Clinical Examination 4 Ediciòn

Clinical Examination
ERRNVPHGLFRVRUJ
Dedication
June, Daniel, Marc, Morris and Nancy

(Owen Epstein)
Harry, George, Josephine, Tom, Ted, Elsie and Ella
(David Perkin)
Anna, Alastair and Fiona
(John Cookson)
Dr Natasha Kapur, my wife and fellow physician. My children
Rohan and Karan.
(Roby Rakhit)
Dr Natasha Arnold, my wife and fellow physician, who shares our
passion for looking after the whole of the patient and is proud
to be called a generalist.
(Andrew Robbins)
Sioban, Calum, Kieran and Brendan.
(Ian Watt)
To Rosemary, my wife for her loving support
(Graham Hornett)
Commissioning Editor: Laurence Hunter

Development Editor: Janice Urquhart, Pru Theaker
Project Manager: Nancy Arnott
Illustration Manager: Gillian Richards
Illustrator: Marion Tasker, MTG and Chartwell
Clinical Examination
Fourth Edition
Owen Epstein MB BCh FRCP
Consultant Physician and Gastroenterologist,
Royal Free Hospital NHS Trust, London, UK
G. David Perkin BA MB MRCP

Emeritus Consultant Neurologist,
Charing Cross Hospital, London, UK
John Cookson MD FRCP

Dean of the Undergraduate School,
Hull York Medical School, University of York, York, UK
Ian S. Watt BSc MB ChB MPH FFPH

Professor of Primary Care,
Hull York Medical School, University of York, York, UK
Roby Rakhit BSc MD MRCP

Consultant Cardiologist and Honorary Senior Lecturer,
Royal Free Hospital, London, UK
Andrew Robins MB MSc MRCP FRCPCH

Consultant Paediatrician,
Whittington Hospital NHS Trust, London, UK
Graham A. W. Hornett MA MB BChir FRCGP

General Practitioner with a Special Interest in ENT,
Surrey Primary Care Trust, UK
Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2008
© 1992 Gower Medical Publishing
© 1997 Times Mirror International Publishers Limited
© 2003, Elsevier Limited. All rights reserved.
© 2008, Elsevier Limited. All rights reserved.
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First edition 1992

Second edition 1997
Third edition 2003
Fourth edition 2008
ISBN 9780723434542
British Library Cataloguing in Publication Data

A catalogue record for this book is available from the British Library
Library of Congress Cataloging in Publication Data

A catalog record for this book is available from the Library of Congress
Note
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knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are
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and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each
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Preface
The fourth edition of Clinical Examination comes at a about health and illness, communication skills and the ability
time of momentous change in medical practice. Gone are to engage in a professional two-way discourse become
the white coats with their dog-eared pockets overflowing increasingly important. The changing emphasis in the
with all the paraphernalia of bedside examination. The clinical encounter is recognized throughout this edition
stethoscope, once peeping subtly from a pocket, in now with the first two chapters emphasizing the Calgary-
draped like a necklace, as much a fashion statement as a Cambridge schema of gathering information, examining the
tool of the trade. The spiral-bound notebook is giving way patient, explaining, planning and closing the consultation.
to the personal digital assistant, the pen for a stylus and For the first time, each chapter has been peer reviewed by
keyboard, and the evocative sound of the bleep is making both a primary care and hospital doctor and two general
way for the ringtones and soundscape of the mobile phone. practitioner authors have contributed chapters to the book.
In the consulting room, the fraying patient file, with its often Where necessary, changes have been made to reflect the
illegible testimony of the patient’s medical journey, is making increasing primacy of general practice and the emergence
way for the electronic patient record, displayed in legible of overlapping roles in modern healthcare practice.
type, and instantly retrievable from cyberspace. The principles that underpinned the first edition remain
The modern era is also blurring the traditional boundaries intact. Each of the systems chapters is introduced with an
which once clearly demarcated the doctor-patient overview of clinical anatomy and physiology. This provides
relationship. Where once the nurse primarily tended for a backdrop for describing history taking and the normal and
patients’ physical and emotional needs, highly trained abnormal examination, and the book spans the age range
practice nurses and nurse specialists now carry stethoscopes from infancy to old age. The text is lavishly illustrated to
and undertake clinical roles previously considered wholly provide a multimedia reading experience and the use of
doctor owned. With improved telecommunication, fax, colour coded icon boxes, including a new ‘red flag’ box,
Internet and email, even medical receptionists and provides quick access to summarized information and a
secretaries have to learn to respond to patients’ questions, revision resource for the ‘night before’ exams. The first two
concerns and needs. To all this is added the panoply chapters introduce the reader to history taking, the general
of new investigations including MRI, spiral CT scanning, examination and the principles of problem-orientated
virtual colonoscopy, virtual bronchoscopy and coronary records. The subsequent chapters are systems-based and
angiography, wireless capsule endoscopy, minimal access include the skin, nails and hair, ears, nose and throat,
surgery and a whole new frontier of genetic profiling respiratory, cardiovascular and abdominal systems, the
and targeted biological therapies. female and male genitalia, bones joints and muscle,
Where does this leave Clinical Examination? In this new neurology and finally, the examination of infants and
edition, the authors have reasserted the centrality and children.
importance of the face-to-face consultation in this fast- Over a decade, Clinical Examination has established
changing medical landscape. Perhaps it is more important its position as a leading text for medical students,
than ever for all those engaged in direct patient care to postgraduates, nurses, physiotherapists and a range of
remain closely connected with the patient’s story and other healthcare professionals. Clinical tutors have found
physical examination. There is no debate about the value of the book and its illustrations a particularly helpful source
skilled history taking and physical examination and its for teaching and learning. This latest edition consolidates its
importance in directing the patient journey and problem position as a rich resource to help learn and teach clinical
solving. Indeed, as patients become more knowledgeable skills in a rapidly changing modern era.
v
Acknowledgements
We wish to thank the following The figures listed below were derived
individuals and organisations for with permission from the following
generously providing illustrative material: sources:
Dr Philip Bardsley, Dr Russell Lane, Dr Mike Morgan, Dr Fig. 11.13 from R. B. Strub and F. William Black: The
P. H. McKee and Dr John Wales; Joan Slack, Dept of Clinical Mental Status Examination in Neurology (F A Davis Co);
Genetics, Royal Free NHS Trust (Figs 2.3–2.7, 2.9–2.16); Figs 11.16, 11.17, 11.19, 11.24–11.26, 11.28–11.41,
Dr Les Berger, Dept of Radiology, Royal Free NHS Trust 11.43–11.45, 11.50, 11.52, 11.62, 11.65) from David
(Figs 2.36, 2.37, 7.16a); Dr Malcolm Rustin (Figs 3.12, 3.15, Spalton: Atlas of Clinical Ophthalmology (Gower Medical
3.23–3.26, 3.30, 3.31, 3.70–3.72); King’s College Hospital Publishing UK, 1984); Fig. 11.41 (right) from Haymaker,
(Figs 3.13, 3.14, 3.16, 3.37, 3.39–3.43, 3.45–3.47, 3.54, Webb: Bing’s Local Diagnosis in Neurological Diseases, 15th
3.65, 3.73, 3.74) for slides reproduced from Anthony du edn (St Louis, The C V Mosby Co, 1989); Figs 11.46 and
Vivier: Atlas of Clinical Dermatology (Gower Medical 11.47 from J. S. Glaser: Neuro-ophthalmology (Harper &
Publishing UK, 1986); Professor Tony Wright (Figs 4.9, 4.12, Row); Figs 11.48 and 11.49 from R. John Leigh and David
4.13); Dr James Entwhistle for Figs 5.5–5.10; Dr C. Richards S. Zee: The Neurology of Eye Movement (F A Davis Co);
for Fig. 5.13; Dame Margaret Turner-Warwick et al (Figs 5.2, Fig. 11.106 from Drs J. W. Lance and J. G. McLeod: A
5.11, 5.12, 5.14, 5.20, 5.29) for slides reproduced from Physiological Approach to Clinical Neurology (Butterworths);
Clinical Atlas of Respiratory Diseases (Gower Medical Fig. 11.103 from Lord Walton of Detchant: Introduction to
Publishing UK, 1989); Professor Robert H. Anderson and Clinical Neuroscience, 2nd edn (Baillière Tindall Ltd);
Dr Sally P. Allwork (Figs 6.4, 6.6, 6.7) for slides reproduced Fig. 11.96 from Professor R. S. Snell: Clinical Neuroanatomy
form Cardiac Anatomy (Gower Medical Publishing UK, for Medical Students, 2nd edn (Little, Brown & Co); Figs
1980); Dr James S. Bingham (Figs 8.37, 8.43–8.46, 9.14, 11.104 and 11.105 from Dr V. B. Brooks: Neural Basis of
9.15, 9.29) for slides reproduced from Sexually Transmitted Motor Control (Oxford University Press); Fig. 11.134 from
Diseases (Gower Medical Publishing UK, 1984); Dr Paul A. ‘Somaesthetic Pathways’ Br Med Bull, 33, 113–120, 1977;
Dieppe et al (Figs 10.8, 10.9, 10.38, 10.42, 10.50–10.52, Fig. 11.142 from Professor Ian A. D. Bouchier CBE and
10.64, 10.66, 10.69, 10.75, 10.77, 10.78, 10.80, 10.81, J. S. Morris; Clinical Skills, 2nd edn (W B Saunders); Figs
10.91) for slides reproduced from Atlas of Clinical 11.150–11.152 from Dr F. Plum: Diagnosis of Stupor and
Rheumatology (Gower Medical Publishing UK, 1986); Mr Coma, 3rd edn (F A Davis Co). Figs 12.1, 12.15–12.26 and
David Spalton et al (Figs 11.24–11.28, 11.30–11.39, 11.52, 12.27 from Dr Caroline Fertleman, UCL Medical School; Figs
11.62, 11.64, 11.65) Atlas of Clinical Ophthalmology 12.3a and b, 12.29, 12.30a–12.30j, 12.30l–12.30n, 12.31,
(Gower Medical Publishing UK, 1984). 12.32, 12.35–12.37 from Dr Heather Mackinnon,
Whittington Hospital. Growth charts reproduced with kind
permission of Castlemead Publications, Welwyn Garden
City; Figs 12.11 and 12.33 with kind permission from Dr T.
Lissauer: Illustrated Textbook of Paediatrics (Mosby); Figs
12.42 and 12.45 from Clement Clarke.
vi
Contents
1. Consultation, medical history 4. Ear, nose and throat 82

and record-taking 1 Graham A. W. Hornett
Ian Watt
Structure of the ear 82
The consultation 1 Symptoms of ear disease 83
Gathering information: the history 3 Examination of the ear 86
Systems review 7 Structure of the nose and sinuses 93
Recording the medical interview 10 Symptoms of diseases of the nose
and sinuses 94
Examination of the nose and sinuses 96
Structure of the throat 98
2. The general examination 20 Symptoms of diseases of the throat 100
Owen Epstein Examination of the throat 101
General examination 20
Formal examination 21
Recognisable syndromes and facies 22 5. The respiratory system 105
Endocrine syndromes 27
John Cookson
The thyroid gland 27
The parathyroid glands 33 Structure and function 105
The adrenal glands 35 Symptoms of respiratory disease 112
The pituitary gland 38 General examination 120
Nutrition 40 Examination of the chest 125
Clinical assessment of vitamin status 43 Common patterns of abnormality 133
Clinical assessment of hydration 44
Clinical assessment of shock 44
Colour 45
Oedema 46 6. The heart and cardiovascular
Temperature and fever 49 system 139
The lymphatic system 50 Roby Rakhit
Structure and function 139
Electrical activity of the heart 144
3. Skin, hair and nails 57 Cardiac arrhythmias 145
Blood supply to the heart 148
Owen Epstein
The arterial system 151
Structure and function 57 The venous system 152
Symptoms of skin disease 59 Clinical history 152
Symptoms of hair disease 60 Occupation and family history 157
Symptoms of nail disease 61 Clinical examination of the cardiovascular
Examination of the skin, hair and nails 61 system 157
Skin infections 71 Examination of the jugular venous pulse 164
Skin manifestations of systemic disease 78 Palpation of the precordium 166
Nail disorders 79 Auscultation of the heart 167
vii
Cardiovascular system and chest The hip 290
examination 173 The knee 295
Cardiovascular system and abdominal The ankle and foot 299
examination 173 Patterns of weakness in muscle diseases 303
Peripheral vascular system 174
Peripheral vascular disease 178
11. The nervous system 307
G. David Perkin
7. The abdomen 186
Owen Epstein The cortex 307
Examination 310
Structure and function 186 Clinical application 314
Symptoms of abdominal disorders 193
Examination of the abdomen 204 The psychiatric assessment 317
Examining the groin 220 Examination 319
Examining the anus, rectum and prostate 221 Clinical application 319
Headache and facial pain 320
8. Female breasts and genitalia 226
The cranial nerves 321
Owen Epstein
The olfactory (first) nerve 321
Breast structure and function 229 Examination 322
Symptoms of breast disease 230 Clinical application 322
Examination of the breast 231 The optic (second) nerve 322
Structure of the genital tract 235 Examination 323
Symptoms of genital tract disease 238 Clinical application 327
Examination of the female genital tract 242
Examination of the abdomen 242 The oculomotor, trochlear and abducens
Examining the external genitalia 243 (third, fourth and sixth) nerves 332
Examination of the vagina 244 Examination 337
Examination of the cervix 246 Clinical application 340
Internal examination of the uterus 248
The trigeminal (fifth) nerve 345
Examination 347
9. The male genitalia 252
Clinical application 349
Owen Epstein
The facial (seventh) nerve 349
Examination 350
Symptoms of genital tract disease 255
Examination of the male genitalia 257
The acoustic (eighth) nerve 353
10. Bone, joints and muscle 265 Examination and clinical application 354
G. David Perkin The glossopharyngeal (ninth) nerve 354
Structure and function 265 Examination 355
Symptoms of bone, joint and muscle Clinical application 355
disorders 267 The vagus (tenth) nerve 355
General principles of examination 269
GALS 272 Examination 355
Regional structure, function and Clinical application 356
examination 274 The accessory (eleventh) nerve 356
Temporomandibular joints 274 Examination 356
The spine 274 Clinical application 357
The shoulder 279
The elbow 282 The hypoglossal (twelfth) nerve 357
The forearm and wrist 283 Examination 357
The hand 286 Clinical application 358
viii
The motor system 359
Examination 362
The cerebellar system 371
Examination 372
The sensory system 374
Examination 377
The unconscious patient 382
Examination 383
12. Infants and children 390

Andrew Robins
Taking a history 390
The examination 392
Growth and development 393
The newborn and very young baby 397
Older babies and toddlers 407
The preschool child 412
The school-aged child 414
Adolescents 416
Index 421
ix
User guide to icon boxes
Differential diagnosis
summarise the common cause of clinical abnormalities
Emergency
outline the implications for history and examination of certain
clinical emergencies
Examination of elderly people

guide the reader through the particular difficulties encountered
when examining the elderly
Questions to ask
list the key questions to ask the patient to help reach a diagnosis
Red flag
represent those symptoms and signs which should be taken
particularly seriously and acted on urgently to rule out potentially
serious pathology; they are also useful in guiding a directed history/
examination if time is short
Review
summarise the most important points to remember about the
examination of each body system
Risk factors
give the basic information on the risk factors associated with a
particular disease
Symptoms and signs

provide the core clinical features of the diseases and disorders
x
1
Consultation, medical history
and record taking
The ability to take an accurate medical history from a Calgary–Cambridge approach. This identifies five main
patient is one of the core clinical skills and an essential stages in a consultation within a framework that provides
component of clinical competence. The medical interview structure and emphasises the importance of building a
or consultation influences the precision of diagnosis and good doctor–patient relationship.
treatment, and studies have indicated that over 80% of This chapter primarily addresses the first two stages:
diagnoses in general medical clinics are based on the initiating the session and gathering information. It
medical history. It is estimated that a doctor might outlines the basics of taking a medical history within
perform 200,000 consultations in a professional lifetime. a framework that is patient-centred and emphasises
All of which supports the need to learn and develop effective communication. In addition, it describes an
effective interviewing technique. approach to recording information from the consultation
The success of the medical consultation depends not in the clinical record.
only on the doctor’s clinical knowledge and interview
skills but also on the nature of the relationship that exists
between doctor and patient. For this reason, increasing
emphasis is being placed on communication skills
The consultation
alongside history-taking in medical training in order to
The medical consultation is the main opportunity for the
enhance the doctor–patient relationship and promote
doctor to explore the patient’s problems and concerns
more effective consultations. How we communicate is
and to start to identify the reasons for their ill health.
just as important as what we say. The patient needs to
Traditionally, medical history-taking has been based on
feel sufficiently at ease to disclose any problems and
a conventional medical model and assumed that disease
express any concerns, and to know they have been
can be fully accounted for by deviations from normal
understood by the doctor. The patient also needs to reach
biological function. It gave little consideration for the
a shared understanding with the doctor about the nature
social, psychological and behavioural dimensions of
of any illness and what is proposed to deal with it.
illness. Consequently, if a patient presented with a history
As well as being more supportive for patients, good
of headaches, for example, the doctor’s questions would
communication skills make history-taking more accurate
be focused mainly on trying to identify the abnormalities
and effective.
of pathophysiology that were causing the symptoms,
In any consultation, the doctor has a number of tasks
such as ‘Where does it hurt?’, ‘When did the headaches
to perform. Ideally, these should be undertaken in a
start?’, ‘What helps relieve the headaches?’.
structured way so as to maximise the efficiency and
Whilst abnormalities of pathophysiology are largely
effectiveness of the process. A number of consultation
common to everyone with the same disease, not everyone
models exist but an increasingly influential model is the
with the same disease experiences it in the same way.
Review
The experiences of each person are unique because their
social, psychological and behavioural perspectives are
The Calgary–Cambridge schema
unique, and interact with abnormal pathophysiology to
• initiating the session cause each patient to experience illness in a very individual
• gathering information way. Thus, more recent approaches to medical consultation
• physical examination stress not just assessment of biomedical abnormality
• explanation and planning but also assessment of psychosocial issues. Questions to
• closing the session identify psychosocial perspectives could include: ‘What
most concerns you about your headaches?’, ‘What do
1
Chapter
1 Consultation, medical history and record taking
your headaches stop you from doing?’, and ‘What do you

think would help these headaches?’.
Unless a doctor can reflect on a patient’s psychosocial
concerns, they risk failing to accurately diagnose the
problem and may ultimately fail to effectively manage the
patient’s illness. The amount of distress an individual
experiences refers not only to the amount of
pathophysiological damage but also to what the illness
means to them and how it relates to their circumstances.
Individuals who have suffered personal upset or are
worried may feel ill even when no demonstrable disease Fig. 1.2 A less than satisfactory seating arrangement. For the more
is present. Good doctors have always known this, but sensitive or nervous patient, it will seem as though an additional
there is now increasing emphasis in medical history- barrier has been placed between him and the doctor, hindering the
exchange of information.
taking that it should be geared to exploring not just the
symptoms of the body’s dysfunction but also the
individual’s perspective of the symptoms. Models of is comfortable and able to engage with you without
history-taking are becoming increasingly patient-centred straining (Fig. 1.3).
and seek to assess both the main components of ill health Time management is important when preparing for
– the biomedical component and the psychosocial the consultation. Ideally you should aim to avoid
component. appearing rushed, and ensure that you set aside adequate
time. Time constraints are often outside a clinician’s
STARTING THE CONSULTATION immediate control and one has to be pragmatic and
comply with clinic appointment times. On the ward,
There are three main aspects to initiating the session:
rest periods and mealtimes are generally regarded as
preparation, establishing initial rapport, and identifying
sacrosanct by the nursing staff, and it is usual courtesy
the patient’s problems and concerns.
to ask permission from them before encroaching on a
Preparation patient’s time.
The patient’s first judgement of any healthcare
In preparing for a consultation, you should plan for
professional is influenced by dress, which plays a role
an optimal setting in which to conduct the interview.
in establishing the early impression in the relationship.
In general practice or in the outpatient department,
Whilst fashions change, most patients have clear
the consulting room should be quiet and free from
expectations of what constitutes appropriate dress and
interruptions. Patients often find that the clinical setting
it is advisable to adopt a dress code that projects a
stokes up anxiety and thought should be given to making
professional image. This may vary according to setting
the environment welcoming and relaxing. For example,
and patient group. For example, children may feel more
arrange the patient’s seat close to yours (Fig. 1.1), rather
at ease with a doctor who adopts a slightly more informal
than confronting them across a desk (Fig. 1.2).
appearance. In addition to dress, you need to pay attention
Hospital wards can be busy and noisy, and it may be
difficult to prevent your consultation being overheard
and maintain confidentiality. If possible, therefore, try
and find a quiet room in which to talk to the patient. If
you consult with a patient at the bedside, sit in a chair
alongside the bed, not on the bed, and ensure the patient
Fig. 1.3 For the bedside interview sit in a chair alongside the bed.
Fig. 1.1 The preferred seating arrangement when interviewing the Ensure that the patient is comfortable and is able to look at you
patient: you are physically closer to the patient, without any barrier. without straining.
2
Chapter
Gathering information: the history 1
to personal hygiene; make sure, for example, that your Symptoms and signs
hands and nails are clean.
Written summary of patient problems
Initial rapport H.M., aged 57, housewife

• Increasing breathlessness for 3 months
On first meeting a patient it is important to establish
• Night-time shortness of breath for 3 weeks
rapport and put the patient at ease. It’s a chance for
• A dry cough for the last 6 days
you to demonstrate from the outset your respect, interest
• Can no longer attend dance lessons
and concern for them. You should greet the patient,
introduce yourself and clarify your role, giving the patient
an outline of what your intentions are. It may sometimes
be appropriate to give an idea of how long the interview
might take. Gathering information: the history
‘Hello, my name is Jean Smith. I’m a medical student EXPLORATION OF THE PATIENT’S PROBLEMS
here at St Elsewhere and I wonder if I could speak You now need to explore each of the patient’s problems
to you about your condition? Your doctor, Dr Brown, in greater detail from both biomedical and psychosocial
has asked me to speak to you.’ perspectives. Gathering information on the patient’s
problems is one of the most important tasks to be
Communication consists not only of verbal discourse but mastered in medicine. The doctor must use a range of
also includes body language, especially facial expression skills to encourage the patient to tell their story as fully
and eye contact. The first contact should also be used to as possible whilst maintaining a degree of control and
obtain or confirm the patient’s name and to check how maintaining a structure in the collection of information.
they prefer to be called. Some people like to be addressed As the history emerges, the doctor must interpret the
by their first name, whilst others may prefer the use of symptom complex. The manner in which the interview is
their surname. conducted, the demeanour of the doctor and the type of
questions asked may have a profound effect on the
Identifying the problems and concerns information revealed by the patient. Obtaining all the
Begin by asking the patient to outline their problems relevant information from the patient can be crucial in
and concerns by using an open-ended question (e.g. helping to formulate a correct diagnosis.
‘Tell me, what has brought you to the doctor today?’). It is important that the patient feels that their welfare
Open-ended questions are designed to introduce an area is central to the doctor’s concern, that their story will be
of enquiry but allow the patient opportunity to answer listened to attentively, and that their information and
in their own way and shape the content of their views will be highly valued. Remember that most patients
response. Closed questions require a specific ‘yes’ or ‘no’ have no knowledge of anatomy, physiology or pathology
response. and it is very important to use appropriate language and
Remember that patients often have more than one avoid medical jargon.
concern they wish to raise and discuss. The order of their
problems may not relate to their importance from either
the patient’s or doctor’s perspective. It is therefore Symptoms and signs
particularly important in this opening phase not to
Five fundamental questions you are trying to
interrupt the patient as this might inhibit the disclosure extract for the history
of important information. Research has shown that
doctors often fail to allow patients to complete their • From which organ(s) do the symptoms arise?
opening statements uninterrupted and yet, when allowed • What is the likely cause?
to proceed without interruption, most people do so in • Are there any predisposing or risk factors?
less then 60 seconds. • Are there any complications?
Once the problems have been identified, it is worth • What are the patient’s ideas, concerns and
reflecting on whether you have understood the patient expectations?
correctly; this can be achieved by repeating a summary
back to them. It is also good practice to check for
additional concerns: ‘Is there anything else you would
like to discuss?’ You may write down a summary of the During the interview it is usual to use a combination
patient’s comments, but constantly maintain eye contact of open-ended and closed questions. Normally, open
and avoid becoming too immersed in writing (or using a questions are more commonly asked at the start of the
computer keyboard). An example of what you may have interview with closed questions asked later, as information
written at this stage is shown in the ‘symptoms and signs’ gathering becomes more focused in an attempt to elicit
box below. more detail.
3
Chapter
Questions to ask
has been necessary to alleviate the pain, whether the pain
interferes with work or other activities and whether the
Examples of open and closed questions
pain wakes the patient from sleep. It is difficult to assess
Open questions pain severity. Offering a patient a numerical score
• Tell me about your headaches. for pain, from ‘0’ for no pain to ‘10’ for excruciating
• What concerns you most about your headaches? pain, may provide a quantitative assessment of the
Closed questions symptom.
• Is the headache present when you wake up?
• Does the headache affect your eyesight?
Symptoms and signs
Pain assessment
• Type
It is also useful to summarise a reflection of the
• Site
information you have gathered at various times in the
• Spread
consultation: ‘So Mrs Smith, if I have understood you
• Periodicity or constancy
correctly, your headaches started two months ago and
• Relieving factors
were initially once a week but now occur almost every
• Exacerbating factors
day. You feel them worse over the back of the head.’ This
• Associated symptoms
is helpful not just because it allows you an opportunity
to check whether you have understood the patient
correctly, but can also provide a stimulus for them to give
further information and clarification. PSYCHOSOCIAL PERSPECTIVE
Information on psychosocial implications of a problem
BIOMEDICAL PERSPECTIVE requires questions to be asked about a person’s ideas,
Questions on the biomedical perspective should seek to concerns, expectations and the effect of the problem on
clarify the sequence of events and help inform an analysis their quality of life. For example, if you wanted to explore
of the cause of the symptoms. a patient’s psychosocial perspectives of their headaches,
Symptoms from an organ system have a typical location potential questions include those listed in the ‘questions
and character: chest pain may arise from the heart, lungs, to ask’ box.
oesophagus or chest wall but the localisation and
character differs. Establish the location of the symptom,
its mode of onset, its progression or regression, its Questions to ask
character, aggravating or relieving factors and associated To explore a patient’s psychosocial perspectives of
symptoms. their headaches
• What concerns you most about the headaches?

• What do you think is causing the headache?
Symptoms and signs • Is there some specific treatment you had in mind?
Symptoms helping distinguish different sources of • How do the headaches affect your daily life?
chest pain
• Myocardial ischaemia – pressure, crushing, pressing

retrosternal pain Some people find it difficult to talk about their feelings
• Pleuritic and chest wall pain – localised, sharp, and concerns and you need to be alert to verbal and
distinct exacerbation with deep inspiration nonverbal cues which might add insight to their thoughts
• Gastro-oesophageal reflux pain – burning and ideas. Following up on such cues can help facilitate
retrosternal discomfort (heart burn) arising from further enquiry and might feel less threatening than more
behind the sternum direct questions: ‘You mentioned that you were frightened
that your headaches could be serious. Did you have
specific cause you were worried about?’.
It is, of course, important to assess the impact of a
For the assessment of pain, use the framework shown problem on daily living by grading severity. For example,
in the pain assessment box. The quality of the pain is if the patient has intermittent claudication, ask how
important in determining the organ of origin. Patients far the patient can walk before pain forces a rest.
often find it difficult to describe the quality of their If breathlessness is a problem, ascertain whether the
symptom, so, if necessary, assist them by offering a list symptom occurs on the flat, climbing stairs, doing chores
of possible adjectives (e.g. cramping, griping, dull, in the home or at rest. Gathering such information will
throbbing, stabbing or vice-like). Ask whether medication allow a clearer understanding of the impact and meaning
4
Chapter
Gathering information: the history 1
of an illness for each individual. Combining information

on psychosocial perspectives with biomedical information A family tree
adds to the diagnosis and provides a foundation to plan
management.
I
BACKGROUND INFORMATION
The information gathered about patient’s problems needs
to be set in context and individualised. The doctor must II
understand and recognise the patient’s background, how
this impacts on the problem(s), and why the patient has
sought help at this particular time. Such contextual III
information requires enquiry into a person’s family
history, their personal and social history, past medical
IV
history as well as their drug and allergy history.
Family history
The family history may reveal evidence of an inherited normal male affected male
disorder. Information about the immediate family may normal female affected female
also have considerable bearing on the patient’s symptoms.
Social partnerships, marriage, sexual orientation and
close emotional attachments are complex systems which mating dead
exert profound influences on health and illness. A useful
starting point might be to ask if the patient has a regular
partner or is married. If so, ask about their health status
or any recent change in health status. If the patient has
children, determine their ages and state of health. Enquire dizygotic propositus monozygotic
whether any near relatives died in childhood and if so, twins twins
from what cause. When there is suspicion of a familial
disorder, it is helpful to construct a family tree (Fig. 1.4). Fig. 1.4 A standard family tree.
If the pattern of inheritance suggests a recessive trait, ask
whether the parents were related – in particular whether
they were first cousins. Education Enquire about the age at which the patient
left school and whether they attained any form of higher
Differential diagnosis education or vocational skill. In addition to providing
Common disorders expressed in families
useful background information, this information provides
a context for assessing diseases and disorders causing
• Hyperlipidaemia (ischaemic heart disease) intellectual deterioration and social function.
• Diabetes mellitus
• Hypertension Employment history Enquire about working conditions
• Myopia as this may be very important if there is suspicion of
• Alcoholism exposure to an occupational hazard.
• Depression Patients may attribute symptoms to work conditions,
• Osteoporosis e.g. a headache from working in front of a computer
• Cancer (bowel, ovarian, breast) screen. Other problems such as depression, chronic
fatigue syndrome and general malaise may also be blamed
on working conditions. Although these associations may
Personal and social history be prejudicial or coincidental, avoid dismissing them too
Just as with families, interactions with wider society can
exert powerful influences on health and well being. We Differential diagnosis
know, for example, that major health inequalities relate
Occupational disease
closely to social class and income, with socially and
financially deprived individuals experiencing poorer • Asbestos workers, builders: asbestosis, mesothelioma
health than people on higher incomes. A detailed social • Coal miners: coal worker’s pneumoconiosis
history includes enquiries about schooling, past and • Gold, copper and tin miners: silicosis
present employment, social support networks, and • Farmers, vets, abattoir workers: brucellosis
leisure. At this point, it is also convenient to ask about • Aniline dye workers: bladder cancer
the use of tobacco and alcohol – the quantity smoked and • Healthcare professionals: hepatitis B
the number of units drunk each week.
5
Chapter
readily. Frequent job changes or chronic unemployment helpful. Certain questions may reveal dependency
may reflect both socioeconomic circumstances and the without asking the patient to specify consumption. Ask
patient’s personality. It is useful to enquire about specific about early morning nausea, vomiting and tremulousness,
stress in the workplace, such as bullying or the fear of which are typical features of dependency. Ask whether
unemployment. they ever drink alone, when they first wake up in the
morning, or during the course of the day as well as in the
Tobacco consumption Patients usually give a fairly
evenings. Do they have alcohol-free days?
accurate account of their smoking. Ask what form of
tobacco they consume and for how long they have been Foreign travel
smoking. If they previously smoked, when did they stop
Ask the patient about recent foreign travel. If so, determine
and for how long did they abstain?
the countries visited and, if the patient has returned from
Alcohol consumption Unlike smoking, alcohol history an area where malaria is endemic, ask about adequate
is often inaccurate with a tendency to underestimate prophylaxis for the appropriate period.
intake. Many patients consider beer and wine to be less
alcoholic than spirits. Establish the type of alcohol the Home circumstances
patient consumes and assess their intake in units. At this stage in the interview, it is useful to ascertain how
the patient was coping until the onset of the illness. The
issue is particularly relevant for elderly patients and
Symptoms and signs individuals with poor domestic and social support
Units of alcohol equivalents networks. Do they live alone? Do they have any support
1 unit is equal to systems provided by either the community or family? If
• 1
/2 a pint of beer the patient’s condition has been present for some time,
• 1 glass of sherry determine the effect on daily living. For example, in
• 1 glass of wine a patient with chronic obstructive pulmonary disease:
• 1 standard measure of spirits Is work still possible? Can the patient climb stairs? If
not, what provisions are required for maintaining
independence? Can the patient attend to personal needs
such as bathing, shaving and cooking? What assistance
If the patient is vague, ask how long a bottle of wine may be on hand during the day or at night? What effects
or spirits might last or the amount they drank over a does the illness have on the financial status of the
specific recent time period (e.g. yesterday or over the last family?
week). Alcohol-dependent patients often deny when
questioned about alcohol consumption and a third party
history from friends and family is often revealing and PAST MEDICAL HISTORY
Patients recall their medical history with varying degrees
of detail and accuracy. Some provide a meticulous history,
Risk factors whilst others need reminding. You can jog a patient’s
Travel-related risks memory by asking if they have ever been admitted to
hospital or undergone a surgical procedure, including
Viral diseases
caesarean sections in women. If the patient mentions
• hepatitis A, B and C
specific illnesses or diagnoses, explore them in more
• yellow fever
detail. For example, if a patient mentions migraine, ask
• rabies
for a full description of the attacks so that you can decide
• polio
whether or not the label is correct.
Bacterial diseases
• salmonella Drug history
• shigella Many patients do not know the names of their medication
• enteropathogenic Escherichia coli and it is useful to ask for the labelled bottles or a written
• cholera medicines list. Remember to ask about nonprescription
• meningitis medicines: NSAIDs commonly cause dyspepsia and
• tetanus codeine-containing analgesics cause constipation. Ask
• Lyme disease about the duration of medication. Remember that
Parasite and protozoan diseases iatrogenic disease is very common and always consider
• malaria drug-related side effects in the differential diagnosis.
• schistosomiasis Ask women of reproductive age about their choice of
• trypanosomiasis contraceptive and postmenopausal women about
• amoebiasis hormone replacement therapy. Ask about, and record,
drug allergies.
6
Chapter
Systems review 1
At this point, it is useful to enquire sensitively about the frequency by beating out the rhythm with a hand?
the use of illicit drugs. This will be influenced by the Do any other symptoms appear such as dizziness, fainting
patient’s age and background; few 80-year-olds smoke or loss of consciousness at or around the time of the
pot or eat magic mushrooms! Broach the subject by palpitation?
first asking about marijuana, LSD and amphetamine
derivatives. If the response suggests exposure, enquire RESPIRATORY SYSTEM
about the use of the harder drugs such as cocaine and
heroin. Cough
Cough is difficult to quantify, particularly if dry. Does the
cough wake the patient from sleep? If productive, assess
Systems review the volume of sputum produced, using a standard
measure like an egg cupful as a reference point. Is the
The other major element of background information sputum mucoid (white or grey) or purulent (yellow or
gathering is to undertake a review of the body’s main green)?
systems. A systems review can provide an opportunity to Haemoptysis
identify symptoms or concerns that the patient may have
failed to mention in the history. Before focusing on If the patient has coughed up blood, ask whether this
individual systems ask some general questions about the is blood staining of the sputum or more conspicuous
patient’s health. Is the patient sleeping well? If not, is frank bleeding. Is it a recent event, or has it happened
there a problem getting to sleep or a tendency to wake periodically over a more prolonged period? Did it follow
in the middle of the night or in the early hours of the a particularly violent bout of coughing? Was it a definite
morning? Has there been weight loss, fevers, rashes or cough or was it vomited (haematemesis)? Was it
night sweats? The questions surrounding the presenting associated with pleuritic chest pain or breathlessness?
complaint will often have completed the systematic Wheezing
enquiry for that organ and there is no need to repeat
questions already asked; simply indicate ‘see above’ in Is the wheezing constant or intermittent, and are there
the notes. Develop a routine to avoid missing out a trigger factors such as exercise? If the patient is using
particular system. bronchodilators, determine the dosage and the frequency
of use.
CARDIOVASCULAR SYSTEM Pain
Chest pain If the patient complains of localised chest pain, ask

whether the painful area is tender to touch as might be
Determine the location of any chest pain, its quality and expected with chest wall pain. Is the pain worse on
its periodicity. Find out if there are specific triggering inspiration? This is a characteristic symptom of pleural,
factors. Does the pain radiate? If the patient describes an or pleuritic, pain.
exercise-induced pain, remember that angina can be
confined to the throat, jaw or medial aspect of the left
arm rather than centring on the chest. GASTROINTESTINAL SYSTEM
Change in weight
Dyspnoea
Ask the patient if there has been any recent weight loss
Ask about breathlessness. Does this occur after climbing or gain. If there is uncertainty about weight change, ask
one or more flight of stairs, after walking on the flat and the patient whether they have noticed any alteration in
after what distance? Does the patient become short of the fit of clothes or belts.
breath on lying flat (orthopnoea) or does the patient
Flatulence and heart burn
wake up breathless in the middle of the night (paroxysmal
nocturnal dyspnoea)? Does the patient complain of flatulence or burping? Is
there heart burn, and, if so, is it aggravated by postural
Ankle swelling
change such as bending? Does the mouth suddenly fill
Has the patient noticed any ankle swelling? Is it confined with saliva (waterbrash)?
to one leg, or does it affect both? Is the swelling persistent
Dysphagia
or only noticeable towards the end of the day?
Has there been difficulty in swallowing? Does this affect
Palpitations
solids more than liquids or both equally? Is the difficulty
Patients may recognise abnormal heart rhythm, swallowing progressive or fluctuant and unpredictable?
particularly one that is rapid or irregular. Try to establish Can the patient identify a site where they believe the
whether the abnormal rhythm is regular or irregular and obstruction occurs (this correlates poorly with the site of
for how long it lasts. Can the patient give you an idea of the relevant pathology).
7
Chapter
Abdominal pain incontinence without warning? Does coughing or

sneezing cause incontinence? Has the urinary stream
Ask about abdominal pain. Determine its site, quality and
become slower, perhaps associated with difficulty in
relationship to food. Does it appear soon after a meal, or
starting or stopping (terminal dribbling)? Does the patient
3 to 4 hours later? Is there any relationship to posture?
have the desire to empty the bladder soon after completing
Can the pain disappear for weeks or months or is it more
micturition?
persistent? Does the pain cause night waking?
Menstruation
Vomiting
Ask about menstrual rhythm. Are they regular and
Ask the patient about nausea and vomiting. Is the
predictable? Use a fraction notation to summarise the
vomiting violent (projectile) or does it represent effortless
duration of menstruation and the number of days
passive regurgitation of stomach contents? Is the vomiting
between each period (e.g. 7/28). Are the periods heavy
lightly bloodstained or does it look like coffee-grounds,
(menorrhagia) or painful (dysmenorrhoea)? Have they
suggesting partly altered blood? Are items of food eaten
changed in quality or quantity?
some hours before still recognisable? Is there recognisable
(green) bile in the vomit? Sexual activity
Bowel habit Although sexual dysfunction is common, few patients
volunteer this information and questions about sexual
Many patients believe they are constipated simply
activity need to be asked sensitively. Ask whether they
because they do not have a daily bowel action. If the
have a sexual partner and whether they are able to achieve
patient has always experienced a bowel movement three
a satisfactory physical relationship. Ask whether the
times a week, and there has been no recent change, there
partner is male or female. Does the patient practise ‘safe
is little likelihood of pathology. A change in bowel habit
sex’? Has the patient ever had a sexually transmitted
can refer to frequency, consistency of stool or both. Has
disease? In addition, ask whether intercourse is painful
the appearance of the stool altered? Are they black
or whether the patient is concerned about a lack of sexual
(suggestive of melaena) or pale and difficult to flush
activity, whether due to loss of libido or to actual
(suggestive of steatorrhoea)? If there has been a change
impotence. Prompting in this manner might prompt the
in bowel habit, ask the patient what drugs they are taking.
patient to volunteer information on libido, potency and
A common cause of constipation is the use of codeine-
pain.
containing analgesics. Has there been rectal bleeding or
mucous discharge? Finally, ask about incontinence or
soiling of underwear. Although this is not uncommon,
NERVOUS SYSTEM
particularly in parous women, few patients volunteer this
symptom. Headache
Most people experience headache. A useful distinguishing
feature is whether the headaches are unusual in either
GENITOURINARY SYSTEM frequency or character. Follow the enquiry you use for
other forms of pain but, in addition, ask if the pain is
Frequency
affected by head movement, coughing or sneezing. This
Determine the daytime (D) and night-time (N) frequency might suggest pain arising from the sinuses. If the patient
of micturition. The findings can be recorded as: D 6–8, mentions migraine, ask the patient to describe the
N 0–1. headaches in detail.
Has there been an increase in the actual volume
passed (polyuria) or, alternatively, a sense of urgency Loss of consciousness
with small volumes passed on each occasion? Does Has the patient lost consciousness? Avoid terms like
the patient wake at night to void urine and is this blackouts even if the patient tries to use them. Enquire
associated with increased thirst (polydipsia) and fluid about prodromal warning symptoms, whether they have
intake? been witnessed and whether they have led to incontinence,
injury or a bitten tongue. Do the episodes occur only in
Pain
certain environments or can they be triggered by certain
Ask whether there is pain either during or immediately activities (e.g. rising rapidly from a lying or sitting
after micturition. Has the patient noticed a urethral position)? How does the patient feel after the attack?
discharge? Is the urine offensive, cloudy or Patients recover rapidly from a simple faint but after an
bloodstained? epileptic seizure, patients often complain of headache
and may sleep deeply for several hours. If the patient
Altered bladder control
mentions epilepsy, ask about the exact nature of the
Determine if there has been urgency of micturition, with attacks. There may be specific symptoms accompanying
or without incontinence. Does the patient have urinary the attack that assist in making an accurate diagnosis.
8
Chapter
Systems review 1
Dizziness and vertigo Diplopia

Dizziness (or giddiness) is a common complaint, If the patient has experienced double vision (diplopia),
describing an ill-defined sense of disequilibrium most determine whether the images were separated horizontally
often without any objective evidence of imbalance. This or in an oblique orientation. Can the patient describe in
symptom is usually episodic, although some patients which direction of gaze the diplopia is most evident? Is
describe a more continuous feeling of dizziness. If the it relieved by covering one eye or the other?
symptom is paroxysmal, does it occur in particular
environments or with particular actions? For instance, Facial numbness
dizziness associated with hyperventilation attacks can Can the patient outline the distribution of any facial
occur with anxiety in crowded places, whereas patients sensory loss? Does the involvement include the tongue,
with postural hypotension will notice dizziness triggered gums and the buccal mucosa.
by sudden change of posture from lying or sitting to
standing. Only use the term ‘vertigo’ if the patient Deafness
describes a sense of rotation, either of the body or the
room or environment. Again, detail any triggering factors. Has the patient become aware of deafness? A useful
In benign positional vertigo, the symptom is induced by reference point is to ask about difficulties using the
lying down in bed at night on one particular side or telephone or listening to the radio/television. Is the
movement of the head from side to side. hearing loss bilateral or unilateral? Is there a history of
chronic exposure to environmental noise or a family
Speech and related functions history of deafness? Is the hearing particularly troublesome
when there is an increased level of background noise? Is
The history will already have provided information about
the hearing problem accompanied by any ringing sound
the patient’s speech. If there is a speech impediment, is
in the ear (tinnitus)?
this a problem of articulation, or does the patient use
wrong words, with or without a reduction in total speech Oropharyngeal dysphagia
output? Note the patient’s handedness, which should
include questions about the limb used for a variety of Has the patient problems with swallowing? Does this
skilled tasks, rather than just writing. Enquire from either principally affect fluids, solids or both? Is there spluttering
the patient or a third party whether there has been and coughing associated with swallowing?
difficulty understanding speech. Has there been any
change in reading or writing skill? Limb motor or sensory symptoms
Is the problem confined to one limb, the limbs on one
Memory
side of the body, the lower limbs alone or all four limbs?
The patient may not complain of memory disturbance Does the patient describe loss of sensation or some
and, if this becomes evident, determine whether this distortion of sensation (e.g. a feeling of tightness round
applies to recent events, to events further back in the the limb)? If the patient complains of weakness, enquire
patient’s youth, or to both. Is the memory problem whether it is intermittent or continuous and, if the latter,
persistent or does the patient have fluctuating memory whether it is progressing. Does the weakness mainly
loss? Impaired memory is a common symptom, although affect the proximal or the distal part of the limb? Has
further enquiry may suggest that it is not interfering with the patient noticed muscle wasting or any twitching of
quality of life or social functioning. limb muscles?
Loss of coordination
CRANIAL NERVE SYMPTOMS Few patients with a cerebellar syndrome will describe
Vision their problem as loss of coordination. Some will complain
of clumsiness, others will simply refer to the problem as
Ask about any visual disturbances. Do these take the weakness. When assessing the loss of limb coordination,
form of visual loss or positive symptoms such as it is useful to ask the patient about everyday activities
scintillations or shimmerings? Most patients assume that such as writing, fastening buttons and using eating
the right eye is concerned with vision to the right and utensils. Ask the patient about the sense of balance. Does
the left eye with vision to the left. Consequently, few the patient tend to deviate to a particular side or in either
will cover-test during attacks of visual disturbance direction? Has the patient had falls as a consequence of
to determine whether the problem is monocular or any imbalance?
binocular. Ask whether the patient has cover-tested
before labelling the account of the visual symptoms.
Is the visual disturbance transient and reversible, ENDOCRINE HISTORY
or continuous? Is it accompanied or followed by The history may provide clues to endocrine disease.
headache? Diabetes mellitus is characterised by weight loss,
9
Chapter
polydipsia and polyuria. An overactive thyroid is suggested In addition, the history may only be complete with a visit
by recent onset heat intolerance, weight loss with to the patient’s home.
increased appetite, irritability and palpitations. An
The hostile patient
underactive thyroid is suggested by constipation, weight
gain, altered skin texture, recent-onset cold tolerance and If a patient is hostile to your attempts to take a history,
depression. back off with dignity and use the experience to try and
analyse the reasons for the reaction. The reaction may
reflect anger at being ill, separated from family and work,
MUSCULOSKELETAL SYSTEM and the doctor or student provides an easy target for the
Has the patient experienced bone or joint pain? Has joint emotion. You may wish to conclude the interview,
pain been accompanied by swelling, tenderness or although you may feel it reasonable to question the
redness? Is the pain confined to a single joint or is it more patient gently about their anger and use the encounter
diffuse? Does the pain predominate on waking or does to restore trust and confidence, allowing you to explore
it appear as the relevant joint is used (e.g. in walking)? the history more formally. If the hostility persists,
Is there a history of trauma to the affected joint and is terminate the interview and discuss the problem with the
there a family history of joint disease? family. Involve another member of the medical or nursing
staff to act as witness.
History-taking in the presence of students
SKIN
Has the patient noticed any rashes? What is the truncal Occasionally, patients find the presence of a group of
and appendicular distribution? Was the rash accompanied students intimidating or an infringement of confidentiality.
by itching? Is there a potential occupational risk of a Although most often an explanation of their presence
chemical contact dermatitis? Enquire about recent change will satisfy the patient, it may be appropriate to leave
in cosmetics which might have provoked a skin reaction. the consultation and allow the patient to continue the
Have metal bracelets or necklaces caused the rash (nickel consultation privately (Fig. 1.6).
allergy)? Does the patient wear protective gloves when Time considerations
using washing up liquid?
The limited time allocated to a consultation might
preclude a full history-taking, and part of the expertise of
DOCUMENTING THE FINDINGS a skilled consulter is the ability to adapt and manage the
interview in the face of time or other constraints. The
It is essential that all the relevant information from the
interview should be efficiently choreographed to maximise
patient interview is accurately recorded in the notes.
the patient’s communication of important and relevant
Deciding what is relevant can be difficult, but, if in any
information. Judgement about which information is
doubt, err on the side of inclusion. A specimen case
relevant can be difficult, and sometimes seemingly
history is illustrated in Figure 1.5.
insignificant details can subsequently prove important to
patient management. It is important to be competent and
PARTICULAR PROBLEMS familiar with the approaches outlined in this and following
chapters even if time constraints make it difficult to apply.
The patient with depression or dementia
It is also important to recognise which symptoms and
It is useful to couple these clinical problems as both signs necessitate prompt or urgent action. To help with
can cause the patient to appear withdrawn and this, Emergency boxes and Red flag boxes can be found
uncommunicative. Patients with depression may dwell throughout the book. Emergency boxes identify those
on symptoms such as insomnia and appetite loss and clinical situations in which immediate action is necessary,
there may be a reluctance to discuss mood or mood whereas Red flag boxes identify symptoms and signs
change. Determine whether there has been any suicidal that necessitate urgent referral for assessment and
intent. Patients with dementia initially retain some insight investigation.
and in particular may have reasonable memory of distant
events. However, recent recall, orientation for ‘person,
place and time’ and logical thought patterns may be Recording the medical interview
obviously dysfunctional. A characteristic feature of
Alzheimer’s dementia is loss of insight and failure of the Almost every encounter between doctor (or student) and
patient to recognise their memory loss. This contrasts patient involves recording information. The initial record
with senile dementias in which the patient is often will include a detailed history and examination, the
concerned at their memory loss. When depression or problem list and plans for investigation and treatment.
dementia interferes with history-taking, family, friends Whenever the results of investigations become available,
and carers become crucially important in the assessment. this new information is added to the record and, at each
10
Chapter
Recording the medical interview 1
Patient history
Mrs G. W. 76-year-old female Allergies: None known

Date of birth: 11/1/36 Retired shop assistant
Travel abroad: Never
Date: 1/6/07
Family history
Patient’s problems:
(1) Constipation
(2) Stomach pain
M. I. 76 66 diabetic complications
History of patient’s problems:
(1) Constipation: Started on 7/4/07. Normally bowels open
76 80 alive and well
once a day, but didn’t go for 6 days. Subsequently has been
going once every 2–4 days.
(2) Stomach pain: Pain started at the same time. Site of pain is
in the left iliac fossa. Patient thought it was due to ‘straining’.
Episodes of pain are of sudden onset and are a ‘sagging dull
ache’.They last 1 hour and occur anything between 2–3 41 38 35
times a day to once every 3 days. There are no alleviating
or exacerbating factors. Pain unrelated to eating or
defecation and there are no preceding events. Pain appears alive and well
not to fluctuate.
Patient went to visit GP after 6 days constipation. GP felt a
mass on abdominal palpatation which on bimanual
examination was thought to be of ovarian origin. Patient No family history of TB.
referred to the gynaecological outpatient department.
Patient does not understand why GP has referred her to Systems review
hospital. Hopes the hospital can just prescribe a laxative and
discharge her. Her children have arranged a holiday for her General:
and her husband in one month’s time and she does not want No weight change, appetite normal, no fevers, night sweats,
to miss it. fatigue or itch.
Social history: Cardiovascular system:

Retired at age of 60 as shop assistant. Married. Husband is a No chest pain, palpitations, exertional dyspnoea, paroxysmal
retired bus driver. Alive and well. Live together in own terraced nocturnal dyspnoea, orthopnoea or ankle oedema.
house. Self-sufficient. No pets.
Respiratory system:
Smoking: No cough, wheeze, sputum or haemoptysis
Ex-smoker, 4–5 a day for 5 years as a teenager.
Gastrointestinal system:
Alcohol: No abdominal swelling noticed by patient, no nausea or
Only on Christmas Day and birthdays. vomiting, no haematemesis. Bowels open once every 2–3 days.
Stool normally formed. No blood or slime. No melaena.
Past obstetric history:
Menarche – 12 Menopause – 50 Gravidity 3 Parity 3 Genitourinary system:
No dysuria, haematuria. Frequency: D 2–3, N1.
(1) Female 41 Spontaneous vaginal delivery full term No vaginal discharge. Not sexually active.
(7 lb)
(2) Female 38 Spontaneous vaginal delivery full term Nervous system:
(8 lb 4 oz) No fits, faints or funny turns. No headache, paraesthesiae,
(3) Female 35 Spontaneous vaginal delivery weakness or poor balance.
39 weeks (6 lb 8 oz)
Musculoskeletal system:
Past medical history: No pain or swelling of joints. Slight stiffness in morning.
Hypertension for last 6 years treated by GP with atenolol.
No previous operations. Summary:
A 76-year-old hypertensive woman, referred to gynaecological
Drug history: Atenolol outpatients with a short history of constipation and stomach
pain. She has no other previous medical history.
Fig. 1.5 A specimen case history taken from a student’s notes. Note the brief summary at the end, the writing of which gives useful practice
in the art of condensing a substantial volume of information.
11
Chapter
PROBLEM-ORIENTATED MEDICAL RECORD

The accuracy of information gathered from a patient
during the course of an illness influences the precision
of the diagnosis and treatment. The POMR stresses
the need to gather all the information, biomedical,
psychosocial, demographic, symptoms and signs and
special tests, and uses this ‘database’ to construct a list of
problems. This problem list not only provides a summary
of the ‘whole’ patient but also offers a resource for
planning management and encourages you to look for
relationships between problems, allowing an integrated
overview of the patient to emerge. Moreover, it
distinguishes problems needing active management from
Fig. 1.6 The patient has to face not only the doctor but a number problems that may be of only historical significance. The
of students. Some patients will have difficulty coping with a ‘mass problem list does not provide a perspective of the relative
audience’.
importance of each problem: this must rely on discussion
with the patient and the skill of clinical judgement. The
follow-up visit, progress and change in management are database and problem list evolve through the course
recorded. The medical record chronicles the patient’s of an illness and changes with each subsequent
medical history from the first illness through to death. presentation.
Over a lifetime, patients present with distinct episodes of In addition to the problem list, the POMR provides a
acute disease and chronic, intractable or progressive framework for standardising the structure of follow-up
conditions. A number of doctors and healthcare notes (Fig. 1.7); this stresses changes in the patient’s
professionals may contribute to the medical record. In symptoms and signs and the evolution of clinical
addition, this multi-authored document may follow the assessment and management plans. The POMR also
patient whenever he or she moves home. provides a flow sheet that records sequential changes in
There is an onus on the author of each medical entry clinical and biochemical measurements.
to recognise the historical importance of each record and
to ensure that the entry conveys a clear and accurate
account which can be easily understood by others.
The medical record has other uses: it is the prime THE HISTORY
resource used in medical audit, a practice widely adopted For generations, there has been little change in the
for quality control in medical practice, and it provides method of recording information from the history. The
much of the evidence used in medicolegal situations; interview is the focal point of the doctor–patient
under judicial examination, your professional credibility relationship and establishes the bonding necessary for
relies solely on the medical record if your memory fails. the patient’s care. The history guides the patient through
Medical records are also a valuable source of data for a series of questions designed to build a profile of the
research. individual and his or her problems. By the end of the
As medical care becomes more specialised and complex first interview you should have a good understanding of
and increasingly dependent on teamwork, it has become the patient’s personality, social habits and clinical
necessary to standardise the approach to clinical record- problems. Additionally, you will have considered a
keeping. The problem-orientated medical record (POMR) differential diagnosis that may explain the patient’s
is a widely accepted framework for both standardising symptoms.
and improving the quality of medical records. The system A new history and examination are recorded in the
encourages a logical approach to diagnosis and notes whenever a patient presents with a fresh problem.
management and addresses the problem of maintaining Some information may remain unchanged over long
order in the multidisciplinary, highly specialised practice periods (previous illness, family history, education and
of modern medical care. The problem-orientated occupation). If these were accurately recorded at the time
approach to medical records was first advocated in of the first presentation, there is no need to re-enter them
1969 by Lawrence Weed and remains relevant today. unless there has been change.
However, it is probably more widely used in hospital Remember, at some time in the future the medical
practice than general practice. There is also increasing history may provide an important source of information,
use of computers to record medical interviews with particularly if a patient is admitted to hospital with, for
software packages that provide a rigid template for example, intense pain, altered consciousness or severe
recording consultation notes. Nevertheless many of the breathlessness and is therefore unable to provide a
principles underlying the POMR provide useful insights history. In these circumstances, a detailed systematic
and guidance to those learning about how to maintain record may provide crucial information. A routine
good medical records. systems enquiry also prompts your patient to remember
12
Chapter
The structure of problem-orientated medical record
History Examination
Database
Problem list
Progress notes Problem-related plans Flow chart
Fig. 1.7 Structure of the problem-orientated medical record (POMR).
events or illnesses that may otherwise have been (problems that have resolved or require no action but
overlooked. may be important at some stage in the patient’s present
or future management). An entry of ‘Peptic ulcer (2006)’
THE EXAMINATION in the ‘inactive’ column will provide a reminder to
someone considering the use of a nonsteroidal anti-
The examination may confirm or refute a diagnosis
inflammatory (NSAID) drug in a patient presenting at a
suspected from the history and by adding this information
later date with arthritis. The problem list is dynamic and
to the database you will be able to construct a more
the page is designed to allow you to shift problems
accurate problem list. Like the history, the examination
between the active and inactive columns (Fig. 1.9).
is structured to record both positive and negative findings
Your entries into the problem list may include
in detail.
established diagnoses (e.g. ulcerative colitis), symptoms
(e.g. dyspnoea), psychosocial concerns (e.g. concern that
THE PROBLEM LIST they will die of stomach cancer like their brother), physical
The problem list is fundamental to the POMR. The entries signs (e.g. ejection systolic murmur), laboratory tests
provide a record of all the patient’s important health- (e.g. anaemia), family and social history (e.g. carer for
related problems, both biomedical and psychosocial. The partner, unemployment) or special risk factors (e.g.
master problem list is placed at the front of the medical smoking, alcohol or narcotic abuse). The diagnostic level
record and each entry is dated (Fig. 1.8). This date refers at which you make the entry depends on the information
to the time of the entry, not the date when the patient available at a particular moment. Express the problem at
first noted the problem (this can be indicated in brackets the highest possible level but update the list if new
alongside the problem). The dates entered into the findings alter or refine your understanding of the problem.
problem list not only provide a chronology of the patient’s The problem list is designed to accommodate change;
health-related problems but also a ‘table of contents’ consequently, it is not necessary to delete an entry once
which serves the medical record. Using the entry date as a higher level of diagnosis (or understanding) is reached.
a reference, there should be no difficulty finding the For example, a patient may present with the problems of
original entry in the notes. In addition to providing a jaundice, anorexia and weight loss. This information will
summary and index, the problem list also assists the be entered into the problem list (Fig. 1.8). If, a few days
development of management plans. later, serological investigation confirms that the patient
was suffering from type A viral hepatitis, this new level
Setting up the problem list
of diagnosis can be entered on a new line in the block
Divide the problems into those that are active (i.e. those reserved for active problem 1 (Fig. 1.9). Other problems
requiring active management) and those that are inactive explained by the diagnosis (anorexia and weight loss)
13
Chapter
Initial problem list
Patient’s name: Hospital no:
No. Active problems Date Inactive problems Date
jaundice (Jan ‘07) 9/1/07

1
anorexia (Dec ‘06) 9/1/07

2
weight loss 9/1/07

3
recurrent rectal bleeding 9/1/07

4
smoking (since 1980) 9/1/07

5
unemployed (Nov ‘06) 9/1/07

6
stutter 9/1/07
7
brother died of colon cancer – patient concerned he may 9/1/07

8 have similar condition (Dec ’06)
duodenal ulcer (1996) 9/1/07

9
10
Fig. 1.8 Problem list entered on 9 January 2007.
should be amended with an arrow and asterisk to indicate that may aid the diagnosis. There are a large number
the connection with the solved problem. At this point, of special tests that may be applicable to a particular
viral hepatitis represents the highest level of diagnosis. problem; therefore, it is useful to evolve a general
Once the disease has resolved, an arrow to the opposite framework for investigation and to adapt this to each
‘inactive’ column will indicate the point during follow-up problem. You can construct a logical flow of investigations
that the doctor noted return of the liver tests to normal by considering bedside tests, side-ward tests, plain
(Fig. 1.9). Unexpected problems may become evident in radiographs, ultrasound, blood tests and specialised
the course of investigation (e.g. hypercholesterolaemia) imaging examinations (Fig. 1.11).
and these are added to the problem list.
Monitoring tests (Mx)
The problem list should be under constant review to
ensure that the entries are accurate and up-to-date. Monitoring information charts the patient’s progress.
Consider whether a particular problem can be monitored
and, if so, document the appropriate tests and the
INITIAL PROBLEM-RELATED PLANS frequency with which they should be performed to
The POMR offers a structured approach to the provide a meaningful flow of information.
management of a patient’s problems. By constructing the
Treatment (Rx)
problem list you will have clearly defined problems
requiring active management (i.e. investigation and Consider each problem in turn with a view to deciding
treatment), so it should be reasonably easy to develop a on a treatment strategy. If drug treatment is indicated,
management plan (Fig. 1.10) by considering four headings note the drug and dosage. Include a plan for monitoring
(see below); all or only some of these headings may be both side effects and the effectiveness of treatment.
applicable to a particular problem.
Education (Ed)
Diagnostic tests (Dx)
An important component of your patient’s management
Enter the differential next to each problem. Adjacent to is education and sharing information and decisions.
each of the possible diagnoses, enter the investigation Patients are able to cope better with their illness if they
14
Chapter
Updated problem list
Patient’s name: Hospital no:
No. Active problems Date Inactive problems Date
jaundice (Jan ‘07) 9/1/07 resolved 14/2/07

1 → type A hepatitis*
anorexia (Dec ‘06) 9/1/07

2 →*1
weight loss 9/1/07

3 →*1
recurrent rectal bleeding 9/1/07

4 → haemorrhoids 13/1/07 haemorrhoid banding 1/2/07
5 smoking (since 1980) 9/1/07
6 unemployed (Nov ‘06) 9/1/07
7 stutter 9/1/07
brother died of colon cancer – patient concerned

8 he may have similar condition (Dec ’06) 9/1/07 resolved Jan 2007
9 9/1/07
duodenal ulcer (1996)
10 hypercholesterolaemia 13/1/07
Fig. 1.9 Problem list updated to 14 February 2007, indicating the diagnosis of hepatitis A on 13 January and return of liver tests to normal by
14 February. The anorexia and weight loss are readily explained by the hepatitis; these problems are arrowed to indicate the relationship to
problem 1 (hepatitis*). Note that the haemorrhoids were diagnosed on 11 January and this problem became ‘inactive’ when banding was
performed on 1 February. The patient’s fears re colon cancer resolved when the diagnosis and causes of symptoms were explained. When the
biochemical tests were returned on 13 January, hypercholesterolaemia was diagnosed for the first time and this was entered into the problem
list on the same day. On 14 February, four unresolved problems remained.
understand its nature, its likely course and the effect of Objective (O)
treatment, and management is most effective when
Record any change in physical signs and investigations
patients are involved in decisions about their care. By
that may influence diagnosis, monitoring or treatment.
including this heading in your plans, you will be reminded
of the need to talk to your patient about the illness and Assessment (A)
involve them in decisions, and encouraged to develop
Comment on whether the subjective and objective
an educational plan for your overall management
information has confirmed or altered your assessment
strategy.
and plans.
PROGRESS NOTES Plan (P)
The POMR provides a disciplined and standardised After making the assessment, and in discussion with the
structure to follow-up notes. These should be succinct patient, consider whether any modification of the original
and brief, focusing mainly on change. There are four plan is needed. Structure this section according to the
headings to guide you through the progress note headings listed earlier (Dx, Mx, Rx and Ed).
(Fig. 1.12). If there is no subjective or objective change from one
visit to the next, simply record ‘No change in assessment
Subjective (S)
or plans’.
Record any change in the patient’s symptoms and, when
necessary, comment on compliance with a particular FLOW CHARTS
regimen (e.g. stopping smoking) or tolerance of drug Clinical investigations and measurements are often
treatment. repeated to monitor the course of acute or chronic illness.
15
Chapter
Problem-related plans
Problem Differential diagnosis Investigation
jaundice liver tests, prothrombin time

acute hepatitis hepatitis screen (A, B and C)
auto-antibodies
(SMA, ANA, AMA)
alcohol mean cell volume, gamma-GT
drugs check with family doctor
Dx
obstructive jaundice ultrasound liver
anorexia see jaundice urea and electrolytes
weight loss see jaundice basal weight
recurrent rectal bleeding haemorrhoids full blood count
polyp or colon cancer proctoscopy
colonoscopy or barium enema
smoking chest radiograph
Problem Monitor
jaundice twice weekly liver tests

anorexia monitor diet and caloric intake
Mx
weight loss twice weekly weight
recurrent rectal bleeding haemoglobin weekly
Problem Treatment
jaundice bed-rest
anorexia encourage calorific intake (favourite foods)
weight loss special high calorific drink supplements
Rx
recurrent rectal bleeding treat cause
(haemorrhoids or tumour) seek surgical opinion
smoking encourage relaxation and stress management
unemployed arrange meeting with social worker
concern recancer discuss concerns, advise refindings of tests and reassure
Problem Education
jaundice discuss differential diagnosis

Ed
anorexia explain association with jaundice
smoking discuss dangers, techniques for coping
rectal bleeding explain need for colonic investigation
Fig. 1.10 Example of a problem-related plan after the creation of a problem list (Dx, diagnostic tests; Mx, monitoring tests; Rx, treatments;
Ed, education.)
For example, patients presenting with diabetic ketoacidosis are relevant to medical record systems in general. The
require frequent checks of blood sugar, urea, electrolytes, POMR encourages all the members of the healthcare
blood pH, urine output and central venous pressure. team to standardise their approach to record-keeping.
In chronic renal failure, the course of the disease and This, in turn, enhances communication and guarantees
its treatment is monitored by repeated measurements that everybody involved in the patient’s care can
of blood urea and electrolytes, creatinine, creatinine contribute to the medical biography. Furthermore, careful
clearance, haemoglobin and body weight. A flow sheet structuring of the problem list, care plans and follow-up
is convenient for recording these data in a format that, at notes encourages logical, disciplined thinking and ensures
a glance, provides a summary of trends and progress (Fig. that the record is comprehensive and accurate. The
1.13). Graphs may be equally revealing (Fig. 1.14) and POMR approach to record-keeping counteracts the
are now often prepared automatically in computerised tendency for the ‘weight’ of a single problem to overwhelm
notes. and to distract from other subsidiary but potentially
important problems.
Peer review and medical audit have become an integral
ADVANTAGES OF THE POMR part of quality assurance and continuing medical
Whilst the POMR may not be followed in all health care education. The structure of the POMR exposes the
settings, its underlying principles represent qualities that clinician’s and patient’s thoughts and their decision-
16
Chapter
Diagnostic test flow chart
electrocardiogram blood glucose

peak flow measurements urine:
fluid aspiration pH
liver/pleural biopsy bedside tests blood
lumbar puncture protein
sigmoidoscopy bilirubin
urobilin
side-ward tests glucose
ketones
specific gravity
radiographs: ultrasound: faecal occult blood
skeleton abdomen
skull/sinuses radiographs pelvis
chest and ultrasound breasts
abdomen neck haematology
biochemistry
endocrine tests
laboratory immunology
tests microbiology
histopathology
endoscopy
CT scanning
magnetic resonance imaging
isotope scanning ‘special’
contrast radiology investigations
lung function tests
exercise electrocardiography
Fig. 1.11 Flow diagram to help plan diagnostic tests.
making processes. This, in itself, is educational for both

Progress notes the clinician and others reading the notes, and makes the
system particularly suited to the process of audit. The
date pressure to record meticulous and detailed information
11/1/07 S – nauseated, fatigued is also of intrinsic value to research workers embarking
on retrospective or prospective clinical studies. Perhaps
O – less jaundiced most importantly, the POMR helps to maintain a
liver less tender perspective of the ‘whole’ patient, thereby providing an
taking adequate calories and fluid
ultrasound liver/biliary tract: normal overview of physical, psychological and social problems
A – seems to be improving and their interaction in health and disease.
no obstruction
P – check liver tests tomorrow
phone laboratory for hepatitis markers CONFIDENTIALITY
13/1/07 S – feels considerably better, appetite improving Clinical notes contain confidential information and it is
O – transaminase levels and bilirubin falling important that you protect this confidentiality. Ensure
IgM antibody to hepatitis A positive that there is control over access to the medical record and
sigmoidoscopy: bleeding haemorrhoids that only individuals directly involved in the patient’s
hypercholesterolaemia
A – resolving hepatitis A care should read or write in the notes. Computerised
rectal bleeding in young patient likely notes should be password protected. In certain
to be haemorrhoids circumstances special security may be necessary. Patients
P – reassess patient, explain hepatitis A with HIV infection and AIDS and individuals attending
consider discharge if next set of liver tests
show sustained improvement; ask surgeon sexually transmitted or psychiatric clinics may have a
to consider treating haemorrhoids separate set of clinical notes that are maintained distinct
recheck cholesterol in 3 months from the general medical records. Access to these
reassure re no evidence of cancer found classified records is usually restricted to doctors working
in that department and the notes never leave the area of
Fig. 1.12 Example of follow-up notes.
the specialist unit.
17
Chapter

Flow sheet
History-taking
7 7 7 7
07 .0 .0 .0 07 .0
Date 9.1. 11.1 13.1 14.1 7.2. 14.2 There are special problems when recording a history
from elderly patients. Consider the following:
Tests
Hearing loss
Bilirubin • Common in the elderly
(<17) 233 190 130 28 10
• May be helped by hearing aid
AST • Important to speak clearly and slowly
(<40) 1140 830 500 52 23 • Face the patient and avoid extraneous sound
• If necessary, write questions in bold letters
ALT
(<45) 1600 650 491 61 31 Visual handicap
• Cataracts, glaucoma and macular degeneration are
Albumin d i s c h a r g e d
common in the elderly
(35–45) 41 40 41 42 43
• Ensure the room is well lit
Pro-time • Engage an assistant or carer to help patients move in
(s) 14/12 14/12 13/12 13/12 12/12 and out of the consulting room and examination
area
Haemoglobin
(11.5–16.2) 12.1 12.3 12.1 12.2 12.6 Dementia
• Often occurs in patients who appear physically fit
Blood urea • Forgetfulness, repetition and inappropriate answers
(3.5–6.5) 3.1 4.2 4.8 6.0 6.2
characterise responses
Blood glucose • Family members, friends and carers often note the
(3.5–6.5) 5.5 6.8 5.0 5.6 6,0 development of dementia
IgM Important aspects of a history from elderly
Hepatitis
screen
Hep A patients include:
+ve • State of the domestic environment and general living
Cholesterol conditions
(3.5–6.8) 8.1 8.4
• Provision of community and social services
• Family support structures
Fig. 1.13 Example of a flow sheet. • Economic status and pension provision
• Mobility (at home and in the local environment)
• Detailed drug history and compliance
• Provision of laundry services
Decreasing bilirubin level • Legal will
240
200
serum bilirubin
160
(μmol/L)
120
80
40
10 20 30 40 50 60
days
Fig. 1.14 Example of the use of a graph to illustrate changes in

serum bilirubin levels following acute type A hepatitis.
18
Chapter
Review
The history
• Welcome • Medicines, drugs and tobacco

