute for experience. If you aren't sure, ask a specialist in that area for advice.
The following are common ‘non-specific’ presentations
is common and, if chronic, most unpleasant.
Local causes: | Systemic: (Do fbc, esr, glucose, lft, u&e, ferritin, tft) | |
Eczema, atopy, urticaria | Liver disease (bile salts, eg pbc) | Old age; pregnancy |
Scabies | Uraemia (eg ckd) | Drugs (eg morphine) |
Lichen planus | Malignancy (eg lymphoma) | Diabetes mellitus |
Dermatitis herpetiformis | Polycythaemia rubra vera | Thyroid disease |
Iron deficiency anaemia | hiv infection | |
Local causes: | Systemic: (Do fbc, esr, glucose, lft, u&e, ferritin, tft) | |
Eczema, atopy, urticaria | Liver disease (bile salts, eg pbc) | Old age; pregnancy |
Scabies | Uraemia (eg ckd) | Drugs (eg morphine) |
Lichen planus | Malignancy (eg lymphoma) | Diabetes mellitus |
Dermatitis herpetiformis | Polycythaemia rubra vera | Thyroid disease |
Iron deficiency anaemia | hiv infection | |
Wheals (urticaria)? Worse at night? Others affected (scabies)? What provokes it? After a bath ≈ polycythaemia rubra vera (p360). Exposure, eg to animals (atopy?) or fibre glass (irritant eczema?).
Scabies burrows in finger webs, lice on hair shafts, knee and elbow blisters (dermatitis herpetiformis).
Splenomegaly, nodes, jaundice, flushed face or thyroid signs?
Treat causes; try soothing bland emollients, eg E45®, ± emollient bath oils ± sedative antihistamines at night, eg chlorphenamine 4mg po.
Common causes of admission in the elderly, and can lead to loss of confidence and independence. Causes are often multifactorial:
typically osteo- or rheumatoid arthritis, but remember fractured neck of femur, cns disease, vision↓, cognitive impairment, depression, postural hypotension, peripheral neuropathy, medication (eg antihypertensives, sedatives), pain, eg arthritis, parkinsonism (eg drugs: prochlorperazine, neuroleptics, metoclopramide), muscle weakness (consider vitamin d deficiency), incontinence, uti, pneumonia, anaemia, hypothyroidism, renal impairment, hypothermia and alcohol.
If there is ataxia, the cause is not always alcohol: other chemicals may be involved (eg cannabis or prescribed sedatives). There may be a metastatic or non-metastatic manifestation of malignancy, or a cerebellar lesion.
Bilateral weak legs may suggest a cord lesion: see p470. If there is associated urinary or faecal incontinence ± saddle anaesthesia or lower limb sensory loss, urgent imaging (mri) and treatment for cord compression may well be needed.
So common that it is a variant of normality. Only 1 in 400 episodes of fatigue leads to visiting the doctor. Don't miss depression (p11). Even if depressed, still rule out common treatable causes—eg anaemia, hypothyroidism, diabetes. After history and examination: fbc, esr, u&e, plasma glucose, tft, ± cxr. Follow up to see what develops, and to address emotional problems. Take a sleep history.
While some night sweating is common in anxiety, drenching sweats requiring changes of night-clothes are a more ominous symptom associated with infection (eg tb, brucellosis), lymphoproliferative disease, or other malignancies. Patterns of fever may be relevant (see p386).
are uncontrolled paroxysms of shivering which occur as a patient's temperature rises rapidly. See p386.
may be primary (eg hidradenitis suppurativa may be very distressing to the patient)—or secondary to fever, pain or anxiety (cold & sweaty) or a systemic condition: the menopause, hyperthyroidism (warm & sweaty), acromegaly, malignancy, phaeochromocytoma, amyloidosis, or neuroleptic malignant syndrome (+hyperthermia). Or it may reflect gabapentin or opiate withdrawal, or a cholinergic or parasympathomimetic side-effect (amitriptyline, bethanechol, distigmine, spider bites)—also hormonal drugs, eg levothyroxine, gonadorelin or somatostatin analogues, vasopressin, and ephedrine. Also amiodarone, ciprofloxacin, l-dopa, lisinopril, rivastigmine, ritonavir, pioglitazone, venlafaxine. At the bedside: Ask about all drugs, examine all over for nodes; any signs of hyperthyroidism? Any splenomegaly? Test the urine; do t°, esr, tsh, fbc & blood culture. ℞: Antiperspirants (aluminium chloride 20%=Driclor®), sympathectomy, or iontophoresis may be tried.
This is trivial—until we ourselves have a few sleepless nights. Then sleep becomes the most desirable thing imaginable, and bestowing it the best thing we can do, like relieving pain. But don't give drugs without looking for a cause.
Self-limiting: Jet lag; stress; shift work; in hospital. We need less sleep as we age.
Psychic: Depression; anxiety; mania; grief; psychomotor agitation/psychosis.
Organic: Drugs (many; eg caffeine; mefloquine; nicotine withdrawal); nocturia; alcohol; pain (eg acid reflux—worse on lying down); itch; tinnitus; asthma; dystonias; obstructive sleep apnoea (p194); dementia; restless leg syndrome (p712, check ferritin). Rarer: encephalitis (eg West Nile virus) and encephalopathy (Whipple's; pellagra; hiv; prion diseases, eg cjd, p710, and fatal familial insomnia).
Hypnotic drugs: give for a few nights only (addictive and cause daytime somnolence ± rebound insomnia on stopping). Warn about driving/machine use. Example: zopiclone 3.75–7.5mg. Obstructive sleep apnoea: p194. Parasomnias, sleep paralysis, etc.: ohcs p392. Narcolepsy: p714.
Signs
Dusky blue skin (peripheral—of the fingers) or mucosae (central—of the tongue), representing 50g/L of Hb in its reduced (hence hypoxic) form, it occurs more readily in polycythaemia than anaemia. Causes:
Lung disease with inadequate oxygen transfer, eg luminal obstruction, asthma, copd, pneumonia, pe, pulmonary oedema—may be correctable by ↑ inspired O2.
Congenital cyanotic heart disease, where there is admixture, eg transposition of the great arteries or right-to-left shunt (eg vsd with Eisenmenger's syndrome; see p150)—cyanosis is not reversed by increasing inspired oxygen.
Rare causes: methaemoglobinaemia, a congenital or acquired red cell disorder.
Acute cyanosis is an emergency. Is there asthma, an inhaled foreign body, a pneumothorax (p763, fig 1) or pulmonary oedema? See p824.
Peripheral cyanosis will occur in causes of central cyanosis, but may also be induced by changes in the peripheral and cutaneous vascular systems in patients with normal oxygen saturations. It occurs in the cold, in hypovolaemia, and in arterial disease, and is therefore not a specific sign.
May be racial or familial—or from anaemia, shock/faints, Stokes–Adams attack (p464, pale first, then flushing), hypothyroidism, hypopituitarism, and albinism. 
If it's just one limb or digit, think of emboli. Anaemia is haemoglobin concentration below the normal range (p318). It may be assessed from the conjunctivae and skin creases. Koilonychia and stomatitis (p24) suggest iron deficiency. Anaemia with jaundice suggests haemolysis.
Generalized hyperpigmentation may be genetic (racial) or due to radiation; ↑acth (cross-reacts with melanin receptors, eg Addison's disease (p218), Nelson's syndrome (p32), ectopic acth in bronchial carcinoma); chronic kidney disease (↑urea, p294); malabsorption; chloasma (seen in pregnancy or with the oral contraceptive pill); biliary cirrhosis; haemochromatosis (‘bronzed diabetes’); carotenaemia; or drugs (eg chlorpromazine, busulfan, amiodarone, gold).
(see ohcs p530)
This is defined by the World Health Organization as a bmi of over 30kg/m2. A higher waist to hip ratio, indicating central fat distribution, is commoner in ♂ and is associated with greater health risks, which include type 2 diabetes mellitus, ihd, dyslipidaemia, ↑bp, osteoarthritis of weight-bearing joints, and cancer (breast and bowel); see p199. The majority of cases are not due to specific metabolic disorders. Lifestyle change is key to treatment, to increase energy expenditure and reduce intake (p236). Medication ± surgery may be considered if the patient fulfils strict criteria. Conditions associated with obesity include: genetic (Prader–Willi syndrome, Lawrence–Moon syndrome), hypothyroidism, Cushing's syndrome and hypothalamic damage (eg tumour or trauma → damage to satiety regions).
Causes of lymphadenopathy are either reactive or infiltrative:
Bacterial: eg pyogenic, tb, brucella, syphilis.
Viral: ebv, hiv, cmv, infectious hepatitis.
Others: toxoplasmosis, trypanosomiasis.
sarcoidosis, amyloidosis, berylliosis, connective tissue disease (eg rheumatoid, sle), dermatological (eczema, psoriasis), drugs (eg phenytoin).
Benign histiocytosis—ohcs p644, lipoidoses.
Haematological: lymphoma or leukaemia: all, cll, aml (p350).
Metastatic carcinoma: from breast, lung, bowel, prostate, kidney, or head and neck cancers.
(see p580)
Oedema around the face has a very different differential; The eyelid skin is very thin so periorbital oedema is usually the first sign—think of allergies (contact dermatitis, eg from eye make-up, stings), angioedema (can be hereditary), infection (orbital cellulitis can be life threatening, refer to hospital immediately if concerned, other infections include ebv and sinusitis); if there is proptosis (p211) think Graves’ disease, connective tissue diseases (eg dermatomyositis, sle, sarcoid, amyloid); and many others. Assess for systemic disease before putting it down to allergies.
ie non-indentable, is lymphoedema due to poor lymphatic drainage. Can be due to radiotherapy, malignant infiltration, infection, filariasis or rarely primary lymphoedema (Milroy's syndrome p720).
This is a feature of chronic disease and depression; also of malnutrition, malignancy, chronic infections (eg tb, hiv/enteropathic aids), diabetes mellitus and hyperthyroidism (typically in the presence of increased appetite). Severe generalized muscle wasting is also seen as part of a number of degenerative neurological diseases and in cardiac failure (cardiac cachexia), although in the latter, right heart failure may not make weight loss a major complaint. Do not forget anorexia nervosa (ohcs p348) as an underlying cause of weight loss.
Rule out treatable causes, eg diabetes is easy to diagnose—tb can be very hard. For example, the cxr may look like cancer so don't forget to send bronchoscopy samples for zn stain and tb culture. Unintentional weight loss should always ring alarm bells, so assess patients carefully.
Examination of the hands
As with any examination routine, begin by introducing yourself, obtaining consent to examine the patient and position them appropriately. Expose the arms, then ask the patient to rest their hands on a pillow. Always ask about pain or tender areas. With the hands, particularly in acute arthritis, the standard joint examination routine of “look, feel, move” is better amended to “look, ask the patient to move, then feel” to avoid causing pain.
On both the palm and the dorsum start by inspecting the skin for:
Colour—pigmentation of creases, jaundice, palmar erythema
Consistency—tight (sclerodactyly), thick (dm, acromegaly)
Characteristic lesions—pulp infarcts, rashes, purpura, spider naevi, telangiectasia, tophi, scars (eg carpal tunnel release)
Examine the muscles for wasting and fasciculations; on the palm look particularly at the thenar and hypothenar eminences.
Thenar wasting = median nerve lesion
Generalized wasting, particularly of the interossei on the dorsum, but sparing of the thenar eminence = ulnar nerve lesion
Also look for Dupuytren’s contracture and perform Tinel’s test (percuss over the distal skin crease of the wrist—tingling suggests carpal tunnel syndrome.
Examine for acute inflammation (swollen, red joints) as well as the characteristic deformities of chronic arthritis:
Ulnar deviation at the wrist
Z deformity of the thumb
On the dorsum, look for the same skin changes as the palm, plus tendon xanthomata, plaques and joint replacement scars, and examine the nails for:
Pitting and onycholysis (p32)
Clubbing (p33)
Nail fold infarcts and splinter haemorrhages
Other lesions, eg Beau’s lines (fig 1, p32), koilonychia, leuconychia
Again, look for muscle wasting, particularly of the dorsal interossei. Examine the joints for characteristic deformities:
By this point, you should know the likely diagnosis, so assess neurological function looking at power, function and sensation:
Wrist and forearm: Extension (prayer position) and flexion (reverse prayer), supination and pronation. Look at the elbows
Small muscles: Pincer grip, power grip (squeeze my two fingers), abduction of the thumb, abduction (spread your fingers) and adduction (grip this piece of paper between your fingers) of the fingers. nb Froment’s sign = flexion of the thumb during grip as ulnar nerve lesion prevents adduction (p456)
Function: Write a sentence, undo a button, pick up a coin
Sensation: Test little finger (ulnar), index finger (median) and anatomical snuff - box (radial) using light touch/pinprick
When you have clinched the diagnosis and functional status, examine each joint, palpating for tenderness, effusions and crepitus. Test sensation (see p73) and examine the elbows. Consider examination of upper limbs and face.
Cross your fingers before the patient grips them, it hurts less!
Don't forget to palpate the radial pulse
Don't forget to look at the elbows for plaques of psoriasis and rheumatoid nodules
Examination of the hands: 2
The hands can give you a wealth of information about a patient, even without needing to examine them directly. Shaking hands can tell you about thyroid disease (warm, sweaty, tremor), anxiety (cold, sweaty), and neurological disease (myotonic dystrophy patients have difficulty relaxing their grip, a weak grip may suggest muscle wasting or peripheral neuropathy), but remember that some patients are not comfortable with physical contact; be guided by your patient. Looking at the nails and skin can give information about systemic disease:
Nail abnormalities
Koilonychia (spoon-shaped nails) suggests iron deficiency, haemochromatosis, infection (eg fungal), endocrine disorders (eg acromegaly, hypothyroidism), or malnutrition.
Mees’ lines are single white transverse bands classically seen in arsenic poisoning but also in chronic kidney disease and carbon monoxide poisoning amongst others.
Terry's nails: Proximal portion of nail is white/pink, nail tip is red/brown (causes include cirrhosis, chronic kidney disease, congestive cardiac failure).
Pitting is seen in psoriasis and alopecia areata.
Splinter haemorrhages are fine longitudinal haemorrhagic streaks (under the nails), which in the febrile patient may suggest infective endocarditis. They may be microemboli, or be normal—being caused, by, for example, gardening.
Nail-fold infarcts are embolic phenomena characteristically seen in vasculitic disorders (ohcs, p414).
Clubbing of the nails occurs with many disorders (p33). There is an exaggerated longitudinal curvature and loss of the angle between nail and nail fold (ie no dip). Also the nail feels ‘boggy’. The cause is unknown but may be due to increased blood flow through multiple arteriovenous shunts in the distal phalanges.
Chronic paronychia is a chronic infection of the nail-fold and presents as a painful swollen nail with intermittent discharge.
Beau's lines, here due to chemotherapy, a new line is seen with each cycle. See p529.
Skin changes
Nodules and contractures
Heberden's node.