• Note the patient’s body language • Alcohol consumption
• Begin with an open-ended question • Foreign travel
• Take a history of the presenting complaints(s) – both • Home circumstances
biomedical and psychosocial perspectives; use closed • Family history
questions to answer the following: • Systems review
• which organ system? • cardiovascular
• likely cause? • respiratory
• predisposing factors? • gastrointestinal
• complications • genitourinary
• Social history • nervous
• Medical history • endocrine
• Education • musculoskeletal
• Employment • skin and hair
19
2
The general examination
The dividing line between the history and examination is 10–15 min, although if you discover an abnormality,
artificial. The examination really begins from the moment considerably more time will be spent refining the findings.
you set eyes on the patient. During the course of the From the outset you should aim to choreograph an
history you will examine the patient’s intellect, personality, economical, aesthetic and complete examination.
family and genetic background, as well as gather
information on the presenting complaint and medical
history. In addition, you will have the opportunity to General examination
assess speech, orientation for person, place and time, and
mood (affect). Throughout the history and examination The general examination permits you to obtain an
you should sense information from the patient’s unspoken overview of the general state of health and provides an
body language. These physical signs are rarely taught, opportunity to examine systems that do not fall neatly
although the patient’s body language may provide many into a regional examination. For the patient, the general
useful signs. The patient’s facial expression and tone of examination is also a gentle introduction to the more
voice often impart more information than verbal intense systems examination to follow.
communication. Hunched shoulders, a slow gait and
poor eye contact may convey a reluctant patient, unable
or unwilling to confront or expose anxieties or fears. FIRST IMPRESSIONS
Facial expression, tone of voice and body attitude may The examination commences as the patient walks into
signal depression, even if the patient does not complain the consulting room or as you sit down at the bedside to
of feeling depressed. Try to look, listen and then write, take a history. At this first encounter, even before you
this will give you the opportunity to see, as well as listen initiate the history, decide whether the patient looks
to, the patient’s complaints. well or not and whether there is any striking physical
The formal physical examination follows on from the abnormality. You will also gain an immediate impression
history and calls on your major senses of sight, touch and of dress, grooming and personal hygiene.
hearing. Inspection, palpation, percussion and auscultation As the patient approaches you in the consulting or
form the foundation of the physical examination and this examination room, observe the posture, gait and character
formula is repeated each time you examine an organ of the stride. Diseases of nerves, muscles, bones and
system. The otoscope and ophthalmoscope extend your joints are associated with abnormal gaits and postures.
vision into the ear and eye, respectively, whereas the You should quickly recognise the slow shuffling gait and
stethoscope provides an amplification system to help you ‘pill rolling’ tremor of Parkinson’s disease or the unsteady
listen to the heart, lung and bowel sounds. With the help broad-based gait of the ataxic patient. Patients with
of technology, we are now able to extend our vision deep proximal muscle weakness may have difficulty rising
into the body: radiographs (including computerised axial from the waiting room chair and their gait may have a
tomography scanning), ultrasound, magnetic resonance waddling appearance. Patients with osteoporosis lose
imaging and fibreoptics greatly broaden our powers of height as the vertebrae progressively collapse: you may
observation. be struck by the typically stooped (kyphotic) appearance
The physical examination begins with a general and ‘round shoulders’ of these patients. Take note if the
examination and is followed by examination of the skin, patient walks with a stick or some form of additional
head and neck, heart and lungs, abdominal organs, physical support. A white stick indicates partial or
musculoskeletal and neurological systems. With practice complete blindness. The gait also conveys body language:
it is possible to perform the ‘routine’ examination in the patient may have a spring in the step, make rapid eye
20
Chapter
Formal examination 2
relief lying with knees drawn towards the chest. Patients

with peritonitis lie motionless, as any abdominal wall
movement causes intense pain. The pain of acute
pyelonephritis or perinephric abscess might be partly
relieved by lateral flexion to the side of the pathology. In
acute pericarditis, the patient finds modest relief by sitting
forward; and in left ventricular failure, patients breath
more easily when lying propped up on three or four
pillows (this is termed orthopnoea).
Formal examination
Fig. 2.1 The handshake serves as a gentle introduction to the
physical contact that will occur during the formal physical On completion of the history, prepare the patient for
examination. the formal examination. Always remain sensitive to the
apprehension most patients feel when laid out naked on
contact and immediately offer a firm handshake. This the examination couch or bed. Imagine yourself in that
contrasts with the patient with drooping shoulders and position, confronted by a near stranger who is about to
a slow (but otherwise normal) step who avoids eye inspect, palpate, percuss and auscultate your body – a
contact. daunting thought. The history should already have
When making your initial acquaintance with the provided you with the opportunity to build a confident
patient, a warm handshake serves a number of functions professional relationship with the patient. It is a cultural
(Fig. 2.1). The touching of hands may reassure the patient and established fact that it is quite acceptable for a doctor
and serve as a gentle and symbolic introduction to to undertake a comprehensive physical examination,
the more intimate physical contact of the examination although remain sensitive to some cultural norms
that follows the history. Before shaking hands, glance where same-sex examinations might be preferable. This
momentarily at the hand to ensure that you will not be acceptance usually extends to medical students who can
grabbing a prosthesis or deformed hand. A well-made be reassured that most patients welcome students and
prosthesis may cause considerable embarrassment as you recognise their need to learn the examination technique.
suddenly realise that the hand you are shaking is hard Explain the necessity of undertaking a full physical
and lifeless. You may also note other abnormalities such examination. The examination adds information to the
as a potentially painful rheumatoid hand or missing clinical database and a thorough examination provides
fingers. The grip of the handshake usually provides considerable reassurance to the patient.
some useful information. A normal grip conveys different
information from a weak, lethargic handshake, which
may imply distal muscle weakness, general ill-health or
depression. The handshake is a useful physical sign in
patients with myotonia dystrophica, a rare autosomal
Growth failure
dominant inherited disease of muscle. A feature of this
disease is the abnormally slow relaxation of the grip on Genetic
completion of the handshake. The syndrome is also • Achondroplasia
characterised by premature frontal balding, testicular • Turner’s syndrome
atrophy and cataracts. • Down’s syndrome
On first contact with the patient, you may be struck Constitutional
by an unusual physical stature. Unusually short stature • Family members who have short stature
may reflect constitutional shortness, a distinct genetic
Endocrine
syndrome or the consequence of intrauterine, childhood
• Hypopituitarism
or adolescent growth retardation. Unusually tall stature
• Hypothyroidism
is most often constitutional, although hypothalamic
tumours in childhood or adolescence may cause excessive Systemic disease
growth hormone release, resulting in abnormally rapid • Crohn’s disease
linear growth and gigantism. If excess growth hormone • Ulcerative colitis
release occurs after the bony epiphyses have fused, body • Renal failure
shape changes (acromegaly). Severe malnutrition and Malnutrition
obesity are readily recognised on the first encounter with • Intrauterine growth retardation
a patient. • Marasmus
In hospitalised patients, posture may provide helpful • Kwashiorkor
information. Patients with acute pancreatitis find some
21
Chapter
2 The general examination
The examination requires full exposure: men and

women should be asked to remove superficial clothing
and vests or undershirts. For a chest examination, women
should be asked to remove their bra. Ensure a clean
and presentable examination gown is available in the
examination room for the patient to don before you enter
the room. When a patient of the opposite sex is to be
examined, always ask the chaperone to check whether
the patient is ready.
SETTING
A separate examination room or adequate screening Fig. 2.2 The position of the patient at the start of the examination.
should be provided to ensure privacy while the patient is
undressing and being examined. The room should be
comfortably warm. Ensure that there are fresh sheets respiratory or cardiac disease, therefore, you should gear
(either linen or disposable) and a clean blanket for cover. the examination towards determining which of these
The examination couch should be positioned to allow possibilities is responsible for the symptoms.
you to examine from the patient’s right side and there Begin with an inspection of overall appearance.
must be good general illumination. You should be
fully equipped to undertake the examination without
disruption. Ensure you have a working penlight torch Symptoms and signs
and stethoscope. Close at hand there must be a
Observation of general appearance
sphygmomanometer, ophthalmoscope, otoscope, tongue
depressors and disposable gloves (for genital and rectal • Does the patient look comfortable or distressed?
examination). Basic equipment for the neurological • Is the patient well or ill?
examination should be available. This includes a patellar • Is there a recognisable syndrome?
hammer, tuning fork, cotton wool buds, an appropriate • Is the patient well nourished?
object for testing pin-prick responses, test tubes to fill • Is the patient well hydrated?
with hot and cold water for temperature testing, and hat
pins with red and white tops to assess visual fields. A
cupful of drinking water should also be available, as you
may ask the patient to swallow a mouthful to check for
a thyroid goitre or other neck swelling.
Recognisable syndromes and facies
As you approach the patient, re-establish both verbal
When inspecting the face, you might be struck by a single
and eye contact. You may ask the patient whether they
sign such as a red eye or the characteristic facies associated
feel comfortable and are prepared for the examination.
with discrete syndromes.
Start the examination with the patient supine and the
head and shoulders raised to approximately 45° above
the horizontal. Most modern examination couches and THE EYE
hospital beds are designed to allow easy adjustment of The history might be helpful in distinguishing possible
the upper body. Most of the examination takes place with causes of the red eye. Ask about duration, previous
the patient comfortably resting in this position (Fig. 2.2). attacks, pain (and its character), photophobia and possible
Three further adjustments will be made in the course of direct causes of traumatic damage. It is useful to
the examination. When auscultating the mitral area of
the heart it is helpful to roll the patient towards the left
lateral position as this brings the apex closer to the Questions to ask
stethoscope. To examine the neck, posterior chest, back
Red eyes
and spine you will ask the patient to sit forward. For
assessing the abdomen, reposition the patient to lie flat, • Is red eye painful or painless?
as this provides optimal access for the abdominal • Is vision affected? Can the patient read ordinary
examination. Plan the examination to ensure the most print with the affected eye(s)?
economical movements for both you and the patient. • Is there foreign body sensation?
Following the history, reflect on which physical signs • Is there photophobia?
may help you confirm or refine your initial assessment. • Is there a discharge other than tears?
Anticipation of physical signs will help you to direct and • Was there trauma?
focus the examination. For example, if a patient complains • Are you a contact lens wearer?
of breathlessness, you may anticipate anaemia or
22
Chapter
Recognisable syndromes and facies 2
distinguish the sensation of a foreign body from less peering through a small hole. In nonrefractive disorders,
specific symptoms such as ‘grittiness’ and ‘itching’. A improvement does not occur.
foreign body sensation feels as if there is something in Next, use a penlight to inspect the pupils and anterior
the eye and is associated with some difficulty opening the segment. In angle closure glaucoma the pupil may be
eye. This symptom is characteristic of an active corneal fixed in mid-dilation and may not respond to light. In
process causing the red eye. corneal abrasion, acute keratitis and iritis, the pupil might
be pinpoint. A purulent discharge suggests bacterial
conjunctivitis or keratitis. The pattern of redness might
Differential diagnosis be helpful. Diffuse injection of both the palpebral and
Main causes of red eye bulbar conjunctivae suggests primary conjunctival
disorders (bacterial, viral, allergic, toxic or associated with
• Conjunctivitis (infective, allergic, toxic)
dry eyes). In contrast, more serious disorders such as
• Keratitis (infective, foreign body, sicca syndrome)
keratitis, iritis and angle closure glaucoma present with
• Acute closed angle glaucoma
a ‘ciliary flush’ with injection most marked at the limbus
• Iritis
(the sclerocorneal junction). A white spot or opacity on
• Subconjunctival haemorrhage
the cornea indicates keratitis and further slit-lamp
examination with fluorescein is required to delineate the
lesion. Hypopyon is seen as a layer of pus in the anterior
Begin the examination by inspecting the eyes. In lid chamber and is associated with infectious keratitis,
and conjunctival disorders, there is no foreign body acute iritis and endophthalmitis and is an ophthalmic
sensation or photophobia and the patient sits in a brightly emergency. Hyphaema refers to the presence of a layer
lit room without discomfort. In bacterial conjunctivitis the of blood in the anterior compartment and is usually
patient complains of pussy discharge (especially in the caused by injury. Subconjunctival haemorrhage is painless
morning on waking) and this might be seen on inspection. and characterised by demarcated areas of extravasated
A foreign body sensation (rather than gritty or itchy blood which resolves in 1–2 weeks.
sensation) is typical of active corneal disease. In infectious
keratitis the patient has difficulty keeping the affected eye
open, and a similar sign occurs with contact lens abrasion.
Red flag – urgent referral
Patients with iritis may present with difficulty keeping
the eye open and some photophobia but without the Indications for emergency referral to
ophthalmology
complaint of a foreign body sensation. In acute angle
closure glaucoma the patient often clutches the affected • Unilateral red eye which is painful with nausea and
eye and complains of associated headache and malaise. vomiting (e.g. acute glaucoma)
Visual acuity may be affected in red eye and should be • Associated loss of vision
assessed. The pinhole test helps distinguish refractive • Corneal infiltrate or hypopion
errors from other causes of visual loss. In refractive visual
disturbances (e.g. myopia), vision is improved when
FACIES AND SYNDROMES

Symptoms and signs Certain diseases are readily identified by a distinctive
Quick testing of visual acuity combination of physical characteristics. There are a large
number of recognisable congenital syndromes that were
• Assess ability of each eye to read newspaper print
probably diagnosed during childhood and should not
• Pinhole test
present as an undiagnosed problem to physicians caring
• Snellen chart
for teenagers or adults. In addition, only a proportion
survives into adulthood. There are several recognisable
genetic or chromosomal syndromes that may present to
Symptoms and signs
clinicians caring for adults; examples include Down’s
syndrome (trisomy 21; Fig. 2.3), Turner’s syndrome (Fig.
Penlight inspection of the red eye
2.4), Marfan’s syndrome (Fig. 2.5), tuberous sclerosis
• Does the pupil react to light? (Figs 2.6, 2.7), albinism (Fig. 2.8), the fragile X chromosome
• Is the pupil smaller than expected or pinpoint? (a common genetic cause of mental subnormality
• Is there a purulent discharge? in which affected males have unusually large testes),
• What is the pattern of the redness? Peutz–Jeghers syndrome (Figs 2.9–2.11), Waardenburg’s
• Is there a corneal ‘white spot’? syndrome (Fig. 2.12), familial hypercholesterolaemia
• Is there hypopyon or hyphema? (Figs 2.13–2.17) and neurofibromatosis. Other readily
recognisable syndromes include the endocrine disorders
23
Chapter
Symptoms and signs

Down’s syndrome (trisomy 21)
• Facies – oblique orbital fissures, epicanthic folds,

small ears, flat nasal bridge, protruding tongue,
Brushfield’s spots on iris
• Short stature
• Hands – single palmar crease, curved little finger,
short hands
• Heart disease (endocardial cushion defects)
• Gap between first and second toes
• Educationally subnormal
Fig. 2.3 Down’s syndrome: epicanthic folds, Brushfield’s spots and
hypertelorism (increased interorbital distance).
Fig. 2.4 Turner’s syndrome: typical facial Fig. 2.5 Marfan’s syndrome. Fig. 2.6 Tuberous sclerosis: flecks of white
appearance, webbed neck and widely hair.
spaced nipples.
Symptoms and signs Symptoms and signs

Turner’s syndrome (XO karyotype) Marfan’s syndrome
• Failure of sexual development • Arm span greater than height

• Short stature • Above average crown-to-heel height
• Facies – micrognathia (small chin), low-set ears, • Long slender fingers
fish-like mouth, epicanthic folds • Hyperextensible joints
• Short, webbed neck with low hairline; widely spaced • Kyphoscoliosis and anterior chest wall deformity
nipples (shield-shaped chest) • High-arched palate
• Heart disease (coarctation) • Aortic incompetence and dissecting aortic aneurysms
• Short fourth metacarpal or metatarsal • Subluxation or dislocation of the lens
• Abnormally wide carrying angle of the elbow
24
Chapter
Recognisable syndromes and facies 2
Symptoms and signs

Tuberous sclerosis (Bourneville’s disease,
autosomal dominant chromosome 9)
• Epilepsy
• Cognitive impairment (67%)
• Skin lesions (facial adenoma sebaceum, shagreen
patch, fibromas near toenails and eyebrows)
• Flecks of white hair
• Retinal haemorrhages
Fig. 2.7 Tuberous sclerosis: shagreen patch.
Symptoms and signs

Oculocutaneous albinism (autosomal recessive)
• Hypomelanosis or amelanosis of skin

• White hair
• Photophobia, nystagmus
• Hypopigmented fundus and translucent iris
Fig. 2.8 Albinism: typical translucent iris.
Fig. 2.9 Peutz–Jeghers syndrome: freckles on lips. Fig. 2.10 Peutz–Jeghers syndrome: pigmentation of the buccal
mucosa.
Symptoms and signs

Peutz–Jeghers syndrome (autosomal dominant)
• Pigmented macules (1–5 mm in diameter)

• Occur in profusion on lips, buccal mucosa and
fingers
• Gastric, small intestinal and colonic hamartoms
polyps that sometimes give rise to abdominal pain,
bleeding and intussusception
Fig. 2.11 Peutz–Jeghers syndrome: pigmentation of the big toe.
25
Chapter
Symptoms and signs

Waardenberg’s syndrome (autosomal dominant)
• Cochlear deafness
• Frontal white lock of hair
• Wide-set eyes
• Different coloured irises (heterochromia)
• White eyelashes
• Piebaldism
Fig. 2.12 Waardenberg’s syndrome: typical white forelock.
Symptoms and signs

Familial hypercholesterolaemia (autosomal
dominant)
• Xanthelasmas, skin xanthomas

• Tendon xanthomas
• Arcus senilis
• Marked artherosclerosis
• Ischaemic heart disease, peripheral vascular disease
Fig. 2.13 Familial hypercholesterolaemia: corneal arcus senilis.
Fig. 2.14 Familial hypercholesterolaemia: tendon xanthomas. Fig. 2.15 Familial hypercholesterolaemia: tendon xanthomas.
26
Chapter
The thyroid gland 2
The endocrine organs
hypothalamus
pituitary
parathyroid gland
thyroid gland
adrenal gland
pancreas (insulin)
Fig. 2.16 Familial hypercholesterolaemia: skin xanthomas.
ovaries
testicles
Fig. 2.18 The positions of the main endocrine organs.
The thyroid gland
Structure and function

The thyroid gland develops from a ventral pouch of the
fetal pharynx. This pouch evolves into the thyroid gland
Fig. 2.17 Familial hypercholesterolaemia: xanthelasmata around by migrating caudally to a resting place in front of the
the eyelids.
trachea. The migration may leave thyroid remnants along
the embryonic tract which extends from the back of the
tongue (where a residual lingual thyroid ‘rest’ may occur).
and major organ failure (liver, heart, lungs and A midline thyroglossal cyst may develop if the migration
kidneys). tract fails to obliterate.
The thyroid gland consists of two lateral lobes joined
by an isthmus. The gland lies in front of the larynx and
Endocrine syndromes trachea with the isthmus overlying the second to fourth
tracheal rings (Fig. 2.19). The lateral lobes extend from
The endocrine glands are scattered throughout the body the side of the thyroid cartilage to the sixth tracheal
(Fig. 2.18). It is practical to consider the examination of ring. Two nerves lie in close proximity to the thyroid
the endocrine glands in the context of the overall general gland: the recurrent laryngeal nerve runs in the groove
examination. Both over- and underactivity of the between the trachea and the thyroid; and the external
endocrine glands can be suspected from the patient’s branch of the superior laryngeal nerve lies deep to the
facies, body build and skin colour; endocrinopathies are upper poles. In thyroid cancer, these nerves may be
often readily recognised in the course of the general invaded and damage may occur in the course of thyroid
examination. surgery.
Distinct clinical syndromes occur in diseases of the
thyroid, parathyroid, adrenal and pituitary glands. An
overview of the structure and function of each of these THYROXINE SYNTHESIS AND SECRETION
organs will help your clinical assessment and syndrome The anterior pituitary hormone, thyroid stimulating
recognition. hormone (TSH), stimulates the synthesis of thyroxine
27
Chapter
Thyroid anatomy Biosynthesis of thyroxine
hyoid bone thyroid hypothalamus

cartilage TRH
+
sternocleido-
mastoid cricoid
muscle cartilage
pituitary
trachea lobe of TSH

thyroid gland +
thyroid
manubrium isthmus of
of the thyroid gland
sternum
capillary
Fig. 2.19 Anatomy of the thyroid gland and surrounding structures. basement
membrane
colloid
colloid
microvilli follicular cell
(T4) (Fig. 2.20). The functioning unit of the thyroid is the
follicle, which consists of epithelial cells lining a central
colloid space. The epithelial cells concentrate iodide, parafollicular
cell
which is oxidised to iodine and incorporated with tyrosine
to form mono-iodotyrosine and di-iodotyrosine. These
TBG T3
two iodinated tyrosines are combined in the colloid to
iodide TBG T4
form either tri-iodothyronine (T3) or tetra-iodothyronine
(T4). The two active hormones, T3 and T4, are stored in T3 T4
the colloid and bound to a specific binding protein
follicular cell
(thyroglobulin). The protein-bound hormones are taken
back up into the follicle epithelium by endocytosis. In the iodine
iodine tyrosine
cells, the colloid droplets are disrupted by proteolytic I peptidase
enzymes, allowing the release of T3 and T4 into the
HO R HO R
circulation where most circulate bound to thyroid binding I I
globulin (TBG). Free hormone levels dictate the metabolic mono-iodotyrosine di-iodotyrosine
(MIT) (DIT)
effects of T4. T4 is synthesised only in the thyroid but T3
can also be produced from conversion of circulating T4 in T3
the liver, the kidney and other tissues. The hepatic thyroglobulin thyroglobulin
conversion of T4 results in two species of T3: an active T3 T4
and an inactive reverse T3.
MIT
thyroglobulin
DIT
Clinical examination of the thyroid gland
and function colloid peroxidase
transaminase
(coupling)
Although considered part of the general examination, the T3
thyroglobulin
thyroid gland is usually examined when examining the T4
head and neck (see Ch. 4).
Like any other organ, the thyroid examination relies
on inspection, palpation, percussion and auscultation.
Examine the thyroid gland with the patient sitting forward Fig. 2.20 The hypothalamus secretes thyroid releasing hormone
(TRH) which stimulates the anterior pituitary to produce thyroid
in bed or seated in a chair. stimulating hormone (TSH). This stimulates the synthesis of thyroxine
Ensure complete exposure of the neck and upper (T4) in the follicles. Iodide taken up into the follicular cell is oxidised
chest. Inspect the thyroid from the front of the neck. The to iodine and then incorporated into tyrosine to form mono-
normal thyroid gland is neither visible nor palpable. An iodotyrosine (MIT) and di-iodotyrosine (DIT), which binds with
enlarged thyroid, or goitre, is seen as a fullness on either thyroglobulin and is secreted into the colloid where T3 and T4 are
synthesised. These are taken back into the follicular cells taken up by
side of the trachea below the cricoid cartilage, or as a endocytosis where the T3 and T4 are split from thyroglobulin and
distinct, enlarged, nodular organ with one or both lobes released into the circulation, where they are bound to T4 binding
easily visible (Figs. 2.21–2.23). If the lobes are visible, globulin (TBG).
28
Chapter
The thyroid gland 2
determine whether they look symmetrical or irregular. symmetry and extent of the goitre. A soft, smooth goitre
Ask the patient to sip a little water and hold it in the may be more easily seen than felt. It is unusual for the
mouth. When you give the instruction to swallow, watch goitre to be tender unless the enlargement is caused by
for the characteristic upward movement of the goitre acute inflammatory thyroiditis. In the course of thyroid
as the pharyngeal muscles contract. This test helps palpation, again ask the patient to take a sip of water and
distinguish a thyroid mass from other neck masses to swallow when you indicate. As the patient gulps,
(e.g. enlarged lymph nodes, which hardly move with you should feel the goitre move beneath your fingers.
swallowing). The midline remnant of the thyroid Complete the palpation by feeling for the carotids, which
(thyroglossal cysts or thyroid remnants) also moves with may be encased by a malignant thyroid gland. Thyroid
swallowing. carcinoma may spread to local neck lymph nodes, so it is
Next, explain to the patient that you wish to feel the important to conclude the palpation by checking for
front of the neck for the thyroid gland. Position yourself palpable regional lymph nodes.
to the right and slightly behind the patient. Feel for the The thyroid gland may also enlarge in a downward
left and right lobes with the finger pulps of both hands direction behind the manubrium sterni. This retrosternal
(Fig. 2.24). Ensure a gentle examination, as your hands goitre may extend deeply into the superior mediastinum
are positioned in a throttling posture; reassure the patient and may even cause compression symptoms (i.e.
by standing to the side rather than at the rear so that you breathlessness and dysphagia). Retrosternal extension
remain in the patient’s peripheral field of vision. Assess can be assessed by percussing over the manubrium and
the texture (hard or soft, single or multiple nodules), upper sternum (Fig. 2.25). Normally, this area resonates,
yet when there is retrosternal enlargement the percussion
note is dull. Auscultate the gland for bruits by applying
the diaphragm of the stethoscope to each lobe in turn
(Fig. 2.26). Ask the patient to stop breathing for a moment
while you listen on either side for a bruit. A soft bruit is
characteristic of the smooth symmetrical hyperthyroid
goitre of Graves’ disease.
Clinical assessment of thyroid function

T4 has a number of important metabolic effects and
over- or underactivity results in characteristic clinical
syndromes that may readily be recognised. Diagnosis of
hyperthyroidism is confirmed by measuring the serum
levels of T4 and T3, whereas in hypothyroidism the serum
Fig. 2.21 Smooth goitre appearing as fullness in the anterior neck. TSH level is elevated and T4 is subnormal.
a b
Fig. 2.22 Readily visible multinodular thyroid goitre. Fig. 2.23 Asymmetrical multinodular
goitre.
29
Chapter
Questions to ask
Hyperthyroidism
• Have you lost weight recently?

• Has your appetite changed (e.g. increased)?
• Have you noticed a change in bowel habit (e.g.
increased)?
• Have you noticed a recent change in heat tolerance?
• Do you suffer from excessive sweating?
• Does your heart race or palpitate?
• Have you noticed a change in mood?
Fig. 2.24 Position for palpation of the lateral lobes of the isthmus Symptoms and signs
of the thyroid.
Hyperthyroidism
• Weight loss, increased appetite

• Recent onset of heat intolerance
• Agitation, nervousness
• Hot sweaty palms
• Fine peripheral tremor
• Bounding peripheral pulses
• Tachycardia, atrial fibrillation
• Lid retraction and lid lag
• Goitre, with or without overlying bruit
• Brisk tendon reflexes
Fig. 2.25 A retrosternal goitre is suggested by dullness to

percussion over the manubrium sterni. masquerades as classical hypothyroidism. In both young
and older thyrotoxic patients, you may be alerted to the
diagnosis by a history of weight loss, recent intolerance
to hot weather, sweating, palpitations, abnormal
irritability and nervousness and increased bowel
frequency. Most hyperthyroid patients feel warm and
sweaty, have a tachycardia, staring eyes (caused by lid
retraction) and abnormally brisk tendon reflexes. A fine
peripheral tremor is common in thyrotoxicosis. This can
be demonstrated by placing a sheet of paper on the back
of the outstretched hand and watching the tremor, which
is amplified by the sheet of paper ‘trembling’ (Fig. 2.27).
Although similar signs of hyperthyroidism may occur in
the young and old, Graves’ disease is more readily
recognisable from the characteristic facial appearance
Fig. 2.26 Auscultation of the thyroid gland. and associated physical signs.
GRAVES’ DISEASE
HYPERTHYROIDISM The facies in Graves’ disease is dominated by a staring
Hyperthyroidism occurs most commonly in young appearance caused by retraction of the upper eyelid.
women presenting with smooth diffuse goitres (Graves’ Normally, during a relaxed forward gaze, the upper lid
disease). However, in elderly people, hyperthyroidism protects the eye by lying in a horizontal position which
may be caused by an autonomous ‘toxic’ adenoma crosses the eye in a plane just above the upper pole of
and, rarely, a functioning carcinoma. Rarely the pupil. In Graves’ disease, autonomic overactivity
factitious hyperthyroidism caused by excessive T4 intake causes increased tone and spasm of levator palpebrae
30
Chapter
The thyroid gland 2
Fig. 2.27 Place a sheet of paper on the outstretched fingers to Fig. 2.28 Bilateral lid retraction in a patient with Graves’ disease.
demonstrate the fine tremor of hyperthyroidism. Note that the upper lid is positioned well above the pupil and the
palpebral fissure is widened.
Symptoms and signs

Hyperthyroidism in Graves’ disease and toxic
nodular goitre
Graves’ disease Nodular goitre

Sex female >> men female = men
Eye signs very common, less severe
exopthalmos
Goitre diffuse, overlying may be multinodular
bruit
Heart tachycardia, atrial also angina,
fibrillation congestive heart
failure Fig. 2.29 Lid lag. With the patient sitting, position yourself on the
Weight may lose weight often profound patient’s right side. Watch how the lid moves with the downward
weight loss movement of the eye as the patient follows your finger moving from
a point approximately 45° above the horizontal to a point below this
plane. Normally there is perfect coordination as the lid follows the
downward movement of the eye.
superioris. This causes retraction of the upper lid, which A Hertel exophthalmometer can be used to make
exposes most, if not all, of the iris, exposing sclera above an accurate baseline measurement of the degree of
the iris and creating the typical staring appearance (Fig. exophthalmos and this measurement is used to monitor
2.28). Spasm of the muscles supplying the upper lid also progression and regression. Other eye signs of Graves’
results in an abnormal following reflex. Normally, if you disease include ophthalmoplegia caused by weakness
ask a patient to follow the movement of an object (e.g. and infiltration of the external ophthalmic muscles.
your fingertip) (Fig. 2.29) from a point above eye level to These patients complain of double vision (diplopia) and
a vertical point below eye level, you will note that as the on examination there is a loss of gaze symmetry.
eye moves, the upper lid follows the upper margin of Conjunctival oedema (chemosis) may also occur. The eye
the pupil in a fully synchronised downward movement. signs can be either bilateral or unilateral (Fig. 2.32),
In hyperthyroidism, this coordination is lost and the although, in the latter, always consider a space-occupying
movement of the upper lid lags well behind the pupil lesion of the orbit. Other features of Graves’ disease
(this is termed ‘lid lag’) (Fig. 2.30). include finger clubbing, onycholysis (separation of the
In progressive Graves’ disease, abnormal connective nail from its bed), pretibial myxoedema (brawny swelling
tissue (especially hyaluronic acid) is deposited in the orbit of lower legs), and periostitis (inflammation of the
and external ocular muscles. The globes are pushed periosteum).
forward, resulting first in proptosis and in the more severe A rare complication of hyperthyroidism is thyroid
form, exophthalmos (defined as >18 mm protrusion). storm. This is an exaggerated manifestation of
To examine for exophthalmos, seat the patient in a chair hyperthyroidism and is life threatening. While thyroid
and inspect the globes from above by looking over storm can develop in patients with longstanding untreated
the forehead or from the side of the profile (Fig. 2.31). hyperthyroidism, it is more often precipitated by an acute
31
Chapter
Fig. 2.30 In hyperthyroidism the downward movement of the lid

lags behind the movement of the bulb as it follows your finger
through an arc.
Fig. 2.32 Graves’ disease: unilateral eye condition.
Emergency
Features of thyroid storm
• Thermoregulation dysfunction
• CNS effects (agitation, delirium, psychosis, epilepsy,
coma)
• Gastrointestinal dysfunction (diarrhoea, vomiting,
abdominal pain)
• Cardiovascular features (tachycardia, high output
cardiac function)
Fig. 2.31 Graves’ disease: proptosis of the eye.
Symptoms and signs

Graves’ disease (autoimmune hyperthyroidism) event such as thyroid or nonthyroid surgery, trauma,
infection or an acute iodine load.
• Diffuse goitre with audible bruit
• Pretibial myxoedema, finger clubbing
• Onycholysis (Plummer’s nails) HYPOTHYROIDISM
• Lid retraction, lid lag
• Proptosis, exopthalmos Hypothyroidism presents insidiously; the diagnosis may
• Conjunctival oedema (chemosis) be readily apparent on general examination. Suspect
hypothyroidism in patients complaining of unexplained
lethargy, weight gain, newly noted cold intolerance,
constipation, generalised hair loss and pain in the hand
suggestive of a carpal tunnel syndrome. Poor memory
Symptoms and signs
and general intellectual deterioration may also be
presenting features. While taking the history you might
Assessment of severity of Graves’ ophthalmopathy
have noticed on unusually coarse voice. The disorder
Class Signs / symptoms may occur at any age, although it is most common
0 no symptoms or signs in elderly individuals. There are a number of possible
I signs but no symptoms causes to consider. On first sight you may notice the
II soft tissue involvement characteristic puffy facial appearance, the pale ‘waxy’
III proptosis skin and diffuse hair loss from the scalp and eyebrows.
IV extraocular muscle involvement Look for other signs to confirm your clinical suspicion
V corneal involvement of myxoedema (Fig. 2.33). The delayed relaxation
VI visual loss (optic nerve damage) phase of the Achilles tendon jerk is especially helpful
(Fig. 2.34).
32
Chapter
The parathyroid glands 2
Fig. 2.34 The ankle jerk in hypothyroidism. Although all the

reflexes show a distinct slowing of the relaxation phase of the
tendon reflex, the sign is best observed and felt with the Achilles
tendon jerk. Ask the patient to kneel on a chair or examination
couch with the feet hanging over the edge. Expose the Achilles
tendon and percuss with a patellar hammer while gently resting one
hand on the sole of the foot. Watch and feel for the delayed return
Fig. 2.33 Myxoedema. of the foot to its resting position after the reflex contraction that
follows the tendon tap.
Hypothyroidism
Questions to ask
Congenital
Hypothyroidism • Congenital absence
• Has your weight changed? • Inborn errors of thyroxine metabolism
• Has your bowel habit changed (e.g. constipation)? Acquired
• Is your hair falling out? • Iodine deficiency (endemic goitre)
• Have you noticed a change in weather preference • Autoimmune thyroiditis (Hashimoto’s disease)
(e.g. cold intolerance)? • Postradiotherapy for hyperthyroidism
• Has there been a change in your voice (e.g. hoarse)? • Postsurgical thyroidectomy
• Do you suffer from pain in your hands (e.g. carpal • Antithyroid drugs (e.g. carbimazole)
tunnel syndrome)? • Pituitary tumours and granulomas
The parathyroid glands
Symptoms and signs

Hypothyroidism Structure and function
• Constipation, weight gain There are usually four parathyroid glands (two superior
• Hair loss and two inferior). Ninety per cent of parathyroid glands
• Angina pectoris lie in intimate contact with the thyroid gland, although
• Hoarse croaky voice in 10% of patients the inferior glands lie in an aberrant
• Dry flaky skin position. These pea-sized glands usually lie embedded
• Balding and loss of eyebrows (beginning laterally) in the posterior aspect of the upper and lower poles
• Bradycardia of the thyroid or superficially on the surface of the
• Xanthelasmas (hyperlipidaemia) thyroid.
• Goitre (especially with iodine deficiency)
• Effusions (pericardial or pleural)
• Delayed relaxation phase of tendon reflexes PARATHYROID HORMONE
• Carpal tunnel syndrome Parathyroid hormone (PTH) is synthesised in a precursor
form known as pre-pro-PTH, which is first cleaved to
33
Chapter
Parathyroid hormone metabolism

parathyroid gland
PRE-PRO-PTH
PRO-PTH
1 32
PTH
1 32 84
NH2 COOH
blood stream
PTH Fig. 2.36 Hyperparathyroidism: a radiograph of the phalanges may
1 32 84
show subperiosteal erosions and bone cysts.
NH2 inactive COOH
32 32
32 84
NH2 COOH
amino-terminal midmolecule carboxy-terminal

fragment fragment fragment
(active) (inactive) (inactive)
Fig. 2.35 Parathyroid hormone (PTH) metabolism. A large precursor

molecule (PRE-PRO-PTH) is cleaved to form an 84 amino acid
molecule PTH which is secreted into the blood stream. The molecule,
which has an amino carboxy terminal, is cleaved to smaller
fragments. Only fragments with the first 32 amino terminal amino
acids are metabolically active.
pro-PTH and then cleaved again to the 84 amino acid

polypeptide, PTH (Fig. 2.35). PTH secretion is regulated
by the level of calcium in the blood; hypocalcaemia
stimulates its release. In the circulation, the 84 amino acid Fig. 2.37 Hyperparathyroidism: skull radiograph shows thinning of
PTH is cleaved to smaller fragments, most of which are the cortex and small osteolytic areas, known as ‘pepper pot’ skull.
inactive; the only active fragment is that containing the
first 32 amino acids. The hormone’s prime effect is on the
renal tubule, where it stimulates calcium resorption from excessive thirst (polydipsia), and symptoms of increased
the tubular fluid and phosphate excretion in the urine. urine output (nocturia and frequency). There may be
PTH also stimulates calcium resorption from bone. profound changes in the mental state and, in severe
cases, drowsiness and even coma may occur. The patient
may complain of gastrointestinal symptoms, including
nausea and constipation. Renal stones are common and
HYPERPARATHYROIDISM
the patient may present with severe acute unilateral renal
Hyperparathyroidism is usually detected by finding an angle pain radiating towards the groin. On examination,
abnormally high serum calcium level on routine blood there may be proximal muscle weakness (due to a
testing or in patients presenting with renal colic caused myopathy), a thin opaque ring around the limbus of the
by stones. Hyperparathyroidism may be caused by cornea, and bone pain or radiological evidence of
hyperplasia or one or more autonomous adenomas hyperparathyroidism (Figs 2.36, 2.37).
(often associated with the multiple endocrine neoplasia
syndromes). In chronic renal failure, longstanding
stimulation may result in loss of feedback and an HYPOPARATHYROIDISM
autonomous secretion of PTH leading to hypercalcaemia Surgical damage or removal of three or four parathyroid
(this is known as tertiary hyperparathyroidism). The glands during neck surgery (usually thyroidectomy) is the
clinical syndrome may be difficult to recognise, because most common cause of hypoparathyroidism. Rarely,
the symptoms (‘moans’) dominate the signs (‘stones and autoimmune destruction may cause hypoparathyroidism.
bones’). The patient complains of tiredness and lethargy, The serum calcium level is low (in the presence of a
34
Chapter
The adrenal glands 2
normal serum albumin). The major symptoms of acute poles of the kidneys abutting the diaphragm. Each gland
hypoparathyroidism are paraesthesiae around the mouth, weighs approximately 4 g and has a rich arterial blood
fingers and toes. Abnormal nerve and muscle irritability supply from vessels derived from the aorta and renal and
can be elicited with Chvostek’s (Fig. 2.38) and Trousseau’s phrenic arteries. A single adrenal vein drains from the
signs (Fig. 2.39). In chronic hypoparathyroidism, the hila of the glands to the inferior vena cava on the right
physical effects develop slowly. The symptoms include and to the renal vein on the left. The gland has an outer
tiredness, fatigue, muscle cramps and epilepsy. Premature cortex derived from mesoderm and central medulla,
cataracts should also alert you to the possibility of which is derived from neuroectoderm.
underlying chronic hypoparathyroidism. The cortex comprises 90% of the gland and consists of
three distinct layers: the subcapsular zona glomerulosa,
the middle zona fasciculata and the zona reticularis,
which lies adjacent to the medulla (Fig. 2.40).
Chvostek’s sign
Cortisol homeostasis
higher centres
hypothalamus
-
Fig. 2.38 Chvostek’s sign. Tap over the facial nerve in front of the
CRH
ear – this causes a momentary twitch of the corner of the mouth on
the same side as the irritable facial muscles contract.
-
ACTH
Trousseau’s sign +
cortisol
adrenal
androgens
aldosterone
reticularis
glomerulosa fasciculata
Fig. 2.39 Trousseau’s sign. Inflate a sphygmomanometer cuff to Fig. 2.40 Secretion of cortisol is stimulated by adrenocorticotrophin
above systolic pressure. Within approximately 4 minutes there is (ACTH) secretion, which is under the influence of hypothalamic
characteristic ‘carpopedal’ spasm of the hand. There is opposition of cortisol releasing hormone (CRH). Both ACTH and CRH are under
the thumb, extension of the interphalangeal joints and flexion of the negative feedback control by circulating cortisol. Aldosterone is
metacarpophalangeal joints. This posture reverses spontaneously secreted from the zona glomerulus by the stimulatory effect of
when the cuff is deflated. angiotensin II.
HORMONE REGULATION
The adrenal glands The adrenal cortex synthesises three steroid hormones:
mineralocorticoids, glucocorticoids and androgens.
Aldosterone is produced in the cells of the zona
Structure and function glomerulosa. Aldosterone secretion is primarily regulated
by the renin–angiotensin system, which in turn is
The high fat content of the adrenal glands gives the organ influenced by the intravascular volume (Fig. 2.41). In
a distinctive yellow colour. The adrenals lie on the upper contrast to the glucocorticoids, mineralocorticoid
35
Chapter
metabolism is not influenced by adrenocorticotrophic

The renin–angiotensin system
hormone (ACTH). When adrenal failure is secondary to
pituitary failure, mineralocorticoid function is preserved,
zona glomerulosa
whereas glucocorticoid function is impaired. Aldosterone
promotes the entry of sodium into cells and the secretion
of potassium from cells; consequently, the overall effect
of aldosterone is to cause sodium retention and potassium
loss. This effect on renal tubular cells plays a central
role in the regulation of sodium, potassium and water angiotensin II aldosterone
balance. Aldosterone-producing tumours of the adrenal angiotensin
cortex cause Conn’s syndrome, which is characterised converting
by hypertension, oedema (due to sodium and water enzyme
retention) and hypokalaemia. angiotensin I
The cells of the zona fasciculata and reticularis
synthesise cortisol and adrenal androgens. Glucocorticoid
renin Na+
synthesis and secretion is under the direct control of retention
ACTH secreted by the anterior pituitary. The secretion of
angiotensinogen K+ loss
ACTH is itself regulated by the release of hypothalamic
corticotrophin releasing hormone (CRH). There is a
feedback loop between the hypothalamus and pituitary
on one side of the axis and the adrenal on the other. renin
blood
Although ACTH stimulates glucocorticoid and adrenal pressure
androgen synthesis and secretion, cortisol (and exogenous
corticosteroids) inhibits ACTH secretion by impairing the Na+
release of CRH and directly inhibiting ACTH release from
the anterior pituitary. Fig. 2.41 Renin–angiotensin system. Renin is secreted from the
The hormones of the adrenal cortex have a circadian juxtaglomerular apparatus of the kidney in response to reduced
rhythm: blood levels of cortisol and aldosterone are serum sodium or reduced renal blood pressure. Renin converts
highest on waking and lowest at and around midnight. angiotensinogen to angiotensin I, which is in turn converted to
angiotensin II by angiotensin converting enzyme (ACE) from the lung.
Glucocorticoids promote the conversion of protein to The angiotensin II stimulates aldosterone release from the zona
glucose (gluconeogenesis) and inhibit the peripheral use glomerulosa cells of the adrenal gland.
of glucose. The corticoids increase blood pressure and
support kidney function by increasing the glomerular
filtration rate. Diagnosis of adrenal disease is based on feature is the rounded, ‘moon-shaped’ face (Fig. 2.42),
measurement of ACTH, blood cortisol and the adrenal an obese body (Fig. 2.43) and thin limbs (Fig. 2.44). A
response to ACTH stimulation. typical cushingoid appearance may also occur in
chronic alcoholism and, in this setting, it is called
HYPERADRENALISM (CUSHING’S SYNDROME) pseudo-Cushing’s syndrome. The diagnosis is suspected
if the physical appearance of Cushing’s syndrome
Excessive glucocorticoids (either endogenous or occurs against a background of excessive alcohol
exogenous) cause a significant change in body appearance consumption. The physical and biochemical abnormalities
which can be readily recognised as Cushing’s syndrome. of pseudo-Cushing’s syndrome regress when alcohol
A cushingoid appearance is most commonly caused by is discontinued.
treatment with exogenous steroids. The most characteristic
Symptoms and signs

Differential diagnosis Cushing’s syndrome
Hyperadrenalism
• Round, moon-shaped plethoric facies
• Iatrogenic, exogenous steroids • Hirsutes
• Bilateral adrenal hyperplasia • Acne
• Benign autonomous adrenal adenoma • Hypertension
• Malignant adrenal adenocarcinoma • Buffalo hump on neck (fatty deposit)
• Nonmetastatic tumour effect (e.g. lung cancer • Central distribution of fat
producing ACTH-like peptide) • Proximal muscle weakness and wasting
• Alcoholism causing pseudo-Cushing’s syndrome • Purple skin striae
36
Chapter
The adrenal glands 2
Fig. 2.42 Cushing’s syndrome: plethoric Fig. 2.43 Cushing’s syndrome: typical Fig. 2.44 Cushing’s syndrome: proximal
‘moon-shaped’ facies. buffalo hump. Recognised as fullness below muscle wasting and central distribution of
the hairline, rather than an actual hump. fat.
HYPOADRENALISM AND ADDISON’S DISEASE

In acute adrenal failure, the clinical features may be
nonspecific and puzzling. The patient usually presents
with malaise, weakness, nausea, vomiting and abdominal
pain with an acute change in bowel habit (constipation
or diarrhoea). The most helpful physical sign is the
profound drop in blood pressure when the patient quickly
changes position from lying to standing (postural
hypotension). Collapse and prostration may occur. As a
result of a mineralocorticoid deficiency, serum potassium
levels are often elevated.
In chronic, progressive adrenal failure there are usually
clinical clues to the diagnosis. Increased pigmentation Fig. 2.45 Hyperpigmentation of the areola in Addison’s disease.
develops in the skin (especially sun-exposed areas,
pressure points, areolae and skin creases) (Fig. 2.45)
and mucous membranes (seen best in the buccal
mucous membrane). In Addison’s disease, patients Hypoadrenalism
may also develop characteristic symmetrical patches Acute
of depigmented skin (vitiligo). Vague abdominal • Rapid withdrawal after exogenous steroid treatment
pain, altered bowel habit, weight loss and weakness • Failure to increase steroid dose when steroid-
also occur. Like the acute disease, postural hypoten- dependent patient is subjected to physiological stress
sion is a helpful clinical sign which, later in the • Septicaemia (especially meningococcus)
course of the disease, may dominate the patient’s Chronic
symptoms. • Autoimmune (Addison’s disease)
• Tuberculosis
• Carcinomatosis with adrenal invasion
37
Chapter
Symptoms and signs

The connection between hypothalamus and pituitary
Presenting features of acute adrenal (Addisonian)
crisis paraventricular,
supraoptic
• Profound dehydration, postural hypotension, shock nuclei produce
• Severe nausea and vomiting associated with ADH and
oxytocin
unexplained weight loss
hypothalamus
• Acute abdominal pain
• Unexplained hypoglycaemia
• Unexplained fever portal venous
• Hypernatraemia, hyperkalaemia, uraemia, connection
hypercalcaemia, eosinophilia transports
releasing axonal transport
• Hyperpigmentation of vitiligo and inhibiting to posterior
hormone to pituitary
anterior posterior
pituitary pituitary
anterior ADH
pituitary oxytocin
The pituitary gland

FSH
LH
GH
TSH
Structure and function ACTH
prolactin
The pituitary gland is suspended from the hypothalamus
by the infundibulum and lies in the pituitary fossa at the
base of the skull (Fig. 2.46). The hypothalamus
Fig. 2.46 The hypothalamus connects to the anterior pituitary by
communicates with the anterior pituitary (or a portal venous network which carries releasing and inhibiting
adenohypophysis) via a unique portal blood system hormones to stimulate the release of hormones into the circulation.
which transports chemical stimuli to the anterior pituitary. By contrast, the posterior pituitary hormones are synthesised in the
A different form of communication occurs with the supraoptic and paraventricular nuclei of the hypothalamus and
transported to the posterior pituitary along axons which discharge
posterior pituitary (or neurohypophysis). The supraoptic
directly into the systemic circulation.
and paraventricular nuclei of the hypothalamus syn-
thesise antidiuretic hormone (ADH) and oxytocin and
these hormones flow along the axons to nerve endings
in the posterior pituitary, where they are released
into the circulation so that they can assert their distant Feedback control of hypothalamus–
effects. anterior pituitary endocrine axis
Hormones synthesised and secreted by the anterior
pituitary include follicle stimulating hormone (FSH), GnRH GHRH CRH TRH
luteinising hormone (LH), growth hormone, prolactin,
TSH and ACTH. These hormones are regulated by the
secretion of specific releasing factors produced in the
hypothalamus and transported to the pituitary by
the hypothalamic–pituitary portal circulation (Fig. 2.47).
The regulation of the anterior pituitary hormones
is controlled by the balance between the stimulating
effects of the release factors and the inhibitory feedback +
from the target circulating hormone. There are also +
FSH/LH
inhibitory hypothalamic hormones (somatostatin and
dopamine). Prolactin release is inhibited by hypothalamic +
+
dopamine; this neurotransmitter is secreted into the GH
portal circulation, causing tonic inhibition of prolactin
TSH
release (Fig. 2.48). ACTH
Hypothalamic osmoreceptors and volume receptors
sense blood osmolality and effective circulating volume
and regulate the secretion of ADH from the posterior Fig. 2.47 Regulation of the hypothalamic–anterior pituitary
pituitary. ADH reduces free water clearance by the distal endocrine axis.
38
Chapter
The pituitary gland 2
Regulation of prolactin secretion
dopamine
hypothalamus
prolactin Fig. 2.49 Acromegaly: typical facial appearance.
Fig. 2.48 Prolactin secretion from the anterior pituitary is inhibited

by the tonic secretion of dopamine from the hypothalamus.
tubules of the nephron, resulting in concentration of

the urine and water conservation. Oxytocin from the
posterior pituitary causes uterine contraction during
childbirth. In addition, the hormone promotes milk
ejection during lactation by stimulating contraction of the
smooth muscles surrounding the mammary gland
ducts.
Pituitary tumours may cause overstimulation
syndromes or destruction of the gland and deficiency
syndromes. Both over- and understimulation cause Fig. 2.50 Acromegaly: large tongue.
recognisable clinical syndromes that can be identified on
general examination. Remember that pituitary tumours
may be associated with other endocrine adenomas, defects. Ask for a previous photograph to compare
especially parathyroid adenomas, which cause physical features. On physical examination, a typical
hypercalcaemia. Diagnosis of pituitary disease depends syndrome reflects the overgrowth of bone and other
on the responsiveness of stimulatory influences (e.g. tissues resulting from growth hormone hypersecretion
effect of administration of hypothalamic releasing (Figs 2.49–2.51).
hormones or insulin-induced hypoglycaemic stress).
Hyperprolactinaemia
SYNDROMES ASSOCIATED WITH Disruption of the tonic inhibition of prolactin release by
OVERPRODUCTION OF PITUITARY HORMONES dopamine results in the syndrome of hyperprolactinaemia.
The syndromes associated with the overproduction
Acromegaly
of prolactin may be dominated by either the effect
Acidophil (or more rarely chromophobe) tumours of the of the prolactin or the destructive effect of the pituitary
anterior pituitary may cause inappropriate release of tumour. Breast secretion (galactorrhoea) may develop
growth hormone, resulting in gigantism if the epiphyses in both women and men. The usual presenting
have not fused and acromegaly in adults when fusion symptom in women is alteration in the menstrual pattern
has occurred. Acromegalic patients may present (usually oligomenorrhoea or amenorrhoea). Men may
complaining that their shoes, gloves or rings no longer present with impotence or with symptoms of pituitary
fit or that they are aware of a change in facial appearance. expansion and malfunction (headaches, visual defects,
There may also be symptoms suggestive of visual field hypothyroidism, hypoadrenalism).
39
Chapter
Symptoms and signs

Acromegaly
• Coarse, prominent facial features

• Prognathoid jaw
• Prominent nose and forehead
• Thickened lips and large tongue
• ‘Spade-shaped’ hands
• Excessive sweating and greasy skin
• Kyphosis
• Hypertension
• Bitemporal hemianopia develops
• Carpal tunnel syndrome
• Impaired glucose tolerance
Fig. 2.51 Acromegaly: spade-shaped hands.
Symptoms and signs Symptoms and signs

Prolactinaemia Hypopituitarism
Women Men Women Men

• Present earlier • Present later • Amenorrhoea, infertility • Loss of libido or
• Galactorrhoea (<30%) • Galactorrhoea • Vaginal atrophy, impotence, infertility
• Infertility • Impotence dyspareunia • Soft atrophic testes and
• Menstrual disorders • Signs of pituitary tumour • Atrophic breasts loss of secondary sexual
• Visual field defects • Loss of axillary and characteristics
• Anterior pituitary failure pubic hair
• TSH deficiency, mild to moderate hypothyroidism
• ACTH deficiency:
– weakness
– postural hypotension
SYNDROMES ASSOCIATED WITH – pallor
PITUITARY HYPOFUNCTION – hypoglycaemia
Hypopituitarism
The syndrome of hypopituitarism may become
recognisable if the pituitary is destroyed by a tumour,
granulomatous disease (e.g. sarcoidosis, tuberculosis,
histiocytosis X), trauma or after a postpartum haemorrhage be confused with compulsive water drinking (i.e. when
(Sheehan’s syndrome). Secondary pituitary failure water deprivation causes appropriate urine concentration)
may also occur with disease of the hypothalamus. The and nephrogenic diabetes insipidus (i.e. when water
clinical features progress in a characteristic sequence. deprivation is associated with dilute urine and high serum
Growth and luteinising hormone failure occurs first, levels of ADH).
followed by FSH and TSH, and finally ACTH (Fig.
2.52).
Impaired ADH secretion causes a typical syndrome Nutrition
known as cranial diabetes insipidus. Patients have
inappropriate polyuria and produce a dilute urine, even Nutritional status may be an important marker of disease
when deprived of water for prolonged periods. Often and the progression or regression of a disorder. Poor
there is no obvious cause for the isolated defect. Head nutrition is readily treatable and nutritional support can
injury or cranial surgery may be complicated by posterior hasten recovery and protect against complications.
pituitary damage and diabetes insipidus. Other rare causes Malnutrition may seriously impair immunological
include pituitary tumours (e.g. destructive adenomas, and healing responses and attention to nutritional
craniopharyngiomas, metastases), granulomatous diseases status may positively influence the course of disease.
(e.g. sarcoidosis, eosinophilic granulomas), infections In contrast, obesity is also associated with morbidity,
(e.g. bacterial meningitis, tuberculosis) and familial so weight loss in these individuals can be
disease. The symptoms of cranial diabetes insipidus can advantageous.
40
Chapter
Nutrition 2
Clinical consequences of hypopituitarism
GH FSH/LH TSH ACTH ADH
children– infertility hypothyroidism loss of diabetes

short stature hypogonadism pigmentation insipidus
adults– reduced sperm count hypoadrenalism
no effect hypogonadism
menstrual
irregularity
Fig. 2.52 Clinical consequences of pituitary failure. Diabetes insipidus is a rare manifestation of the hypopituitary syndrome (GH, growth
hormone; FSH, follicle stimulating hormone; LH, luteinising hormone; TSH, thyroid stimulating hormone; ACTH, adrenocorticotrophin;
ADH, antidiuretic hormone).
ASSESSMENT OF NUTRITION
The clinical assessment of nutritional status includes Height/weight norms
overall appearance, weight, height, muscle and fat bulk,
height height
and vitamin, mineral and haematinic status. (cm) (ft/in)
Either at the beginning or conclusion of the first 186 6'1"
examination, you should weigh the patient and measure 183 6'
180 5'11"
the height. This provides useful baseline information, as 178 5'10"
standard growth charts are available to help you judge 175 5'9"
173 5'8"
whether the patient falls within the normal range of 170 5'7"
weight for height (Fig. 2.53). Always adopt a standard 168 5'6"
165 5'5"
procedure for weighing the patient. In the outpatient 163 5'4"
department, it is customary to weigh the patient in socks 160 5'3"
158 5'2"
and basic clothing. Patients in hospital can be weighed 155 5'1"
152 5'
either naked or with a light linen gown. Ensure that all 149 4'11"
subsequent weighings are performed in a standard
44 57 70 83 95 108 120 134 146
manner. Standard weight charts indicating expected weight (kilograms)
percentiles and norms for height assume that the patient
has been weighed naked. Body mass index (BMI) is the underweight fat
acceptance very fat
preferred method for assessing weight as it considers overweight
both weight and height. This is calculated from the
formula:
Fig. 2.53 Chart indicating height and weight norms in adults.
weight (kg)/height (m)2
The normal BMI range is 20–25.

Standardise the method for measuring height. The is also useful; from the teens to adulthood, this height
height measurement is usually made on the vertical should be near 50% of the total height. In osteoporosis,
height ruler attached to the scale. Ensure that the patient the collapse of vertebrae causes shortening, which is
stands bolt upright with heels firmly on the surface and reflected in a reduction of the sitting height. Arm span
back flush against the rule. Measure the height by sliding may occasionally be helpful. Ask the patient to extend
the height marker to touch the crown. The sitting height the arms and hands fully and measure the distance
41
Chapter
between the tips of the middle fingers. This distance Symptoms and signs
should equal the linear height. In Marfan’s syndrome, the
Biochemical and immunological markers of
arm span exceeds the height. malnutrition
When the patient is exposed during the course of the
physical examination, take the opportunity to evaluate • Haemoglobin (iron, B12, folate deficiency)
whether the patient is of usual body build, unusually thin • Low serum albumin
or overweight. Weight loss and ‘wasting’ are suggested • Low serum transferrin
by indrawing of the cheeks and unusual prominence • Reduced creatinine (reflects reduced muscle bulk)
of the cheek-bones, head of humerus and major joints, • Creatinine : height ratio reduced
the rib cage and bony landmarks of the pelvis (Fig. • Reduced white cell count
2.54). Muscle wasting may exaggerate the skeletal • Impaired delayed cell-mediated immunity (skin tests)
prominence. Atrophy of the deltoid muscles may be
particularly striking. Hypoalbuminaemia may cause
white nails (leukonychia) and loss of capillary osmotic
pressure results in pedal oedema. Iron deficiency may Symptoms and signs
cause spooning of the nails (koilonychia). Other Vitamin deficiency syndrome
features of nutritional deficiency include inflammation
and cracks at the angle of the mouth (angular stomatitis), Fat-soluble Clinical features of deficiency
a smooth tongue lacking in papillae (atrophic glossitis) vitamin
(Fig. 2.55) and skin rashes (e.g. pellagra) (Fig. 2.56). A Dry eyes and skin, night blindness,
Although a visual assessment provides a relatively corneal thinning (keratomalacia)
accurate assessment of general nutritional status, more D Proximal muscle weakness, bone pain,
objective measures, both clinical and biochemical, are osteomalacia
necessary – especially when it is important to establish a K Easy bleeding, bruising
baseline for nutritional support and when progress needs
monitoring.
MIDARM MUSCLE CIRCUMFERENCE

This measurement provides an estimate of muscle and
fat status. The standard position for measurement is
the midpoint between the tip of the olecranon and
Fig. 2.55 Smooth shiny tongue of atrophic glossitis (especially iron

deficiency).
Fig. 2.54 Malnutrition in liver disease. Muscle wasting is readily

recognised by the prominence of the skeleton due to loss of muscle
bulk and fatty tissue. Fig. 2.56 Pellagra: photosensitive ‘crazy paving’ skin rash.
42
Chapter
Clinical assessment of vitamin status 2
Fig. 2.57 Measurement of the midarm muscle circumference. Fig. 2.58 Measurement of triceps skinfold thickness.
acromial process. The patient’s arm should be relaxed Symptoms and signs
and flexed to a right angle. Take the measurement by Water-soluble vitamin deficiency
wrapping the tape-measure around the upper arm
midpoint (Fig. 2.57), taking care not to pull too tight B1 (thiamine)
or to leave excessive slackness. Take three measurements • Wet beriberi
at the same point and calculate the average. The – peripheral vasodilatation
measurement is itself a useful baseline measure for – high output cardiac failure
follow-up purposes. In addition, the single measurement – oedema
can be compared with percentiles in standard age and • Dry beriberi
sex charts. – sensory and motor peripheral neuropathy
• Wernicke’s encephalopathy
– ataxia, nystagmus, lateral rectus palsy
TRICEPS SKINFOLD THICKNESS – altered mental state
• Korsakoff’s psychosis
In adults, the skin overlying the triceps muscle can be – retrograde amnesia
lifted and subcutaneous tissue can be distinguished – confabulation
from the underlying muscle bulk. This fold of skin and
subcutaneous tissue (the fat fold) provides an indirect B2 riboflavin
assessment of fat stores. Measure the fat fold thickness • Inflamed oral mucous membranes
from the patient’s rear and make the measurement at the • Angular stomatitis
same midarm landmark used for measuring the midarm • Glossitis, normocytic anaemia
muscle circumference. It is useful to mark this point so B3 niacin
that you can lift the skinfold between your thumb and • Pellagra
index finger and position the jaws of the calipers on • Dermatitis (photosensitive)
either side of the midarm mark on the raised skinfold • Diarrhoea
(Fig. 2.58). As with the tape measurement of midarm • Dementia
muscle circumference, ensure that the caliper jaws are B6 pyridoxine
neither too tight nor too loose. Repeat the measurement • Peripheral neuropathy
three times and take the average to compare with standard • Sideroblastic anaemia
tables. B12
• Megaloblastic, macrocytic anaemia
• Glossitis
• Subacute combined degeneration of the cord
Clinical assessment of vitamin status
Folic acid
Vitamins are essential cofactors obtained from the diet. • Megaloblastic, macrocytic anaemia
Reduced dietary intake may result in recognisable • Glossitis
deficiency syndromes. Specific deficiencies of the fat- C
soluble vitamins (A, D and K) occur in patients with • Scurvy
chronic steatorrhoea due to chronic cholestasis and – perifollicular haemorrhage
malabsorption syndromes complicated by steatorrhoea. – bleeding gums, skin purpura
Deficiencies of water-soluble vitamins occur in all – bleeding into muscles and joints
forms of malnutrition. The syndromes are especially • Anaemia
prevalent in malnutrition due to famine, malnourished • Osteoporosis
alcoholic patients, patients on chronic renal dialysis and
43
Chapter
in underdeveloped countries where processing of staple Symptoms and signs

foods reduces vitamin content.
Measuring the capillary refill time
• Patient’s hand placed level with heart

Clinical assessment of hydration • Distal phalanx of the middle finger compressed for
5 seconds
Fluid and electrolyte balance is carefully regulated. The • Release pressure
intake of fluid and electrolytes is closely matched by loss • Measure time to regain normal colour (refill time)
in urine, stool and sweat. Dehydration can occur if there – normal filling time is 2–3 seconds (2–4 seconds on
is a mismatch between fluid intake and loss. Ill patients the elderly)
may be anorexic and fail to take in the minimal fluid
intake necessary to maintain fluid balance; the kidney
may lose its ability to regulate the quality and quantity of
urine; and there may be excessive gastrointestinal fluid skin immediately springs back to its original position,
loss (diarrhoea and vomiting) or abnormal sweating whereas in dehydration the skinfold only slowly returns
(pyrexia). back to normal. This sign is unreliable in elderly patients
The history may be helpful when assessing hydration. whose skin may have lost its normal elasticity. Urine
Dehydration rapidly provokes thirst, the first clinical output falls and the urine is concentrated. In severe
symptom of dehydration. Ask patients whether they feel dehydration, the patient may be profoundly hypotensive
abnormally thirsty and whether they have noticed a dry, and anuric, and renal failure caused by tubular necrosis
parched mouth. Physical signs of dehydration are usually may occur.
only apparent with moderate to severe dehydration.
Inspect the tongue and note whether the mucosa is wet
and glistening. Touching the tongue may help you assess Clinical assessment of shock
its moistness. Look at the eyes, which should have a
glistening, shiny appearance; this sparkle is lost as The clinical presentation of shock varies both with the
dehydration develops. With moderate dehydration, the type and the cause, but there are several common features.
eyes may appear sunken into the orbits; the pulse rate Any patient suspected of developing shock should have
may increase to compensate for intravascular volume continuous assessment of the peripheral and central
loss. Blood pressure falls in hypovolaemic patients and circulation. In the earliest phase (preshock), the pulse
the demonstration of postural hypotension is a cardinal rate rises and the blood pressure may be maintained by
sign of significant intravascular fluid loss. In addition, the peripheral vasoconstriction, resulting in cool peripheries,
capillary refill time can be used to assess the circulatory skin pallor and reduced capillary refill time. Blood
effects of volume depletion. pressure measurement is very helpful in assessing shock,
With marked dehydration skin turgor is lost. This and postural (orthostatic) hypotension antedates the
can be demonstrated by gently pinching a fold of skin development of recumbent hypotension (systolic BP
on the neck or anterior chest wall, holding the fold for a <90 mmHg or a drop of 40 mmHg in previous hypertensive
few moments (Fig. 2.59) and letting it go. Well-hydrated patients). Once the blood pressure has fallen, oliguria
Symptoms and signs

Measurement of postural change in blood
pressure
• Lie the patient supine for 2 min

• Record pulse rate and blood pressure in supine
position
• Ask the patient to stand upright
• Wait 1 min
• Measure standing heart rate and blood pressure at
1 and 3 min
• Heart normally increases by 8–12 beats/min
• Systolic blood pressure drops by 3–4 mmHg
• Diastolic blood pressure increases by 3–7 mmHg
• Postural hypotension when systolic drops by Fig. 2.59 To test for moderate to severe dehydration, assess skin
20 mmHg and/or diastolic drops by 10 mmHg turgor by lifting the skin, pinching it and observing the rate at which
it springs back to its normal position.
44
Chapter
Colour 2
develops. Cerebral hypoperfusion results in altered

mental state, characterised initially by agitation and
progressing to confusion, delirium, obtundation and
coma. Initially patients might hyperventilate, causing
a short, transient respiratory acidosis, but this is
soon replaced by metabolic acidosis reflecting renal
hypoperfusion and impaired clearance of lactate by the
liver, kidney and muscle.
Shock
• Hypovolaemic shock
– GI bleeding Fig. 2.60 Evert the lower lid to inspect the palpebral conjunctiva
– trauma for pallor.
– ruptured aneurysm
– burns
– haemorrhagic pancreatitis PALLOR
– fractures (e.g. neck of femur) The cardinal sign of anaemia is pallor. Severe anaemia
– diarrhoea and vomiting may be readily recognised by a pale facial appearance and
• Cardiogenic shock shortness of breath on exertion. The red colour of arterial
– acute myocardial infarction blood is easiest to assess where the horny layer of the
– acute arrythmias epidermis is thinnest; this includes the palpebral
– acute rupture of valve cusp conjunctiva, nail bed, lips and tongue. Inspect the
– pericardial tamponade palpebral conjunctiva by gently everting the lower eyelid
• Distributive shock (Fig. 2.60). The palpebral conjunctiva is normally a healthy
– Gram-negative sepsis red colour but, in anaemia, it appears a pale pink.
– toxic shock syndrome Experience will teach you to distinguish normal from
– anaphylaxis abnormal. Conjunctival pallor should be accompanied
– Addisonian crisis by pallor of the nail bed and palmar skin creases (only
– spinal cord/major brain injury assess this if the hands are warm). Pallor is an unreliable
sign in cold or shocked patients because peripheral
vasoconstriction causes skin and conjunctival pallor even
when not associated with blood loss.
Assessment of shock PLETHORA
• Rise in pulse occurs early This refers to a ruddy ‘weather beaten’ facial appearance
• Reduced pulse volume/pressure where the skin has an unusually red or bluish (cyanosed)
• Orthostatic hypotension appearance. Facial plethora is usually caused by
• Recumbent hypotension an abnormally high haemoglobin concentration
• Cool, pale peripheries (polycythaemia). This is usually caused by chronic
• Delayed capillary refill time cyanotic lung disease in which hypoxia stimulates
• Dry mucous membranes erythropoietin release from the macula densa of the
• Oliguria proximal renal tubule cells. This hormone stimulates the
• Altered mental state marrow to increase red cell production with consequent
• Signs of metabolic acidosis increase in haemoglobin concentration. The plethora
causes a bloated facial appearance and, together with the
cyanosis, these patients have a typical ‘blue bloater’
appearance.
Polycythaemia rubra vera is a myeloproliferative
Colour disorder that causes very high haemoglobin levels
and plethora occurs in the absence of hypoxic cyanosis.
Once you have assessed nutrition and hydration, look The conjunctiva has a characteristic ‘plum’ colour and
at the patient’s ‘colour’. Look for pallor or plethora, on fundoscopy the increased blood viscosity causes
central and peripheral cyanosis, jaundice and skin the venules to assume a thickened ‘sausage-shaped’
pigmentation. appearance.
45
Chapter
Fig. 2.61 Peripheral cyanosis; note the bluish discoloration of

the fingers.
CYANOSIS
Cyanosis refers to a bluish or purplish discoloration of
the skin or mucous membranes caused by excessive
amounts of reduced haemoglobin in blood. At least
5 g/dl of reduced haemoglobin is necessary for cyanosis
to appear. In peripheral cyanosis, the extremities are
cyanosed (Fig. 2.61) but the tongue retains a healthy pink
colour. This is caused by any condition resulting in
slowing of the peripheral circulation. In cold weather, Fig. 2.62 Typical skin pigmentation in chronic cholestasis (primary
there is reflex peripheral vasoconstriction with slowing of biliary cirrhosis).
the circulation, allowing more time for the extraction of
oxygen from haemoglobin. A similar mechanism accounts
for peripheral cyanosis in heart failure, peripheral vascular large amounts of carrots or other carotene-containing
disease, Raynaud’s phenomenon and shock. A reduction vegetables or substances causes carotenaemia, which can
in arterial oxygen saturation results in central cyanosis. be confused with jaundice. The yellow discoloration is
The extremities are cyanosed and the tongue and mucous prominent in the face, palms and soles but, in contrast to
membranes also have a bluish or purple discoloration. jaundice, the sclera remains white.
Central cyanosis may develop in any lung disease in
which there is a mismatch between ventilation and PIGMENTATION
perfusion. In right-to-left shunts caused by congenital
heart disease, the admixture of venous blood to the Sunburn is the most common cause of increased
systemic circulation causes cyanosis. pigmentation and this should be readily distinguished
from the history. In iron overload (haemochromatosis),
the skin colour may appear slate grey. A silver-grey
JAUNDICE colour develops in silver poisoning (argyria). In
Skin pigmentation influences the ease with which chronic cholestasis (e.g. primary biliary cirrhosis), skin
jaundice can be detected. The yellow discoloration is hyperpigmentation may develop, especially over pressure
most easily recognised in fair-skinned individuals and is points (Fig. 2.62). A marked increase in pigmentation
more difficult to detect in darkly pigmented patients. occurs after bilateral adrenalectomy for adrenal
Bilirubin has a high affinity for elastic tissue. This, together hyperplasia. This condition (Nelson’s syndrome) is caused
with the sclera’s white colour, makes the sclera the most by unopposed pituitary stimulation. Addison’s disease
sensitive area for looking for the yellow discoloration of may also be associated with deepening pigmentation,
jaundice. especially skin creases and pressure points.
Mild jaundice is best seen in natural daylight. Expose
the sclera by gently holding down the lower lid
and asking the patient to look upwards. With progression, Oedema
the yellow discoloration becomes obvious on the
truncal skin. In chronic, severe obstructive jaundice, Fluid movement between the intravascular and
the skin develops a yellow-green appearance. Eating extravascular space occurs through the walls of capillaries.
46
Chapter
Oedema 2
results in a fall in the effective intravascular volume,

Starling forces across the capillary which, in turn, activates the renin–angiotensin system.
venular end arteriolar end These factors all contribute to the fluid retention that
complicates portal hypertension. Ascites complicating
oncotic >> >> oncotic portal hypertension usually only develops when there
pressure hydrostatic pressure pressure
is hypoalbuminaemia and a fall in oncotic pressure
(Fig. 2.64).
Inflammation increases capillary permeability, allowing
movement of albumin and other colloidal proteins as
well as fluid into the interstitial space. The increase in
tissue oncotic interstitial oncotic pressure encourages the shift of fluid
pressure pressure
of and electrolytes out of the capillaries into the interstitium.
interstitial This causes the swelling that invariably accompanies the
fluid
inflammatory response. Lymph is particularly rich in
net inflow of fluid net outflow of fluid protein and, when lymphatic flow is obstructed, the
and electrolytes and electrolytes abnormal accumulation of lymph in the interstitial space
increases the interstitial oncotic pressure, with consequent
retention of interstitial fluid.
Fig. 2.63 The Starling forces across the capillary bed. At the
arteriolar end the hydrostatic and interstitial oncotic pressures exceed The distribution of excess fluid depends on its
the plasma oncotic pressure, resulting in efflux of fluid and underlying cause, the shifting effect of gravity and the
electrolytes. At the venular end plasma oncotic pressure exceeds capacity of the tissue in which it accumulates. In
hydrostatic pressure, resulting in net influx. congestive heart failure, patients often notice marked
ankle swelling (dependent oedema) which becomes more
noticeable as the day wears on and appears to resolve
The efflux of fluid across the capillary wall is governed through the night. In the upright posture, increased
mainly by the hydrostatic pressure transmitted by the capillary pressure is transmitted to the lower limbs: this
arterial blood pressure through the precapillary arteriole, favours the regional accumulation of excess fluid in
and also by the capillary permeability and the opposing the loose connective tissue around the ankles. At night,
osmotic (oncotic) pressure exerted by the serum proteins the recumbent position causes redistribution of the
(especially albumin). In addition, the oncotic pressure of transcapillary and gravitational forces so that by early
the interstitial fluid may contribute to the efflux of morning the oedema is most prominent in the sacral
intravascular fluid. The reabsorption of interstitial fluid is region and appears to have resolved from around the
driven primarily by the plasma oncotic pressure, the ankles. When the left ventricle fails, interstitial oedema
hydrostatic pressure in the interstitial space (known as accumulates in the lungs, causing pulmonary oedema.
the tissue pressure) and the fall in hydrostatic pressure at The fluid settles in the most dependent (basal) areas of
the venular end of the capillary. These forces (known as the lung, causing the basal alveoli to collapse during
the Starling forces) determine the movement of fluid and expiration. The opening of these collapsed alveoli during
electrolytes between the intravascular and interstitial inspiration can be heard with a stethoscope as ‘crackles’.
compartments (Fig. 2.63). Facial and periorbital tissue is particularly compliant. In
Any imbalance of the Starling forces will cause superior vena caval obstruction and chronic renal failure,
expansion of the interstitial space. In heart failure, the facial ‘puffiness’ is prominent, especially on waking.
increased central venous pressure causes increased Anasarca refers to the gross, generalised oedema that
capillary pressure, reduced resorption and oedema; renal accompanies profound hypoproteinaemic states.
hypoperfusion also stimulates the renin–angiotensin
system, which, in turn, causes inappropriate sodium
and water retention, and further contributes to oedema.
When serum albumin levels fall there is a loss of plasma SYMPTOMS OF OEDEMA
oncotic pressure. This favours the movement of fluid into If the oedema is generalised, patients may notice tight-
the interstitial space. The consequent fall in intravascular fitting shoes, frank swelling of the legs or an unexplained
volume causes activation of the renin–angiotensin system, increase in weight. There may be associated symptoms
which adds further to fluid retention and oedema. linked to underlying diseases such as heart failure and
Hypoalbuminaemia occurs in nephrotic syndrome liver, kidney, bowel or nutritional disease. Localised
(albuminuria, hypoalbuminaemia, hyperlipidaemia and oedema may be obvious if there is venous thrombosis,
oedema), liver failure, malabsorption syndromes, protein- regional lymphatic obstruction or a painful, inflamed area
losing enteropathy, severe burns and malnutrition. of swelling. Fluid accumulation in the pleural space
In liver disease complicated by portal hypertension, (hydrothorax or pleural effusion) may cause breathlessness.
there is pooling of blood in the splanchnic bed with Ascites may be noticed as an increase in girth, weight
increased splanchnic capillary pressure. The pooling gain or the eversion of the umbilicus.
47
Chapter
The pathophysiology of oedema
liver disease
portal hypertension
nephrotic syndrome heart failure

splanchnic pooling
effective arterial
blood volume
albuminuria
renal hypoperfusion
renin-angiotensin
system
hypoalbuminaemia Na & water central

retention venous pressure
oncotic
pressure plasma volume capillary pressure
transudation
oedema
Fig. 2.64 The formation of oedema in liver disease with portal hypertension, cardiac failure and nephrotic syndrome.
SIGNS OF OEDEMA oedema. Press the ball of your thumb or the tips of your
index and middle fingers into the posterior malleolar
In ambulant patients, generalised oedema is readily space and maintain moderate pressure for a few seconds.
demonstrated in the tissue space behind the medial The skin has a ‘boggy’ feel. The extrinsic pressure will
malleolus. Fluid accumulates in the loose connective squeeze oedema fluid away from the pressure point. On
tissue of this dependent area; the skin between the medial removing your thumb or fingers, the finger impression
malleolus and Achilles tendon is normally concave but remains imprinted in the skin for a short while before
with fluid accumulation it becomes flattened and then fading as the oedema redistributes. Repeat the compression
convex. You may notice a skin impression made by tight- test more proximally to assess the upper margin of
fitting socks. In longstanding oedema, the skin may oedema (Fig. 2.65).
become shiny, thin, and even ulcerated due to poor local In the recumbent posture, oedema is less obvious
tissue circulation. Mild pedal oedema may not be obvious around the ankles and most prominent over the sacrum
on inspection. Palpation is, however, a sensitive test for and lower back. This is often forgotten when examining
48
Chapter
Temperature and fever 2
a b
Fig. 2.65 Finger indentation to demonstrate ankle oedema.
patients confined to bed. Ask the patient to sit well sample suggests malignancy; cytology, pH, protein
forward in bed and expose the lower back and sacral content, neutrophil count and Gram and direct stains for
region. Press the thumb or fingers into the skin over the tuberculosis can facilitate a rapid diagnosis. Pleural
midsacrum. Like pedal oedema, abnormal fluid retention effusions are readily detected on clinical examination and
is indicated by the residual impression left at the pressure chest radiograph (see Ch. 5). Like ascites, an aspiration
point. In anasarca, the signs of oedema extends to the sample can provide valuable diagnostic information.
thighs, scrotum and anterior abdominal wall. Anasarca
occurs in hypoproteinaemic states (especially nephrotic
syndrome, malnutrition and malabsorption), severe Temperature and fever
cardiac or renal failure and when there is a generalised
increase in capillary permeability (e.g. severe allergic In all warm-blooded animals, core body temperature is
reactions). set within closely regulated limits and is stabilised by a
The veins of the lower legs have valves that protect the combination of convection, conduction and evaporation.
vessels from the pressure effect of the column of blood The major regulatory organ for heat loss and retention is
from the right ventricle. Damaged and incompetent the extensive vascular plexus in the subcutaneous tissue.
valves in the deep and perforating veins of the lower Although metabolism produces most of the body heat,
limb cause a marked increase in hydrostatic pressure to ventilation and ingestion of hot or cold substances also
the lower limb veins, causing varicose veins and pedal make a small contribution to heat exchange in the body.
oedema. Localised oedema may occur in deep venous Vasodilatation of skin vessels allows dissipation of heat
thrombosis of the leg veins. The affected limb becomes transferred from the deep organs. Sweating facilitates
swollen and if there is thrombophlebitis and rapid muscle heat loss through evaporation; the eccrine sweat glands
swelling, the calf muscle may be tender to palpation are innervated by cholinergic sympathetic nerve fibres.
(Homan’s sign). Conservation of heat by adrenergic autonomic stimuli
Lymphatic oedema has a high protein content and the reduces blood flow through the subcutaneous vascular
oedema is localised to the area drained by the lymphatics. plexus. The integrated response to temperature regulation
The swelling is pronounced and on palpation the skin has is under the control of the hypothalamus.
an indurated, thickened feel. This ‘brawny’ oedema is the
clinical hallmark of lymphoedema (filariasis is a common MEASURING TEMPERATURE
cause of brawny oedema in certain tropical countries). Temperature may be measured by placing a thermometer
Surgical removal of axillary lymph nodes in the treatment under the tongue, in the rectum or under the axilla. If you
of breast cancer commonly results in troublesome use a mercury thermometer, shake it to ensure that the
lymphoedema of the arm. mercury is well below 37°C and leave for at least 90s.
Ascites is characterised by abdominal distention Electronic temperature sensors are now widely available,
(especially in the flanks) and, on examination, there is providing more rapid stabilisation.
shifting dullness. Look for signs of abdominal disease
such as peritoneal infection, peritoneal carcinomatosis or
liver disease with portal hypertension (e.g. splenomegaly NORMAL TEMPERATURE
or liver flap). Removing a small volume of ascitic fluid is Temperature depends on the site of measurement. The
often helpful in reaching a diagnosis. A bloodstained mouth, rectum and axilla are common sites. ‘Normal’ oral
49
Chapter
temperature is usually considered to be 37°C. Rectal CHILLS AND RIGORS

temperature is 0.5°C higher than the mouth and the axilla High fever may be accompanied by a subjective sensation
0.5°C lower. Remember that ‘normal’ temperature is not of chill, which may be accompanied by goose pimples,
set at a precise level and there are small variations shivering and chattering of the teeth. As the fever
between individuals (which may range from 35.8 to subsides, the defervescence is accompanied by hot
37.1°C). There is also a distinct diurnal variation: oral sensations and intense sweating. When shivering is
temperature is usually about 37°C on waking in the extreme, the presentation is dominated by the rigors.
morning, rising to a daytime peak between 6.00 and Severe rigors and spiking fevers are characteristic of
10.00 p.m. and falling to a low point between 2.00 and biliary and renal bacterial infections and malaria.
4.00 a.m. In menstruating women, ovulation is
accompanied by a 0.5°C increase in body temperature.
Daily temperature measurement can be used as an Differential diagnosis
accurate marker of ovulation. Rigors
• Biliary sepsis (Charcot’s triad)

FEVER – jaundice
Abnormally high body temperature is an important – right hypochondrial pain and tenderness
physical sign. Pathological temperatures often show an – fever and rigors
exaggerated diurnal pattern with evening high points and • Pyelonephritis
the lowest temperatures in the early morning. Fever may • Visceral abscesses
be caused by microbes, immunological reactions, hormones • Malaria
(e.g. T4 and progesterone), inability to lose heat (e.g.
absence of sweat glands and scaling of the skin – ichthyosis),
drugs (e.g. penicillin and quinidine) and malignancy (e.g.
HYPOTHERMIA
Hodgkin’s disease and hypernephroma).
Sequential recording of temperature may show a Hypothermia usually occurs with prolonged exposure
variety of patterns (Fig. 2.66). These patterns are neither to winter cold. Predisposing factors include old age,
specific nor sensitive signs of individual diseases. Typhoid myxoedema, pituitary dysfunction, Addison’s disease
fever may show a ‘stepwise’ increase in temperature and abuse of drugs or alcohol. Patients are pale, the skin
associated with a relative bradycardia. Occasionally, feels cold and waxy and the muscles are stiff. Consciousness
patients with Hodgkin’s disease have a Pel–Ebstein fever, is depressed and when the temperature drops to
characterised by 4–5 days of persistent fever, followed by below 27°C, consciousness is lost. A special low-reading
a similar period when the temperature hovers around the thermometer is required to establish the baseline
normal baseline. Abscess and collections of pus often temperature. The most convenient measuring device is a
present with a high spiking fever. rectal probe (thermocouple) which provides real-time
temperature measurement.
Sequential temperature variation Hypothermia
• Environmental exposure
40° • Hypothyroidism
• Increased cutaneous heat loss – burns, toxic
epidermal necrolysis
• Drugs (alcohol, opiates, barbiturates, phenothiazines,
lithium)
• Altered thermoregulation (sepsis, hypothalamic
37°
disease, spinal cord injury)
The lymphatic system

0600 1800 0600
hours
intermittent persistent
remittent spiking Examination of the lymphatic system
Fig. 2.66 Temperature may be described as intermittent, remittent, As the lymphoreticular system is widespread, it is
persistent or spiking. convenient to consider its examination in the general
50
Chapter
The lymphatic system 2
Primary and secondary lymphoid tissue The lymphatic drainage system
primary secondary external

lymphoid organs lymphoid organs ring cervical nodes
right lymphatic
thymus duct thoracic duct
Waldeyer’s lymph nodes
ring tonsils and
Kupffer cells adenoids right left
subclavian subclavian
vein vein
lymph nodes axillary
nodes
spleen mesenteric and
para-aortic mediastinal
mesenteric nodes nodes
lymph nodes
iliac nodes inguinal
Peyer’s patch nodes
lymph nodes
popliteal
bone marrow nodes
Fig. 2.67 The primary lymphoid organs include bone marrow Fig. 2.68 Regional drainage of the lymphatic system. The right
(which produces B lymphocytes) and the thymus (which produces T upper quadrant drains via the right thoracic duct into the right
lymphocytes). The secondary lymphoid organs provide a ‘base camp’ subclavian vein. The remainder of the lymphatic network drains into
for interaction between lymphocytic subtypes and antigens (i.e. the left subclavian vein via the thoracic duct.
macrophages, antigen presenting cells, T and B lymphocytes). The
immune response is generated in the secondary lymphoid tissues.
vein, with the remainder of the body ultimately draining

examination. You may choose to examine for enlargement to the thoracic duct, which drains into the left subclavian
of the lymph nodes (lymphadenopathy) as part of the vein (Fig. 2.68). Fat from the small intestine is not
preliminary general examination, although most clinicians absorbed into the portal circulation. Triglyceride in the
integrate the examination into the regional examination enterocyte is coated with protein to form chylomicrons
of the head and neck, chest and abdomen. and these are absorbed into mesenteric lymphatics which
drain through the thoracic duct into the systemic
Structure and function of circulation.
the lymphatic system The lymph nodes are comprised of lymphocyte-rich
lymphoid follicles and sinuses that are lined with
The lymphatic system drains the interstitial space, reticuloendothelial cells (histiocytes and macrophages).
facilitates antigen presentation, produces antibodies and The follicles in the cortex of the node have a germinal
phagocytes, and provides a pathway for chylomicron centre populated by rapidly dividing B lymphocytes and
absorption from enterocytes. It comprises the lymphatic macrophages. The germinal centre is surrounded by a
ducts, lymph nodes, spleen, tonsils, adenoids and the cuff of T lymphocytes. Antigens from a distant region
thymus gland (Figs 2.67, 2.68). Lymphoid tissue is also drain through the lymphatic vessels into the regional
present in the Peyer’s patches of the terminal ileum. The nodes, where they are presented to the lymphocytes,
lungs contain significant islands of lymphoid tissue and which respond by proliferating into antibody-producing
the hepatic reticuloendothelial cells are an integral B lymphocytes or antigen-specific T lymphocytes (Fig.
component of the lymphoreticular system. 2.69).
A network of lymphatic ducts accompanies the blood Lymphadenopathy may be caused by proliferation
vessels; these lymphatics transport lymph from the of cells in response to antigen challenge. Abnormal
interstitial tissues to the lymph nodes. Lymph is an cells may populate the nodes. Malignant transformation
opalescent fluid derived from the protein-rich fluid, of the lymphoid cells in lymphomas may cause
enriched with lymphocytes, which bathes the interstitial lymphadenopathy. The glands may become populated by
space. The lymphatic vessels drain distinct regions of the leukaemic cells or metastatic carcinoma. In the lipid
body into groups of regional lymph nodes. Efferent lymph storage diseases, lipid-laden macrophages may infiltrate
vessels leave the regional nodes, converging to form and enlarge the nodes.
larger vessels. Ultimately, the larger lymphatic vessels Before setting out to examine the lymphatic system, it
converge into two main lymph vessels – the lymphatic is important to know the regional arrangement of the
trunk drains the right upper body into the right subclavian major groups of superficial nodes (Fig. 2.68).
51
Chapter
Anatomy of the lymph node Lymph nodes of the head and neck
preauricular
primary subcapsular medulla (T and B cells)
follicle (marginal) tonsillar
(B cells) sinus posterior
paracortex (T cells, auricular
antigen
presenting
cells)
occipital
blood
submaxillary
capsule efferent
lymphatic
lymphocyte submental
traffic to superficial
cervical
artery deep cervical chain
posterior
vein cervical (deep to the
cortex sternomastoid)
supraclavicular
medullary cords
(plasma cells)
other
afferent lymphatic secondary
trabecula lymphoid
lymph from organs
interstitial Fig. 2.70 Horizontal ring of facial nodes and the vertical chain of
space cervical neck nodes.
germinal centre of
secondary
follicle
submental, submandibular, preauricular (superficial

Fig. 2.69 Structure of the lymph node.
parotid), posterior auricular (mastoid) and occipital
nodes. The vertical nodes also drain the deep structures
of the head and neck. The deep cervical chain extends
Differential diagnosis along the internal jugular vein from the base of the skull
Some causes of localised lymphadenopathy to the root of the neck (deep to sternocleidomastoid) and
then to the thoracic and right lymphatic ducts. A chain
• Local acute or chronic infections of superficial cervical nodes lies along the external jugular
• Metastatic carcinoma (especially breast, lung, head vein, draining the parotid glands and the inferior portion
and neck, kidney) of the ear. This chain drains into the deep cervical nodes.
• Hodgkin’s disease The tip of the tongue drains to the submental nodes, the
anterior two-thirds to the submental and submandibular
nodes, and then to the lower deep cervical nodes; the
posterior tongue drains to the tonsillar nodes at the upper
limit of the deep cervical chain.
General lymphadenopathy The lymphatics of the hand and arm drain to the
• Lymphoma axillary and infraclavicular group of nodes (Fig. 2.71). The
• Acute and chronic lymphatic leukaemia epitrochlear node is the most distal node in the arm.
• Viral infections (HIV/AIDS, infectious mononucleosis, The anterior chest wall (and breast) drains medially to
cytomegalovirus) the internal mammary chain and laterally to the axillary
• Bacterial infections (tuberculosis, brucellosis, syphilis) and brachial nodes. The lung parenchyma and visceral
• Toxoplasmosis pleura drain to the hilar nodes, whereas the parietal
• Sarcoidosis pleura drains to the axillary nodes (this is why the axilla
• Phenytoin pseudolymphoma, serum sickness is palpated in the course of the lung examination). The
• Autoimmune diseases (systemic lupus erythematosus, lymphatics of the lower limb drain to the popliteal nodes
rheumatoid arthritis) and then up to the vertical group of superficial inguinal
nodes lying close to the upper portion of the great
saphenous vein (Fig. 2.72). The perineum, scrotal skin,
penis, lower vagina and vulva, and lower trunk and the
The lymph nodes of the head and neck are grouped back below the umbilicus drain into the horizontal group
in an encircling and vertical arrangement (Fig. 2.70). lying below the inguinal ligament. The tests drain to the
The circle of nodes drains the superficial structures of para-aortic nodes, whereas the female genitalia drain to
the head and neck. This ring of nodes includes the pelvic, intra-abdominal and para-aortic nodes.
52
Chapter
(lymphadenitis) and the overlying skin may be red and

Lymphatic system of the arm inflamed. When superficial lymphatic vessels leading to
a group of nodes are inflamed (lymphangitis), the
channels can be seen as thin red streaks leading from a
more distal site of inflammation.
infraclavicular
Use your fingertips to palpate the regional nodes. Feel
for the node by applying moderate pressure over the
axillary region and moving your fingers in an attempt to feel a
node or nodes slipping under your fingers. Normal nodes
are not palpable. If you feel nodes, assess their size
(length and width), consistency (soft, firm, rubbery, hard
or craggy), tenderness and mobility to surrounding nodes
epitrochlear and tissues. Whenever you discover an enlarged node,
inspect the draining area in an attempt to find a source.
Painful, tender nodes usually indicate an infected source
that may be hidden from obvious view (e.g. infected
cracks between toes). Malignant lymph nodes (either
primary or secondary) are not usually tender. Malignant
nodes vary in size from tiny, barely palpable structures to
large glands 3–4 cm in size. Malignant lymph nodes may
feel unusually firm (often described as ‘rubbery’) or hard
and irregular. Fixation to surrounding tissue is highly
suspicious of malignancy. Matted glands may occur in
tuberculous lymphadenitis.
Often, in the course of routine examination, you will
discover one or more small, mobile, nontender ‘pea-
sized’ lymph nodes. The ‘significance’ of these ‘shotty’
nodes may be difficult to assess. Before embarking
on a major exercise to diagnose the cause of the
Fig. 2.71 Lymphatic drainage of the arm. lymphadenopathy, it is reasonable to re-examine the
node a few weeks later. If there is no change in symptoms
and signs or gland size over this period, it is reasonable
to consider the node a relic of a previous illness.
Structures draining to inguinal nodes On completion of the lymphoreticular examination,
it should be clear whether the lymphadenopathy is
localised or generalised. This, in turn, helps with the
from lower abdomen
below umbilicus differential diagnosis. If there is widespread adenopathy,
from buttock
and back consider HIV infection and AIDS, lymphomas and
from skin of leukaemia.
penis, scrotum,
perineum.
lower vagina
horizontal vulva, anus HEAD AND NECK NODES
group
First, examine the nodes encircling the lower face
and neck. Sit the patient forward. You may choose to
vertical
group examine these nodes from the front (Fig. 2.73) or back
(Fig. 2.74). Both left and right sides can be examined
simultaneously using the fingers of your left and right
hands. Palpate the nodes in sequence, starting with the
Fig. 2.72 Inguinal nodes drain the lower limbs, lower trunk, penis, submental group in the midline behind the tip of the
scrotum, perineum, lower vagina and anus. mandible. Next, feel for the submandibular nodes midway
and along the inner surface of the inferior margin of the
mandible. Feel for the tonsillar node at the angle of the
jaw, the preauricular nodes immediately in front of
Examination of the lymph nodes the ear, the postauricular nodes over the mastoid process
and, finally, the occipital nodes at the base of the skull
Examination of the lymph nodes involves inspection posteriorly.
and palpation. Large nodes may be clearly visible on Follow this examination with palpation of the vertical
inspection. Infected nodes are enlarged and tender groups of neck nodes. It may be helpful to flex the
53
Chapter
a
a
b
b Fig. 2.74 Examination of the lymph nodes from the posterior:
(a) submandibular nodes, (b) cervical nodes.
Fig. 2.73 Examination of the lymph nodes of the head and neck
from the patient’s front: (a) submandibular nodes, (b) occipital
nodes, (c) deep cervical nodes.
Fig. 2.75 Palpation of the supraclavicular nodes in the

patient’s neck slightly to relax the strap muscles. Feel for supraclavicular fossa.
the superficial cervical nodes along the body of
sternocleidomastoid (Fig. 2.70). The posterior cervical
nodes run along the anterior border of trapezius. The EPITROCHLEAR AND AXILLARY NODES
deep cervical chain is difficult to feel as the nodes are To palpate the epitrochlear node, passively flex the
deep to the long axis of sternocleidomastoid; explore for patient’s relaxed elbow to a right angle. Support this
these nodes by palpating more firmly through the body position with one hand while feeling with your fingers
of this muscle. Conclude the examination by probing for for the epitrochlear nodes which lie in a groove above
the supraclavicular nodes which lie in the area bound and posterior to the medial condyle of the humerus (Fig.
by the clavicle inferiorly and the lateral border of 2.76). The axillary group includes anterior, posterior,
sternocleidomastoid medially (Fig. 2.75). A palpable left central, lateral and brachial nodes. Examine the axillary
supraclavicular node (Virchow’s node) should always nodes from the patient’s front. The technique for
alert you to the possibility of stomach cancer. examining this region is described in Chapter 8.
54
Chapter
Fig. 2.76 Palpation of the epitrochlear nodes which lie in a groove

above and posterior to the medial condyle of the humerus.
Fig. 2.78 Palpation of the popliteal nodes.
INGUINAL AND LEG NODES

Examine these nodes with the patient lying down (Fig.
2.77). The superficial inguinal nodes run in two chains.
Palpate the horizontal chain which runs just below the
line of the inguinal ligament and the vertical chain which
runs along the saphenous vein. Relax the posterior
popliteal fossa by passively flexing the knee. Explore the
fossa for enlarged popliteal nodes by wrapping the hands
around either side of the knee and exploring the fossa
with the fingers of both hands (Fig. 2.78).
Remember that the spleen and liver are important
components of the lymphoreticular system. Both may
enlarge in lymphoreticular diseases. The examination of
Fig. 2.77 Palpation of the inguinal nodes. these organs is covered in Chapter 6.

Nutrition in the elderly
• Elderly at special risk of nutritional compromise • Age-related norms for height, weight, midarm muscle
• Contributory factors: circumference and triceps skinfold thickness
– socioeconomic unavailable for elderly people
– inability to shop • Nutrition best assessed by careful dietary assessment
– loneliness (using third party to validate information)
– loss of smell, taste and teeth • Assessment of hydration affected by loss of elastic
tissue in skin
55
Chapter
Review
Framework for the routine physical examination
General examination • Lungs (inspect, palpate, percuss, auscultate)

• First impressions • Heart (evidence of cor pulmonale)
• Clinical syndromes (including endocrinopathies) Abdominal examination
• Nutritional status • Hands (flapping tremor, nails, palms)
• Hydration • Jaundice and signs of liver failure
• ‘Colour’ • Parotids
• Oedema • Mouth and tongue
• Temperature • Chest (gynaecomastia, spiders, upper body of liver)
• Lymphoreticular examination • Abdomen (inspect, palpate, percuss, auscultate)
Skin examination • Groins
• Skin inspection • Rectal examination
• Palpation Male genitalia
• Description of lesions • Sexual development
• Hair • Penis
• Nails • Scrotum
Ear, nose and throat examination • Testes and spermatic cord
• Inspection of outer ear and ear drum, test hearing and • Inguinal region
balance Female breasts and genitalia
• Inspection of nose and palpation/percussion of sinuses • Sexual development
• Inspection of lips, teeth, tongue, oral cavity and • Breast (inspection, palpation)
pharynx, inspection and palpation of salivary glands • Vulva (inspection, palpation)
• Palpation of regional lymph nodes • Vagina (inspection, palpation)
Cardiovascular examination • Uterus and adnexae (palpation)
• Hands (splinters, clubbing) Musculoskeletal examination
• Pulses • Proximal and distal muscles (inspection, palpation)
• Blood pressure • Large joints
• Jugular blood pressure • Small joints
• Heart (inspect, palpate, auscultate) • Spine
• Lungs (basal crackles, effusions)
Neurological examination
• Abdomen (liver pulsation)
• Psychological profile
• Extremities (peripheral circulation, oedema)
• Mental status
Respiratory examination • Cranial nerves
• Hands (clubbing, cyanosis, CO2 retention) • Motor and sensory examination (central and
• Blood pressure (pulsus paradoxus) peripheral), cerebellar examination
• Neck (JVP, trachea) • Autonomic nervous system
56
3
Skin, hair and nails
This chapter aims to familiarise you with the clinical layer of the stratum corneum) where the cells lose their
features of skin disease and illustrates some of the more nuclei and form a tough superficial barrier (Fig. 3.1). The
common skin disorders. migratory cycle from the basal to horny layer takes
The relatively sparse distribution of hair in the human approximately 30 days, with the cornified cells shedding
species contrasts starkly with most other mammals and from the surface some 14 days later. Abnormalities of this
reflects an evolutionary event that must, in some way, transit time may lead to certain skin diseases such as
have been advantageous. Perhaps human nakedness psoriasis, in which the migration rate is greatly accelerated.
provided a strong stimulus for developing alternative Epidermal cells are linked by structures known as
‘coats’ and from this emerged the creative attributes that desmosomes. The epidermis rests on a thin basement
characterise the species. membrane and is anchored to the dermis by
The environment in which we live is harsh, variable hemidesmosomes and other anchor proteins such as
and unpredictable. In contrast, the efficiency with which laminin, basement membrane proteoglycan and type IV
the body operates is set within narrow limits of collagen. These and other proteins are of importance in
temperature and hydration. Skin has evolved to the pathogenesis of diseases occurring at the epidermal–
encapsulate, insulate and thermoregulate. Recently, other dermal junction (e.g. bullous pemphigoid and
functions have been recognised: the skin is an important epidermolysis bullosa).
link in the immune system, and the Langerhans cells Melanocytes develop among the basal cells. These
of the dermis are closely related to monocytes and cells are derived from neural crest cells and synthesise
macrophages and are probably important in delayed melanin pigment which is transferred to keratinocytes
hypersensitivity reactions and allograft rejection. Skin through dendritic processes. Melanin is responsible for
also has an important endocrine function, being skin and hair pigmentation. The pigment protects the
responsible for the modification of sex hormones skin from the potentially harmful effects of ultraviolet
produced by the gonads and adrenals. In addition, skin irradiation. Skin colour is determined by the total number,
is the site of vitamin D synthesis. size and distribution of melanin granules, not the number
of melanocytes. Hereditary failure to synthesise melanin
results in albinism.
Dermis
SKIN This layer provides the supporting framework on which
The skin comprises two layers: the epidermis, derived the epidermis rests and consists of a fibrous matrix of
from embryonic ectoderm, and the dermis and collagen and elastin set in a ground substance of
hypodermis, derived from mesoderm. glycosaminoglycans, hyaluronic acid and chondroitin
sulphate (Fig. 3.1). The skin appendages are set in the
Epidermis
dermis. Nerves, blood vessels, fibroblasts and various
This layer consists of a modified stratified squamous inflammatory cells also populate this layer. The dermis is
epithelium and arises from basal, germinal columnar divided into two layers: the papillary dermis apposes the
keratinocytes that evolve as they migrate towards the undulating dermal–epidermal junction, whereas the
surface through a prickle cell layer (where the cells acquire reticular dermis lies beneath, forming the bulk of collagen,
a polyhedral shape) and a granular cell layer (where elastic fibres and ground substance. Dermal fibroblasts
the nucleated cells acquire keratohyalin granules) and synthesise and secrete the dermal collagen subtypes (I
eventually form the superficial keratinised layer (horny and III) and elastin. If there is disruption of dermal elastin,
57
Chapter
3 Skin, hair and nails
midline of the back and the perineum. Sebum contains

triglyceride, scalene and wax esters and functions to
Structure of the epidermis, dermis
and hypodermis waterproof and lubricate the skin, as well as inhibiting
the growth of skin flora and fungi. Skin disorders such as
horny granular spinous basement acne vulgaris and rosacea occur in areas where sebaceous
layer layer layer membrane glands concentrate.
(prickle cells) basal layer
(germinal Apocrine and eccrine glands
keratinocytes)
The apocrine glands are concentrated in the axillae,
hair areolae, nipples, anogenital regions, eyelids and external
exfoliation
ears. These glands become functionally active at puberty
14 days and are responsible for an odourless secretion which is
acted on by skin flora, causing characteristic body odour
30 days to develop. The eccrine sweat glands are widely distributed
and are extremely important in heat regulation and fluid
superficial
vascular plexus
balance. Whereas the eccrine cells secrete an isotonic
fluid, the duct cells modify the fluid to render it hypotonic.
arrector pili
muscle Secretion and its modification are under cholinergic and
hormonal control. Sweating in response to temperature
reticular
dermis change is under hypothalamic control.
sebaceous
gland
deep HAIR
vascular
plexus In most mammals, hair is important in the control of
hair follicle temperature. In humans, however, hair is mainly
important as a tactile organ which also has a sensual
hypodermis function, important in both sexual attraction and
stimulation. Hair covers all of the body except the palms,
capillaries soles, prepuce and glans and inner surface of the labia
minora. During gestation the fetus is covered by a fine
coat of lanugo hair which is lost shortly before birth,
except for the scalp, eyebrows and lashes. Hair may be
Fig. 3.1 Section through full thickness of skin showing the structure vellus, which is short, fine and unpigmented, or terminal
of the epidermis, dermis and hypodermis.
hair, which is thicker and pigmented. Puberty is
characterised by the development of coarse, pigmented
hair in a pubic, axillary and facial distribution.
disorders such as wrinkles and a loose skin syndrome Hair is formed by specialised epidermal cells that
(cutis laxa) occur. invaginate deep into the dermal layer. Hair develops
Hypodermis from the base of the hair follicle where the papilla, a
network of capillaries, supports the nutrition and growth
The dermis rests on the hypodermis, which is the of the hair. Hair growth is cyclical: the active growth
subcutaneous layer of fat and loose connective tissue. phase is termed anagen; involution of the hair, catagen;
This layer serves both as a fat store and an insulating and the resting phase, telogen.
layer. The hair shaft consists of a cuticle, cortex and medulla.
The arrectores pilorum muscles anchor in the papillary
SKIN APPENDAGES dermis and insert into the perifollicular tissue (Fig. 3.1).
Contraction of these muscles causes goose pimples (cutis
Sebaceous glands
anserina) to occur. Hair colour is determined by the
Skin sebaceous glands can function throughout life, density of melanosomes within the cortex of the hair
although activity is latent between birth and puberty. shaft; none is present in white hair, whereas grey hair has
These glands are partly responsible for the production of a reduced number. Red hair has different melanosomes
vernix caseosa which covers and waterproofs the fetus to black hair, both chemically and structurally.
during the latter stages of gestation. The glands become
particularly active during puberty. The secretion is
holocrine (i.e. caused by complete degeneration of the THE NAIL
acinar cells) and is stimulated by androgens and opposed Nail is a specialised skin appendage derived from an
by oestrogens. Sebaceous glands are absent from the epidermal tuck that invaginates into the dermis. The
palms and soles and are concentrated on the face, scalp, highly keratinised epithelium is strong but flexible and
58
Chapter
Symptoms of skin disease 3
or domestic toxins or chemicals. Ask whether waterproof

Structure of nail gloves are worn when washing dishes or dusting and
nail bed
cleaning the home. Question the patient about recent
nail plate exposure to medicines, especially antibiotics which often
cause skin rashes. Cosmetics are an important cause of
skin sensitisation so enquire about the use of new soaps,
deodorants and toiletries. Ask about hobbies (e.g.
gardening, model building and photographic developing),
eponychium posterior foreign travel and insect bites. Ascertain whether or not
nail fold the skin complaint is seasonal.
body of nail
nail matrix nail root

Questions to ask
nail plate
Skin history
paronychium
lunule • Was the onset sudden or gradual?
cuticle
• Is the skin itchy or painful?
eponychium
• Is there any associated discharge (blood or pus)?
• Where is the problem located?
• Have you recently taken any antibiotics or other
drugs?
• Have you used any topical medications?
Fig. 3.2 Structure of nail.
• Were there any preceding systemic symptoms (fever,
sore throat, anorexia, vaginal discharge)?
provides a sharpened surface for fine manipulation, • Have you travelled abroad recently?
clawing, scraping or scratching. • Were you bitten by insects?
The nail has three major components: the root, the nail • Any possible exposure to industrial or domestic
plate and the free edge (Fig. 3.2). The proximal and lateral toxins?
nail folds overlap the edges of the nail and a thin cuticular • Any possible contact with sexually transmitted
fold, the eponychium, overlies the proximal nail plate. disease or HIV?
The lunule is the crescent-shaped portion of the proximal • Was there close physical contact with others with
nail formed by the distal end of the nail matrix. The skin disorders?
free margin of the distal nail is continuous along its
undersurface with the hyponychium, a specialised area
of thickened epidermis. The nail plate lies on the highly
vascularised nail bed, which gives the nail its pink Differential diagnosis
appearance. The paronychium is the soft, loose tissue
Systemic diseases causing pruritus
surrounding the nail border; it is particularly susceptible
to bacterial or fungal infection infiltrating from a breach • Intrahepatic and extrahepatic biliary obstruction
in the eponychium (a paronychia). Fingernails grow (cholestasis)
approximately 0.1 mm per day, with more rapid growth • Diabetes mellitus
in summer compared with winter. • Polycythaemia rubra vera
• Chronic renal failure
• Lymphoma (especially Hodgkin’s disease)
Symptoms of skin disease
The history should evaluate possible precipitating factors
and determine whether the skin problem is localised or Systemic disorders may also present with skin
a manifestation of systemic illness. symptoms. Infectious diseases often present with skin
The skin is readily examined and for this reason the rashes or lesions. Ask about a recent sore throat, as
history often assumes less importance than with other streptococcal infection may be accompanied by typical
systems. However, a thorough history may unearth rash (scarlet fever), painful red nodules on the extensor
crucial information to aid diagnosis. Attempt to gain surface (erythema nodosum) or guttate psoriasis. In a
some insight into the patient’s social conditions, as cutaneous candidal infection, the patient often complains
overcrowding and close physical contact are important of an itchy rash and sore tongue or, in women, a vaginal
when considering infectious disorders such as scabies discharge. Candida albicans infection often follows a
and impetigo. Enquire in some depth about possible course of broad-spectrum antibiotics. Skin rashes
precipitating factors, especially contact with occupational developing in sun-exposed areas (in the absence of strong
59
Chapter
sunburn, known as photosensitive rashes) should raise

the possibility of systemic lupus erythematosus, porphyria
or drugs. If the patient complains of skin lesions around
the genitalia, enquire about possible contact with sexually
transmitted disease. AIDS may present with the nodular
lesions characteristic of Kaposi’s sarcoma or thrush
affecting the mucosa or skin. Therefore, it is important to
take a history of risk factors (e.g. male homosexuality,
high-risk heterosexual contact, blood transfusion and
intravenous drug abuse). Skin itching (pruritus) in the
absence of an obvious rash should alert you to an
underlying systemic disorder.
Topical steroids and other topical substances are
commonly prescribed to treat a variety of skin lesions. Fig. 3.3 Alopecia.
Always ask about topical treatment as this may alter the
appearance of a skin lesion, making the diagnosis more
difficult.
Symptoms of hair disease

HAIR THINNING
Balding (alopecia) worries patients and you will often be
asked to assess scalp hair loss. Male pattern baldness
is common; the patient will note the slow onset of hair
loss with the hairline receding from the frontal and
temporal scalp and crown. Ask about a family history of
baldness as male alopecia is an expression of autosomal
dominance and may begin early in life. After the
menopause, many women note thinning of the hair
(Fig. 3.3); this is often associated with growth of facial Fig. 3.4 Alopecia areata characterised by localised patches of hair
hair. loss.
Questions to ask causing a local area of thinning or baldness. Severe illness

Hair history and malnutrition, as well as sudden psychological shock,
• Was the hair loss sudden or gradual?
may be associated with hair loss, which usually recovers
• Does the loss occur only on the scalp or is the body
once the stress has been resolved.
hair involved as well?
• Is the baldness localised or general, symmetrical or ABNORMAL HAIR GROWTH
asymmetrical? Remember to warn patients undergoing cytotoxic
• Is there a family history of baldness (especially in treatment for cancer that they can expect generalised hair
men)? loss. Failure to develop axillary and pubic hair at the
• What drugs have you taken recently? expected time of puberty should alert you to the possibility
• Any recent illnesses, stress or trauma? of pituitary or gonadal dysfunction.
• Are there other systemic symptoms (e.g. symptoms Abnormal facial hair growth (hirsutism) is a distressing
of hypothyroidism)? symptom in women. It is important to recognise that
a certain degree of facial hair growth occurs naturally
in postpubertal women. There are racial differences:
physiological hirsutism is least apparent in Japanese and
Hair loss may also be a feature of disease and the Chinese women and most apparent in women of
characteristics of the alopecia may be helpful. Patients Mediterranean, Middle Eastern, Indian and Negroid
complaining of localised alopecia (alopecia areata) (Fig. extraction. The unexpected occurrence of hirsutism,
3.4) may have an autoimmune disease (e.g. Hashimoto’s especially if accompanied by other symptoms and signs
thyroiditis with myxoedema). Patients with stress or of virilism, should alert you to the possibility of a hormonal
anxiety neurosis may nervously pluck hair from the scalp, imbalance.
60
Chapter
Examination of the skin, hair and nails 3
Questions to ask
areas like the axillae, inner thighs and buttock with
its natal cleft. Many skin lesions can be diagnosed by
Hirsutism
their appearance and localisation. Unlike any other
• Is there a family history of hirsutism? organ system, the examination relies almost entirely on
• Are your menstrual periods normal or absent careful inspection and meticulous use of descriptive
(or scanty)? terminology.
• Is there a history of primary or secondary infertility? Measurement of the length and breadth of skin lesions
• Do you experience visual disturbances or headaches is useful, especially when monitoring progression or
(pituitary disease)? regression. A broad beam torch or electric light helps to
• What medications do you take (e.g. phenytoin, define the outline of the border of a skin lesion; a thin
anabolic steroids, progestogens)? beam is helpful if you wish to check whether or not a
lesion transilluminates. A fluid-filled but not solid lesion
emits a red glow when the torch light shines through it.
A Wood’s lamp helps to distinguish a fluorescing lesion;
Differential diagnosis by shining the lamp at a suspect lesion, it may be possible
Hirsutism to show the characteristic blue-green fluorescence of
fungal infections.
• Racial variation in hair distribution
• Hormonal imbalance Skin colour
– polycystic ovaries
Skin colour varies between individuals and races and is
– ovarian failure or menopause
usually even and symmetrical in distribution. Normal
– virilising adrenal tumours
variations occur in freckling and sun-exposed areas.
• Drugs
During pregnancy, there may be darkening of the skin
– phenytoin
overlying the cheek bones (melasma) and the areolae
– progestogens
surrounding the nipple (chloasma).
– anabolic steroids
– ciclosporin Abnormal skin colour
Generalised changes in skin colour occur in jaundice,
iron overload, endocrine disorders and albinism. The
yellow tinge of jaundice is best observed in good daylight,
Symptoms of nail disease appearing initially as yellowing of the sclerae and then as
a yellow discoloration on the trunk, arms and legs.
Whereas examination of the nails may be very revealing, Jaundice is less apparent in unconjugated as opposed to
nail-related symptoms are usually nonspecific. Patients conjugated hyperbilirubinaemia. In longstanding, deep
may relate symptoms suggestive of bacterial infection obstructive jaundice, the skin may turn a deep yellow-
along the nail edge; these include intense pain, swelling green. Remember that people eating large quantities of
and often a purulent discharge. Complaints of brittleness, carrots or other forms of vitamin A may develop yellow
splitting or cracking provide little diagnostic information. skin pigmentation (carotenaemia) and that the absence
Ask specifically about skin disease that may affect the of scleral discoloration distinguishes this syndrome from
nail, such as psoriasis, severe eczema, lichen planus or a jaundice.
susceptibility to fungal skin infection. Iron overload (haemosiderosis and haemochromatosis)
causes the skin to turn a slate-grey colour. The astute
observer may recognise this metabolic disease by the
Examination of the skin, hair and nails characteristic skin pigmentation. Addison’s disease
(autoimmune adrenal destruction) is characterised by
EXAMINING THE SKIN darkening of the skin, occurring first in the skin creases
When examining the skin, there is a tendency to focus of the palms and soles, scars and other skin creases. The
on the local area noticed by the patient. Nonetheless, you mucosa of the mouth and gums also becomes pigmented.
should consider the skin as an organ in its own right and, Striking pigmentation also arises after bilateral
like any other examination, the whole organ should be adrenalectomy for adrenal hyperplasia: this syndrome
examined to gain maximum information. The patient (Nelson’s syndrome) is caused by unopposed pituitary
should be stripped to the underwear, covered with a overstimulation. In hypopituitarism, the skin is soft, pale
gown or blanket and the examination area should be well and wrinkled.
lit (preferably natural daylight or fluorescent light). Albinism is an autosomal recessive disorder caused by
failure of melanocytes to produce melanin. The skin and
Inspection and palpation
hair are white and the eyes are pink because of a lack
Scan the skin, looking for skin lesions and noting both of pigmentation of the iris, and there may also be
position and symmetry. Remember to expose hidden nystagmus.
61
Chapter
Fig. 3.8 Typical appearance of petechial haemorrhage in a patient

Fig. 3.5 Depigmented skin (vitiligo): white discoloration of brown with thrombocytopenia.
hand.
Fig. 3.9 Telangiectasia on the tongue.

Fig. 3.6 Café-au-lait patches with neurofibromas.
Telangiectasia refers to fine blanching vascular lesions

caused by superficial capillary dilatation (Fig. 3.9).
Localised skin lesions
Careful descriptions of size, shape, colour, texture and
position of lesions are helpful in skin diagnosis. Try
to ascertain a primary and secondary description of
the skin lesion. To establish the primary nature of the
skin lesion decide whether the lesion is flat, nodular or
fluid-filled. Flat circumscribed changes in colour are
termed macules if less than 1 cm or patches if more than
1 cm. If the lesion is raised and can be palpated, assess
whether the mass is a papule, plaque, nodule, tumour
or wheal. If a circumscribed elevated lesion is fluctuant
Fig. 3.7 Café-au-lait patches in neurofibromatosis.
and fluid-filled, describe whether it is a vesicle, bulla or
pustule (Fig. 3.10). If possible, describe the arrangement
Common localised abnormalities of skin pigmentation of the lesions; that is, whether linear, annular (ring-
include vitiligo (Fig. 3.5), café-au-lait spots (Figs 3.6, 3.7), shaped) or clustered. In shingles (herpes zoster), the
pityriasis versicolor and idiopathic guttate hypomelanosis. rash occurs in the distribution of one or more skin
Erythema of the skin is caused by capillary dilatation; dermatomes.
when pressure is applied the red lesion blanches and Add to the primary description any secondary
reforms. When examining a patient, you may notice an characteristics such as superficial erosions, ulceration,
erythematous flush in the necklace area which is caused crusting, scaling, fissuring, lichenification, atrophy,
by anxiety. Purpura is the term used for red-purplish excoriation, scarring, necrosis or keloid formation.
lesions of the skin caused by seepage of blood from skin Palpation is used to decide whether a lesion is flat,
blood vessels. Unlike erythema, these lesions do not raised or tender. Compression may be helpful (e.g.
blanch with pressure. If the lesions are small (<5 mm) demonstration of the characteristic arteriolar dilatation of
they are called petechiae (Fig. 3.8), whereas larger lesions spider naevi occurring in decompensated liver disease)
are purpura. Traumatic bruises are called ecchymoses. (Fig. 3.11). Use the back of your hand to assess
62
Chapter
Primary localised lesions

macule patch papule wheal
<1cm >1cm
vesicle plaque nodule bulla
Fig. 3.10 Primary localised skin lesions.
index finger and thumb. Hold firmly for a few seconds

and then release. Healthy, well-hydrated skin immediately
springs back into its resting position. In significant
dehydration or when skin elastic tissue is lost (e.g.
ageing), the skin behaves like putty and only slowly
reshapes to its resting position. Skin oedema can be
demonstrated by pressing your thumb or fingers into the
skin, maintaining the pressure for a short while and then
releasing. Your thumb or finger impression will remain
indented in the skin if there is excessive fluid (‘pitting’
oedema).
Although most disorders can be diagnosed from their
Fig. 3.11 Spider naevi in hepatocellular disease. appearance, special techniques such as microscopy of
skin biopsies or skin scrapings, immunofluorescent
staining and culture of specimens may be required to
temperature. Inflamed lesions (e.g. cellulitis) are hotter confirm diagnosis.
than surrounding tissue, whereas skin overlying a lipoma
Common skin lesions
(subcutaneous fat tumours) is cooler than adjacent tissue.
Skin turgor may be used as a measure of moderate to Skin lesions are often readily recognisable and you should
severe hydration. Pinch a small area of skin between be able to distinguish some common conditions.
63
Chapter
Fig. 3.12 Papules, pustules and scarring in acne vulgaris. Fig. 3.13 Rosacea: papules and pustules occur on the face.
Acne vulgaris
This common disorder of the pilosebaceous unit occurs
at puberty. Plugging of the duct, increased sebum
production, bacterial growth and hormonal changes all
predispose to the condition. Acne presents with greasy
skin, blackheads (comedones), papules, pustules and
scars (Fig. 3.12). The lesions are common and vary in
severity and most teenagers recognise the problem before
visiting the doctor. The disorder affects the face, chest
and back. Acne usually subsides in the third decade.
Rosacea
This facial rash usually presents in the fourth decade,
although in women it may present after the menopause. Fig. 3.14 Rosacea: lesions occur on the nose, cheeks and chin.
Papules and pustules erupt on the forehead, cheeks,
bridge of the nose and the chin. The erythematous
patients taking more than one drug, because it may be
background highlights the rash (Figs 3.13, 3.14).
difficult to decide which the offending agent is. Also,
Comedones do not occur, distinguishing the condition
remember that drugs may cause secondary skin eruptions:
clinically from facial acne. Occasionally, the rash may
broad-spectrum antibiotics may encourage the growth of
be localised to the nose. Eye involvement is characterised
candida, which, in turn, can present as a ‘drug-related’
by grittiness, conjunctivitis and even corneal ulceration.
skin rash. Drug reactions may occur within minutes or
There appears to be vasomotor instability and patients
hours of taking the medication but there may also be
flush readily in response to stimuli such as hot drinks,
delays of up to 2 weeks for the reaction to manifest. This
alcohol and spicy foods. If this disorder is treated with
may even follow the discontinuation of the drug (well
potent topical corticoids there may be a temporary
known with ampicillin). It is important to recognise
response, but a marked relapse occurs on cessation of
different expressions of drug sensitivity.
treatment. It is important to check carefully whether or
not steroids have been applied and to dissuade your
patient from using this treatment (like acne vulgaris, Differential diagnosis
antibiotics are the treatment of choice).
Skin lesions associated with drug sensitivity
Drug reactions
• Toxic erythema
Drugs are probably the most common cause of acute skin • Exfoliative dermatitis
disease and your history must include a complete history • Urticaria
of all drugs the patient may have been exposed to over • Angioneurotic oedema
the preceding month. Antibiotics such as ampicillin, • Erythema nodosum
penicillin and sulphonamides commonly cause drug • Erythema multiforme
rashes. It may be difficult to distinguish between a drug • Fixed drug reaction
reaction and the manifestations of the disease under • Photosensitive drug reactions
treatment. In addition, drug reaction may closely mimic • Pemphigus
skin diseases. Diagnosis may be further confused in
64
Chapter
Toxic erythema Questions to ask

Profuse eruptions affect most of the body. Red macules Exfoliative dermatitis
appear and overlap and coalesce to give the appearance
• Is there any loss of hair or nails?
of diffuse erythema (Fig. 3.15). The erythematous skin
• Have you ever had psoriasis or eczema?
desquamates as it heals. This condition is most often
• What drugs have you taken recently (barbiturates,
caused by ampicillin but also by sulphonamides (including
sulphonamides, phenylbutazone, streptomycin)?
co-trimoxazole), phenobarbital and infections.
• Do you have a fever?
Exfoliative dermatitis
Also known as erythroderma, this form of dermatitis
is characterised by diffuse erythema and desquamation
of the epithelium. If severe, the patient may lose both
heat and fluids. Many drugs are implicated, although
barbiturates, sulphonamides, streptomycin and gold are Urticaria
especially predominant. This presents with intense itching and localised swellings
of the skin that may occur anywhere on the body.
Typically, wheals occur that are red at the margins with
paler centres (Fig. 3.16). The characteristic feature of the
rash is its tendency to disappear within a few hours.
Angio-oedema usually occurs in association with urticaria
and is characterised by swelling of the face and hands.
Erythema nodosum
Symmetrical in distribution, the acute crops of painful,
tender, raised red nodules usually affect the extensor
surfaces, especially the shins but also the thighs and
upper arms (Figs 3.17, 3.18). Over 7–10 days, the lesions
change colour from bright red through shades of purple
to a yellowish area of discoloration. Erythema nodosum
is caused by vasculitis, may be recurrent, and is
most commonly associated with sulphonamides, oral
Fig. 3.15 Toxic erythema. contraceptives and barbiturates.
Fig. 3.16 Urticaria: lesions vary in size and Fig. 3.17 Erythema nodosum: painful, Fig. 3.18 Erythema nodosum: the nodules
shape. smooth red nodules on the lower leg. are raised and tender.
65
Chapter
Erythema nodosum
Infections
• Streptococcal infections
• Tuberculosis
• Leprosy
• Syphilis
• Deep fungal diseases
Drugs
• Sulphonamides
• Barbiturates
• Oral contraceptives
Systemic diseases
• Sarcoidosis
• Inflammatory bowel disease
Fig. 3.19 Erythema multiforme: the lesions are widespread on this

patient.
Erythema multiforme
This is characterised by symmetrical, round (annular)
lesions occurring especially on the hands and feet but
which may extend more proximally (Figs 3.19, 3.20).
Central blistering may occur, giving the appearance of
‘target’ lesions. In severe forms, bullae may appear. This
skin disease occurs with drugs, vaccination and, frequently,
with a herpes simplex infection.
Stevens–Johnson syndrome
This is a severe blistering form of erythema multiforme
with blistering and ulceration affecting the mucous
membranes of the mouth and often affecting the eyes
and nasal and genital mucosa (Fig. 3.21).
Fixed drug eruption Fig. 3.20 Erythema multiforme.
This presents with one or more red blotches that

may become swollen and even bullous. The rash always
recurs in the same anatomical site: usually the mouth,
a limb or genital area. The rash fades, leaving an
area of skin discoloration (Fig. 3.22). Associated
with many drugs but especially phenolphthalein
(common in laxatives), sulphonamides, tetracycline and
barbiturates.
Photosensitive drug rashes

This rash occurs in sun-exposed areas (face, necklace
region and extensor surfaces of limbs). It may appear
as erythema, oedema, blistering or an eczematous Fig. 3.21 Stevens–Johnson syndrome: ulceration is present on the
rash. lips and in the mouth.
66
Chapter
Fig. 3.22 Fixed drug eruption, with hyperpigmentation of the Fig. 3.23 Eczema: note the vesicle formation.
breasts.
Photosensitive skin reactions
Drugs
• Tetracyclines
• Sulphonamides
• Phenothiazines
• Psoralens
• Hydroxychloroquinones
Systemic disorders
• Pellagra (nicotinic acid deficiency)
• Systemic lupus erythematosus
• Porphyria cutanea tarda Fig. 3.24 Acute eczema: red exudative eruption which is painful.
• Erythema multiforme
Eczema
This common skin abnormality is caused by a number
of different mechanisms and the disease may be acute,
subacute or chronic, all of which may coexist. Itching is
a major symptom. Acute eczema is characterised by
oedema, vesicle formation (Fig. 3.23), exudation (weeping)
(Fig. 3.24) and crusting. In chronic eczema there are
dry, scaly, hyperkeratotic patches and thickening and
fissuring of the skin (Fig. 3.25). The appearance of
eczema is often modified because the patient scratches,
causing secondary changes such as excoriation and Fig. 3.25 Chronic eczema: the skin is dry and scaly.
secondary infection. The boundaries of an area of
chronic eczema are less well defined than psoriasis and
this may be a helpful sign in the differential diagnosis and does not have the characteristic scales typical of
(Fig. 3.26). psoriasis.
Discoid (nummular) eczema Unlike other forms of Atopic eczema This usually presents in infancy, although
eczema, this subtype has a well-defined, coin-shaped (L. it does occasionally present for the first time in adulthood.
nummularius = of money) outline and may be confused There is normally a family history of eczema or some
with psoriasis. However, nummular eczema tends to other atopic disorder (e.g. asthma, hay fever, urticaria).
occur on the back of the fingers and hands. It also weeps The rash is symmetrical, usually starting on the face
67
Chapter
Fig. 3.28 Seborrhoeic dermatitis in an infant.

Fig. 3.26 Typical appearance of eczematous lesion. Note that the
boundary is less distinct than plaques of psoriasis.
Fig. 3.29 Seborrhoeic dermatitis occurs most commonly on the

face.
Fig. 3.27 Contact dermatitis caused by shampoo.
and migrating to the trunk and limbs (where it tends the appearance of the primary lesion. The scalp is most
to affect the flexures of the elbows, knees, wrists and commonly involved and the condition is distinguished
ankles). from dandruff by the associated erythema of the skin due
to inflammation. Other regions involved include the
Contact dermatitis This variant of eczema is caused
central areas of the face, eyelid margins, nasolabial folds,
by an exogenous irritant (Fig. 3.27). The lesion may
cheeks, eyebrows and forehead. Involvement of the
be a primary irritant phenomenon, occurring almost
outer ear occurs (otitis externa). The vulva may also be
predictably when skin contact is made with a concentrated
affected.
toxic agent, or an allergic contact dermatitis which only
occurs in patients who generate a delayed (type IV) Pompholyx Pompholyx is another variant of eczema
immune response to a substance in contact with the skin. affecting the hands and feet (Figs 3.30, 3.31). This variant
The distribution of the eczema may provide an important is characterised by the eruption of itchy vesicles, especially
clue to the nature of the topical irritant. Individuals on the lateral margins of the fingers and toes, as well as
who regularly immerse their hands in water containing the palms and soles.
detergents or other sensitising substances will present
with the rash restricted to the hands. Jewellery may Varicose eczema This subtype occurs in patients with
cause an allergic contact dermatitis; nickel is an longstanding varicose veins. The eczematous patches
important sensitising agent. Rubber, dyes, cosmetics affect the lower leg and may or may not be associated
and industrial chemicals are common allergens implicated with other skin disorders caused by varicose veins; for
in this immune-mediated form of eczema. Plants example, venous ulcers that occur in the region of the
such as primulas and chrysanthemums have also been medial malleolus, pigmentation and oedema.
implicated.
Psoriasis
Seborrhoeic dermatitis This is an eczematous condition
occurring in infants (Fig. 3.28), adolescents and young The lesions are well-defined, slightly raised and
adults. There is erythema and scaling with a symmetrical erythematous. In the chronic phase, silvery scales cover
rash (Fig. 3.29). Secondary infection may occur, altering the surface. The lesions vary in size from small (guttate)
68
Chapter
Fig. 3.30 Typical itchy vesicles of pompholyx. Fig. 3.33 Acute guttate psoriasis.
Fig. 3.31 Pompholyx: pruritic vesicles on the hand. Fig. 3.34 Psoriatic plaque covered with a silvery scale.
Fig. 3.32 Guttate (teardrop) psoriasis. Fig. 3.35 Psoriatic plaque. Note the scaly, shiny surface and the
sharp border.
(Figs 3.32, 3.33) to large plaques (Figs 3.34, 3.35). These traumatised (the Koebner phenomenon). If you gently
guttate (1–3 cm) lesions are widely distributed over scratch the surface of a psoriatic plaque, tiny bleeding
the body and may either resolve or persist as chronic points appear.
psoriasis. Guttate psoriasis may follow streptococcal
Pustular psoriasis Pustular psoriasis is a variant, usually
pharyngitis.
confined to the palms (Fig. 3.36) and soles, although
Chronic psoriasis The plaques of chronic psoriasis have some are occasionally more diffuse. The pustules, 2–5 mm
a predilection for the scalp, elbows, knees, perineum, in diameter, are yellow (Fig. 3.37). On the palms and
umbilicus and submammary skin. The lesions are usually soles they become pigmented and hyperkeratotic. Rarely,
symmetrical. A characteristic feature of psoriasis is the psoriasis may be so extensive that most of the skin is
development of new psoriatic lesions where the skin is involved and exfoliation occurs.
69
Chapter
Fig. 3.36 Pustular psoriasis of the palm with well-defined scaling Fig. 3.38 Pitting of the nails in psoriasis.
and erythema.
Fig. 3.37 Pustular psoriasis of the foot. The yellow pustules turn Fig. 3.39 Pityriasis rosea: the pink papules become oval macules.
brown.
Psoriatic arthropathy In psoriatic arthropathy, the characteristic appearance (Figs 3.40, 3.41). The rash
distal interphalangeal joints are affected. Large joints resolves spontaneously within approximately 6 weeks.
may also be affected, either singly or symmetrically.
Rarely, patients may have sacroiliitis or even spinal Lichen planus
ankylosis. The nails may be involved even in the absence This is another itchy rash that can usually be diagnosed
of skin disease. The typical features include pinpoint at the bedside by its typical appearance (Fig. 3.42).
pitting of the nail (Fig. 3.38) and onycholysis (lifting of Occasionally, a lichenoid rash may be associated with
the distal nail from the nail bed). Unlike fungal nail systemic disorders (e.g. primary biliary cirrhosis, chronic
lesions, nail psoriasis is symmetrical. Severe nail dystrophy graft versus host disease) or drugs (e.g. penicillamine
may occur. and gold) but most commonly there is no associated
disease.
Pityriasis rosea
The rash affects both the skin and mucous membranes.
This is a common skin disorder in the younger patient. It has a predilection for the volar (front) aspect of the
A single patch rash occurs days or even weeks before forearm and wrists, the dorsal (back) surface of the hands,
the more general eruption. This ‘herald patch’ may be the shins, ankles and lower back region. The rash is
confused with ringworm. The full blown rash affects the symmetrical and characterised by small, shiny, purple or
upper arms, trunk and upper thighs (‘shirt and shorts’ violaceous papules which have a polygonal rather than
distribution). Pink papules evolve into 1–3 cm itchy oval rounded outline. A network of white lines on the surface
macules (Fig. 3.39) that scale near the edge, giving a of the papules is termed Wickham’s striae (best seen after
70
Chapter
Skin infections 3
Fig. 3.40 In pityriasis rosea, the typical lesions are ovoid macules Fig. 3.43 Lichen planus: linear lesion of the Koebner syndrome.
with scaling.
Fig. 3.41 Pityriasis rosea with obvious scaling. Fig. 3.44 Buccal involvement in lichen planus.
coating the lesion with mineral oil). As the papules

resolve, the affected skin becomes pigmented. Eruptions
occur after trauma (Koebner phenomenon) (Fig. 3.43)
and linear lesions are tell-tale signs occurring in scratched
areas. The buccal mucous membrane is commonly
involved (Fig. 3.44). Use a spatula and light to inspect the
mouth, looking for the lace-like network of white lines
or spots. The scalp is usually, although not always, spared.
The disease may affect the nails and penis.
Skin infections
BACTERIAL
Impetigo
Fig. 3.42 Polygonal papules in lichen planus.
This is a highly contagious skin lesion caused by β-
haemolytic streptococci. The face is most commonly
infected (Fig. 3.45). The lesions start as a papular eruption
around the mouth and nose that then evolves into a
vesicular eruption and spreads locally. The lesion breaks
71
Chapter
Fig. 3.46 Erysipelas. Note the erythema and oedema.
Fig. 3.45 Facial impetigo with crusting of the lesion.
down to leave a typical honey-coloured crust. Secondary

infection with Staphylococcus aureus is common.
Furuncle (boil)
A furuncle is an infection of a hair follicle, caused by S.
aureus, that spreads locally into the surrounding tissue.
A head of pus may be obvious at its apex. Furuncles
usually affect adolescents. A local collection of furuncles
is called a carbuncle. A stye (or hordeolum) is a small
furuncle affecting an eyelash.
Erysipelas and cellulitis Fig. 3.47 Erythema and oedema associated with cellulitis.
Infection of the superficial skin layers by Streptococcus
pyogenes is termed erysipelas, whereas an infection of the
deeper skin layers is called cellulitis. The lower limbs are
most commonly affected. Erysipelas is characterised by
the abrupt onset of a well-demarcated slightly raised and
tender erythematous rash (Fig. 3.46). Left untreated, the
margins of the lesion advance rapidly. The patient is
usually pyrexial and toxic. The infection responds quickly
to antibiotics. The margin of an area of cellulitis is less
well defined than erysipelas; in addition, superficial bullae
may develop in the centre of an affected area of skin (Fig.
3.47).
Syphilis
There are numerous skin manifestations of syphilis and
Fig. 3.48 Primary chancre in syphilis.
you should always suspect this disease when confronted
with an unexplained, non-itchy rash, especially when
the patient is generally unwell or when there is a high occur in the mucous membrane of the mouth (snail-track
risk of sexually transmitted disease. In primary syphilis, ulcers). In the tertiary stage, granulomas form (gummas);
a painless ulcer with an indurated edge (primary chancre) these can be felt as skin nodules which are prone to
(Figs 3.48, 3.49) appears at the site of infection (usually degenerate and ulcerate.
on the genitalia but occasionally on the lips or even
fingers). Approximately 2 months after the appearance of VIRAL
the chancre, the secondary rash appears: a pink macular
Warts
rash on the trunk (Fig. 3.50) that becomes papular,
affecting the genital skin, palms and soles. In the anal Common warts caused by papilloma viruses are self-
and groin regions, the moistness may cause erosions limiting and generally occur in the young patient. Warts
(condylomata accuminata) (Fig. 3.51). Raised oval patches usually occur on the fingers and hands as discrete papules
72
Chapter
Skin infections 3
Fig. 3.49 Primary syphilitic chancre on the frenulum. Fig. 3.52 Finger warts.
Fig. 3.53 ‘Fever blister’ caused by herpes simplex.
with a typical irregular surface (Fig. 3.52). Plantar warts

occur on the pressure-bearing areas of the feet and are
consequently flattened rather than raised.
Fig. 3.50 The maculopapular rash of secondary syphilis. Molluscum contagiosum
This is a common infection caused by a member of the
pox virus group. The lesions appear as flesh-coloured,
dome-shaped papules varying in size from pinpoint to
1 cm in diameter. The most characteristic feature of the
lesion is umbilication (a central depression of the surface).
In children, the lesions are especially common on the
face and trunk, whereas in adults, the genitalia may be
affected. As the lesions resolve, an area of induration
often develops in the surrounding skin.
Herpes simplex
There are two types of herpes simplex virus (HSV). Type
1 virus normally affects the mouth and lips (Fig. 3.53),
whereas type 2 usually affects the genitals. Crossover
infections do sometimes occur. The primary HSV infection
presents with crops of painful superficial vesicles
surrounded by an area of erythema. The vesicles erode
superficially, then crust and finally heal without scarring.
After the primary infection, the virus lies dormant in the
dorsal root nerve ganglion, with recurrences occurring
Fig. 3.51 Condylomata accuminata. predictably in the same area as the initial infection.
73
Chapter
Reactivation is heralded by a tingling sensation in the immunosuppressed patients and diabetics, and after
skin which is followed within 1–2 days by the eruption treatment with antibiotics. Candidosis is a major
of a crop of vesicles. Exacerbations may be precipitated manifestation of AIDS. Look for candidosis in the mouth;
by infection, stress, fever (hence the term fever blisters), the oral infection is characterised by white or off-white
abnormal exposure to sunlight, menstruation and trauma. plaques that can be scraped off, leaving a raw red base.
Often, no obvious precipitating cause is discovered. Other manifestations include angular stomatitis, vulval
and vaginal infections and involvement of contact
Herpes zoster (shingles)
surfaces (e.g. the natal cleft, inner thighs, scrotum and
After an attack of chicken pox, the varicella-zoster virus inframammary fold – intertrigo).
lies dormant in a dorsal root or cranial nerve ganglion.
Reactivation of the virus causes a localised eruption called
Pityriasis versicolor (tinea versicolor)
shingles. The cause of reactivation is often not apparent,
although immunosuppression, lymphomas and ageing This common condition of young adults is caused by
may be implicated. Malassezia furfur and presents as small pigmented or
The patient complains of pain or discomfort in a hypopigmented macules on the upper trunk and arms.
localised area of skin and, within a few days, a crop of The macules tend to coalesce, resulting in lesions that
vesicles appears in a characteristic dermatomal distribution vary in size and shape. Scales can be demonstrated by
(Fig. 3.54). Over 2–3 weeks, the vesicles evolve into scraping or teasing the lesions with a scalpel blade. In
pustules, scab, then heal. Often there is some residual sunburnt areas, the lesions appear to be hypopigmented
scarring. In order of frequency, the thoracic, cervical, in comparison to the surrounding skin.
lumbar and sacral dermatomes are affected. If the
ophthalmic branch of the trigeminal nerve is involved,
Dermatophytes (tinea)
there may be serious damage to the cornea. This is
associated with a typical distribution of the vesicles on The dermatophytes inhabit the stratum corneum and the
the tip and side of the nose. Involvement of the geniculate dead keratin of the nails and hair. Hair infection (tinea
ganglion of the facial nerve causes a facial palsy with capitis) presents with localised patches of hair loss and
involvement of the outer ear (Ramsay Hunt syndrome). skin inflammation. Skin infection (tinea corporis) affects
The most debilitating long-term effect of shingles, even the unhairy parts of the body. This presentation is often
when healing has occurred, is chronic pain and referred to as ‘ringworm’, because the lesion has an
hyperaesthesia in the affected dermatome. inflamed annular edge with a paler central area of healing
(Fig. 3.55). Athlete’s foot (tinea pedis) appears as a scaling
erythematous rash between the toes. A nail infection
FUNGAL
(tinea unguium) is often asymmetrical and affects the
Candida albicans toenails more often than the fingernails. The nail becomes
This is a common infection of the skin and mucous yellow and thick; there is onycholysis and, at a later stage,
membranes. Oral candidosis tends to occur in the nail crumbles and breaks. If suspected, take nail
clippings for mycology.
Fig. 3.54 Herpes zoster: note the haemorrhagic lesions (distribution

of L2). Fig. 3.55 Ringworm rash with inflamed periphery.
74
Chapter
Skin infections 3
INFESTATIONS haemorrhagic and then degenerate, causing erosions that

Pediculosis are susceptible to secondary infection (Fig. 3.59). Healing
occurs without scarring.
Infestation with lice causes skin irritation. Head lice
infestation (pediculosis capitis) is common in children. Pemphigus
The diagnosis is made by careful inspection of the hair This autoimmune disorder occurs most commonly in
for eggs (nits) which, unlike dandruff, cannot be shaken middle-aged Ashkenazi Jews. The onset is usually
off the hair. Scratching may give rise to secondary insidious and the earliest lesions often start in the mouth
inflammation and itching. Body lice infestation (pediculosis or genital mucous membrane; however, patients usually
corporis) is rare and almost always occurs in malnutrition present to the doctor once the skin is involved. Pemphigus
and when hygiene is poor. Infection of the pubic hair is characterised by painful, flaccid blisters that rupture
(pediculosis pubis) is caused by the crab louse and is to reveal a raw base that heals slowly (Figs 3.60, 3.61).
usually sexually transmitted. Like other lice infections, The skin adjacent to the bullous lesion slides
the infestation causes intense pruritus and the nits (and over the underlying dermis (Nikolsky’s sign). The
lice) are seen with the naked eye. umbilicus, trunk, intertrigenous areas and scalp are most
Scabies commonly affected. The clinical diagnosis is confirmed
by typical immunofluorescent staining, which shows
Consider scabies in any patient presenting with immunoglobulin G (IgG) and complement deposition in
widespread pruritus. The mite (Sarcoptes scabei) burrows the epidermis.
into the skin, where the female lays her eggs. The burrows
can be seen on inspection; look for these along the sides
of the fingers, the webs (Fig. 3.56) and the wrist. The
burrows are linear and just palpable and the white dot of
the mite can often be seen. The lesions may develop into
inflamed papules and may affect the elbows, axillae and
genitalia. Scratching causes secondary excoriation and
infection.
BLISTERING LESIONS
Bullous pemphigoid
This disorder occurs most commonly in elderly people.
The lesions are itchy and appear as tense, mainly
symmetrical blisters overlying and surrounded by an area
of erythema (Fig. 3.57). The blisters are initially small but
enlarge to a considerable size over a few days (Fig. 3.58).
Although truncal involvement also occurs, the blisters
appear mainly on the limbs, especially along the inner Fig. 3.57 Bullous pemphigoid with surrounding erythema.
aspects of the thighs and arms. The blisters become
Fig. 3.56 Chronic scabies in the webs between fingers. Fig. 3.58 Tense blisters of bullous pemphigoid.
75
Chapter
Fig. 3.62 The skin lesions of dermatitis herpetiformis.
Fig. 3.59 Haemorrhagic blisters of bullous pemphigoid.
Fig. 3.63 Junctional naevus.
Healing leaves tell-tale areas of hyperpigmentation. The

disorder is almost always associated with gluten-sensitive
Fig. 3.60 Skin pemphigus.
enteropathy (coeliac disease). Although almost all
patients have villous atrophy, it is unusual for them to
present with features of malabsorption.
Naevi
There are numerous skin blemishes collectively called
naevi. Pigmented naevi cause the greatest concern
because of the seriousness of malignant change. The
junctional naevus is distinguished as a flat or slightly
raised smooth lesion which has a uniform colour and
varies in size up to about 1 cm (Fig. 3.63). A compound
naevus is a raised, rounded, pigmented papular lesion
from which hairs may project (Fig. 3.64). Dermal naevi
are raised, flesh-coloured, dome-shaped lesions with a
wrinkled surface, occurring most commonly on the face
Fig. 3.61 Oral mucous membrane involvement in pemphigus. (Fig. 3.65).
Café-au-lait patches
These are flat, coffee-coloured patches (see Fig. 3.7),
Dermatitis herpetiformis
usually centimetres in size, which may occur as a
This disorder usually occurs in the third and fourth benign blemish or a marker of neurofibromatosis (Von
decades and is characterised by strikingly symmetrical Recklinghausen’s disease). The presence of five or more
groups of intensely itchy vesicles which most commonly of these patches is a sure sign of the disorder.
erupt on the elbows, below the knees, buttocks, back and Neurofibromas appear as soft, sessile, pedunculated
scalp (Fig. 3.62). Scratching causes local excoriation. lesions or discrete subcutaneous nodules.
76
Chapter
Skin infections 3
Fig. 3.66 Squamous cancer of the lip.