Thoracic: | GI: | Cardiovascular: |
• Inflammatory bowel disease (especially Crohn's) • Cirrhosis • gi lymphoma • Malabsorption, eg coeliac Rare: • Familial • Thyroid acropachy (p564) | • Cyanotic congenital heart disease • Endocarditis • Atrial myxoma • Aneurysms • Infected grafts | |
Unilateral clubbing: | ||
• Hemiplegia • Vascular lesions, eg upper-limb artery aneurysm, Takayasu's arteritis, brachial arteriovenous malformations (including iatrogenic— haemodialysis fistulas)  Fig 3. Finger clubbing.  Fig 4. Testing for finger clubbing. |
Thoracic: | GI: | Cardiovascular: |
• Inflammatory bowel disease (especially Crohn's) • Cirrhosis • gi lymphoma • Malabsorption, eg coeliac Rare: • Familial • Thyroid acropachy (p564) | • Cyanotic congenital heart disease • Endocarditis • Atrial myxoma • Aneurysms • Infected grafts | |
Unilateral clubbing: | ||
• Hemiplegia • Vascular lesions, eg upper-limb artery aneurysm, Takayasu's arteritis, brachial arteriovenous malformations (including iatrogenic— haemodialysis fistulas) Fig 3. Finger clubbing. Fig 4. Testing for finger clubbing. |
The cardiovascular system: history
History
(see also p88) Ask about age, occupation, hobbies, sport, exercise and ethnic origin.
| Presenting symptoms | Direct questions |
|---|---|
Site? Central? Onset? (sudden? What was the patient doing?) Character? Ask patient to describe pain (crushing? heavy?) Radiation? Ask specifically if moves to arm, neck or jaw? Associations? Ask specifically about shortness of breath, nausea, sweating. Timing? Duration? Exacerbating and alleviating factors? Worse with respiration or movement (less likely to be angina)? Relieved by gtn? Worse on inspiration and better when sitting forwards (pericarditis)? Severity: out of 10? Also ask if patient is known to have angina or chest pain in the past; better/worse/same as usual pain; is it more frequent? Decreasing exercise tolerance? nb: ‘heartburn’ more likely if ‘burning’, onset after eating/drinking, worse lying flat, or associated with dysphagia. | |
‘Ever aware of your own heartbeat’? When and how did it start/stop? Duration? Onset sudden/gradual? Associated with blackout (how long)? Fast/slow? Regular/irregular? Ask patient to tap out the rhythm. Related to eating/drinking (especially coffee, tea, wine, or chocolate)? | |
Duration? At rest? On exertion? Determine exercise tolerance (and any other reason for limitation, eg arthritis). nyha classification (p131)? Worse when lying flat, how many pillows does the patient sleep with (orthopnoea)? Does the patient ever wake up in the night gasping for breath (paroxysmal nocturnal dyspnoea), and how often? Any ankle swelling? | |
Did patient lose consciousness, and for how long (short duration suggests cardiac while longer duration suggests a neurological cause)? Any warning (pre-syncope)? What was patient doing at the time? Sudden/gradual? Associated symptoms? Any residual symptoms? How long did it take for patient to return to ‘normal’? Any tongue biting (p464–465), seizure, incontinence? Witnessed? | |
Claudication | socrates? Specifically foot/calf/thigh/buttock? Quantify ‘claudication distance’, ie how long can patient walk before onset of pain? Rest pain? |
| Presenting symptoms | Direct questions |
|---|---|
Site? Central? Onset? (sudden? What was the patient doing?) Character? Ask patient to describe pain (crushing? heavy?) Radiation? Ask specifically if moves to arm, neck or jaw? Associations? Ask specifically about shortness of breath, nausea, sweating. Timing? Duration? Exacerbating and alleviating factors? Worse with respiration or movement (less likely to be angina)? Relieved by gtn? Worse on inspiration and better when sitting forwards (pericarditis)? Severity: out of 10? Also ask if patient is known to have angina or chest pain in the past; better/worse/same as usual pain; is it more frequent? Decreasing exercise tolerance? nb: ‘heartburn’ more likely if ‘burning’, onset after eating/drinking, worse lying flat, or associated with dysphagia. | |
‘Ever aware of your own heartbeat’? When and how did it start/stop? Duration? Onset sudden/gradual? Associated with blackout (how long)? Fast/slow? Regular/irregular? Ask patient to tap out the rhythm. Related to eating/drinking (especially coffee, tea, wine, or chocolate)? | |
Duration? At rest? On exertion? Determine exercise tolerance (and any other reason for limitation, eg arthritis). nyha classification (p131)? Worse when lying flat, how many pillows does the patient sleep with (orthopnoea)? Does the patient ever wake up in the night gasping for breath (paroxysmal nocturnal dyspnoea), and how often? Any ankle swelling? | |
Did patient lose consciousness, and for how long (short duration suggests cardiac while longer duration suggests a neurological cause)? Any warning (pre-syncope)? What was patient doing at the time? Sudden/gradual? Associated symptoms? Any residual symptoms? How long did it take for patient to return to ‘normal’? Any tongue biting (p464–465), seizure, incontinence? Witnessed? | |
Claudication | socrates? Specifically foot/calf/thigh/buttock? Quantify ‘claudication distance’, ie how long can patient walk before onset of pain? Rest pain? |
(Screen for presenting symptoms before proceeding to past history.)
Past history
Ask specifically about: angina, any previous heart attack or stroke, rheumatic fever, diabetes, hypertension, hypercholesterolaemia, previous tests/procedures (ecg, angiograms, angioplasty/stents, echocardiogram, cardiac scintigraphy, coronary artery bypass grafts (cabg)).
Drug history
Particularly note aspirin/gtn/β-blocker/diuretic/ace-i/digoxin/statin use.
Family history
Enquire specifically if any 1st-degree relatives having cardiovascular events (especially if <60yrs).
Social history
Smoking, impact of symptoms on daily life.
Smoking
Diabetes mellitus/raised bmi
Family history (1st-degree relative <60yrs old with ihd)
Hypertension
Hyperlipidaemia
Renal disease
Deprivation
An awareness of the heartbeat. Have the patient tap out the rate and rhythm of the palpitations.
Irregular fast palpitations are likely to be paroxysmal af, or atrial flutter with variable block.
Regular fast palpitations may reflect paroxysmal supraventricular tachycardia (svt) or ventricular tachycardia (vt).
Dropped or missed beats related to rest, recumbency, or eating are likely to be atrial or ventricular ectopics.
Regular pounding may be due to anxiety.
Ask about associated chest pain, dyspnoea, and faints, suggesting haemodynamic compromise. Ask when it occurs: anxious people may be aware of their own heartbeat at night. Reassurance is vital and can often be therapeutic. Check a tsh and consider a 24h ecg (Holter monitor, p102). An event recorder, if available, is better than 24h ecgs, which miss some attacks.
At night on my pillow the syncopated staggerOf the pulse in my ear. Russian roulette:Every heartbeat a fresh throw of the dice …Hypochondria walked, holding my armLike a nurse, her fingers over my pulse …The sudden lapping at my throat of loose blood.Ted Hughes, Birthday Letters.
Faber & Faber, by kind permission.
is a loose term, so try to clarify if your patient means:
Vertigo (p466), the illusion of rotation of either the patient or their surroundings ± difficulty walking/standing, patients may fall over.
Imbalance, a difficulty in walking straight but without vertigo, from peripheral nerve, posterior column, cerebellar, or other central pathway failure.
Faintness, ie ‘light-headedness’, seen in anaemia, ↓bp, postural hypotension, hypoglycaemia, carotid sinus hypersensitivity, and epilepsy.
The cardiovascular system: examination
As with any examination routine, begin by introducing yourself, obtaining consent to examine the patient and position them appropriately: for the cardiovascular system, lying on a bed but sitting up at 45°. Expose them to the waist (for female patients, delay this until examining the praecordium). Explain what you are doing throughout.
A = Aortic
P = Pulmonary
T = Triscuspid
M = Mitral
Assess general state (ill/well)
Look for clues (oxygen, gtn spray)
Colour (pale, cyanosed, flushed)
Short of breath?
Scars on chest wall?
Temperature: capillary refill time
Inspect:
Skin: tobacco staining, peripheral cyanosis, tendon xanthomata, Janeway lesions, Osler’s nodes (signs of infective endocarditis)
Nails: clubbing, splinter haemorrhages, nailbed pulsation (Quinke’s sign of aortic regurgitation)
Radial: rate, rhythm; radio–radial delay (palpate pulse bilaterally simultaneously), radiofemoral delay (palpate ipsilateral pulses simultaneously), collapsing pulse (hold pulse with fingers of one hand, wrap the fingers of other hand around forearm, check “any pain in arm/shoulder?”, lift arm up straight collapsing pulse, felt as ‘waterhammer’ pulsation in forearm).
Brachial: (just medial to tendonous insertion of biceps). Waveform character.
Hyper or hypotensive?
Pulse pressure (wide = aortic regurgitation, narrow = aortic stenosis)
Carotid pulse: inspect (visible carotid = Corrigan’s sign of aortic regurgitation), and palpate volume and character on one side then the other.
The jvp.
Colour: pale, flushed, central cyanosis
Features: corneal arcus (fig 2), xanthelasma
Pallor of the conjunctiva (anaemia)
Malar flush (mitral stenosis)
Dental hygiene
Corneal arcus.
Scars: midline sternotomy, lateral thoractomy (mitral stenosis valvotomy).
Apex beat (lowermost lateral pulsation): usually 5th intercostal space in mid-clavicular line; measure position by counting intercostal spaces (sternal notch = 2nd intercostal space). Undisplaced/displaced? Character: impalpable (?dextrocardia/copd), tapping (palpable S1), double impulse, sustained/strong. Count rate if pulse irregular (af, p124).
Heaves’ and ‘thrills’: place the heel of the hand flat on chest to left then right of sternum. Heave: sustained, thrusting usually felt at left sternal edge (= right ventricular enlargement). Thrill: palpable murmur felt as a vibration beneath your hand.
(palpate carotid pulse at the same time)
At apex with bell, ask the patient to “Roll over onto your left side, breathe out, and hold it there” (a rumbling mid-diastolic murmur—mitral stenosis).
Lower left sternal edge (tricuspid area) and pulmonary area (left of manubrium in the 2nd intercostal space): if suspect right-sided mumur, listen with patient’s breath held in inspiration.
Right of manubrium in 2nd intercostal space (aortic area) ejection systolic murmur radiating to the carotids—aortic stenosis.
Sit the patient up and listen at the lower left sternal edge with patient held in expiration (early diastolic murmur: aortic regurgitation?).
Palpate for sacral and ankle oedema (fig 3).
Auscultate the lung bases for inspiratory crackles.
Examine the abdomen for a pulsatile liver and aortic aneurysm.
Check peripheral pulses, observation chart for temperature and O2, sats, dip urine, perform fundoscopy.
Pitting oedema, apply firm pressure for a few seconds.
The hand can be used as a manometer to estimate jvp/cvp if you cannot see the neck properly (eg central line in situ). Hold the hand palm down below the level of the heart until the veins dilate (patient must be warm!), then lift slowly, keeping the arm horizontal. The veins should empty as the hand is raised. Empty veins below the level of the heart suggests a low cvp, if they remain full it suggests a normal/high cvp.
The cardiovascular system: examination
General inspection
Ill or well? In pain? Dyspnoeic? Are they pale, cold, and clammy? Can you hear the click of a prosthetic valve? Inspect for scars: median sternotomy (cabg; valve replacement; congenital heart disease). Inspect for any pacemakers. Look around the bed for oxygen and gtn spray.
Hands
Finger clubbing occurs in congenital cyanotic heart disease and endocarditis. Splinter haemorrhages, Osler's nodes (tender nodules, eg in finger pulps) and Janeway lesions (red macules on palms, fig 3, p145) are signs of infective endocarditis. If found, examine the fundi for Roth's spots (retinal infarcts, p386, fig 1). Are there nail fold infarcts (vasculitis, p558) or nailbed capillary pulsation (Quincke's sign in aortic regurgitation)? Is there arachnodactyly (Marfan's) or polydactyly (asd)? Are there tendon xanthomata (fig 3, p36; hyperlipidaemia)?
Pulse
See p42. Feel for radio-femoral delay (coarctation of the aorta) and radio-radial delay (eg from aortic arch aneurysm).
Blood pressure
(see box) Systolic bp is the pressure at which the pulse is first heard as on cuff deflation (Korotkov sounds); the diastolic is when the heart sounds disappear or become muffled (eg in the young). The pulse pressure is the difference between systolic and diastolic pressures. It is narrow in aortic stenosis and hypovolaemia, and wide in aortic regurgitation and septic shock. Defining hypertension is problematic: see p132. Examine the fundi for hypertensive changes (p133). Shock may occur if systolic <90mmHg (p804). Postural hypotension is defined as a drop in systolic >20mmHg or diastolic >10mmHg on standing (see box).
Face
Is there corneal arcus (fig 2, p37) or xanthelasma (fig 1, p705, signifying dyslipidaemia, p704)? Is there a malar flush (mitral stenosis, low cardiac output)? Are there signs of Graves’ disease, eg bulging eyes (exophthalmos) or goitre—p210)? Is the face dysmorphic, eg Down's syndrome, Marfan's syndrome (p720)—or Turner's, Noonan's, or William's syndromes (p143)?
Carotid pulse
Praecordium
Palpate the apex beat. Normal position: 5th intercostal space in the mid-clavicular line. Is it displaced laterally? Is it abnormal in nature: heaving (caused by outflow obstruction, eg aortic stenosis or systemic hypertension), thrusting (caused by volume overload, eg mitral or aortic incompetence), tapping (mitral stenosis, essentially a palpable 1st heart sound), diffuse (lv failure, dilated cardiomyopathy) or double impulse (h(o)cm, p146)? Is there dextrocardia? Feel for left parasternal heave (rv enlargement, eg in pulmonary stenosis, cor pulmonale, asd) or thrills (transmitted murmurs).
Auscultating the heart
Also auscultate for bruits over the carotids and elsewhere, particularly if there is inequality between pulses or absence of a pulse. Causes: atherosclerosis (elderly), vasculitis (young, p558).
Lungs
Examine the bases for creps & pleural effusions, indicative of cardiac failure.
Oedema
Examine the ankles, legs, sacrum, and torso for pitting oedema. (You may prefer to examine ankles whilst standing at the foot of the bed as it is a good early clue that there may be further pathology to be found.)
Abdomen
Hepatomegaly and ascites in right-sided heart failure; pulsatile hepatomegaly with tricuspid regurgitation; splenomegaly with infective endocarditis.
Fundoscopy
Roth spots (infective endocarditis).
Urine dipstick
Haematuria.
Signs of heart failure?
Clinical evidence of infective endocarditis?
Sinus/abnormal rhythm?
Heart sounds normal, abnormal or additional?
Murmurs?
Optimal cuff width is 40% of the arm circumference. If you suspect a bp reading to be anomalous, check the equipment and review the observation chart for previous readings and other vital signs. Consider taking a manual reading with a different set yourself.Hypovolaemia (early sign); drugs, eg nitrates, diuretics, antihypertensives; antipsychotics; Addison's (p218); hypopituitarism (↓acth), autonomic neuropathy (p509, dm, multisystem atrophy, p498), after a marathon run (peripheral resistance is low for some hours); idiopathic.
Lie down if feeling faint.
Stand slowly (with escape route: don't move away from the chair too soon!).
Consider referral to a ‘falls clinic’, where special equipment is available for monitoring patient under various tilts.
Manage autonomic neuropathy, p509.
↑Water and salt ingestion can help (eg 150mmol Na+/d), but Na+ has its problems.
Physical measures: leg crossing, squatting, elastic compression stockings (check dorsalis pedis pulse is present), and careful exercise may help.
If post-prandial dizziness, eat little and often; ↓carbohydrate and alcohol intake.
Head-up tilt of the bed at night ↑renin release, so ↓fluid loss and ↑standing bp.
If these fail, turn things on their head and ask: is this really supine hypertension?
Localized deposits of fat under the skin, occurring over joints (fig 3, p36), tendons, hands, and feet. They are a sign of dyslipidaemia (p704). Xanthelasma refers to xanthoma on the eyelid (p705, fig 1). Corneal arcus (fig 2, p37) is a crescentic- shaped opacity at the periphery of the cornea. Common in those over 60yrs, can be normal, but may represent hyperlipidaemia, especially in those under this age.
The jugular venous pressure
The internal jugular vein acts as a capricious manometer of right atrial pressure. Observe 2 features: the height (jugular venous pressure, jvp) and the waveform of the pulse. jvp observations are often difficult. Do not be downhearted if the skill seems to elude you. Keep on watching necks, and the patterns you see may slowly start to make sense—see fig 2 for the local venous anatomy. Relating the waveform to the arterial pulse (by concomitant palpation) will help to decipher patterns.
The jugular venous system.
The height
The waveform
See box 1.
Abnormalities of the jvp
Raised jvp with normal waveform: Fluid overload, right heart failure.
Fixed raised jvp with absent pulsation: svc obstruction (p526).
Large a wave: Pulmonary hypertension, pulmonary stenosis.
Cannon a wave: When the right atrium contracts against a closed tricuspid valve, large ‘cannon’ a waves result. Causes: complete heart block, single chamber ventricular pacing, ventricular arrhythmias/ectopics.
Absent a wave: Atrial fibrillation.
Large v waves: Tricuspid regurgitation—look for earlobe movement.
Constrictive pericarditis: High plateau of jvp (which rises on inspiration—Kussmaul's sign) with deep x and y descents.
Absent jvp: When lying flat, the jugular vein should be filled. If there is reduced circulatory volume (eg dehydration, haemorrhage) the jvp may be absent.
Pulses
Assess the radial pulse to determine rate and rhythm. Character and volume are best assessed at the brachial or carotid arteries. A collapsing pulse may also be felt at the radial artery when the patient's arm is elevated above his head. See fig 3.
Arterial pulse waveforms.
Rate
Rhythm
An irregularly irregular pulse occurs in af or multiple ectopics. A regularly irregular pulse occurs in 2° heart block and ventricular bigeminus.
Character and volume
Bounding pulses are caused by CO2 retention, liver failure, and sepsis.
Small volume pulses occur in aortic stenosis, shock, and pericardial effusion.
Collapsing (‘waterhammer’) pulses are caused by aortic incompetence, av malformations, and a patent ductus arteriosus.
Anacrotic (slow-rising) pulses occur in aortic stenosis.
Bisferiens pulses occur in combined aortic stenosis and regurgitation.
Pulsus alternans (alternating strong and weak beats) suggests lvf, cardiomyopathy, or aortic stenosis.
Jerky pulses occur in h(o)cm.
Pulsus paradoxus (systolic pressure weakens in inspiration by >10mmHg) occurs in severe asthma, pericardial constriction, or cardiac tamponade.
Peripheral pulses
The jugular venous pressure wave. The jvp drops as the x descent during ventricular systole because the right atrium is no longer contracting. This means that the pressure in the right atrium is dropping and this is reflected by the jvp.
A venous pulse:
Is not usually palpable.
Is obliterated by finger pressure on the vessel.
Rises transiently with pressure on abdomen (abdominojugular reflux) or on liver (hepatojug-ular reflux).
Alters with posture and respiration.
Usually has a double pulse for every arterial pulse.
The waterhammer was a popular toy that consisted of a vacuum tube half-filled with water. On inversion, the whoosh of water produced an intriguing hammer-blow as it rushed from end to end. This is the alternative name for Corrigan's collapsing pulse—ie one in which the upstroke is abrupt and steep, whose peak is reached early and with abnormal force—before a rapid downstroke (as blood whooshes back into the left ventricle through an incompetent aortic valve).
The heart sounds
Listen systematically: sounds then murmurs. While listening, palpate the carotid artery: S1 is synchronous with the upstroke.
Heart sounds
The 1st and 2nd sounds are usually clear. Confident pronouncements about other sounds and soft murmurs may be difficult. Even senior colleagues disagree with one another about the more difficult sounds and murmurs. See fig 1.