Fig. 3.64 Cellular naevus.
Fig. 3.65 Dermal naevus.
TUMOURS Fig. 3.67 Leukoplakia of the vulva (the pubic area has been
shaved).
Squamous cell carcinoma
There is usually a risk factor predisposing to this cancer.
Consider excessive sun exposure, carcinomatous change
in a chronic leg ulcer and areas of leukoplakia. The
tumour presents as an ulcer or nodule with a firm
indurated margin; the ulcer margin is often everted (Fig.
3.66). The cancer usually occurs in sun-exposed areas
(face, back of the hands and forearm) or, in women, in
an area of vulval leukoplakia (Fig. 3.67).
Basal cell carcinoma
This tumour most commonly affects the face and, like
squamous carcinoma, sun exposure is an important
predisposing factor. The ‘rodent’ ulcer starts as a small
painless papule (Fig. 3.68) which ulcerates. The ulcer
margin is well-defined and rolled at the edges. The Fig. 3.68 Papular form of basal cell carcinoma.
tumour bleeds and scabs. Your index of suspicion must
be aroused if any skin ulcer fails to heal.
associated with a pre-existing pigmented lesion but
Malignant melanoma
approximately one-third are associated with a junctional
This is less common than squamous or basal cell pigmented naevus. The tumour is usually pigmented and
carcinoma but is the most serious, because it spreads presents either as a nodule or a spreading area of
by the lymphatics and blood. Most lesions are not pigmentation (Fig. 3.69). Consider the diagnosis if a
77
Chapter
Fig. 3.69 Spreading malignant melanoma.
pigmented lesion is nodular, grows, darkens in colour,

changes shape or bleeds. The back is a common site Fig. 3.70 Kaposi’s sarcoma in a black African. The nodules are
in men, whereas in women the legs are the most multiple and dark blue in colour.
common site.
Red flag
Features suspicious of malignant melanoma
• Asymmetry with irregular border

• Irregular colorations
• Diameter usually > 0.5 cm
• Irregular elevation
• Loss of skin markings
Risk factors
Malignant melanoma
• New mole, change in pre-existing mole

• Prior melanoma or family history of melanoma
• Caucasian
• Oral psoralens and PUVA for psoriasis
• Immunosuppression
• Excessive sun exposure
• Red hair, blond hair, green or blue eyes
Fig. 3.71 Kaposi’s sarcoma in an Ashkenazi Jew. The purple

Kaposi’s sarcoma plaques particularly occur on the lower legs and feet.
This tumour was once restricted to equatorial black
Africans (Fig. 3.70) and elderly Ashkenazi Jews (Fig.
3.71). Immunosuppression is an important predisposing
factor and the sarcoma occurs in transplant recipients on
immunosuppressive drugs and is particularly associated
with AIDS (Fig. 3.72). The Kaposi’s lesion is characterised
by red-blue nodules, especially affecting the lower legs
but also involving the hands.
Skin manifestations of systemic disease

Many systemic disorders involve the skin and careful
examination of the skin often helps in diagnosis.
Fig. 3.72 Kaposi’s sarcoma in an immunosuppressed AIDS patient.
78
Chapter
Nail disorders 3
lines) (Fig. 3.76) which grow out with normal nail growth
Nail disorders
on recovery. Infection of the skin adjacent to the nail is
Examination of the nails can provide useful and often called paronychia and is characterised by pain, swelling,
diagnostic physical signs. Patients often complain of redness and tenderness of the skin at its interface with
cracking, ridging and brittleness of the nail. This may the nail (Fig. 3.77). Fungal infection of the nail causes
be caused by nail-biting, picking and poor nail care opacification and distortion of the nail. Spooning of the
rather than disease. In addition, nails may have white nail (koilonychia) occurs in iron deficiency (Figs 3.78,
spots which have no significance. First examine the 3.79).
nail face-on. Asymmetrical splinter-like lesions (splinter
haemorrhages) may indicate microemboli from infected
heart valves (subacute bacterial endocarditis) or vasculitis.
Remember that manual labourers may have traumatic
nail lesions that resemble splinter haemorrhages. Pitting
of the nail occurs in psoriasis (Fig. 3.73) and may even
occur in the absence of the typical skin rash. Premature
lifting of the distal nail is called onycholysis (Fig. 3.74).
This occurs in many chronic nail disorders and is
also associated with hyperthyroidism (Plummer’s nails).
White nails with loss of the lunule (leukonychia) is typical
of hypoalbuminaemia and severe chronic ill health
(Fig. 3.75).
Acute severe illness may be associated with the later
appearance of transverse depressions in the nail (Beau’s
Fig. 3.75 Leukonychia in a patient with liver disease and

hypoalbuminaemia.
Fig. 3.73 Pitting and onycholysis of the nail caused by psoriasis.
Fig. 3.76 Beau’s lines.
Fig. 3.74 Onycholysis caused by hyperkeratotic psoriasis beneath

the nail. Fig. 3.77 Bacterial paronychia.
79
Chapter
Finger clubbing
Lung disease
• Pyogenic (abscess, bronchiectasis, empyema)
• Bronchogenic carcinoma
• Fibrosing alveolitis
Heart disease
• Cyanotic congenital heart disease
• Subacute bacterial endocarditis
Gastrointestinal
• Cirrhosis
• Ulcerative colitis
Fig. 3.78 Koilonychia with spooning of the nail in a patient with • Crohn’s disease
chronic iron deficiency anaemia.
Idiopathic/congenital
Symptoms and signs

Skin manifestations of systemic disease
Disease Skin findings

Sarcoidosis Erythema nodosum, lupus pernio,
nodules in scars
Systemic lupus Facial ‘butterfly’ rash (malar
erythematosus erythema over cheeks and bridging
nose); occurs in 50% of patients on
exposure to UV rays. Also alopecia
areata and discoid lupus
Scleroderma Thickened tight skin (especially
Fig. 3.79 Spooning of the nails.
fingers), skin telangiectasia, calcified
skin nodules
Hyperlipidaemia Xanthelasmata of eyelids, xanthomas
Clubbing
of elbows, knuckles, buttock, soles
floating increased angle and palms, and Achilles tendon
nail base (180°) Diabetes mellitus Necrobiosis lipoidica – symmetrical
plaques on shins with atrophic,
yellow appearance and waxy feel;
cutaneous candida, ulcers on feet
Hyperthyroidism Pretibial myxoedema – thickened
skin on front of skin, clubbing
Cushing’s Purple striae, thin skin, easy bruising
early clubbing syndrome
Ulcerative colitis/ Pyoderma gangrenosum – large
Fig. 3.80 Clubbing. The angle is increased and filled in and the nail Crohn’s disease ulcer
base has a spongy consistency. Dermatomyositis Oedema and mauve discoloration of
eyelid, erythema of the knuckles and
Always examine the lateral outline of the nails and other bony parts such as elbow and
fingertip to check for clubbing. The normal angle between shoulder tip; photosensitive
the fingernail and nail base is 160° (Fig. 3.80) and the ‘butterfly rash’ on face
base is firm to palpation. Clubbing occurs when abnormal Cancer Acanthosis nigricans – brown,
connective tissue and capillaries fill this angle. In early velvet-like thickening of skin in axilla
clubbing, the angle increases and if you press the nail and groin; tylosis – thickening of
base the nail appears to ‘float’. In severe clubbing, such palms/soles; ichthyosis – fish-skin
as occurs with lung cancer, the fingers may have a appearance
drumstick appearance and may be associated with wrist
pain and tenderness due to periostitis (hypertrophic
pulmonary osteoarthropathy).
80
Chapter
Nail disorders 3
Examination of elderly people Review

Skin changes in elderly people Skin examination
• Skin becomes increasingly wrinkled with loss of • Always expose the patient to allow examination of
elastic tissue and collagen the whole skin organ
• Skin becomes fragile and even minor trauma can • Ensure good illumination (preferably natural light)
cause wounding and secondary infection • Measure dimensions of skin lesions (especially helpful
• Loss of spring makes it more difficult to use tissue when assessing progression and regression)
turgor as a sign for assessing hydration • Attempt to transilluminate larger swellings
• Capillary fragility results in easy intradermal bleeding (fluid-filled)
(senile purpura and ecchymosis) • Assess skin colour and variations
• Warty pigmented lesions (senile keratosis) may • Describe the primary morphology of a localised skin
become widespread and disfigure skin lesion
• Sunburnt area increasingly predisposed to malignant – macule
change in the elderly (squamous and basal cell – patch
carcinomas) – papule
• Pressure sores (decubitus ulcers) are a particularly – plaque
serious complication of immobility; predisposing – wheal
factors include capillary occlusion, friction and – vesicle
secondary infection – nodule
• Pressure sores most commonly develop over bony – petechiae or ecchymosis
prominences, especially the heels and sacrum – bulla
– telangiectasia, spider naevus
• Describe the secondary characteristics
– superficial erosion
– ulceration
– crusting
– scaling
– fissuring
– lichenification
– atrophy
– excoriation
– scarring or keloid
• Describe the distribution of a more widespread rash
or colour change
• Assess the temperature of the affected area
• Perform a general examination, looking for evidence
of systemic disease
81
4
Ear, nose and throat
The ear reflex) reflects back to the observer. This arc is directed
antero-inferiorly.
Structure of the ear THE MIDDLE EAR

This extends from the inner surface of the tympanic
A diagrammatic cross-section of the external, middle and
membrane to the temporal bone and includes the air
inner parts of the ear is shown in Figure 4.1.
filled cavities containing the three ossicles (from proximal
to distal to the observer these are the malleus, incus
and stapes; see Fig. 4.4), the Eustachian tube and the
THE EXTERNAL EAR mastoid air cells. The function of the middle ear is
The externally visible part of the external ear is the pinna to magnify sound-waves sensed by the tympanic
(Fig. 4.2). This is a structure covered by skin with an membrane and forms an important part of conductive
internal structure of cartilage (which is absent in the hearing. This magnification of sound is done by the three
lowest part, the tragus). ossicles, the last of which is the stapes whose foot-plate
As well as the pinna, the external ear includes the fits in the oval window which is connected to the cochlea
external canal and peripheral surface of the tympanic of the inner ear. The function of the Eustachian tube is
membrane. The skin of the external canal contains normal to aerate the middle ear so that the pressure in the middle
epithelium with hair follicles and apocrine glands. It is ear is equal to the outside pressure (in the external canal)
the combination of desquamated skin and the ceruminous and thus allow the tympanic membrane to vibrate
secretions of the apocrine glands that form wax. Wax is freely.
protective to the ear but over-accumulation or impaction There are two important nerves that pass through the
reduces the conductive element of hearing. The external medial wall of the middle ear. These are the facial nerve
canal is straight in children (making the tympanic and its off-shoot, the chorda tympani (concerned with
membrane easier to see) but in adulthood the canal taste from the tongue on the same side and with
passes through an angle of descent distal to the observer. submandibular and sublingual salivary glands). The facial
The angle formed by the tympanic membrane and the nerve passes in the bone above and behind the stapes
external canal makes an acute-angled recess (the anterior footplate, whereas the chorda tympani emerges through
recess) which can be difficult to visualise, and wax, the posterior wall of the middle ear and passes between
discharge or a foreign body may be difficult to locate and the malleus and incus.
remove. This difficulty may be compounded by the
isthmus if it is narrow. The isthmus is the junction
between the outer cartilaginous two-thirds of the external THE INNER EAR
canal and the bony inner one-third. The inner ear is that part of the auditory mechanism
The tympanic membrane (Fig. 4.3) is a translucent within the petrous temporal bone. The inner ear is called
membrane visible at the inner extremity of the external the labyrinth and is comprised of the cochlea, vestibule
canal. In its normal state the membrane appears grey and and semi-circular canals. The cochlea is the organ of
shiny and through it the handle of the malleus is visible hearing and the semicircular canals are the organ of
with its inferior pole (the umbo) pointing posteriorly. The balance. The sensorineural part of hearing is located here
umbo can be seen fairly close to the centre of the tympanic in the inner ear, whereas conductive hearing is managed
membrane. Inferior to the umbo, an arc of light (the light by the external and middle parts of the ear. The sensori-
82
Chapter
The ear 4
Cross-section of the ear Anatomy of normal tympanic membrane
posterior lateral
temporalis semicircular malleolar folds process
muscle auditory ossicles canal anterior
malleus incus stapes malleolar attic
fold
vestibular
nerve
posterior anterior mesotympanum

cochlea
nerve
external auditory canal hypotympanum
cochlea
pars tensa umbo cone of handle of

light malleus
tympanic
cavity
pars flaccida
tympanic
membrane eustachian Fig. 4.3 Anatomy of normal tympanic membrane.
tube
lobule
Fig. 4.1 Cross-section of the whole structure of the ear.
Auditory ossicles
Pinna
helix triangular short head

fossa process
incus
external long
auditory process
antihelix meatus lateral malleus
process
tragus
manubrium
(handle)
concha foot crus head
plate
lobule
(ear lobe) stapes
Fig. 4.4 The auditory ossicles.
Fig. 4.2 The pinna.
connected to the eyes and cerebellum. The eyes,

proprioception and cerebellum, together with the cerebral
part of hearing occurs within the cochlea, whereas the cortex, form the central balance control.
neuro- part occurs within the eighth (VIII) nerve and
beyond.
The cochlea records the transmission of sound via hair Symptoms of diseases of the ear
cells which convert the signal received into electrical
impulses. These are transmitted by the auditory (VIII) VISIBLE SYMPTOMS
nerve to the cerebral cortex. Patients may present with symptoms of visible external
The semicircular canals or balance organ form the abnormalities. The conditions that may be seen usually
peripheral balance organ. There are three canals: the present because of concern about the cosmetic appearance
superior, lateral and posterior. The organ is neurologically of the ear.
83
Chapter
4 Ear, nose and throat
Differential diagnosis Questions to ask

Cosmetic presentations Otalgia
• Bat ears • Where is the pain and does it radiate?

• Preauricular sinus • How long has the pain been present?
• Accessory auricles • Is the pain constant or intermittent?
• Anotia and microtia • Does anything provoke or relieve it?
• Cauliflower ear (untreated haematoma) • Is there any swelling, discharge, deafness or vertigo?
• Chondrodermatitis nodularis helicis • Has anything been put in the ear?
• Basal cell carcinoma • Is there a past history of ear problems?
• Squamous cell carcinoma • Is there a problem in other areas – teeth, pharynx,
cervical spine?
PAIN IN THE EAR (OTALGIA)

Pain in the ear may arise from the ear itself (usually
unilateral) but may arise from other sources. The cause
can usually be determined on history and clinical DISCHARGING EAR (OTORRHOEA)
examination. The possible causes of otalgia are summarised
The ear naturally discharges wax which is a mixture of
in the differential diagnosis box.
skin debris and apocrine gland secretion.
Pathological discharge from the ear varies in nature
Differential diagnosis from watery to foul-smelling or blood-stained. A
green-coloured discharge often indicates pseudomonas
Otalgia
infection, whereas a blackened discharge may indicate
Pinna Perichondritis, cellulits fungal infection.
Neoplasm (basal cell or squamous cell) With foul-smelling discharge, or with the presence of
External canal Furuncle, furunculosis pseudomonas infection, middle ear disease (and therefore
Otitis externa a perforated tympanic membrane) should be suspected.
Impacted wax In the rare instance of a cerebrospinal fluid (CSF) leak,
Foreign body due to trauma or surgery, the discharge will be watery. A
Herpes zoster (Ramsay Hunt syndrome) mucoid discharge is suggestive of middle ear disease.
Neoplasm Purulent discharge is commonly from infection of the
Middle ear Acute otitis media and its rare external canal.
sequelae (mastoiditis, meningitis and A most common cause of a bloodstained discharge
cerebral abscess) is infection, but the rare instance of a squamous cell
Secretory otitis media (glue ear) carcinoma may present with this.
Eustachian tube obstruction Discharge is often associated with otalgia and
Barotraumas the timing of the two symptoms will often indicate
Neoplasm the origin. Otalgia from middle ear disease is usually
Other sites Teeth, tongue, pharynx (including relieved when the tympanic membrane ruptures
tonsils and hypopharynx), sinuses, and discharges mucopus, whereas continuing pain
temporomandibular joint, cervical associated with discharge usually indicates external ear
spine inflammation.
To fully assess causes of otalgia it is necessary to

exclude causes of referred pain. The clinician should
directly question whether the patient has any problem Questions to ask
with other structures such as teeth, the pharynx or cervical
Otorrhoea
spine.
To assess aural causes of the symptom of otalgia, ask • How long has it been present?
about any associated swelling, discharge, deafness, • What is its relationship to pain?
giddiness or vertigo. Any history of excessive contact with • Has it occurred previously?
water such as by swimming, bathing or showering is • What is its colour and consistency?
relevant and it is wise to check that the patient has not • Is it blood-stained?
been putting anything into the external canal (cottonwool • Is it offensive?
buds, pins).
84
Chapter
The ear 4
conduction and magnification of sound to the cochlea.
For sound to be conducted, the external canal must be
Discharging ear
patent. It may be impeded by malformation, wax or
Site Diagnosis discharge. The tympanic membrane should be intact and
External ear Otitis externa – bacterial, fungal or the middle ear aerated and free of discharge or adhesions.
secondary to middle ear discharge The ossicular chain in the middle ear must be intact and
Middle ear Acute suppurative otitis media, chronic move freely. Testing of the integrity of middle ear function
suppurative otitis media, mastoid is explained in the section on examination of the ear
disease (rare), neoplasm (rare) (pages 90–92).
Inner ear Fracture (CSF leak)
Sensorineural deafness
HEARING LOSS (DEAFNESS) The sensory part of the ear is the cochlea, but for full
Hearing loss is recognised as being either conductive or function the neural element is required. This comprises
sensorineural. It varies in degree from minor to profound the auditory nerve and cerebral cortex. To distinguish
and affects all age groups. Poor hearing is significant in between the sensory and neural element can be
infants because of the association with slow or abnormal difficult.
development of speech. Assessment of hearing in infants Hearing loss in the elderly (presbyacusis) is mainly due
and young children is difficult (see p. 92). The clinician to degeneration of the cochlea. The cochlea may be
should take careful note of parents’ concerns. Hearing damaged during life in other ways. This may be by
loss of old age is called presbyacusis. There are many infection, vascular ischaemia, noise, drugs, surgery, or
causes of hearing loss. Ménière’s disease.
The red flag symptom to alert the clinician is unilateral
Conductive deafness
deafness as this may indicate an acoustic neuroma. Early
Conductive deafness is the term used to indicate that treatment of this space-occupying lesion lessens morbidity
hearing is being impaired by a malfunction in the and mortality.
Hearing loss
Age group Causes Type of loss

Infants Congenital Conductive or sensorineural
Secretory otitis media (glue ear) Conductive
Young children Congenital Conductive or sensorineural
Secretory otitis media (glue ear) Conductive
Postinfective (meningitis, viral) Sensorineural
Adolescents Congenital Conductive or sensorineural
Malingering —
Postinfective (meningitis, viral) Sensorineural
Acoustic trauma or drugs Sensorineural
20–40 years Postinfective (meningitis, viral) Sensorineural
Otosclerosis Conductive
Acoustic neuroma Sensorineural
Ménière’s disease Sensorineural
Postoperative complications Conductive or sensorineural
40–60 years Acoustic trauma or drugs Sensorineural
Otosclerosis Conductive
Ménière’s disease Sensorineural
60+ years Presbyacusis Sensorineural
85
Chapter
TINNITUS but is manifest by a feeling of unsteadiness and is not

Tinnitus is the symptom of noise in the ears. It is difficult usually associated with nausea or vomiting. One possible
to investigate because it is a subjective symptom. It may cause of this is a hypotensive state, perhaps caused by
be heard as a continuous, pulsatile or episodic sound. The drugs in the management of hypertension. Vertigo of
sound may be difficult for the patient to describe but is vestibular (peripheral) origin is almost always accompanied
often noted as whistling, buzzing or crackling. The sounds by nausea and/or vomiting, whereas this is less common
experienced are not complex auditory hallucinations as in central vertigo. Another distinguishing feature is that
found in certain psychoses. peripheral vertigo is usually intermittent and is not
The most common cause of tinnitus is the onset of progressive. Giddiness of central origin is often constant
sensorineural deafness associated with degeneration of and progressive.
the cochlea. However, anything which interferes with the The red flag sign in vertigo, requiring urgent
hearing mechanism (even wax) may produce tinnitus. All investigation or referral, is the possibility of a transient
the possible causes of hearing loss should be considered ischaemic attack (TIA) or vertebrobasilar ischaemia. The
when tinnitus is present. It is one of the triad of symptoms other associated signs suggesting these conditions as
that are observed in Ménière’s disease, the others being a possible cause are raised blood pressure, dysarthria,
vertigo and loss of hearing. Tinnitus may arise from the visual disturbance, neck problems and loss of
Eustachian tube, which is also the site of the rare condition coordination.
of palatal myoclonus.
In present day usage it is unusual to see tinnitus caused Questions to ask
by drugs, but it may be seen in the treatment of rheumatic
Vertigo
fever by high dose aspirin and is a recognised side-effect
of aminoglycosides. High doses of nonsteroidal anti- • How would you describe the giddiness?
inflammatory drugs may also induce tinnitus. This form • How long has it been present?
of drug-induced tinnitus is usually reversible on stopping • Is it intermittent?
the medication. • How long does it last?
A red flag sign is when the tinnitus is unilateral. As • What precipitates it (e.g. change of posture or head
with unilateral deafness, an acoustic neuroma must be movement)?
considered and investigated. • Are you on any medication (ototoxic or lowering
blood pressure)?
• Do you have any nausea or vomiting?
VERTIGO (DIZZINESS)
• Have you ever had ear problems or surgery?
Vertigo is a symptom of imagined spinning or unsteadiness. • Do you have any deafness or tinnitus?
The patient feels they or their surroundings are moving.
This is true vertigo and is caused by inner ear, vestibular,
dysfunction. Vertigo arising from the vestibular mechanism
is known as peripheral vertigo. Differential diagnosis
Acute labyrinthine dysfunction Central and peripheral vertigo
Acute labyrinthine dysfunction is the term used for severe Diagnosis Site
episodic vertigo of sudden onset. Its cause includes Acute labyrinthine dysfunction Peripheral
diagnoses such as viral, idiopathic or vascular labyrinthitis. Benign positional vertigo Peripheral
The disorder may last for days and may be prolonged in Ménière’s disease Peripheral
benign positional vertigo. Multiple sclerosis Central
Transient ischaemic attack (TIA) Central
Benign positional vertigo
Vertebrobasilar ischaemia Central
Benign positional vertigo is recognised by the short- Head injury Central or peripheral
lasting onset of vertigo with movement of the head. It
may be one of the sequelae of acute labyrinthine
dysfunction. Other causes are trauma or idiopathic.
Central causes of vertigo Examination of the ear
Other manifestations of giddiness arise from different
sites. The vestibular (inner ear) cause of vertigo is THE AUROSCOPE
known as peripheral vertigo and that arising from other Use the largest aural speculum that fits in the external
sites is termed central vertigo. Inputs from the eyes, canal comfortably. Hold the auroscope at its point of
proprioception, cerebellum, brainstem, cerebrum and balance (centre of gravity). Balance it lightly in the hand.
reticular formation all have a function in balance. The loss Do not grab it like a screwdriver! Use the same hand as
of balance in central vertigo is not of the rotational type the ear (left hand for left ear) (see Fig. 4.5). When inserting
86
Chapter
The ear 4
Preauricular sinus
preauricular
sinus
tragus
Fig. 4.5 How to hold the auroscope.
the auroscope retract the pinna posteriorly with the free

hand (right hand for left ear). This opens the canal for
easier inspection. Always examine the pinna before Fig. 4.6 Site of preauricular sinus.
examining the external canal.
Do not rush to insert the auroscope and, when inserting
it, look at the canal throughout its whole length. Observe
for any anatomical abnormality and note the external Accessory auricles
appearance of any discharge or eczema. The appearance
of discharge, if mucoid, may indicate middle ear disease
rather than otitis externa, whereas evidence of eczematous
skin in the pinna (or psoriasis) may indicate that otitis
externa will be found in the canal.
tragus
Look also for scars of mastoid surgery (pre- or post-
auricular) because passing the auroscope too hastily into
the ear may result in a large posterior mastoid cavity accessory
being overlooked. auricle(s)
EXTERNAL EAR
Pinna
Minor congenital abnormalities Bat ears is the term
given to ears which do not lie flat against the head but
protrude outwards. They occur in about 2% of the Fig. 4.7 Site of accessory auricles.
population and if to be surgically corrected this is best left
until after six years of age.
to the pinna should be treated with systemic antibiotics.
Pre-auricular sinus is a defect in embryological
Infections of the pinna include cellulitis and perichondritis,
development and usually occurs antero-superiorly to the
where the underlying cartilage is infected.
tragus (Fig. 4.6).
Cauliflower ears are the result of previous untreated
Accessory auricles occur anterior to the tragus (Fig.
traumatic haematoma of the pinna. Early surgical
4.7) and are another embryonic fault.
treatment of the initial haematoma may prevent lasting
Gross congenital deformities are rare and include
deformity.
anotia (complete absence of the pinna). The conditions
Chondrodermatitis nodularis helicis is a benign
can occur with normal or abnormal development of the
nodular condition usually of the helix of the ear. The
middle and inner ear.
aetiology is unknown but, as it occurs in later life, may
Skin changes Eczema or psoriasis are common conditions be related to sun damage. It can only be differentiated
which may involve the pinna and external canal. Like from malignant conditions by biopsy.
any skin condition, secondary infection is a possible Basal cell carcinomata and squamous cell carcinomata
complication and is more likely to occur in the external are tumours most commonly seen on the pinna and
ear because of the accumulation of debris. require appropriate surgical treatment.
Infection/inflammation can be severe with pain, Chondromata arise from cartilage, which forms the
redness and swelling. The infection may be an extension outer one-third of the canal. They may vary in size
of infection from the external canal but even if localised from being quite small to obstructing the whole canal.
87
Chapter
They rarely need attention but may make it difficult to

remove wax and observe the inner part of the canal
and the tympanic membrane. To the inexperienced eye
chondromata may appear alarming and arouse concern
about malignancy. They are swellings that are covered by
normal epithelium and vary greatly in size from minor
swellings to those obstructing most of the external
canal.
External canal
The diameter of the canal is very variable and even in
some adults may be very narrow. In a child the canal is
straight and the tympanic membrane is easily seen. In
adults the distal part of the canal, close to the tympanic
membrane, narrows (the isthmus) in its final third and
Fig. 4.8 Instruments useful in the removal of wax. From left to
deflects downwards. This results in a recess inferiorly right: Jobson Horne probe, wax hook, crocodile forceps, aural
with an acute angle being formed between canal and forceps, aural speculum, aural sucker.
tympanic membrane. It is thus more difficult to see the
whole tympanic membrane and debris or foreign bodies a Jobson Horne probe (tipped with cotton wool) to dry
are more easily concealed from the clinician in the recess the outer part of the external canal. In addition to the
(see Fig. 4.1). Jobson Horne probe, useful instruments for removing
Wax Wax is the natural accumulation of skin debris and wax include a wax hook, crocodile forceps and aural
secreted oil from the apocrine glands of the external canal forceps (Fig. 4.8).
and unless causing symptoms does not need to be Water used to irrigate wax should be at 37°C (hand
removed. Before full examination of the external canal temperature). Variation in this temperature may stimulate
can be complete, the ear should be cleaned of wax. Wax, the labyrinth, causing temporary giddiness.
impacted or otherwise, is one of the commonest The ENT specialist will have access to microsuction,
conditions of the ear dealt with by the general physician. which is light suction applied by an aural cannula under
It may present with a difficulty in hearing or even with operating-microscope vision.
pain. Whatever method is used to clean the external canal,
The production and accumulation of wax (rather than this must be done before any external canal or middle ear
its natural expulsion) is dependent on occupational and disease can be diagnosed.
genetic factors (gene on chromosome 16). The removal Otitis externa
of impacted wax gives the greatest relief (in both hearing
and discomfort) to an afflicted patient. Otitis externa is an infection of the external canal. Infections
The most common method used to clear wax is by include furuncle or generalised furunculosis and otitis
syringing or the now more acceptable irrigation (by an externa, bacterial or fungal. Otitis externa causes discharge,
electrical pulsed pump). There are contraindications to irritation and often pain. The colour of the discharge is
syringing. discussed in the section on symptoms (see p. 83) but when
observing the discharge the possible presence of the spores
of a fungal growth should be noted.
Review Furunculosis
Contraindications to syringing A single furuncle or generalised furunculosis of the
• Previous ear surgery – mastoid, tympanoplasty, external canal is usually painful and may be extremely so.
stapedectomy Furuncles can be recognised as a small boil in the external
• Previous otitis externa canal. The lesion may be quite distal and it may be easily
• Perforation missed if the auroscope is inserted too deeply without
• Tinnitus observing the whole length of the canal. Furunculosis is
• Labyrinthine disturbance recognised by the appearance of multiple boils or
abscesses in the canal and is associated with severe
pain and swelling of the external canal which may be
completely occluded.
Water in the ears is a common trigger for otitis externa
Myringitis bullosa
and it is important that the ears are fully cleaned if
possible so that no water is trapped behind any remaining This is a manifestation of viral otitis externa where blisters
wax. The ears should be carefully dried after syringing are to be seen on the epithelial surface of the tympanic
and it is useful to have an operator trained in the use of membrane.
88
Chapter
The ear 4
Suppurative acute otitis media

Suppurative otitis media is one of the possible sequelae
of acute otitis media. With this the tympanic membrane
ruptures and releases the mucopus formed by the acute
otitis media infection. Again this condition usually
resolves spontaneously because of the release of the
mucopus.
Chronic suppurative otitis media
This can be defined as a continuing discharging tympanic
membrane perforation. The tympanic perforation of acute
suppurative otitis media may remain, together with the
discharge and become chronic. Referral to an ENT
specialist is then indicated so that the possible extension
of the infection into the mastoid and beyond (meninges
and brain) can be assessed.
Fig. 4.9 Normal tympanic membrane.

Acute mastoiditis, meningitis and cerebral abscess
Though rare, these are all possible sequelae of acute otitis
media and should be considered when there is continuing
fever, otorrhoea, otalgia and any suspicion of cerebral
THE MIDDLE EAR signs present. Acute mastoiditis may be detected by
Tympanic membrane examination of the mastoid bone for swelling, redness or
tenderness.
The whole circumference of the membrane should be
It should be noted that these conditions may progress
visualised. In its normal state the membrane appears grey
very rapidly from an attack of acute otitis media.
and shiny and through it the handle of the malleus
is visible with its inferior pole (the umbo) pointing Eustachian tube dysfunction
posteriorly. Inferior to the umbo, an arc of light reflects
This may present with otalgia, reduced or distorted
back to the observer. This arc is directed antero-inferiorly
hearing, or with tinnitus. As the condition advances,
(Fig. 4.9).
vascular infiltration of the tympanic membrane along the
Any vascular infiltration should be noted and this may
handle of the malleus develops and the malleus becomes
occur either along the handle of the malleus or involve
more prominent as the increasing negative pressure
the tympanic membrane as a whole.
in the middle ear causes retraction of the tympanic
Superior to the handle of the malleus is the pars
membrane.
flaccida. This is the part of the tympanic membrane that
As a result of the negative pressure in the middle ear,
is mobile and will move either by instigating a Valsalva
and blockage of the Eustachian tube, the mobility of the
manoeuvre or by using an auroscope with pneumatic
pars flaccida is lost. This can be demonstrated by asking
attachment. Demonstration of the mobility of the pars
the patient to perform the Valsalva manoeuvre and
flaccida will assure the clinician of aeration of the middle
observing for movement (or lack of) in the pars flaccida.
ear and therefore of patency of the Eustachian tube. The
This can be replicated by use of the puffer with a
main area of the tympanic membrane is called the pars
pneumatic auroscope. Graphical demonstration of
tensa and comprises the largest part of the membrane. It
Eustachian tube dysfunction can be obtained using
is in this part that a perforation may be noted. Here also
tympanometry.
chalk patches (tympanosclerosis) may be seen.
Tympanometry Tympanometry (Figs 4.10, 4.11) provides
Acute otitis media
a good method for detecting middle ear effusion. A
This is the most common middle ear infection and is flat trace on the tympanogram indicates an immobile
particularly common in childhood. The presenting tympanic membrane suggestive of middle ear effusion.
symptoms are fever and otalgia. In infancy, otalgia is
Secretory otitis media (glue ear)
recognised by the child being restless and crying. The
onset is rapid and is usually associated with an upper This is a condition of mucoid secretions in the middle ear
respiratory tract virus infection. which results primarily in reduction in hearing. It occurs
On clinical examination of the ear, the tympanic as a result of poor aeration of the middle ear caused by
membrane is inflamed and the epithelium of the Eustachian tube dysfunction. It is mainly a disease of
membrane is often distorted (‘pavement’ epithelium) or children in whom adenoidal obstruction of the Eustachian
bulging. The condition normally resolves with or without tube is a prominent feature. However it can occur in
treatment. adults whose nasal airway is compromised.
89
Chapter
Fig. 4.10 Tympanometer in use.
1.5 left ear

Fig. 4.12 Ventilation tube (grommet) in situ.
2
Uea (+200)
1.0
Yd (mmhO)
0.5
0
0
–400 – 200 0 +200
pressure (daPa)
Fig. 4.11 Normal tympanogram showing tympanic membrane
response to pressure.
Clinical diagnosis is made in several ways. Bubbles of

mucous may be seen on examination of the tympanic
membrane. Otherwise all the clinical aspects of Eustachian
tube dysfunction may be elicited (see above).
The importance of this condition is for children in Fig. 4.13 Large tympanic membrane perforation. Incudostapedial
whom speech, language or educational development joint just visible posterosuperiorly; round window visible posteriorly.
may be delayed due to reduction in hearing. If there is
evidence of such delay in development, or if there is
a persistent (longer than three months) reduction of
hearing, referral to an ENT specialist is advisable for Deafness
consideration of grommet insertion (Fig. 4.12) and Tuning fork tests Tuning forks are the first and an
adenoidectomy. important tool to investigate deafness (Fig. 4.14). A
Dry perforation tuning fork with a frequency of 256 Hz (C256, middle C
on the piano) can be used to undertake the Rinne and
This may occur due to trauma or as a result of a previous Weber tests (see below) with which it should be relatively
middle ear infection and may be of varying size from very easy for the clinician to differentiate conductive from
small to involving the vast majority of the tympanic sensorineural deafness.
membrane and exposing structures in the middle ear It is also most helpful to have a high-tone tuning fork
(Fig. 4.13). of about 4096 Hz. In deafness of old age (presbyacusis)
it is the high tones that the patient first loses the ability
THE INNER EAR to hear. Holding a sounding tuning fork of 4096 Hz a few
centimetres away from the entrance of the external ear
Information about inner ear disease is mainly obtained
will ascertain whether there is a degree of high-tone
from the history of the condition that the patient gives,
hearing loss.
whether it is deafness, tinnitus or giddiness. The inner
ear cannot be examined directly and information on its • Weber test. This test is performed by placing a tuning
function is obtained by various methods and tests. fork (C256) on the midline of the skull, usually on the
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Chapter
The ear 4
mastoid bone. It will be heard less well than if the

tuning fork is placed close to the external canal. If it is
heard louder on the mastoid bone, the test is negative
and indicates that the ossicular chain is not magnifying
the sound for some reason.
A false negative Rinne test may occur if the ear has a
profound sensorineural deafness. With an ear conducting
normally the test should be positive, but the bone
conduction (the tuning fork placed on the mastoid bone)
sound may be picked up by the opposite ear and therefore
thought by the patient to be louder than air conduction;
whereas such profound deafness in the tested ear negates
the test for conduction (false negative Rinne). This finding
will be supported by the fact that the Weber test will be
referred to the other (less deaf) ear.
As already explained, in conductive deafness there
is an interruption of sound, and/or sound magnification,
Fig. 4.14 Tuning forks: left, 4096 Hz; right, 256 Hz. in the external or middle ear. Sensorineural deafness
indicates a problem with the cochlea or auditory nervous
system.
Weber test
Rinne negative (conductive deafness)
Obstruction of Impacted wax

external canal Exostosis
Debris (otitis externa)
Foreign body
Canal atresia
Middle ear pathology Perforation of tympanic
L R L R
membrane
Ossicular chain problem
– congenital
– otosclerosis
– trauma
Fig. 4.15 Weber test. – post-infective adhesions
– Eustachian tube dysfunction
forehead (Fig. 4.15). With normal hearing the sound of
the tuning fork is heard centrally (equally in both ears).
If it is referred to one side, that side either has a Audiometry The definitive test for hearing acuity is by
conductive deafness or has a better sensorineural audiometry. There may be subjective errors in the tuning
hearing than the other side. fork tests. There may also be subjective anomalies in
audiometric testing but these are less likely. Audiometric
testing shows in graphic form both bone and air
conduction (Fig. 4.17).
Weber test The normal annotation used when producing an
Conductive deafness Weber referred to side of audiogram is as follows:
conductive deafness • X refers to air conduction in the left ear
Sensorineural deafness Weber referred to better ear • O refers to air conduction in the right ear
• ⊃ refers to bone conduction in the left ear
• ⊂ refers to bone conduction in the right ear
• Rinne test. This test clarifies whether or not there is The horizontal axis indicates the frequency of the sound
conductive deafness (Fig. 4.16). It tests the efficiency of in Hz and the vertical axis indicates the hearing level in
the ossicular chain. In a normal ear the Rinne test will decibels (dB). Levels of hearing recorded between zero
be positive. A tuning fork (C256) is first placed on the and 20 dB are considered to be within normal limits.
91
Chapter
Rinne‘s test
a b c d
Fig. 4.16 Rinne test: (a) bone conduction, (b) air conduction, (c) perceptive deafness, (d) conductive deafness.
air conduction right left
bone conduction unmasked B masked right left

nominal masking levels
–20 –20
–10 –10
0 0
10 10
20 20
hearing level (dB)
hearing level (dB)
30 30
40 40
50 50
60 60
70 70
80 80
90 90
100 100
110 110
120 120
125 250 500 1000 2000 4000 8000 125 250 500 1000 2000 4000 8000
frequency (Hz) frequency (Hz)
Fig. 4.17 A blank audiogram.
Oto-acoustic emissions test (to screen for deafness the affected side, although the nystagmus is named to
in infancy) the side of the fast element. Thus nystagmus (fast) to the
right indicates an affected left labyrinth.
This is a screening test for neonates. It is non-invasive
The caloric test is carried out by irrigating the ear canal
and relies on a sound transmitted to a baby’s ear
with cold or warm water. This induces nystagmus. Lack
producing an auto-acoustic emission or echo. This echo
of response indicates no function in the labyrinth of the
can be measured by computer. A negative response may
side tested. This finding may be indicative of Ménière’s
indicate infant hearing impairment, but the test can give
disease.
false readings. The infant can then be referred for the
more accurate auditory brain-stem response test.
Benign positional vertigo
Labyrinthine dysfunction
Hallpike (Dix–Hallpike) test This is a definitive test for
Nystagmus occurs with stimulation of the vestibular benign positional vertigo. If vertigo is induced by the
system. The direction of the nystagmus indicates the side manoeuvre, the test is deemed positive. The manoeuvre
affected. The direction of the fast element is away from is performed by sitting the patient on a couch with their
92
Chapter
The nose 4
legs extended. The clinician turns the head 45° to one

side and lays the patient fully on their back and slightly
The nose and paranasal sinuses
extends the neck. The test is positive if nystagmus is
provoked by this. The cause of the vertigo can then be inferior view of nose external nose
established as peripheral (in the labyrinth) as opposed to tip
central.
ala nasi bridge
The ear vestibule
anterior
naris tip
• Sudden onset of unilateral deafness
ala nasi
• Unilateral deafness even if not of sudden onset
• Persistent unilateral tinnitus columella columella
• Unresolving ear discharge
nasal septum
• Acute and unremitting otalgia not responding to
treatment cranial frontal sinus
• Vertigo if TIA or vertebrobasilar ischaemia a sphenoid cavity
sinus bony portion
possibility of nasal
septum
pituitary
fossa
The nose
septal
vomer cartilage
hard palate
Structure of the nose and sinuses nasopharynx

lateral wall of nose
Diagrams of the nose and paranasal sinuses are shown
in Figure 4.18. cranial
sphenoid cavity frontal sinus
sinus
superior
EXTERNAL NOSE turbinate
The external appearance of the nose (before it may be
middle
distorted by injury or disease) is variable due to genetic turbinate
factors. It is dependent on the shape of the cartilage and vestibule
bone structure.
hard palate inferior
The external structure of the nose consists of skin
turbinate
overlying a bone and cartilaginous support. This skin
continues into the anterior nares (the vestibule). The skin coronal section of nasal cavity and sinuses
of the nose contains many sebaceous glands and within
the vestibule the skin contains both hair and sebaceous ethmoidal air orbit
cells. The proximal one-third of the nose is constructed cells
middle
of bone while the distal two-thirds is cartilage. meatus
middle inferior
NASAL CAVITY turbinate meatus
The interior structure is called the nasal cavity. After the maxillary
vestibule, the surface is lined with ciliated columnar inferior sinus
turbinate (antrum)
epithelium except in its upper part, which is lined with
olfactory epithelium. The ciliated columnar epithelium
lines the whole respiratory tract, indicating the importance
of the nose in this system. The sinuses are also lined with Fig. 4.18 Diagrams of nose and paranasal sinuses.
ciliated columnar epithelium.
The central pillar at the entrance to the nose is the Turbinates extend from the lateral wall of the nasal
columella from which the nasal septum extends poster- cavity and act as air-warming processes. These are the
iorly. This is cartilaginous in its outer structure, becoming inferior, middle and superior turbinates. The inferior
bony after about half its length. The bony part is formed turbinate is easily seen through the vestibule by elevating
by perpendicular plate of the ethmoid and inferiorly by the tip of the nose. Drainage of the nasolacrimal duct
the vomer, which is an extension of the maxillary crest. occurs under the inferior turbinate; of the maxillary,
The septum is often not straight in its development. anterior ethmoid and frontal sinuses from under the
93
Chapter
middle turbinate; of the posterior and sphenoidal sinuses

from under the superior turbinate. Symptoms of diseases of the nose
and sinuses
BLOOD SUPPLY ANOSMIA (COMPLETE LOSS OF
The blood supply of the nose is abundant and is derived SENSE OF SMELL)
from both internal and external carotid arteries. The Happily this is a fairly rare condition but it is very upsetting
lateral nose is supplied by the sphenopalatine artery and to those who suffer it. Hyposmia is when the sense of
the anterior and posterior ethmoid arteries. The septum smell is partially lost and occurs more commonly than
is supplied by these arteries. The anterior part of the the complete anosmia. Dysosmia is an altered perception
septum also receives a supply from the superior labial of smell and is usually a hallucination.
artery and the posterior part from the greater palatine.
The area of maximal confluence of these vessels is at
Little’s area, which is an area at the antero-inferior part
of the nasal septum.
Venous drainage of the nose follows the arterial supply Risk factors
but is important in that they drain directly into the Disturbance of smell
cavernous sinus. This is a route of potential infection into
the cranium. • Nasal polyps or chronic sinus disease
• Viral upper respiratory tract infections
• Trauma or toxic chemicals
SINUSES • Idiopathic
The sinuses – maxillary, ethmoidal, frontal and sphenoidal • CNS dysfunction (Alzheimer’s)
– are air-filled cavities (Fig. 4.19). All but the frontal • Hallucinogenic (epilepsy, schizophrenia)
sinuses are present at birth. All are represented
bilaterally although the sphenoidal sinus is central
with a separating septum. The importance of this sinus
is that its posterior wall is the anterior wall of the
pituitary fossa. The frontal sinuses border the orbit and EPISTAXIS (NOSE BLEED)
anterior cranial fossa. The ethmoid sinuses are closely
It is important to distinguish a frank blood loss from a
related to the orbit and the anterior cranial fossa and the
bloody nasal discharge as the latter may have more
maxillary sinuses are close to the orbit and teeth. Their
serious implications.
drainage has been described in the section on the nasal
Epistaxis usually occurs spontaneously or is caused by
cavity.
direct trauma. Associated conditions are vestibulitis or
The function of the sinuses is unknown but they form
rhinitis, nose-picking or a foreign body. In the elderly,
part of the respiratory tract and are susceptible to
degenerative vascular disease or hypertension may be
infection.
linked to the epistaxis, thus bleeding may be more severe
in the elderly.
Bleeding is more common if there is an associated
bleeding diathesis or if the patient is taking medication
such as anticoagulants, aspirin or a nonsteroidal anti-
Paranasal sinuses
inflammatory drug.
ethmoidal
sinuses
frontal
sinus Questions to ask
Epistaxis
• How long and how severe is the bleeding?

• Which side did the bleeding start?
• Have you had nosebleeds before?
maxillary
sinus • Do you have hypertension?
(antrum) • Are you on any medication? (specify these)
• Have you had nasal surgery in the recent past?
• Do you have a personal or family history of a
bleeding disorder?
Fig. 4.19 Topographical representation of the paranasal sinuses.
94
Chapter
The nose 4
Emergency
occurs as a result of injury which may be of cartilage or
fracture of the nasal bone. Abnormal development of the
Epistaxis
nasal septum may be congenital or due to a disease
• Bleeding brisk and prolonged process such as collapse of the septum caused by cocaine
• Ongoing (>30 minutes) or other chemicals. It may result from previous surgery.
• Shortness of breath The rare congenital obstruction of the nose seen
• Clinically anaemic in infants and young children is choanal atresia. The
• Shock (tachycardia, hypotension, sweating) communication between the nose and pharynx may be
absent in one or both nares.
RUNNY NOSE (RHINORRHOEA) Questions to ask

The type of nasal discharge may suggest the diagnosis. Rhinorrhoea and blocked nose
Rhinorrhoea may be intermittent, varying with the
• What is the colour of any nasal discharge?
clock, or with contact with animals, dust, chemicals,
• Is the discharge from one nostril or both?
certain foods or heat. It may also be intermittent and
• Is any nasal obstruction one sided or both?
related to the season, typically in hay fever (seasonal
• Do you suffer from both nasal discharge and
allergic rhinitis). The differential diagnosis of these
obstruction?
presentations is discussed in the examination of the nose
• Do the symptoms vary with the time of day or night,
section (p. 98).
or with the time of year?
Unilateral nasal discharge may signify a serious cause,
• Does anything aggravate your symptoms?
whether it is an otherwise unrecognised foreign body in
• Do you have any pets?
a child or neoplasm in an adult, and must always be
• Has any medication relieved your symptoms?
thoroughly investigated.
• Do you have any known allergies?
• Have you had any previous nasal surgery?
Symptoms and signs

Nasal discharge
NASAL DEFORMITY
Type of discharge Potential causes
Watery or mucous Perennial allergic rhinitis Deformity of the nose may be congenital or acquired.
Seasonal allergic rhinitis Patients will either present with a nose that has always
Vasomotor rhinitis dissatisfied them or with one that has become misshapen
Viral infection due to an injury or possibly due to a disease process.
Mucopurulent Bacterial infection When taking a history, the patient should be asked
Foreign body about any injury and the length of time the deformity has
Serous Cerebrospinal fluid leak been present. Any other associated symptoms should be
Bloody Epistaxis noted such as the presence of obstruction or discharge.
Foreign body The use of cocaine or contact with chemicals (such as
Trauma chromium) should be noted.
Neoplasia
Bleeding diathesis PAINFUL NOSE AND FACE
Other than as a result of direct trauma or acute
inflammation, it is unusual for nasal pain to be present
as a symptom. If it is, care should be taken to establish
BLOCKED NOSE the cause.
This condition is often associated with rhinorrhoea and Facial pain may be caused by acute sinus infections but
so taking the history is the same in both conditions. is often associated with causes other than the nose or
As with unilateral nasal discharge, unilateral nasal sinuses. Sites to be considered in particular are the teeth
obstruction may have a significant cause. The examiner and the trigeminal nerve.
must establish whether the nasal obstruction is a true Maxillary sinus pain is usually always associated with
obstruction or intermittent. If the obstruction is nasal obstruction or discharge and is typically worse on
intermittent, and even varying from one side to the other, bending down. Frontal sinus pain is felt above the orbit
it is more likely to be caused by a physiological reaction and is usually accompanied by periorbital swelling. This
rather than mechanical obstruction. condition requires urgent referral because of the closeness
Mechanical nasal obstruction may be due to nasal of the lateral sinus and it communication with the
septal, turbinate or other causes. Nasal septal distortion brain.
95
Chapter

The nose
• Unilateral nasal discharge, especially if blood-stained

(>2/52)
• Unilateral nasal obstruction (>2/52)
• Nasal pain with no obvious aetiology (>2/52)
• Unexplained facial pain (>2/52)
• Epistaxis, heavy and lasting longer than 30 minutes
• Periorbital swelling and pain
Fig. 4.20 Manual examination of the nasal vestibule and lower

Examination of the nose and sinuses cavity.
EXTERNAL APPEARANCE OF THE NOSE

The general appearance of the nasal structure and the THUDICUM SPECULUM OR AUROSCOPE
skin overlying the nose should be observed. Any redness
This useful instrument allows a good view of the vestibule
or abnormal swelling or shape should be noted. Swelling
and lower part of the nasal cavity, while the clinician has
around the maxilla or orbit may indicate severe sinus
one hand free to, for example, remove a foreign body.
infection but maxillary swelling may also highlight
Figure 4.21 illustrates how to use the thudicum.
a dental abscess. The nose is not an uncommon site
If a speculum is not available, an auroscope is a useful
for skin tumours such as basal or squamous cell
and simple alternative.
carcinomas.
NASENDOSCOPE
SEBORRHOEIC DERMATITIS
A more complete view of the nasal cavity can be obtained
This is a common skin condition often first seen at the
with the use of a rigid (Fig. 4.22) or flexible (Fig. 4.23)
side of the nose close to the alae. It is manifest by redness
nasendoscope. In particular the flexible nasendoscope
and scaling of the skin.
allows a view of the whole cavity and can be advanced
into the postnasal space, and beyond (Figs 4.24, 4.25).
ACNE ROSACEA
While this skin condition is well recognised to be a DEFORMITIES OF THE NOSE
redness of the skin seen in adults on various areas of the
Genetic causes, injury or disease may result in structural
face, it may occur on the lower part of the nose.
deformities. Injury may result in fracture or dislocation of
the nasal bone or cartilage. These may be visible from
RHINOPHYMA observing the external appearance or more usually from
This condition is thought to be an extension of acne examining the nasal cavity.
rosacea. The excessive swelling and growth of the nose The nasal structure may also be damaged by conditions
can be quite disfiguring. It is important to note that which collapse the nasal bridge such as contact with
there is an increased incidence of skin neoplasia in this various chemicals, notably cocaine. The structure may
condition. also be distorted by syphilis, tuberculosis or neoplasms
within the cavity of the nose.
Most deformities of the nose involve the midline
NASAL CAVITY septum and such deformities are detected both externally
The nasal cavity can be visualised in a variety of ways and by examining the nasal septum.
and this depends on the equipment available to the The most common problem with the septum is
clinician. deviation from the central position, often termed as
deflection.
MANUAL EXAMINATION
In children and adolescents the nasal vestibule and lower SEPTAL PERFORATION
cavity can be easily seen by elevating the tip of the nose The finding of a septal perforation should prompt the
(Fig. 4.20). clinician to seek any possible pathology, although there
96
Chapter
The nose 4
Fig. 4.22 Rigid endoscope.

a
Fig. 4.23 Flexible endoscope.
d
Fig. 4.24 Flexible endoscope in use.
Fibreoptic nasendoscopy
Fig. 4.21 (a) The thudicum nasal speculum. (b) Place thudicum
on left index finger with the flanges pointing towards the wrist.
(c) Rotate the hand so that the arms of the speculum are between
the third and fourth fingers such that the flanges are protected
from spreading too wide. (d) Flex the wrist and the speculum is
ready for use. (e) Speculum in use.
Fig. 4.25 Fibreoptic examination of the postnasal space (transnasal).
97
Chapter
may be none. Perforations usually occur low in the way to vasomotor rhinitis. Vascularity of the turbinates is
septum and should be visible to the nonspecialist by use increased causing turbinate swelling and watery nasal
of a thudicum speculum or auroscope. discharge.
ATROPHIC RHINITIS
Aetiology
The mucosa in this condition is very different to the other
Septal perforation
types of rhinitis. It is atrophied, dry and crusted. As a
• Idiopathic result, halitosis is often present.
• Iatrogenic (previous cauterisation or surgery)
• Infection (tuberculosis, syphilis)
SINUSES
• Neoplastic (basal or squamous cell carcinoma,
malignant granuloma) Acute maxillary sinusitis
• Chemicals (cocaine, chromic salts) The diagnosis of acute sinusitis is usually made on the
history of facial pain, blocked nose and purulent nasal
discharge. It is usually associated with an upper respiratory
tract infection and fever may be a feature. On examination
VESTIBULITIS
the clinician may elicit maxillary tenderness. Diagnostically,
Inflammation and crusting in the area of the nasal however, mucopus should be observed coming from
vestibule indicates a bacterial infection. Such infection beneath the middle turbinate. A CT scan is the most
will cause dilatation of blood vessels, in particular in the helpful investigation to confirm the condition.
plexus of Little’s area which can result in epistaxes.
Acute frontal sinusitis
EPISTAXIS It is unusual for this condition to occur without associated

maxillary sinusitis. Supraorbital tenderness, swelling and
The large majority of epistaxes come from Little’s area on even redness may be observed. Again mucopus should
the nasal septum where there is a plexus of blood vessels. be detected drained from under the middle turbinate.
The clinician will be able to see dilated vessels in this
area with simple instrumentation. Only by use of a Chronic sinusitis
nasendoscope will it be possible to detect bleeding points The diagnosis of this condition is similar to acute sinusitis
higher in the nose. but the condition will have lasted longer and may be
more associated with halitosis.
ALLERGIC RHINITIS
Allergic rhinitis may be seasonal (hay fever) or perennial.
It can be recognised by observing the prominent inferior The throat
turbinates which will be swollen and oedematous. There
will be a watery nasal discharge and sneezing may be a
feature. Seasonal allergic rhinitis will be related to the
Structure of the throat
seasons. Perennial allergic rhinitis will be related to dusts,
cats, feathers or other allergens and will occur throughout
ORAL CAVITY
the year.
The structures within the oral cavity are the gums, teeth,
tongue and tonsils (Fig. 4.26). The anterior border of
VASOMOTOR RHINITIS the oral cavity is formed by the gums and its posterior
(NONALLERGIC RHINITIS) boundary is the oropharynx. The surface of the cavity is
The signs on examination are similar to allergic rhinitis lined by mucous membrane.
but it is not related to any allergy. Profuse watery nasal The salivary glands open into the oral cavity. The
discharge is a feature, as is nasal obstruction. It is due to parotid glands open into the buccal mucosa at the level
increased vascularity of the nasal mucosa. The difference of upper second molar and the submandibular glands
from allergic rhinitis is that the turbinates may appear open into the floor of the mouth lateral to the frenulum
more reddened. The symptoms may be enhanced by a of the tongue.
dry atmosphere, heat or hot foods, alcohol and certain
chemicals.
TEETH
There are 10 upper and 10 lower deciduous or milk teeth.
RHINITIS MEDICAMENTOSA In the adult there are 16 upper teeth and 16 lower teeth.
The result of this condition is that by the misuse of nasal Their average times of eruption are shown in Figures 4.27
sympathomimetic sprays the mucosa behaves in a similar and 4.28.
98
Chapter
The throat 4
Examination of the mouth and throat
hard palate opening of

parotid duct
uvula soft palate undersurface of

tongue
posterior posterior
pharyngeal wall pillar submandibular
duct
vallate
papillae tonsil
buccal
opening of mucosa
dorsum anterior submandibular
of tongue pillar duct frenulum
Fig. 4.26 Structure of the oral cavity.
Average eruption times of deciduous teeth Average eruption times of permanent teeth
edcba abcde 87654321 12345678

edcba abcde 87654321 12345678
d d 4 4
a a 6 months d d 14 months 1 1 6 years 4 4 10 years
6 6 53 53
a a c c 6 6 6 years 53 53 11–13 years
7 months c c 18 months
1 1 7 7
b b e e 7 years 7 7 12 years
b b 8–9 months e e 24 months
Fig. 4.27 Average eruption times of the deciduous teeth. 8 8

2 2 8 years 8 8 18–25 years
TONGUE
The tongue is a muscular organ whose ventral or under 2 2
surface is mucous membrane. The dorsal or upper surface 9 years
is of squamous epithelium in which are papillae containing
taste buds. It has a rich blood and nerve supply. The Fig. 4.28 Average eruption times of the permanent teeth.
anterior two-thirds of the tongue is divided from the
posterior one-third by a V-shaped sulcus terminalis.
In the posterior third of the tongue the papillae are crypts which commonly contain harmless exudate, or
particularly prominent. food debris. Lymphoid tissue is also found in the
The tongue has a central band of tissue tethering its nasopharynx (adenoids) and posterior to the tongue
ventral surface; this is called the frenulum. (lingual tonsil). All lymphoid tissue in the pharynx tends
to regress with age.
TONSILS
The tonsils are lymphoid tissue that lie posterolaterally PHARYNX AND LARYNX
to the tongue between the anterior and posterior falces. The pharynx forms the space posterior to the oral cavity.
The lymphoid tissue contains many mucus-secreting It is anatomically divided into three parts.
99
Chapter
Questions to ask
Sore throat or mouth
• How long have you had the pain?

• Does anything aggravate or relieve the pain?
• Where do you feel the pain and does it radiate?
• Is the pain constant or does it vary?
• How is your swallowing?
• Have you any other symptoms?
• Have you been or are you presently taking any
medication?
Fig. 4.29 Fibreoptic view of normal larynx, showing epiglottis, cords • Do you smoke or drink alcohol?
and arytenoid cartilages (courtesy of Wonersh Surgery).
The nasopharynx is the part of the pharynx that forms LUMP IN THE NECK
the postnasal space above the soft palate and in which,
in children, lie the adenoids. The choanae of the nose Thyroid swellings are dealt with in Chapter 2. There are
form its anterior border. other sites in the neck where swelling may arise. The
The oropharynx is the posterior extension of the oral clinician should establish the position of any mass and
cavity. palpate the lumps presented (see ‘Examination of the
The hypopharynx, or laryngopharynx, extends from the throat’ p. 101). It is not uncommon in infections of the
oropharynx to the cricoid cartilage which lies distal to the throat for the anterior cervical glands to be tender and
vocal cords. The internal structures to be observed here enlarged. Posterior cervical gland enlargement (posterior
are the epiglottis and larynx. The main structures of the to the sternomastoid muscle) may be of more sinister
larynx are the vocal cords and their suspensory cartilages, significance.
the arytenoid cartilages. Above the cords is the ventricular Neck lumps may be a sign of generalised disease and
sinus which is bordered proximally by mucous membrane the possibility of other systems being involved must be
folds (false chords). There is a recess posterior to the considered.
tongue but anterior to the epiglottis, the vallecula. The
pyriform fossae are two recesses which lie either side of Questions to ask
the larynx.
Lump in the neck
The larynx (Fig. 4.29) is enclosed in the thyroid cartilage
(Adam’s apple) and beneath (and above and connecting • How long has it been present?
it to the cricoid cartilage) is the cricothyroid membrane • Has the lump changed in size?
(a site for tracheostomy). • Is the lump painful?
• Do you have a cough?
• Have you any problem with your mouth or throat?
Symptoms of diseases of the throat • Have you lost weight recently?
• How is your general health?
BLOOD IN THE MOUTH
• Do you have any problem with sweating?
Patients may present with a history of finding blood in • Do you have any thyroid symptoms?
their mouth or throat. This should be distinguished from
blood arising from vomiting (haematemesis) or coughing
(haemoptysis). STRIDOR
The most common site for bleeding of the throat is
from inflamed gums. Lesions from other sites in the oral Stridor is a harsh sound made on inspiration. It is
cavity and pharynx where neoplasm might be concealed associated with narrowing of the upper airway, usually
should be excluded. of the glottic or vocal cord area. It should be distinguished
from the expiratory wheeze of asthma. It is often
associated with hoarseness and the age of the patient is
SORE THROAT
relevant to the diagnosis.
Pain can arise from all the structures in the mouth and
pharynx, from teeth to larynx. In the mouth the cause
may be readily seen. It is important to establish the HOARSE VOICE
severity of the symptoms and if there is any associated Hoarseness is a term describing an altered voice. It may
fever. It is also important to establish the effect of the pain be extreme, in that there is little or no voice production.
on swallowing solids and liquids. It is frequently associated with an upper respiratory
Soreness in the throat may present as the feeling of a tract infection and any symptoms of that should be
lump in the throat. elucidated.
100
Chapter
The throat 4
The clinician should ascertain whether the voice has has been found. Associated factors in aphthous ulcer
been overused (frequent singing or shouting) and obtain formation are listed in the ‘differential diagnosis’ box.
information about smoking and the use of alcohol. Other causes of buccal lesions are Vincent’s angina
(acute ulcerative stomatitis) and the more chronic
infections of tuberculosis and syphilis.
Questions to ask
Carcinoma in the mouth usually presents as an ulcer
Hoarse voice and may occur on any part of the mucosa or tongue.
• How long have you been hoarse? Kaposi sarcoma may involve the buccal mucosa and
• Is it persistent or intermittent? appear as small, firm, cytic-shaped, bluish lesions.
• Have you any other symptoms (cold or fever)?
• Have you been projecting your voice for any reason?
• Do you smoke or drink alcohol and how much?
• What is your job; do you work in dusty
surroundings?
DYSPHAGIA
Difficulty on swallowing of oesophageal origin is dealt
with in Chapter 7. It should be distinguished from
oropharyngeal causes of pain or difficulty in swallowing.
The anatomical level of discomfort and any associated
symptoms should be ascertained when taking a history
(see ‘Questions to ask, sore throat or mouth’ p. 100).
Fig. 4.30 Technique of indirect laryngoscopy.
Examination of the throat

INSTRUMENTS
It would be unusual for a nonspecialist clinician to have
access to fibreoptic equipment. Important requirements
for a primary care physician are a good light source,
tongue depressor and possibly an indirect laryngoscopy
mirror (Figs 4.30–4.34).
BUCCAL MUCOSA
Ulceration
Ulceration is where there is loss of epithelium. There are Fig. 4.31 Technique of examination of nasopharynx using postnasal
mirror.
many conditions that may cause ulceration of the buccal
mucosa. Most causes are infective in origin but perhaps
the most common are aphthous ulcers for which no cause
Posterior rhinoscopy
Aphthous ulcers
• Viral (herpes simplex)

• Allergies to foodstuffs or certain chemicals found in
toothpastes and mouthwashes
• Stress
• Medication such as nonsteroidal anti-inflammatory
drugs, beta-blockers
• Medical conditions such as vitamin deficiencies,
Crohn’s disease, Behçet’s syndrome, blood dyscrasias
(agranulocytosis)
• Mechanical trauma
Fig. 4.32 Posterior rhinoscopy.
101
Chapter
recognised by random areas of desquamation which may

Indirect laryngoscopy concern the patient.
Hairy tongue
The tongue in this condition may be black in colour. It is
caused by hypertrophy of filiform papillae and may be
related to social factors such as smoking or drinking tea
and coffee.
Fissured tongue
In this condition there is an exaggeration of fissures in
the epithelium of the tongue. It may be a manifestation
of iron-deficiency anaemia but is more often of genetic
origin.
Fig. 4.33 Indirect laryngoscopy. TONSILS AND OROPHARYNX

Pharyngitis
Inflammation of the pharynx without an associated
tonsillitis is recognised by a redness and oedema of the
soft palate and fauces. Its cause may be viral or bacterial
Fibreoptic nasendoscopy and it is usually associated with fever and swelling of the
anterior cervical glands.
Tonsillitis
When there is infection of the tonsils it is notoriously
difficult for the clinician to determine whether the
causative organism is viral or bacterial. Commonly
tonsillar exudates are seen and every organism may
produce these. Although exudates are commonly seen in
infective mononucleosis (glandular fever) these can be
seen in any inflammatory condition of the tonsil. The
tonsils, as well as producing exudates, may enlarge with
inflammation.
Fig. 4.34 Fibreoptic examination of the larynx (transnasal).
Unilateral enlargement of the tonsils
This is a significant finding and is a red flag indication for
referral (see box).
If there is obvious redness, oedema and uvular
White lesions displacement, a peritonsillar abscess (quinsy) should be
White lesions on the buccal mucosa are not uncommon suspected. Associated signs will be fever and anterior
in the oral cavity. cervical gland enlargement.
Candidiasis is the most common cause. This condition Lymphoma of the tonsil may present in a similar
more commonly occurs in infants and frail elderly but fashion but usually without the signs of fever and
also may be seen in those on antibiotic treatment or in inflammation.
immunocompromised patients.
Lichen planus and leucoplakia may be similar in
appearance to candida and, if candida fails to respond to
treatment, a biopsy may be necessary to distinguish these Red flag – urgent referral
other two possibilities. All these lesions may present with The throat
some ulceration.
• Unilateral tonsillar enlargement
• Child with fever, cough, stridor and respiratory
TONGUE distress
• Child with fever, drooling and respiratory distress
Geographical tongue
• Airways obstruction in any age group
The tongue has various conditions of unknown aetiology • Hoarseness lasting longer than 4 weeks
and of no pathological importance. This condition can be
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Chapter
The throat 4
LARYNX Laryngitis
Infective causes involving the larynx may occur at any age In the adult, laryngitis is usually diagnosed by its
but there are two conditions in children of particular symptoms. Cough, throat discomfort and hoarseness of
importance. voice together with fever are the usual presenting
symptoms. If the causative organism is bacterial, there
Acute laryngotracheobronchitis (croup) will be an associated purulent sputum. Most cases
The usual organism causing this condition is the however are viral.
parainfluenza virus. It most commonly occurs in children Voice production, hoarseness or aphonia, may be due
under the age of 5 years and is of sudden onset. It to misuse or overuse. There may also be symptoms in the
is recognised by the presence of a barking cough, larynx of pain or voice alteration caused by a psychological
stridor (inspiratory wheeze), and hoarse voice. There element (hysterical dysphonia and globus syndrome).
will usually be fever present and symptoms are These conditions can only be diagnosed in the absence
most prominent at night. The condition lasts about of direct or indirect laryngoscopy by the history and lack
48 hours. of infective signs.
Severe cases may cause acute respiratory distress A patient in whom the hoarseness has lasted for longer
(tachycardia, rapid respirations and possibly cyanosis) than 4 weeks should be referred to a specialist for
and require urgent admission to hospital. investigation.
Diagnosis of croup is mainly made on the symptoms
alone. Tumours of the larynx
Laryngeal carcinoma should be excluded in anyone with
Epiglottitis (supraglottitis) a persistent hoarse voice, which is the cardinal symptom
This infection extends into a slightly older age group and of this condition. There may be an associated history of
the mean age is around 5 years old, and therefore older smoking or a family history of the disease.
children may be affected. Again, onset is sudden and Not all tumours of the larynx are malignant, however
diagnosis is made mainly on the symptomatology. Cough – singer’s nodes and polyps are happily a more common
in this condition is much less of a feature. Drooling finding. Vocal cord palsy may indicate a malignant
of saliva is frequently present, as well as difficulty in bronchial tumour.
swallowing and respiratory distress. As with any infection,
fever may be present.
If this condition is suspected in a child, urgent
admission is necessary as deterioration in the airway may
be rapid.

The ear
• Wax removal may greatly help hearing The nose

• Ear irrigation is perfectly acceptable as long as there • Epistaxis in the elderly is usually more difficult to
are no contraindications control due to arteriosclerosis, so there should be a
• Presbyacusis (sensorineural deafness of old age) may lower threshold for referral criteria
occur over 60 years of age; it is the most common • Epistaxis in the elderly is more likely to be from higher
cause of deafness in old age in the nose than Little’s area and will be more difficult
• Presbyacusis is usually first recognised clinically by a for the primary care physician to control
high tone hearing loss • Incidence of carcinoma of the nose and sinuses
• Unilateral deafness may indicate significant pathology, increases with age
so refer The throat
• Unilateral tinnitus may indicate significant pathology, • Voice change occurs in the elderly due to loss of tissue
so refer elasticity
• Persisting unilateral otalgia may indicate significant • The incidence of carcinoma of the larynx increases
pathology, so refer with age and so hoarseness lasting longer than 4
• Persisting discharge from a perforated tympanic weeks should be referred to a specialist urgently
membrane may indicate significant pathology, • Malignancies may cause hoarseness by involving the
so refer vocal cords directly or by recurrent laryngeal nerve
palsy from a carcinoma in the hilum of the lung
103
Chapter
Review
Framework for the routine examination of the ear, nose and throat
A useful guide to a student of ear, nose and throat • Rhinorrhoea and nasal obstruction are the most
examination is to always take particular note of common symptoms of the nose presented to the
symptoms and signs that are unilateral. clinician
The ears • Allergic rhinitis is the most common reason for those
• Always examine the pinna and entrance to the symptoms
external canal before inserting the auroscope into the • Distinguishing allergic rhinitis from atrophic or
ear vasomotor rhinitis is made on the history and findings
• Irrigation of ears is a safe procedure except in defined in the nose
circumstances • Nasal fractures do not need correcting if there is no
• The temperature of the water used should be 37°C cosmetic deformity or if the nasal airway is unimpeded
otherwise the onset of a convection current in the • Unilateral nasal discharge in children may indicate a
labyrinth may result in temporary vertigo foreign body
• Water is a significant irritant of otitis externa and of • Unilateral nasal discharge in an adult may indicate
the middle ear if there is a perforation and therefore neoplasm
irrigation should not be used in such circumstances • Uncontrolled epistaxis, lasting over 30 minutes, should
• Unilateral symptoms, such as sudden onset deafness be seen in a specialist clinic especially if the patient is
or tinnitus, may be significant and should be referred elderly
– urgently in the case of sudden onset deafness The throat
• Presbyacusis is signalled by an initial high tone hearing • Unilateral tonsillar enlargement may be significant.
loss Consider lymphoma or, if there is inflammation,
• Continuing discharge from an ear should be referred peritonsillar abscess (quinsy)
to a specialist. If the discharge is from the external • In children with stridor indicating acute
ear, aural toilet will speed resolution; if the discharge laryngotracheitis and signs of respiratory distress admit
is from the middle ear specialist management is to a specialist unit urgently
needed • In children with fever, drooling and respiratory distress
The nose suspect epiglottitis and admit to a specialist unit
• Look into the nose frequently. Use an auroscope if urgently
nasal speculae are not available. Get used to what is • Hoarse voice lasting more than 4 weeks should be
normal referred for specialist examination to exclude
• Nasal polypi are white and pearly and should not be malignancy
confused with the appearance of a swollen inferior
turbinate
104
5
The respiratory system
Disease of the respiratory tract accounts for more Structure and function
consultations with general practitioners than any other
of the body systems. It is also responsible for more new The respiratory tract extends from the nose to the alveoli
spells of inability to work and more days lost from and includes not only the air-conducting passages but
work. the blood supply as well. The arrangement of the major
For example, asthma now affects approximately 10% airways is shown in Figure 5.1. An appreciation of this
of the population of many Western countries; lung cancer arrangement helps in the interpretation of radiographs
is the most common male cancer and in some places has (Fig. 5.2) and is essential for the bronchoscopist. More
already exceeded breast cancer as the most common important for the examiner is the arrangement of the
female malignancy. Tuberculosis, for so long the staple lobes of the lungs (Fig. 5.3). It will be seen that both lungs
of the respiratory physician is, after a long period of are divided into two and the right lung is divided again
decline, increasing again. The respiratory complications to form the middle lobe. The corresponding area on the
of HIV infections have added to the burden. Increases in left is the lingula, a division of the upper lobe. Figure 5.4
pollution, new industrial processes and the growing transposes this pattern on to a person, outlining the
worldwide consumption of tobacco all have implications surface markings of the lungs. Examination of the front
for the lungs. The average family practitioner, therefore, of the chest is largely that of the upper lobes, examination
is likely to spend more of the working day examining the of the back the lower lobes. It will be seen how much
respiratory system than any other. more lung there is posteriorly than anteriorly, so it comes
Respiratory disease is common in hospital practice. It as no surprise that lung disease that primarily affects the
accounts for approximately 4% of all hospital admissions bases is best detected posteriorly. Note how much lung
and approximately 35% of all acute medical admissions. is against the lateral chest wall. Students often examine
Surgeons and anaesthetists are very interested in ensuring a narrow strip of chest down the front and the back.
an adequate respiratory system in any patient who needs Many signs are found laterally and in the axilla.
a general anaesthetic. Computerised tomography (CT) adds an extra
Radiologists, pathologists and microbiologists are dimension to visualisation of the chest (Figs 5.5–5.10).
intimately involved in the diagnosis of lung conditions. The fine detail of the airways is beautifully illustrated
Consequently, doctors in many branches of medicine by wax injection models (Fig. 5.11). The same technique
spend a very substantial portion of their professional can be used to illustrate the intimate relationships
working life in the diagnosis and treatment of lung between the supply of blood and air to the lungs
disease. (Fig. 5.12).
As with any other disease, a good history is the basis
for a diagnosis of lung disease, particularly as examination
may be normal even in advanced disease. A good history LUNG DEFENCE AND HISTOLOGY
is aided by a knowledge of structure and function. The lung is exposed to 6 litres of potentially infected and
Fortunately, two fairly straightforward techniques, irritant-laden air every minute. There are, therefore,
radiography and spirometry (the analysis of the volume numerous defence mechanisms to ensure survival. The
of expired air over time), illustrate normality and help the nose humidifies, warms and filters the air and contains
physician to understand the abnormal. lymphocytes of the B series which secrete immunoglobulin
105
Chapter
5 The respiratory system
The bronchial tree
trachea
right main bronchus left main bronchus
apical apical
posterior posterior
upper lobe
anterior (apicoposterior)
upper lobe
(intermediate) anterior
lateral (superior division)
middle lobe
medial superior lingular
medial basal apical inferior lingular
anterior basal anterior basal
lower lobe lower lobe
lateral basal lateral basal
posterior basal posterior basal
Fig. 5.1 The arrangement of the major airways.
The lobes of the lung
upper upper
lobe lobe
middle
lobe
lower lower
lobe lobe
Fig. 5.2 Normal radiograph: posteroanterior view (left) and right
lateral view (right).
upper upper
lobe lobe
A. The epiglottis protects the larynx from inhalation of
material from the gastrointestinal tract.
middle
The cough reflex is both a protective and a clearing lower lobe lower
mechanism. Cough receptors are found in the pharynx, lobe lobe
larynx and larger airways. A cough starts with a deep
inspiration followed by expiration against a closed glottis.
Glottal opening then allows a forceful jet of air to be
expelled.
Fig. 5.3 Lobes of the lung: anterior view (upper) and lateral view
The main clearance mechanism is the remarkable (lower).
mucociliary escalator. Bronchial secretions from bronchial
glands and goblet cells, together with secretions from
deeper in the lungs, form a sheet of fluid which is The chief defence of the alveoli is the alveolar
propelled upwards continuously by the beat of the cilia macrophage (Fig. 5.15), which, in conjunction with
lining the bronchial epithelium (Figs 5.13, 5.14). This complement and immunoglobulin, ingests foreign
cilial action can fail either from the rare immotile cilia material that is then transported either up the airways or
syndromes or commonly from cigarette smoke. into the pulmonary lymphatics. T and B lymphocytes are
106
Chapter
superior ascending
vena aorta
cava pulmonary
trunk
UL UL left
right
pulmonary
ML pulmonary
artery
artery descending
aorta
LL LL
Fig. 5.7 CT scan at level of carina.
a b
heart
right
superior descending
pulmonary oesophagus aorta
vein
UL
ML UL
LL
LL
Fig. 5.8 CT scan at level of mid left atrium.
right
main
bronchus
left
main
c d bronchus
Fig. 5.4 Surface markings of the lobes of the lung: (a) anterior,
right
(b) posterior, (c) right lateral and (d) left lateral (UL, upper lobe; ML, oblique left
middle lobe; LL, lower lobe). fissure oblique
fissure
right left
brachiocephalic brachiocephalic Fig. 5.9 CT scan – lung windows at level of carina.
vein vein
left
carotid
artery
innominate left
artery subclavian
artery
Fig. 5.5 CT scan at level of thoracic inlet.
internal
superior mammary
vena vessels
cava
aortic arch
azygos
vein
Fig. 5.6 CT scan at level of aortic arch. Fig. 5.10 Shaded surface display of reconstruction of dynamic
magnetic resonance angiography of pulmonary and great vessels.
107
Chapter
Fig. 5.11 A cast of the bronchial tree with the segments outlined in Fig. 5.12 Injection model showing bronchi (white), arteries (red but
different colours. carrying deoxygenated blood) and veins (blue but carrying
oxygenated blood).
Epithelium
Connective tissue
Epithelium
Glandular ducts
Mucous glands
Cartilage
Lung tissue Connective tissue Cartilage
Fig. 5.13 (a) Low-power photomicrograph of a bronchus. (b) High-power photomicrograph of normal bronchial wall.
present throughout the lung substance and most of the mechanisms within the brainstem. These can be
immunoglobulin in the lung is made locally. The blood influenced voluntarily from higher centres and from
supplies neutrophils that pass into the lung structure in the effect of chemoreceptors. The medullary or central
inflammation. chemoreceptors in the brainstem respond to changes in
partial pressure of carbon dioxide in the blood (PCO2).
Chemoreceptors in the aortic and carotid body respond
LUNG FUNCTION to low partial pressure of oxygen (PO2) but only when this
The function of the lung is to oxygenate the blood and to falls below 8 kPa. Thus, alteration in PCO2 is the most
remove carbon dioxide. To achieve this, ventilation of the important factor in respiratory control in health.
lungs is performed by the respiratory muscles under the The sensitivity of the medullary chemoreceptor to
control of the respiratory centre in the brain. The rhythm PCO2 can be reset either upwards in prolonged ventilatory
of breathing depends on various inhibitory and excitatory failure or downwards, as when a patient is placed on a
108
Chapter
Lung volumes
volume
total
lung
capacity
tidal
volume
vital
capacity functional
residual
residual capacity
volume
time
Fig. 5.14 Electron micrograph of bronchial cilia and the mucus Fig. 5.16 Subdivisions of lung volume.
sheet.
muscles, spine, ribs and diaphragm are all involved.

Moreover, the lung tissue itself must overcome its own
inertia and stiffness. Malfunction of any of these can lead
to respiratory failure.
Diaphragm function is in two parts: contraction leads
to descent of the diaphragm and the costal parts elevate
the lower ribs. A common consequence of chronic airflow
limitation and hyperinflation is a low flat diaphragm
which may pull the ribs inwards rather than out.
ASSESSING RESPIRATORY FUNCTION

As the function of the lungs is to add oxygen to the blood
and to remove carbon dioxide, it might be thought that
measurement of the PO2 and PCO2 in the blood would
Fig. 5.15 Normal lung. Occasional pigment-containing be an adequate assessment of its efficiency. However,
macrophages are present within the alveolar spaces. Haematoxylin the lung has such an enormous reserve capacity that it
and eosin stain (× 25).
can sustain considerable damage before blood gases are
affected. There are, nonetheless, a number of other tests
mechanical ventilator. The first situation is most of lung function that are briefly described here. These are
commonly seen in chronic airflow limitation (chronic tests of static lung volumes, ventilation or dynamic lung
obstructive pulmonary disease) when patients may volumes and gas exchange across the alveolar–capillary
become dependent on hypoxic drive to maintain membrane.
respiration. The injudicious administration of oxygen can Although some tests of pulmonary function are quite
then lead to ventilatory failure and death. In the second complex, most problems only need the simpler tests to
situation, ‘weaning’ a patient away from a ventilator is diagnose. Spirometry and peak flow measurements can
difficult because the medullary centre demands a low be made available in many primary care centres.
PCO2 that cannot be maintained by the patient unaided.
Static lung volumes
Ventilation is largely performed by nerve impulses in
the phrenic nerve acting to contract the diaphragm and When attempting to take as deep an inspiration as
expand the volume of the chest. Scalene and intercostal possible we are eventually stopped partly by the
muscles act mainly by stabilising the chest wall. The resistance of the chest wall to further deformation and
result is to decrease the pressure in the pleura (already partly by the inability to stretch the lung tissues any
less than atmospheric). As the air inside the airways is at further (Fig. 5.16). Total lung capacity (TLC) at one end
atmospheric pressure, the lungs must follow the chest is, therefore, largely influenced by this ‘stretchability’ or
wall through pleural apposition and expand, sucking in elasticity of the lung. The stiffer the lung, as in fibrosis or
air. Expiration is largely a passive process: when the scarring, the less distensible it will be. Conversely, damage
muscles relax the lung recoils under the influence of its to the elastic tissue of the lung (e.g. emphysema) with
own elasticity. Ventilation is, therefore, much more than destruction of the alveolar walls will make it more
just forcing air through tubes. Higher brain centres, the distensible, leading to an increase in TLC. TLC is also
brainstem, spinal cord, peripheral nerves, intercostal high is some patients with asthma and chronic obstructive
109
Chapter
bronchitis, probably because the lungs are overexpanded

in an attempt to widen the airways. The expiratory spirogram
As already indicated, breathing out from TLC is largely
passive by progressive retraction of the lung; this process volume
(litres)
will end at functional residual capacity (FRC) when the
tendency of the lung to contract is balanced by the thorax 5
resisting further deformation. This point is also the
end of normal expiration. Further expiration is an active 4
process involving expiratory muscles. By using these
muscles, more air can be forced out until, at least in older
3
individuals, the limiting factor is closure of the small
VC = 4.0 l
airways which have been getting smaller along with the
FEV1 = 3.0 l
alveoli. Beyond this the lungs can only become smaller 2 FEV1% = 75
by direct compression of gas (Boyle’s law) by the
expiratory muscles. At this point, the amount of air left
1
in the lung is designated residual volume (RV).
In chronic bronchitis, the small airways are narrowed
and inflamed; in emphysema, the elastic tissue supporting 0
the small airways is lost and they collapse in expiration. 0 1 2 3 4 5 6
time (seconds)
Both mechanisms lead to an increase in RV. Conversely,
if the lungs are stiffer (fibrosis), the increased tension in
Fig. 5.17 Normal expiratory spirogram.
the lung tissue holds the airways open with closure
occurring later in expiration, thus reducing the RV.
In summary, stiff lungs from fibrosis cause a low TLC
and low RV, emphysema causes a high TLC and a high
RV and chronic bronchitis causes a high RV. Vital capacity
(VC) depends on the relative changes in RV and TLC but
usually the overall effect in lung disease is a reduction.
Dynamic lung volumes
Assessment of airflow involves measuring the volume
exhaled in unit time by use of a spirometric trace (Fig.
5.17). This is produced by a forced exhalation from TLC
to RV. The conventional parameters derived from this
trace are the forced vital capacity (FVC) and the forced
expiratory volume in 1 second (FEV1). FVC is the amount
exhaled forcefully from a single deep inspiration, FEV1 is
the fraction of that volume exhaled in the first second.
These are then expressed as a ratio of the FEV1 over the
FVC (FEV1%). This is normally approximately 75%, which
indicates that a normal person can exhale forcibly three-
quarters of their VC in 1 second. VC and FVC, one in slow Fig. 5.18 The Mini-Wright Flow Meter in use.
expiration and the other in fast expiration, give similar
results in normal individuals, although FVC is reduced
in many disease states because of premature airway figure is extrapolated over 1 minute. It can be measured
closure. easily by a variety of portable devices (Fig. 5.18) and serial
In diseases causing airways obstruction, the proportion recordings can be very useful in the diagnosis and
of the VC that can be exhaled in 1 second is reduced and monitoring of asthma (Fig. 5.19).
the FEV1% falls. Conversely, in restrictive lung disease
Gas exchange
the airways are held open by the stiff lungs and the
FEV1% is normal, even increased. Nevertheless, the FVC The transfer factor (TF) is a measurement of gas
will be reduced because the TLC is reduced. In restrictive transference across the alveolar–capillary membrane. For
lung disease, FEV1 is reduced in proportion to FVC; in technical reasons carbon monoxide is used as the test gas
airways obstruction, it is reduced disproportionately. but oxygen is affected in a similar way. TF is reduced
when there is destruction of the alveolar–capillary bed,
Peak flow
as in emphysema, and also when there is a barrier to
The peak expiratory flow rate (PEFR) is the flow generated diffusion. This may occur when the alveolar–capillary
in the first 0.1 seconds of a forced expiration; the resulting membrane is thickened or where there is lack of
110
Chapter
Peak flow recordings in asthma

600
500 cough cough cough cough
400
300
200
100
time 2 610 2 610 2 6102 610 2 610 2 6102 610 2 610 2 610 2 610 2 610 2 6102 610 2 610
date 8 9 10 11 12 13 14
Fig. 5.19 Peak flow chart in a child with asthma whose main
symptom was cough. The dips coincide with the symptoms.
homogeneity in the distribution of blood and air at

alveolar level. Both mechanisms are important in lung
fibrosis. Fig. 5.20 Perfusion (upper) and ventilation (lower) scans in
The TF will naturally be reduced if the lungs are pulmonary emboli. Note the multiple perfusion defects but the
normal ventilation pattern.
small or if one has been removed (pneumonectomy).
The transfer coefficient (KCO or DLCO divided by
alveolar volume, calculated separately) is a more useful
measurement because it reflects the true situation in
the ventilated lung. labelled with technetium-99m, and injected into a
peripheral vein. These microaggregates form small emboli
within the lung and the radioactivity they give off is a
LUNG VOLUMES IN DISEASE measure of blood distribution. These tests are most useful
In summary, it is possible to distinguish two main patterns in the diagnosis of pulmonary embolism when perfusion
of abnormal lung function. An ‘obstructive pattern’ is to an area of lung is reduced but ventilation is maintained
seen in asthma, chronic obstructive bronchitis and (Fig. 5.20). If both ventilation and perfusion are reduced,
emphysema. FVC, FEV1 and FEV1% are all reduced and then the defect probably lies within the airways and is a
RV increased; TLC is often reduced but high in failure of ventilation with secondary changes in the blood
emphysema. TF is low in emphysema but otherwise supply.
normal. A ‘restrictive pattern’ is seen in lung fibrosis,
such as occurs in cryptogenic fibrosing alveolitis. TLC,
BLOOD GASES
VC, FEV1, RV and TF are all reduced but FEV1% is normal
or high. Blood gases can be measured directly by electrodes in
When other results do not give a clear pattern, RV can blood obtained by arterial puncture. The results are
be very helpful, being high in airways obstruction and expressed as partial pressure of gas in the plasma (PO2
low in fibrosis. and PCO2). It is important to realise that this is not the
same as the amount of gas carried by the blood. If all the
red cells were removed, the PO2 would be unchanged, yet
DISTRIBUTION OF VENTILATION the patient would be in a perilous state. The haemoglobin
AND PERFUSION in the red cell packages and transports oxygen and carbon
Distribution of air within the lung is best assessed for dioxide just as a subway train packages and transports
clinical purposes by radioactive isotopes. The usual tracer passengers.
gas is radioactive xenon. The measurement of radioactivity The relationship between PO2 and saturation of the
over the lung gives a measure of the distribution and also haemoglobin by oxygen (and hence the volume of oxygen
the rate at which gas enters and leaves various parts of carried) is given by the oxygen dissociation curve (Fig.
the lung. Thus, it can be used to detect ‘air trapping’ or 5.21). It will be seen that the PO2 can drop significantly
absence of ventilation. Perfusion of blood can be measured before there is a drop in the saturation, clearly a good
in a similar way, usually by microaggregates of albumin thing in the early stages of lung disease. Nevertheless, it
111
Chapter
The oxygen dissociation curve The carbon dioxide dissociation curve

CO2
O2 content saturation content
(ml/l) (%) (ml/l)
200 100 600
90
500
160 80
400
70
120 60 300
50
200
80 40
30 100
40 4 6 8 10 12 kPa
20 0
10 4 8 12 kPa 10 20 30 40 50 60 70 80 90 mmHg
0 0 arterial carbon dioxide pressure
10 30 50 70 90
(mmHg)
arterial oxygen pressure Fig. 5.22 Carbon dioxide dissociation curve relating partial pressure
of gas in the blood to amount carried.
Fig. 5.21 Oxygen dissociation curve relating the partial pressure of
oxygen in the blood to saturation of haemoglobin and amount of
oxygen carried (assuming haemoglobin is normal).
means that overventilation of the lung’s good parts the pH towards normal. Retention or secretion of carbon
cannot fully compensate for underventilation of bad parts dioxide as a result of lung disease (respiratory acidosis
because the good parts on the flat part of the curve cannot and alkalosis) alters pH, which is then secondarily
increase the carriage of oxygen in the blood supplied to restored by excretion or retention of bicarbonate by the
them beyond a certain maximum. Thus, when there is a kidney. Thus, changes in arterial PCO2 (whether primary
shunt of blood from the right to the left heart, either or secondary) can be regarded as functions of the lung,
directly through the heart or through unventilated lung, and changes in bicarbonate (again, either primary or
the total amount of oxygen carried is bound to be reduced secondary) can be regarded as functions of the kidney.
and cannot be restored to normal either by increasing
ventilation or administering oxygen.
The steep part of the curve indicates that a small Symptoms of respiratory disease
increase in inspired oxygen gives a large increase in the
amount of oxygen carried – clearly useful for oxygen History-taking must follow the principles outlined
therapy in sick patients. It also indicates how readily earlier. Here, we are concerned with the analysis of the
hypoxic tissues can remove large amounts of oxygen from main symptoms of respiratory disease in turn. These are
the blood. dyspnoea, cough, sputum, haemoptysis, pain and
The dissociation curve for carbon dioxide is very wheeze.
different to that for oxygen; lowering the PCO2 continuously
lowers the saturation and hence the volume of gas carried
(Fig. 5.22). This means that overventilation in one part of Questions to ask
the lung can compensate for underventilation elsewhere.
Essential questions
Arterial PCO2 is a good measure of overall alveolar
ventilation, being increased in alveolar hypoventilation • Do you get short of breath?
(e.g. severe chronic airflow limitation) and decreased in • how much can you do?
alveolar hyperventilation (e.g. anxiety states, heart failure, • Do you have a cough?
pulmonary embolus, asthma), in which hypoxia and • do you cough anything up?
other factors stimulate an increase in ventilation. • what colour is it?
The lungs help to regulate the acid–base balance by • is there any blood?
their ability to excrete or to retain carbon dioxide. In cases • Do you have any (chest) pain?
of metabolic acidosis (e.g. diabetic ketoacidosis, renal • where is it?
failure), the lungs can ‘blow off’ carbon dioxide to restore • does it hurt to breathe?
the pH towards normal. In cases of metabolic alkalosis • Do you wheeze?
(e.g. prolonged vomiting with loss of acid from the • does it come and go or is it there all the time?
stomach), the retention of carbon dioxide again restores
112
Chapter
Symptoms of respiratory disease 5
DYSPNOEA Differential diagnosis

Most lung diseases will cause dyspnoea or difficulty in Duration of breathlessness
breathing. Patients will express this in different ways as
‘shortness of breath’, ‘shortwindedness’, ‘can’t get my Immediate (minutes)
breath’ or in terms of functional disability (‘can’t do the • Pulmonary embolism
housework’). • Pneumothorax
Some patients will talk about ‘tightness’. It may not • Pulmonary oedema
be immediately clear whether they are describing • Asthma
breathlessness or pain. If the complaint is really a pain Short (hours to days)
then this may well be angina, which is in itself sometimes • Pulmonary oedema
associated with breathlessness. If asked directly, patients • Pneumonia
can usually tell you whether their tightness means pain • Asthma
or breathlessness. Some patients with pleuritic pain • Pleural effusion
complain of breathlessness, but what they really mean • Anaemia
Long (weeks to years)
• Chronic airflow limitation
• Cryptogenic fibrosing alveolitis
Questions to ask
• Extrinsic allergic alveolitis
Dyspnoea • Anaemia
• Is the breathlessness recent or has it been present
for some time?
• Is it constant or does it come and go?
• What can’t you do because of the breathlessness?
• What makes the breathing worse?
• Does anything make it better? is that they are unable to take a deep breath because
of pain. It is of interest to consider why patients
complain of breathlessness. Most normal people do
not regard themselves as ill when they are short of
breath, say when running for a bus. It seems probable
that the sensations reported by patients are the same
Some causes of breathlessness as the rest of us but they recognise that the work
Control and movement of the chest wall and pleura the lungs are being asked to do is disproportionate
• Hyperventilation syndrome to the task the body is performing, that is, it feels
• Hypothalamic lesions inappropriate.
• Neuromuscular disease
• Kyphoscoliosis Causes of breathlessness
• Ankylosing spondylitis The causes of breathlessness may be listed as those
• Pleural effusion and thickening to do with the control and movement of the chest
• Bilateral diaphragm paralysis wall, lung disease itself and problems with the blood
Diseases of the lungs and its supply to the lungs. The control of breathing can
• Airways disease start with psychological factors in the brain, problems
– chronic bronchitis and emphysema with the control centre in the medulla (rare) and the
– asthma increased effort needed to overcome the effects of spinal
– bronchiectasis cord disease (trauma or degeneration), neuropathies
– cystic fibrosis (e.g. Guillain–Barré syndrome), myopathies and
• Parenchymal disease chest wall problems (e.g. kyphoscoliosis, ankylosing
– pneumonia spondylitis).
– cryptogenic fibrosing alveolitis Lung diseases may require more work to overcome
– extrinsic allergic alveolitis obstruction to airflow (e.g. chronic obstructive bronchitis,
– primary and secondary tumour emphysema, asthma) or to stretch stiff lungs (e.g.
– sarcoidosis pulmonary oedema, lung fibrosis).
– pneumothorax Hypoxia needs to be severe to stimulate respiration
– pulmonary oedema but may be the mechanism in pneumonia, severe heart
• Blood supply failure and other causes of pulmonary oedema. Pulmonary
– pulmonary embolism embolism leads to wasted ventilation in the affected area.
– anaemia Severe anaemia reduces the oxygen-carrying capacity of
the blood.
113
Chapter
J receptors are vagal nerve endings and are adjacent to Questions to ask
pulmonary capillaries. Stimulation of these by pulmonary
Asthma
oedema, fibrosis and lung irritants is an additional
mechanism causing breathlessness. • Does anything make any difference to the asthma?
• What happens if you are worried or upset?
Duration of dyspnoea
• Does your chest wake you at night?
The duration of dyspnoea may give a clue to the cause • Does cigarette smoke make any difference?
and can conveniently be divided into immediate (over • Do household sprays affect you?
minutes), short (hours to days) and long (weeks to years). • What happens when sweeping or dusting the
There is some overlap but contrast, for example, the house?
patient with a large pulmonary embolism who collapses • Does exposure to cats or dogs make any difference?
in minutes in acute distress compared with the progressive • Have you lost time from work/school?
relentless disability extending over a decade in the patient
with smoking-related airflow limitation. Some patients
find it difficult to remember duration accurately. Many
report symptoms as lasting for only ‘a few weeks’ when
they mean ‘worse for a few weeks’. A question like ‘When Symptoms and signs
could you last run for a bus?’ may reveal problems Allergic and nonallergic factors in asthma
stretching back for years. A spouse is often more accurate
Allergic
in this respect than the patient.
• House dust mite
• Animals (especially cats)
Variability of dyspnoea
• Pollens (especially grass)
Questions about variability can be couched as ‘Does it Nonallergic
come and go or is it much the same?’ or ‘Do you have • Exercise
good days and bad days or is it much the same from one • Emotion
day to another?’. A reply suggesting variability is highly • Sleep
characteristic of variable airflow limitation, that is, asthma. • Smoke
If asthma is suspected, this can be followed-up by • Aerosol sprays
questions on aggravating factors. Follow this up with • Cold air
some more directed questions about particular factors. • Upper respiratory tract infections
These are important not only as potentially preventable
causes but because positive replies strengthen the
diagnosis. The house dust mite is the most common
allergen; patients will report worsening of symptoms on
sweeping, dusting or making the beds. Exercise, at least Severity of dyspnoea
in children, is a potent trigger of asthma but exercise will
also make other forms of breathlessness worse. The Severity can be assessed by rating scales, although it is
difference is that in asthma the attack is caused by the much better to use some functional measure. Ask the
exercise, may indeed follow it and may last for 30 min or patient in what way their breathlessness restricts their
more. In other causes of breathlessness, recovery starts activities: can they go upstairs, go shopping, wash the car
as soon as exercise stops. or do the garden? If they are troubled with stairs, how
many flights can they manage? Do they stop half way up
or at the top? Questions about gardening are useful, at
Asthma
least in the summer, as it is possible to grade activity from
Asthma due solely to emotional causes probably does not pulling out a few weeds to digging the potato patch. It is
exist; nonetheless, most patients who have asthma are important to be certain that any restriction is caused by
worse if emotionally upset. Patients may feel that breathlessness and not some other disability (e.g. an
admitting to stress is respectable when they would deny arthritic hip or angina).
other emotions. Nocturnal asthma is very common. Few
Orthopnoea and paroxysmal nocturnal dyspnoea
asthmatics smoke because they know it makes them
worse. Ask what happens if they go into a smoky room. Orthopnoea and paroxysmal nocturnal dyspnoea need
Many will say they are unable to do so because of the special consideration. Both are usually regarded as
effects of the smoke. The response to household aerosol manifestations of left ventricular failure, yet this
sprays can be helpful. Many breathless patients with a is an oversimplification. Orthopnoea is defined as
variety of illnesses will think it logical, rightly or wrongly, breathlessness lying flat but relieved by sitting up. It is
that ‘dust’ or ‘fumes’ will make them worse but only common in patients with severe fixed airways obstruction,
true asthmatics seem to notice a deterioration with the as in some chronic bronchitics who may admit to not
ubiquitous domestic spray can. having slept flat for years. Normal people, when they lie
114
Chapter
flat, breathe more with the diaphragm and less with the ketosis or renal failure may produce tachypnoea which
chest wall. In patients with airways obstruction, the may be felt as dyspnoea. Many patients think that if they
diaphragm is often flat and inefficient and may even draw are short of breath, they must be short of oxygen. This is
the ribs inwards rather than out. Thus, when they lie sometimes the case but, as mentioned earlier, hypoxia
down the diaphragm cannot provide the ventilation only stimulates respiration when relatively severe. To
required. illustrate the distinction between hypoxia and dyspnoea,
The term paroxysmal nocturnal dyspnoea is self- consider that many patients with airflow limitation from
explanatory and is a feature of pulmonary oedema from chronic bronchitis have hypoxia severe enough to cause
left ventricular failure. However, many asthmatics develop right-sided heart failure, yet they have relatively little
bronchoconstriction in the night and wake with wheeze dyspnoea (blue bloaters). In contrast, some patients with
and breathlessness very similar to the symptoms of left emphysema seem to need to keep their blood gases
ventricular failure. In contrast, patients with severe fixed normal by a heroic effort of breathing (pink puffers); they
flow limitation usually sleep well even if they do have to are very dyspnoeic.
be propped up.
The hyperventilation syndrome COUGH
Cough arises from the cough receptors in the pharynx,
The hyperventilation syndrome is more common than
larynx and bronchi; it, therefore, results from irritation of
is generally realised but produces a distinct pattern of
these receptors from infection, inflammation, tumour
symptoms. It is usually associated with anxiety and
or foreign body. Cough may be the only symptom in
patients overbreathe inappropriately. The initial complaint
asthma, particularly childhood asthma. Cough in children
is often, although not always, of breathlessness. The
occurring regularly after exercise or at night is virtually
hyperventilation is the response to this sensation. It may
diagnostic of asthma. Many smokers regard cough as
be described by the patient as a ‘difficulty in breathing
normal: ‘only a smoker’s cough’ or may deny it completely
in’ or an inability to ‘fill the bottom of the lungs’. The
despite having just coughed in front of the examiner. In
hyperventilation induces a reduction in the PCO2, creating
these patients, a change in the character of the cough can
a variety of other symptoms: paraesthesiae in the fingers,
be highly significant.
tingling around the lips, ‘dizziness’, ‘lightheadedness’
Patients can often localise cough to above the larynx
and sometimes frank tetany. Chest pain is the probable
(‘a tickle in the throat’) or below. Postnasal drip from
consequence of increased chest wall movement. The
rhinitis can cause the former and may be accompanied
onset is often triggered by some life event; especially
by sneezing and nasal blockage.
work related (e.g. redundancy or dismissal). The diagnosis
Laryngitis will cause both cough and a hoarse voice.
can be confirmed by asking the patient to take 20 deep
Recurrent laryngeal nerve palsy causes a hoarse voice and
breaths, which will reproduce the symptoms.
an ineffective cough because the cord is immobile. The
usual cause is involvement of the left recurrent laryngeal
Symptoms and signs nerve by tumour in its course in the chest. Cough from
Features suggestive of the hyperventilation tracheitis is usually dry and painful. Cough from further
syndrome down the airways is often associated with sputum
production (bronchitis, bronchiectasis or pneumonia).
• Breathlessness at rest
In the latter, associated pleurisy makes coughing very
• Breathlessness as severe with mild exertion as with
distressing and reduces its effectiveness. Other possibilities
greater exertion
are carcinoma, lung fibrosis and increased bronchial
• Marked variability in breathlessness
responsiveness (this is an inflammatory condition of the
• More difficulty breathing in than out
airways, thought to be part of the mechanism underlying
• Paraesthesiae of the fingers
asthma and often made worse by the factors listed in the
• Numbness around the mouth
‘symptoms and signs’ box on allergic and nonallergic
• ‘Lightheadedness’
factors in asthma). A cause of cough, which is often
• Feelings of impending collapse or remoteness from
overlooked, is aspiration into the lungs from gastro-
surroundings
oesophageal reflux or a pharyngeal pouch. Cough will
• Chest wall pain
then follow meals or lying down. Prolonged coughing
bouts can cause both unconsciousness from reduction of
venous return from the brain (cough syncope) and also
Dyspnoea and hypoxia vomiting. Sometimes the history of cough is omitted,
making diagnosis difficult!
Dyspnoea should be distinguished from tachypnoea
(increased rate of breathing) and from hypoxia. It is a
symptom, not a sign, and is not necessarily an indication SPUTUM
of lung disease. Psychological factors, such as the Patients may understand the term ‘phlegm’ better than
hyperventilation syndrome, and acidosis from diabetic sputum. It is the result of excessive bronchial secretion;
115
Chapter
itself a manifestation of inflammation and infection. Like Sticky ‘rusty’ sputum is characteristic of lobar
cough, smokers may not acknowledge its existence. pneumonia, and frothy sputum with streaks of blood is
Children usually swallow their sputum. It is essential to seen in pulmonary oedema.
be certain that the complaint relates to the chest, because Highly viscous sputum, sometimes with plugs, is
some patients have difficulty in distinguishing sputum characteristic of asthma and in some patients with chronic
production from gastrointestinal reflux, postnasal drip or bronchitis. Small bronchial casts, like twigs, may be
saliva. Sometimes asking the patient to ‘show me what described by a patient with the condition of
you have to do to get phlegm up’ can be helpful. If the bronchopulmonary aspergillosis associated with asthma.
patient denies sputum, a cough producing a rattle (a
‘loose cough’) suggests that it is present.
HAEMOPTYSIS
Sputum caused by chronic irritation is usually white or
grey, particularly in smokers; if infected, it becomes The coughing up of blood is often a sign of serious lung
yellow from the presence of leucocytes and this may turn disease. Nevertheless, it is common in trivial respiratory
to green by the action of the enzyme verdoperoxidase. infections. Like sputum production, it is essential to
Yellow or green sputum in asthma can be caused by the establish that it is coming from the lungs and not the
presence of eosinophils rather than infection. Questions nose or mouth or being vomited (haematemesis).
on frequency are most useful in the diagnosis of chronic Bleeding from the nose may run into the pharynx and be
bronchitis, an epidemiological definition of this is ‘sputum coughed out but usually the patient will also describe
production on most days for three consecutive months bleeding from the anterior nares. Bleeding in the mouth
for two successive years’. Sputum production is common causes confusion, it is usually related to brushing the
in asthmatics and is occasionally the main complaint. The teeth (gingivitis).
diagnosis of bronchiectasis is made on a story of daily The blood in haemoptysis is usually bright red at
sputum production stretching back to childhood. first, then followed by progressively smaller and darker
Patients can often give an estimate of the amount amounts. This would be unusual in haematemesis.
of sputum they bring up each day, usually in terms of a
cup or teaspoon and so on. Large amounts occur in Differential diagnosis
bronchiectasis and lung abscess and in the rare Haemoptysis
bronchioloalveolar cell carcinoma.
Common
• Infection including bronchiectasis
• Bronchial carcinoma
• Tuberculosis
• Pulmonary embolism and infarction
Sputum • No cause found
White or grey Uncommon
• Smoking • Mitral stenosis and left ventricular failure
• Simple chronic bronchitis • Bronchial adenoma
• Asthma • Idiopathic pulmonary haemosiderosis
Yellow or green • Anticoagulation and blood dyscrasias
• Acute bronchitis
• Acute on chronic bronchitis
• Asthma Differential diagnosis
• Bronchiectasis Pointers to the significance of an episode
• Cystic fibrosis of haemoptysis
Frothy, blood-streaked
• Pulmonary oedema Probably serious
• Middle-aged or elderly
• Spontaneous
• Previous or current smoker
• Recurrent
• Large amount
Questions to ask
Probably not serious
Sputum
• Young
• What colour is the phlegm? • Recent infection
• How often do you bring it up? • Never smoked
• How much do you bring up? • Single episode
• Do you have trouble getting it up? • Small amount – if single episode
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Chapter
All haemoptysis is potentially serious, although the with sleep usually indicates malignant disease involving
most important cause is carcinoma of the bronchus. the chest wall. Moreover, spinal disease and herpes zoster
Repeated small haemoptyses every few days over a period may cause pain in a root distribution round the chest.
of some weeks in a middle-aged smoker is virtually Pleural pain is usually localised accurately by the
diagnostic of bronchial carcinoma. patient, yet if the pleura overlying the diaphragm is
Other serious causes are pulmonary embolism (sudden involved pain may be referred either to the abdomen
onset of pleuritic chest pain and dyspnoea followed by from the costal part of the diaphragm or to the tip of the
haemoptysis), tuberculosis (weight loss, fever, cough and shoulder from the central part because the pain fibres run
sputum) and bronchiectasis (long history of sputum in the phrenic nerve (C3–5). Pain may subside when an
production and the haemoptysis associated with an effusion develops.
exacerbation and increased sputum purulence). Blood- Although the lungs are insensitive to pain, the
tinged sputum in pneumonia and pulmonary oedema mediastinal structures are not. Cancer of the lung and
has already been mentioned. other central lesions produce a dull, poorly localised pain
– presumably from pressure on mediastinal structures.
A third type of pain is a central soreness over the
Risk factors
trachea in acute tracheitis.
Pulmonary embolism
• Previous DVT or PE WHEEZE AND STRIDOR

• Surgery
Wheeze
• Immobility, especially stroke and heart failure
• Malignancy Most patients will understand wheeze as a high-pitched
• Pregnancy whistling sound, although some require a demonstration
• Leg trauma by the doctor before they recognise it. It occurs in both
• Haematological abnormalities inspiration and expiration but is always louder in the
latter. Spouses sometimes pick this up better than
patients, particularly if the wheeze is mainly at night. It
implies airway narrowing and is, therefore, common in
asthma and chronic obstructive bronchitis. In asthma, the
PAIN wheeze is episodic and clearly associated with shortness
The lungs and the visceral pleura are devoid of pain of breath, fulfilling the definition of ‘variable wheezy
fibres, whereas the parietal pleura, chest wall and breathlessness’. Nevertheless, some asthmatics may have
mediastinal structures are not. The characteristic ‘pleuritic little wheeze and acute severe attacks can be associated
pain’ is sharp, stabbing, worse on deep breathing and with a ‘silent chest’. In chronic obstructive bronchitis
coughing and arises from either pleural inflammation or and emphysema, the associations are less clear-cut, with
chest wall lesions. Pain from the pleura is caused by the wheeze, shortness of breath, cough and sputum occurring
two pleural surfaces rubbing together. The pain may in various proportions.
interfere with breathing: ‘I have to catch my breath’.
Stridor
Inflammation of the pleura occurs chiefly in pneumonia
and pulmonary infarction from pulmonary emboli. Stridor is a harsh inspiratory and expiratory noise which
Pneumothorax can produce acute transient pleuritic can be imitated by adducting the vocal cords and
pain. breathing in and out. It is often more evident to the
Most pains from the chest wall are caused by localised observer than the patient.
muscle strain or rib fractures (persistent cough can cause
the latter). These pains are often worse on twisting or
turning or rolling over in bed; an uncommon feature of OTHER IMPORTANT POINTS IN THE HISTORY
other disease. Bornholm disease is thought to be a viral
Other body systems
infection of the intercostal muscles and produces very
severe pain. True pleuritic pain is often accompanied by The lungs do not exist in isolation from the rest of the
a pleural rub; this is absent in chest wall pain but there body. Lung disease can affect other structures, and
may be striking local rib tenderness reproducing the disease elsewhere can affect the lungs. The closest
symptoms. Unfortunately, this is not entirely reliable, for relationships are naturally with the heart. Lung disease
pleurisy can be associated with local tenderness. A can affect the right side of the heart (cor pulmonale). An
particular type of chest wall pain is caused by swelling of early manifestation is peripheral oedema (ankle swelling),
one or more of the upper costal cartilages (Tietze’s which is likely to be accompanied by a raised jugular
syndrome); however, this is rare and it is much more venous pressure and an enlarged liver. Disease of the left
common to find tenderness without swelling. Severe heart causes pulmonary oedema (orthopnoea, paroxysmal
constant pain not related to breathing but interfering nocturnal dyspnoea, cough and frothy sputum). Diseases
117
Chapter
of other systems that affect the lungs include rheumatoid PREVIOUS DISEASE
arthritis, other connective tissue disease (scleroderma A history of tuberculosis may explain abnormal shadowing
and dermatomyositis), immune deficiency syndromes on a chest radiograph. Current symptoms may be caused
(including AIDS) and renal failure. A variety of by relapse, especially if the patient was treated before
neuromuscular diseases and skeletal problems affect the the start of the antibiotic era (1950). Some operations
mechanics of breathing. for tuberculosis from those days (thoracoplasty and
Weight loss is an important manifestation of lung phrenic crush) produce lifelong chest or radiographic
carcinoma, although by the time it occurs there are deformity. Bronchial damage from tuberculosis can lead
usually metastatic deposits in the liver. Less well known to bronchiectasis.
as a cause is chronic airflow limitation, presumably from BCG vaccination reduces the risk of tuberculosis but
the increased respiratory effort impairing appetite and one degree of protection is disputed. In some areas in the
diverting calories to the respiratory muscles. Chronic UK it is performed at school at the age of 12 or 13 years.
infection, particularly tuberculosis, causes weight loss. Babies born to immigrant mothers often receive it at
Gain in weight may be a cause of increased dyspnoea and birth. For children, tuberculin testing to assess sensitivity
sleep apnoea (see below). One cause is steroid therapy is performed first. A history of these procedures helps in
for lung disease (iatrogenic Cushing’s syndrome). the assessment of a possible case of tuberculosis.
Fever must be distinguished from feeling hot or A history of wheeze in childhood suggests asthma.
sweating and generally implies infection, particularly This may have gone into remission and been forgotten
pneumonia or tuberculosis. Less commonly, it is caused only to occur in later life. Whooping cough or pneumonia
by malignancy or connective tissue disease affecting the in childhood may lead to bronchiectasis and patients may
lungs. If pulmonary embolism is suspected, pain or have been told by their parents that their problems started
swelling in the legs suggests a deep venous thrombosis. with such an episode.
Sleep Chest injuries, operations or pneumonia can all lead
to permanent radiographic changes which otherwise
Sleep disturbance may be caused by pain, breathlessness
would be very difficult to explain. Previous radiographs
and cough from airways obstruction or from depression.
can be invaluable in these circumstances and may be
In the sleep apnoea syndrome, patients are aroused
available. ‘Health checks’ may have included chest
repeatedly in the night from obstruction of the upper
radiography. Many patients will have had chest
airways. The cause is not always clear but obesity is very
radiography before an operation.
common and hypertrophied tonsils often contribute.
Sudden obstruction leads to greater and greater inspiratory
efforts by the patient who, in a half-awake state, will SOCIAL HISTORY
thrash around and eventually overcome the obstruction
Smoking
to the accompaniment of loud snoring noises. This may
be repeated many times during the night. Wives (the The importance of enquiry about smoking in lung disease
patients are usually men) will describe this in graphic can hardly be overemphasised (Figs 5.23, 5.24). Smoking
detail! The poor quality of sleep leads to daytime is, for practical purposes, the cause of chronic bronchitis
somnolence and the carbon dioxide retention to morning and carcinoma of the bronchus and neither diagnosis is
headaches. likely to be correct in a lifelong nonsmoker. Patients seem
Many diseases of the respiratory system produce to be generally accurate about their tobacco consumption
lasting disability and some are fatal. Therefore, depression contrasting sometimes with alcohol.
and anxiety are to be expected and may influence the It is important not to appear censorious when enquiring
history. about smoking. Tobacco is highly addictive and most
patients would give up if only they could and are not
being perverse when they continue despite evidence of
lung damage. You should be aware that some patients
claim to be nonsmokers when they only stopped last
Symptoms and signs
month, last week or even on the way to hospital! Ask
Clinical features suggesting the sleep
apnoea syndrome
nonsmokers: ‘Have you smoked in the past?’. The risk of
disease increases with the amount smoked. Cigarettes
• Excessive daytime somnolence are the most dangerous; pipes and cigars are not free of
• Intellectual deterioration and irritability risk. Risk declines steadily when smoking stops; it takes
• Early morning headaches 10–20 years for the risk of lung cancer to equal that of
• Snoring lifelong nonsmokers.
• Restless nights Inhalation of another person’s smoke at home or at
• Social deterioration (e.g. job, marriage, driving work is increasingly recognised as a factor in lung disease.
difficulties) This is particularly true for asthma. Children in households
with smokers have more respiratory infections.
118
Chapter
100 Pets and hobbies

For many asthmatics, cats and dogs are common sources
80 Japan
of allergen. The allergen may remain in the house long
(percentage of smokers) after the offending animal has been banished.
60 Exposure to racing pigeons, budgerigars, parrots and
UK
male
other caged birds can cause extrinsic allergic alveolitis.

The cause is protein material derived from feathers and
40
USA droppings. Acute symptoms are usually seen in pigeon
fanciers who, a few hours after cleaning out their birds,
20 develop cough, breathlessness and ‘flu-like’ symptoms.
Recovery takes place over the next day or two unless
0 there is re-exposure. Chronic symptoms are seen in
1960 1970 1980 1990 2000 budgerigar owners, presumably because they are exposed
year
continuously to low doses of antigen. Their complaint is
60
(percentage of smokers)
of progressive breathlessness.
UK Parrots and related species transmit the infectious
40 agent of psittacosis, a cause of pneumonia. You may need
female
USA
to extend your enquires beyond the home because
20 patients may be exposed to birds belonging to friends and
Japan relations.
0 Occupation
1960 1970 1980 1990 2000
year The question ‘What work do you do?’ is more important
Fig. 5.23 Smoking trends in selected countries, based on data from for respiratory disease than for any other. The nature of
the World Heath Organization. the job and not just the title is important because the
latter may convey no meaning to you at all. The question
is important in two ways. Respiratory disease may affect
Mortality ratios and smoking
a patient’s ability to perform a job but may also be the
result of the occupation. Any job involving exposure to
mortality noxious agents of a respirable size is potentially damaging;
ratio the most obvious example is pneumoconiosis in coal
3
miners.
Risk factors
2
Some occupational causes of lung disease
Occupation Agent Disease
1 Mining Coal dust Pneumoconiosis
Quarrying Silica dust Silicosis
Foundry work Silica dust Silicosis
0 Asbestos (mining, Asbestos fibres Asbestosis
s
rs
er
heating, building, Mesothelioma

ok
ok
0
9
m
–2
–3
m
+
9
demolition, ship Lung cancer

ns
ls
10
21
40
1–
no
al
building)
cigarette consumption per day
Farming Actinomycetes Alveolitis
Fig. 5.24 Mortality ratios and smoking. Paint spraying Isocyanates Asthma
Plastics manufacture Isocyanates Asthma
Soldering Colophony Asthma
Risk factors
Enquiry may need to be searching and, if occupational
Lung cancer
lung disease is suspected, then a full list of all jobs
• Smoking performed will need to be constructed. For example, in
• Atmospheric pollution the case of asbestos there can be an interval of 30 years
• Asbestos exposure between exposure, say in shipyard work, and the
• Radon exposure (natural and occupational) development of asbestosis or mesothelioma. Some will
• Work in gas and coke industry deny working with asbestos but nevertheless were
exposed when others were performing lagging (putting
119
Chapter
asbestos on pipes) or stripping (taking it off). Other that this is now becoming more common in the
occupations in which exposure may not be obvious, heterosexual population, especially in individuals who
although real nonetheless, are building and demolition have travelled abroad, particularly to Africa and Asia.
work, electrical repair work, railway engineering and gas
mask and cement manufacture. Environmental exposure,
DRUG HISTORY
including that of wives of asbestos workers, seems
important occasionally. The most useful questions are those concerning past
The easiest way to diagnose pneumoconiosis is to ask treatment. Successful use of bronchodilators and
the patient. Miners in the UK undergo regular chest corticoids in airways obstruction will indicate asthma.
radiography while working. If significant pneumoconiosis Aspirin and sometimes other nonsteroidal anti-
is diagnosed the patient will be told. inflammatory drugs and β-adrenergic receptor blockers
can make asthma worse, and angiotensin-converting
Occupational asthma enzyme inhibitors cause chronic dry cough. Steroid
The list of causes of occupational asthma grows longer therapy predisposes to infections, including
yearly. A good screening question to any asthmatic is: tuberculosis.
‘Does your work make any difference to your symptoms?’.
Follow this up with questions about improvement at PATIENT PERSPECTIVE
weekends or on holiday. The latter is important because
symptoms caused at work may not be manifest until the Many lung conditions are chronic and most of these
evening or night and sometimes changes take place over are progressive. It is therefore particularly important
days or even weeks. to understand patients’ reactions to the prospect of
Common causes are isocyanates (paint hardeners increasing disability and sometimes death. Ask about
and plastic manufacture) and colophony (soldering and patients’ hopes and fears for the future and how the
electronics). The lack of an obvious culprit should not put disease is affecting their lives and that of their families.
you off the scent if the evidence is otherwise suggestive.
Much detective work is necessary in individual cases.
Extrinsic allergic alveolitis General examination
Extrinsic allergic alveolitis can be caused by occupation Examination starts on first encounter. You should be able
as well as by exposure to birds. The best example is to continually pick up and store clues while talking and
farmer’s lung: the agent is the microorganism thermophilic listening to the patient. As with all body systems, a good
actinomycetes contaminating stored damp hay. The story look at the patient as a whole will provide important
is of shortness of breath, cough and chills a few hours evidence that will be missed in a rush to lay a stethoscope
after forking out fodder for cattle in the winter. Other on the chest. Your findings should be divided into first
occupations with similar risks are mushroom workers, impressions, then a more directed search for signs outside
sugar workers (bagassosis – mouldy sugar cane), the chest likely to be helpful in lung disease and, finally,
maltworkers and woodworkers, although the antigens examination of the chest itself.
vary in each case. There are a number of circumstances when the
examination may have to be focused on particular areas
rather than attempting a comprehensive examination.
FAMILY HISTORY
This may be because the patient is too unwell or because
The most common lung disease with a genetic basis is the history only requires a specific confirmatory sign, say
asthma, although the development of the disease in an the presence or absence of wheeze. It may be difficult
individual is much more complicated. A family history of to undress some patients fully, particularly in primary
asthma and the related conditions of hay fever or eczema care.
are often found but these diseases are so prevalent
that enquiry beyond the immediate family is of little
value. Other diseases that run in the family include cystic FIRST IMPRESSIONS
fibrosis and α1-antitrypsin deficiency, a rare cause of How breathless does the patient appear? Is it consistent
emphysema. with the story? If seen in the clinic or office, can the
Tuberculosis is usually passed on within families. In patient walk in comfortably and sit down or does the
the UK, tuberculosis is common in Asian and African patient struggle to get in? Perhaps the patient is in a
migrants, particularly in their first 10 years in the country, wheelchair; if so, is it because of breathing troubles or
and in individuals who have revisited the subcontinent. something else? Can the patient carry on a conversation
Most of the increased incidence of the disease seen in with you or do they break up their sentences? How
recent years has occurred in conditions of poverty. breathless is the patient when getting undressed? Details
Enquiry into sexual habits will be necessary if the of breathing patterns are considered later but is the
illness could be a manifestation of AIDS, remembering patient obviously distressed or quite comfortable? Is
120
Chapter
there stridor or wheeze? Is there cough, confirming or the nail from the side against a white background, say
perhaps at variance with the history? Is there evidence of the bedsheets. Not surprisingly, there can be considerable
weight loss suggesting carcinoma or weight gain from disagreement about the presence or absence of clubbing
steroid therapy? in the early stages. When normal nails are placed ‘back
Do not ignore clues around the patient. An air to back’ there is usually a diamond-shaped area between
compressor by the bed will be used to deliver bronchodilator them. This is obliterated early in clubbing (Fig. 5.27).
drugs. A packet of cigarettes in the pyjama jacket will In the next stage, the normal longitudinal curvature
have the opposite effect. In hospital you will be deprived of the nail increases. Some normal nails have a
of some of these features but not how the patient is pronounced curve but in clubbing the increase in soft
positioned – does the patient have to sit up to breathe tissue in the nail beds needs to be present as well. In the
(confirming a history of orthopnoea)? Is the patient final stage, the whole tip of the finger becomes rounded
receiving oxygen? (a club) (Fig. 5.28). Clubbing less commonly affects the
After extracting as much information as you can, if it toes.
is feasible and appropriate position the patient comfortably The pathogenesis of clubbing is unknown. There is
on the bed or couch with enough pillows to support increased vascularity and tissue fluid and this seems to
the chest at an angle of approximately 45° and begin the be under neurogenic control because it can be abolished
formal examination. This can conveniently start with the by vagotomy.
hands and a search for clubbing. Clubbing is sometimes associated with hypertrophic
pulmonary osteoarthropathy; this presents with pain in
Clubbing
the joints – particularly the wrists, ankles and knees.
This refers to an increase in the soft tissues of the nail The pain is not in the joint itself but over the shafts of
bed and the finger tip. The earliest stage is some softening the long bones adjacent to the joint. It is caused by
of the nail bed which can be detected by rocking the nail subperiosteal new bone formation, which can be seen
from side to side on the nail bed (Fig. 5.25). This sign can on a radiograph (Fig. 5.29). The condition is almost
be present to some extent in normal individuals but is invariably associated with clubbing, although it can
exaggerated in the early stages of clubbing. Next, the soft occur alone. Any cause of clubbing can also cause
tissue of the nail bed fills in the normal obtuse angle hypertrophic pulmonary osteoarthropathy; however, it is
between the nail and the nail bed. This is usually usually associated with a squamous carcinoma of the
approximately 160° but the area becomes flat, even bronchus. The condition is often mistaken for arthritis,
convex in clubbing (Fig. 5.26). This is seen best by viewing with consequent delay in diagnosis. Successful treatment
Fig. 5.25 Rocking the nail on the nail bed Fig. 5.26 Mild clubbing. The nail on the left shows obliteration of the angle at the nail fold
in clubbing. compared with a normal nail on the right.
Fig. 5.27 Clubbing, showing how the diamond-shaped area formed between two normal Fig. 5.28 Gross clubbing.
nails (left) is obliterated (right).
121
Chapter
periosteal
bone
Fig. 5.29 Hypertrophic pulmonary osteoarthropathy.
Some common causes of clubbing
Pulmonary
• Bronchial carcinoma Fig. 5.30 Cyanosis in a patient with chronic airflow limitation.
• Chronic pulmonary sepsis
– empyema
– lung abscess produce cyanosis, even though there is enough oxygenated
– bronchiectasis haemoglobin to maintain a normal oxygen-carrying
– cystic fibrosis capacity.
• Cryptogenic fibrosing alveolitis Cyanosis can be divided into central and peripheral
• Asbestosis varieties. Central cyanosis is caused by disease of the
Cardiac heart or lungs and the blood leaving the left heart
• Congenital cyanotic heart disease is blue. Peripheral cyanosis is caused by decreased
• Bacterial endocarditis circulation and increased extraction of oxygen in the
Other peripheral tissues. Blood leaving the left heart is
• Idiopathic/familial normal.
• Cirrhosis Central cyanosis Although the whole patient may
• Ulcerative colitis appear cyanosed, the best place to look is the mucous
• Coeliac disease membranes of the lips and tongue (Fig. 5.31). Good
• Crohn’s disease natural light is best. Any severe disease of the heart and
lungs will cause central cyanosis but the most common
causes are severe airflow limitation, left ventricular failure
and pulmonary fibrosis.
of the cause will relieve clubbing and the pain of
hypertrophic pulmonary osteoarthropathy. While Peripheral cyanosis Here, the peripheries, the fingers
searching for clubbing, note any nicotine staining of the and the toes, are blue with normal mucous membranes.
fingers. The usual cause is reduced circulation to the limbs, as
seen in cold weather, Raynaud’s phenomenon or
Cyanosis
peripheral vascular disease. The peripheries are also
Cyanosis, a bluish tinge to the skin and mucous usually cold. There may be an element of peripheral
membranes, is seen when there is an increased amount cyanosis in heart failure when the perfusion of the
of reduced haemoglobin in the blood (Fig. 5.30). extremities is reduced.
Traditionally, it is thought to become visible when there Cyanosis can rarely be caused by the abnormal
is approximately 5 g/dl or more of reduced haemoglobin, pigments methaemoglobin and sulphaemoglobin.
corresponding to a saturation of approximately 85%; Arterial oxygen tension is normal.
however, there is a good deal of interobserver variation.
Tremors and carbon dioxide retention
Severe anaemia and cyanosis cannot coexist otherwise
most of the haemoglobin would be reduced. Conversely, The most common tremor in patients with respiratory
in polycythaemia, in which there is an increase in red cell disease is a fine finger tremor from stimulation of
mass, there may be enough reduced haemoglobin to β-receptors in skeletal muscle by bronchodilator
122
Chapter
Fig. 5.32 Superior vena caval obstruction showing a swollen face

and neck, dilated veins over the trunk and the site of a lymph node
biopsy.
fibrosis. The tumour compresses the superior vena cava

Fig. 5.31 Central cyanosis of the tongue. near the point where it enters the right atrium. The
resulting high pressure in the superior vena cava causes
distension of the neck, fullness and oedema of the face,
drugs. Carbon dioxide retention is seen in severe chronic dilated collateral veins over the upper chest (Fig. 5.32)
airflow limitation. Clinically, it can be suspected by a and chemosis or oedema of the conjunctiva. The internal
flapping tremor (indistinguishable from that associated jugular vein is, of course, distended but may be difficult
with hepatic failure), vasodilatation manifested by to see because it does not pulsate (the ‘dog-in-the-night-
warm peripheries, bounding pulses, papilloedema and time’ syndrome). The external jugular vein should be
headache. visible. The patient may have noticed that shirt collars
have become tighter.
Pulse and blood pressure
Lymphadenopathy
Pulsus paradoxus is a drop in blood pressure on
inspiration. A minor degree occurs normally. Major Lymph nodes may enlarge either because of generalised
degrees occur in pericardial effusion and constrictive disease (e.g. lymphoma) or from local disease spreading
pericarditis but also in severe asthma. However, it through the lymphatics to the nodes. Both may be
probably adds nothing to other measures of severe important in respiratory disease. Palpation of lymph
asthma. For further discussion see Chapter 6. nodes is considered in Chapter 2, so here the examination
of only those lymph nodes draining the chest is
Jugular venous pulse and cor pulmonale
considered.
The jugular venous pulse may be raised in cor pulmonale Lymphatics from the lungs drain centrally to the hilum
(right-sided heart failure due to lung disease). The then up the paratracheal chain to the supraclavicular
common cause in the UK is chronic airflow limitation (scalene) or cervical nodes. Chest wall lymphatics,
leading to hypoxia. The main mechanism is pulmonary especially from the breasts, drain to the axillae. Lung
vasoconstriction. Other signs are peripheral oedema disease, therefore, rarely involves the axillary nodes.
(probably as much due to renal hypoxia as back Examination of the cervical chain can be carried out by
pressure from the right heart), hepatomegaly and a palpation from the front of the patient. Supraclavicular
left parasternal heave, indicating right ventricular lymphadenopathy is best detected from behind the
hypertrophy. In severe cases, functional tricuspid patient by placing your fingers either side of the neck
regurgitation will lead to a pulsatile liver, large V waves behind the tendon of the sternomastoid muscle. It helps
in the jugular venous pulse and a systolic murmur in the if the neck is bent slightly forward (Fig. 5.33). Cervical
tricuspid area (see Ch. 6). Sometimes overinflation of the nodes can be palpated this way too.
lungs will displace the liver downwards and also obscure It is sometimes difficult to examine in the supraclavicular
the cardiac signs, leaving the jugular venous pulse as the area because lymph nodes may be only slightly enlarged.
only sign. If palpable, the nodes are usually the site of disease.
Obstruction of the superior vena cava is a common Careful comparisons should be made between the two
presentation of carcinoma of the bronchus but can rarely sides. If lymph nodes are enlarged then biopsy or
be caused by lymphoma, benign tumours and mediastinal aspiration may be a simple way to confirm a diagnosis.
123
Chapter
Beware of performing a cervical node biopsy too readily. metastatic carcinoma are hard and fixed. Tuberculous
Throat cancer can involve these nodes and painstaking nodes, common in Asian patients in the UK, are soft and
block dissection is the correct treatment. matted and may have discharging sinuses. Healing and
Respiratory diseases that involve these nodes are calcification leave small hard nodes.
carcinoma, tuberculosis and sarcoidosis. Nodes containing Examination of the axillary nodes is shown in Figure
5.34. Abduct the patient’s arm, place the fingers of your
hand high up in the axilla, press the tips of the fingers
against the chest wall, relax the patient’s arm and draw
your fingers downwards over the ribs to roll the nodes
Common respiratory causes of supraclavicular
lymphadenopathy between your fingers and the ribs.
• Lung cancer
• Lymphoma Skin
• Tuberculosis The early stages of sarcoidosis and primary tuberculosis
• Sarcoidosis are often accompanied by erythema nodosum (Fig. 5.35):
• HIV infection painful red indurated areas usually on the shins; although
occasionally more extensive, they fade through bruising.
Severely affected patients may also have arthralgia.
Sarcoidosis can also involve the skin, particularly old
scars and tattoos, with nodules and plaques. Lupus pernio
is a violaceous swelling of the nose from involvement by
sarcoid granuloma.
Eyes
Horner’s syndrome [miosis (contraction of the pupil),
enophthalmos (backward displacement of the eyeball in
the orbit), lack of sweating on the affected side of the face
and ptosis (drooping of the upper eyelid; see also Chapter
11)] is usually due to involvement of the sympathetic
chain on the posterior chest wall by a bronchial
carcinoma.
Sarcoidosis and tuberculosis can cause iridocyclitis.
Fig. 5.33 Palpation of the supraclavicular lymph nodes from Miliary tuberculosis can produce tubercles visible
behind. on the retina by ophthalmoscopy. Papilloedema can
Fig. 5.34 Palpation of the axillary lymph nodes. Fig. 5.35 Erythema nodosum, showing
raised red lumps on the shins.
124
Chapter
Examination of the chest 5
Fig. 5.36 ‘Barrel chest’. Note the increased Fig. 5.37 Pectus excavatum, showing the depressed sternum.
anteroposterior diameter of the chest.
Erythema nodosum
Infections
• Streptococci
• Tuberculosis
• Systemic fungal infections
• Leprosy
Others
• Sarcoidosis
• Ulcerative colitis
• Crohn’s disease
• Sulphonamides
• Oral contraceptive pill and pregnancy
be caused by carbon dioxide retention and cerebral

metastases. Fig. 5.38 Thoracoplasty with secondary changes in the spine.
Examination of the chest

Barrel chest is seen in states of chronic airflow limitation,
You should follow the classical sequence of inspection, with the degree of deformity correlating with its
palpation, percussion and auscultation, not forgetting severity.
contemplation (Osler). In pectus excavatum (‘funnel chest’; Fig. 5.37), the
sternum is depressed. The condition is benign and
needs no treatment but can produce unusual chest
INSPECTION OF THE CHEST WALL radiographic appearances, with the heart apparently
First look for any deformities of the chest wall. In ‘barrel enlarged and displaced to the left. In pectus carinatum
chest’ the chest wall is held in hyperinflation (Fig. 5.36). (‘pigeon chest’), the sternum and costal cartilages project
In normal people the anteroposterior diameter of the outwards. It may be secondary to severe childhood
chest is less than the lateral diameter but in hyperinflation asthma.
the anteroposterior diameter may be greater than the Examine the chest wall for any operative scars or the
lateral. The amount of trachea palpable above the changes of thoracoplasty. This was an operation performed
suprasternal notch is reduced. The normal ‘bucket handle’ in the 1940s and 1950s for tuberculosis and designed to
action of the ribs moving upwards and outwards, pivoting reduce the volume of the chest. It can produce marked
at the spinous processes and the costal cartilages, is distortion of the chest wall, more clearly seen from the
converted into a ‘pump handle’ up-and-down motion. back (Fig. 5.38).
125
Chapter
Emergency
Signs of asthma in adults
Signs of acute severe asthma in adults

• Unable to complete sentences
• Pulse >110 beats/min
• Respirations >25 breaths/min
• Peak flow <50% predicted or best
Signs of life-threatening asthma in adults
• Silent chest
• Cyanosis
• Bradycardia
• Exhaustion
• Peak flow <33% predicted or best
• SpO2 <92%, PaO2 <8 Kpa
Fig. 5.39 Kyphoscoliosis. acidosis from renal failure, diabetic ketoacidosis and
aspirin overdosage will have deep sighing (Kussmaul)
respirations as they try to excrete carbon dioxide. Acute
massive pulmonary embolism gives a similar pattern.
Flattening of part of the chest can be due either to Is the breathing regular? Cheyne–Stokes respiration is
underlying lung disease (which usually has to be a waxing and waning of the respiratory depth over a
longstanding) or to scoliosis. minute or so from deep respirations to almost no
Kyphosis is forward curvature of the spine and scoliosis breathing at all. It is thought to be caused by a failure of
is a lateral curvature (Fig. 5.39). Both, but scoliosis in the central respiratory control to respond adequately to
particular, can lead to respiratory failure. changes in carbon dioxide and is often seen in patients
Air in the subcutaneous tissue is termed surgical with terminal disease. Patients may seem unaware of the
emphysema, although it is as commonly associated with condition.
a spontaneous pneumothorax as trauma to the chest. The Is there any prolongation of expiration? The typical
tissues of the upper chest and neck are swollen, sometimes patient with airflow limitation has trouble breathing out.
grossly so (Michelin man), although the condition is not Inspiration may be brief, even hurried, but expiration is
dangerous in itself. The tissues have a characteristic a prolonged laboured manoeuvre. Many of these patients
crackling sensation on palpation. In pneumothorax, the breathe out through pursed lips as if they were whistling;
air probably tracks from ruptured alveoli, through the this mechanism maintains a higher airway pressure and
root of the lungs to the mediastinum, thence up into keeps open the distal airways to allow fuller although
the neck. On auscultation of the precordium, you may longer expiration.
hear a curious extra sound in time with the heart Note if the chest expands unequally. If this is so and
(mediastinal crunch) but this can occur in pneumothorax there is no structural abnormality of the chest or spine to
without pneumomediastinum. Mediastinal air may be account for it, then air is probably not entering the lung
visible on a radiograph. so well on the affected side. The difference has to be
marked to be appreciated. The causes will be considered
under palpation. It is possible to measure overall
BREATHING PATTERNS expansion with a tape-measure (the result is of little value
A good deal can be learnt from simple observation of the and certainly no substitute for measures of lung volume).
chest wall movements. Note rate, depth and regularity. Breathing mainly from the diaphragm suggests chest
Does the chest move equally on the two sides? Does wall problems (e.g. pleural pain, ankylosing spondylitis).
breathing appear distressing? Is it noisy? Breathing mainly with the rib cage suggests diaphragm
Counting the respiratory rate is often neglected and paralysis, peritonitis or abdominal distension. Normally,
the precise rate is rarely of practical importance. However, as the diaphragm descends in inspiration the anterior
changes can be of great help in the absence of other abdominal wall will move outwards. If it moves inwards
information. You should note an increase in rate or depth. (abdominal paradox) then the diaphragm is probably
An increase in rate may occur in any severe lung disease paralysed. Similarly, in tetraplegia, when the chest
and in fever and sepsis. Patients with hyperventilation wall muscles are paralysed but phrenic nerve function
may breathe both faster and more deeply, although the preserved, descent of the diaphragm produces indrawing
increase can be subtle and easily missed. Patients with of the chest wall (chest wall paradox).
126
Chapter
Is the patient distressed by breathing? Can the patient

carry on a normal conversation or does he or she have to
break up sentences, even perhaps to single words at a
time? Patients with severe respiratory distress use their
accessory muscles of respiration. They fix the position of
the shoulder girdle by pressing the hands on the nearest
fixed object and throw back their heads. This gives a
purchase for accessory muscles of respiration, mainly the
sternomastoids.
Does the patient breathe more comfortably in certain
positions? Can the patient lie flat or does he or she have
to be propped up? Patients with pulmonary oedema and
severe airflow limitation will be unable to lie down for
long but then most patients with breathing difficulty
are more comfortable sitting up. Is breathing audible?
Wheeze is a prolonged expiratory noise often audible to
the patient as well as the doctor and implies airflow Fig. 5.40 A ‘blue bloater’ showing ascites from marked cor
pulmonale.
limitation. Stridor is a harsh inspiratory and expiratory
noise and implies obstruction in the central airways.
This may be at laryngeal level when the voice is usually
hoarse but otherwise implies tracheal or major bronchial
obstruction. In children, croup and foreign bodies are
the usual causes; in adults, carcinoma or extrinsic
compression.
‘Pink puffers’ and ‘blue bloaters’

The terms ‘pink puffers’ and ‘blue bloaters’ are applied
to the overall appearances of some patients with chronic
airflow limitation. They describe polar groups and most
patients are in between. ‘Blue boaters’ (Fig. 5.40) are
cyanosed from hypoxia and bloated from right-sided
heart failure. Further investigation shows features of
chronic obstructive bronchitis. Cough and sputum are
common but breathlessness less so. Carbon dioxide
retention is a feature. ‘Pink puffers’ (Fig. 5.41) are not
cyanosed and are thin. Investigation shows features
associated with emphysema. Cough and sputum are less
common, but the patients are breathless. Carbon dioxide
levels in the blood are normal or low.
Fig. 5.41 ‘Pink puffer’. Note the pursed-lip breathing.
PALPATION
Trachea and mediastinum
Start palpation by feeling for the position of the trachea.
Do this from the front by placing two fingers either side
of the trachea and judging whether the distances between
it and the sternomastoid tendons are equal on the two
sides (Fig. 5.42). An alternative is to examine the patient
from behind and hook your fingers round the tendons to
meet the trachea. The trachea may be displaced by masses
in the neck such as thyroid enlargement. Nonetheless,
the trachea gives an indication about the position of the
mediastinum, although often you will only be confident
about tracheal displacement after you have seen the
radiograph. Fig. 5.42 Palpation of the trachea.
127
Chapter
Chest wall
Mediastinal displacement If the patient complains of chest pain, then you should
gently palpate the chest for local tenderness. If present,
fibrosis this usually indicates disease of bones, muscles or
cartilage. As indicated earlier, one variety is called Tietze’s
syndrome, in which there is pain and swelling of one or
more of the upper costal cartilages, but much more
commonly than this syndrome there is merely pain and
tenderness of the cartilage but no swelling. Chest wall
tenderness may also be present in pleurisy; point
tenderness over a rib or cartilage is almost always due to
collapse
benign local disease and the worried patient can be
pull reassured.
pneumothorax
A SYSTEMATIC APPROACH
From this point on, as with most parts of the physical
examination, comparison is made between the two sides
of the body as abnormality is likely to be confined to one
side. Start from the front at the apex of the lung and work
downwards, comparing each side immediately with the
effusion other. Remember that the heart will influence the result
fluid on the left. Do not forget the lateral sides and the axillae.
push Then sit the patient forwards and examine the back.
Sometimes you will need an assistant to help a sick
patient to lean forwards. When examining from the back,
place the arms of the patient forwards in the lap. This will
Fig. 5.43 Mediastinal displacement. move the scapulae laterally and uncover more of the
chest wall.
Differential diagnosis Vocal fremitus

Mediastinal displacement This is performed by placing either the edge or the flat of
Away from the lesion your hand on the chest and asking the patient to say
• Pneumothorax ‘ninety-nine’ or count ‘one, two, three’. The vibrations
• Effusion (large) produced by this manoeuvre are transmitted through the
lung substance and are felt by the hand. The test is crude
Towards the lesion
and the mechanism and the alterations in disease are the
• Lung collapse from central airway obstruction same as for vocal resonance.
• Localised fibrosis
Chest expansion
The purpose of this test is to determine if both sides of
The position of the apex beat also gives information the chest move equally. Students often have difficulty
about the position of the mediastinum so long as the with this examination. A good method is to put the
heart is not enlarged. The trachea moves with the upper fingers of both your hands as far round the chest as
part of the mediastinum, the apex beat with the lower. possible and then to bring the thumbs together in the
The mediastinum may be pushed or pulled to either side. midline but to keep the thumbs off the chest wall.
Large effusions push the position of the apex beat but The patient is then asked to take a deep breath in;
very large effusions are needed to displace the trachea. the chest wall, by moving outwards, moves the fingers
Pneumothorax pushes the mediastinum even though the outwards and the thumbs are in turn distracted away
lung collapses. This is because the pressure in the pleural from the midline (Fig. 5.44). The thumbs must be free:
space (usually negative) approaches or even exceeds if they are also fixed to the chest wall they will not
atmospheric pressure, that is, increases. Lung collapse move. It is important to keep your fingers and thumbs
and fibrosis pull the mediastinum (Fig. 5.43). Tumour, in the same relationship to each other, for it is easy to
especially the pleural tumour mesothelioma, may ‘fix’ move the thumb the way you think it ought to go.
the mediastinum so that it cannot move despite these Examination can be performed on both the front and the
changes. back.
128
Chapter
Fig. 5.44 Assessing chest expansion in expiration (left) and inspiration (right).
Fig. 5.45 Percussion over the anterior chest. Fig. 5.46 Direct percussion of the clavicles for disease in the lung
apices.
Expansion can be reduced on both sides equally. This the middle finger of the other hand (Fig. 5.45); it must
is difficult to detect as there is no standard of comparison be removed again immediately, like the clapper inside
but is produced by severe airflow limitation, extensive a bell, otherwise the resultant sound will be damped.
generalised lung fibrosis and chest wall problems (e.g. The striking movement should be a flick of the wrist
ankylosing spondylitis). and the striking finger should be at right angles to the
Unilateral reduction implies that air cannot enter other finger. As well as hearing the percussion note,
that side and is seen in pleural effusion, lung collapse, vibrations will be felt by your hand on the chest wall.
pneumothorax and pneumonia. Again, each side is compared with the equivalent
area on the other from top to bottom. Do not forget the
sides.
The finger on the chest should be parallel to the
expected line of dullness (e.g. in an effusion, parallel to
Dullness to percussion the floor). This will then produce a clearly defined change
Moderate in note from normal to dull; a finger straddling the
• Consolidation demarcation will not do this. It should be placed in the
• Fibrosis intercostal spaces. Do not percuss more heavily than is
• Collapse necessary: it gives no more information and can be
distressing to patients. The apex of the lung can be
‘Stony’
examined by tapping directly on the middle of the clavicle
• Pleural fluid
(Fig. 5.46). Remember that the lung extends much further
down posteriorly than anteriorly (see Fig. 5.4).
The degree of resonance depends on the thickness of
the chest wall and on the amount of air in the structures
PERCUSSION underlying it. The possibilities are increased resonance,
The purpose of percussion is to detect the resonance or dullness and ‘stony dullness’. Obese patients and
hollowness of the chest. Use both hands, placing the individuals with thick chest walls show less resonance,
fingers of one hand on the chest with the fingers separated yet it is equal on the two sides. In contrast, patients with
and strike one of them with the terminal phalanx of overinflated lungs, particularly those with emphysema,
129
Chapter
have increased resonance; however, it is generalised and they do. To help them you may have to press gently on
without a reference point is difficult to grade. It might be the jaw to open it. Some take enormous slow deep
thought that air in the pleural space (pneumothorax) breaths that, although otherwise satisfactory, do prolong
would increase resonance but the difference is often the examination. A quick demonstration of what you
insufficient to identify which is the affected side from want will resolve any problems.
percussion alone. The breath sounds are produced in the large airways,
Resonance is decreased moderately in consolidation transmitted through the airways and then attenuated by
and fibrosis of the lung and markedly if there is fluid of the distal lung structure through which they pass. The
any kind between the lung and the chest wall, that is, sounds you hear at the lung surface are therefore different
stony dullness. A collapsed lobe can compress to a very from the sounds heard over the trachea and are modified
small volume and compensatory overinflation of the further if there is anything obstructing the airways, lung
other lobe fills the space. The percussion note may then tissue, pleura or chest wall. When reporting on auscultatory
be normal. A whole lung cannot collapse completely changes, you must distinguish between the breath sounds
(unless there is also a pneumothorax) so the chest will be and the added sounds. Breath sounds are termed either
dull. Percussion can also be used to determine movement vesicular or bronchial and the added sounds are divided
of the diaphragm because the level of dullness will into crackles, wheezes and rubs.
descend as the patient breathes in (tidal percussion).
Dullness is to be expected over the liver, which anteriorly Vesicular breath sounds
reaches as high as the sixth costal cartilage, and over the
This is the sound heard over normal lungs; it has a rustling
heart. Resonance in these areas, again a subjective finding,
quality and is heard on inspiration and the first part
implies increased air in the lungs and is common in
of expiration (Fig. 5.48). Reduction in vesicular breath
overinflation and emphysema. Bilateral basal dullness is
sounds can be expected with airways obstruction as in
more usually due to failure or inability to take a deep
asthma, emphysema or tumour. The so-called ‘silent
breath, to obesity or to abdominal distension than to
chest’ is a sign of severe asthma: so little air enters the
bilateral pleural effusions. The right diaphragm is
lung that no sound is produced. The breath sounds can
normally higher than the left so expect a slightly higher
be strikingly reduced in emphysema, particularly over a
level of dullness.
bulla. Generalised reduction in breath sounds also occurs
with a thick chest wall or obesity.
Anything interspersed between the lung and the chest
AUSCULTATION
wall (air, fluid or pleural thickening) will reduce the
Many doctors prefer to use the diaphragm of the breath sounds; this is likely to be unilateral and therefore
stethoscope for auscultation of the chest (Fig. 5.47). In more easily detected.
thin bony chests, the bell may give a more airtight fit and Avoid the term ‘diminished air entry’ when you mean
is less likely to trap hairs underneath, which produce a diminished breath sounds. The two are not necessarily
crackling sound. synonymous.
Ask the patient to take deep breaths through the
mouth, then listen in sequence over the chest as before. Bronchial breathing
Start at the apices and compare each side with the other.
Some patients fail to understand the instruction to breathe Bronchial breathing causes much confusion because the
through the mouth but the sounds are much clearer if essential feature of bronchial breathing, the quality of
the sound, is difficult or impossible to put into words.
Traditionally, it is described by its timing as occurring in
both inspiration and expiration with a gap in between
(Fig. 5.49). In this way it is contrasted with vesicular
breathing. These features are undoubtedly true but lead
to the confusion in the mind of the student that if anything
is heard in middle or late expiration it must be bronchial
breathing. Many normal people and individuals with
airways obstruction have a prolonged expiratory
component to the breath sounds (this is sometimes
designated ‘bronchovesicular’ but this term increases
the confusion rather than diminishing it). It is best to
forget about the timing and concentrate on the essential
feature, the quality of the sound. It can be mimicked to
some extent by listening over the trachea with the
stethoscope, although a better imitation can be obtained
Fig. 5.47 Auscultation of the chest using the diaphragm. by putting the tip of your tongue on the roof of your
130
Chapter
Vesicular breathing Bronchial breathing in the upper lobes

upper lobe
bronchial breathing
transmitted
expiration from trachea
inspiration
Fig. 5.48 Timing of vesicular breathing.
lower lobe
no bronchial breathing
Bronchial breathing
Fig. 5.50 Bronchial breathing may be heard over the upper lobes
even if the bronchus is blocked.
inspiration expiration
over an effusion will be diminished but bronchial
breathing may be heard over its upper level, perhaps
because the effusion compresses the lung.
Bronchial breathing is only heard over a collapsed lung
if the airway is patent. This is rare as the collapse
is usually caused by an obstructing carcinoma.
Nevertheless, there is an exception with the upper lobes
Fig. 5.49 Timing of bronchial breathing. (see above).
Bronchial breathing has been divided into tubular,
cavernous and amphoric but attempts to score points on
mouth and breathing in and out through the open ward rounds by using these terms are best left to
mouth. others.
Bronchial breathing is heard when sound generated in
Vocal resonance
the central airways is transmitted more or less unchanged
through the lung substance. This occurs when the lung This is the auscultatory equivalent of vocal fremitus. Place
substance itself is solid, as in consolidation, but the air the stethoscope on the chest and ask the patient to
passages remain open. Sound is conducted normally to say ‘ninety-nine’. Normally the sound produced is
the small airways but then, instead of being modified by ‘fuzzy’ and seems to come from the chest piece of the
air in the alveoli, the solid lung conducts the sound better stethoscope. The changes in disease should by now be
to the lung surface and, hence, to the stethoscope. If the predictable. The sound is increased in consolidation
central airways are obstructed by, say, a carcinoma, then (better transmission through solid lung) and decreased if
no transmission of sound will take place and no bronchial there is air, fluid or pleural thickening between the lung
breathing will occur even though the lung may be solid. and the chest wall. The changes of vocal fremitus are the
An exception is seen in the upper lobes. Here, if same. Both tests are of little value in themselves, yet a
the bronchi to either lobe are blocked, sounds from the refinement of vocal resonance can be very useful.
central airways can still be transmitted directly from Sometimes the increased transmission of sound is so
the trachea through the solid lung to the chest wall marked that even when the patient whispers, the sound
(Fig. 5.50). is still heard clearly over the affected lung (whispering
The main cause of bronchial breathing is consolidation, pectoriloquy). When this is well developed there is a
particularly from pneumonia – so much so that in the striking difference between the normal side, where the
minds of most clinicians the three terms are synonymous. sound appears to come from the end of the stethoscope,
Lung abscess, if near the chest wall, can cause bronchial and the abnormal side, where the syllables are much
breathing, probably because of the consolidation around clearer and seem as if they are being whispered into your
it. Dense fibrosis is an occasional cause. Breath sounds ear.
131
Chapter
Bronchial breathing and whispering pectoriloquy have Crackles

the same mechanism so commonly occur together.
In a sense the term crackles is self-explanatory. Problems
Consequently, if you are in doubt about the presence
arise because of various descriptions that are often
of bronchial breathing then whispering pectoriloquy
added, such as coarse, medium, fine, wet or dry. These
may confirm it. Like bronchial breathing, whispering
add little to our understanding; nonetheless, it is possible
pectoriloquy is characteristic of consolidation but can also
to distinguish two main types. The first occurs when
occur with lung abscess and above an effusion.
there is fluid in the larger bronchi and a coarse bubbling
sound can be heard that clears or alters as the secretions
Added sounds causing the sound are shifted on coughing or deep
There are three types of added sounds: wheezes, crackles breathing.
and pleural rubs. Much confusion has been generated The sound of other ‘fine’ crackles can be imitated by
in the past by other terms such as rhonchi, which are rolling the hairs of your temple together between your
equivalent to wheezes, and crepitations and rales, which fingers. They occur in inspiration and are high-pitched,
are equivalent to crackles. Further subdivision is often explosive sounds. The mechanism of their production
attempted but is of very limited value. is thought to be as follows. Many conditions lead to
premature closure of the small airways at the end of
Wheezes expiration. During the succeeding inspiration, these units
can only be reopened by overcoming the surface tension
These are prolonged musical sounds largely occurring on that keeps them closed. When they eventually ‘pop open’
expiration, sometimes on inspiration, and are due to crackles are produced. During inspiration, larger bronchi
localised narrowing within the bronchial tree. They are will open before smaller ones so crackles from chronic
caused by the vibration of the walls of a bronchus bronchitis and bronchiectasis tend to occur early.
near to its point of closure. Most patients with wheeze Conditions that largely involve the alveoli, such as left
have many, each coming from a single, narrowed area. ventricular failure, fibrosis and pneumonia, tend to
As the lung gets smaller on expiration, so the airways get produce crackles later on inspiration. This distinction is
smaller too; each narrowed airway reaches a critical phase of clinical value.
when it produces a wheeze then ceases to do so. Thus,
during expiration, numerous narrowings produce
numerous wheezes in sequence and together. A single
wheeze can occur and may then suggest a single Differential diagnosis
narrowing, often caused by a carcinoma or foreign body Crackles
(fixed wheeze).
• Left ventricular failure
Wheezes are typical of airway narrowing from any
• Fibrosing alveolitis
cause. Asthma and chronic bronchitis are the most
• Extrinsic allergic alveolitis
common and the narrowing is caused by a combination
• Pneumonia
of smooth muscle contraction, inflammatory changes in
• Bronchiectasis
the walls and increased bronchial secretions. Sometimes
• Chronic bronchitis
patients with these conditions have few or no wheezes.
• Asbestosis
If so, ask the patient to take a deep breath and then to
blow out hard. This may produce a marked wheeze.
Occasionally, wheezing is heard in pulmonary oedema,
presumably because of bronchial wall oedema.
The term bronchospasm suggests narrowing caused Note whether the crackles are localised. This would be
only by smooth muscle contraction and should be avoided expected in pneumonia and mild cases of bronchiectasis.
as the bronchial narrowing is usually multifactorial. Pulmonary oedema and fibrosing alveolitis typically affect
Wheeze-like breath sounds can disappear in severe both lung bases equally.
asthma and emphysema because of low rates of airflow. Normal people, especially smokers, may have a few
The amount of wheeze is not a good indicator of the basal crackles; these often clear with a few deep
degree of airways obstruction. Peak expiratory flow breaths.
measurement is much better. Pleural rub
This is caused by the inflamed surfaces of the pleura
Stridor
rubbing together. The sound has been likened to new
Stridor may be heard better without a stethoscope by leather when it is bent or, more vividly, to the creaking
putting your ear close to the patient’s mouth and asking noises made in a sailing ship heeling to the wind, which
the patient to breathe in and out. As indicated earlier, it you may have experienced from films if not in reality.
is a sign of large airway narrowing in the larynx, trachea Some idea of the quality of the sound can be obtained by
or main bronchi. placing one hand over the ear and rubbing the back of
132
Chapter
Common patterns of abnormality 5
Red flag – urgent referral Differential diagnosis