The cardiac cycle.
The 1st heart sound
(S1) represents closure of mitral (M1) and tricuspid (T1) valves. Splitting in inspiration may be heard and is normal.
Loud S1 In mitral stenosis, because the narrowed valve orifice limits ventricular filling, there is no gradual decrease in flow towards the end of diastole. The valves are therefore at their maximum excursion at the end of diastole, and so shut rapidly leading to a loud S1 (the ‘tapping’ apex). S1 is also loud if diastolic filling time is shortened, eg if the pr interval is short, and in tachycardia.
Soft S1 occurs if the diastolic filling time is prolonged, eg prolonged pr interval, or if the mitral valve leaflets fail to close properly (ie mitral incompetence).
The intensity of S1 is variable in av block, af, and nodal or ventricular tachycardia.
The 2nd heart sound
(S2) represents aortic (A2) and pulmonary valve (P2) closure. The most important abnormality of A2 is softening in aortic stenosis.
A2 is said to be loud in tachycardia, hypertension, and transposition, but this is probably not a useful clinical entity.
P2 is loud in pulmonary hypertension and soft in pulmonary stenosis.
Splitting of S2 in inspiration is normal and is mainly due to the variation of right heart venous return with respiration, delaying the pulmonary component.
Wide splitting occurs in right bundle branch block (bbb), pulmonary stenosis, deep inspiration, mitral regurgitation, and vsd.
Wide fixed splitting occurs in asd.
Reversed splitting (ie A2 following P2, with splitting increasing on expiration) occurs in left bundle branch block, aortic stenosis, pda (patent ductus arteriosus), and right ventricular pacing.
A single S2 occurs in Fallot's tetralogy, severe aortic or pulmonary stenosis, pulmonary atresia, Eisenmenger's syndrome (p150), large vsd, or hypertension.
nb: splitting and P2 are heard best in the pulmonary area.
Additional sounds
A 3rd heart sound
(S3) may occur just after S2. It is low pitched and best heard with the bell of the stethoscope. S3 is pathological over the age of 30yrs. A loud S3 occurs in a dilated left ventricle with rapid ventricular filling (mitral regurgitation, vsd) or poor lv function (post mi, dilated cardiomyopathy). In constrictive pericarditis or restrictive cardiomyopathy it occurs early and is more high pitched (‘pericardial knock’).
A 4th heart sound
(S4) occurs just before S1. Always abnormal, it represents atrial contraction against a ventricle made stiff by any cause, eg aortic stenosis or hypertensive heart disease.
Triple and gallop rhythms
A 3rd or 4th heart sound occurring with a sinus tachycardia may give the impression of galloping hooves. An S3 gallop has the same rhythm as ‘Ken-tucky’, whereas an S4 gallop has the same rhythm as ‘Tenne-ssee’. When S3 and S4 occur in a tachycardia, eg with pulmonary embolism, they may summate and appear as a single sound, a summation gallop.
An ejection systolic click
is heard early in systole with bicuspid aortic valves, and if bp↑. The right heart equivalent lesions may also cause clicks.
Mid-systolic clicks
occur in mitral valve prolapse (p138).
An opening snap
precedes the mid-diastolic murmur of mitral (and tricuspid) stenosis. It indicates a pliable (non-calcified) valve.
Prosthetic sounds
are caused by non-biological valves, on opening and closing: rumbling sounds ≈ ball and cage valves (eg Starr–Edwards); single clicks ≈ tilting disc valve (eg single disc: Bjork Shiley; bileaflet: St Jude—often quieter). Prosthetic mitral valve clicks occur in time with S1, aortic valve clicks in time with S2.
Cardiac murmurs
(see also Heart murmurs in children, ohcs p137)
Always consider other symptoms and signs before auscultation and think: “What do I expect to hear?” But don't let your expectations determine what you hear.
Use the stethoscope correctly: remember that the bell is good for low-pitched sounds (eg mitral stenosis) and should be applied gently. The diaphragm filters out low pitches, making higher-pitched murmurs easier to detect (eg aortic regurgitation). nb: a bell applied tightly to the skin becomes a diaphragm.
Consider any murmur in terms of character, timing, loudness, area where loudest, radiation, and accentuating manoeuvres.
When in doubt, rely on echocardiography rather than disputed sounds. (But still enjoy trying to figure out the clinical conundrum!)
Character and timing (see fig 1)
An ejection-systolic murmur (esm, crescendo–decrescendo) usually originates from the outflow tract and waxes and wanes with the intraventricular pressures. esms may be innocent and are common in children and high-output states (eg tachycardia, pregnancy). Organic causes include aortic stenosis and sclerosis, pulmonary stenosis, and h(o)cm.
A pansystolic murmur (psm) is of uniform intensity and merges with S2. It is usually organic and occurs in mitral or tricuspid regurgitation (S1 may also be soft in these), or a ventricular septal defect (p150). Mitral valve prolapse may produce a late systolic murmur ± midsystolic click.
Early diastolic murmurs (edm) are high pitched and easily missed: listen for the ‘absence of silence’ in early diastole. An edm occurs in aortic and, though rare, pulmonary regurgitation. If the pulmonary regurgitation is secondary to pulmonary hypertension resulting from mitral stenosis, then the edm is called a Graham Steell murmur.
Mid-diastolic murmurs (mdm) are low pitched and rumbling. They occur in mitral stenosis (accentuated presystolically if heart still in sinus rhythm), rheumatic fever (Carey Coombs’ murmur: due to thickening of the mitral valve leaflets), and aortic regurgitation (Austin Flint murmur: due to the fluttering of the anterior mitral valve cusp caused by the regurgitant stream).
Intensity
All murmurs are graded on a scale of 1–6 (see table), though in practice diastolic murmurs, being less loud, are only graded 1–4. Intensity is a poor guide to the severity of a lesion—an esm may be inaudible in severe aortic stenosis.
| Grade | Description |
|---|---|
1/6 | Very soft, only heard after listening for a while |
2/6 | Soft, but detectable immediately |
3/6 | Clearly audible, but no thrill palpable |
4/6 | Clearly audible, palpable thrill |
5/6 | Audible with stethoscope only partially touching chest |
6/6 | Can be heard without placing stethoscope on chest |
| Grade | Description |
|---|---|
1/6 | Very soft, only heard after listening for a while |
2/6 | Soft, but detectable immediately |
3/6 | Clearly audible, but no thrill palpable |
4/6 | Clearly audible, palpable thrill |
5/6 | Audible with stethoscope only partially touching chest |
6/6 | Can be heard without placing stethoscope on chest |
Area where loudest
Though an unreliable sign, mitral murmurs tend to be loudest over the apex, in contrast to the area of greatest intensity from lesions of the aortic (right 2nd intercostal space), pulmonary (left 2nd intercostal space) and tricuspid (lower left sternal edge) valves.
Radiation
The esm of aortic stenosis classically radiates to the carotids, in contrast to the psm of mitral regurgitation, which radiates to the axilla.
Accentuating manoeuvres
Movements that bring the relevant part of the heart closer to the stethoscope accentuate murmurs (eg leaning forward for aortic regurgitation, left lateral position for mitral stenosis).
Expiration increases blood flow to the left side of the heart and therefore accentuates left-sided murmurs. Inspiration has the opposite effect.
Valsalva manoeuvre (forced expiration against a closed glottis) decreases systemic venous return, accentuating mitral valve prolapse and h(o)cm, but softening mitral regurgitation and aortic stenosis. Squatting has exactly the opposite effect. Exercise accentuates the murmur of mitral stenosis.
Non-valvular murmurs
A pericardial friction rub may be heard in pericarditis. It is a superficial scratching sound, not confined to systole or diastole. Continuous murmurs are present throughout the cardiac cycle and may occur with a patent ductus arteriosus, arteriovenous fistula, or ruptured sinus of Valsalva.
Typical waveforms of common heart murmurs.
The following grading is commonly used for murmurs—systolic murmurs from 1 to 6 and diastolic murmurs from 1 to 4, never being clinically >4/6.
All types produce a degree of outflow obstruction and thus have an esm. Tilting single disc (eg Bjork Shiley) and bileaflet (eg St Jude) valves do not completely close and allow a regurgitant stream during diastole; hence they have a low-intensity diastolic murmur. The intensity of this murmur increases as the valve fails. Ball and cage valves (eg Starr–Edwards) and tissue valves do close completely in diastole and so any diastolic murmur implies valve failure.
Ball and cage valves project into the left ventricle and can cause a low-intensity esm as they interfere with the ejected stream. Tissue valves and bileaflet valves can have a low-intensity diastolic murmur. Consider any systolic murmur of loud intensity to be a sign of regurgitation and ∴ failure.
de Musset's sign—head nodding in time with the pulse
Muller's sign—systolic pulsations of the uvula
Corrigan's sign—visible carotid pulsations
Quincke's sign—capillary nailbed pulsation in the fingers
Traube's sign—’pistol shot’ femorals, a booming sound heard over the femorals
Duroziez's sign—to and fro diastolic murmur heard when compressing the femorals proximally with the stethoscope
Peripheral vascular system: examination
Arterial
Inspection Look for scars of previous surgery and signs of peripheral arterial disease; loss of hair, pallor, shiny skin, cyanosis, dry skin, scaling, deformed toenails, ulcers, gangrene. Be sure to inspect the pressure points, ie between the toes and under the heel.
Palpation Skin temperature will be low in peripheral arterial disease. Is there a level above which it is warm? Delayed capillary refill (>2s) also indicates arterial disease. Are peripheral pulses palpable or not? ‘If you cannot count it, you are not feeling it.’ Note down on a quick stick-man diagram where they become palpable. Check for atrial fibrillation or other arrhythmias, as these can be the cause of embolic disease. Palpate for an enlarged abdominal aorta and attempt to assess size. (Though don't press too firmly!) An expansile pulsatile mass in the presence of abdominal symptoms is a ruptured aneurysm until proven otherwise.
Auscultation The presence of bruits suggests arterial disease. Listen over the major arteries—carotids, abdominal aorta, renal arteries, femorals.
Special tests Buerger's angle is that above the horizontal plane which leads to development of pallor (<20° indicates severe ischaemia). Buerger's sign is the sequential change in colour from white to pink, upon return to the dependent position; if the limbs become flushed red (reactive hyperaemia) this is indicative of more severe disease.
Complete your examination by measuring the abpi (p658), us Doppler assessment for presence of pulses that were not palpable, and a neurological examination of the lower limbs.
Venous
(see also p660)
Inspection Look for any varicosities and decide whether they are the long saphenous vein (medial), short saphenous vein (posterior, below the knee), or from the calf perforators (usually few varicosities but commonly show skin changes). Ulcers around the medial malleolus are more suggestive of venous disease, whereas those at the pressure points suggest arterial pathology. Brown haemosiderin deposits result from venous hypertension. There may also be atrophy and loss of skin elasticity (lipodermatosclerosis) in venous disease.
Palpation Warm varicose veins may indicate infection. Are they tender? Firm, tender varicosities suggests thrombosis. Palpate the saphenofemoral junction (sfj) for a saphena varix which displays a cough impulse. Similarly, incompetence at the saphenopopliteal junction (spj) may be felt as a cough impulse. If ulceration is present, it is prudent to palpate the arterial pulses to rule out arterial disease.
Tap test A transmitted percussion impulse from the lower limit of the varicose vein to the saphenofemoral junction demonstrates incompetence of superficial valves.
Auscultation Bruits over the varicosities means there is an arteriovenous malformation.
Doppler Test for the level of reflux. On squeezing the leg distal to placement of the probe you should only hear one ‘whoosh’ if the valves are competent at the level of probe placement.
Tourniquet test This is the more ‘classical’ test for the level of reflux. If the varicosities are controlled by the tourniquet then the level of incompetence is above the tourniquet. Note that all veins will refill eventually via the arterial system but rapid refill signifies superficial reflux. (Also Trendelenburg's test and Perthes’ test, p661.)
Complete examination by examining the abdomen, pelvis in females and external genitalia in males (for masses).
Arterial
Introduction, consent, patient sitting back at 45°. Inspect skin (hair loss, etc.). Look between toes and lift up heels to inspect for ulcers.
Temperature bilaterally in thighs, legs, and feet.
Capillary refill: Press/squeeze great toe until blanches, release, and measure time for colour to return (normal <2s).
Peripheral pulses: Radial, brac hial, carotid, femoral (mid-inguinal point), popliteal (flex patient’s knees slightly and press into centre of popliteal fossa; fig 1), posterior tibial (just posterior & inferior to medial malleolus) and dorsalis pedis (between bases of 1st & 2nd metatarsals); assess whether palpable bilaterally. Detect rate and rhythm. For brachial and carotid determine volume and character.
Abdominal aorta: Palpate midline above umbilicus; position fingers either side of outermost palpable margins (fig 2).
Peripheral pulses: popliteal.
Pulses: abdominal aorta. a) Expansile (aneurysm?) b) transmitted.
for carotid, femoral, renal and aortic bruits.
Buerger’s test: Lift both legs to 45° above the horizontal, supporting at heels. Allow a minute for legs to become pale. If they do, ask patient to sit up and swing around to lower legs to ground—observe colour change.
Doppler probe to detect pulses and measure ankle –brachial pressure index; conduct neurological examination of lower limbs.
Venous
Introduction, consent, patient sitting back at 45°. Inspect for varicosities and skin changes.
Temperature of varicosities
Ask patient to cough while you palpate for impulse at sfj and spj.
Percuss lower limit of varicosity and feel for impulse at sfj.
Listen for bruits over any varicosities.
Place probe over sfj, squeeze calf and listen. Repeat with probe at spj.
Elevate leg and massage veins to empty varicosities. Apply tourniquet to upper thigh. Ask patient to stand. If not controlled, repeat, placing tourniquet below knee.
of abdomen; rectum; pelvis (♀); genitals (♂).
The respiratory system: history
History
Age, race, occupation (the latter is essential for respiratory disease).
| Presenting symptoms | Direct questions |
|---|---|
• Cough (see box) | Duration? Character (eg barking/hollow/dry)? Nocturnal (≈asthma, ask about other atopic symptoms, ie eczema, hayfever)? Exacerbating factors? Sputum (colour? How much?) Any blood/haemoptysis? |
• Haemoptysis (see box) | |
Duration? Steps climbed/distance walked before onset? nyha classification (p131)? Diurnal variation (≈asthma)? Ask specifically about circumstances in which dyspnoea occurs (eg occupational allergen exposure). | |
Eg due to laryngitis, recurrent laryngeal nerve palsy, Singer's nodules, or laryngeal tumour. | |
socrates (see p34), usually ‘pleuritic’ if respiratory (ie worse on inspiration?). |
| Presenting symptoms | Direct questions |
|---|---|
• Cough (see box) | Duration? Character (eg barking/hollow/dry)? Nocturnal (≈asthma, ask about other atopic symptoms, ie eczema, hayfever)? Exacerbating factors? Sputum (colour? How much?) Any blood/haemoptysis? |
• Haemoptysis (see box) | |
Duration? Steps climbed/distance walked before onset? nyha classification (p131)? Diurnal variation (≈asthma)? Ask specifically about circumstances in which dyspnoea occurs (eg occupational allergen exposure). | |
Eg due to laryngitis, recurrent laryngeal nerve palsy, Singer's nodules, or laryngeal tumour. | |
socrates (see p34), usually ‘pleuritic’ if respiratory (ie worse on inspiration?). |
(Screen for presenting symptoms before proceeding to past history.)
Past history
Ask about: pneumonia/bronchitis; tb; atopy5 (asthma/eczema/hay fever); previous cxr abnormalities; lung surgery; myopathy; neurological disorders. Connective tissue disorders, eg rheumatoid, sle.
Drug history
Respiratory drugs (eg steroids, bronchodilators)? Any other drugs, especially with respiratory se (eg ace inhibitors, cytotoxics, β-blockers, amiodarone)?
Family history
Atopy?5 Emphysema? tb?
Social history
Quantify smoking in ‘pack-years’ (20 cigarettes/day for 1 year = 1 pack-year). Occupational exposure (farming, mining, asbestos) has possible compensatory implications. Pets at home (eg birds)? Recent travel/tb contacts?
Inspiratory sound due to partial obstruction of upper airways. Obstruction may be due to something within the lumen (eg foreign body, tumour, bilateral vocal cord palsy), within the wall (eg oedema from anaphylaxis, laryngospasm, tumour, croup, acute epiglottitis, amyloidosis), or extrinsic (eg goitre, oesophagus, lymphadenopathy, post-op stridor, after neck surgery). It's an emergency (p786) if gas exchange is compromised. nb: wheeze is an expiratory sound.
Coughing is relatively non-specific, resulting from irritation anywhere from the pharynx to the lungs. The character of a cough may, however, give clues as to the underlying cause:
Loud, brassy coughing suggests pressure on the trachea, eg by a tumour.
Hollow, ‘bovine’ coughing is associated with recurrent laryngeal nerve palsy.
Barking coughs occur in croup.
Chronic cough: Think of pertussis, tb, foreign body, asthma (eg nocturnal).
Dry, chronic coughing may occur following acid irritation of the lungs in oesophageal reflux, and as a side-effect of ace inhibitors.
Do not ignore a change in character of a chronic cough; it may signify a new problem, eg infection, malignancy.
Blood is coughed up, eg frothy, alkaline, and bright red, often in a context of known chest disease (vomited blood is acidic and dark).