Respiratory disease Some causes of pneumonia
• Haemoptysis. May be a symptom of cancer, • Streptococcus pneumoniae

although most are due to infection. Chest x-ray • Mycoplasma pneumoniae
required. • Haemophilus influenzae
• Persistent symptoms of chest infection. May be • Influenza virus
underlying cancer. Chest x-ray required. • Legionella pneumophila
• Right lower lobe collapse. Enquire about choking fit. • Psittacosis
May be foreign body. • Q fever
• Absent breath sounds and wheeze in a breathless • Chemical (for example, aspiration of vomit)
patient. Not necessarily a good sign. May imply • Radiation
severe asthma with little air movement.
• Equal inspiratory and expiratory wheeze may in fact
be stridor from a central obstruction. If there is also
a hoarse voice consider laryngeal carcinoma.
• In a patient with apparently mild COPD (chronic an alveolar-filling process with no presumption about
obstructive pulmonary disease) who develops aetiology. To a pathologist it means a heavy airless lung
oedema or excessive sleepiness consider type 2 and to a clinician it means bronchial breathing that is
respiratory failure. usually equated with pneumonia. To use pneumonia as
• In a patient with a ‘fat face’ and full neck consider an example, the affected lung or lobe is the same size or
SVC (superior vena cava) obstruction and look for very slightly larger than normal lung. The alveoli are full
dilated veins over the chest wall. of exudate, yet the air passages are open. The pleura
• If clubbing develops in a patient with COPD this is are inflamed. The ‘differential diagnosis’ box lists some
likely to be due to a carcinoma. causes. Note that not all are infections.
Inspection of the chest may show diminished
movement on the affected side, palpation shows no shift
of the mediastinum but expansion is reduced, vocal
that hand with the fingers of the other. Pleural rubs are fremitus may be increased, percussion note will be
usually heard on both inspiration and expiration. At first moderately impaired, breath sounds will be bronchial
you may think that you are moving the stethoscope on over the affected area with whispering pectoriloquy and
the chest. Sometimes coarse crackles can sound like rubs; there may be a pleural rub. Early and late in the disease
a cough will shift the former. If there is any pain, ask the process there may also be crackles and these may be
patient to point to the site of the pain, this often localises the only auscultatory change in mild cases. In lobar
the rub too. Rubs are heard in all varieties of pleural pneumonia, the changes are localised to a lobe, which
inflammation, such as in pneumonia and pulmonary means that the signs are detected either anteriorly or
embolism. Any effusion will separate the pleura and the posteriorly but not usually both. More widespread
rub may well go but sometimes remain above the changes suggest ‘bronchopneumonia’, a complication of
effusion. chronic bronchitis, or ‘atypical pneumonia’ caused by
viruses, mycoplasma and other organisms. Radiology
may show an ‘air bronchogram’ – air in the bronchi
Common patterns of abnormality outlined by fluid in the alveoli (Fig. 5.51).
This section summarises what has been said before PLEURAL FLUID
but from the perspective of the disease process. The
diagnosis itself will need the integration of the history Whether this be from an increase in pleural transudate,
and any other information. The processes considered are pleural exudate from inflammation, blood, pus or lymph,
consolidation, pleural fluid, pneumothorax, chronic the signs are the same. A large amount of fluid is needed
airflow limitation, lung or lobar collapse and fibrosis. Not to displace the heart and an even larger amount, filling
all the signs are present in every case and often there is most of the hemithorax, to displace the trachea. The
more than one disease process at a time. The radiograph displacement is away from the fluid. Expansion is
often illustrates the anatomical nature of the process, so diminished on the affected side, vocal fremitus is
examples are shown. reduced, percussion note is markedly reduced, ‘stony
dullness’, and breath sounds are absent or markedly
reduced. Bronchial breathing and a rub may be heard at
CONSOLIDATION the upper level of the effusion. An effusion, if large
Consolidation is a confusing term as it means different enough, is detected both anteriorly and posteriorly
things to different specialists. To a radiologist it means (Figs 5.52, 5.53).
133
Chapter
Mediastinum central
Expansion ↓
Percussion note ↓
Breath sounds bronchial
Whispering pectoriloquy
Crackles
Pleural rub
Fig. 5.51 Consolidation (unusual because it affects both lungs). Enlarged view showing air bronchogram (arrow).
Mediastinum usually central

Expansion ↓
Percussion ↓
Breath sounds ↓
Sometimes bronchial breathing
or a pleural rub at upper level
Fig. 5.52 Small effusion.
Mediastinum displaced
Expansion ↓
Percussion ↓
Breath sounds ↓
Fig. 5.53 Large effusion with mediastinal displacement.
134
Chapter
Differential diagnosis Risk factors

Some causes of pleural fluid Some causes of pneumothorax
Transudates • No cause found

• Congestive cardiac failure • Apical blebs
• Cirrhosis • Chronic bronchitis and emphysema
• Nephrotic syndrome • Staphylococcal pneumonia
Exudates • Asthma
• Tumours – primary, secondary and lymphomas • Tuberculosis
• Pneumonia • Cystic fibrosis
• Tuberculosis • Trauma
• Rheumatoid arthritis and other connective tissue
disorders
• Pulmonary embolism and infarction
Blood there is also dullness to percussion. Vocal resonance is
• Trauma reduced and there are no added sounds (Fig. 5.54). Some
• Pulmonary embolism causes of pneumothorax are given in the ‘risk factors’
• Tumours box.
Pus
• Pneumonia CHRONIC AIRFLOW LIMITATION
• Trauma This term covers the entities of chronic obstructive
Lymph bronchitis, emphysema and asthma, which are not always
• Tumours, especially lymphoma readily distinguishable from each other. There may be
hyperinflation of the chest, pursed lip breathing and use
of accessory muscles of respiration. Expansion may well
be reduced but usually equally so. The mediastinum is
PNEUMOTHORAX not displaced. Vocal fremitus is normal, percussion is
usually normal but there may be increased resonance and
The pressure in the pleural space is normally negative reduced hepatic and cardiac dullness. Breath sounds are
with respect to atmospheric pressure. In a pneumothorax, vesicular and sometimes reduced, presumably from low
the affected side is at a higher pressure, that is, less flow rates; the added sounds are wheezes and often
negative. This pressure tends to displace the mediastinum crackles. The radiograph is usually normal but sometimes
to the opposite side, and if there is a flap valve effect shows overinflation with low flat diaphragms (Fig.
producing a tension pneumothorax this can be extreme 5.55).
and dangerous. The affected side moves less well, vocal
fremitus is reduced and the percussion note is normal.
The expected increased resonance can be difficult to LUNG AND LOBAR COLLAPSE
detect and it is the conjunction of diminished breath The usual cause is a central bronchial carcinoma, although
sounds with a normal percussion note that distinguishes a foreign body has the same effect. If the lung or lobe
it from other causes of diminished breath sounds when is not ventilated, the air within it is absorbed by the
Mediastinum sometimes
displaced
Expansion ↓
Percussion normal or ↑
Breath sounds ↓
No added sounds
Fig. 5.54 Pneumothorax on right.
135
Chapter
Hyperinflation
Mediastinum central
Hepatic and cardiac dullness ↓
Vesicular breath sounds
Wheezes and crackles
Radiograph often normal but
here shows overinflation
and low flat diaphragms
Fig. 5.55 Chronic airflow limitation.
Mediastinum displaced
Expansion reduced
Percussion normal or ↓
Breath sounds vesicular
but ↓ or sometimes
bronchial
Fig. 5.56 Right middle and lower lobe collapse.
blood and the lung collapses. If the whole lung is involved, of direct transmission of sound from the trachea. Bronchial
then the degree of collapse is limited by the capacity breathing is also heard in collapse of other lobes if
of the chest to shrink, but if a lobe is involved, then (unusually) the airways remain patent (Fig. 5.56). Crackles
the other lobe can fill the space and the affected lung and wheeze may be present if the cause is damage from
may come to occupy only a very small area. Lung an old infection.
collapse can also follow infection: tuberculosis and
bronchiectasis are good examples. Here the airways
remain open.
The findings on examination depend on whether the LUNG FIBROSIS
whole lung or only one lobe is involved. There is This may be the end result of many lung conditions
diminished movement on the affected side, with the and minor degrees are undetectable clinically. Localised
mediastinum deviating to that side. The percussion note changes produce similar signs to lung collapse. Generalised
is markedly reduced if the whole lung is involved but can disease is best illustrated by cryptogenic fibrosing
be difficult or impossible to detect if only a lobe is involved alveolitis. The lungs are stiff, expansion may be reduced,
and has shrunk to a small space. Breath sounds are but equally, and the mediastinum is central. Vocal
diminished but remain vesicular in lobar collapse and fremitus is normal, percussion note is normal or
may be absent if the whole lung is involved. Vocal slightly reduced, breath sounds are vesicular, although
resonance is decreased. As already indicated, bronchial occasionally bronchial, yet there are marked crackles,
breathing, increased vocal resonance and whispering initially confined to the bases but later extending up the
pectoriloquy can be heard in upper lobe collapse because chest (Fig. 5.57).
136
Chapter
Mediastinum central
Expansion equally ↓
Percussion normal or ↓
Breath sounds vesicular
(occasionally bronchial)
Crackles
Fig. 5.57 Cryptogenic fibrosing alveolitis.
Emergency
Bedside assessment of acute respiratory failure
Bedside diagnosis of acute respiratory failure is difficult • Consider parenchymal lung disease (e.g. pneumonia,
but: pulmonary oedema, alveolitis)
• Look first for respiratory rate, cyanosis, respiratory – look for crackles, bronchial breathing
distress, use of accessory respiratory muscles, ankle • Consider pleural problems (e.g. effusion,
swelling pneumothorax)
• Consider upper airways obstruction (e.g. anaphylactic – look for displaced trachea, dullness with silence,
shock, laryngeal tumour, foreign body, obstructive resonance with silence
sleep apnoea) • Consider chest wall problems (e.g. ankylosing
– look for swelling of lips and tongue, stridor, hoarse spondylosis, neurological disease)
voice, snoring – look for scoliosis, upper limb weakness, poor chest
• Consider central airways obstruction (e.g. tumour) wall movement, poor diaphragm movement,
– look for stridor, unilateral reduced breath sounds muscle fasciculations.
• Consider generalised airway narrowing (e.g. asthma, Further analysis depends crucially on vital capacity,
COPD) chest radiograph, arterial blood gases, oxygen saturation
– look for flapping tremor, wheeze, prolonged
expiration, silent chest, perform PEF
Respiratory examination
• Be aware of multiple problems • Respiratory and cardiac disease often coexist

• Occupational history still valid • Right ventricular failure as a consequence of lung
– mesothelioma occurs long after exposure disease is difficult to distinguish from congestive
– pneumoconiosis changes persist for life cardiac failure
• Not all breathless elderly patients have chronic • Disability may be multifactorial
obstructive pulmonary disease
137
Chapter
Review
Framework for the routine examination of the respiratory system
1. While taking the history, watch for respiratory 9. Palpate the front of the chest for vocal fremitus and
distress, particularly while talking. Note any clues for right ventricular hypertrophy
from the patient’s surroundings 10. Assess expansion of the chest from the front and
2. Look at the hands for clubbing, cyanosis and note any inequalities
evidence of carbon dioxide retention 11. Percuss the front of the chest comparing one side
3. Look at the mucous membranes for central with the other and noting any areas of dullness;
cyanosis include the axillae
4. Check the jugular venous pulse for evidence of cor 12. Auscultate the chest similarly and decide on the
pulmonale presence and nature of the breath sounds
5. Palpate for supraclavicular lymph nodes 13. Test for vocal resonance and, where appropriate,
6. Inspect the chest wall for deformities and whispering pectoriloquy
inequalities 14. Note any added sounds
7. Note the pattern of breathing 15. Repeat last six steps on the back of the chest
8. Palpate the trachea for any displacement 16. If appropriate, measure the peak flow rate
138
6
The heart and cardiovascular
system
The cardiovascular system is fundamental to the
functioning of almost every other organ system. Despite
the availability of many sophisticated imaging techniques,
The adult heart (Fig. 6.1) consists of two pumps working
which will be discussed later, the fundamental simplicity
in series. The ‘right heart’, comprising the right atrium,
and accessibility of the structure and function of the heart
tricuspid valve, right ventricle, pulmonary valve and
and vascular system make its physical examination both
pulmonary artery, is a low pressure pump receiving blood
important and extremely rewarding.
The chambers of the heart
pulmonary pulmonary
artery vein aortic valve
blood from blood to

right right left left
systemic systemic
atrium ventricle atrium ventricle
veins arteries
aorta
tricuspid valve mitral valve

pulmonary
valve
aorta pulmonary
artery
superior
vena cava
pulmonary
veins
pulmonary
valve
right mitral valve

atrium
tricuspid
valve
aortic valve
right
ventricle
inferior left
vena cava ventricle
Fig. 6.1 Arrangement of the heart chambers as a flow diagram (above) and in their approximate anatomical positions (below).
139
Chapter
6 The heart and cardiovascular system
pulmonary left atrial Fig. 6.2 Most of the anterior surface of the
aorta artery appendage heart is formed by the right ventricle and
pulmonary artery. The tip of the left ventricle and
the left atrial appendage also appear on the left
border of the heart.
right left
right left
ventricle ventricle
Fig. 6.3 Computerised tomography scan of the heart showing the

position of the heart within the chest cavity. Viewed from below.
Fig. 6.4 A ‘corrosion cast’ of the chambers of the heart, made by
filling the chambers with wax or plastic and dissolving away the
muscle.
from the systemic veins and pumping it to the lungs. The tip or apex of the heart (Fig. 6.2). The way the heart is
left heart, comprising the left atrium, mitral valve, left situated within the chest cavity is also well demonstrated
ventricle, aortic valve and aorta, is a high pressure pump on the computerised tomographic scan of the chest
receiving blood from the lungs and pumping it round the shown in Figure 6.3. Note that the heart lies obliquely in
body. In the early embryo, the heart forms as a simple the chest and that its long axis, the planes of the interatrial
tube down the midline of the body. As the embryo grows, and interventricular septum, and the planes of the various
the tube elongates more rapidly than the tissues around valves, are not aligned with any of the conventional
it and thus develops a loop and a twist. It also becomes anatomical planes. The chambers of the heart can be
divided into left and right chambers by the growth of a examined after death by injecting wax or plastic and
partition or septum down the middle. dissolving away the muscle (Fig. 6.4). They can also be
In the ninth week of gestation, the fetal heart rotates examined during life by injecting radio-opaque contrast
in a clockwise direction until the right ventricle comes to medium through catheters placed in the various chambers
rest anteriorly behind the sternum. Most of the left of the heart and taking cine radiographs. By tilting the
ventricle comes to lie posteriorly, apart from a small x-ray tube and image detector appropriately, it is possible
portion of left ventricular muscle which forms the left to obtain detailed pictures of the full extent of the
heart border when seen from the front and the extreme ventricular cavities (Fig. 6.5).
140
Chapter
HEART MUSCLE
Ventricles
Heart muscle or myocardium is a special type of muscle
that is extremely resistant to fatigue. As a result of the
higher pressures that it normally generates, the wall of
the left ventricle is much thicker than the wall of the right
ventricle. In a section taken through both ventricles, left
ventricular myocardium, including the intraventricular
septum, has a roughly circular outline with the right
ventricle appearing to be wrapped around one side of it
(Fig. 6.6). The muscle fibres of the heart are arranged in
a complicated spiral arrangement so that when they
contract (systole) not only is blood forced out of the
ventricles but the heart also elongates and rotates on the
fixed base provided by the attachment of the major blood
Fig. 6.5 Left ventricular cine-angiogram made by injecting radio- vessels. It is this movement that is felt as the beating of
opaque contrast medium into the heart through a catheter passed the heart by a hand placed on the chest. The heart
via the femoral artery and aorta. The x-ray tube and image intensifier normally lies in its own serous cavity, the pericardium,
are tilted into the ‘right anterior oblique’ position to outline the full
which allows it to move without friction. Apart from
extent of the left ventricle.
moving with each heart beat, the position of the
pericardium and the heart can be altered by the phase of
respiration or by rolling from one side to the other.
Atria
The atria of the heart are also muscular but are much
thinner walled than the ventricles (Fig. 6.7). They contract
Transverse (’short axis’) view of the heart
‘Long axis’ view of the heart
0.4–0.6 cm 0.8–1.5 cm
right
ventricle left right aorta
ventricle ventricle
wall
left
ventricle
left
septum atrium
0.8–1.5 cm
0.2–0.3 cm
Fig. 6.6 ‘Short axis’ view of the heart. In the short axis or transverse
section, the thinner (low pressure) right ventricle is ‘wrapped around’
the left ventricle. Fig. 6.7 Relative thickness of muscle in different parts of the heart.
141
Chapter
a fraction of a second before the ventricles and, in HEART VALVES

doing so, they assist in the filling of the ventricles, There are four heart valves. They fall anatomically and
particularly when there is a need for increased cardiac functionally into two groups: the inflow or atrioventricular
output. The atrial component of cardiac filling can valves and the outflow or ‘semilunar’ valves. The tricuspid
contribute up to 30% of cardiac output. Patients in whom, and mitral valves separate right atrium and right ventricle
as a result of disease, the atria are paralysed or are beating and left atrium and left ventricle, respectively. Both
out of synchrony with the ventricles are usually develop from the endocardial cushions of the embryonic
comfortable at rest but may become short of breath on heart and are composed of thin flexible leaflets that are
exercise. prevented from prolapsing back into the atrium when
the ventricle contracts by being attached by chordae
tendineae to specialised portions of ventricular muscle,
CARDIAC HYPERTROPHY AND DILATATION
the papillary muscles (Fig. 6.9). The hydrodynamic
Like any muscle, cardiac muscle responds to an increased efficiency of the mitral and tricuspid valves is very high.
workload by growth. The heart responds in different Their pliable edges smooth out eddies and turbulence in
ways to pressure load and volume load. Pressure load is blood flow and allow the rapid transfer of blood from
caused by an increased resistance to ejection of blood atrium to ventricle with a very small pressure differential.
from the heart. The response to pressure load is cardiac The aortic and pulmonary valves develop from two spiral
hypertrophy, initially without dilatation of the chamber ridges that divide the single great vessel leaving the
involved. For example, in aortic stenosis, the left embryonic heart into aortic and pulmonary trunks. Each
ventricular wall becomes excessively thickened but the normally has three cusps whose arrangement reflects
left ventricular cavity remains of normal size. Eventually, their embryonic origin (Fig. 6.10). As each cusp is shaped
when the pressure load is extreme or growth of the heart like a half moon, they are sometimes called the semilunar
muscle has outstripped its blood supply, failure of the valves.
muscle occurs and the cavity begins to enlarge.
The heart responds to a volume load, for example, a
HEART SOUNDS
leaking mitral or aortic valve, an arteriovenous fistula or
left-to-right shunt, by both hypertrophy of the myocardium Closure of the heart valves at different stages of the
and dilatation of the chamber involved. This is to cardiac cycle gives rise to sounds that are readily audible
accompany the increased stroke volume that is required through a stethoscope. The sounds are normally described
to deal with the volume load. The chest radiograph shows as ‘lub-dup’. The first heart sound (‘lub’) is caused by
cardiac enlargement (Fig. 6.8) and this is also found on the closure of the mitral and tricuspid valves, and
echocardiography. Ventricular hypertrophy produces the second heart sound, the rather higher pitched (‘dup’),
characteristic electrocardiographic changes and it is is caused by the closure of aortic and pulmonary
possible to identify the cardiac chamber involved from valves. The relationship between the heart sound, the
the electrocardiographic appearances. electrocardiogram and the arterial pulse wave is shown
in Figure 6.11. In children or in young adults, the
Fig. 6.8 Chest radiograph showing cardiac enlargement in response Fig. 6.9 Postmortem specimen showing attachment of valve cusps
to a volume load chronic mitral regurgitation (compare with Fig. 6.2). to papillary muscles by chordae tendineae.
142
Chapter
Development of the aortic and pulmonary (semilunar) valves
pulmonary
artery
left
coronary
artery
spiral course
brings the
pulmonary artery
primitive ‘trunk’ develops right to cross in front
four spiral ridges coronary artery of the aorta
aorta
spiral ridges separate the aorta from the

pulmonary artery and also from cusps of
aortic and pulmonary valves
Fig. 6.10 The common ‘great vessel’ of the fetal heart is divided into aorta and pulmonary artery by the growth of the spiral ridges.
Pulse, heart sounds and ECG
Increased pressure load (afterload) on the heart
Right ventricular pressure load

• Pulmonary valve stenosis
• Increased pulmonary vascular resistance
R
• chronic hypoxia
• chronic lung disease
• secondary to left heart failure
• Eisenmenger’s syndrome aortic pressure left ventricle
• primary pulmonary hypertension pressure
Left ventricular pressure load
• Aortic valve stenosis
• Subaortic stenosis
• Supravalvar aortic stenosis
• Hypertrophic obstructive cardiomyopathy
• Coarctation of the aorta
first sound second sound
• Systemic hypertension
second heart sound splits into two components during

inspiration (‘lub da-dup’) and comes together again in P Q S
expiration. This physiological splitting of the second heart
sound is the result of minor changes in the stroke volume P wave QRS width
of left and right ventricles during the normal respiratory <0.12 s <0.10 s
cycle.
During inspiration, venous return to the right side of PR interval QT interval <0.42 s
the heart is increased, thus increasing right ventricular <0.20 s at rate of 60 beats/min
stroke volume and delaying pulmonary valve closure. At
the same time, pooling of blood in the pulmonary veins
reduces filling of the left ventricle and makes aortic valve Fig. 6.11 Relationship between heart sounds, electrocardiogram
closure slightly earlier than in expiration. The split may and arterial pulse.
143
Chapter
Splitting of the second heart sound Electrical conduction in the heart
Inspiration Expiration spread of

electrical
Normal S activity
1 a2P2 S1 S2 through
atria
sinoatrial
node left
Wide, fixed Atrial septal
splitting S1 a2 P2 S1 a2 P2 defect atrium
atrioventricular
node
Pulmonary
Wide split stenosis
but varies right bundle
S1 a2 P2 S1 a2 P2 right
with inspiration branch block atrium
fibrous ring
Hypertrophic ‘insulating’
Reversed
cardiomyopathy ventricles
splitting S1 S2 S1 P2 a2
from atria right bundle of left
bundle His bundle
Fig. 6.12 Beat to beat variations in left and right ventricular stroke branch branch
volume cause splitting of the second heart sound in phase with
breathing. Splitting of the second sound with inspiration is normal. Fig. 6.13 Paths of the spread of electrical impulses in the heart
Other patterns may indicate cardiac abnormalities. (note that there are no specific electrical pathways in the atria).
be widened by other factors that delay right ventricular cells in other parts of the heart. The electrical impulse
contraction, such as right bundle branch block or spreads out from the sinoatrial node (Fig. 6.13) through
pulmonary valve stenosis. Conversely, anything that the cardiac muscle of the atria. The atria and the ventricles
delays left ventricular contraction, such as left bundle are separated by a fibrous ring of tissue to which the
branch block, hypertrophic obstructive cardiomyopathy tricuspid and mitral valves are attached and which
or severe aortic stenosis, may so delay the aortic does not support conduction of the cardiac impulse. The
component of the second heart sound that the normal only electrical pathway through this ring is through the
relationship is reversed and there is increasing splitting atrioventricular node, a localised area of specialised
of the second heart sound on expiration with the sounds conducting tissue lying between the tricuspid valve and
coming together on inspiration. This is known as the aorta. There is a delay of 0.12–0.20s while the impulse
paradoxical splitting of the second heart sound. Finally, passes through the atrioventricular node, ensuring the
in an atrial septal defect, there is a characteristically fixed correct delay between atrial and ventricular contraction.
splitting of the second heart sound because the hole in Once through the atrioventricular node, the electrical
the intra-atrial septum means that left and right atrial impulse is rapidly conducted to ventricular tissue through
pressure remains equal throughout the respiratory cycle specialised conducting fibres which form the bundle of
(Fig. 6.12). His and its branches.
ELECTROCARDIOGRAM
Electrical activity of the heart
The electrocardiogram (ECG) is an electrical and structural
The signal for contraction of each heart muscle cell is the map of the heart and is an invaluable aid to studying
electrical depolarisation of its membrane. The electrical normal heart rhythm and its disturbances. It works by
signal is transmitted from cell to cell in an orderly way so sensing and amplifying the very small electrical potential
that under normal circumstances the heart contracts in changes between different points on the surface of
an orderly fashion. The physiological cardiac pacemaker the body caused by the cyclical depolarisation and
comprises a small group of cells in the sinoatrial node repolarisation of the heart cells. Electrical potentials are
situated close to where the right atrium joins the superior picked up by electrodes that are attached to the skin. The
vena cava. Normally, these cells undergo cyclical points at which the electrodes are attached and the
repolarisation and depolarisation at a faster rate than conventional ways in which they are connected enable
144
Chapter
Cardiac arrhythmias 6
The ECG ‘complex’

The multilead ECG
electrical activity
from sinoatrial node
too small to detect
aVR aVL
R
Q T
1 2 P S
I 3 4
III
1 P wave – atrial activation

2 PR interval – delay in conduction through AV node
II 3 QRS complex – ventricular activation
4 T wave – ventricular recovery
Fig. 6.15 Different parts of an ECG ‘complex’.
aVF
Fig. 6.14 How the ECG ‘looks at’ the heart from different
directions (a concept due to Goldberger and Wilson).
the ECG to ‘look at’ the heart from a sequence of different

directions (Fig. 6.14). The cycle of electrical changes
during a single heart beat is termed an ECG complex.
Different parts of the ECG complex reflect the activation
of different parts of the heart. The P wave signals atrial
activity and the QRS complex indicates ventricular activity
(Fig. 6.15).
In patients suspected of intermittent arrhythmias, the
ECG may be displayed as a continuous monitor trace Fig. 6.16 ECG trace displayed on a monitor at the nursing station
(Fig. 6.16). In patients outside hospital, the ECG can be or bedside.
recorded continuously digitally for periods of 24–48 h
and then played back to analyse any rhythm disturbances.
This process is called ‘ambulatory ECG’ or ‘Holter
monitoring’. The ECG can be used to detect hypertrophy Differential diagnosis
of the different chambers of the heart (Fig. 6.17), abnormal Autonomic effects on the heart
rhythms and cardiac damage. Vagal tone (slows the heart)
• Increased in: children, athletes
• Stimulated by:
Cardiac arrhythmias • carotid baroreceptors, pain, trauma (via
hypothalamus)
Abnormalities of heart rhythm can be divided into those • ventricular stretch receptors (fainting reflex)
in which the heart goes too slowly (bradycardia) and • Excessive in:
those in which the rate is abnormally rapid (tachycardia). • malignant vasovagal syncope
Physiologically, heart rate can vary in a normal young • carotid sinus syncope
adult from 40 beats/min during sleep to 180 beats/minute • Blocked by: atropine
or more during vigorous exercise. The physiological Sympathetic tone (speeds up the heart)
control of heart rate is due to a balance between • Increased by: fear, pain, hypovolaemia, heart failure,
sympathetic nervous activity, which speeds the heart physical activity
rate, and vagal activity, which slows it down. • Decreased: during sleep
There are two principal mechanisms of arrhythmia • Blocked by: β-adrenoceptor blockers
generation: automaticity and re-entry phenomena. The
145
Chapter
Effect of cardiac chamber hypertrophy on the ECG
left
atrium left
right atrium
atrium right
P>3 mm atrium
P >0.12 s
right atrial hypertrophy: tall ‘peaked’ P wave left atrial hypertrophy: wide ‘M-shaped’ P wave
e.g. pulmonary stenosis e.g. mitral stenosis
V2
V2 = deep
S wave
normal V1
V5
V5 = large
right ventricular R wave
hypertrophy:
right ventricular hypertrophy dominant left ventricular hypertrophy also QRS 0.1 s
R wave in V1 wide and
T wave inversion
Fig. 6.17 Electrocardiographic changes can be used to identify hypertrophy of the cardiac chambers.
latter comprises 90% of arrhythmias. Automaticity implies

normal conduction tissue or abnormal conduction Heart block
(ectopic) tissue that is repetitively firing faster than usual.
Re-entry phenomenon is described under tachycardia
below.
BRADYCARDIA
Bradycardia may be caused by drugs, particularly β-
adrenoceptor blocking drugs (‘beta-blockers’); it may
also be a physiological finding in fit young athletes with
a high vagal tone. Extreme bradycardia may be caused by
heart block with failure of conduction of the electrical
impulse, most often as it passes through the atrioventricular
P P P P P P P
node or bundle of His (Fig. 6.18).
QRS QRS
TACHYCARDIA
Ectopic beats
Fig. 6.18 Heart block is one cause of bradycardia; there is failure of
As all heart muscle and not only the sinoatrial node conduction of the electrical impulses from atrium to ventricle.
exhibits the capacity for spontaneous depolarisation, it is
not uncommon to find an ‘ectopic focus’ of electrical
activity which can initiate extra beats out of time
with the normal cardiac cycle. These extra beats or infarction or during a viral infection of the heart,
extrasystoles may be generated in the atrium or they may act as markers for metabolic damage and,
ventricle. In otherwise healthy people, extrasystoles consequently, excessive irritability of the heart muscle
are usually benign and harmless. Following myocardial (Fig. 6.19).
146
Chapter
Cardiac arrhythmias 6
Sustained tachycardia
Ventricular and atrial extrasystoles
A persistent tachycardia may be caused by several ectopic
beats occurring in sequence (e.g. as the manifestation of
a particularly irritable ectopic focus). This is called a ‘focal
atrial
focus
tachycardia’.
A more common mechanism for sustained tachycardia
is, however, the phenomenon of re-entry (Fig. 6.20). The
ventricular focus basic principle of a re-entry tachycardia is that there are
usually scarred two alternative pathways for the conduction of the
or injured electrical impulse; these pathways differ both in their
myocardium
speed of conduction and their refractory period. Under
normal conditions, the cardiac impulse will be conducted
R R R R V by both pathways but an exceptionally early beat may
find one pathway still refractory to conduction and
therefore the impulse will be conducted down the other
atrial ectopic same shape ventricular ectopic different
as normal complex shape from normal complex one alone. However, by the time it reaches the end of
compensatory pause same compensatory pause less this pathway, the other pathway will have recovered and
as normal RR interval than normal RR interval be able to conduct the impulse in the reverse direction.
This sets up the possibility of a ‘circus movement’ or
Fig. 6.19 Extrasystoles are caused by an ectopic focus of electrical oscillation and the re-entry circuit can act as a focus for
activity.
Re-entry tachycardia
normal conduction
pathway via
atrioventricular
node 1 1 2 3 3
tachycardia
2
abnormal
conduction via
‘bypass tract’
3
(bundle of Kent)
conducting entirely via

normal pathway (short
refractory period,
slow conducting) 4
conducting entirely
through bypass pathway
(longer refractory period, 4
fast conducting)
1. Abnormal beats conducted through both normal (blue)
and accessory (red) pathways
conducting through both 2. A premature atrial beat finds the red pathway refractory but is
normal and bypass conducted down the blue pathway
pathways
3. By the time the impulse reaches the ventricle, the red
pathway has recovered and now conducts rectogradely to
stimulate the atria and set up a re-entry tachycardia
Fig. 6.20 Mechanism of a re-entry tachycardia, based on the ‘paradigm’ of the Wolff–Parkinson–White syndrome. The left hand diagram
shows the ECG pattern produced when conduction is all along the bypass pathway, when it is all along the normal pathway and when it is
along both simultaneously.
147
Chapter
generating a tachycardia. This tachycardia may continue because the atrioventricular node acts as a ‘filter’,
until one of the pathways fatigues and cannot conduct preventing the ventricles from being stimulated at too
fast enough to maintain the circuit or until the process is rapid a rate. Ventricular fibrillation is, however, rapidly
interrupted by an electrical stimulus which breaks the lethal because the rapidly contracting ventricles are
circuit and re-establishes normal conduction (Fig. 6.21). ineffective and unable to pump any blood into the
circulation. The only treatment for ventricular fibrillation
Fibrillation
is to pass an artificial competing electric current through
The most extreme form of arrhythmia occurs when the the heart. This technique is referred to as defibrillation
coordinated conduction of impulses between cells and causes momentary extinction of all electrical activity,
completely breaks down and individual cells contract allowing the whole system to reset (Fig. 6.22).
haphazardly. This process is termed fibrillation. Atrial
fibrillation is common but not particularly hazardous
Blood supply to the heart
Heart muscle needs a supply of blood to support both
Terminating a re-entry tachycardia its basal metabolic needs and the increased oxygen
requirements of exercise. The blood supply must be
capable of increasing to meet the heart’s demands during
exercise because heart muscle, unlike skeletal muscle, can
only work aerobically. The arterial blood supply to the
heart is provided by the right and left coronary arteries.
The right coronary artery supplies mainly the right
ventricle and the inferior surface of the left ventricle. It
divides at the end of its course into the posterolateral
branch and the posterior descending branch, which
supplies the posterior and lateral parts of the left ventricle
The left coronary has a common trunk (the left main
stem) which divides soon after its origin into the left
anterior descending coronary artery, which supplies
the interventricular septum, the anterior surface and the
apex of the left ventricle, and the circumflex coronary
Fig. 6.21 A critically timed extra stimulus can terminate a re-entry artery, which supplies the lateral part of the left ventricle
tachycardia by making both pathways refractory. (Fig. 6.23).
Fig. 6.22 A defibrillator (a). An electrical charge is built up within the machine and discharged through paddles applied to the
patient’s chest (b).
148
Chapter
Blood supply to the heart 6
LAD LM
CA
LMCA Cx
Cx RCA
LAD
Fig. 6.23 Cine-angiograms to show (left and middle) the left coronary artery and (right) the right coronary artery (RCA) (Cx, left circumflex
artery; LAD, left anterior descending artery; LMCA, left main coronary artery).
The fetal circulation Changes from fetal to adult circulation
active constriction
pulmonary aorta arterial of ductus
artery duct pulmonary aorta arteriosus
artery
2
foramen ovale
1. Blood passes from

left fall in right
the right atrium to the left
atrium atrial pressure
right left atrium through atrium
closes valve
atrium the foramen ovale
right of foramen
atrium ovale
1 2. Blood passes from
the pulmonary artery
to the aorta through
the arterial duct
right left
ventricle ventricle right left
ventricle ventricle
Fig. 6.24 In the fetal circulation, oxygenated blood from the Fig. 6.25 Changes that occur in the fetal circulation at birth. The
umbilical vein bypasses the liver through the ductus venosus; a ductus arteriosus constricts and the fall in right arterial pressure as
portion is shunted from the right to left atrium through the foramen the lungs expand closes the foramen ovale.
ovale and a further portion passes through the arterial duct.
In common with other arteries in the body, coronary the right ventricle or through a hole in the intra-atrial
arteries are prone to atheroma which predisposes to septum, the foramen ovale. Blood entering the right
thrombosis and coronary artery occlusion. The clinical ventricle is pumped into the pulmonary artery, with only
features of coronary thrombosis and the myocardial a small proportion of it entering the lungs. The remainder
infarction are described later. passes via the ductus arteriosus into the aorta
(Fig. 6.24).
After birth, as the lungs inflate with air, intrapulmonary
INTRACARDIAC SHUNTING vascular resistance of the lungs rapidly falls. The
In the fetus, the placenta, rather than the lungs, subsequent fall in right atrial pressure and rise in left
participates in respiratory gas exchange and the atrial pressure creates a pressure change which forces the
unexpanded lungs offer a high resistance to blood flow. valve-like foramen ovale to close and seals the interatrial
Both sides of the fetal heart work to pump a mixture of septum. At the same time, the ductus arteriosus constricts
deoxygenated blood from the systemic veins and and closes (Fig. 6.25). This separates the work of the right
oxygenated blood from the placenta into the aorta and and left sides of the heart and causes them to work in
thus to the rest of the body. Blood entering in the right series rather than in parallel. However, abnormalities in
atrium may pass either through the tricuspid valve into the process of transition from fetal to adult circulation, or
149
Chapter
Examples of left to right shunts: atrial septal defect Left to right shunt: ventricular septal defect
pulmonary
pulmonary aorta
aorta artery
artery
atrial septal
defect: shunt left increased mitral
pulmonary from higher atrium valve flow: may
flow left pressure left cause diastolic
murmur atrium atrium to right
murmur
right right atrium atrium
atrium
increased flow left left
at tricuspid ventricle ventricle
valve may
ventricular septal
cause diastolic
right dilated hyperdynamic right dilated defect: causes
murmur
ventricle right ventricle ventricle hyperdynamic loud pansystolic
right ventricle murmur
a b
Fig. 6.26 (a) Left to right shunt atrial septal defect. Blood passes
Left to right shunt: persistent ductus arteriosus from the left to right atrium. The overall result is an increase in
pulmonary blood flow. (b) Left to right shunt: ventricular septal
defect. Blood passes from the high pressure left ventricle to the
right to left shunt lower pressure right ventricle. (c) Left to right shunt: persistent
pulmonary through persistent ductus arteriosus. Blood passes from the high pressure aorta to the
artery ductus arteriosus: lower pressure pulmonary artery.
aorta continuous murmur
below right clavicle
the heart has to cope with the extra load of blood

shunted from the left. A two-to-one shunt means that
the output at the right side of the heart is twice that of
the left side of the heart and the increased workload
left
atrium on the right side of the heart may lead to heart failure.
right Alternatively, the excessively high blood flow through
atrium the lungs may lead to irreversible damage to the
pulmonary vasculature and the development of
pulmonary hypertension. Examples of left to right
shunts are shown in Figure 6.26.
right left
c ventricle ventricle
Right to left shunt
If a septal defect or persistent ductus arteriosus is
combined with a further lesion that raises the pressure
on the right side of the heart then, instead of blood
anatomical defects in the partitions or ‘septa’ dividing the flowing from the left-sided chamber to the right-sided
right and left sides of the heart, may lead to short-circuits chamber, it will flow in the opposite direction, from the
or ‘shunts’. right side of the heart to the left. The most common
example of congenital heart disease causing a right to
left shunt is Fallot’s tetralogy (Fig. 6.27) which is
Left to right shunt
physiologically equivalent to a ventricular septal defect
A congenital or acquired defect in the interatrial septum, plus pulmonary valve stenosis. A right to left shunt can
interventricular septum or failure of closure of the occur when pulmonary vascular damage occurs in a
ductus arteriosus will produce a left to right shunt. Blood patient with a severe left to right shunt. The resistance of
follows the path of least resistance from the high pressure the pulmonary arteries rises, resulting in increased
left-sided chamber to the lower pressure right-sided pressure on the right side of the heart and a reversal
chamber. The result is that, instead of matching left of the shunt. This is called Eisenmenger’s syndrome
and the right sided cardiac outputs, the right side of (Fig. 6.28).
150
Chapter
The arterial system 6
Fallot’s tetralogy Eisenmenger’s syndrome
pulmonary vascular
pulmonary damage causes
artery aorta raised pulmonary
artery pressure
aorta
‘over-rides’
septal defect
ventricular
stenosed septal defect
pulmonary left
shunt reverses
valve atrium
right to become
atrium right to left
left
ventricle
hypertrophied
right ventricle right raised right ventricular pressure
ventricle secondary to pulmonary
hypertension
Fig. 6.27 Fallot’s tetralogy is the most common ‘congenital’ cause Fig. 6.28 Eisenmenger’s syndrome is caused by a secondary rise in
of a right to left shunt. (The ‘tetralogy’ comprises pulmonary pulmonary vascular resistance as a consequence of pulmonary
stenosis, ventricular septal defect, over-riding aorta and right damage from increased blood flow initially due to a left to right
ventricular hypertrophy.) (Note that cyanosis sometimes develops shunt. (In some children, the pulmonary vasculature may never
several weeks after birth because dynamic hypertrophy of muscle in develop normally in the presence of such a shunt.)
the right ventricular outflow tract worsens the obstruction.)
The striking clinical feature about patients with right

to left shunts is central cyanosis due to the admixture
of desaturated venous blood with saturated blood
coming from the pulmonary vein. It differs from
cyanosis caused by lung disease or pulmonary oedema
as it is not corrected by administering supplemental
oxygen.
In patients with right to left shunts clinical signs of
long-term adaptation to chronic reduction in systemic
arterial oxygen saturation include finger clubbing (Fig.
6.29), polycythaemia and acne (particularly in adolescent
children).
Fig. 6.29 Cyanosis and finger clubbing in a girl with Eisenmenger’s
syndrome.
Factors that affect the shape of the pulse
• Velocity of cardiac ejection The arterial system

• Stroke volume (decreased with tachycardia, heart
failure or hypovolaemia) The arterial system distributes oxygenated blood from the
• Peripheral resistance (low peripheral resistance leads heart to the tissues and organs of the body. At the points
to ‘collapsing’ pulse) where arteries pass close to the body surface or can be
• Left ventricular outflow obstruction (‘slow rising’ compressed against the bony skeleton, they can be felt
pulse in aortic stenosis) as ‘pulses’ (Fig. 6.30). During each cardiac cycle, the left
• Elasticity of peripheral vessels (inelastic vessels, e.g. ventricle ejects blood into the aorta and initiates a pulse
in elderly people, may ‘sharpen’ pulse waves) wave that is transmitted to the periphery. It is important
• Reflection of pulse waves from the periphery to remember that the pulse wave travels to the periphery
much more rapidly than the actual flow of blood.
151
Chapter
The arterial pulses The pulse wave
superficial 100 mg systole

temporal
carotid
brachial diastole
femoral
radial
skin
fat
ulna
vessel
popliteal
bone
Fig. 6.31 Relationship between the pulse and the arterial

tibialis waveform.
posterior
dorsalis
pedis
are the small muscular arteries and arterioles; larger

Fig. 6.30 Some of the points at which arterial pulsation can be felt. blood vessels such as the femoral, carotid or radial arteries
(Note the similarity to first-aiders’ ‘pressure points’.)
are conduits and play little or no role in the control of
blood pressure.
The major veins of the body are shown in Figure 6.32.
An intra-arterial recording of pressure against time Systemic veins collect blood from the tissues and return
indicates the shape of the pulse wave, which approximates it to the right atrium of the heart. The venous return
to that which would be felt by a finger placed on the from the gut is specialised because it flows into the
arterial wall (Fig. 6.31). The shape of the arterial pulse hepatic portal vein and first enters the liver before flowing
wave depends on many factors (see ‘differential diagnosis’ out through the hepatic veins into the inferior vena cava.
box). The venous system operates at a much lower pressure
than the arterial system. Veins draining the chest and
abdomen drain passively into the vena cava, either
directly or via the azygos vein. In the upright position,
The venous system
venous drainage from the head and neck is assisted
by gravity. Passive venous drainage alone is inadequate
The most important mechanism allowing individual
for the limbs and, in particular, the lower limbs. Here,
organs to adjust their blood supply according to
the venous system is divided into superficial and
metabolic need is by decreasing or increasing the
deep veins (Fig. 6.33) separated by one-way valves.
arteriolar resistance to inflow (i.e. very small arteries
Contraction of the arm and leg muscles during normal
200–300 mm in diameter). Thus, food ingestion
activities massage the deep veins and this pumping action
considerably reduces gut vascular resistance and increases
actively propels blood back towards the heart. The one-
gut blood flow. Similarly, exercising skeletal muscle
way valve system between the deep and superficial
strikingly reduces its vascular resistance, thereby
venous systems of the lower limb ensures unidirectional
increasing local blood flow. Alteration of blood flow to
blood flow.
the skin is one of the important mechanisms controlling
heat loss or conservation. The arteriolar resistance in
the skin and the gut is under autonomic sympathetic
nervous system control; sympathetic nervous system Clinical history
stimulation causes arteriolar constriction resulting in a
rise in blood pressure. The most important blood vessels A carefully taken history sets the scene for the subsequent
contributing to control of peripheral vascular resistance physical examination. Particular symptoms that need to
152
Chapter
Clinical history 6
be enquired of in the cardiovascular history include

Venous drainage breathlessness, chest pain, palpitation, syncope and
claudication. The presence or absence of these symptoms
provides clues to the likely findings anticipated on
physical examination.
superior
vena cava
BREATHLESSNESS
inferior Patients with heart disease characteristically experience
vena cava breathlessness during physical exertion (exertional
gut
dyspnoea) and sometimes when lying flat (known as
drains positional dyspnoea or orthopnoea). There is evidence
via hepatic that orthopnoea is caused by stimulation of fine nerve
portal vein endings in the lungs as a result of increased pulmonary
capillary pressure, caused by redistribution of fluid
between peripheral tissues and the lungs when the
patient lies flat. Sometimes, the patient wakes extremely
breathless from sleep and has to sit up gasping for breath,
artery femoral vein
(deep) a symptom known as paroxysmal nocturnal dyspnoea. In
extreme forms, this may be accompanied by a cough
productive of white frothy sputum indicative of pulmonary
saphenous oedema.
vein
vein (superficial)
deep veins in
forearm and legs run as Questions to ask
‘venae comitantes’ Breathlessness
alongside arteries
• Do you ever feel short of breath?
Fig. 6.32 Principal veins of the body. • Does this happen on exertion?
• How much can you do before getting breathless?
• Do you ever wake up gasping for breath?
• If so, do you have to sit up or get out of bed?
• How many pillows do you sleep on?
• Do you cough or wheeze when you are short of
Veins in the leg breath?
skin
deep veins
(running with
The mechanism of exercise-associated dyspnoea is
arteries)
fascia controversial. It may be partly due to the same mechanism
as orthopnoea, with increased venous return from
tibia
fibula
exercising muscles raising left atrial pressure. However,
in exercising patients, the sensation of breathlessness
great does not always correlate well with directly measured
saphenous short left atrial pressure. Other factors such as reduced
vein saphenous arterial blood oxygen saturation and alteration of muscle
vein
function in chronic heart failure have also been invoked
venous as mechanisms contributing to the sensation of
spaces in perforating
calf vein with one
breathlessness.
muscle way valve A commonly used classification of exercise tolerance
in heart failure is that proposed by the New York
Heart Association (NYHA). This is commonly used in
Fig. 6.33 Veins in the leg form a ‘muscle pump’ in conjunction clinical trials and has been shown to correlate with
with the calf muscles. Muscle contraction forces blood from
prognosis. For practical purposes, when taking the history,
superficial to deep veins, and from periphery to centre.
it is helpful to record the symptoms verbatim. Reflecting
the patient’s description of symptoms over time can be
particularly useful in assessing progress. Left ventricular
failure may present with associated wheezing. However,
cardiac asthma should always be distinguished from
153
Chapter
obstructive airways disease; both history and examination

should be helpful in distinguishing heart failure from Sites of anginal pain
asthma.
Symptoms and signs

New York Heart Association classification of
heart failure
Grade I No symptoms at rest, dyspnoea only on

vigorous exertion
Grade II No symptoms at rest, dyspnoea on
moderate exertion
Grade III May be mild symptoms at rest, dyspnoea
on mild exertion, severe dyspnoea on
moderate exertion
Grade IV Significant dyspnoea at rest, severe
dyspnoea even on very mild exertion.
Patient often bed bound Fig. 6.34 Characteristic distribution of anginal pain.
pain are listed in the ‘symptoms and signs’ box and its
It can sometimes be difficult to decide whether distribution is illustrated in Figure 6.34.
dyspnoea is caused by heart disease or lung disease.
Paroxysmal nocturnal dyspnoea or orthopnoea points
more to left ventricular failure, whereas wheezing or
productive cough accompanying dyspnoea and risk Symptoms and signs
features for lung disease would favour a pulmonary Anginal pain
cause.
• Brought on by physical or emotional exertion
• Relieved by rest
• Usually crushing, squeezing or constricting in nature
• Usually retrosternal (Fig. 6.34)
Differential diagnosis • Often worse after food or in cold winds
Dyspnoea • Often relieved by nitrates
• Heart failure
• Ischaemic heart disease (atypical or ‘silent’ angina)
• Pulmonary embolism
• Lung disease The characteristic feature of angina is exercise-induced
• Severe anaemia chest pain that remits soon after the exertion is
discontinued. It is usually described as a crushing,
squeezing or constricting pain (the Greek word from
which it is derived means ‘choking’). Most patients
with angina have stenosis of one or more coronary
Anxiety should always be considered in the differential arteries and the retrosternal pain is precipitated when
diagnosis of breathlessness. The pattern described by the physical or emotional exertion increases the metabolic
patient is different; they might describe the sensation of demand. The discomfort and pain are caused by
suddenly feeling the need to take a deep breath unrelated an imbalance between myocardial blood supply and
to physical exertion, excessive sighing or a feeling of air the metabolic demand resulting in anaerobic
hunger. metabolism. Less often, angina may be a symptom of
aortic stenosis, hypertrophic cardiomyopathy and other
CHEST PAIN rare causes such as syndrome X (angina with normal
coronary arteries) and Prinzmetal’s angina (due to
Chest pain caused by myocardial ischaemia
coronary spasm).
Angina pectoris is the most common presenting Pain similar in nature to angina but occurring at rest
cardiac chest pain. The characteristic features of anginal may be caused by the acute coronary syndrome, otherwise
154
Chapter
Clinical history 6
Questions to ask
Pericarditis
Angina Pericarditis is an inflammation of the pericardium, the
serous sac surrounding the heart. It may be a complication
• Do you get pain in your chest on exertion (e.g.
following myocardial infarction or may result from a viral
climbing stairs)?
or bacterial infection or uraemia. The patient usually
• Whereabouts in the chest do you feel the pain?
complains of pain that is perceived as a constant
• Is it worse in cold weather?
retrosternal soreness and which is often aggravated by
• Is it worse if you exercise after a big meal?
deep breathing. The pain of pericarditis is characteristically
• Is it bad enough to stop you from exercising?
aggravated by change in posture (e.g. turning over in
• Does it go away when you rest?
bed) rather than physical exertion and sometimes radiates
• Do you ever get similar pain if you get excited or
to the left shoulder tip.
upset?
Musculoskeletal chest pain
Pain arising in the chest wall or thoracic spine is often
mistaken for cardiac pain. Characteristically, it is described
Differential diagnosis as an aching pain, the onset of which may relate to a
Chest pain on exertion postural movement and the pain is usually present at rest.
Costochondritis, or Tietze syndrome, should also be
• Angina caused by coronary atheroma
considered in patients presenting with chest pain. The
• Aortic stenosis
anterior chest pain is usually present at rest and associated
• Hypertrophic cardiomyopathy
with localised tenderness over the costal cartilages and
• ’Syndrome X’ (anginal syndrome with normal
costochondral joints. This syndrome is due to local
coronary arteries)
inflammation which may be viral in origin or occur
spontaneously. A variant of musculoskeletal pain is the
precordial catch syndrome, in which the patient describes
a sudden, sharp needle-like jabbing pain in the precordium.
known as unstable angina or myocardial infarction. The The pain is short-lasting but may recur. The cause is
pain of myocardial infarction is severe, persistent and unknown and the symptom runs a benign course.
often accompanied by autonomic symptoms including
nausea, vomiting and sweating (diaphoresis). Some Dissecting aortic aneurysm
patients describe a feeling of impending death.
Dissecting aneurysm of the thoracic aorta is a rare cause
of chest pain which has a characteristic presentation. The
pain is usually described at the outset as a ‘tearing’
Differential diagnosis sensation. It is often felt between the shoulder blades or
in the mid-back and is usually severe, persistent and
Chest pain at rest
readily mistaken for the pain of myocardial infarction.
• Myocardial infarction
• Unstable angina Other chest pains
• Dissecting aortic aneurysm Other chest pains that may masquerade as cardiac pain
• Prinzmetal’s angina (due to coronary spasm) include the pain of pleurisy, acute pneumothorax or
• Oesophageal pain herpes zoster (shingles).
• Pericarditis
• Pleuritic pain
• Musculoskeletal pain PALPITATION
• Herpes zoster (shingles) Palpitation is defined as abnormal awareness of the heart
beat. This may be perceived with exercise, when it is quite
normal, or when there is an irregularity of the heart beat.
It may be helpful to ask the patient to tap out the heart
rhythm on the table. Ask about the duration of the
palpitations and whether they end abruptly. In patients
Chest pain
with extrasystoles, it is often not the extra beat itself that
• Chest pain at rest lasting >15–20 min the patient perceives, but rather the following beat, which
• Recent onset crescendo angina symptoms is characterised by a longer than usual pause and an
• Unresponsive to GTN (glyceryl trinitrate) excessively forceful beat. The patient may describe a
• Associated autonomic symptoms (nausea, vomiting, jumping sensation or the feeling that the heart is about
sweating) to stop. Ask about precipitating factors such as exercise,
emotion or foods, in particular tea, coffee, alcohol and
155
Chapter
chocolates. You should also ask carefully about any epilepsy. Key features in the history that distinguish
medication, particularly over-the-counter decongestants cardiogenic syncope from epilepsy includes lack of
and ‘cold cures’ which often contain sympathomimetic warning or aura, colour change (patients look pale during
drugs. the event and flushed upon recovery due to hyperaemia)
Ectopic beats are often more apparent when the and rapid recovery. Remember that generalised
background heart rate is slow (e.g. when the patient convulsions can also occur following cerebral anoxia if
lies down to rest). Paroxysmal tachycardias are often the blood supply to the brain is interrupted for long
precipitated by exercise or by particular movements such enough. Common causes of syncope include simple
as stooping down to open a drawer or reaching to remove fainting (vasovagal syncope), its variants such as
an item from a high shelf. micturition and cough syncope, postural hypotension,
vertebrobasilar insufficiency and cardiac arrhythmias,
particularly intermittent heart block.
Questions to ask Simple fainting is caused by a vagally mediated
Palpitation bradycardia combined with sudden reflex vasodilatation.
It is usually caused by a combination of diminished
• Please tap out on the table the rate at which you
venous return (e.g. standing still on a hot parade ground),
think your heart goes during an attack
coupled with increased sympathic drive caused by
• Is the heart beat regular or irregular?
excitement, fear or disgust. Malignant vasovagal syncope
• Is there anything that sets an attack off?
is a rare disorder characterised by an exaggerated
• Can you do anything to stop an attack?
tendency to faint, resulting in recurrent episodes of
• What do you do when you have an attack?
unexpected syncope. Micturition syncope characteristically
• Are there any foods that seem to make symptoms
occurs at night in middle-aged or elderly men with a
worse?
degree of prostatic obstruction, in whom the fall in venous
• What medicines are you taking?
return is caused by straining to empty the bladder
accompanied by the sympathic stimulation of the
consequences of not doing so. Cough syncope is an
Differential diagnosis exaggerated vagal response to violent coughing and,
Palpitation
uncommonly, is a cause of syncope in patients with
chronic lung disease.
• Extrasystoles The Stokes–Adams attack is a term used by some
• Paroxysmal atrial fibrillation physicians to describe cardiogenic syncope. It was
• Paroxysmal supraventricular tachycardia originally defined as syncope due to cortical hypoper-
• Thyrotoxicosis fusion caused by transient asystole or a ventricular
• Perimenopausal tachyarrhythmia.
The need to treat an arrhythmia is usually dictated by Differential diagnosis

its haemodynamic effects. Enquire whether the arrhythmia
Stokes–Adams versus epilepsy
is simply a transient inconvenience or whether the patient
has to stop their activity and perhaps even lie down. Stokes–Adams Epilepsy
Cardiac arrhythmias may cause loss of consciousness No aura or warning Aura often present
(cardiac syncope). Transient loss of Prolonged loss of consciousness
Many patients with paroxysmal tachycardia learn to consciousness
use a modified Valsalva manoeuvre to terminate an Pale during attack Tonic/clonic phases
attack. This might be achieved by forcibly exhaling with Rapid recovery Prolonged recovery/drowsy
the nose and the mouth held shut or even by head Hot flush on recovery No hot flush on recovery
immersion in cold water. Some patients with tachycardia
describe a period of excessive urination following the
palpitation. This is due to the release of atrial natriuretic
hormone (ANP) during the tachycardia. In fainting, loss of consciousness is seldom abrupt. The
patient appears pale both before and immediately
afterwards and both consciousness and motor power
are rapidly restored by elevating the legs. In contrast,
SYNCOPE (FAINTING, BLACKOUTS) syncope caused by heart block is sudden, unheralded
Syncope is defined as loss of consciousness resulting and complete and is usually witnessed as a drop
from a transient failure of blood supply to the brain. The attack. The patient looks pale while collapsed and
presentation is readily confused with certain forms of recovery, which is often equally sudden, may be
156
Chapter
Clinical examination of the cardiovascular system 6
heralded by a pink flush. Vertebrobasilar insufficiency specific family members are still alive or about the
is common in elderly patients. There is often restricted circumstances of their death because the significance
neck movement and active or passive movements of this may not be apparent to the patient. For
of the neck may precipitate symptoms. Postural example, early death from stroke may indicate a family
hypotension is more common in elderly patients and susceptibility to hypertension. The significance of cardiac
may be exacerbated by antihypertensive medication, disease may be very relevant to the patient’s occupation;
particularly diuretics. Important clinical questions in an example would be an airline pilot or heavy goods
taking the history are highlighted in the ‘questions to vehicle driver where clinical coronary artery disease
ask’ box. or arrhythmias might be incompatible with safety at
work.
Questions to ask
HABITS
Syncope
Do not forget to enquire specifically about cigarette
(Wherever possible history should be taken from a smoking, alcohol intake and any medication the patient
family member or observer as well as the patient.) may be taking.
• What were the exact circumstances of the blackout?
• Did you have any warning of the attack?
• How quickly did you recover? Questions to ask
• Did you go pale or red during or after the attack? Family history
• Are you taking any medication?
• Is there any heart disease in the family?
• Are your parents still alive?
• Did they live to a good age?
Red flag – urgent referral • Do you know what they died from?
• Have you any brothers or sisters?
Syncope
• Do any of them have a heart problem?
• Complete loss of consciousness
• Associated injury
• Recurrent syncope
• Known aortic stenosis Clinical examination of the
• Family history of premature sudden cardiac death cardiovascular system
<40 years of age
There are three interlinking facets to the cardiovascular
examination. First, the examination routine should ensure
CLAUDICATION that the cardiovascular system is examined smoothly
and efficiently and in appropriate detail. Second, the
Intermittent claudication is the term given to a condition examination should aim to build on the clinical clues
where the patient experiences pain in one or both derived from the history. Third, the discovery of an
legs on walking and which eases when the patient unexpected sign, such as a heart murmur or anaemia,
rests. Just as angina is the usual initial symptom of might alter the interpretation of the history and the
atheromatous disease of the coronary arteries, so differential diagnosis.
intermittent claudication is usually the earliest symp-
tom of narrowing of the arteries supplying the legs.
The pain is usually described as ‘aching’ felt in the GENERAL OBSERVATION
calf, thigh or buttocks. Intermittent claudication The position of the patient on the examination couch is
is more common in men and most common in important. The patient should lie comfortably at 45°, with
smokers. the head supported and the body exposed to the waist.
Prior to starting the formal examination, spend a few
moments observing the patient as important signs can be
Occupation and family history elicited from inspection alone. Is the patient comfortable
at rest or distressed? Is the patient able to lie flat? Is the
The family history is important in evaluating patients patient breathless or cyanosed and, if cyanosed, is this
with heart disease as many cardiac diseases have an peripheral or central cyanosis? (See ‘symptoms and signs’
underlying genetic predisposition (e.g. towards box.)
hyperlipidaemia). The relevance of a positive family Blood appears bluish or purplish when there is more
history of coronary heart disease applies to first degree than 5 g of reduced haemoglobin in the circulation. In
relatives only. Sometimes it is more helpful to ask whether peripheral cyanosis, the prolonged capillary circulation
157
Chapter
Symptoms and signs midline

sternotomy
General observation
• Tachypnoea at rest
• Central or peripheral cyanosis
• Mitral facies
lateral closed
• Scars (sternotomy, lateral thoracotomy, closed mitral
thoracotomy mitral
valvotomy, saphenous vein graft harvest) valvotomy
• Dentition (as a possible source of bacterial
endocarditis)
• Xanthelasma
• Corneal arcus
• Anaemia Fig. 6.35 Location of surgical incisions.
the circulation and is indicative of anatomical or

time caused by peripheral vasoconstriction results in functional shunting of venous blood into the arterial
excessive haemoglobin desaturation whilst the normal circulation.
circulation time in the warm tongue and oral mucous Is there evidence of previous cardiac surgical scars?
membranes does not predispose to excessive The commonest cardiac scar is a mid-line sternotomy
deoxygenation. Central cyanosis indicates the presence scar; also, check the legs for scars from veins stripped for
of more than 5 g of reduced haemoglobin throughout use as bypass grafts. A lateral thoracotomy scar is often
used in thoracic surgery. A small scar in the subclavicular
region is a tell-tale site for a permanent pacemaker and
Symptoms and signs a small scar under the left breast may indicate a previous
Cyanosis closed mitral valvotomy (Fig. 6.35). Patients with mitral
stenosis sometimes have a pink flushed colouration of
Peripheral cyanosis
the face, the so-called ‘mitral facies’.
• Cold fingers and toes
• Not dyspnoeic or tachypnoeic
• Peripheral vasoconstriction THE HANDS IN HEART DISEASE
• Bluish or purple discoloration of fingers and toes Hand temperature gives a guide to the extent of peripheral
• Normal pink coloured tongue vasodilatation. Patients in heart failure are usually
Central cyanosis vasoconstricted and their hands feel cold and sometimes
• Dyspnoea and tachypnoea sweaty from increased sympathetic drive. The fingernails
• Polycythaemia (secondary) may reveal splinter haemorrhages (Fig. 6.36) suggestive
• Bluish or purple discolouration of the fingers and of subacute infective endocarditis. Finger clubbing is a
toes sign of endocarditis and is a classical sign of cyanotic
• Similar discoloration of the tongue and oral mucous congenital heart disease.
membranes
• Deoxygenated Hb level >5 g/dl
Cyanosis
Peripheral cyanosis
• Cold ambient temperature
• Shock with vasoconstriction
• Raynaud’s phenomenon
• Beta-blocker drugs
Central cyanosis
• Severe chronic obstructive pulmonary disease
• Severe pulmonary infection
Fig. 6.36 Splinter haemorrhage in the ring finger of a man with
• Severe pulmonary embolism infective endocarditis. There is an older, fading ‘splinter’ under the
• Congenital right to left shunt nail of the index finger. Splinter haemorrhages are often smaller and
darker than this.
158
Chapter
PALPATING THE PERIPHERAL PULSES

The radial pulse
The right radial pulse is usually best felt with the fingers
of the examiner’s left hand (Fig. 6.37) and is used to
assess heart rate and rhythm. As the radial pulse is distant
from the heart, it is an unsatisfactory landmark from
which to attempt to assess pulse character. If there is
suspicion of an abnormality in the aortic arch or the
brachial artery on either side, it may be helpful to feel
both radial pulses and simultaneously compare their
volume and timing. In patients with suspected coarctation
of the aorta, it is helpful simultaneously to feel the radial
and the femoral pulse. In the presence of coarctation not
only is the volume of the femoral pulse diminished but it Fig. 6.39 Using the thumb to assess the character of the brachial
is also appreciably delayed compared with the radial pulse. The artery lies just medial to the tendinous insertion of the
pulse (Fig. 6.38). As the blood flow leaving the aorta biceps muscle and deep to the fascial insertion of this muscle. It was
called the ‘grâce à dieu’ (thanks be to God) fascia by medieval
meets the restriction of a coarctation, there is dilatation barber surgeons because it saved them from fatally damaging the
of proximal collaterals and blood flows through intercostal artery when blood letting at the elbow!
Pulse character
Name Feels like Associated with
Normal
Slow rising Aortic stenosis
Bisferiens Mild aortic stenosis

(’two peaks’) plus reflux
Aortic reflux
Collapsing Persistent ductus
arteriosus
No pulse Occluded bronchial

or axillary artery
Fig. 6.37 Feeling the right radial pulse.
Fig. 6.40 Different pulse waveforms are associated with different
cardiac or vascular abnormalities.
collaterals to rejoin the aorta distally. The extended route

of the collateral circulation is the reason for radial femoral
delay.
The brachial pulse
The right brachial pulse is best palpated using the thumb
of the right hand, applied to the front of the elbow just
medial to the biceps tendon with the fingers cupped
round the back of the elbow (Fig. 6.39). The use of the
thumb for feeling the pulse is helpful as it is the character
Fig. 6.38 Simultaneous palpation of the radial and femoral pulses: of the pulse rather than rate or rhythm which is important
a delayed femoral pulse is a feature of aortic coarctation. at this point (Fig. 6.40).
159
Chapter
Fig. 6.41 Palpation of the carotid artery using the thumb. Fig. 6.42 Palpation of the carotid artery by different means.
Aortic stenosis Hypertrophic cardiomyopathy
hypertrophied
interventricular
aorta
septum
papillary
muscle
in systole, hypertrophied septum

bulges into and obstructs left
ventricular ejection aorta
mitral valve
meeting septum
pulse wave ‘truncated’ by sudden

obstruction in early systole
Fig. 6.44 Hypertrophic cardiomyopathy. A ‘jerky’ carotid pulse may

Fig. 6.43 Pulse wave changes in aortic stenosis. result from dynamic left ventricular outflow obstruction.
the cause may be aortic stenosis because the pulse form

The carotid pulse
becomes more ‘normal’ the nearer the periphery it is felt
The carotid pulse is even closer to the heart than the (Fig. 6.43). Another sign best appreciated at the carotid
brachial pulse and therefore even better for assessing is the jerky pulse of hypertrophic cardiomyopathy. This
pulse character as a reflection left ventricular mechanics. starts normally and then suddenly peters out as the
The best way to feel the patient’s right carotid artery is contracting left ventricular outflow tract obstructs ejection
to locate the tip of the left thumb against the patient’s (Fig. 6.44).
larynx and then gently but firmly press directly backwards
The femoral pulse
so that the carotid artery is felt against the precervical
muscles (Fig. 6.41). Alternatively, the carotid pulse can be The femoral pulse is almost as valuable as the carotid
felt from behind by curling the fingers around the side of pulse in assessing cardiac performance. It is more likely
the neck (Fig. 6.42). In severe aortic stenosis, there is to be weak or absent in patients with disease of the aorta
characteristically a slow rising carotid pulse, usually called or iliac arteries. It is best examined with the patient
a ‘plateau’ pulse. If the carotid pulse is difficult to feel in exposed and lying flat with the thumb or finger placed
a patient whose radial and brachial pulses are easily felt, directly above the superior pubic ramus and midway
160
Chapter
Fig. 6.45 Palpation of the femoral artery. Fig. 6.47 Palpation of the dorsalis pedis pulse.
Fig. 6.46 Palpation of the popliteal artery.
Fig. 6.48 Palpation of the tibialis posterior pulse.