1 Infective | |
2 Neoplastic | Primary or secondary. |
3 Vascular | Lung infarction (pe); vasculitis (anca-associated; ra; sle); hereditary haemorrhagic telangiectasia; av malformation; capillaritis. |
4 Parenchymal | Diffuse interstitial fibrosis; sarcoidosis; haemosiderosis; Goodpasture's syndrome; cystic fibrosis. |
5 Pulmonary hypertension | Idiopathic, thromboembolic, congenital cyanotic heart disease (p150), pulmonary fibrosis, bronchiectasis. |
6 Coagulopathies | Any—eg thrombocytopenia, p338; dic; warfarin excess. |
7 Trauma/foreign body | Eg post-intubation, or an eroding implanted defibrillator. |
8 Pseudo-haemoptysis | Munchausen's (p720); aspirated haematemesis; red pigment (prodigiosin) from Serratia marcescens in sputum. |
1 Infective | |
2 Neoplastic | Primary or secondary. |
3 Vascular | Lung infarction (pe); vasculitis (anca-associated; ra; sle); hereditary haemorrhagic telangiectasia; av malformation; capillaritis. |
4 Parenchymal | Diffuse interstitial fibrosis; sarcoidosis; haemosiderosis; Goodpasture's syndrome; cystic fibrosis. |
5 Pulmonary hypertension | Idiopathic, thromboembolic, congenital cyanotic heart disease (p150), pulmonary fibrosis, bronchiectasis. |
6 Coagulopathies | Any—eg thrombocytopenia, p338; dic; warfarin excess. |
7 Trauma/foreign body | Eg post-intubation, or an eroding implanted defibrillator. |
8 Pseudo-haemoptysis | Munchausen's (p720); aspirated haematemesis; red pigment (prodigiosin) from Serratia marcescens in sputum. |
(see also p796)
Subjective sensation of shortness of breath, often exacerbated by exertion.
Lung—airway and interstitial disease. May be hard to separate from cardiac causes; asthma may wake patient, and cause early morning dyspnoea & wheeze.
Cardiac—eg ischaemic heart disease or left ventricular failure (lvf), mitral stenosis, of any cause. lvf is associated with orthopnoea (dyspnoea worse on lying; “How many pillows?”) and paroxysmal nocturnal dyspnoea (pnd; dyspnoea waking one up). Other features include ankle oedema, lung crepitations and ↑jvp.
Anatomical—eg diseases of the chest wall, muscles, pleura. Ascites can cause breathlessness by splinting the diaphragm, restricting its movement.
Others Any shocked patient may also be dyspnoeic (p804 & p609)—dyspnoea may be shock's presenting feature. Also anaemia or metabolic acidosis causing respiratory compensation, eg ketoacidosis, aspirin poisoning. Look for other clues—dyspnoea at rest unassociated with exertion, may be psychogenic: prolonged hyperventilation causes respiratory alkalosis. This causes a fall in ionized calcium leading to apparent hypocalcaemia. Features include peripheral and perioral paraesthesiae ± carpopedal spasm. Speed of onset helps diagnosis:
| Acute | Subacute | Chronic |
|---|---|---|
Foreign body | Asthma | copd and chronic parenchymal diseases |
Parenchymal disease, eg alveolitis pneumonia | ||
Pulmonary embolus | Non-respiratory causes, eg cardiac failure anaemia | |
Acute pulmonary oedema | Effusion |
The respiratory system: examination I
As with any examination routine, begin by introducing yourself, obtaining consent to examine the patient and position them appropriately: for the respiratory system, lying on a bed but sitting up at 45°. Expose them to the waist (for female patients, delay this until examining the chest itself). Explain what you are doing throughout.
Assess general state (ill/well/cachexic)
Look for clues (oxygen, inhalers)
Colour (pale, cyanosed, flushed)
Short of breath? Accessory muscle use?
Scars on chest wall? Ask the patient to take a deep breath in, watch chest movement and symmetry, any coughing?
Inspect: Tobacco staining, peripheral cyanosis, clubbing, signs of systemic disease (systemic sclerosis, rheumatoid arthritis)
Asterixis: Ask the patient to hold their hands out and cock their wrists back, fig 1
Asterixis.
Time pulse rate, with fingers still on the pulse, check respiratory rate (this can increase if the patient is aware you are timing it)—and pattern (p53)
Bounding pulse (CO2 retention)?
Check blood pressure
Trachea: feel in sternal notch (deviated?), assess cricosternal distance in fingerbreadths and feel for tracheal tug
Lymphadenopathy: from behind with patient sat forward palpate lymph nodes of head and neck
jvp raised in cor pulmonale, fixed and raised in superior vena cava obstruction
Inspect: for signs of Horner’s, conjunctival pallor, central cyanosis (ask patient to stick out tongue), pursed lip breathing
Apex beat.
Expansion: Ask patient to “breathe all the way out”, place hands as in fig 2, “now a deep breath in”, and note distance of thumbs to midline, is expansion equal? Repeat with hands laid on upper chest, equal?
Tactile vocal fremitus: Ask patient to repeat “99” each time they feel your hand while palpating the chest wall with your fingertips. This is rarely used as more information can be gained from vocal resonance.
Percussion: Percuss over diff erent respiratory segments, comparing right and left.
Auscultation: Ask patient to “take steady breaths in and out through your mouth” and listen with diaphragm from apices to bases, comparing right and left.
Vocal resonance: Repeat auscultation, asking patient to repeat “99” each time they feel the stethoscope. If marked ↑ resonance heard, repeat with asking patient to whisper “99”; if clearly heard this is termed ‘whispering pectoriloquy’ and is a sensitive sign for consolidation. Outside of exams, the choice of vocal resonance or tactile vocal fremitus is a personal preference. Many clinicians prefer vocal resonance as it is an easier skill to master and provides more information than tactile vocal fremitus.
Placement of the hands for testing chest expansion: anchor with the fingers and leave the thumbs free-floating.
Expansion
Tactile vocal fremitus
Percussion
Auscultation
Vocal resonance
Palpate for sacral and ankle oedema
Check peripheral pulses, observation chart for temperature and O2 sats
Examine the sputum pot and check pefr
The respiratory system: examination II
General inspection
”Comfortable at rest” or unwell? Cachectic? Respiratory distress? (see minibox; occurs if high negative intrathoracic pressures are needed to generate air entry). Stridor? Respiratory rate, breathing pattern (see box). Look for chest wall and spine deformities (see p55). Inspect for scars of past surgery, chest drains, or radiotherapy (skin thickening, tattoos for radiotherapy). Chest wall movement: symmetrical? (if not, pathology on restricted side). Paradoxical respiration? (abdomen sucked in with inspiration; seen in diaphragmatic paralysis, see p506).
Hands
Clubbing, peripheral cyanosis, tar stains, fine tremor (β-agonist use), wasting of intrinsic muscles (t1 lesions, eg Pancoast's tumour, p722). Tender wrists (hypertrophic pulmonary osteoarthropathy—cancer). Asterixis (CO2 retention). Pulse: paradoxical (respiratory distress), bounding (CO2 retention).
Face
Neck
Trachea:: Central or displaced? (towards collapse or away from large pleural effusion/tension pneumothorax; slight deviation to right is normal). Cricosternal distance <3cm is hyperexpansion. Tracheal tug: descent of trachea with inspiration (severe airflow limitation). Lymphadenopathy: tb/Ca? jvp: ↑ in cor pulmonale.
Examining the chest:
Palpation
Apex beat: impalpable? (copd/pleural effusion/dextrocardia?) Expansion: <5cm on deep inspiration is abnormal. Symmetry? Tactile vocal fremitus: ↑ implies consolidation (< sensitive than vocal resonance).
Percussion
Dull percussion note: collapse, consolidation, fibrosis, pleural thickening, or pleural effusion (classically ‘stony dull’). Cardiac dullness usually detectable over the left side. Liver dullness usually extends up to 5th rib, right mid-clavicular line; below this, resonant chest is a sign of lung hyperexpansion (eg asthma, copd). Hyperresonant percussion note: pneumothorax or hyperinflation (copd).
Auscultation
Normal ‘vesicular’ breath sounds have a rustling quality. Bronchial breathing: Harsh with a gap between inspiration and expiration, occurs where lung tissue has become firm/solid, eg consolidation, localized fibrosis, above a pleural effusion, or large pericardial effusion (Ewart's sign, p148). May be associated with increased vocal resonance and whispering pectoriloquy. Diminished breath sounds: Pleural effusions, pleural thickening, pneumothorax, bronchial obstruction, asthma, or copd. Silent chest: In life-threatening asthma severe bronchospasm prevents adequate air entry. Added sounds: Wheezes (rhonchi): caused by air expired through narrowed airways. May be monophonic (single note, signifying a partial obstruction of one airway, eg tumour) or polyphonic (multiple notes, signifying widespread narrowing of airways of differing calibre, eg asthma, copd). Wheeze is also heard in lvf (‘cardiac asthma’). Crackles (crepitations): caused by re-opening, during inspiration, of small airways which have become occluded during expiration. May be fine and late in inspiration if coming from distal air spaces (eg pulmonary oedema, fibrosing alveolitis) or coarse and mid-inspiratory if they originate more proximally (eg bronchiectasis). Early inspiratory crackles suggest small airways disease (eg copd), whereas late/pan-inspiratory crackles suggest disease confined to alveoli. Crackles disappearing on coughing are insignificant. Pleural rubs: caused by movement of visceral pleura over parietal pleura, when both surfaces roughened, eg by inflammatory exudate. Causes include adjacent pneumonia or pulmonary infarction.
Tachypnoea
Nasal flaring
Tracheal tug (pulling of thyroid cartilage towards sternal notch in inspiration)
Use of accessory muscles (sternocleidomastoid, platysma, infrahyoid)
Intercostal, subcostal and sternal recession
Pulsus paradoxus (p40)
Pneumothorax click: produced by shallow left pneumothorax between layers of parietal pleura overlying heart, heard during cardiac systole.
Further examination
Sputum (see box), temperature charts, O2 sats, pefr.
may be fast (tachypnoea, ie >20 breaths/min) or deep (hyperpnoea, ie tidal volume ↑). Hyperpnoea is not unpleasant, unlike dyspnoea. It may cause respiratory alkalosis, hence paraesthesiae ± muscle spasm (Ca2+↓). The main cause is anxiety: there is associated dizziness, chest tightness/pain, palpitations, and panic. Rare causes: response to metabolic acidosis; brainstem lesions.
Neurogenic hyperventilation is produced by pontine lesions.
nb: the anxious patient in a&e with hyperventilation and a respiratory alkalosis may actually be presenting with an aspirin overdose (p856).
Breaths get deeper and deeper, then shallower (±episodic apnoea) in cycles. Causes: Brainstem lesions or compression (stroke, icp↑). If the cycle is long (eg 3min), the cause may be a long lung-to-brain circulation time (eg in chronic pulmonary oedema or ↓cardiac output). It is enhanced by opioids.
Always inspect any sputum produced, however unpleasant this task may be. Send suspicious sputum for microscopy (Gram stain and auramine/zn stain, if indicated), culture, and cytology.
Black carbon specks in the sputum suggests smoking, the most common cause of increased sputum production.
Yellow/green sputum suggests infection, eg bronchiectasis, pneumonia.
Pink frothy sputum suggests pulmonary oedema.
Bloody sputum (haemoptysis) may be due to malignancy, tb, infection, or trauma, and requires investigation for these causes. See p49.
Clear sputum is probably saliva.
The respiratory segments supplied by the segmental bronchi.
The respiratory system: important presentations
Physical signs on chest examination.
Barrel chest: ap diameter↑, tracheal descent and chest expansion↓, seen in chronic hyperinflation (eg asthma/copd).
Pigeon chest (pectus carinatum): See fig 2.
Funnel chest (pectus excavatum): Developmental defect involving local sternum depression (lower end). See fig 3.
Kyphosis: ‘Hump-back’ from ↑ ap thoracic spine curvature.
Scoliosis: Lateral curvature (ohcs p672); all of these may cause a restrictive ventilatory defect.
Pectus carinatum (pigeon chest). Prominent sternum, from lung hyperinflation while the bony thorax is still developing, eg in chronic childhood asthma. Often seen with Harrison's sulcus, a groove deformity caused by indrawing of lower ribs at the diaphragm attachment site. This usually has little functional significance in terms of respiration but can have significant psychological effects: see box.
Pectus excavatum; the term for funnel or sunken chest. It is often asymptomatic, but may cause displacement of the heart to the left, and restricted ventilatory capacity ± mild air-trapping. Associations: scoliosis; Marfan's; Ehlers–Danlos syndrome.
Herr Minty and his pigeon chestThe gastrointestinal system: history
| Presenting symptoms | Direct questions |
|---|---|
‘socrates’ (p34) | |
Distension (see box 3) | |
Nausea, vomiting (see box 1) | Timing? Relation to meals? Amount? Content (liquid, solid, bile, blood)? |
Frequency? Fresh (bright red)/dark/’coffee grounds’? Consider neoplasia (weight loss, dysphagia, pain, melaena?), nsaids/warfarin? Surgery? Smoking? | |
Dysphagia (p240) | Level? Onset? Intermittent? Progressive? Painful swallow (odynophagia)? |
Indigestion/dyspepsia/reflux (p242) | Timing (relation to meals)? |
Recent change in bowel habit | Consider neoplasia (weight loss, dysphagia, pain, melaena?) |
Pain on defecation? Mucus? Fresh/ dark/black? Mixed with stool/on surface/on paper/in the pan? | |
Appetite, weight change | Intentional? Quantify. Dysphagia? Pain? |
Jaundice (p250) | Pruritus? Dark urine? Pale stools? |
| Presenting symptoms | Direct questions |
|---|---|
‘socrates’ (p34) | |
Distension (see box 3) | |
Nausea, vomiting (see box 1) | Timing? Relation to meals? Amount? Content (liquid, solid, bile, blood)? |
Frequency? Fresh (bright red)/dark/’coffee grounds’? Consider neoplasia (weight loss, dysphagia, pain, melaena?), nsaids/warfarin? Surgery? Smoking? | |
Dysphagia (p240) | Level? Onset? Intermittent? Progressive? Painful swallow (odynophagia)? |
Indigestion/dyspepsia/reflux (p242) | Timing (relation to meals)? |
Recent change in bowel habit | Consider neoplasia (weight loss, dysphagia, pain, melaena?) |
Pain on defecation? Mucus? Fresh/ dark/black? Mixed with stool/on surface/on paper/in the pan? | |
Appetite, weight change | Intentional? Quantify. Dysphagia? Pain? |
Jaundice (p250) | Pruritus? Dark urine? Pale stools? |
(Screen for all above presenting symptoms before proceeding to past history.)
Past history
Peptic ulcer disease, carcinoma, jaundice, hepatitis, blood transfusions, tattoos, previous operations, last menstrual period (lmp), dietary changes.
Drug history
Especially steroids, nsaids, antibiotics.
Family history
Irritable bowel syndrome (ibs), inflammatory bowel disease (ibd), peptic ulcer disease, polyps, cancer, jaundice.
Social history
Smoking, alcohol, recreational drug use, overseas travel, tropical illnesses, contact with jaundiced persons, occupational exposures, high-risk sexual behaviour.
History is vital. Associated symptoms and past medical history often indicate cause. Examine for dehydration, distension, tenderness, abdominal mass, succussion splash in children (pyloric stenosis), or tinkling bowel sounds (intestinal obstruction).
Gastrointestinal | cns | Metabolic/endocrine |
• Gastroenteritis • Peptic ulceration • Pyloric stenosis • Intestinal obstruction • Paralytic ileus • Acute cholecystitis • Acute pancreatitis | • Meningitis/encephalitis • Migraine • ↑Intracranial pressure • Brainstem lesions • Motion sickness • Ménière's disease • Labyrinthitis | • Uraemia • Hypercalcaemia • Hyponatraemia • Pregnancy • Diabetic ketoacidosis • Addison's disease |
Alcohol and drugs | Psychiatric | Others1 |
• Antibiotics • Opiates • Cytotoxics • Digoxin | • Self-induced • Psychogenic • Bulimia nervosa | • Myocardial infarction • Autonomic neuropathy • Sepsis (uti; meningitis) |
Gastrointestinal | cns | Metabolic/endocrine |
• Gastroenteritis • Peptic ulceration • Pyloric stenosis • Intestinal obstruction • Paralytic ileus • Acute cholecystitis • Acute pancreatitis | • Meningitis/encephalitis • Migraine • ↑Intracranial pressure • Brainstem lesions • Motion sickness • Ménière's disease • Labyrinthitis | • Uraemia • Hypercalcaemia • Hyponatraemia • Pregnancy • Diabetic ketoacidosis • Addison's disease |
Alcohol and drugs | Psychiatric | Others1 |
• Antibiotics • Opiates • Cytotoxics • Digoxin | • Self-induced • Psychogenic • Bulimia nervosa | • Myocardial infarction • Autonomic neuropathy • Sepsis (uti; meningitis) |
How to remember the chief non-gi causes of vomiting? Try abcdefghi: Acute kidney injury Addison's disease; Brain (eg ↑icp); Cardiac (myocardial infarct); Diabetic ketoacidosis; Ears (eg labyrinthitis, Ménière's disease); Foreign substances (alcohol; drugs, eg opiates); Gravidity (eg hyperemesis gravidarum); Hypercalcaemia/Hyponatraemia; Infection (eg uti, meningitis).
Varies depending on the underlying cause. Examples: irritation of the mucosa (acute gastritis), smooth muscle spasm (acute enterocolitis), capsular stretching (liver congestion in ccf), peritoneal inflammation (acute appendicitis) and direct splanchnic nerve stimulation (retro-peritoneal extension of tumour). The character (constant or colicky, sharp or dull), duration, and frequency depend on the mechanism of production. The location and distribution of referred pain depend on the anatomical site. Time of occurrence and aggravating or relieving factors such as meals, defecation, and sleep also have special significance related to the underlying disease process. The site of the pain may provide a clue:
Epigastric Pancreatitis, gastritis/duodenitis, peptic ulcer, gallbladder disease, aortic aneurysm.
Left upper quadrant Peptic ulcer, gastric or colonic (splenic flexure) cancer, splenic rupture, subphrenic or perinephric abscess, renal (colic, pyelonephritis).
Right upper quadrant Cholecystitis, biliary colic, hepatitis, peptic ulcer, colonic cancer (hepatic flexure), renal (colic, pyelonephritis), subphrenic/perinephric abscess.
Loin (lateral ⅓ of back between thorax and pelvis—merges with the flank, p567) Renal colic, pyelonephritis, renal tumour, perinephric abscess, pain referred from vertebral column. Causes of flank pain are similar (see index for fuller list).
Left iliac fossa Diverticulitis, volvulus, colon cancer, pelvic abscess, inflammatory bowel disease, hip pathology, renal colic, urinary tract infection (uti), cancer in undescended testis; zoster—wait for the rash! (p458). Gynae: Torsion of ovarian cyst, salpingitis, ectopic pregnancy.
Right iliac fossa pain All causes of left iliac fossa pain plus appendicitis and Crohn's ileitis, but usually excluding diverticulitis.
Pelvic Urological: uti, retention, stones. Gynae: Menstruation, pregnancy, endometriosis (ohcs p288), salpingitis, endometritis (ohcs p274), ovarian cyst torsion.
Generalized Gastroenteritis, irritable bowel syndrome, peritonitis, constipation.
Central Mesenteric ischaemia, abdominal aneurysm, pancreatitis.
Remember referred pain: Myocardial infarct → epigastrium; pleural pathology.
Enid Blyton's Famous Five characters can generally solve any crime or diagnostic problem using 1950s methodologies steeped in endless school holidays, copious confectionladen mid-night feasts, and lashings of homemade ginger beer.
Let's give them the problem of abdominal distension. The sweets and drinks used by the Famous Five actually contribute to the distension itself: fat, fluid, faeces, flatus, and fetus. If you think it far-fetched to implicate ginger beer in the genesis of fetuses, note that because it was homemade, like the fun, there was no limit to its intoxicating powers in those long-gone vintage summers. The point is to think to ask “When was your last period?” whenever confronted by a distended abdomen.
Flatus will be resonant on percussion. Fluid will be dull, and can be from ascites (eg from malignancy or cirrhosis: look for shifting dullness), distended bladder (cannot get below it) or an aortic aneurysm (expansile). Masses can be pelvic (think of uterine fibroids or ovarian pathology) or tumours from colon, stomach, pancreas, liver, or kidney. Also see causes of ascites with portal hypertension (p606), hepatomegaly (p63), splenomegaly, and other abdominal masses (p606).
Gastrointestinal symptoms
This is common in the elderly. Do your best to help, and get social services involved if concerned. Continence depends on many factors—mental function, stool (volume and consistency), anatomy (sphincter function, rectal distensibility, anorectal sensation and reflexes). Defects in any area can cause loss of faecal continence.
often multifactorial. Is it passive faecal soiling or urgency-related stool loss? Consider the following:
Sphincter dysfunction:
Vaginal delivery is the commonest cause due to sphincter tears or pudendal nerve damage.
Surgical trauma, eg following procedures for fistulas, haemorrhoids, fissures.
Impaired sensation: diabetes, ms, dementia, any spinal cord lesions (consider cord compression if acute faecal incontinence).
Faecal impaction: overflow diarrhoea, extremely common, especially in the elderly, and very easily treated.
Idiopathic: although there is often no clear cause found, especially in elderly women, this is usually multifactorial, including a combination of poor sphincter tone and pudendal damage leading to poor sensation.
Do pr (overflow incontinence? poor tone?) and assess neurological function of legs, particularly checking sensation.
Never let your own embarrassment stop you from offering help. Knowledge and behaviour are key factors:
Ensure toilet is in easy reach. Plan trips away in the knowledge of toilet locations.
Obey call-to-stool impulses (esp. after meal, ie the gastro-colic reflex).
Ensure access to latest continence aids and advice on use, refer to continence nurse specialist for assessment.
If all sensible measures fail, try a brake-and-accelerator approach: enemas to empty the rectum (twice weekly) and codeine phosphate, eg 15mg/12h, on non-enema days to constipate. It's not a cure, but makes the incontinence manageable.
This is a sensation in the rectum of incomplete emptying after defecation. It's common in irritable bowel syndrome (p276), but can be caused by tumours.
Gastric and oesophageal contents are regurgitated effortlessly into the mouth—without contraction of abdominal muscles and diaphragm (so distinguishing it from true vomiting). It may be worse on lying flat, and can cause cough and nocturnal asthma. Regurgitation is rarely preceded by nausea, and when due to gastrooesophageal reflux, it is often associated with heartburn. An oesophageal pouch may cause regurgitation. Very high gi obstructions (eg gastric volvulus, p613) cause non-productive retching rather than true regurgitation.
These are pale stools that are difficult to flush, and are caused by malabsorption of fat in the small intestine and hence greater fat content in the stool.
Ileal disease (eg Crohn's or ileal resection), pancreatic disease, and obstructive jaundice (due to ↓excretion of bile salts from the gallbladder).
Smoking, drugs (disulfiram; isosorbide), lung disease, hangovers.
Try to eliminate anaerobes:
Good dental hygiene, dental floss, tongue scraping.
0.2% aqueous chlorhexidine gluconate.
The very common halitosis arising from the tongue's dorsum is secondary to overpopulated volatile sulfur compound-producing bacteria. Locally retained bacteria metabolize sulfur-containing amino acids to yield volatile (∴ smelly) hydrogen sulfide and methylmercaptane, which perpetuate periodontal disease. At night and between meals conditions are optimal for odour production—so eating regularly may help. Treat by mechanical cleansing/scraping using tongue brushes or scrapes plus mouthwashes. Oral care products containing metal ions, especially Zn, inhibit odour formation, it is thought, because of affinity of the metal ion to sulfur. It is possible to measure the level of volatile sulfur-containing compounds in the air in the mouth directly by means of a portable sulfide monitor.
Examination of the abdomen
As with any examination routine, begin by introducing yourself, obtaining consent to examine the patient and position them appropriately. To examine the abdomen, lie the patient down as flat as possible, ideally exposing from ‘nipples to knees’ although in practice keep the groin covered and examine separately for hernias, etc.
Assess general state (ill/well/cachexic)
Look for clues (vomit bowl, stoma bags)
Colour (pale, jaundiced, uraemic)
Body mass index?
Scars on the abdomen? Stomas?
Ask the patient to lift their head off the bed, or cough, looking for bulges, distension or pain
Inspect: clubbing, koilonychia, leuconychia, Muehrcke’s lines, palmar erythema, Dupuytren’s contracture, pigmentation of the palmer creases
Asterixis: (see fig 1, p50)
Check pulse and blood pressure
Look in the distribution of the svc (arms, upper chest, upper back) for spider naevi
Check for track marks, bruising, pigmentation, scratch marks, arteriovenous fistulae (see p295 for signs seen in patients with chronic kidney disease)
Examine cervical and supraclavicular lymph nodes (see fig 1)
jvp raised in fluid overload (renal dysfunction, liver dysfunction), tricuspid regurgitation (may cause pulsatile hepatomegaly)
Scars from tunnelled haemodialysis lines (see p295) or other central venous access
Cervical and supraclavicular nodes.
Skin and eyes: jaundice, conjunctival pallor, Kayser–Fleischer rings, xanthelasma, sunken eyes (dehydration)
Mouth: angular stomatitis, pigmentation, telangiectasia, ulcers, glossitis
Scars—previous surgery, transplant, stoma
Visible masses, hernias or pulsation of aaa
Visible veins suggesting portal hypertension
Gynaecomastia, hair loss, acanthosis nigricans
Squat by the bed so that the patient’s abdomen is at your eye level. Ask if there is any pain and examine this part last. Watch the patient’s face for signs of discomfort. Palpate the entire abdomen (see p567):
Light palpation: If this elicits pain, check for rebound tenderness. Any involuntary tension in muscles (‘guarding’)? See p608.
Deep palpation: To detect masses.
Liver: Using the radial border of the index finger aligned with the costal margin start palpation from the rif. Press down and ask patient to take a deep breath. Continue upwards towards the costal margin until you feel the liver edge.
Spleen: Start palpation from the rif and work towards the left costal margin asking the patient to take a deep breath in and feeling for the edge of the spleen—much like palpating the liver.
Aorta: Palpate midline above umbilicus, is it expansile? (fig 2, p47).
Liver: Percuss to map upper & lower border of liver.
Spleen: Percuss from border of spleen as palpated, around to mid-axillary line.
Bladder: If enlarged, suprapubic region will be dull.
Ascites: Shifting dullness: Percuss centrally to laterally until dull, keep your finger at the dull spot and ask patient to lean onto opposite side. If the dullness was fluid, this will now have moved by gravity and the previously dull area will be resonant.
Bowel sounds: Listen just below the umbilicus.
Bruits: Listen over aorta and renal arteries (either side of midline above umbilicus)
Palpate for ankle oedema, examine the hernial orifices, external genitalia and perform a rectal examination
Check the observation chart for temperature and dipstick the urine
If you think there is a spleen tip, roll the patient onto their right side and feel again. This tips the spleen forward and allows you to percuss around to the back (try to do this at the same time as shifting dullness to look super slick)
Don't forget to check the back for spider naevi, even if the chest appears clear, you can miss a valuable sign (look for nephrectomy scars as you do this)
Light palpation really should be light, a quick check for tenderness and very large masses, watching the patient's face throughout
The gastrointestinal system: examination
Inspection
Does your patient appear comfortable or in distress? Look for abnormal contours/distension. Tattoos? Cushingoid appearance may suggest steroid use post-transplant or ibd. Inspect (and smell) for signs of chronic liver disease:
Look for signs of malignancy (cachexia, masses), anaemia, jaundice, Virchow's node. From the end of the bed inspect the abdomen for:
Visible pulsation (aneurysm, p656)
Striae (stretch marks, eg pregnancy)
Peristalsis
Distension
Scars
Genitalia
Masses
Herniae
If abdominal wall veins look dilated, assess direction of flow. In inferior vena caval (ivc) obstruction, below the umbilicus blood flows up; in portal hypertension (caput medusae), flow radiates out from the umbilicus.
The cough test:
While looking at the face, ask the patient to cough. If this causes abdominal pain, flinching, or a protective movement of hands towards the abdomen, suspect peritonitis.
Hands
Clubbing, leuconychia (whitening of the nails due to hypoalbuminaemia), koilonychia (‘spooning’ of the nails due to iron, B12, or folate deficiency), Muehrcke's lines (transverse white lines due to hypoalbuminaemia), blue lanulae (bluish discolouration seen in Wilson's disease). Palmar erythema (chronic liver disease, pregnancy), Dupuytren's contracture (thickening and fibrous contraction of palmar fascia (see fig 1, p713; alcoholic liver disease)). Hepatic flap/asterixis (hepatic encephalopathy, uraemia from renal disease), check pulse (and respiratory rate) (infection/sepsis?), palpate for arteriovenous fistulae in the forearm (access for haemodialysis in end-stage renal failure).
Face
Assess for jaundice, anaemia, xanthelasma (pbc, chronic obstruction), Kayser–Fleischer rings (green-yellow ring at corneal margin seen in Wilson's disease). Inspect mouth for angular stomatitis (thiamine, B12, iron deficiency), pigmentation (Peutz–Jeghers syndrome, p723, fig 3), telangiectasia (Osler–Weber–Rendu syndrome/hereditary haemorrhagic telangiectasia, p723, fig 1), ulcers (ibd), glossitis (iron, B12, or folate deficiency).
Cervical lymph nodes
Palpate for enlarged left supraclavicular lymph node (Virchow's node/Troisier's sign) (gastric carcinoma?).
Abdomen
Inspect:
Look around to the flanks for nephrectomy scars.
Palpate:
Palpating the liver:
Assess size (see box), regularity, smoothness, and tenderness. Pulsatile (tricuspid regurgitation)? The scratch test is an another way to find the lower liver edge (if it is below the costal margin): start with diaphragm of stethoscope at right costal margin. Gently scratch the abdominal wall, starting in the right lower quadrant, working towards the liver edge. A sharp increase in transmission of the scratch is heard when the border of the liver is reached.
Palpating the spleen:
If suspect splenomegaly but cannot detect it, assess patient in the right lateral position with your left hand pulling forwards from behind the rib cage.
Palpating the kidneys:
see fig 1. Enlarged? Nodular?
Ballottement of the kidneys.
Palpating the aorta:
Normally palpable transmitted pulsation in thin individuals.
Percussion
Auscultation
Bowel sounds: absence implies ileus; they are enhanced and tinkling in bowel obstruction. Listen for bruits in the aorta, renal and femoral arteries.
Further examination
(For hepatosplenomegaly, see p606)
Malignancy: Metastatic or primary (usually craggy, irregular edge).
Hepatic congestion: Right heart failure—may be pulsatile in tricuspid incompetence, hepatic vein thrombosis (Budd–Chiari syndrome, p710).
Anatomical: Riedel's lobe (normal variant).
Infection: Infectious mononucleosis (glandular fever), hepatitis viruses, malaria, schistosomiasis, amoebic abscess, hydatid cyst.
Haematological: Leukaemia, lymphoma, myeloproliferative disorders (eg myelofibrosis), sickle-cell disease, haemolytic anaemias.
Others: Fatty liver, porphyria, amyloidosis, glycogen storage disorders.
Abnormally large spleen.
See p606. If massive, think of: chronic myeloid leukaemia, myelofibrosis, malaria (or leishmaniasis).
Cannot get above it (ribs overlie the upper border of the spleen).
Dull to percussion (kidney is usually resonant because of overlying bowel).
Moves towards rif with inspiration (kidney tends to move downwards).
May have palpable notch on its medial side.
The genitourinary system: history
| Presenting symptoms | Direct questions |
|---|---|
Dysuria (see box 1) | Pain: socrates (p34). Fever? Sexual history. |
Lower urinary tract symptoms (luts) | Abnormal looking urine? Previous problems. |
Must rule out testicular torsion (p654). | |
Menses (ohcs, p250) | Ask about menarche, menopause, length of periods, amount, pain? Intermenstrual loss? 1st day of last menstrual period (lmp)? |
| Presenting symptoms | Direct questions |
|---|---|
Dysuria (see box 1) | Pain: socrates (p34). Fever? Sexual history. |
Lower urinary tract symptoms (luts) | Abnormal looking urine? Previous problems. |
Must rule out testicular torsion (p654). | |
Menses (ohcs, p250) | Ask about menarche, menopause, length of periods, amount, pain? Intermenstrual loss? 1st day of last menstrual period (lmp)? |
Detecting outflow obstruction
(see box 5) eg prostatic hyperplasia; stricture; stone). Ask about luts (lower urinary tract symptoms)
On trying to pass water, is there delay before you start? (Hesitancy)
Does the flow stop and start? Do you go on dribbling when you think you've stopped? (Terminal dribbling)
Is your stream getting weaker? (Poor stream)
Is your stream painful and slow/‘drop-by-drop’? (Strangury, eg from bladder stone)
Do you feel the bladder is not empty after passing water?i
Do you ever pass water when you do not want to? (Incontinence—p650)
On feeling an urge to pass water, do you have to go at once? (Urgency)i
Do you urinate often at night? (Nocturia)i In the day? (Frequency)i How often?
i = irritative (or ‘filling’) symptoms: they can be caused by, for example, uti, as well as obstructions.
Past history
Renal colic, urinary tract infection, diabetes, bp↑, gout, analgesic use (p306), previous operations.
Drug history
Anticholinergics.
Family history
Prostate carcinoma? Renal disease?
Social history
Smoking, sexual history.
Voiding difficulty is a sign of outflow obstruction, eg from an enlarged prostate, or urethral stricture (commonly post-traumatic, post-gonococcal). Other features: straining to void, poor stream, urinary retention, and incontinence. Strangury is urethral pain, usually referred from the bladder base, causing a constant distressing desire to urinate even if there is little urine to void.
Aim to differentiate ↑urine production (eg diabetes mellitus and insipidus, polydipsia, diuretics, alcohol, renal tubular disease, adrenal insufficiency) from frequent passage of small amounts of urine (eg in cystitis, urethritis, neurogenic bladder), or bladder compression or outflow obstruction (pregnancy, bladder tumour, enlarged prostate).
Oliguria is defined as a urine output of <400mL/24h or <0.5mL/kg/hour and can be a sign of shock (eg post-op, p578) or acute kidney injury: causes: p290. Anuria is defined as <50mL/24h. In a catheterized patient with sudden anuria consider catheter blockage, with slow decline of oliguria to anuria renal dysfunction is more likely.
Increased urine volume, eg >3L/24h.
Over-enthusiastic iv fluid therapy; diabetes mellitus & insipidus (diabetes is Greek for fountain); ↑Ca2+; psychogenic polydipsia/pip syndrome (p232); polyuric phase of recovering acute tubular necrosis.