between the pubic tubercle and anterior superior iliac
spine (Fig. 6.45). the foot lateral to the extensor hallucis longus tendon
The popliteal pulse (Fig. 6.47); the tibialis posterior pulse is felt with the
fingers cupped round the ankle just posterior to the
Assessment of the popliteal and foot pulses is important medial malleolus (Fig. 6.48).
in the examination of patients suspected of having
peripheral arterial disease (see p. 178).
The popliteal pulse lies deep within the popliteal fossa MEASURING BLOOD PRESSURE
but is readily felt by compressing the artery against the The most convenient way of measuring blood pressure is
posterior surface of the distal end of the femur. The with a stethoscope and sphygmomanometer. To measure
patient lies flat with the knee slightly flexed. The fingers the blood pressure reliably, all clothing must be removed
of one hand are used to press the tips of the fingers of from the arm and the sphygmomanometer cuff smoothly
the other hand into the popliteal fossa to feel the popliteal applied (Fig. 6.49). The patient’s arm should be supported
artery against the back of the knee joint (Fig. 6.46). at heart level by an arm rest or by the examiner. For
Palpating the popliteal artery is routinely used to evaluate accurate measurement, pressure in the cuff should be
arterial flow in patients with symptoms of intermittent reduced slowly, ideally at about 1 mmHg/s. Mercury
claudication. manometers must be upright and not tilted. Aneroid
manometers invariably become inaccurate with time and
The dorsalis pedis and tibialis posterior pulses
should be regularly recalibrated. Most practitioners now
Like the popliteals, these peripheral pulses are examined use automated devices as standard. This includes an
to assess the adequacy of the peripheral arterial tree in electronic monitor with a pressure sensor, a digital display
suspected peripheral vascular disease. The dorsalis pedis and an upper arm cuff that is inflated by an electrically
pulse is felt with the fingers aligned along the dorsum of driven pump.
161
Chapter
It is good practice to check the systolic pressure roughly can be heard with a stethoscope placed over the brachial
by palpation of the radial artery before applying the artery at the elbow. These sounds are called the Korotkoff
stethoscope. As the pressure in the sphygmomanometer sounds after the Russian physician who first described
cuff increases above the brachial artery systolic pressure, them. The generation of the Korotkoff sounds is shown
the artery is compressed and the radial pulse becomes diagrammatically in Figure 6.50. As pressure in the cuff
impalpable. As the pressure in the cuff is gradually is lowered, the first appearance of the sound (phase 1)
lowered, a pressure is reached where the blood is able to corresponds to the systolic blood pressure. The Korotkoff
force its way past the obstruction created by the inflated sounds then become louder and more ringing in character
cuff. Initially, this creates the sound of turbulent flow that due to further increased turbulence (phase 2/3) before
becoming muffled (phase 4). Finally, at the point where
the flow again becomes linear, rather than turbulent, the
audible sounds disappear altogether. Although the point
of muffling of the sounds (phase 4) corresponds most
closely to the diastolic pressure, as measured by an
indwelling arterial cannula, the point of disappearance of
the Korotkoff sounds (phase 5) is now used to define
diastolic pressure for clinical and epidemiological
purposes. This is because phase 5 readings are more
reproducible amongst different observers.
Most people consciously or unconsciously round off
the blood pressure reading to the nearest 5–10 mmHg,
but this should be avoided. The most accurate method
for assessing blood pressure is to use a random zero
sphygmomanometer in which the operator presses
levers to indicate when he or she thinks systolic and
diastolic pressures have been reached and then opens the
back of the instrument to read the results off a concealed
scale.
Fig. 6.49 Measuring blood pressure using a sphygmomanometer
and stethoscope. The sphygmomanometer cuff is smoothly applied Important points about the measurement of blood
around the unclothed upper arm and the examiner supports the pressure are summarised in the ‘symptoms and signs’
patient’s arm at ‘heart height’. box.
Taking the blood pressure
Intra-arterial Artery under Cuff Sounds

pressure the cuff pressure
mmHg
cuff above no sounds,
systolic pressure pulse absent
artery occluded
systolic
cuff at
systolic pressure
artery just opens sounds audible
cuff between systolic

artery open for more and diastolic
of systole sounds audible
cuff at
diastolic diastolic pressure sounds audible
artery open for
nearly all of systole
cuff just below
diastolic pressure sounds disappear
artery open all (phase 5)
the time
Fig. 6.50 The relationship between cuff pressure, Korotkoff sounds and arterial pressure.
162
Chapter
Symptoms and signs

a tendency for both systolic and diastolic pressures to
increase with age, although this does not necessarily
Important points about measuring blood pressure
apply to other populations, particularly peoples in whom
• Remove all clothing from arm there is a low salt intake. Most authorities accept a blood
• Support arm comfortably at heart level pressure of over 140/90 mmHg on repeated measurement
• Use correct size of cuff: wide cuff for obese arms, as defining a hypertensive population. In the diabetic
paediatric cuff for children population the corresponding level defining hypertension
• Check systolic pressure by palpitation is a reading consistently greater than 130/80 mmHg.
• Release pressure no faster than 1 mmHg/second A diastolic pressure of greater than 120 mmHg and
• Take phase 5 (disappearance of sounds) as diastolic evidence of end-organ damage would define patients
pressure with severe hypertension. Accelerated phase or malignant
hypertension is a rare form of severe uncontrolled blood
pressure associated with retinal haemorrhages and
requires immediate hospital admission.
Patients with very high blood pressure often have
other evidence of hypertensive disease. End-organ
damage includes retinal changes, left ventricular Red flag – urgent referral
hypertrophy and proteinuria due to hypertensive renal Hypertension
damage. In the absence of end-organ signs, it is important
not to make a final diagnosis of hypertension based on a • Severe hypertension (BP >200/120 mmHg)
single blood pressure recording. Repeated blood pressure • Retinal haemorrhages and cottonwool spots
measurements will nearly always show some tendency to • Proteinuria
regress towards normal. Some patients have high blood • Left ventricular hypertrophy on ECG
pressure when measured in a hospital clinic, yet • Headache
measurement in their own home or by continuous blood
pressure monitoring reveals a more normal pattern. This
is sometimes referred to as ‘white coat hypertension’. Use The converse of hypertension is hypotension or low
of a 24-hour ambulatory blood pressure monitor is blood pressure. Although a systolic blood pressure of less
employed to distinguish artefactual from true essential than 100 mmHg is part of the definition of shock,
hypertension. hypotension is usually characterised by its consequences
such as impaired cerebral or renal function rather than
by an arbitrary pressure level. Postural hypotension,
Differential diagnosis which most commonly presents as dizziness, is
Systemic hypertension
precipitated by changing posture from a recumbent or
sitting position to a standing position. The diagnosis is
Primary: ‘Essential’ hypertension made by measuring the blood pressure with the patient
Secondary: Aortic coarctation lying supine at rest and then re-measuring the systolic
Hormonal: Congenital and blood pressure 2 minutes after changing the position
– adrenal hyperplasia to standing.
– 11-hydroxylase deficiency
Acquired
– phaeochromocytoma Differential diagnosis
– Conn’s syndrome Hypotension
– Cushing’s syndrome Impaired cardiac output
Renal: Polycystic kidneys • Myocardial infarction
Renal artery stenosis • Pericardial tamponade
Acute glomerulonephritis • Massive pulmonary embolism
Chronic renal disease • Acute valve incompetence
Drug-related: Steroids
Hypovolaemia
Contraceptive pill
• Haemorrhage
Non-steroidal anti-inflammatory drugs
• Diabetic pre-coma
Ciclosporin
• Dehydration from diarrhoea or vomiting
Excessive vasodilatation
• Anaphylaxis
The definition of what constitutes high blood pressure • Gram-negative septicaemia
has long been a subject for controversy. In any given • Drugs
population, the distribution of systolic and diastolic blood • Autonomic failure
pressures is continuous. In Western populations, there is
163
Chapter
Emergency Examination of the jugular venous pulse

Severe hypotension (shock)
Evaluation of the jugular venous pulse is a key clinical
Emergency medical assessment of the patient with sign used to assess the performance of the ‘input’ side
severe hypotension (shock): of the heart. The internal jugular vein is in direct
History (from patient, relatives or attendants) communication with the superior vena cava and the right
• Has there been any trauma, haemorrhage or atrium. The normal pressure in the right atrium is
substance abuse? equivalent to that exerted by a 10–12 cm column of blood.
• Has onset been sudden or gradual (over hours or Therefore, when standing or sitting upright the internal
days, e.g. diabetic ketoacidosis, dysentery)? jugular vein is collapsed, when lying flat it is completely
• Has there been any pain (i) in the chest (myocardial filled by a gravitational effect. If the patient lies supine at
infarction, dissecting aneurysm) or (ii) elsewhere (e.g. approximately 45°, the point at which jugular venous
headache in meningococcal septicaemia)? pulsation becomes visible is usually just above the clavicle;
• Is there any other relevant history (e.g. bed rest, this is the position usually chosen for examination of the
airline travel in massive pulmonary embolism)? jugular venous pulse (Fig. 6.51). To examine the pulse,
Clinical examination the patient rests the head comfortably against a pillow,
• Before starting the examination, check that the with the neck slightly flexed and looking straight ahead.
patient’s airway is safe and, if possible, attach an It is important not to tense the sternomastoid muscles
ECG monitor because the internal jugular vein lies directly beneath this
• Check whether the patient is more comfortable muscle. Reliable ways of telling the jugular venous pulse
sitting up (think of pulmonary oedema) or lying flat from the carotid arterial pulse are listed in the ‘differential
(think of hypovolaemia or pulmonary embolism) diagnosis’ box.
• Remove external clothes and conduct a quick but
thorough examination for signs of trauma or
haemorrhage if appropriate. Usually the skin in shock Differential diagnosis
is pale and cold but if it is warm or red think of Distinction between jugular venous and
septicaemia or allergy carotid pulses
• Assess the pulse. Normally it would be fast (100–120
beats/min) in shock, if very slow think of heart block, Venous
if more rapid consider an arrhythmia • Most rapid movement inward
• Quickly assess the major pulses (carotid, femorals). If • Two peaks per cycle (in sinus rhythm)
asymmetrical, think of dissecting aortic aneurysm • Affected by compressing abdomen
• Try and assess the jugular venous pressure. A very • May displace earlobes (if venous pressure raised)
high jugular venous pressure suggests pulmonary Arterial
embolism or cardiac tamponade • Most rapid movement outward
• Check that the trachea is central and that air entry • One peak per cycle
can be heard on both sides of the chest (if not, think • Not affected by compressing abdomen
of tension pneumothorax). If there are widespread • Never displaces earlobes
crackles in the lungs, think of pulmonary oedema
• Listen to the front of the chest for murmurs or
abnormal heart sounds (often very difficult if the
heart rate is rapid)
• Gently palpate the abdomen for tenderness or
pulsation (think of ruptured aortic aneurysm)
• If appropriate consider rectal or vaginal examination
for hidden haemorrhage
Investigation
• As soon as possible record an ECG (diagnosis of
myocardial infarction, arrhythmia, pulmonary
embolism) and take a chest radiograph (and if
appropriate other radiographs, e.g. in the case of
trauma). Consider emergency echocardiography if
diagnosis is still in doubt
Fig. 6.51 Assessing the jugular venous pressure. With the patient
lying supine at 45°, jugular pulsation is normally just visible above
the clavicle.
164
Chapter
Examination of the jugular venous pulse 6
Measuring the height of the jugular venous pulse Venous pressure waveforms
a v a v
a v
normal waveform
jugular
venous position
sternal angle
v v v
mid-right atrium atrial fibrillation
45°
TR TR
Fig. 6.52 Relationship of the jugular venous pulsation, right atrium tricuspid regurgitation (striking systolic
and manubriosternal angle. waves that are both larger and earlier
than normal ‘v’ waves)
It is sometimes said that jugular venous pulsation can

a a
be obliterated by gentle finger pressure and that the
jugular pulse is never palpable. Whilst generally true,
a v v v a
both statements are refuted in patients with severe
tricuspid regurgitation where the venous pulse can be right ventricular hypertrophy with
palpated. exaggerated ‘a’ waves (e.g. pulmonary
Once the jugular venous pulse has been identified, hypertension or pulmonary stenosis)
both its mean height above right atrial level and the
waveform are assessed. As it is not possible to see or feel
the right atrium, it is usual to express the height of jugular
venous pulsation by its height above the manubriosternal ‘x’ ‘x’ ‘x’
angle (Fig. 6.52). A normal jugular venous pressure is
conventionally reported if less than 4 cm above the
manubriosternal angle. constrictive pericarditis high jugular
The waveform of the normal jugular venous pressure venous pulse with exaggerated descent
is biphasic with an ‘a’ wave and a ‘v’ wave (Fig. 6.53). corresponding to onset of systole
Changes in the waveform reflect changes in right atrial
pressure. The ‘a’ wave is a reflection of the pressure
caused by atrial contraction and is therefore absent in
Fig. 6.53 Examples of different jugular pressure waveforms.
atrial fibrillation. The ‘v’ wave is due to atrial filling
against the closed atrioventricular valve and therefore
occurs immediately after the first heart sound. sitting bolt upright. Even sitting the patient upright may
Distinguishing ‘a’ from ‘v’ waves is best made by timing fail to expose a very high venous pressure. When this is
with the aortic pulse pressure because the ‘a’ wave is not suspected, a rough estimate can be made by raising the
synchronous with the arterial pulse pressure whereas the patient’s outstretched hand to a horizontal position at the
‘v’ wave is synchronous. level of the sternomanubrial angle and then slowly raising
In patients with a very high jugular venous pressure, the hand and watching carefully for the point at which
such as occurs in pericardial tamponade or constrictive the veins on the back of the hand collapse. At this point,
pericarditis, the internal jugular vein may be completely the difference in height between the hand and the right
filled with the patient positioned at 45°. In the setting, it atrium or sternal angle is a crude reflection of right atrial
is necessary to sit the patient bolt upright to visualise the pressure.
apex of the pulsation. As a quick rule of thumb, the By far the most common cause of a raised jugular
jugular venous pressure must be raised if jugular venous venous pressure is congestive heart failure, in which the
pulsation is visible above the clavicle with the patient raised venous pressure reflects right ventricular failure
165
Chapter
and a raised right atrial pressure. Examples of different

jugular pressure waveforms are shown in Figure 6.53. In
practice, the waveform that accompanies tricuspid
regurgitation is the most common and most important
abnormality of wave pattern. Free retrograde flow of
blood from the right ventricle into the right atrium and
jugular vein causes the characteristic large ‘CV’ wave that
may even be palpable and provides a clue to the likelihood
of discovering tricuspid regurgitation on direct examination
and auscultation of the heart. Circumstances where the
atrium contracts against a closed tricuspid valve give rise
to a ‘cannon’ ‘a’ wave. This occurs in complete heart
block and ventricular tachycardia. A raised but non-
pulsatile jugular venous pressure should raise the
suspicion of superior vena cava obstruction. Fig. 6.54 Palpating the precordium. For locating the apex beat,
the patient should lie flat on the back but to assess the quality of
the impulses the patient should be rolled onto the left side.
Causes and characteristics of raised jugular
venous pressure Types of apex beat
Common
• Congestive heart failure
• Tricuspid regurgitation Normal
• Normal wave pattern usually preserved
• Large ‘V’ waves
Less common
• Pericardial tamponade
• Massive pulmonary embolism
• Iatrogenic fluid overload ‘Sustained’ or ‘heaving’ apex
beat of left ventricular
Rare hypertrophy, often associated
• Superior vena cava obstruction with a double impulse from
• Constrictive pericarditis concomitant left atrial hypertrophy
atrial component
• Tricuspid stenosis
‘Tapping’ apex in
mitral stenosis
Palpation of the precordium
Palpate the precordium by laying the flat of the hand with
outstretched fingers on the chest wall to the left of the
Diffuse or dyskinetic
sternum (Fig. 6.54). The first manoeuvre is to locate the apex beat after
apex beat, which coincides with the tip of the left ventricle. anterior myocardial
The apex beat is the furthest outward and downward infarction
point at which cardiac pulsation is palpable. With the
patient lying supine at 45°, the normal adult apex beat
Fig. 6.55 Types of apical impulse.
lies in the fifth or sixth left intercostal space, extending
no further than the midclavicular line. Remember that
the heart has some mobility within the thorax, so if you In addition to demarcating the position of the apex
roll the patient onto, for example, the left side, the apex beat, it is important to evaluate the quality of the impulse
beat will displace further outwards. There are circumstances (Fig. 6.55). The quality of the normal apex beat and the
where the apex beat is difficult to palpate. This occurs in range of abnormality is learnt by experience. A thrusting,
markedly obese patients and patients with chronic forceful or heaving apex beat, palpated within the
airways disease and hyperinflated chests such as occurs midclavicular line, indicates a hypertrophic myocardial
in emphysema. In this setting, you might need to roll the response to increased left ventricular workload. This is
patient onto the left side in order to feel the apex beat – characteristic of the myocardial response to hypertension
and even then the pulsation might be undetectable. and aortic stenosis prior to the development of cardiac
166
Chapter
Auscultation of the heart 6
positioning the thenar eminence of the flat of your hand
just to the left of the lower half of the sternum.
Left ventricular hypertrophy
While palpating the heart, the examining hand will
• Hypertension occasionally detect a vibration or ‘thrill’. Thrills are
• Aortic stenosis ‘palpable murmurs’ and are always accompanied by an
• Hypertrophic cardiomyopathy easily heard murmur on auscultation. A diastolic thrill,
which conveys a sensation akin to that felt when stroking
a purring cat, can occasionally be felt in patients
with mitral stenosis. Systolic thrills may accompany
decompensation. Displacement of the apex beat lateral aortic stenosis, ventricular septal defect or mitral
to the midclavicular line indicates left ventricular regurgitation.
dilatation. A diffuse, displaced, poorly localised apex beat
is indicative of more profound damage to the ventricular
muscle. This occurs in extensive myocardial infarction, as Auscultation of the heart
a result of cardiomyopathy and in particular, in patients
with severe aortic incompetence. This diffuse impulse can The stethoscope was originally introduced into medical
often be seen on inspection of the precordium. Another practice by the French physician Laennec at the beginning
characteristic sign that can be detected on pulsation is the of the nineteenth century. In its original form it consisted
tapping apex beat of mitral stenosis. This is partly caused of a wooden cylinder with a small hole drilled from end
by left atrial enlargement causing displacement of the left to end. In addition to introducing a decorous distance
ventricle nearer to the examining hand and, partly, due between the head of the physician and the chest of the
to a loud first heart sound which becomes both palpable patient, the stethoscope has two principal functions.
and audible if the valve cusps are still pliable. Right First, it transmits sounds from the patient’s chest and,
ventricular hypertrophy or dilatation is felt as a parasternal second, it selectively emphasises sounds of certain
heave close to the left sternal border. This is felt by frequencies, enabling the examiner to interpret the
Cardiac auscultation
below left clavicle: upper left sternal border:

continuous murmur of second heart sound, opening
ductus arteriosus well snap, pulmonary valve
heard here. Also radiating murmurs, ventricular septal
pulmonary valve murmurs defect murmur
axilla:
upper right sternal border: 4 murmur of mitral
3
left ventricular outflow regurgitation of sound
murmurs (e.g. aortic stenosis) often radiates here
2
heard here, also radiate to
the neck
1 apex:
good for first heart sound,
murmurs from mitral or
lower left sternal border:
aortic valves
tricuspid regurgitation, aortic radiation of murmurs
third heart sound
regurgitation often heard here 1 mitral regurgitation:
fourth heart sound
apex–axilla
2 aortic regurgitation:
lower left sternal border
3 pulmonary stenosis:
upper left sternal border clavicle
4 aortic stenosis:
apex upper right sternal border neck
Fig. 6.56 Cardiac auscultation; the best sites for hearing sounds and murmurs depend on where the sound is produced and to where
turbulent blood flows radiate.
167
Chapter
auditory information. Indiscriminate amplification of the

sound coming from the chest, as would be produced by
a sensitive high fidelity microphone, actually produces a
signal that is very hard for the human ear to interpret.
The ear pieces of the stethoscope should be angled
forwards to match the direction of the examiner’s external
auditory meati. They should fit snugly but comfortably
and the tubing should not be too long. The bell and
diaphragm selectively emphasise sounds of different
frequencies. The bell is more efficient for listening to low-
pitched sounds such as the mid-diastolic murmur of
mitral stenosis or the third heart sound of cardiac failure.
In contrast, the diaphragm filters out low-pitched sounds
and, therefore, emphasises high-pitched ones. The
diaphragm is best for analysing the second heart sound,
ejection murmurs, ejection and mid-systolic clicks and
the soft but high-pitched early diastolic murmur of aortic
regurgitation.
When auscultating the heart, you should listen at the
apex (known as the mitral area), the tricuspid area
(between the apex and the sternum) and the aortic and
pulmonary areas which are located respectively in
the second intercostal space to the right and left of the
sternum (Fig. 6.56). If an abnormal heart is heard, the
stethoscope can be moved around until the abnormality
is heard most clearly. Relate the auscultatory findings to Fig. 6.57 Simultaneously listening to the heart sounds and timing
the cardiac cycle by simultaneously palpating the carotid them against the carotid pulse.
artery while listening to the heart (Fig. 6.57). A useful
technique is to listen sequentially to the heart sounds.
Initially, focus on auscultating the first heart sound in the on the pulmonary and aortic components of the second
mitral and tricuspid areas. Follow this with a similar focus heart sounds. Once the first and second heart sounds
have been assessed, listen systematically for a third or
fourth heart sound, systolic and diastolic murmurs and,
Differential diagnosis where appropriate, ejection clicks. On discovering a
Factors that might influence the intensity of systolic or diastolic murmur, determine whether there is
the heart sounds radiation of the sound. The pansystolic ejection murmur
of mitral incompetence typically radiates towards the
Loud first sound
axilla whilst the ejection systolic murmur of aortic stenosis
• Hyperdynamic circulation (fever, exercise)
characteristically radiates to the carotids.
• Mitral stenosis
• Atrial myxoma (rare)
Soft first sound HEART SOUNDS
• Low cardiac output (rest, heart failure)
First and second heart sounds
• Tachycardia
• Severe mitral regurgitation The mechanics of the first and second heart sounds and
Variable intensity of first sound the mechanism and physiology of splitting the second
• Atrial fibrillation heart sound have already been described. The first heart
• Complete heart block sound can be easily identified with both the bell and
• Ventricular tachycardia diaphragm but the diaphragm is more efficient for
auscultating and analysing the second heart sound, with
Loud aortic component of second sound
the stethoscope usually best placed at the midleft sternal
edge. It is usual to record the heart sounds in a shorthand
• Dilated aortic root
notation which is derived from the recording made by
Soft aortic component of second sound phonocardiography (Fig. 6.58). Factors causing a change
• Calcific aortic stenosis in the intensity of the heart sounds are summarised in
Loud pulmonary component of second sound the ‘differential diagnosis’ box.
• Pulmonary hypertension The most common causes of a loud first heart sound
include any cause of increased cardiac output and mitral
168
Chapter
Shorthand notation for heart sounds The fourth heart sound
S1
S2
S4
first and second
heart sounds
S1 S2
first and da lub dup

(physiologically)
split second sound
S1 S2
first, second and

third heart sounds
S1 S2 S3
P R T
first, second and
fourth heart sounds
S4
Fig. 6.59 The fourth heart sound.
diastole systole diastole
heart sound usually indicates severe impairment of

left ventricular function and in particular, occurs with
left ventricular dilatation. Consequently, a third heart
sound might be anticipated in patients with dilated
cardiomyopathy, following acute myocardial infarction or
in acute massive pulmonary embolism, when the third
Fig. 6.58 Shorthand notation (derived from phonocardiography) for
recording the heart sounds. heart sound originates from the right ventricle and is
consequently best heard during inspiration. A pathological
third heart sound is usually accompanied by a tachycardia
and, because the phenomenon occurs in the presence of
stenosis (with pliable valve cusps). The most common left ventricular dilatation, the first sound is usually soft
causes of an abnormally quiet first heart sound are because of failure to generate sufficient power to cause
reduced cardiac output, severe mitral valve incompetence full closure of the mitral valve. The cadence of first, second
and the acoustic effect of a thick chest wall or hyperinflated and third heart sounds is usually described by the sound
lungs. The second heart sound is usually softer in the ‘da-da-boom’ and the timing is likened to the sound of
second left interspace than the equivalent right interspace, ‘Kentucky’. The combined sound pattern of first, second
reflecting the lower closing pressure of the pulmonary and third sound has been described by the term ‘gallop
compared to the aortic valve. A louder than expected rhythm’.
ringing second heart sound may be auscultated in A fourth heart sound is an additional heart sound
systemic hypertension or, occasionally, pulmonary occurring late in diastole. This sound coincides with atrial
hypertension. contraction and reflects the contraction of the left atrium
against a raised left ventricular end diastolic pressure.
Third and fourth heart sounds
Consequently, a fourth heart sound can be anticipated in
These are additional heart sounds that convey important patients with left ventricular hypertrophy such as occurs
haemodynamic information. The third heart sound is a in systemic hypertension. A fourth heart sound is also
low-pitched, thudding sound that occurs in early diastole often heard in the early phase following acute myocardial
and coincides with the end of the rapid phase of infarction when the left ventricle is ‘stunned’, less
ventricular filling. It is important to recognise that a third compliant and consequently develops a raised end-
heart sound may be either physiological or pathological. diastolic pressure. A fourth sound sounds a little like
A physiological third heart sound occurs in young fit ‘da-lub-dup’ and timed like ‘Tennessee’ (Fig. 6.59).
adults in circumstances of increased cardiac output (e.g.
Other extra heart sounds
in athletes, in the presence of a fever or during pregnancy).
In this setting, the discovery of a third heart sound is Ejection clicks This is a high-pitched ringing sound that
of no pathological significance. A pathological third usually follows very shortly after the first heart sound
169
Chapter
(Fig. 6.60). An ejection click is a feature of aortic or

Extra heart sounds pulmonary valve stenosis, where it is probably generated
by the sudden opening of the deformed valve. Sometimes,
patients with a dilated pulmonary artery or ascending
click
aorta may have an ejection click without a stenotic
ejection click (plus valve.
ejection systolic murmur)
S1 S2
Opening snap This is a diastolic sound heard in mitral
stenosis caused by the snappy opening of a stenosed but
0.5
still pliable mitral valve under the influence of the higher
opening snap (plus a than normal left atrial pressure. A fibrosed and nonpliable
diastolic murmur of mitral mitral valve will generate only a soft opening snap or no
S1 S2 stenosis) snap at all. The opening snap is best heard to the left of
the sternum and sounds rather like the second component
click
mid-systolic click (plus of a widely split second heart sound.
late systolic murmur of
mitral valve prolapse)
Mid-systolic clicks These are most often associated with
S1 S2 mitral valve prolapse and are caused by the tensing of the
prosthetic mitral valve long and redundant chordae tendineae of these valves.
closing opening
sounds: opening sound The clicks may or may not be associated with a late
analogous to opening systolic murmur (Figs 6.61, 6.62).
snap, closing sound
coincides with S1 Sounds from artificial heart valves The ball, disc or
S4
poppet in an artificial heart valve usually makes a noise
prosthetic aortic valve both when it opens and closes. The closing sound is
opening closing sounds: opening sound
analagous to ejection usually louder than the opening sound. Thus, an aortic
click, closing sound prosthesis will have a soft opening click just after the first
S4
coincides with S2 heart sound and a loud closing click which contributes to
the second heart sound. Conversely, a mitral valve will
give a soft opening click in a similar position to the
Fig. 6.60 Extra heart sounds. opening snap of mitral stenosis and a loud closing click
which contributes to the first heart sound.
Murmurs
Murmurs are musical sounds caused by turbulent flow
occurring at specific points in the cardiac cycle. The
Pansystolic murmur
mitral regurgitation ventricular septal defect
dilated left atrium

atrial fibrillation left
aorta ventricle
pansystolic left common
murmur atrium
S1 S2 S1 S2
left
right ventricle
ventricle
murmur best heard murmur best heard
at apex; radiates arterial pulse at left sternal edge arterial pulse
to axilla but often radiates widely. in adults congenital ventricular septal
Large VSD causes defects are always small or else present
hyperdynamic right with Eisenmenger’s syndrome.
ventricle and mitral Large VSD in adults is usually a sequel to
diastolic flow murmur septal rupture in myocardial infarction
Fig. 6.61 Pansystolic (holosystolic) murmurs: mitral regurgitation (left), ventricular septal defect (right).
170
Chapter
Ejection systolic murmur
aortic stenosis pulmonary stenosis
ejection systolic ejection systolic

murmur aorta murmur
left
atrium soft S2 S1 A2P2
second sound
may be
ejection click split but
in children and varies with
left young adults respiration
ventricle
murmur best heard hypertrophied

at apex and wall slow rising right ventricular normal arterial
upper right carotid pulse heave to left pulse
sternal edge of sternum
radiating to neck
exagerated ‘a’ wave

in jugular phase
Fig. 6.62 Ejection systolic murmurs: aortic stenosis and pulmonary stenosis.
important points in analysing a murmur include its timing Systolic murmurs Systolic murmurs result from one of
in the cardiac cycle, what it sounds like, where it is best three causes: leakage of blood through a structure that is
heard, where it radiates to and what happens during normally closed during systole (e.g. mitral or tricuspid
manoeuvres like deep breathing. valves or the interventricular septum), blood flow through
a valve normally open in systole but which has become
abnormally narrowed (e.g. aortic or pulmonary stenosis),
Symptoms and signs
or increased blood flow through a normal valve (a flow
murmur).
Grading the intensity of murmurs
Murmurs that are due to leakage of blood through an
Grade 1 – just audible with a good stethoscope in a incompetent mitral or tricuspid valve or a ventricular
quiet room septal defect are usually of similar intensity throughout
Grade 2 – quiet but readily audible with a stethoscope the length of systole and are termed pansystolic or
Grade 3 – easily heard with a stethoscope holosystolic murmurs (Fig. 6.61). Occasionally, a valve is
Grade 4 – a loud, obvious murmur competent at the onset of systole but starts to leak halfway
Grade 5 – very loud, heard not only over the through. This occurs in mitral valve prolapse and results
precordium but elsewhere in the body in a murmur that starts in mid or late systole and is
termed a mid-systolic or late systolic murmur.
Sites of radiation of murmurs
Cause ‘Primary’ site Radiation

Tricuspid regurgitation Lower left sternal edge Lower right sternal edge, liver
Pulmonary stenosis Upper left sternal edge Towards left clavicle, beneath left scapula
Mitral regurgitation Apex Left axilla, beneath left scapula
Aortic regurgitation Left sternal edge Down left sternal edge towards apex
Aortic stenosis Apex Towards upper right sternal edge, over carotids
Ventricular septal defect Left sternal edge All over pericardium
Mitral stenosis Apex Does not radiate
171
Chapter
following characteristics: always systolic and quiet; usually
best heard at the left sternal edge; not associated with
Systolic murmurs
ventricular hypertrophy; associated with normal heart
• Ejection systolic sounds, pulses, chest radiology and electrocardiography.
• Innocent systolic murmur
Diastolic murmurs Diastolic murmurs can be divided
• Aortic stenosis
into early and mid-diastolic murmurs. An early diastolic
• Pulmonary stenosis
murmur is characteristic of aortic and pulmonary valve
• Hypertrophic cardiomyopathy
incompetence. Its cadence is maximal at the onset of
• Flow murmurs
diastole when aortic or pulmonary pressure is highest
• atrial septal defect
and the murmur rapidly becomes quieter as pressure in
• fever
the aortic or pulmonary artery falls (decrescendo) (Fig.
• athlete’s heart
6.63). The sound of an aortic diastolic murmur has aptly
Pansystolic murmurs been described as like a whispered letter ‘r’.
• Tricuspid regurgitation A mid-diastolic murmur is usually caused by blood
• Mitral regurgitation flow through a narrowed mitral valve (or, rarely, the
• Ventricular septal defect tricuspid valve). Occasionally, a similar murmur is
generated when there is increased blood flow through
one of these valves. Characteristically, this occurs in
children with atrial septal defect where the tricuspid valve
is anatomically normal but where increased flow derived
Murmurs caused by blood flow through a narrowed
from the shunt creates turbulence. The characteristic
aortic or pulmonary valve or due to increased blood flow
murmur of mitral stenosis is a low-pitched, rumbling
through a normal calibre aortic or pulmonary valve tend
murmur heard during diastole (Fig. 6.64). Sometimes, in
to initiate quietly at the beginning of systole, rise to a
patients in sinus rhythm, the murmur intensifies just
crescendo in midsystole and then quieten again towards
prior to the onset of systole. This phenomenon is caused
the end of systole. These diamond-shaped murmurs are
by atrial contraction increasing the blood flow through
called ejection systolic murmurs (Fig. 6.62).
the narrowed valve and is termed ‘presystolic accentuation’.
Innocent murmurs Innocent murmurs are murmurs Sometimes patients with aortic regurgitation have a mid-
not associated with any cardiac structural abnormality diastolic murmur known as an Austin Flint murmur. As
nor with any haemodynamic disturbance. They occur a result of the aortic valvular incompetence, a regurgitant
commonly in children and young adults and have the jet of blood creates a vibration of the anterior leaflet of
Aortic regurgitation Mitral stenosis
blood pressure early diastolic mid-diastolic

usually shows murmur murmur
wide pulse
‘tapping’
pressure
apex beat
e.g. 170/60
opening
snap
sometimes
better
heard at
base (like
murmur usually best widely split murmur best heard
opening
heard at left sternal occasionally a S2) at apex with patient snap
edge with patient mid-diastolic murmur rolled on left side
sitting up, leaning is caused by murmur often very sometimes mid-diastolic
forward and breathing the regurgitant localised and louder murmur
in expiration jet disturbing does not radiate just before
the mitral leaflets systole
collapsing arterial pulse pulse–atrial fibrillation 80%
Fig. 6.63 Aortic regurgitation as an example of an early diastolic Fig. 6.64 Mitral stenosis as an example of a mid-diastolic murmur.
murmur.
172
Chapter
Cardiovascular system and abdominal examination 6
the mitral valve and also causes mild functional mitral arising on the left side of the heart tend to sound quieter
narrowing, both of which contribute to this functional during inspiration and appear louder in expiration.
murmur. Asking the patient to perform a Valsalva manoeuvre
Murmurs are usually most obvious over the site of by forcibly expiring against a closed glottis makes
the causative lesion and there may be radiation in the most murmurs quieter, as cardiac output is diminished.
direction of the turbulent bloodstream that generates the However, the ejection murmur of hypertrophic obstructive
sound. It is sometimes possible to intensify the murmur cardiomyopathy arising from obstruction the left
by positioning the patient appropriately. The murmur of ventricular outlet tract tends to intensify as the degree of
mitral stenosis is best heard when the patient is rolled obstruction increases. The mid-diastolic murmur of mitral
onto the left side and the stethoscope bell applied to the stenosis is often easier to hear if the patient is made to
cardiac apex (Fig. 6.65). The murmur of aortic regurgitation exercise before listening for it.
is more intense and best heard if the patient is asked to
sit up, lean forward and breathe out fully while the
stethoscope is applied at the left side of the lower part of
the sternum (Fig. 6.66). Differential diagnosis
The behaviour of murmurs during the respiratory cycle Behaviour of murmurs in respiration
provides further clues to their origin and nature. Murmurs
arising from the right side of the heart, such as pulmonary Louder immediately on inspiration
stenosis flow murmurs or tricuspid regurgitation • Pulmonary stenosis
pansystolic murmurs, tend to get louder during inspiration • Pulmonary valve flow murmurs
and quieter during expiration. Conversely, murmurs Quieter immediately on inspiration (may become
louder later)
• Mitral regurgitation
• Aortic stenosis
Louder during Valsalva manoeuvre
• Hypertrophic obstructive cardiomyopathy
• The murmur of mitral prolapse may become louder
or softer during inspiration
Cardiovascular system and

chest examination
The most important pulmonary sign in patients with
cardiac disease is the presence of crackles at the lung
bases. These occur during inspiration and are an early
Fig. 6.65 Mitral diastolic murmurs are best heard using the bell,
with the patient rolled onto the left side. sign of pulmonary oedema. Crackles are believed to be
derived from the sound of collapsed alveoli snapping
open. In mild heart failure, crackles are confined to the
lower zones posteriorly but in severe failure they may be
heard throughout the chest. Patients with severe heart
failure and peripheral oedema may also develop pleural
effusions. Examination of the chest is discussed in detail
in Chapter 5.
Cardiovascular system and

abdominal examination
In patients with cardiovascular disease, the abdominal
examination (see Ch. 7) can add useful information. For
example, in patients with biventricular or right ventricular
failure and raised right atrial pressure, congestion caused
Fig. 6.66 Aortic diastolic murmurs may be heard more easily if the by impaired hepatic venous outflow might cause liver
patient sits up, leans forward and holds the breath in expiration. enlargement. The patient may complain of right upper
173
Chapter
quadrant pain and the hepatomegaly is smooth and Abdominal ultrasound examination provides an accurate
tender. In patients with significant tricuspid incompetence, method for confirming the diagnosis of aortic aneurysm
the enlarged liver may also be pulsatile, reflecting the and of measuring its size.
transmitted impulse from the right ventricle. The
abdominal examination might also reveal an abdominal
aortic aneurysm and, in patients with systemic Peripheral vascular system
hypertension, a renal artery bruit or the presence of
enlarged kidneys might implicate this organ in the Because blood flow to the skin determines the skin
aetiology of the raised blood pressure. The presence of a temperature, temperature change is a common sign
renal artery bruit can be sought by applying the diaphragm of peripheral vascular disease. In the lower limbs,
of the stethoscope to a point 2.5 cm lateral and superior it is often possible to determine the level where the
to the umbilicus on either side. The most common cause skin temperature changes from warm to cold and this
of probable large kidneys is polycystic disease of the should be documented. Trophic skin changes also occur
kidney which inevitably results in hypertension and as a result of arterial insufficiency and this is
chronic renal failure. Ascites occurs rarely in very severe characterised by thin, smooth and hairless skin which
heart failure as a result of generalised fluid retention and is easily traumatised. Examination of the femoral,
the effect of impaired hepatic venous outflow on hepatic popliteal, posterior tibial and dorsalis pedis pulses
and splanchnic haemodynamics. helps determine whether vascular disease is due to
Rarely, splenomegaly may be apparent in patients large or small vessel disease. Look for varicose veins, the
with severe congestive heart failure. This is due to passive characteristic mottled discoloration caused by postphlebitic
congestion. The presence of an enlarged spleen in patients changes, and the presence of varicose ulcers, which
with cardiac disease should also alert to the possibility of localise to the medial aspect of the lower limb and are
subacute bacterial endocarditis where splenomegaly relatively painless.
develops as part of the immune response in this
disease.
OEDEMA
Aneurysm of the abdominal aorta is common,
particularly in men over the age of 60 years. It is important Oedema reflects the abnormal accumulation of fluid
to detect because early elective surgery carries a much in the interstitial space. Fluid in the interstitial space
lower mortality than emergency surgery. On examination, is normally in dynamic equilibrium with plasma, so
the characteristic finding is pulsation at about the level of that the amount of fluid escaping from and re-entering
the umbilicus. It is often possible to feel the normal aorta the capillary network and lymphatic system is normally
at this level, particularly in thin patients. If the abdominal finely balanced (Fig. 6.68). The oedema of heart failure
aorta is aneurysmal, the aorta feels wider than normal is largely the result of increased venous pressure
(Fig. 6.67) and there may be an associated aortic bruit. creating increased end capillary pressure, but factors
such as a slightly reduced plasma albumin concentration
and abnormal capillary permeability may also play a
role.
The oedema of heart failure can be divided into
Abdominal aortic aneurysms pulmonary oedema and peripheral oedema. Peripheral
Oedema
>4 cm
1 2 3 4
1 excessive vasodilatation 3 acute venous obstruction

or chronic venous
2 increased capillary permeability insufficiency
low plasma albumin
increased renal salt retention 4 lymphatic obstruction or
congenital absence
Fig. 6.67 Abdominal aortic aneurysm is felt as an ‘expansile
swelling’ in the abdomen. Fig. 6.68 The factors contributing to oedema formation.
174
Chapter
oedema is the characteristic feature of right-sided heart

failure or biventricular congestive cardiac failure.
Peripheral oedema characteristically accumulates at the
lowest gravitational parts of the body and is known as
‘dependent oedema’. Consequently, when patients are
ambulant, the oedema tends to accumulate in the feet
and ankles. In the recumbent position, there is
redistribution of fluid with less pedal oedema and an
increase in interstitial fluid in the back, especially the
presacral region – where it is termed ‘sacral oedema’. The
more severe the oedema the further up the leg it tends
to extend. In severe and untreated cardiac failure, the
oedema may extend to involve the thigh, the scrotum and
the lower part of the abdominal wall. This phenomenon
is known as anasarca. Severe oedema is frequently
accompanied by increased transudation of fluid into the
serous cavities and may cause ascites and pleural
effusions. It is virtually unknown for cardiac oedema to
involve the facial tissues.
Clinically, peripheral oedema is detected by swelling
that can be displaced by firm finger pressure which leaves Fig. 6.69 Chest radiograph of acute left heart failure caused by
a pitted impression when the finger is removed. This is mitral stenosis. (Note that left heart failure does not equate with left
known as ‘pitting oedema’. The main differential diagnosis ventricular failure: the left ventricle in mitral stenosis is fine!)
of cardiac oedema is stasis oedema, which occurs in
elderly or immobile patients. This is caused by lack of
muscle pump activity, in addition to chronic damage to
cough and in severe left ventricular failure may even
venous valves and possibly a degree of lymphatic
produce frothy pink-stained sputum. The characteristic
obstruction. The distinction is best made by looking for
clinical sign of pulmonary oedema is the presence of
other signs of cardiac failure. In a patient who has a
widespread crepitations or crackling sounds, usually best
normal jugular venous pressure, peripheral oedema is
heard at the base of the lungs. The chest radiograph
seldom the result of heart failure.
shows white fluffy shadows in both lungs (Fig. 6.69). In
severe disease, both lung fields become almost opaque.
HEART FAILURE With acute right-sided heart failure, such as occurs as a
consequence of acute massive pulmonary embolism,
Heart failure refers to the inability to generate a cardiac
there is no pulmonary oedema but the jugular venous
output adequate to satisfy the body’s needs. The European
pressure is markedly elevated and blood pressure is very
Society of Cardiology (2001) definition broadly
low.
encompasses the different facets of the clinical syndrome
including symptoms of exercise intolerance, signs of fluid
retention and response to therapy, accompanied by
objective evidence of cardiac dysfunction at rest. Heart Symptoms and signs
failure can be subdivided into acute and chronic heart
Acute heart failure
failure and also into left-sided, right-sided or mixed heart
failure, depending on the cause. • Acute dyspnoea (pulmonary oedema)
• Hypotension (may be marked by general
vasoconstriction)
Acute heart failure
• Cold clammy skin (peripheral vasoconstriction)
One of the most common manifestations of acute heart • Anxiety
failure is tachycardia and a low systemic blood pressure • Confusion (impaired cerebral blood flow,
– although sometimes intense peripheral vasoconstriction hypoxaemia)
supports a normal or even increased blood pressure • Oliguria
despite a very much reduced cardiac output. Acute left
heart failure is accompanied by pulmonary oedema,
tachycardia and a third heart sound. Pulmonary oedema
is caused by a rise in pulmonary venous pressure to a
Chronic heart failure
point where there is net movement of fluid into the
interstitial, and ultimately, alveolar spaces of the lungs. In chronic heart failure, the body invokes physiological
The patient becomes extremely breathless, develops a responses to compensate for the cardiac insufficiency. In
175
Chapter
Mixed or 'congestive' heart failure
raised (2) reflux pulmonary

jugular vasoconstriction
venous secondary to
pressure raised pulmonary
venous pressure
(3) secondary right

(1) initially left-
heart failure
sided heart
resulting
failure, e.g. from
from pulmonary
left ventricular
hypertension
damage due to
myocardial
infarction
Fig. 6.71 Treadmill exercise testing is best used to confirm a clinical

crepitations at enlarged salt and diagnosis of angina and to get an objective estimate of exercise
lung bases tender liver water retention tolerance.
sometimes peripheral
pleural effusions oedema
Fig. 6.70 Mixed or ‘congestive’ heart failure starts as left heart

principal manifestations: angina, the acute coronary
failure, but secondary pulmonary vasoconstriction then causes right
heart failure. syndrome (myocardial infarction) and chronic heart
failure. The characteristic features of angina have already
been described in the section on taking a cardiac
history.
Symptoms and signs Physical examination of the angina patient is frequently
Chronic heart failure normal. Nonetheless, the examiner should seek signs of
• Fatigue on minimal exertion hyperlipidaemia, such as corneal arcus, tendon xanthomata
• Exertional dyspnoea and xanthelasma. Because the resting ECG is frequently
• Peripheral oedema entirely normal in patients with angina, confirmation of
• Abdominal discomfort (from hepatic distension) myocardial ischaemia is usually made by ECG exercise
• Nocturia (reversal of diurnal rhythm) testing (Fig. 6.71). Other tests used commonly for the
• Weight loss and cachexia diagnosis of coronary artery disease include myocardial
perfusion scanning (Fig. 6.72) and coronary arteriography
(Fig. 6.73).
chronic left heart failure, there is often a reflex elevation

of pulmonary vascular resistance, protecting the patient
from pulmonary oedema but at the cost of generating Risk factors
secondary right heart failure. This combination is Coronary artery disease
sometimes called mixed, biventricular or congestive heart Inherited
failure (Fig. 6.70). • Familial hyperlipidaemia
Another important compensatory mechanism is fluid • High lipoprotein a (e.g. Indo origin)
retention mediated by the renin–angiotensin system • Others*
which increases renal salt and water reabsorption. This
Acquired
has the effect of increasing cardiac filling pressure
• Smoking
(manifested by a raised jugular venous pressure) at the
• Acquired hyperlipidaemia
cost of increased oedema.
• Diabetes
• Hypertension
• Physical inactivity
CORONARY ARTERY DISEASE
Angina *This includes many common polymorphisms with small
(but cumulative) effects and some rare polymorphisms
Coronary artery disease is the most common form (e.g. pseudoxanthoma elasticum) with large effects.
of heart disease in the Western world. It has three
176
Chapter
ECG in myocardial infarction
Normal
P Q S T
Acute myocardial damage
Massive S-T
segment
Fig. 6.72 Myocardial perfusion scan showing evidence of anterior elevation
reversible ischaemia. loss of R wave
Resolving myocardial infarction
terminal
T inversion
Q wave
Old myocardial infarct
T wave
inversion
Q wave
Fig. 6.73 Coronary arteriogram showing left main coronary stenosis
(arrow).
Fig. 6.74 ECG showing features of acute myocardial infarction.
Symptoms and signs

Hyperlipidaemia Acute coronary syndrome
Common Acute coronary syndromes are nearly always caused by
• Corneal arcus (nonspecific in patients over 50 years coronary thrombosis. The coronary thrombosis occurs at
old) the site of disruption of an atheromatous plaque triggered
• Xanthelasma (nonspecific in patients over 50 years by inflammation. Three distinct clinical syndromes are
old) currently recognised including unstable angina, non-ST
• Tendon xanthomas (mainly in familial segment elevation myocardial infarction (NSTEMI) and
hypercholesterolaemia) ST segment elevation myocardial infarction (STEMI).
Less common However, the clinical presentation is identical. STEMI is
• Palmar xanthomas associated with typical electrocardiographic changes of
• Eruptive xanthomas ST elevation and Q wave formation due to transmural
• Ejection systolic murmur (familial myocardial ischaemia (Fig. 6.74) and is always associated
hypercholesterolaemia) with myocardial necrosis confirmed by a rise in plasma
• Lipaemia retinalis level of cardiac enzymes including creatine kinase or
troponin.
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Chapter
Unstable angina and NSTEMI are associated with a from thrombosis or much more rarely from embolism
variety of electrocardiographic changes including a from the heart.
normal ECG, T wave inversion or ST segment depression. Acute arterial obstruction presents with a cold, white,
Unstable angina can be distinguished from NSTEMI by painful, pulseless limb. The site of obstruction is usually
the absence of myocardial necrosis. NSTEMI patients obvious from examining the pulses but confirmation by
have a rise in cardiac enzymes (but without ST elevation) vascular imaging is generally necessary, especially prior
due to sub-endocardial ischaemia. The patient may to planned surgery. Check all the pulses of the unaffected
previously have suffered from angina, but frequently this limbs, as there might be some clinical evidence of more
is not the case. The hallmark of an acute coronary diffuse or chronic peripheral vascular disease. This might
syndrome is angina pain at rest, often associated manifest as reduced pulse volumes or absent pulses
with autonomic symptoms including nausea, vomiting where a collateral circulation maintains function and
and sweating. In a small proportion of patients, tissue viability. Embolism to multiple sites may be the
particularly elderly people and individuals with first clue to a cardiac disease such as atrial myxoma.
diabetes mellitus, myocardial ischaemia and infarction Chronic arterial insufficiency occurs most commonly
can be painless and might present with dyspnoea in the lower limb and usually presents as intermittent
alone. claudication. The patient is aware of exercise-induced
pain in the leg, thigh or buttock. Characteristically the
pain relieves rapidly on stopping to rest. Examination of
the leg reveals weak or absent foot, knee and sometimes
Symptoms and signs femoral pulses. There may be a murmur or bruit over the
femoral artery because of turbulence caused by upstream
Acute myocardial infarction
narrowing in the internal or external iliac arteries. As the
Symptoms disease progresses, the time to claudication reduces until
• Severe pain finally the patient experiences rest pain. Pain is often
• Pain persists despite rest worse at night. Patients with severe chronic arterial
Physical signs insufficiency in the leg often gain partial relief by hanging
• Signs of sympathetic activation (pallor, sweating) the leg over the side of the bed outside the bedclothes.
• Narrow pulse pressure Paradoxically, this often makes perfusion of the foot
• May be extrasystoles worse. Chronically ischaemic skin tends to become
• May be added (third) heart sound discoloured and shiny, and hair is lost from the foot.
Infection, is often initiated by a minor injury such as that
occurring during toenail clipping and infection
characteristically spreads rapidly. Eventually, gangrene
may affect the toes and foot (Fig. 6.75).
An early complication of STEMI is ventricular fibrillation Patients with diabetes mellitus are particularly
which is the most serious of cardiac arrhythmias, often susceptible to peripheral arterial disease. As diabetes
requiring urgent defibrillation. Late complications include affects both large and small blood vessels as well as the
other cardiac arrhythmias such as ventricular tachycardia, intercellular tissue matrix, peripheral tissue damage tends
atrial fibrillation or bradycardia, cardiac failure, cardiac to be disproportionately more severe than would be
rupture (myomalacia), severe mitral valve regurgitation expected from the clinical assessment of the large vessels.
and, occasionally, the development of ventricular septal The damage potential is further aggravated when there
defect or mild mitral regurgitation due to papillary muscle
fibrosis. These complications are now less common since
the advent of prompt reperfusion therapy.
Chronic heart failure due to ischaemic heart disease
has the clinical features of any other form of chronic heart
failure and diagnosis can usually be made on the basis of
the history of effort dyspnoea and orthopnoea.
Peripheral vascular disease

Peripheral vascular disease refers to disease of both
the peripheral arterial and venous systems. Peripheral
arterial disease results mainly from acute or chronic
impairment of peripheral blood supply to a limb. This
may result from atheromatous narrowing of the artery, Fig. 6.75 Gangrene of toes in peripheral vascular disease.
178
Chapter
is also accompanying diabetic sensory neuropathy, and prevent blood flowing back from the femoral vein by
indeed, diabetic patients may sustain injuries giving rise tying a tourniquet around the upper thigh. Identification
to infection without noticing much discomfort until the of the site of perforating veins is an important step in
infection is well established. treating varicose veins by injecting a sclerosant solution
The main aids to clinical diagnosis of peripheral arterial around incompetent perforators. Very advanced varicose
disease are Doppler ultrasound examination, which veins may require ligation and stripping of the long (and
evaluates both vessel diameter and blood flow, and either sometimes the short) saphenous vein. The importance of
contrast or magnetic resonance angiography. the long saphenous vein as a source of vascular tissue in
coronary bypass surgery makes it important to preserve
this vessel if possible.
DISEASES OF THE PERIPHERAL VEINS
The principal diseases of the peripheral veins are varicose Chronic venous insufficiency
veins, thrombophlebitis and deep venous thrombosis.
Failure or inadequacy of the ‘muscle pump’ mechanism
Varicose veins may also lead to chronic oedema of the legs and feet. This
is more common in elderly, obese and sedentary patients
Varicose veins are readily apparent as excessively dilated
and tends to become self-perpetuating because the legs
superficial leg veins. In adopting an upright posture, the
are often painful and underused. The oedema is often
human species has a special adaptation to ensure
relatively firm or ‘brawny’ and pits only reluctantly on
adequate venous drainage from the legs towards the
pressure. The oedema is readily distinguished from heart
heart. A system of one way valves in the venous system
failure because the jugular venous pressure is normal.
of the lower limbs ensures flow toward the heart
Sometimes chronic venous insufficiency is associated
orchestrated by the pump action of the lower limb
with obstruction of the inferior vena cava but in this
muscles. Varicose veins usually result from defects in the
setting there are usually grossly distended collateral veins
valvular system that normally directs the venous blood
visible on the abdominal wall.
flow from the legs via the deep veins against the force of
gravity. The two major causes of varicose veins are Varicose ulceration and eczema
defective valves in the ‘perforating veins’ which connect
the deep and superficial venous systems in the calf, and Chronic venous insufficiency results in a rise in tissue
defective valves in the upper part of the long saphenous pressure affecting skin and subcutaneous tissue attrition.
vein where it joins the femoral vein at the thigh. This may lead to skin necrosis and ulceration, most
Commonly, the problem is initiated by incompetent commonly at the ankle just above the medial malleoli.
valves in the perforating veins and saphenofemoral The skin is often dusky and indurated. Scarring as part
incompetence is secondary to the resulting dilatation of of the healing process tends to impair the microcirculation
the superficial venous system. further and the condition may become self-perpetuating
(Fig. 6.76).
Thrombophlebitis
Risk factors
Superficial thrombophlebitis refers to inflammation
Varicose veins and thrombosis of a superficial vein. This commonly
• Obesity results either from local trauma or from an intravenous
• Stasis from sitting or standing (position) infusion but may occur spontaneously. There is local
• Pregnancy pain, redness and tenderness over the course of the vein.
• Pelvic venous obstruction The condition is usually benign and self-limiting but
• Damage to deep veins from thrombosis septic thrombophlebitis from a drip site infection can lead
• Trauma to short or long saphenous vein to septicaemia.
• Hereditary
Deep vein thrombosis
Thrombosis of the deep veins in the calf or pelvis usually
occurs as a result of a combination of intravascular stasis
Varicose veins are always most apparent when the and damage of the endothelial lining. Inactivity is the
patient is standing upright and the dilated veins empty major predisposing factor and it is well known that bed
completely when the legs are raised above heart level. By rest, hospitalisation and long haul flights place individuals
elevating the legs to empty the veins and then watching at particular risk. Until measures were taken to prevent
them refill as the leg is lowered, it is often possible to inactivity by encouraging early mobilisation and using
localise the sites of incompetent perforating veins and low dosage low molecular weight heparin, deep venous
control them by local finger pressure. If the saphenofemoral thrombosis was a common and potentially fatal
junction is incompetent, it may be necessary first to complication of major surgery. Deep vein thrombosis
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Chapter
The diagnosis of deep vein thrombosis needs to be

confirmed by either Doppler ultrasound scanning or
venography. It is important to remember that deep vein
thrombosis, particularly in elderly people, may be
accompanied by very few clinical signs and often goes
unnoticed until it presents as pulmonary embolism.
Deep vein thrombosis
Pain and swelling in the leg may be caused by:

• deep vein thrombosis
• ruptured head of gastrocnemius muscle
• ruptured osteoarthritic cyst (Baker’s cyst) or knee
joint
• anterior compartment syndrome (skin splints)
Pulmonary embolism is the most important

complication of deep venous thrombosis. If extensive
thrombosis occurs in the deep veins of the lower limb, a
distal fragment may become detached and travel through
Fig. 6.76 Severe varicose ulceration of the leg. the great veins to the heart, where it may either lodge in
the right ventricle or in the pulmonary artery. Clinically,
pulmonary embolism may present as a pulmonary infarct,
acute massive pulmonary embolus and a more chronic
may also occur in the absence of any obvious predisposing pulmonary thromboembolic disease.
factor. On more extensive investigation, these patients
may have abnormalities of the blood clotting and Acute pulmonary infarction
fibrinolytic systems (thrombophilia) and should be further This is usually the consequence of a relatively small
investigated. Hereditary causes of thrombophilia include pulmonary embolus lodging in a branch of the pulmonary
the Factor V Leiden, prothrombin gene mutation, Protein artery. As a result of vasospasm and reduced air entry, a
C and S deficiency, anti-phospholipid antibody syndrome wedge-shaped section of the lung downstream of the
and anti-thrombin III deficiency. block becomes necrotic. This, in turn, causes inflammation
The characteristic clinical features of deep vein of the pleura straddling the infarct and this results in the
thrombosis in the leg are pain, swelling and occasionally characteristic presentation with sudden onset pleuritic
redness. The pain is a deep aching pain which is worse pain. The patient may complain of dyspnoea and
on activity but persists at rest. Often, the pain is absent tachypnoea might be evident on examination. There is
despite the presence of extensive venous thrombosis. Leg seldom hypotension. A further clue to the diagnosis is
swelling can be assessed clinically by comparison of calf profound arterial hypoxaemia with normal partial
diameters at a fixed point below the patella. There is often pressure of carbon dioxide. The chest radiograph may
dilatation of the superficial veins and warm skin resulting show a wedge-shaped opacity with its base along the
from diversion of blood flow from the deep to the pleural edge. The diagnosis is supported by an isotopic
superficial veins. Pain in the calf can sometimes be ventilation and perfusion lung scan which often shows
produced by dorsiflexing the foot (Homan’s sign) but this other perfusion defects.
sign is most often absent in patients with deep venous
Acute massive pulmonary embolism
thrombosis. If pain and swelling are mainly below the
knee, it is likely that the thrombosis is in the calf veins. This occurs most commonly in postoperative patients.
If the swelling and tenderness extends to the thigh or the The patient suddenly becomes extremely breathless,
groin, then the thrombosis may involve the femoral or profoundly hypotensive and may not be able to sit
iliac veins: this is potentially more serious because upright. There is often an accompanying urge to evacuate
thromboembolism from these sites is frequently the bowels. The jugular veins are markedly distended and
massive. the liver may also be enlarged by congestion. Heart
The main differential diagnosis of deep vein thrombosis sounds are usually quiet because of the reduced cardiac
of the legs is spontaneous rupture of the gastrocnemius output and there might be a third sound best heard to
muscle and rupture of a Baker’s cyst in the popliteal fossa. the left of the sternum. The chest radiograph is usually
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Chapter
unhelpful but the ECG shows a characteristic pattern of INFECTIVE ENDOCARDITIS

acute right ventricular strain (S-wave in standard lead I, Infection of the endocardium of the heart is known as
Q waves in standard lead III associated with an inverted infective endocarditis. There are three principal clinical
T wave). Echocardiography shows a dilated, poorly types of endocarditis: acute, subacute, and postoperative
contracting right ventricle and a small underfilled left endocarditis.
ventricle. Definitive diagnosis is by isotopic ventilation
perfusion scanning and/or CT pulmonary angiography.
Acute endocarditis
Chronic pulmonary thromboembolic disease
Acute endocarditis is the result of endocardial infection
Chronic thromboembolic disease results from the occurring in a normal or abnormal heart with a virulent
showering of multiple small pulmonary emboli over a organism such as Staphylococcus aureus or Streptococcus
period of time. The clinical features are those of chronic pneumoniae. The infection usually involves one of the
pulmonary hypertension (see below). The diagnosis heart valves but may involve the endocardium adjacent
should be suspected in patients who develop chronic to a defect such as a ventricular septal defect. The infection
pulmonary symptoms or right-sided heart failure against may destroy valve tissue, or result in abscess formation
a background of chronic or recurrent deep vein thrombosis or the formation of large vegetations composed of an
or evidence of thrombophilia. aggregation of bacteria, platelets and thrombin. The
patient is usually seriously ill with a fever and profound
PULMONARY HYPERTENSION systemic symptoms. One of the characteristic clinical
findings is rapidly developing or changing cardiac
Pulmonary hypertension is defined by a mean pulmonary murmurs, indicative of the destructive underlying process.
arterial pressure >25 mmHg and can be caused by Other signs include finger clubbing and splinter
obstruction or increased vascular tone at any point in the haemorrhages. The cardiac vegetations are a potential
pulmonary vascular tree. In order to better understand source of septic systemic emboli that may be carried
pulmonary hypertension, it is useful to divide causes into through the circulation to reach distant parts of the
those predominantly precapillary, capillary or postcapillary. body.
Precapillary pulmonary hypertension is due to pathology
involving the pulmonary arteries and arterioles including
chronic pulmonary thromboembolic disease, primary Subacute endocarditis
pulmonary hypertension and pulmonary vasculitis.
Capillary pulmonary hypertension occurs in conditions Subacute endocarditis may result from a more indolent
associated with parenchymal lung disease including intercurrent infection of an already diseased heart
cystic fibrosis and other chronic lung diseases such as valve or septal defect. The time course of the illness is
chronic obstructive pulmonary disease. Postcapillary much more insidious than acute endocarditis. The most
pulmonary hypertension is caused by left heart failure common organism associated with subacute endocarditis
due to primary left ventricular myocardial dysfunction or is Streptococcus viridans. Another cause of subacute
ventricular failure secondary to aortic and/or mitral valve endocarditis is partial treatment of acute endocarditis
disease. Symptoms may be insidious, beginning with with inadequate doses of antibiotics.
exertional dyspnoea which becomes progressively more Patients present with fatigue and tiredness, depression,
severe. Rarely, chest pain occurs, which is sometimes unexplained fever, and symptoms related to the
called right ventricular angina. Progressive right heart progressive valve destruction or systemic emboli. There
failure supervenes and this is detected by the signs of is nearly always a heart murmur and the combination of
right heart failure and fluid overload (see ‘symptoms and fever and a heart murmur should always raise the
signs’ box). suspicion of endocarditis. Like acute endocarditis, the
murmurs may change but this usually occurs over a time
course of days or weeks rather than hours. Finger clubbing
and splinter haemorrhages are common cardinal physical
Symptoms and signs
signs. In untreated cases there may be anaemia and
pigmentation of the skin. There is often splenomegaly,
Pulmonary hypertension
reflecting of the involvement of the immune system in
• Loud pulmonary component of the second sound this subacute infection. Other signs include localised
• Parasternal (right ventricular) heave subconjunctival haemorrhages, tender swellings in the
• Dominant a wave in jugular venous pressure finger pulps (Osler’s nodes), painless macules on the
• Tricuspid regurgitation palms and soles (Janeway lesions) and haemorrhagic
• Pulmonary regurgitation spots in the retina characterised by an area of central
• Signs of right heart failure (pedal oedema, ascites, pallor (Roth spots). Many of the systemic features of
pleural effusion) subacute endocarditis are due to immune complex
deposition and systemic vasculitis.
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Chapter
Postoperative endocarditis
Postoperative endocarditis most commonly follows Hypertrophic cardiomyopathy
open heart surgery and may involve artificial heart valves
or other implanted material. The most common organism
is a coagulase-negative staphylococcus. The clinical sometimes
reverse splitting hypertrophied
features may resemble those of acute or subacute left atrium causes
of S2
endocarditis. fourth sound and
double apical impulse
S 4 S1
MYOCARDITIS midsystolic
Myocarditis is an inflammatory infection of heart muscle, murmur
usually resulting from a virus infection. Clinically,
myocarditis usually presents with heart failure or an
arrhythmia. There is often cardiac dilatation, a third heart
sound and there may be a pansystolic apical murmur jerky pulse
arising from ‘functional’ mitral incompetence caused by
dilatation of the ventricle and consequent stretching of
the chordae tendinae and papillary muscles. hypertrophied septum hypertrophied left
may bulge into left ventricle:
ventricular outflow ‘sustained’ apex beat
CARDIOMYOPATHY tract causing obstruction
giving systolic murmur
Cardiomyopathy is a general term meaning ‘heart muscle and jerky pulse
disease’. Clinically, cardiomyopathy can be classified into
hypertrophic, dilated and restrictive types.
Not all cases of hypertropic cardiomyopathy have left
Hypertrophic cardiomyopathy ventricular out-flow obstruction. In those that do,
obstruction is made worse by isoprenaline, vasodilators,
Hypertrophic cardiomyopathy is characterised by Valsalva manoeuvre, ectopic beats and improved
abnormal cardiac muscle hypertrophy in the absence of by beta blockers and vasoconstrictors.
a stimulus such as hypertension. The hypertrophy may
be ‘asymmetrical’, that is, it specifically affects the
Fig. 6.77 Findings in hypertrophic cardiomyopathy.
interventricular septum, which bulges into the left
ventricular outflow tract and causes obstruction to blood
flow during ventricular systole. This variant, called
hypertrophic obstructive cardiomyopathy (HOCM), has Restrictive cardiomyopathy
been associated with sudden death, often occurring This is a rare condition in Western countries. The clinical
during sport or exercise. The clinical features of presentation mimics constrictive pericarditis and the
hypertrophic obstructive cardiomyopathy are summarised differential is readily made by echocardiography. Causes
in Figure 6.77. of restrictive cardiomyopathy include systemic amyloidosis
Dilated cardiomyopathy and eosinophilic heart disease.
Dilated cardiomyopathy is characterised by a global

impairment of left ventricular function, leading to ACUTE RHEUMATIC FEVER
progressive dilatation of the ventricles. Most commonly, Acute rheumatic fever is caused by a throat infection with
the cause is unknown and this is termed idiopathic dilated certain strains of beta-haemolytic streptococci. Many
cardiomyopathy. Similar pathology can occur in alcoho- of the features are a consequence of an autoimmune
lic patients and patients with systemic diseases such as response to this organism. Whilst rheumatic fever is now
sarcoidosis, haemochromatosis, thyrotoxicosis and uncommon in Western countries, the condition remains
myocarditis; a very rare form occurs in pregnancy prevalent in the developing world. The long-term
(peripartum cardiomyopathy). Dilated cardiomyopathy consequences of the acute infection and the immunological
has been associated with certain drugs, especially response remains an important cause of chronic valvular
anthracyclines used in chemotherapy. The clinical heart disease. Clinically, acute rheumatic fever presents
presentation is dominated by symptoms and signs of in children or young adults either with pharyngitis, an
biventricular heart failure. The apex beat is displaced acute, migratory polyarthritis or with Sydenham’s chorea.
laterally, indicating left ventricular dilatation, and Other features include an erythematous non-itchy skin
invariably there is a gallop rhythm (third and fourth heart rash called erythema marginatum which is fleeting,
sounds). There may be mitral or tricuspid regurgitation variable and has a serpiginous margin and subcutaneous
caused by stretching of the chordae tendinae and papillary rheumatic nodules which are pathognomonic and located
muscles attached to the dilated utricular wall. on the extensor surfaces of the knees and elbows.
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Chapter
Cardiac involvement is caused by a pancarditis affecting usually varies in intensity when listened to interpretively
the endocardium, myocardium and pericardium. over a period of a few hours. Patients with acute
Endocardial involvement is usually signalled by the pericarditis are often pyrexial and may feel systemically
development of a pansystolic murmur caused by unwell.
regurgitation of blood through an incompetent
Pericardial effusion
oedematous mitral valve. Another important murmur is
a soft mid-diastolic murmur resembling the murmur of Normally, there is only just sufficient fluid in the
mitral stenosis and caused by oedema of the mitral valve pericardial cavity to lubricate the visceral and parietal
and platelet vegetations. Listening at different times of pericardial surfaces during cardiac movement. Excessive
the day, this murmur varies in intensity and is called a accumulation of pericardial fluid is called a pericardial
Carey Coombs murmur. Its presence has prognostic effusion.
significance as in these patients the acute valvulitis
invariably progresses to a fibrotic mitral stenosis. Differential diagnosis
Myocarditis usually manifests as prolongation of the PR
Pericardial effusion
interval of the ECG.
Infection
• Viral pericarditis
Symptoms and signs • Bacterial pericarditis (streptococcus)
• Tuberculous pericarditis
Criteria for the diagnosis of rheumatic fever
Myocardial infarction
Major criteria • Peri-infarct pericarditis
• Carditis • Cardiac rupture
• Polyarthritis • Dressler’s syndrome
• Subcutaneous rheumatic nodules
Malignant pericarditis
• Sydenham’s chorea
• Secondary (common) or primary (rare) tumours
• Erythema marginata
• Leukaemia
Minor criteria
Autoallergic
• Prolonged PR interval
• Acute rheumatic fever
• Recent history of a throat infection
• Rheumatoid arthritis
• Serological evidence of recent streptococcal infection
• Arthralgia Other
• Raised ESR • Myxoedema
• Trauma (stab wounds)
• After cardiac surgery
Diagnosis requires the presence of either two major

criteria or one major criterion and two minor criteria.
The clinical features of a pericardial effusion depend
both on the amount of fluid and the speed with which it
PERICARDIAL DISEASE accumulates. A large amount of fluid or the very rapid
The heart normally contracts within a smooth, closely accumulation of fluid causes compression of the heart,
fitting serous cavity – the pericardium. The principal particularly the right ventricle, causing a substantial
pericardial diseases are acute pericarditis, pericardial reduction in cardiac output. This is termed ‘cardiac
effusion and chronic constrictive pericarditis. tamponade’ and is a medical emergency. The patient is
often very ill, hypotensive and peripherally vasoconstricted.
Acute pericarditis
There may be pulsus paradoxus which is a variation in
The symptoms of acute pericarditis have already been pulse volume with respiration (Fig. 6.78). The jugular
discussed under chest pain. The most characteristic venous pressure (JVP) is very high but this may be difficult
physical sign on examination is the pericardial rub. This to see because the patient may be too hypotensive to sit
is often mistaken for a murmur but usually has a distinct upright. Whereas normally the upper level of the JVP falls
scratchy quality that sounds like two leather surfaces during inspiration as blood is sucked into the chest and
being rubbed together. In sinus rhythm, the rub is returned to the right heart, in pericardial tamponade, the
rhythmic and occurs in the presystolic, systolic and upper level rises paradoxically due to obstructed passage
diastolic phases of cardiac contraction. Pericardial rubs of the increased venous inflow occurring in inspiration.
may be best heard with the patient sitting up, leaning Even a small amount of fluid, acuminating rapidly, can
forward and holding their breath in deep expiration cause cardiac tamponade. In this setting, the usual signs
(similar to the position for hearing aortic diastolic of a pericardial effusion, including increased area of
murmurs). The pericardial rub is usually evanescent and dullness to percussion in the front of the chest and an
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Chapter
Pulsus paradoxus
pulmonary veins are

outside pericardium: during
inspiration pulmonary venous
return is inadequate to fill
left ventricle properly
pericardial fluid
tends to raise
left ventricular
diastolic pressure
pericardial fluid under pressure

compresses right atrium and right ventricle,
reducing output of right side of heart
Fig. 6.79 Characteristic diastolic equalisation of right and left

ventricular pressures leading to ‘dip and plateau’ appearance.
15–20 mmHg
difference
between inspiration
inspiration
and expiration If pericardial fluid accumulates slowly over days or
expiration
weeks, this is often accommodated by stretching of the
pericardium rather than cardiac tamponade. A chronic
Fig. 6.78 Pulses paradoxus, or the apparent diminution of the pulse
pericardial effusion may be detected accidentally or, more
on inspiration, is a feature of pericardial tamponade.
commonly, it presents as chronic right-sided cardiac
failure, with marked peripheral oedema and, sometimes,
enlarged globular cardiac shadow on a chest radiograph, ascites. Breathlessness is conspicuously absent despite
are unreliable in diagnosing cardiac tamponade. Bedside the signs of right heart failure. The jugular venous pressure
echocardiography is the best way of confirming the is usually markedly elevated and there is paradoxical
diagnosis of a pericardial effusion and, if necessary, this movement with respiration. There is often an enlarged
can be followed by pericardiocentesis. area of dullness on percussion to the left of the sternum.
Depending on the volume of effusion there may or may
not be a pericardial rub. In the presence of a large effusion,
the apex beat will be impalpable and the heart sounds
soft or virtually inaudible. There may be a pulsus
Cardiac tamponade paradoxus, but this is often less prominent than in acute
Causes cardiac tamponade. Chest radiography shows cardiac
• Any cause of pericardial effusion (see ‘pericardial enlargement and echocardiography is the simplest
effusion differential diagnosis’ box) investigation to confirm the diagnosis.
• Pneumonia Chronic constrictive pericarditis
• Trauma
Chronic inflammation of the pericardium may lead to a
Clinical presentation
thickened fibrotic pericardial membrane that constricts
• Hypotension
and compresses the heart. Worldwide, tuberculous
• Oliguria
pericarditis remains the most common cause, although it
• Raised jugular venous pulse
may also follow acute viral pericarditis, cardiac surgery or
• Paradoxical pulse
chest wall or lung radiation.
Diagnosis The clinical features of chronic constrictive pericarditis
• Chest radiograph: enlarged heart shadow are similar to those of chronic pericardial effusion.
• ECG: small voltages, ‘electrical alternans’ There are readily visible signs of right-sided heart failure,
• Echo: effusion with collapse of right ventricle often with severe and widespread oedema. Abdominal
Treatment distension is common and due to ascites. The jugular
• Pericardiocentesis venous pressure is elevated and often has a characteristic
• Surgical drainage waveform, with a very rapid dip in the pulse as the
tricuspid valve opens, followed by an equally abrupt
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Chapter
termination as filling of the ventricle is curtailed. In by echocardiography or at cardiac catheterisation. There

longstanding severe constrictive pericarditis, the is a characteristic ‘dip and plateau’ or ‘square root’ sign
pericardium may become adherent to the ribcage and the in the pressure curves of the right and left ventricles and
examiner can feel a tugging on the posterior ribs in time equalisation of pressure in the range of 5 mmHg or less
with the heart beat (pericardial rub). Diagnosis is made (Fig. 6.79).