(see also p644)
Symptoms of prostate enlargement are miscalled ‘prost-atism’; it is better to talk about irritative or obstructive bladder symptoms, as bladder neck obstruction or a stricture may be the cause.
Urgency, dysuria, frequency, nocturia6 (the last two are also associated with causes of polyuria).
Reduced size and force of urinary stream, hesitancy and interruption of stream during voiding and terminal dribbling—the usual cause is enlargement of the prostate (prostatic hyperplasia), but other causes include a urethral stricture, tumour, urethral valves, or bladder neck contracture. The maximum flow rate of urine is normally ∼18–30mL/s.
Dribbling at the end of urination, often seen in conjunction with incontinence following incomplete urination, associated with prostatism.
Cloudy urine suggests pus (uti) but is often normal phosphate precipitation in an alkaline urine. Pneumaturia (bubbles in urine as it is passed) occurs with uti due to gas-forming organisms or may signal an enterovesical (bowel–bladder) fistula from diverticulitis, Crohn's disease or neoplastic disease of the bowel. Nocturia occurs with ‘irritative bladder’, diabetes mellitus, uti, and reversed diurnal rhythm (seen in renal and cardiac failure). Haematuria (rbc in urine) is due to neoplasia or glomerulonephritis (p300) until proven otherwise.
This includes poor flow, straining to void, hesitancy, intermittent stream, incontinence (eg overflow), retention (acute or chronic), incomplete emptying (±uti from residual urine). Remember faecal impaction as a cause of retention with overflow.
The breast: history
| Presenting symptoms | Direct questions |
|---|---|
Breast lump | Previous lumps? Family history? Pain? Nipple discharge? Nipple inversion? Skin changes? Change in size related to menstrual cycle? Number of pregnancies? First/last/latest period? Postnatal? Breast feeding? Drugs (eg hrt)? Consider metastatic disease (weight loss, breathlessness, back pain, abdominal mass?) |
Breast pain (see box 1) | socrates (p34). Bilateral/unilateral? Rule out cardiac chest pain (p88 & p798). History of trauma? Any mass? Related to menstrual cycle? |
Nipple discharge (see box 2) | Amount? Nature (colour? consistency? any blood?) |
| Presenting symptoms | Direct questions |
|---|---|
Breast lump | Previous lumps? Family history? Pain? Nipple discharge? Nipple inversion? Skin changes? Change in size related to menstrual cycle? Number of pregnancies? First/last/latest period? Postnatal? Breast feeding? Drugs (eg hrt)? Consider metastatic disease (weight loss, breathlessness, back pain, abdominal mass?) |
Breast pain (see box 1) | socrates (p34). Bilateral/unilateral? Rule out cardiac chest pain (p88 & p798). History of trauma? Any mass? Related to menstrual cycle? |
Nipple discharge (see box 2) | Amount? Nature (colour? consistency? any blood?) |
(Screen for all above presenting symptoms before proceeding to past history.)
Past history
Any previous lumps and/or malignancies. Previous mammograms, clinical examinations of the breast, uss, fine-needle aspirate (fna)/core biopsies.
Drug history
Ask specifically about hrt and the Pill.
Family history
See p524.
Social history
Try to gain an impression of support network if suspect malignancy.
Is it premenstrual (cyclical mastalgia, ohcs p254)? Breast cancer (refer, eg, for mammography if needed)? If non-malignant and non-cyclical, think of:
Tietze's syndrome7
Bornholm disease8
Angina
Gallstones
Lung disease
Thoracic outlet syndrome
Oestrogens/hrt
If none of the above, wearing a firm bra all day may help, as may nsaids.
Duct ectasia (green/brown/red, often multiple ducts and bilateral), intraductal papilloma/adenoma/carcinoma (bloody discharge, often single duct), lactation.
Diagnose the cause (mammogram, ultrasound, ductogram); then treat appropriately. Cessation of smoking reduces discharge from duct ectasia. Microdochectomy/total duct excision can be considered if other measures fail, though may give no improvement in symptoms.
The breast: examination
Inspection Assess size and shape of any masses as well as overlying surface. Which quadrant (see fig 2)? Note skin involvement; ulceration, dimpling (peau d'orange), and nipple inversion/discharge.
Palpation of the breast Confirm size, and shape of any lump. Is it fixed/tethered to skin or underlying structures (see box)? Is it fluctuant/compressible/hard? Temperature? Tender? Mobile (more likely to be fibroadenoma)?
Palpation of the axilla for lymph nodes Metastatic spread? Ipsilateral/bilateral? Matted? Fixed?
Further examination Examine abdomen for hepatomegaly, spine for tenderness, lungs (metastatic spread).
Always have a chaperone present when examining the breast.
Introduction, consent, position patient sitting at edge of bed with hands by her side, expose to waist. Inspect both breasts for obvious masses, contour anomalies, asymmetry, scars, ulceration, skin changes, eg peau d’orange (orange peel appearance resulting from oedema). Look for nipple inversion and nipple discharge. Ask her to “press hands on hips” and then “hands on head” to accentuate any asymmetrical changes. Whilst patient has her hands raised inspect axillae for any masses as well as inspecting under the breasts.
Position patient sitting back at 45° with hand behind head (ie right hand behind head when examining the right breast—see fig 1). Ask patient if she has any pain or discharge. Examine painful areas last and then ask her to express any discharge. Examine each breast with the ‘normal’ side first. Examine each quadrant in turn as well as the axillary tail of Spence (fig 2) or use a concentric spiral method (fig 3) using a flat hand to roll breast against underlying chest wall. Define any lumps/lumpy areas. If you discover a lump, to examine for fixity to the pectoral muscles ask the patient to push against your hand with her arm outstretched.
Correct patient position for breast examination.
The quadrants of the breast with the axillary tail of Spence.
Methods for systematic breast palpation.
Examine both axillae. When examining right axilla, hold the patient’s right arm with your right hand and examine axilla with left hand.
5 sets of axillary nodes:
apical (palpate against glenohumeral joint)
anterior (palpate against pectoralis major)
central (palpate against lateral chest wall)
posterior (palpate against latissimus dorsi)
medial (palpate against humerus)
Complete examination by palpating down spine for tenderness, examining abdomen for hepatomegaly, and lungs for signs of metastases. Thank patient and wash hands.
The thyroid: examination
Inspection The key questions to ask oneself when presented with a lump in the neck are: Is this lump thyroid related or not? What is the patient's thyroid status? Inspect the neck; the normal thyroid is usually neither visible nor palpable. A midline swelling should raise your suspicion of thyroid pathology. Look for scars (eg collar incision from previous thyroid surgery). Examine the face for signs of hypothyroidism (puffiness, pallor, dry flaky skin, xanthelasma, corneal arcus, balding) as well as overall body habitus. Assess the patient's demeanour; do they appear anxious, nervous, agitated, fidgety (hyperthyroid)? Or slow and lethargic (hypothyroid)?
Tongue protrusion test A thyroglossal cyst will move up on tongue protrusion.
Palpation (By this stage of the examination if the evidence is in favour of the lump not rising from the thyroid it is acceptable to examine the lump like any other (p596); assess site, size, shape, smoothness (consistency), surface (contour/edge/colour), and surroundings, as well as transilluminance, fixation/tether-ing, fluctuance/compressibility, temperature, tenderness and whether it is pulsatile.) If a thyroid mass is suspected, standing behind the patient provides an opportunity to check for any proptosis (hyperthyroidism). Proceed to palpate each lobe, attempting to decide whether any lump is solitary or multiple, nodular or smooth/diffuse as well as site, size, etc. Repeating the swallow test whilst palpating allows you to confirm the early finding, but also attempt to ‘get below the lump’. If there is a distinct inferior border under which you can place your hand with the entire lump above it then the goitre is unlikely to have retrosternal extension. Examining for ‘spread’ to the lymph nodes is particularly important if you suspect a thyroid malignancy (p602). Complete palpation by assessing if the presence of the lump has caused the trachea to deviate from the midline.
Percussion A retrosternal goitre will produce a dull percussion note when the sternum is percussed.
Auscultation A bruit in a smooth thyroid goitre is suggestive of Graves’ disease (p210).
The next stages of the exam are to examine the systemic signs of thyroid status.
Hands Clubbing (‘thyroid acropachy’) is seen in Graves’ disease. Palmar erythema and a fine tremor are also signs of thyrotoxicosis. Assess temperature (warm peripheries if hyperthyroid) and the radial pulse; tachycardia and atrial fibrillation are seen in hyperthyroidism, while bradycardia is seen in hypothyroidism).
Eyes The ‘normal’ upper eyelid should always cover the upper eye such that the white sclera is not visible between the lid and the iris. In hyperthyroidism with exophthalmus there is proptosis as well as lid retraction and ‘lid lag’ may also be detected. If the patient reports double vision when eye movements are being tested this indicates ophthalmoplegia of hyperthyroidism.
Asking the patient to stand allows you to assess whether there is any proximal myopathy (hypothyroidism). Look for pretibial myxoedema (brown swelling of the lower leg above the lateral malleoli in Graves’ disease). Finally, test the reflexes; these will be slow relaxing in hypothyroidism and brisk in hyperthyroidism.
Thank the patient and consider whether the lump is a goitre, and if so whether it is single/multiple, diffuse/nodular, as well as the patient's thyroid status. Decide on a diagnosis (p602).
Introduction, consent, position patient sitting on a chair (with space behind), adequately expose neck. Inspect from front and sides for any obvious goitres or swellings, scars, signs of hypo-/hyperthyroidism.
Standing in front of the patient ask them to “sip water…hold in your mouth …and swallow” to see if any midline swelling moves up on swallowing.
Ask patient to "stick out your tongue". Does the lump move up?
If evidence favours lump not arising from thyroid, examine lump like any other (p596)
Stand behind the patient.
Proptosis: (p211) whilst standing behind the patient ask them to tilt their head back slightly; this will give you a better view to assess any proptosis than when assessing the other aspects of eye pathology from front on, as in 8)
The thyroid gland: ask the patient “any pain?” Place middle 3 fingers of either hand along midline below chin and ‘walk down’ to thyroid. Assess any enlargement/ nodules
Swallow test: repeat as before, now palpating; attempt to ‘get under’ the lump
Lymph nodes: examine lymph nodes of head and neck (p60). Stand in front of the patient
Trachea: palpate for tracheal deviation from the midline.
Percuss the sternum for dullness of retrosternal extension of a goitre.
Listen over the goitre for a bruit.
Inspect: for thyroid acropachy (clubbing) and palmar erythema
Temperature
Pulse: rate and rhythm
Fine tremor: ask patient to “hold hands out”, place sheet of paper over outstretched hands to help.
Exophthalmos: inspect for lid retraction and proptosis (p211)
Lid lag: ask patient to “look down following finger” as you move your finger from a point above the eye to below
Eye movements: Ask patient to follow your finger, keeping their head still, as you make an ‘H’ shape. Any double vision?
Ask patient to stand up from the chair to assess for proximal myopathy, look for pretibial myxoedema, test ankle reflexes (ask patient to face away from you with knee resting on chair). Thank patient and wash hands.
The neurological system: history
History
This should be taken from the patient and if possible from a close friend or relative as well for corroboration/discrepancies. The patient's memory, perception, or speech may be affected by the disorder, making the history difficult to obtain. Note the progression of the symptoms and signs: gradual deterioration (eg tumour) vs intermittent exacerbations (eg multiple sclerosis) vs rapid onset (eg stroke). Ask about age, occupation and ethnic origin. Right- or left-hand dominant?
Presenting symptoms
Headache: (p460 & p794) Different to usual headaches? Acute/chronic? Speed of onset? Single/recurrent? Unilateral/bilateral? Associated symptoms (eg aura with migraine, p462)? Any meningism (p832)? Worse on waking (↑icp)? Decreased conscious level? Take a ‘worst-ever’ headache very seriously. (See p763)
Muscle weakness: (p470) Speed of onset? Muscle groups affected? Sensory loss? Any sphincter disturbance? Loss of balance? Associated spinal/root pain?
Visual disturbance: (ohcs p410) eg blurring, double vision (diplopia), photophobia, visual loss. Speed of onset? Any preceding symptoms? Pain in eye?
Change in other senses: Hearing (p468), smell, taste? Abnormalities are not always due to neurological disease, consider ent disease.
Dizziness: (p466) Illusion of surroundings moving (vertigo)? Hearing loss/tinnitus? Any loss of consciousness? Positional?
Speech disturbance: (p80) Difficulty in expression, articulation, or comprehension (can be difficult to determine)? Sudden onset or gradual?
Dysphagia: (p240) Solids and/or liquids? Intermittent or constant? Difficulty in coordination? Painful (odynophagia)?
Fits/faints/‘funny turns’/involuntary movements: (p472) Frequency? Duration? Mode of onset? Preceding aura? Loss of consciousness? Tongue biting? Incontinence? Any residual weakness/confusion? Family history?
Abnormal sensations: eg numbness, ‘pins & needles’ (paraesthesiae), pain, odd sensations. Distribution? Speed of onset? Associated weakness?
Tremor: (p71) Rapid or slow? Present at rest? Worse on deliberate movement? Taking β-agonists? Any thyroid problems? Any family history? Fasciculations?
Cognitive state
1 Tell patient an address to recall at the end (eg 42 West Street) 2 Age 3 Time (to nearest hour) 4 What year is it? 5 Recognize 2 people (eg doctor & nurse) 6 Date of birth 7 Dates of the Second World War 8 Name of current monarch/prime minister 9 Where are you now? (Which hospital?) 10 Count backwards from 20 to 1 | A score of ≤6 suggests poor cognition, acute (delirium), or chronic (dementia). amts correlates well with the more detailed Mini-Mental State Examination (mmse™), though recent copyright means that its use has become more restricted. nb: deaf, dysphasic, depressed, and uncooperative patients, as well as those who do not understand English, will also get low scores (tym test: see p85). |
1 Tell patient an address to recall at the end (eg 42 West Street) 2 Age 3 Time (to nearest hour) 4 What year is it? 5 Recognize 2 people (eg doctor & nurse) 6 Date of birth 7 Dates of the Second World War 8 Name of current monarch/prime minister 9 Where are you now? (Which hospital?) 10 Count backwards from 20 to 1 | A score of ≤6 suggests poor cognition, acute (delirium), or chronic (dementia). amts correlates well with the more detailed Mini-Mental State Examination (mmse™), though recent copyright means that its use has become more restricted. nb: deaf, dysphasic, depressed, and uncooperative patients, as well as those who do not understand English, will also get low scores (tym test: see p85). |
Past medical history
Ask about meningitis/encephalitis, head/spine trauma, seizures, previous operations, risk factors for vascular disease (p474, af, hypertension, hyperlipidaemia, diabetes, smoking), and recent travel, especially exotic destinations. Is there any chance that the patient is pregnant (eclampsia, ohcs p48)?
Drug history
Any anticonvulsant/antipsychotic/antidepressant medication? Any psychotropic drugs (eg ecstasy)? Any medication with neurological side-effects (eg isoniazid which can cause a peripheral neuropathy)?
Social and family history
Diuretics (? from K+↓), domperidone, salbutamol/terbutaline ivi, ace-i, telmisartan, celecoxib, lacidipine, ergot alkaloids, levothyroxine.
‘Pins and needles’, numbness/tingling, which can hurt or ‘burn’ (dysaes-th-esia).
↓Ca2+ (perioral); PaCO2↑; myxoedema; neurotoxins (tick bite; sting).
Arterial emboli; Raynaud's; dvt; high plasma viscosity.
ace-i.
Thalamic/parietal lesions.
Tremor is rhythmic oscillation of limbs, trunk, head, or tongue. 3 types:
Resting tremor—worst at rest—eg from parkinsonism (±bradykinesia and rigidity; tremor is more resistant to treatment than other symptoms). It is usually a slow tremor (frequency of 3–5Hz), typically ‘pill-rolling’ of the thumb over a finger.
Intention tremor—worst on movement, seen in cerebellar disease, with past-pointing and dysdiadochokinesis (see p503). No effective drug has been found.
Neck | Cervical disc pathology |
Bone/sinuses | Sinusitis; neoplasia |
Eye | Glaucoma; iritis; orbital cellulitis; eye strain; avm |
Temporomandibular joint | Arthritis or idiopathic dysfunction (common) |
Teeth/gums | Caries; broken teeth; abscess; malocclusion |
Ear | Otitis media; otitis externa |
Vascular/vasculitis |
Neck | Cervical disc pathology |
Bone/sinuses | Sinusitis; neoplasia |
Eye | Glaucoma; iritis; orbital cellulitis; eye strain; avm |
Temporomandibular joint | Arthritis or idiopathic dysfunction (common) |
Teeth/gums | Caries; broken teeth; abscess; malocclusion |
Ear | Otitis media; otitis externa |
Vascular/vasculitis |
Neurological examination of the upper limbs
The neurological system is usually the most daunting examination, so learn at the bedside from a senior colleague, preferably a neurologist. Keep practising. Be aware that books present ideal situations: often one or more signs are equivocal or even contrary to expectation; consider signs in the context of the history and try re-examining the patient, as signs may evolve over time. The only essential point is to distinguish whether weakness is upper (umn) or lower (lmn) motor neuron (p451). Position the patient comfortably, sitting up at 45° and with arms exposed. The general order of examination should be Tone, Reflexes, Power, Coordination, Sensation.
Abnormal posturing, asymmetry, abnormal movements (fasciculation/tremor/dystonia/athetosis), muscle wasting (especially small muscles of the hand)—symmetrical/asymmetrical? Local/general?
Ask patient to "relax/go floppy like a rag-doll". Ask if patient has any pain in hands/arm/shoulder before passively flexing and extending limb while also pronating and supinating the forearm. Any spasticity or rigidity?
Testing tone.
Direct patient to adopt each position and follow commands while you as the examiner stabilise the joint above and resist movements as appropriate to grade power. Test each muscle group bilaterally before moving on to the next position.
“Shrug your shoulders and don’t let me push down; push your arms out to the side against me; try to pull them back in”
“Hold your arms up like this and pull me towards you, now push me away”
“Hold your hand out flat, don’t let me push it down; now don’t let me push it up”
Offer the patient two of your fingers and ask them to “squeeze my fingers”
Ask patient to “spread your fingers and stop me pushing them back together”, then hand the patient a piece of paper to grip between two fingers. You as the examiner should grip the paper with your corresponding fingers whilst asking patient to “grip the paper and don’t let me pull it away”.
Testing limb power.
For each reflex, test right, then left and compare. If absent, attempt to elicit with ‘reinforcement’ by asking patient to clench their teeth on a count of 3 at which time you strike. Decide whether reflexes are absent/present (with reinforcement)/normal/ brisk/exaggerated.
Biceps: (C5,6)
Triceps: (C7)
Supinator: (C6). See below.
Holding your finger in front of the patient instruct “touch my finger then your nose…as fast as you can”. Look for intention tremor and ‘past pointing’.
Test for dysdiadokokinesis: Ask patient to repeatedly pronate and supinate forearm, clapping the hands each time. Test both limbs. You may have to demonstrate. Failure to perform rapidly alternating movements is dysdiadokokinesis.
Test for pronator drift: with patient’s eyes closed and arms outstretched tap down on their up-facing palms and look for a failure to maintain supination.
Testing tendon reflexes in biceps.
Light touch: Use cotton wool, touch it to sternum first—"this is what it should feel like, tell me where you feel it and if it feels diff erent". Proceed to test with cotton wool in all dermatomes (see p458), comparing left and right.
Pin prick: Repeat as above using a neurological pin, asking patient to tell you if it feels sharp or dull.
Temperature: Repeat as above, alternating hot and cold probes. Can the patient tell hot from cold?
Vibration: Using a 128Hz tuning fork confirm with patient that they “can feel a buzzing” when you place the tuning fork on their sternum. Proceed to test at the most distal bony prominence and move proximally by placing the buzzing fork on the bony prominence, then stopping it with your fingers. Ask the patient to tell you when the buzzing stops.
Proprioception: With the patient’s eyes closed grasp distal phalanx of the index finger at the sides. Stabilize the rest of the finger. Flex and extend the joint, stopping at intervals to ask whether the finger tip is up or down.
Use the tendon hammer like a pendulum, let it drop, don't grip it too tightly
Ensure you are testing light touch, not stroke sensation
Neurological examination of the lower limbs
If the patient is able to walk, the best way to begin your examination is to ask the patient to remove their lower garments down to underwear, and to walk across the room. Gait analysis (p471) gives you more information than any other test. If they aren't able to walk, start with them lying down, legs fully exposed. The general routine should be Gait, Tone, Reflexes, Power, Coordination, Sensation.
Ask patient to walk a few metres, turn and walk back to you. Note use of walking aids, symmetry, size of paces, arm swing. Ask patient to “walk heel-to-toe as if on a tightrope” to exaggerate any instability. Ask patient to walk on tiptoes, then on heels. Inability to walk on tiptoes indicates S1 or gastroc nemius lesion. Inability to walk on heels indicates L4,5 lesion or foot drop.
Ask patient to stand unaided with arms by their sides and close their eyes (be ready to support them). If they sway/ lose balance the test is positive and indicates posterior column disease/ sensory ataxia.
Abnormal posturing, muscle wasting, fasciculation (lmn lesion?), deformities of the foot (eg pes cavus of Friedreich’s ataxia or Charcot–Marie–Tooth disease). Is one leg smaller than the other (old polio, infantile hemiplegia)?
Ask patient to “relax/go floppy like a rag-doll”. Ask if they have any pain in feet/legs/hips before passively flexing and extending each limb while also internally and externally rotating. Hold the patient’s knee and roll it from side to side. Put your hand behind the knee and raise it quickly. The heel should lift slightly from the bed if tone is normal. Any spasticity/rigidity?
(fig 1) Plantar flex the foot then quickly dorsiflex and hold. More then 5 ‘beats’ of plantar flexion is sustained clonus and is abnormal. Hypertonia and clonus suggest an upper motor neuron lesion.
Ankle tone: testing for clonus.
For each reflex, test right, then left and compare. If absent, attempt to elicit with ‘reinforcement’. Decide whether reflexes are absent/ present (with reinforcement)/normal/brisk/exaggerated.
Knee: (L3,4) Strike on the patella tendon, just below the patella.
Ankle: (L5,S1) Several accepted methods; ideally ask the patient to slightly bend the knee, then drop it laterally, grasp the foot and dorsiflex, then strike the Achilles tendon. If hip pain limits mobility, dorsiflex the foot with a straight leg and strike your hand, feeling for an ankle jerk.
Plantar reflexes: (L5, S1, S2) Stroke the patient’s sole with an orange stick or similar. The normal reflex is downward movement of the great toe. Babinski’s sign is positive if there is dorsiflexion of the great toe (this is abnormal (upper motor neuron lesion) if patient age >6 months)
Direct patient to adopt position and follow commands below while you as the examiner resist movements as appropriate to grade power (p451). Test each muscle group bilaterally before moving on to the next position.
Hip flexion: “Keeping your leg straight, can you lift your leg off the bed, don’t let me push it down”
Hip extension: “And now using your leg, push my hand into the bed”
Hip abduction: Position hands on outer thighs—“push your legs out to the sides”
Hip adduction: Position hands on inner thighs—“and push your legs together”
Knee flexion and extension: “Bend your knee and bring your heel to your bottom, don’t let me pull it away… and now kick out against me and push me away”
Ankle plantar flexion: With your hand on the underside of the patient’s foot ask them to “bend your foot down, pushing my hand away”
Ankle dorsiflexion: Put your hand on the dorsum of the foot and ask them to “lift up your foot, point your toes at the ceiling, don’t let me push your foot down”
Using your finger on the patient’s shin to demonstrate, instruct patient to “put your heel just below your knee then run it smoothly down your shin, lift it up and place it back on your knee, now run it down again”, etc. Repeat on the other side.
As upper limbs (p73)
Light touch: Lower limb dermatomes (p458)
Pin prick
Temperature
Vibration
Joint position sense: With the patient’s eyes closed grasp distal phalanx of the great toe at the sides. Stabilize the rest of the toe. Move the joint up and tell patient “this is up”, and down, saying “this is down”. Flex and extend the joint, stopping at intervals to ask whether the toe is up or down.
If you are limited for time, gait is the most useful test to start with
Make sure you test each muscle group individually by stabilising above the joint you are testing
Test vibration by putting a buzzing tuning fork on the bony part of a joint with the patient's eyes closed then ask them to tell you when the buzzing stops (pinch the tuning fork to stop it) to distinguish vibration from pressure sensation
Cranial nerve examination
Approach to examining the cranial nerves
Where is the lesion? Think systematically. Is it in the brainstem (eg ms) or outside, pressing on the brainstem? Is it the neuromuscular junction (myasthenia) or the muscles (eg a dystrophy)? Cranial nerves may be affected singly or in groups. Face the patient (helps spot asymmetry). For causes of lesions see box.
Smell: Test ability of each nostril to distinguish familiar smells, eg coffee.
Acuity: Test each eye separately, and its correctability with glasses or pin-hole; use Snellen chart if possible, or the one inside the cover of this book. Visual fields: Compare with your own fields or formally via perimetry testing. Any losses/inattention? Sites of lesions: ohcs p428. Pupils: (p79) Size, shape, symmetry, reaction to light (direct and consensual) or accommodation. Swinging light test for relative afferent pupillary defect. Ophthalmoscopy: (ohcs, p412) This is best learnt from an ophthalmologist. Darken the room, warn the patient you will need to get close to their face. Focus the lens on the optic disc (pale? swollen?). Follow vessels outwards to view each quadrant. If the view is obscured, examine the red reflex, with your focus on the margin of the pupil, to look for a cataract. Try to get a view of the fovea by asking the patient to look directly at the ophthalmoscope Pathology here needs prompt ophthalmic review. If in doubt, ask for slit lamp examination or photography of the retina.
10, iv & vi Eye movements. IIIrd nerve palsy: Ptosis, large pupil, eye down and out. IVth nerve palsy: Diplopia on looking down and in (often noticed on descending stairs)—head tilting compensates for this (ocular torticollis). VIth nerve palsy: Horizontal diplopia on looking out. Nystagmus is involuntary, often jerky, eye oscillations. Horizontal nystagmus is often due to a vestibular lesion (acute: nystagmus away from lesion; chronic: towards lesion), or cerebellar lesion (unilateral lesions cause nystagmus towards the affected side). If it is more in whichever eye is abducting, ms may be the cause (internuclear ophthalmoplegia, p78). If also deafness/tinnitus, suspect a peripheral cause (eg viiith nerve lesion, barotrauma, Ménière's, p466). If it varies with head position, suspect benign positional vertigo (p466). If it is up-and-down, ask a neurologist to review—upbeat nystagmus classically occurs with lesions in the midbrain or at the base of the 4th ventricle, downbeat nystagmus in foramen magnum lesions. Nystagmus lasting ≤2 beats is normal, as is nystagmus at the extremes of gaze.
Motor palsy: “Open your mouth”: jaw deviates to side of lesion.
Sensory: Check all 3 divisions. Consider corneal reflex (lost first).
10 Facial nerve lesions cause droop and weakness. As the forehead has bilateral representation in the brain, only the lower two-thirds is affected in umn lesions, but all of one side of the face in lmn lesions. Ask to “raise your eyebrows”, “show me your teeth”, “puff out your cheeks”. Test taste with salt/sweet solutions.
10 & x10 Gag reflex: Ask the patient to say “Ah”. xth nerve lesions also cause the palate to be pulled to the normal side on saying “Ah”. Ask them to swallow a sip of water. Consider gag reflex—touch the back of the soft palate with an orange stick. The afferent arm of the reflex involves ix; the efferent arm involves x.
Trapezii: “Shrug your shoulders” against resistance. Sternocleidomastoid: “Turn your head to the left/right” against resistance.
Tongue movement: The tongue deviates to the side of the lesion.
olfactory
optic
oculomotor
trochlear
trigeminal
ophthalmic division
maxillary division
mandibular division
abducens
facial
vestibulocochlear
glossopharyngeal
vagus
accessory
hypoglossal
Any cranial nerve may be affected by diabetes mellitus; stroke; ms; tumours; sarcoidosis; vasculitis, p558, eg pan (p558), sle (p556); syphilis. Chronic meningitis (malignant, tb, or fungal) tends to pick off the lower cranial nerves one by one.
Trauma; respiratory tract infection; meningitis; frontal lobe tumour.
Field defects may start as small areas of visual loss (scotomas, eg in glaucoma). Monocular blindness: Lesions of one eye or optic nerve eg ms, giant cell arteritis. Bilateral blindness9: Any cause of mononeuritis, eg diabetes, ms; rarely methanol, neurosyphilis. Field defects—Bitemporal hemianopia: Optic chiasm compression, eg pituitary adenoma, craniopharyngioma, internal carotid artery aneurysm (fig 1, p452). Homonymous hemianopia: Affects half the visual field contralateral to the lesion in each eye. Lesions lie beyond the chiasm in the tracts, radiation, or occipital cortex, eg stroke, abscess, tumour. Optic neuritis (pain on moving eye, loss of central vision, relative afferent pupillary defect, disc swelling from papillitis10). Causes: Demyelination (eg ms); rarely sinusitis, syphilis, collagen vascular disorders.
Ischaemic papillopathy: Swelling of optic disc due to stenosis of the posterior ciliary artery (eg in giant cell arteritis).
Papilloedema (bilaterally swollen discs, fig 3, p562): most commonly ↑icp (tumour, abscess, encephalitis, hydrocephalus, idiopathic intracranial hypertension); rarer: retro-orbital lesion (eg cavernous sinus thrombosis, p484).
Rare. Polio, syringomyelia, tumour, stroke, bulbar palsy, trauma, tb.
If the patient is able to shake their head, there is no meningism.
Cranial nerve lesions of the eye
Internuclear ophthalmoplegia (ino) and its causes. To produce synchronous eye movements, cranial nerves iii, iv, and vi communicate through medial longitudinal fasciculus in midbrain. In ino, a lesion disrupts communication, causing weakness in adduction of the ipsilateral eye with nystagmus of the contralateral eye only when abducting. There may be incomplete or slow abduction of the ipsilateral eye during lateral gaze. Convergence is preserved. Causes: ms or vascular (rarely: hiv; syphilis; Lyme disease; brainstem tumours; phenothiazine toxicity).
Drooping of the upper eyelid. Best observed with patient sitting up, with head held by examiner. Oculomotor nerve (cn iii) innervates main muscle concerned (levator palpebrae), but nerves from the cervical sympathetic chain innervate superior tarsal muscle, and a lesion of these nerves causes mild ptosis which can be overcome on looking up.
cn iii lesions cause unilateral complete ptosis: look for other evidence of a cn iii lesion: ophthalmoplegia with ‘down and out’ deviation of the eye, pupil dilated and unreactive to light or accommodation. If eye pain too, suspect infiltration (eg by lymphoma or sarcoidosis). If t°↑ or consciousness°↓, suspect infection (any tick bites?)
Sympathetic paralysis usually causes unilateral partial ptosis. Look for other evidence of a sympathetic lesion, as in Horner's syndrome (p716): constricted pupil = miosis, lack of sweating on same side of the face (=anhidrosis).
Myopathy, eg dystrophia myotonica, myasthenia gravis (cause bilateral partial ptosis).
Congenital; usually partial and without other cns signs.
Get ophthalmology help. See ohcs p434–p455. Consider:
Is the eye red? (glaucoma, uveitis p563)
Pain? Giant cell arteritis: severe temporal headache, jaw claudication, scalp tenderness, ↑esr: urgent steroids (p558). Optic neuritis: eg in ms.
Is the cornea cloudy: corneal ulcer (ohcs p432), glaucoma (ohcs p430)?
Is there a contact lens problem (infection)?
Any flashes/floaters? (tia, migraine, retinal detachment?)
Is there a visual field problem (stroke, space-occupying lesion , glaucoma)?
Are there any focal cns signs?
Any valvular heart disease/carotid bruits (emboli)? Hyperlipidaemia (p704)?
Is there a relative afferent pupillary defect (p79)?
Any past history of trauma, migraine, hypertension, cerebrovascular disease, ms, diabetes or connective tissue disease?
Any distant signs: eg hiv (causes retinitis), sle, sarcoidosis?
Acute glaucoma
Retinal detachment
Vitreous haemorrhage (eg in diabetic proliferative retinopathy)
Central retinal artery or vein occlusion
Migraine
cns: tia (amaurosis fugax), stroke, space-occupying lesion
Optic neuritis (eg ms)
Temporal arteritis
Drugs: quinine/methanol
Pituitary apoplexy.
Optic atrophy
Chronic glaucoma
Cataracts
Macular degeneration
Tobacco amblyopia.
Key questions:
Equal, central, circular, dilated, or constricted?
React to light, directly and consensually?
Constrict normally on convergence/accommodation?
Anterior uveitis (iritis), trauma to the eye, syphilis.
cn iii lesions (inc. ↑icp, p840) and mydriatic drugs. Always ask: is this pupil dilated, or is it the other that is constricted?
Old age, sympathetic nerve damage (Horner's, p716, and ptosis, p78), opiates, miotics (pilocarpine drops for glaucoma), pontine damage.
may be due to unilateral lesion, eye-drops, eye surgery, syphilis, or Holmes–Adie pupil. Some inequality is normal.
Test: cover one eye and shine light into the other obliquely. Both pupils should constrict, one by direct, other by consensual light reflex (fig 2). The lesion site is deduced by knowing the pathway: from the retina the message passes up the optic nerve (cnii) to the superior colliculus (midbrain) and thence to the cniii nuclei on both sides. The iiird cranial nerve causes pupillary constriction. If a light in one eye causes only contralateral constriction, the defect is ‘efferent’, as the afferent pathways from the retina being stimulated must be intact. Test for relative afferent pupillary defect: move torch quickly from pupil to pupil. If there has been incomplete damage to the afferent pathway, the affected pupil will paradoxically dilate when light is moved from the normal eye to the abnormal eye. This is because, in the face of reduced afferent input from the affected eye, the consensual pupillary relaxation response from the normal eye predominates. This is the Marcus Gunn sign, and may occur after apparent complete recovery from the initial lesion.
Light reflex. Action potentials go along optic nerve (red), traversing optic chiasm, passing synapses at pretectal nucleus, en route to Edinger–Westphal nuclei of cniii. These send fibres to both irises’ ciliary muscles (so both pupils constrict) via ciliary ganglion (also relays accommodation and corneal sensation, and gets sympathetic roots from C8–T2, carrying fibres to dilate pupil).
If the patient first looks at a distant object and then at the examiner's finger held a few inches away, the eyes will converge and the pupils constrict. Afferent fibres in each optic nerve pass to the lateral geniculate bodies. Impulses then pass to the pretectal nucleus and then to the parasympathetic nuclei of the iiird cranial nerves, causing pupillary constriction.
Holmes–Adie (myotonic) pupil: The affected pupil is normally moderately dilated and is poorly reactive to light, if at all. It is slowly reactive to accommodation; wait and watch carefully: it may eventually constrict more than a normal pupil. It is often associated with diminished or absent ankle and knee reflexes, in which case the Holmes–Adie syndrome is present. Usually a benign incidental finding. Rare causes: Lyme disease, syphilis, parvovirus b19, hsv, autoimmunity. ♀>♂.
Hutchinson pupil: This is the sequence of events resulting from rapidly rising unilateral intracranial pressure (eg in intracerebral haemorrhage). The pupil on the side of the lesion first constricts then widely dilates. The other pupil then goes through the same sequence. See p840.
Speech and higher mental function
Have mercy on those with dysphasia: it is one of the most debilitating neurological conditions, and the more frustrating when cognitive function is intact.
Dysphasia
(Impairment of language caused by brain damage)
Assessment:
If speech is fluent, grammatical and meaningful, dysphasia is unlikely.
Comprehension: Can the patient follow one, two, and several step commands? (touch your ear, stand up, then close the door).
Repetition: Can the patient repeat a sentence?
Naming: Can they name common and uncommon things (eg parts of a watch)?
Reading and writing: Normal? They are usually affected like speech in dysphasia. If normal, the patient is unlikely to be aphasic—could they be mute?
Classification:
Broca's (expressive) anterior dysphasia: Non-fluent speech produced with effort and frustration with malformed words, eg ‘spoot’ for ‘spoon’ (or ‘that thing’). Reading and writing are impaired but comprehension is relatively intact. Patients understand questions and attempt to convey meaningful answers. Site of lesion: inferolateral dominant frontal lobe (see box).
Wernicke's (receptive) posterior dysphasia: Empty, fluent speech, like talking ragtime with phonemic (‘flush’ for ‘brush’) and semantic (‘comb’ for ‘brush’) paraphasias/neologisms (may be mistaken for psychotic speech). The patient is oblivious of errors. Reading, writing, and comprehension are impaired (replies are inappropriate). Site of lesion: posterior superior dominant temporal lobe.
Conduction aphasia: (Traffic between Broca's and Wernicke's area is interrupted.) Repetition is impaired; comprehension and fluency less so.
Nominal dysphasia: Naming is affected in all dysphasias, but in nominal dysphasia, objects cannot be named but other aspects of speech are normal. This occurs with posterior dominant temporoparietal lesions.
Mixed dysphasias are common. Discriminating features take time to emerge after an acute brain injury. Speech therapy is important, but may not help.
Dysarthria
Difficulty with articulation due to incoordination or weakness of the musculature of speech. Language is normal (see above).
Assessment: Ask to repeat ‘British constitution’ or ‘baby hippopotamus’.
Cerebellar disease: Ataxia speech muscles cause slurring (as if drunk) and speech irregular in volume and staccato in quality (see minibox).
Extrapyramidal disease: Soft, indistinct, and monotonous speech.
Bulbar palsy: Lower motor neuron (eg facial nerve palsy, Guillain–Barré, mnd, p510)—any associated palatal paralysis gives speech a nasal character.
Dysphonia
Dyspraxia
Poor performance of complex movements despite ability to do each individual component. Test by asking the patient to copy unfamiliar hand positions, or mime an object's use, eg a comb. The term ‘dyspraxia’ is used in 3 other ways:
Dressing dyspraxia: The patient is unsure of the orientation of clothes on his body. Test by pulling one sleeve of a sweater inside out before asking the patient to put it back on (mostly non-dominant hemisphere lesions).
Constructional dyspraxia: Difficulty in assembling objects or drawing, eg a 5-pointed star (non-dominant hemisphere lesions, hepatic encephalopathy).
Gait dyspraxia: More common in the elderly; seen with bilateral frontal lesions, lesions in the posterior temporal region, and hydrocephalus.
Start by having a conversation with the patient, asking questions they need to phrase an answer to (ie not just yes/no) as this tests fluency and reception, understanding, and allows assessment of articulation. Eg How did you travel here today? I came by bus. Then assess dysphasia by asking: What is this eg pen (tests for nominal dysphasia), repeat British Constitution (tests for conduction dysphasia and dysarthria). Then ask patient to follow one, two and three step commands ensuring these ‘cross the midline’ eg make a fist with your right hand then extend your right index finger and touch your left ear.
is due to a lesion in the putamen, causing slow sinuous writhing movements in the hands, which are present at rest. Pseudoathetosis refers to athetoid movements in patients with severe proprioceptive loss.
means dance (hence ‘choreography’)—a flow of jerky movements, flitting from one limb to another (each seemingly a fragment of a normal movement). Distinguish from athetosis/pseudoathetosis (above), and hemiballismus (p472).
basal ganglia lesion (stroke, Huntington's, p716); streptococci (Sydenham's chorea; St Vitus’ dance, p136); sle (p556); Wilson's (p269); neonatal kernicterus; polycythaemia (p360); neuroacanthocytosis (genetic, with acanthocytes in peripheral blood, chorea, oro-facial dyskinesia, and axonal neuropathy); hyperthyroidism (p210); drugs (levodopa, oral contraceptives/hrt, chlorpromazine, cocaine—’crack dancing’). The early stages of chorea may be detected by feeling fluctuations in muscle tension while the patient grips your finger.
Dopamine antagonists, eg tetrabenazine 12.5mg/12h (/24h if elderly) po; increase, eg to 25mg/8h po; max 200mg/d.
is uncontrolled unilateral flailing movements of proximal limb joints caused by contralateral subthalamic lesions. See p472.
Speech: Slurred/ataxic/staccato
Eye movements: Nystagmus
Tone and power: Hypotonia and reduced power
Coordination: Finger-to-nose test; test for dysdiadochokinesis, p503
Gait: Broad based, patients fall to the side of the lesion. Romberg's test: ask patient to stand with eyes closed. If he loses balance, the test is positive and a sign of posterior column disease. Cerebellar disease is Romberg negative.
(Remember DASHING: Dysdiadochokinesis, Ataxia, Slurred speech, Hypotonia and reduced power, Intention tremor, Nystagmus, broad based Gait).
Psychiatric assessment
Introduce yourself, ask a few factual questions (precise name, age, job, and who is at home). These may help your patient to relax, but be careful that you do not touch on a nerve, eg if job recently lost, marriage recently ended so living alone.
Presenting problem
Ask for the main problems that have led to this consultation. Sit back and listen. Don't worry whether the information is in a convenient form or not—this is an opportunity for the patient to come out with worries, ideas, and preoccupations unsullied by your expectations. After >3–5min it is often good to aim to have a list of all the problems (each sketched only briefly). Read them back to the patient and ask if there are any more. Then ask about:
History of presenting problem
For each problem obtain details, both current state and history of onset, precipitating factors, and effects on life.
Check of major psychiatric symptoms
Check those that have not yet been covered: depression—low mood, anhedonia (inability to feel pleasure), thoughts of worthlessness/hopelessness, sleep disturbance with early morning waking, loss of weight and appetite. Ask specifically about suicidal thoughts and plans: “Have you ever been so low that you thought of harming yourself?”, “What thoughts have you had?” Hallucinations (“Have you ever heard voices or seen things when there hasn't been anyone or anything there?”) and delusions (“Have you ever had any thoughts or beliefs that have struck you afterwards as bizarre?”); anxiety and avoidance behaviour (eg avoiding shopping because of anxiety or phobias); obsessional thoughts and compulsive behaviour, eating disorders, alcohol (see p283 for alcohol screening tests) and other drugs.
Present circumstances
Housing, finance, work, relationships, friends.
Family history
Ask about health, personality, and occupation of parents and siblings, and the family's medical and psychiatric history.
Background history
Try to understand the context of the presenting problem.
Biography: relationships with family and peers as a child; school and work record; sexual relationships and current relationships; and family. Previous ways of dealing with stress and whether there have been problems and symptoms similar to the presenting ones.
Premorbid personality: mood, character, hobbies, attitudes, and beliefs.
Past medical and psychiatric history
Mental state examination This is the state now, at the time of interview.
Appearance: Clothing, glasses, headwear? Unkempt/normal/meticulous?
Observable behaviour: Eg excessive slowness, signs of anxiety, gesture, gaze or avoiding gaze, tears, laughter, pauses (while listening to voices?), attitude (eg withdrawn).
Mode of speech: Include the rate of speech, eg retarded or gabbling (pressure of speech). Note its content. Flight of ideas? Knight's move thinking? (See box)
Mood: Note thoughts about harming self or others. Gauge your own responses to the patient. The laughter and grand ideas of manic patients are contagious, as to a lesser extent is the expression of thoughts from a depressed person.
Beliefs: Eg about himself, his own body, about other people, and the future. Note abnormal beliefs (delusions), eg that thoughts are overheard, and abnormal ideas (eg persecutory, grandiose).
Unusual experiences or hallucinations: Note modality, eg visual, auditory.
Orientation: In time, place, and person. What is the date? What time of day is it? Where are you? What is your name?
Short-term memory: Give a name and address and test recall after 5min. Make sure that he has got the address clear in his head before waiting the 5min.
Concentration: Months of the year backwards.
Note the degree of your rapport and the patient's insight into his current state.
There are many different ways to think about psychiatric symptoms. One simple approach can be to consider negative and positive symptoms. Negative symptoms involve the absence of a behaviour, thought, feeling or sensation (eg lack of appetite, apathy, and blunted emotions in depression), whereas positive symptoms involve their presence when not normally expected (eg thought insertion, ie “Someone is putting thoughts into my head”). Understanding the difference between psychosis and neurosis is vital. Psychosis entails a thought disorder (eg thought insertion, thought broadcasting) ± delusions (abnormal beliefs which are held to despite all reasoning, and which run counter to the patient's cultural background) and abnormal perceptions (eg hallucinations). Neurosis entails insight—if there are intrusive ideas or odd experiential phenomena, the person knows that they are false or illusory (and may be triggered by stress, etc.).
Interesting abnormalities of speech include flight of ideas, in which the speech races through themes, switching whimsically or through associations, eg ‘clang’ association: “Yesterday I went down to the local shop. I didn't hop (clang), but I walked. Kangaroos hop, don't they? My friend Joey wasn't there, though …”. Knight's move is an unexpected change in the direction of speech or conversation (akin to the lateral component of the move of the knight's piece in chess) and neologism is the formation of new words. They may be normal or indicate an organic brain condition or a psychosis.
Many psychiatric symptoms in isolation, to a lesser degree of severity, or even in a different culture, may well be considered part of ‘normal’ behaviour. For example, a vision from a religious figure may be considered normal, whereas one from an alien may not. Consider your patient in their cultural and religious context. As with so many aspects of medicine, in psychiatry there is a vast spectrum of behaviour, thought and perception, at least one extreme of which is considered to be ‘abnormal’. It is in part our challenge to attempt to interpret these symptoms with relevance, insight and impartiality so that we may best benefit our patients and not form opinions that are set in stone. On acute medical wards psychiatric symptoms are often due to stress, drug or alcohol withdrawal, u&e imbalance, or medication. When in doubt, ask a psychiatrist to help.
Beware of simplistic formulations, eg If you talk to God, you are praying. If God talks to you, you have schizophrenia (Dr Thomas Szasz). It is not the auditory phenomenon that makes the diagnosis of psychosis: what matters is what the patient believes about the phenomenon, and whether they are associated with a thought disorder or a delusion.
Method and order for routine examination
Look at the patient. Healthy, unwell, or in extremis? This vital skill improves with practice. Beware those who are sicker than they look, eg cardiogenic shock; cord compression; non-accidental injury.
pulse, bp, O2 sats, t°.
Examine nails, hands, conjunctivae (anaemia), and sclerae (jaundice). Consider: Paget's, acromegaly, endocrine disease (thyroid, pituitary, or adrenal hypo- or hyper-function), body hair, abnormal pigmentation, skin.
Examine mouth and tongue (cyanosed; smooth; furred; beefy, eg rhomboid area denuded of papillae by Candida, after prolonged steroid inhaler use).
Examine the neck from behind: lymph nodes, goitre.
Make sure the patient is at 45° to begin cvs examination in the neck: jvp; feel for character and volume of carotid pulse.
The praecordium. Look for abnormal pulsations. Feel the apex beat (character; position). Any parasternal heave or thrill? Auscultate (bell and diaphragm) apex in the left lateral position, then the other 3 areas (p39) and carotids. Sit the patient forward: listen during expiration.
Whilst sitting forward, look for sacral oedema.
Begin the respiratory examination with the patient at 90°. Observe (and count) respirations; note posterior chest wall movement. Assess expansion, then percuss and auscultate the chest.
Sit the patient back. Feel the trachea. Inspect again. Assess expansion of the anterior chest. Percuss and auscultate again.
Examine axillae and breasts, if indicated (+chaperone for all intimate examinations).
Lie patient flat (1 pillow) to inspect, palpate, percuss, and auscultate abdomen.
Look at the legs: any swellings, perfusion, pulses, or oedema?
cns exam: Cranial nerves: pupil responses; fundi; visual fields; visual acuity. Consider corneal reflexes. “Open your mouth; stick your tongue out; screw up your eyes; show me your teeth; raise your eyebrows.” Limbs (most signs are due to central not peripheral nerve lesions): Look for wasting and fasciculation. Test tone in all limbs. “Hold your hands out with your palms towards the ceiling and fingers wide. Now shut your eyes.” Watch for pronator drift. “Keep your eyes shut and touch your nose with each index finger.” “Lift your leg straight in the air. Keep it there. Put your heel on the opposite knee (eyes shut) and run it up your own shin.” You have now tested power, coordination, and joint position sense. Tuning fork on toes and index fingers to assess vibration sense.
Examine gait and speech. Any abnormalities of higher mental function to pursue?
Consider rectal and vaginal examination.
Examine the urine with dipstick if appropriate (p383).
In general, go into detail where you find (or suspect) something to be wrong.
So now we have a template for the all-important history and examination, but it is no more than a rough guide, you must flesh it out with your own learning. We start out nervous of missing some question or sign, but what we should really be nervous about is losing our humanity in the hurly-burly of a time-pressed interview. Here is how one student put some flesh on the bones—for a man in a wheelchair: she asked all about the presenting complaint, and how it fitted in with his cns condition and life at home—and then found out that his daughter had had a nervous breakdown at the start of his illness, 5 years ago. “How is she now?” she asked “Fine—I've got two lovely grand-children…Jim is just learning to walk…” “Oh…you must be so busy!” the student said with a joyful smile. This man had not been busy for 5 years, and was fed up with his passive dependency. The thought of being busy again made his face light up—and when the student left he rose up out of his wheelchair to shake her by the hand, a movement we doctors thought was impossible. Jim and his grandfather were learning to walk, but this student was up and running—far ahead of her teachers.
The tym (Test Your Memory) test
In one preliminary study,12 the controls’ average score was 47/50. Those with Alzheimer's disease (ad) scored an average of 33/50. The tym score correlates highly with other standard tests, but, uniquely, it is quick and can be self-administered. A score of <42/50 had a sensitivity of 93% and specificity of 86% for ad. tym is more sensitive at detecting ad than the mini-mental exam (mmse), detecting 93% of patients compared with 52% for mmse. Negative and positive predictive values (p674) of tym with a cut-off of 42 were 99% and 42% (if prevalence of ad is 10%). If non-Alzheimer dementia, score was 39/50 (mean). This new test should not make any diagnosis—but it may suggest when further referral might help.
Animals beginning with ‘S’:
‘Shark’ and mythical creatures not allowed.
Carrot/potato:
Reasonable but less precise answer than “…vegetables…”, eg “food”, scores 1 point. 2 such statements score 2, eg “grows in ground…fierce” or “…food…4 legs…” scores 2 in total.
Jacket-naming:
Answers are collar, lapel, tie, pocket, button. 1 point each. Shirt is acceptable for item 1; jacket or blazer is ok for 2 or 4 (but not both).
Circles task:
1 point if all circles joined even if not a letter W.
Clockface:
All numbers ok 1; correct number position 1; correct hands 1.
Sentence:
1 point for each word remembered up to a maximum of 5.
Use a different approach in paediatrics, and for autosomal or sex-linked disease. Ask if parents are related (consanguinity ↑risk of recessive diseases). This page owes much to Dr Helen Firth, who we thank.
This sign was first described by Pasteur in 1885 in the context of tricuspid incompetence.
Atopy implies predisposition to, or concurrence of, asthma, hay fever and eczema with production of specific IgE on exposure to common allergens (eg house dust mite, grass, cats).
In the elderly, nocturia (1–2/night) may be ‘normal’ because of: i) loss of ability to concentrate urine; ii) peripheral oedema fluid returns to the circulation at night; iii) circadian rhythms may be lost; iv) less sleep is needed and waking may be interpreted as a need to void (a conditioned Pavlovian response).
Tietze's syndrome is costochandritis plus swelling of the costal cartilage.
Bornholm disease (Devil's grip) is due to Coxsackie b virus, causing chest and abdominal pain, which may be mistaken for cardiac pain or an acute surgical abdomen. It resolves within ∼2 weeks.
Remember the commonest cause of monocular or binocular blindness is not a cranial nerve lesion but a problem with the eye itself (cataracts, retinal problems). Neurological disorders more commonly cause loss of part of the visual field.
While abstract words activate a sub-region of the left inferior frontal gyrus more strongly than concrete words, specific activity for concrete words can also be observed in the left basal temporal cortex.
tym for detection of Alzheimer's disease: cross sectional study. Brown J, Dawson K, Pengas G 2009 bmj 338 1426.