Cardiovascular examination
• General approach and techniques unaltered • Cardiac arrhythmias are common and do not generally
• Some stress tests may be impractical but there are require investigation unless symptomatic
alternatives • Causes of dizziness or transient loss of consciousness
• Likely to be multisystem disease include postural hypotension (often drug induced),
• Common problems are hypertension, ischaemic heart vertebrobasilar insufficiency, arrhythmias (especially
disease and peripheral vascular disease bradycardia)
• Ischaemic heart disease may be asymptomatic • Multiple drug therapy may be the cause of the
• Acute myocardial infarction may be ‘silent’ problem – nonsteroidals cause fluid retention and
• Ankle swelling usually a clue to venous insufficiency hypertension
not heart failure
• Aortic stenosis is common and difficult to diagnose
but worth treating if severe
Review
Framework for the routine examination of the cardiovascular system
1. Observe the patient. Are they comfortable at rest? 9. Palpate the precordium, locate the apex beat and
Watch for features of breathlessness or cyanosis. assess its character. Assess the feel of the rest of
Look out for any cardiac scars that may be relevant. the precordium and the presence of any abnormal
2. Take the patient’s hand and assess warmth, vibrations or thrills.
sweating and peripheral cyanosis; examine the nails 10. Listen with the stethoscope and assess heart sounds
for clubbing or splinter haemorrhages. and murmurs systematically in the four valve areas:
3. Palpate the radial pulse and assess the rate and mitral, tricuspid, pulmonary and aortic. If
rhythm. appropriate, listen over the carotid artery for
4. Locate and palpate the brachial pulse and assess its radiating murmurs or bruits.
character. Measure the blood pressure. If there is 11. Percuss and auscultate the chest both front and
any suspicion of a problem with the aortic arch, back looking for pleural effusions. Listen for
compare pulses in both arms. crepitations at the lung bases.
5. Palpate the carotid pulse and assess its volume and 12. Lie the patient flat and palpate the abdomen,
character. feeling in particular for the liver and any dilatation
6. With the patient lying supine at 45°, assess the of the abdominal aorta.
height of the jugular venous pressure and the 13. Assess the femoral pulses and the popliteal and
jugular venous pulse waveform. foot pulses. Look for ankle or sacral oedema.
7. Take an opportunity for a closer look at the face, 14. If appropriate, assess the patient’s exercise tolerance
the conjunctivae, the tongue and the inside of the by taking the patient for a short walk.
mouth. 15. Test the urine.
8. With the patient’s chest exposed, inspect the
precordium and assess the breathing pattern and
the presence of any abnormal pulsation.
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7
The abdomen
The abdominal examination follows that of the heart and the abdominal cavity (Fig. 7.1) The liver, gallbladder and
lungs. Diseases of the abdominal organs may already be spleen lie protected under cover of the lower thoracic
apparent from the general examination: for example, you ribs, whereas the stomach, 6 m of small intestine and
may have noticed jaundice when examining the skin and 1.5 m of large bowel cover and cushion the pancreas,
eyes and in patients with obstructive jaundice, scratch kidneys and ureters. The urinary bladder, and in women
marks may be apparent. You may have been aware of the ovaries and adnexae, lie hidden deep in the protective
abnormal weight loss, signs of malnutrition or anaemia. wall of the pelvis.
Underlying iron deficiency may be revealed by a smooth,
atrophic tongue and by cracks at the angles of the mouth GASTROINTESTINAL TRACT
(cheilosis), which may also suggest a vitamin B group Mouth and oesophagus
deficiency.
Digestion begins in the mouth where food is chewed and
moistened with saliva. The salivary fluid is a cocktail of
Structure and function enzymes, including amylase and lingual lipase and
bicarbonate and lysozyme. Saliva is secreted by the
The symptoms and signs of abdominal disease reflect parotid, submandibular and sublingual glands, with a
disorder in the anatomy and physiology of the major small contribution from the labial glands on the inner
abdominal organs. These organs are packed neatly into aspects of the lips.
The major digestive organs The vagal supply to the oesophagus
glossopharyngeal
nerve
swallowing
centre
transverse
gallbladder colon vagus
pharynx nerve
descending
colon
ascending
colon small
intestine epiglottis
caecum sigmoid
colon trachea
appendix bladder oesophagus
peristalsis
Fig. 7.1 The anatomical relationships of the major digestive organs. Fig. 7.2 The innervation of the oesophagus.
186
Chapter
Gastric secretions Stimuli for gastric acid secretion

stomach
pepsin lumen food
vagus nerve
mucus HCI +
chief cells mucous pepsinogen

pepsinogen
neck cells
+ +
+ acid
gastrin
–
parietal pepsin
cells
to G-cells
intrinsic
superficial terminal
factor
epithelial ileum
cells
Fig. 7.3 Cells found in the mucosa of the stomach body are Fig. 7.4 The control of gastric acid secretion by food, vagal
responsible for the principal gastric secretions. stimulation and gastrin. Pepsinogen is activated to pepsin at low pH.
Swallowing is controlled by a medullary centre in the stomach mucosa, protecting it from self-inflicted injury
brainstem which relays to and from the pharynx and by acid and pepsin.
oesophagus via the glossopharyngeal and vagus nerves Regurgitation of gastric contents into the oesophagus
(Fig. 7.2). There is also an intrinsic innervation within the is prevented by an antireflux mechanism at the gastro-
smooth muscle of the oesophagus. There are three phases oesophageal junction. This includes the intrinsic tone of
to the swallowing reflex: oral, pharyngeal and oesophageal. the lower oesophageal sphincter, the flap-valve effect of
During the oral phase, the tongue presses the bolus the angle of His and the squeezing effect of intra-
up against the hard palate and drives the food into abdominal pressure on the small segment of oesophagus
the pharynx. In the pharyngeal phase, the respiratory that protrudes through the diaphragm into the abdomen
tract closes off, the upper pharyngeal sphincter (Fig. 7.5). If one or more of these antireflux mechanisms
(cricopharyngeus) relaxes and the upper, middle and breaks down, gastric contents may regurgitate into the
lower pharyngeal constrictors propel the food into the lower oesophagus, damaging the mucosa and causing
oesophagus. In the oesophageal phase, a powerful heartburn.
peristaltic wave propels the bolus towards the stomach.
Small intestine
The lower oesophageal sphincter has intrinsic tone that
prevents regurgitation of the gastric contents: it relaxes The small intestine comprises the duodenum, the jejunum
in advance of the peristaltic wave and remains relaxed for and the ileum. It fills most of the anterior abdomen and
a few seconds after the wave has passed. is framed by the ascending, transverse and descending
Difficulty swallowing (dysphagia) may be caused by colon. Blood is supplied by the superior mesenteric
damage to the neural control, abnormalities of the vessels (Fig. 7.6). The principal role of the small intestine
oesophageal muscle or obstruction of the lumen. is digestion and absorption, which is achieved by a
combination of macroscopic and microscopic folds
creating a vast absorptive area (Fig. 7.7).
Stomach
Most of the enzymes necessary for the digestion of fat,
The churning action of the antrum continues the mixing protein and carbohydrate are present in the duodenum.
process started in the mouth and prepares food for its Enterocytes develop in the base of the crypts of Lieberkuhn
journey into the duodenum. The parietal cells in the body and migrate to the tip of the finger-shaped villi (Fig. 7.8).
of the stomach (Fig. 7.3) secrete hydrochloric acid, which Both the enterocyte’s capacity to produce specialised
sterilises the meal, and intrinsic factor, which is necessary digestive enzymes on the brush border membrane and
for the absorption of vitamin B12 in the terminal ileum. its absorptive properties develop progressively as the cell
The chief cells secrete pepsinogen which is converted to migrates towards the villous tip, at which point these
the proteolytic enzyme pepsin by the low pH of the functions are maximally developed.
stomach lumen. The secretion of acid is stimulated by the Carbohydrate digestion is initiated by salivary and
vagus nerve, distension of the stomach with food and pancreatic amylase. Enzymes, such as lactase and sucrase,
the secretion of the hormone gastrin from the G-cells of on the brush border membranes of the enterocytes,
the gastric antrum (Fig. 7.4). A mucous layer coats the complete the digestion of complex polysaccharides and
187
Chapter
7 The abdomen
The antireflux mechanism The fold forming the surface of the bowel
lower oesophageal
sphincter fold
intra-abdominal flap effect

segment of of angle
oesophagus of His
acid
pepsin
bile
microvillus
villus membrane
goblet
cell
Fig. 7.5 The antireflux mechanism comprises the intrinsic tone of

the lower oesophageal sphincter, the acute angle formed at the
oesophagogastric junction (angle of His) and the pressure on the
intra-abdominal oesophagus.
Blood supply to the intestine

pancreas
superior
mesenteric
absorptive
artery and vein
cell
second
part of jejunum
duodenum
muscularis mucosa
Fig. 7.7 The large surface area of the small intestine is formed by
ileum the duodenal folds, the villi and the microvillus membrane of the
caecum enterocyte.
terminal
appendix ileum
transverse colon
hepatic splenic
flexure flexure
descending
ascending colon
colon
right
inferior
colic
mesenteric
artery
artery
caecum
Fig. 7.8 Duodenal enterocytes develop in the crypts and migrate

terminal rectum towards the villus tip.
ileum
Fig. 7.6 The blood supply of the small intestine, colon, sigmoid and
rectum.
188
Chapter
Digestion of carbohydrate, fat and protein Table 7.1 Principal effects of gastrointestinal hormones
intestinal lumen portal blood Hormone Function

salivary and enterocyte Gastrin Stimulates gastric acid secretion
pancreatic amylase
Cholecystokinin Stimulates gallbladder contraction
and pancreatic enzyme secretion
starch maltose passive
Secretin Stimulates secretion of pancreatic
sucrose brush border diffusion fluid and bicarbonate
disaccharidases
lactose Gastric inhibitory Potentiates the insulin response to
polypeptide glucose
glucose Enteroglucagon Trophic to small intestine
galactose Vasoactive intestinal Secretin-like effect on pancreas
fructose polypeptide (VIP) Affects intestinal motility and
membrane membrane mesenteric blood flow
transport transport
Motilin Stimulates intestinal motility
between meals
Somatostatin Inhibits secretion of gastrin, other
short chain gut hormones and pepsin
fatty acids Stimulates gastric mucus production
fatty acid + Insulin Lowers blood glucose
dietary mono- diglyceride
triglyceride glyceride Stimulates glycogen synthesis
Stimulates protein and fat anabolism
bile triglyceride Pancreatic glucagon Promotes glucogenolysis, lipolysis,
acids
lymph
gluconeogenesis
pancreatic and Slows intestinal motility
salivary lipase chylomicron
Pancreatic Inhibits pancreatic secretion
protein phospholipid polypeptide Relaxes the gallbladder
Ghrelin Stimulates appetite
lacteal
pancreatic
peptidases passive
diffusion 7.9). These triglycerides, as well as absorbed cholesterol,
brush border
oligopeptides
are formed into fat aggregates (chylomicrons) that are
dietary amino acids
absorbed into the lymphatics and discharged into the
proteins oligopeptides
circulation through the thoracic duct. The fat-soluble
enzymes cytosolic
peptidases vitamins A, D, K and E are absorbed in a similar manner
dipeptides to other lipids.
tripeptides Proteolysis is initiated in the stomach by pepsin, yet
the bulk of protein digestion is mediated by trypsin and
other pancreatic peptidases in the small intestine (Fig.
liver 7.9). The action of these enzymes produces small peptides
with 4–6 amino acids that undergo further processing to
Fig. 7.9 Digestion in the small intestine. Digestion of complex amino acids, dipeptides and tripeptides by oligopeptidases
carbohydrates occurs in the lumen and at the brush border on the enterocyte brush border membrane. These are
membrane. Monosaccharides can then be absorbed through the absorbed into the enterocytes where the final digestion
brush border membrane into the portal circulation. Fat digestion to single amino acids occurs. The amino acids are
occurs in the lumen and triglyceride is reconstituted in the enterocyte
transported to the liver by the portal blood.
before absorption. Proteins are digested in the lumen and at the
brush border membrane. Amino acids are then absorbed into the The addition of pancreatic juice and bile, which are
enterocyte and portal circulation. secreted through the ampulla of Vater, modifies and
enriches the chyme (semi-liquid food) entering the
duodenum from the stomach.
disaccharides to monosaccharides, which are then Absorption of nutrients occurs in the jejunum and
transported through the enterocyte by specialised ileum, along with the production and secretion of a range
transporters on the brush border and basolateral of hormones. The terminal ileum absorbs vitamin B12 and
membranes (Fig. 7.9). Pancreatic lipase hydrolyses bile acids.
triglycerides to fatty acids and monoglycerides. These The small intestine has a considerable functional
products are emulsified by bile acids which help form reserve and only fails when there is less than 100 cm of
micelles. The micelles are then taken up at the brush bowel following surgical resection.
border membrane and diffuse passively into the Table 7.1 lists the principal effects of gastrointestinal
enterocyte, where the triglyceride is reconstituted (Fig. hormones.
189
Chapter
7 The abdomen
Colon
The lobes of the liver
The ileum enters the caecum through the ileocaecal valve,
which prevents reflux of colonic contents into the
small intestine. Whereas the small intestine is relatively
microbe free, the colon is heavily colonised by bacteria.
Approximately 1.5 litres of ileal fluid empties into the
caecum each day. Most of this effluent is reabsorbed as
it passes through the ascending, transverse and descending
colon. The colon concentrates the ileal outflow so that right lobe
the daily stool output on a Western diet averages 200 g; left lobe
75% of stool weight is water and the remainder is
unabsorbed food and bacteria. The colonic mucosa is rich
in glands producing mucus, which provides constant
lubrication for the passage of faeces and protects the
mucosa from bacterial enzymes. The rectum is the storage
organ for stool.
Infection or inflammation of the colonic mucosa may gallbladder
provoke fluid and electrolyte secretion and interfere with
absorption, causing diarrhoea and dehydration. Diarrhoea
may also occur in small bowel disease when the volume
of ileal effluent exceeds the colon’s absorptive capacity.
Liver quadrate
lobe
The liver is the largest intra-abdominal organ. The
falciform ligament divides the liver into a large right lobe right lobe
and a smaller left lobe (Fig. 7.10). Two smaller lobes, the left lobe
anterior quadrate and posterior caudate, are squeezed
between the left and right lobes on the visceral surface of
the liver.
The liver is the focal point of intermediary metabolism caudate
and energy production and it lies in a strategic position lobe
between the gut and the systemic organs. The products Fig. 7.10 The gross anatomy of the liver.
of digestion are absorbed into the mesenteric veins which
drain into the portal vein and ultimately into the hepatic
sinusoids (Fig. 7.11). Specialised macrophages (Kupffer
cells) straddle the sinusoids and mount an almost The portal venous system
impenetrable defence against unwanted microbes or
matter that has escaped the first line of defence in the
bowel. Nutrient-rich plasma filters through the small liver
holes (fenestrae) in the endothelial cells lining the
sinusoids and passes into the space of Disse, which lies
left branch splenic
between the endothelial cells and hepatocytes (Fig. 7.12).
vein spleen
The plasma filtrate bathes these highly adaptable cells,
right branch portal vein
which are enriched with a range of enzymes able to
metabolise the wide variety of incoming digestion
products. Three hepatic veins collect the sinusoidal
outflow and deliver it into the inferior vena cava. umbilical vein
Hepatocytes perform a remarkable array of synthetic
inferior
and catabolic functions, with many clinical features of pancreas mesenteric vein
liver disease resulting from derangement of these
processes. They convert glucose to glycogen (which can superior
be stored and later reconverted, on demand, to glucose), mesenteric vein
synthesise a range of proteins (including albumin and digestion products
the clotting factors), degrade protein to amino acids,
Fig. 7.11 The anatomy of the portal venous system. The vessels
synthesise urea from ammonia, and manufacture drain into the liver sinusoids carrying nutrients from the intestine,
cholesterol and bile acids. The lateral borders of pancreatic hormones from the islets of Langerhans and antibodies
hepatocytes are modified to form bile canaliculi which from the spleen.
190
Chapter
Microanatomy of the liver Bilirubin metabolism

portal blood flow
foreign bodies reticuloendothelial cell
Kupffer cells (trapped by tight
Kupffer cell) junction haemoglobin catabolism
hepatocyte
bilirubin
plasma
space of Disse
conjugation with
systemic circulation
glucuronic acid
bile
duct
portal
endothelial digestive vein
cell fenestra
products urobilinogen small
sinusoid
intestine
kidney
Fig. 7.12 Microanatomy of the liver sinusoids, the space of Disse bilirubin bacterial
and hepatocytes. Tight junctions adjacent to the bile canaliculi bind oxidation
the hepatocytes together.
urobilinogen
interconnect and eventually converge as the left and right large intestine
main hepatic ducts at the liver hilum. The liver cells urobilinogen
in urine urobilin in stool
secrete bile into the canaliculi. Bile is a fluid comprising
bile salts, cholesterol and bilirubin. Bilirubin is a
pigment derived from haemoglobin released from Fig. 7.13 Bilirubin is a product of haemoglobin catabolism.
dead erythrocytes. It cannot be excreted in bile until it
has been rendered water-soluble by conjugation with
glucuronic acid in the liver (Fig. 7.13).
The liver is an important storage site for iron and
vitamins and plays a central role in the hydroxylation of Anatomy of the pancreatic and bile ducts
vitamin D. Other functions include the conjugation and cystic
excretion of steroid hormones, the detoxification of drugs Hartmann’s
duct right hepatic duct
pouch
and the conversion of fat-soluble waste products to
water-soluble substances for excretion by the kidneys. left hepatic duct
main hepatic duct

Gallbladder body
common bile duct
The gallbladder is a pear-shaped organ with a fundus, a
body and a neck that narrows to give rise to the cystic fundus
duct. It lies protected beneath the lower surface of the
liver in the gallbladder fossa that separates the right and
quadrate lobes. The gallbladder concentrates and stores
main pancreatic
bile and, under the influence of cholecystokinin, it pumps duct
the bile through the cystic duct into the common bile duct
and through the ampulla of Vater into the duodenum, ampulla of
where it blends with the other products of digestion Vater
duodenal
(Fig. 7.14). papilla
Pancreas
The pancreas is an elongated retroperitoneal organ that Fig. 7.14 The gallbladder and related ducts. Bile and pancreatic
lies in the transpyloric plane with its head end tucked juice both enter the duodenum through the ampulla of Vater.
into the C-shaped loop of the duodenum and its tail
end abutting the spleen (Fig. 7.15). Its posterior position
places the organ well out of reach of the examining
191
Chapter
7 The abdomen
hand and diagnosis of pancreatic diseases is promotes the secretion of fluid and bicarbonate from duct
largely dependent on the use of special imaging cells. The mucosa of the duodenum synthesises both
techniques such as CT scanning, magnetic resonance these hormones. The endocrine secretion of the pancreas
cholangiopancreatography (MRCP) and endoscopic arises from the islets of Langerhans, which secrete insulin,
retrograde cholangiopancreatography (ERCP) (Fig. glucagon, somatostatin and pancreatic polypeptide into
7.16). the pancreatic and portal veins.
The pancreas has mixed exocrine and endocrine Blockage of the main pancreatic duct by a carcinoma,
functions. The duct cells secrete bicarbonate which or diffuse damage caused by pancreatitis, may cause
protects the duodenum from gastric acid and ensures an maldigestion of protein, fat and carbohydrate. Patients
optimum pH for digestive enzyme activity. The exocrine with pancreatic exocrine failure pass pale, fatty stools that
acinar cells secrete lipase, phospholipase, amylase and are difficult to flush (steatorrhoea).
peptidases (trypsinogen, chymotrypsinogen, elastase
and carboxypeptidase). All the pancreatic enzymes are Spleen
secreted in an inactive precursor form and are only
The spleen is a highly modified lymphoid organ which
cleaved to their active forms in the duodenum by
also regulates the destruction of red blood cells.
enterokinase, which is fixed on the enterocyte brush
Reticuloendothelial cells populate the bulk of the spleen,
border membranes. The hormone cholecystokinin
forming the white pulp. These cells provide an important
mediates pancreatic enzyme secretion, whereas secretin
line of defence and the organ is a major site of antibody
production. The remainder of the spleen, the red pulp,
consists of capillaries and venous sinuses that act as a
The pancreas sump for the storage of red blood cells, white blood cells
and platelets. When the spleen enlarges, excessive
stomach pooling of these cells may occur, causing a fall in the
peripheral blood count. The splenic venous outflow
drains into the portal vein, adding a rich supply of
kidney antibodies to the portal blood entering the liver.
spleen
pancreas
Kidneys
tail
The kidneys control fluid electrolyte balance and produce
body
the hormones erythropoietin and renin. Each kidney
contains approximately 1.2 million nephrons. The
head structural and functional arrangement of a typical
nephron is shown in Figure 7.17.
The capillary loops of the glomerulus form between
the afferent and efferent arterioles supplying each
glomerulus; the capillary tuft is embedded in the
mesangium, which consists of a matrix and specialised
duodenum mesangial cells. The basement membrane of the capillary
tuft impinges on the epithelium of Bowman’s capsule via
Fig. 7.15 The anatomical relationships of the pancreas. foot processes (podocytes) that arise from the visceral
a b
Fig. 7.16 (a) CT scan showing a normal pancreas and the surrounding structures; (b) the pancreatic duct visualised after ERCP injection of
radio-opaque contrast medium through the ampulla of Vater.
192
Chapter
collecting ducts are normally impermeable to water but

The nephron they are rendered permeable by the action of antidiuretic
cortex hormone (ADH), which is secreted by the pituitary. This
afferent proximal distal collecting allows water to be reabsorbed passively down the osmotic
arteriole convoluted convoluted duct gradient that exists between the duct lumen and interstitial
glomerulus
tubule tubule fluid. The permeability of the collecting duct is modified
in response to body water requirements and is important
for the fine tuning of fluid balance. Failure to produce
efferent ADH or insensitivity of the renal tubule to ADH causes
arteriole inappropriate loss of water through the kidneys and
medulla excess urine secretion (polyuria), a syndrome known
as diabetes insipidus. Sodium is also actively reabsorbed
loop of in the collecting tubules under the influence of
descending Henle ascending aldosterone.
limb limb
Symptoms of abdominal disorders

Structure Function
GASTROINTESTINAL DISEASES
Glomerulus Filtration
Proximal convoluted tubule Reabsorption of 85% of filtrate The principal symptoms of gastrointestinal disease
Ascending loop of Henle Generation of medullary include dysphagia, heartburn, abdominal pain, loss of
hypertonicity ‘fine tuning’ appetite, nausea and vomiting, weight loss, constipation
Distal convoluted tubule Fine tuning of Na+ and pH
Collecting duct Water reabsorption (ADH control)
or diarrhoea and rectal bleeding.
Dysphagia
Fig. 7.17 The structure and function of a typical nephron.
Difficulty in swallowing is the principal symptom of
oesophageal disease. Patients can usually indicate the
level of obstruction but this does not always correspond
cells. This complex anatomical relationship allows a to the actual level. Determine whether the dysphagia
protein-free fluid to filter under pressure from the developed suddenly or gradually over weeks or months.
blood into the proximal convoluted tubule, where Enquire whether the symptom is constant or intermittent
specialised epithelium allows the reabsorption of sodium, and whether the dysphagia occurs with both solids and
water, bicarbonate, glucose and amino acids into the liquids. Associated symptoms such as weight loss and
efferent arteriole. Approximately two-thirds of the
glomerular filtrate is reabsorbed in the proximal
convoluted tubule. Differential diagnosis
The fluid entering the descending limb of the loop of
Dysphagia
Henle is isosmotic. The proximal and distal limbs of this
loop are highly differentiated in their ability to secrete • Benign oesophageal stricture
water, chloride and sodium and this, together with the • Carcinoma of the oesophagus
spatial orientation of the loop, is responsible for the • Oesophageal motor disorders
progressive increase in the sodium chloride concentration • Systemic sclerosis
gradient between the cortex and medulla. This medullary • Old age (presbyoesophagus)
hyperosmolality is vital for the further reabsorption of • Bulbar and pseudobulbar palsy
water. The thin descending limb of the loop of Henle is
permeable to the outflow of water but not to that of
sodium and chloride, so as the filtrate approaches the
hairpin bend in the loop it becomes hypertonic. The thick Questions to ask
ascending limb of the loop is impermeable to the efflux
Dysphagia
of water, yet permeable to the efflux of sodium which
follows the active secretion of chloride ions. In the • At what level does food stick?
ascending limb, the tubular fluid becomes hypotonic • Has the symptom developed over weeks, months or
while medullary interstitium becomes hypertonic. More longer?
sodium is reabsorbed from the distal convoluted tubule • Is the dysphagia intermittent or progressive?
in exchange for potassium under the modulating influence • Are both food and drink equally difficult to swallow?
of aldosterone. • Is there a history of reflux symptoms?
The final composition of urine is determined by the • Has there been weight loss?
collecting ducts that course through the medulla. The
193
Chapter
7 The abdomen
pain or cough with swallowing may help you construct a

differential diagnosis.
The more common causes of dysphagia include
oesophageal cancer, benign stricture caused by
longstanding acid reflux, and motility disorders including
achalasia of the cardia (where there is increased tone in
the lower oesophageal sphincter and failure of oesophageal
peristalsis). The history may indicate the underlying
cause, although special tests such as barium swallow,
oesophagoscopy and manometry are required to make a
definitive diagnosis.
Dysphagia caused by a carcinoma usually progresses
rapidly over 6–10 weeks and is worse for solids than
liquids. Profound weight loss results from reduced food
intake and the wasting effect of the cancer.
Patients with a benign ‘peptic’ stricture often have a
long history of heartburn, a slower rate of progression
and less marked weight loss. In dysmotility syndromes
the dysphagia often varies in intensity and is not
accompanied by profound weight loss. Solids and fluids
may be equally difficult to swallow. When dysphagia Fig. 7.18 Barium meal showing a sliding hiatus hernia with the
is caused by disease of the swallowing centre in gastro-oesophageal junction and a segment of stomach prolapsing
the brainstem (e.g. pseudobulbar palsy) or damage to the into the chest.
vagus nerve (e.g. bulbar palsy caused by polio), the
symptom is accompanied by coughing and spluttering as
food spills into the larynx and trachea.
A common cause of heartburn is a hiatus hernia,
Heartburn
in which the oesophagogastric junction prolapses
Malfunction of the antireflux mechanism of the gastro- into the chest through the oesophageal hiatus (Fig. 7.18).
oesophageal junction allows gastric acid, pepsin and bile The heartburn is often provoked by postures which
to reflux into the oesophagus, causing damage to the raise intra-abdominal pressure, such as stooping,
mucosa, muscle spasm and pain felt behind the sternum. bending or lying down. The diagnosis may be suspected
Most people have experienced heartburn: the pain is a in overweight patients but confirmation relies on
scalding or burning sensation that wells up behind the visualising the hernia, either by barium meal or
sternum and radiates towards the throat. An acid or bitter endoscopy, and assessing the response to treatment
taste may develop in the mouth and reflex salivation may with antacids.
cause it to fill with saliva (water brash). The patient’s Heartburn may result from a particular diet and
description is often accompanied by a hand gesture that lifestyle: chocolate, alcohol consumption and cigarette
illustrates the upward radiation of the pain behind the smoking relax the lower oesophageal sphincter, allowing
sternum. Heartburn is rapidly relieved by antacids. reflux to occur. It is a common symptom in the later
Retrosternal chest pain caused by reflux or oesophageal months of pregnancy. This is due both to the increase in
spasm may closely mimic the pain of myocardial intra-abdominal pressure and the loss of sphincter tone
ischaemia. caused by high oestrogen levels.
Distinguishing clinical features of reflux and myocardial ischaemic pain
Position Character Associated Aggravating Relieving

features factors factors
Reflux Radiates towards the Burning, scalding Water brash Bending, lying Antacids
chest from the down, eating
epigastrium
Myocardial Radiates across the Gripping vice-like Nausea, shortness Exercise Ceasing exercise,
ischaemia chest, into the pressure of breath nitrates
jaw and down
the left arm
194
Chapter
Pain on swallowing (odynophagia) Dyspepsia and indigestion

Chest pain caused by swallowing has a deep ‘boring’ Most people have experienced ‘indigestion’ or ‘dyspepsia’.
quality which differs from heartburn, although both may Patients and doctors use these terms rather loosely
occur together. The symptoms suggest deep inflammation and interchangeably to describe a range of subjective
or ulceration of the oesophageal wall or intense spasm of abdominal symptoms. This term applies to a sensation
the oesophagus; it may be provoked by obstruction or an of pain, discomfort or fullness in the epigastrium,
intrinsic motor disorder causing abnormal, intense and often accompanied by belching, nausea and early satiety.
uncoordinated contraction (‘nutcracker’ oesophagus). Dyspepsia should focus your attention on foregut
disorders.
Loss of appetite (anorexia)
Loss of appetite is a nonspecific symptom that commonly
accompanies both acute and chronic ill health; return
of appetite usually heralds recovery. Prolonged or
unexplained anorexia, especially when accompanied by Dyspepsia
weight loss, should alert you to a serious underlying • Nonulcer dyspepsia
disease. Anorexia may be a prominent feature of digestive • Peptic ulcer disease
diseases, failure of the major organs (kidneys, liver, heart • Gastritis
and lungs) and generalised debilitating illnesses (e.g. • Gallstones
cancer, tuberculosis). • Chronic pancreatitis
Profound anorexia occurs in anorexia nervosa, a
psychiatric disorder occurring mainly in young women.
Anorexia in these patients results in marked weight
loss, malnutrition and cessation of menstruation
(amenorrhoea). Suspect anorexia nervosa in teenagers Risk factors
and young adults, otherwise healthy, who present with Dyspepsia
an eating disorder associated with depression, vomiting
• Cigarette smoking
or purgative abuse.
• Alcohol
Weight loss • Aspirin
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
Weight loss is an important but rather unspecific symptom
• Corticosteroids and NSAIDs
of gastrointestinal and other diseases. Enquire about
• Oral bisphosphonates
appetite, eating habits and average daily diet. When
• Helicobacter pylori infection
eating causes pain (as in gastric ulceration, mesenteric
angina or pancreatitis), the inclination to eat is suppressed.
Weight loss may be caused by inappropriate wastage
of calories due to steatorrhoea, thyrotoxicosis or
diabetes mellitus. Marked weight loss accompanies Red flag – urgent referral
serious diseases such as chronic pancreatitis, advanced Dyspepsia
malignancy, chronic infections and failure of the
major organs. • Weight loss
• Vomiting
• Haematemesis or melaena
• Dysphagia
Questions to ask • Anaemia
Weight loss
• Is your appetite normal, increased or decreased?

• Over what time span has the weight been lost?
Nausea
• Do you enjoy your meals?
• Describe your usual breakfast, lunch and supper Nausea describes the sensation experienced before
• Is the weight loss associated with nausea, vomiting vomiting, although it often occurs without vomiting.
or abdominal pain? Nausea may last hours or days, usually comes in waves
• Are your motions normal in colour and consistency? and is often associated with belching. It may be relieved
• Has there been a fever? by vomiting. The symptom may be provoked by
• Do you pass excessive volumes of urine? unpleasant sights, smells and tastes or by abnormal
• Have you noticed a recent change in weather stimulation of the inner ear labyrinths (motion sickness).
tolerance? Nausea may be accompanied by other complaints such
as abdominal pain and diarrhoea (Fig. 7.19). It is a
195
Chapter
7 The abdomen
Causes of nausea and vomiting
Gastrointestinal bleeding
Cause Frequency (%)

autonomic
labyrinthine Gastric ulcer 30
stimuli from
stimulation Duodenal ulcer 21
major organs hepatitis or
motion
sickness gallbladder Gastritis or erosions 9
labyrinthitis disease Oesophagitis or oesophageal ulcer 8
Duodenitis 4
Varices 3
vomiting
Tumours 2
centre
Mallory–Weiss tear 1
Others 22
sights morphine
smells digoxin
sounds gastritis or duodenitis alcohol
taste peptic ulceration
pyloric obstruction Emergency
Assessment of patient presenting with
haematemesis and melena
Fig. 7.19 The causes of nausea and vomiting.
• Pulse rate (consider whether on beta-blockers)
• Respiratory rate
characteristic of the prodromal phase of viral hepatitis • Recumbent blood pressure
and often accompanies biliary diseases (e.g. cholecystitis). • Evidence of postural hypotension and reduced
Drugs causing gastric irritation (e.g. nonsteroidal capillary filling time
analgesics) or those stimulating the vomiting centre (e.g. • Hydration (dry tongue, sunken eyes, reduced skin
digoxin, morphine and anticancer drugs) cause nausea. turgor)
Early morning nausea commonly occurs during the first • Pallor (caused by shock and peripheral
trimester of pregnancy. vasoconstriction or anaemia)
• Urine output
Vomiting and haematemesis • Stigmata of liver disease (flap, jaundice, spider naevi)
A wave of nausea usually heralds vomiting and the causes
of nausea and vomiting are similar. Vomiting may occur
in diseases of the gastrointestinal and biliary tracts, as
well as in a variety of systemic and metabolic disorders. Questions to ask
It may also be the presenting symptom of psychological Vomiting
disorders such as anorexia nervosa, bulimia and fear.
Suspect an iatrogenic cause in patients taking digoxin or • Is the vomiting worse in the mornings?
morphine and in individuals undergoing cancer treatment • Does the vomiting occur in relation to meals?
with cytotoxic drugs. Try to establish whether the vomit • Is there associated abdominal pain?
is bile-stained because this indicates patency between the • Is the vomit blood- or bile-stained?
stomach and duodenum. The presence of undigested • Is there recognisable food or ‘coffee-grounds’ in the
food and a lack of bile suggest pyloric obstruction. Early vomit?
morning nausea and vomiting are characteristic of early • What drugs are being taken?
pregnancy and alcoholism.
Vomiting blood (haematemesis) indicates bleeding
from the oesophagus, stomach or duodenum. If the
bleeding is brisk the vomit may be heavily bloodstained of coincident liver disease, consider oesophageal varices
but if bleeding is slower or vomiting delayed, gastric acid to be the cause of bleeding. Weight loss may suggest
reacts with haemoglobin, turning it a dark brown or bleeding from a gastric cancer, and a history of epigastric
‘coffee-ground’ colour. The patient’s history often yields pain or heartburn suggests bleeding from a peptic ulcer
clues to the cause of haematemesis. If the bleeding is or ulcerated oesophagus.
preceded by repeated bouts of retching or vomiting,
consider as the cause a Mallory–Weiss tear which results
Abdominal pain
from mechanical disruption of the mucosa at the gastro-
oesophageal junction. Enquire about ingestion of alcohol Pain is an important symptom of abdominal disease
or other gastric irritants (e.g. aspirin). If there is evidence that may present in various forms, ranging from a
196
Chapter
Diagnostic features of abdominal pain
Disorder Localisation Character Aggravating Relieving Visceral Major physical Diagnostic test
factors factors symptoms signs
Acute Epigastric and Severe, constant May improve Nausea, vomiting Tachycardia, Raised serum
pancreatitis left hypo- pain when sitting shock, tender and urinary
chondrium forward upper abdomen amylase
radiating to back with guarding.
Bruising in flanks
Acute Right hypo- Initially colicky, Palpation over Nausea, vomiting, Tender right Biliary tract
cholecystitis/ chondrium/ becomes the gallbladder may have fever hypochondrium, ultrasound,
biliary colic epigastrium continuous. bed (below 10th and rigors positive Murphy's ERCP
radiating to Patient writhes rib in right upper sign, may be
right scapula quadrant) jaundiced
and shoulder
Renal colic Loin pain Very intense Nausea, vomiting, Microscopic or Abdominal
(ureteric stones) radiating to colicky pain. frequency obvious radiograph (90%
groin, and in Patient writhes haematuria stones visible),
males the ultrasound intra-
scrotum venous urogram
Intestinal Large bowel: Colic Food, drink Large bowel: Abdominal Radiograph of
obstruction lower constipation, distension, abdomen shows
abdomen vomiting occurs empty rectum air–fluid levels in
Small intestine: later bowel
periumbilical Small intestine:
vomiting,
constipation
occurs later
Acute Initially, Initially dull, Movement, hip Lying still Nausea, anorexia, Fever, tenderness Laparoscopy
appendicitis periumbilical pain, later intense extension vomiting and guarding in
later localises to the right
right iliac fossa iliac fossa
Perforated Sudden onset of Severe, persistent Movement Lying still Nausea, vomiting Fever, tachycardia, Chest radiograph
peptic epigastric pain. hypotension, reveals air under
ulcer May radiate to the shock, rigid the diaphragm
shoulder and abdomen with
extend to rebound
whole abdomen tenderness
Ruptured ectopic Lower abdomen Sudden onset, Movement Lying still Tachycardia, Positive
pregnancy severe pain hypotension, pregnancy test,
shock. Lower anaemia,
abdominal ultrasound
tenderness may
become
generalised.
Guarding and
rebound
tenderness,
tender cervix
Ruptured aortic Pain radiating Moderately severe Pulsatile tender Abdominal

aneurysm to the back Nausea, mass, hypo- radiograph
sweating tension, shock, (calcification),
oliguria/aneuria ultrasound
angiography
Fig. 7.20 The characteristics of abdominal pain which may help in making a differential diagnosis.
dull ache to cramp, colic and peritonitis. A differential Differential diagnosis

diagnosis can often be constructed from the position,
Pancreatitis
character and timing, the aggravating and relieving
factors and other distinctive or associated features • Idiopathic
(Fig. 7.20). When taking a history of abdominal pain, aim • Toxic (alcohol, drugs)
to distinguish between visceral, parietal and referred • Common bile duct stone
pain. • Abdominal trauma
Visceral pain is caused by stretching or inflammation • Mumps
of a hollow muscular organ (gut, gallbladder, bile duct,
197
Chapter
7 The abdomen
Localisation of foregut, midgut and hindgut pain
foregut pain localises to

epigastric area
midgut pain localises to

periumbilical area
hindgut pain localises to

suprapubic areas
Fig. 7.21 Perception of visceral pain is localised to the epigastric, umbilical or suprapubic region according to the embryological origin of the
diseased organ.
ureters, uterus). It is often described as a ‘dull ache’

or a ‘gnawing’ or ‘cramping’ sensation that is perceived Radiation of pain
near the midline, irrespective of the location of the organ.
The pain can usually be localised to the epigastric,
periumbilical or suprapubic areas, depending on whether
the affected organ is derived from the embryological right
foregut, midgut or hindgut (Fig. 7.21). Pain arising from shoulder
foregut is felt in the epigastrium; midgut pain is perceived
tip of
around the umbilicus; pain arising from the hindgut scapula
is felt in the suprapubic area. Visceral pain may also
diaphragm
radiate to specific sites and this helps to establish its
origin (Fig. 7.22). It is commonly accompanied by
nonspecific, ‘visceral’ symptoms (e.g. anorexia, nausea,
pallor, sweating).
Colic is a characteristic manifestation of visceral pain
and is caused by concerted and excessive smooth muscle
contraction. It signifies obstruction of a hollow, muscular gallbladder
organ, such as the intestine, gallbladder, bile duct or gallbladder pain ureter
ureter, and consists of recurring bouts of intense,
cramping, visceral pain which build to a crescendo diaphragmatic
pain inguinal
and then fade away. When the smaller organs such
canal
as the gallbladder, bile duct or ureters are acutely uteric pain
obstructed by a stone, the cyclical nature of colic
soon gives way to a continuous visceral pain caused Fig. 7.22 Characteristic radiation of pain from the gallbladder,
by the inflammatory effect of the impacted stone or diaphragm and ureters. The pain is not always felt in the organ
secondary infection. Movement does not aggravate concerned.
visceral pain, so the patient may writhe or double-up in
response to it.
Unlike the visceral peritoneum, the parietal peritoneum as possible. Palpation over the area is extremely painful,
is innervated by pain-sensitive fibres. Therefore, pain with the overlying muscles contracting to protect the
arising from the parietal peritoneum is well localised to peritoneum (guarding). When the pressure of the
the area immediately overlying the area of inflammation examining hand is suddenly released, the pain is further
or irritation. Parietal pain is aggravated by stretching or aggravated and the patient winces. This sign is known as
moving the peritoneal membrane; the patient lies as still ‘rebound tenderness’.
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Chapter
Questions to ask
occurs with a hiatus hernia, peptic ulceration and chronic
gallbladder disease. The symptom may be accompanied
Abdominal pain
by a feeling of abdominal distension. Intestinal gas is
• Describe the position, character and radiation of the produced by fermentation of certain foods, especially
pain legumes, in the colon and your history should seek to
• Has the pain been present for hours, days, weeks, identify a possible dietary cause of excessive flatus and
months or years? flatulence.
• Is the pain constant or intermittent?
• Have you noticed specific aggravating or relieving CHANGE IN BOWEL HABIT
factors?
• Is the pain affected by eating or defecation? Constipation
• Does the pain awake you from sleep? Most people on a Western diet expect bowel actions
• Is there associated nausea or vomiting? once or twice daily. Consequently, constipation usually
• Has there been associated weight loss? implies failure to produce a stool over 24 h. However,
• Is there a history of ulcerogenic drugs? normal expectations vary between individuals and
• Has there been a change in bowel habit? cultures; some healthy individuals evacuate every other
day or even only three times a week, whereas others,
particularly people on high roughage diets, expect up
to three bulky bowel actions daily. Constipation is
Abdominal pain may progress from a visceral sensation described more precisely as a disorder of bowel habit
to a parietal pain. Acute appendicitis provides an excellent characterised by straining and the infrequent passage of
example of this transition. When this midgut structure small, hard stools. Constipated patients often complain
becomes inflamed and obstructed, a dull pain localises to that they are left dissatisfied, with a sense of incomplete
the periumbilical area and the patient may feel nauseous evacuation (tenesmus). Patients with troublesome
and sweaty. As the inflammation advances through the constipation often seek medicinal relief and a history of
visceral covering to the parietal peritoneum, the pain laxative use may be a helpful guide to the severity of the
appears to shift to the right iliac fossa where it localises condition.
over McBurney’s point. The character of the pain also When constipation has troubled a patient for years or
changes from dull to sharp. The area overlying the even decades, the cause is likely to be functional rather
appendix is very tender and palpation causes reflex than obstructive and it may be attributed to diet, lifestyle
guarding and rebound tenderness. or psychological make-up. Lack of exercise, inadequate
fibre intake, irritable bowel syndrome and depression
may all cause constipation.
Mesenteric angina
When constipation presents as a recent change, and
When the mesenteric arteries are stenosed by especially if it is associated with colic, suspect an organic
atherosclerosis the blood supply to the bowel may be cause such as malignancy or stricture formation. Enquire
impaired. The collateral supply to the bowel is well about constipating drugs (e.g. codeine-containing
developed and the pain of bowel ischaemia usually analgesics, aluminium-containing antacids) and about
becomes apparent only on eating, when the metabolic rectal bleeding, an alarm symptom that raises the
demands of digestion and absorption require an increase suspicion of cancer. Consider hypothyroidism or
in the blood supply. Patients complain of a severe visceral electrolyte abnormalities. Anal pain caused by a fissure
periumbilical pain occurring soon after meals (mesenteric
angina). The pain causes anorexia, which, together with
damage to the bowel mucosa, results in considerable Differential diagnosis
weight loss. Constipation
• Low-residue diet
Wind
• Motility disorder (irritable bowel syndrome)
Most gas in the gastrointestinal tract is swallowed, with • Physical immobility
a smaller contribution arising from fermentation of • Drugs (especially opiates and antidepressants)
cellulose in the colon. Small, imperceptible amounts of • Depression and dementia
gas constantly escape from the bowel via the mouth and • Organic disease
anus. Excessive belching (flatulence) or the passage of – colon cancer
wind through the anus (flatus) are common symptoms – diverticular stricture
that cause considerable distress. These symptoms are – Crohn’s stricture
rather unspecific and occur in both functional and organic – hypothyroidism
disorders of the gastrointestinal tract. Flatulence is usually – electrolyte imbalance
caused by excessive air swallowing (aerophagy) and often
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Chapter
7 The abdomen
Questions to ask Questions to ask

Constipation Diarrhoea
• What is the normal stool frequency? • What is the normal stool frequency?
• Do you strain at stool? • How many stools daily?
• How long have you been constipated? • How long have you had diarrhoea?
• Is there associated abdominal pain, distension, • Are you awoken from sleep to open the bowels?
nausea or vomiting? • What is the colour and consistency of stools?
• Are the stools large or small and pellet-shaped? • Are blood and mucus present?
• Have you noticed intercurrent diarrhoea (spurious • Any travel abroad or contact with diarrhoea?
diarrhoea)? • Is there associated nausea, vomiting, weight loss or
• Are any constipating drugs, such as codeine or other pain?
opiates, being used? • Any purgative abuse?
• Any antibiotics?
or a thrombosed pile may cause profound constipation

because of the patient’s fear of pain at stool.
Rectal bleeding
Constipation caused by chronic partial obstruction
may be punctuated by periods of loose or watery stool. Rectal bleeding is a symptom common to several disorders
This ‘spurious diarrhoea’ occurs in elderly patients with (Fig. 7.23) and the history is not of much diagnostic value.
faecal impaction and also when colon cancer causes a Bright-red rectal bleeding usually arises from the sigmoid
partial obstruction. The proximal bowel dilates and fills colon or rectum and more proximal colonic bleeding is
with liquid, which then seeps around the obstruction, often a darker red or maroon colour. The blood usually
presenting as liquid diarrhoea. coats the stool, although in haemorrhoidal bleeding the
blood may be most noticeable on the toilet paper. Colon
cancer and polyps often present with intermittent rectal
Differential diagnosis bleeding, whereas patients with inflammatory bowel
Steatorrhoea disease pass blood, often mixed with mucus, with each
stool. Torrential haemorrhage may occur from diverticular
• Chronic pancreatitis
disease and marked bleeding may occur in mesenteric
• Gluten enteropathy
vascular disease when the ischaemic colonic mucosa
• Small bowel bacterial overgrowth
ulcerates and bleeds. Microscopic blood loss (occult
• Blind loops
• Short bowel syndrome
Colonic causes of blood in stool

Diarrhoea
polyp diverticular
The usual stool weight is 200–300 g/day. Diarrhoea disease
implies increased stool volume and frequency and a
change in consistency from formed to semiformed,
semiliquid or liquid. Always enquire about the presence
of blood and mucus and establish whether or not there
is accompanying pain or colic. There is a wide differential
diagnosis and the history may give some leads. Functional
ischaemic
diarrhoea caused by anxiety, stress or the irritable bowel colitis
syndrome does not wake the patient from sleep, nor is it
associated with rectal bleeding. Recent travel abroad, villous
adenoma
eating out or an outbreak among people living in close carcinoma
proximity suggests an infective cause.
Enquire about colour; in fat malabsorption, the stool
is pale, malodorous, poorly formed and difficult to flush. angiodysplasia
Blood and mucus mixed in the stool suggest an infective
colitis or inflammatory bowel disease. When a cause is haemorrhoids inflammatory
bowel
not readily apparent, consider laxative abuse and recent
disease
broad-spectrum antibiotic treatment, both of which may
precipitate diarrhoea. Thyrotoxicosis may present with Fig. 7.23 Potential causes of bright-red or maroon-coloured rectal
increased stool frequency and weight loss. bleeding.
200
Chapter
bleeding) usually presents with symptoms of anaemia.

Always consider a diagnosis of gastric, caecal or colon Venous collaterals in portal hypertension
cancer in older patients with unexplained iron deficiency
anaemia. Haemorrhoids are common, so always consider nodular cirrhotic
liver oesophageal
other causes of bleeding in patients aged 45 and over. varices
Questions to ask
Gastrointestinal bleeding
• Is there a past history of abdominal pain or other

gastrointestinal symptoms?
• Is there a history of chronic alcoholism or excessive
intake?
• Is there a past history of haematemesis, melaena or
anaemia?
fundal
• Are any nonsteroidals, steroids or proprietary varices
medicines being taken?
• Was the bleeding preceded by intense retching?
• Has there been ingestion of iron or bismuth that
Fig. 7.24 Cirrhosis of the liver. When portal pressure rises, collateral
may stain the stools?
veins open and blood bypasses the liver through dilated fundal and
oesophageal varices that eventually drain into the azygos vein and
superior vena cava.
The passage of sticky, black stools with the colour diversion of portal blood through collaterals (Fig. 7.24).
and consistency of tar (melaena) usually indicates A collateral circulation is established through the veins of
bleeding from the oesophagus, stomach or duodenum. the oesophagus. At endoscopy these abnormally dilated
The characteristic appearance and smell is attributed to oesophageal veins are seen as tortuous, dilated veins
the denaturing effect of gastric acid and enzymes on (varices). Oesophageal varices are prone to rupture and
blood. Treatment with iron and certain drugs (e.g. may cause torrential haemorrhage.
bismuth-containing preparations) also blackens the stool Gut bacteria metabolise unabsorbed protein, releasing
and this cause must be distinguished from melaena. potentially neurotoxic breakdown products into the portal
blood. The liver normally detoxifies these gut-derived
products but in patients with portal hypertension, portal
LIVER DISEASE
blood bypasses the liver (portosystemic shunting), and
The background symptoms of liver disease may reflect the brain is exposed to gut-derived products which
damage to the parenchymal liver cells (hepatocellular depress brain function, causing a characteristic neurological
disease) or obstruction of the biliary tree (intrahepatic or syndrome known as hepatic encephalopathy.
extrahepatic cholestasis). Patients may also complain A further clinical consequence of portal hypertension
of symptoms related to the development of portal is fluid retention in the abdominal cavity (ascites). The
hypertension. Liver cell damage and obstruction of the combination of high portal pressure and low serum
bile duct both have numerous clinical consequences, the albumin allows fluid to escape and to accumulate in the
most striking of which are jaundice, pale stools and abdominal cavity.
darkening of the urine. When sufficient hepatocyte
damage occurs, the patient becomes jaundiced because
bilirubin excretion fails and the pigment deposits in
tissues. When hepatocytes are damaged or dead, enzymes Risk factors
leak into the blood, where they can be measured. The
Factors predisposing to hepatitis B
high plasma activity of these enzymes is the basis of
biochemical tests for liver damage. • Intravenous drug abuse
In cirrhosis, liver architecture is severely disturbed, • Exposure to contaminated blood or blood products
with regenerating nodules distorting and compressing • Reuse of hypodermic needles, ritual scarification
the sinusoids and intrahepatic portal venous radicals. In • Unprotected sex
addition, collagen is deposited between the sinusoidal • Needle-stick injury from infected individual
lining cells and the hepatocytes, causing gradual • Vertical transmission from mother to newborn
obliteration of the space of Disse. Blood flow through the • Horizontal transmission between children at play,
liver is partially obstructed and pressure rises in the portal toothbrushes, razors
vein. Resistance to blood flow through the liver encourages
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Chapter
7 The abdomen
Liver cell damage Questions to ask

The earliest symptoms of liver damage are not very specific Jaundice
and include malaise, fatigue, anorexia and nausea. Viral
• Have you travelled to areas where hepatitis A is
hepatitis is preceded by prodromes such as fatigue, nausea
endemic?
and a profound distaste for alcohol and cigarettes. Before
• Is there a history of alcohol or intravenous drug abuse?
the onset of jaundice the patient may notice darkening of
• Have you ever had a blood transfusion?
the urine and lightening of stool colour. This is caused by
• Have you had contact with jaundiced patients?
failure of the liver cells to excrete conjugated bilirubin.
• Have you experienced skin itching?
Enquire about the principal causes of liver damage.
• What medication has been used recently (including
Calculate the number of units (or grams) of alcohol
nonprescription drugs)?
consumed in a week as this provides a good guide to the
• Have you had occupational contact with hepatotoxins?
risk of liver damage (see Ch. 1). Ask about any foreign
• Is there pain and weight loss?
travel, intravenous drug abuse or exposure to blood
• What colour are the stools and urine?
products, and establish the patient’s sexual orientation.
• Is there a family history of liver disease?
Enquire about drugs that may cause liver damage and ask
about a family history of liver disease.
The principal complications of chronic liver cell damage
are jaundice, cirrhosis and portal hypertension. The
patient may notice increasing girth and weight gain. This duct, whereas ‘painless’ jaundice suggests either a more
is caused by the accumulation of ascites. If encephalopathy chronic obstruction of the common bile duct (e.g. cancer
occurs, the sleep pattern may be reversed and the patient of either the bile duct or head of the pancreas) or damage
may undergo a change in personality. to the intrahepatic biliary tree (e.g. primary biliary
cirrhosis, sclerosing cholangitis, drugs). Impaired bile
flow into the duodenum causes fat malabsorption and
BILIARY OBSTRUCTION
steatorrhoea; marked weight loss may occur.
The principal symptom is itching (pruritus) and this may
occur long before the patient becomes jaundiced. The PANCREATIC DISEASE
cause of pruritus is unknown, although the deposition of
Acute pancreatitis presents with the onset of upper
bile acids in the skin has been suggested. As with viral
abdominal pain that is most prominent in the epigastrium
hepatitis, lightening of the stools and darkening of the
and left upper quadrant. The pain may radiate through
urine often precedes jaundice. The history may not help
to the back, with its intensity varying from mild to severe.
distinguish between the different causes of intrahepatic
It is persistent and often lasts a few days before abating.
and extrahepatic obstruction. Severe epigastric and right
The pain is commonly accompanied by nausea and
hypochondrial pain accompanied by fever and jaundice
vomiting; some relief may be obtained by sitting forward.
suggests impaction of a gallstone in the common bile
Ask about alcohol intake and drugs (e.g. azathioprine,
furosemide, corticoids) and consider underlying
Differential diagnosis gallstones, which may precipitate acute pancreatitis.
Jaundice Recurrent attacks of acute pancreatitis may result
in chronic pancreatitis. This is often characterised by
Prehepatic or unconjugated hyperbilirubinaemia persistent, severe upper abdominal pain that may radiate
• Haemolytic anaemias circumferentially to the back. Progressive loss of exocrine
• Gilbert’s syndrome function eventually leads to steatorrhoea and weight loss.
Hepatocellular disease Endocrine failure with diabetes is a late manifestation.
• Viral hepatitis (types A, B, C, D and E) Occasionally, chronic pancreatitis develops insidiously
• Alcoholic hepatitis and presents with weight loss and steatorrhoea.
• Autoimmune hepatitis (lupoid) Progressive fibrosis may occlude the lower bile duct
• Drug hepatitis (halothane, paracetamol) causing jaundice.
• Decompensated cirrhosis
Intrahepatic cholestasis KIDNEY AND BLADDER DISEASE
• Drugs (phenothiazines) The principal symptoms of diseases affecting the kidneys,
• Primary biliary cirrhosis ureters and bladder are pain and an alteration in the
• Primary sclerosing cholangitis volume and frequency of bladder emptying.
Extrahepatic cholestasis
Frequency and urgency
• Bile duct stricture (benign and malignant)
• Common duct stone Frequency refers to the desire to pass urine more often
• Cancer of the head of the pancreas than normal, although there is not necessarily an increase
in the volume of voided urine. Urgency may accompany
202
Chapter
frequency (i.e. a strong urge to urinate even though only Hesitancy

small amounts of urine are present in the bladder).
Hesitancy is a delay between attempting to initiate
Nocturia urination and the actual flow of urine. It is a characteristic
sign of bladder outlet obstruction (e.g. as a result of
It is unusual to be woken from sleep to pass urine
prostatic hypertrophy).
(nocturia) but this may occur in patients with daytime
frequency or individuals producing excessive quantities Oliguria and anuria
of urine (polyuria). Incomplete bladder voiding caused by
Patients may complain of passing only small volumes
prostatism often presents with nocturia.
of urine. The term oliguria is used if less than 500 ml of
Incontinence urine is passed over 24 h. The subjective assessment
of urine volume is often inaccurate and requires
Incontinence is an involuntary leakage of urine. If the
confirmation by 24 h urine collection and measurement.
symptom is provoked by increased intra-abdominal
Apparent oliguria may occur in patients with bladder
pressure (coughing, sneezing or laughing), it is referred
muscle (detrusor) failure. Consequently, it may be
to as ‘stress incontinence’.
necessary to pass a catheter to confirm true oliguria.
Diseases causing excessive bladder filling (e.g. bladder
outlet obstruction or damage to the nervous supply of the Pain
bladder) may cause ‘overflow incontinence’ which reflects
Pain may originate in the kidneys, ureter, bladder or
spill-over from an overfilled, hypotonic bladder.
urethra. Infection of the kidneys (pyelonephritis) causes
pain and tenderness in the renal angles, usually associated
Symptoms and signs with fever, anorexia and nausea. Obstruction of the
Some renal symptoms and their causes ureters by stones, sloughed papillae or blood may cause
intense pain in the renal angle. This pain may radiate
Frequency towards the groins and, in men, into the testes. Renal
• Irritable bladder ‘colic’ caused by stones in the ureters is extremely painful,
– infection, inflammation, chemical irritation often causing the patient to double-up or roll around in
• Reduced compliance a futile attempt to find relief. Bladder pain may occur in
– fibrosis, tumour infiltration severe cystitis. The pain is of moderate severity, localised
• Bladder outlet obstruction to the suprapubic region and associated with urgency
– in prostatism, detrusor failure may limit the and frequency.
volume voided
Dysuria
Polyuria
• Ingestion of large volumes of water, beverages or Dysuria describes a stinging or burning sensation that
alcohol occurs when passing urine. It is often accompanied by
• Chronic renal failure (loss of concentrating power) frequency and urgency. The most common cause of
• Diabetes mellitus (osmotic effect of glucose in urine) dysuria is cystitis.
• Diabetes insipidus (caused by a lack of ADH or
Haematuria
tubules insensitive to circulating ADH)
• Diuretic treatment Blood in urine may be obvious, associated with a cloudy
Dysuria colour or only apparent on chemical testing (microscopic
• Bacterial infection of the bladder (cystitis) haematuria). Whether the passage of blood is painful or
• Inflammation of the urethra (urethritis) painless may be of diagnostic assistance.
• Infection or inflammation of the prostate (prostatitis)
Incontinence
• Sphincter damage or weakness after childbirth Differential diagnosis
• Sphincter weakness in old age
Haematuria
• Prostate cancer
• Benign prostatic hypertrophy Painful
• Spinal cord disease, paraplegia • Kidney stones
Oliguria or anuria • Urinary tract infection
• Hypovolaemia (dehydration or shock) • Papillary necrosis
• Acute renal failure caused by acute Painless
glomerulonephritis • Infection
• Bilateral ureteric obstruction (retroperitoneal fibrosis) • Cancer of the urinary tract
• Detrusor muscle failure (bladder outlet obstruction or • Acute glomerulonephritis
neurological disease) • Contamination during menstruation
203
Chapter
7 The abdomen
resembling a ‘noughts and crosses’ matrix (Fig. 7.29).

Examination of the abdomen These segments are useful landmarks for ensuring a
complete and systematic examination of the abdomen. A
Before beginning your examination ask the patient to lie
vertical line is dropped from the midclavicular points on
flat, with the head resting comfortably on a pillow, arms
either side and these are crossed by a horizontal line
lying loosely on either side. According to the demands of
drawn in the subcostal plane and by a line joining the
the particular procedure you are performing, try to expose
anterior superior iliac spines.
the patient as little as possible. The ‘classical’ arrangement
When locating or describing the position of the
is shown in Figure 7.25 but until you gain experience it
abdominal organs it is useful to recognise the anterior
will help to have the visual clues provided by the
anatomical planes and their correlation with vertebral
landmarks of the entire abdomen and lower chest;
levels (Fig. 7.30). The xiphisternum corresponds to the
subsequent illustrations reflect this.
The abdominal examination depends largely on the
palpation and percussion of organs that normally lie out
of reach of the examining hands. As with all other
examinations, it is important to become completely Examination of the liver and spleen
familiar with the clinical anatomy of the abdomen.
The costal margin demarcates the superficial boundary
between the chest and abdomen, although the domes of
the diaphragm rise behind the ribs to accommodate the
liver and spleen, so a full abdominal examination also
includes examination of the lower half of the chest (Fig.
7.26). Familiarise yourself with the bony landmarks of the
abdomen (Fig. 7.27). Feel the xiphisternum at the lower
end of the sternum, then trace the outline of the costal
margin formed by the seventh costal cartilage at the
liver stomach
xiphisternum to the tip of the 12th rib. Note a distinct
step in the costal margin which provides a useful landmark gallbladder spleen
because it coincides with the tip of the 10th rib. Turn your pancreas
attention to the bony margins of the lower abdomen. The duodenum
iliac crest has a distinct anterior prominence, the anterior costal
superior iliac spine, from which the inguinal ligament margin
runs downward and medially to attach to a lateral
prominence on the pubic bone (the pubic tubercle). Fig. 7.26 The liver and spleen lie protected under the ribs and so
For descriptive purposes the anterior abdominal wall the lower one-half of the chest must be exposed in order to examine
may be divided into four quadrants (Fig. 7.28). Trace the them.
imaginary lines demarcating the left and right upper
and lower quadrants. A vertical line extends from the
xiphisternum to the pubic symphysis in the midline and
a horizontal line is drawn through the umbilicus. The
abdomen may also be divided into nine segments
Fig. 7.25 The patient should be exposed as little as possible during

your examination. Fig. 7.27 The bony landmarks of the anterior abdominal wall.
204
Chapter
Examination of the abdomen 7
level of T9. The transpyloric plane lies midway between subcostal plane coincides with the level of L3 and is
the suprasternal notch and the pubis, approximately a defined by a line joining the lowest point of the thoracic
hand’s breadth below the xiphoid cartilage. This plane cage on either side. A line joining the highest points of
corresponds to the vertebral level of L1 and passes the iliac crest corresponds to the level of L4.
through the pylorus, the long axis of the pancreas, the
duodenojejunal flexure and the hila of the kidneys. The
INSPECTION OF THE ABDOMEN
Contours
Expose the patient to the groins and observe the symmetry
Quadrants of the abdomen
of the abdomen from the foot of the bed. The normal
abdomen is concave and symmetrical and moves gently
with respiration. Next, move to the patient’s right and
view the abdomen tangentially. From this position it is
easier to pick out the subtle changes of contour and
shadow. In thin individuals you may notice the pulsation
of the abdominal aorta in the midline above the umbilicus.
Ask the patient to raise the head a few inches off the
xiphisternum pillow. This tenses the rectus abdominis, which becomes
firm and prominent on either side of the midline.
Abnormal contours and distension of the abdomen
may be caused by a number of mechanisms (Fig. 7.31).
right upper left upper
quadrant quadrant
Establish whether the swelling is generalised or localised.
Fluid and gaseous distension is generalised and
symmetrical (Fig. 7.32). Fluid gravitates towards the
right lower left lower flanks causing the loins to bulge, and the umbilicus,
quadrant quadrant which is normally inverted, may become everted when
massive ascites distends the abdomen beyond its normal
compliance. In thin individuals, the contour of an enlarged
liver may be visible below the right costal margin. A
pubic symphysis midline fullness in the upper abdomen may indicate
disease of the stomach (e.g. carcinoma), pancreas (e.g.
Fig. 7.28 The quadrants of the anterior abdominal wall. pancreatic cysts) or an abdominal aortic aneurysm.
Segmental anatomy of the abdomen The transverse planes of the abdomen
xiphisternum
(T9)
right left transpyloric plane (L1)

hypochondrium epigastrium hypochondrium
subcostal plane (L3)
right left iliac crest (L4)
lumbar umbilical lumbar
region region region
right suprapubic left
inguinal region inguinal
region region
Fig. 7.29 The nine segments of the anterior abdominal wall. Fig. 7.30 The transverse planes and their equivalent vertebral levels.
205
Chapter
7 The abdomen
Abnormal abdominal contours (on inspection)
linea alba
hernia
paraumbilical
hernia
incisional divarication
hernia hernia
Fig. 7.31 Some abnormal abdominal contours.
a b
Fig. 7.32 The characteristic appearance of gross ascites: (a) lateral,
(b) anterior view.
Fig. 7.33 Striae gravidarum appear after childbirth.

Suprapubic fullness may reflect an enlarged uterus
(pregnancy or fibroids), ovaries (cysts or carcinoma) or a
full bladder. The periodic rippling movement of bowel pressure is raised by coughing. Surgical scars are potential
peristalsis may be observed in intestinal obstruction, points of weakness in the abdominal wall and incisional
especially in thin individuals. This is referred to as a herniae may develop under the scar.
visible peristalsis.
Abnormal bulges may appear when intra-abdominal Skin
pressure is raised and may be revealed by tensing the During pregnancy the abdominal wall skin is stretched
abdominal muscles. If the muscles of the recti are and after childbirth many women are left with tell-tale
abnormally separated on either side of the midline stretch lines (striae gravidarum) that arc across the mid-
(divarication of the recti), tensing the abdominal muscles and lower abdominal wall on either side of the midline
causes a longitudinal bulge to appear in the midline (Fig. (Fig. 7.33). Stretch marks similar to those occurring after
7.31). The appearance of a more localised bulge just pregnancy may occur in patients successfully treated
above or below the umbilicus occurs with a paraumbilical for ascites. In Cushing’s syndrome, excessive adrenal
hernia (Fig. 7.31). Direct and indirect inguinal herniae corticoid secretion thins the skin and purplish striae
may also become prominent when intra-abdominal appear on the abdominal wall even in the absence of a
206
Chapter
Determining the direction of blood flow in abdominal wall veins

place two fingers at one end of the vein
and apply occlusive pressure
move one finger along the vein, thus

emptying a section
blood flow direction is indicated by

whether or not the vein refills once the
finger is removed
(a) (b) (c)
Fig. 7.34 Determining the direction of blood flow in abdominal veins. (a) Normal blood flow pattern and those characteristic of (b) portal
hypertension and (c) obstruction of the inferior vena cava.
pregnancy. In acute haemorrhagic pancreatitis, there

may be a bluish discoloration of either the flanks (Grey Surgical incisions
Turner’s sign) or the periumbilical area (Cullen’s sign),
which results from seepage of bloodstained ascitic fluid
along the fascial planes and into the subcutaneous tissue.
A similar appearance may occur after rupture of an ectopic
pregnancy.
Look for veins coursing over the abdominal wall: they
are rarely prominent in health. If veins are visible, map
the direction of flow by emptying the vein with the index
finger of one hand while attempting to prevent refilling
by applying occlusive pressure more proximally over the
vein. The direction of flow helps distinguish normal from right
abnormal flow patterns (Fig. 7.34). In portal hypertension subcostal midline
incision incision
and inferior vena caval obstruction, the venous return to
the liver or vena cava is redirected through abdominal paramedian loin incision
wall collaterals that provide an alternative route to the incision
right atrium. These veins dilate and may be seen coursing suprapubic
across the abdominal wall. It is possible to distinguish incision
appendectomy
collaterals caused by portal hypertension from those scar hernia
caused by inferior vena caval obstruction by mapping the repair
direction of flow in these vessels.
Look for surgical scars, which should have a fleshy red Fig. 7.35 Surgical scars seen commonly on the abdomen.
or pink colouring in the first year after an operation,
becoming white as the scar tissue matures. Common
locations of surgical scars are shown in Figure 7.35. provide substantial clinical information. These procedures
are difficult to perform if the patient is not relaxed. If
the abdominal wall muscles are tense, ask the patient to
PALPATION OF THE ABDOMEN bend the knees and flex the hips (Fig. 7.36). This helps
Although the intra-abdominal organs are normally to relax the abdomen. Always warm your hands before
impalpable, in diseased states palpation and percussion palpating the abdomen and use the fingertip and palmar
207
Chapter
7 The abdomen
aspects of the fingers; a single-handed technique may the patient flinches on even the lightest palpation and
be used but you may prefer to use both hands, the there is reflex rigidity, guarding and rebound tenderness.
upper hand applying pressure, while the lower hand Light palpation may localise an area of peritoneal
concentrates on feeling (Fig. 7.37). inflammation, thereby helping to establish a differential
diagnosis. It is unusual to feel the abdominal organs or
Light palpation
large masses on light palpation unless they are grossly
Before laying a hand on the abdomen ask the patient to enlarged.
localise any areas of pain or tenderness. If these are
Deep palpation
present, begin the examination in the segment furthest
from the discomfort. Start light palpation by gently Once you have used light palpation to explore for areas
pressing your fingers into each of the nine segments, of tenderness and muscle tension, the sequence is
sustaining the light pressure for a few seconds while repeated using firm but gentle deep pressure with the
gently exploring each area with the fingertips. Tenderness palmar surface of the fingers. Deep palpation is helpful
may be reflected by grimacing, so with every move of for palpating abdominal masses, and healthy individuals
your hand briefly look to see the patient’s facial often report pain on deep pressure of the abdomen. If the
response. patient is relaxed it is usually possible to press deeply into
Gentle palpation will detect tenderness caused by the abdomen. While doing so try to imagine the anatomy
inflammation of the parietal peritoneum. In peritonitis, underlying your hand (Fig. 7.38). In thin individuals, the
descending and sigmoid colon may be felt as an elongated
tubular structure in the left loin and lower quadrant. The
Palpation of the abdomen sigmoid is mobile and can readily be rolled under the
fingers. The colon can usually be distinguished from
other structures because of its firm stool content. It has
a putty-like consistency and can be indented with the
fingertips. The ‘mass’ also becomes less obvious after the
passage of stool. In thin individuals, the abdominal aorta
may be felt as a discrete pulsatile structure in the midline,
above the umbilicus. The rectus muscles may be mistaken
for an abnormal fullness or the edge of a mass. Tensing
the abdominal muscles causes the rectus to become more
prominent, whereas intra-abdominal masses are less
easy to feel.
Abdominal masses and enlargement of the liver,
spleen and kidneys may also be felt by deep palpation.
Any abnormal fullness, firmness or discrete mass should
be localised by careful palpation of shape, mobility,
consistency and movement with respiration. Localisation
helps determine which organ may be involved. Determine
Fig. 7.36 Palpation of the abdomen may be aided if the patient is
whether there is any deep tenderness, suggesting
asked to flex the hips. This helps to relax the anterior abdominal stretching of the capsule of either the liver or kidney,
wall. or early peritoneal inflammation or infiltration. A large
a b
Fig. 7.37 Light abdominal palpation is performed using one (a) or both hands (b).
208
Chapter
Structures that may be felt on deep palpation Distinction between aortic pulsation and movement
of an overlying structure
liver
lower
pole of right abdominal
kidney aorta
caecal
squelch descending
and/or
sigmoid
colon
uterus
bladder
Fig. 7.38 On deep palpation of the abdomen, these structures may

be felt.
pulsatile structure in the midline above the umbilicus

indicates an aortic aneurysm or a transmitted impulse
to a mass overlying the aorta. These can usually be
distinguished using the index finger of either hand to
Fig. 7.39 Palpating the aorta. The direction of the pulsation
sense whether the movement is pulsatile or transmitted indicates whether it arises directly from the aorta (above) or is
(Fig. 7.39). transmitted by a mass overlying the tissues (below).
PALPATION OF THE ORGANS

The surface anatomy of the liver
The solid organs (liver, pancreas, kidneys and spleen) are
normally out of reach of the examining hand. The
stomach, small intestine and colon are soft, pliable and
impalpable. In chronic fibrosing diseases of the liver
(e.g. micronodular cirrhosis) or kidneys (e.g. chronic
glomerulonephritis), these organs shrink even further
from reach. However, they may become palpable when
enlarged.
EXAMINING THE LIVER nipple line

Palpating the liver
Examine the liver with the surface anatomy in mind.
Visualise its upper margin as a line passing just below 10th rib
each nipple on either side and imagine the lower margin
spanning a line from the tip of the 10th rib on the right
Fig. 7.40 The surface anatomy of the liver.
to a point just below the left nipple (Fig. 7.40). The upper
surface of the organ is tightly apposed to the undersurface
of the diaphragm and examination takes advantage of the smaller left lobe nestles under the lower left rib cage and
movement of the liver with respiration. The initial aim of is often impalpable even when the organ is generally
the examination is to define the outline of the lower edge enlarged.
of the right lobe, which is normally tucked along the Examine from the patient’s right and use either the
inner surface of the right costal margin. The edge of the fingertips or the radial side of the index finger to explore
209
Chapter
7 The abdomen
Fig. 7.42 Positioning of the hand when percussing for the lower
border of the liver.
At this point in the examination it is useful to percuss

for the lower liver edge. With the long axis of your middle
finger positioned parallel to the right costal margin,
percuss from the point where you started palpating for
the liver (Fig. 7.42). This point normally overlies bowel
and should sound resonant. Repeat the percussion in a
stepwise manner, each time moving the finger closer to
the costal margin until the note becomes duller. This
should coincide with the costal margin. Ask the patient
b to inspire deeply; the dullness should move down as the
Fig. 7.41 Liver palpation. A two-handed (a) and single-handed (b) liver descends.
technique using the radial surface of the index finger(s) to feel for Next, find the position of the upper margin of the liver
the lower liver edge as it descends during inspiration. so that you can assess the liver span. The upper margin
cannot be palpated because it lies high in the dome of
the diaphragm, but it can be located by noting the change
for the liver edge under the costal margin. Point the ends in percussion note from the resonance of the lungs to the
of the index, middle and ring fingers in an upward dullness of the liver. The upper margin of the liver usually
position, facing the liver edge, at a point midway between lies deep to the sixth intercostal space. Percuss the third
the costal margin and iliac crests, lateral to the rectus space and then percuss each succeeding interspace until
muscle (Fig. 7.41). Press the fingertips inwards and you detect the transition from resonance to dullness (Fig.
upwards and hold this position while the patient takes 7.43). On deep inspiration the percussion interface should
a deep inspiration. Near the height of inspiration relax descend by either one or two interspaces as the lungs
the inward pressure slightly but maintain upward expand and the liver descends. Liver size is proportional
pressure. As the fingers drift upwards feel for the liver to body size. Measure the liver span in the midclavicular
edge slipping under them as the organ descends. If line; in women this should measure 8–10 cm and in men,
no edge is felt, repeat the manoeuvre in a stepwise 10–12 cm.
fashion, each time moving the starting position a little
Downward displacement of the liver In patients who
closer to the costal margin. If the liver is impalpable
have hyperinflated lungs (e.g. emphysema), the
at this point, you should repeat the procedure more
diaphragm is flattened and the liver is pushed down so
laterally in line with the anterior axillary line. In patients
that the edge may be easily palpable below the costal
of thin or medium build a normal liver edge may be
margin (Fig. 7.44). Percussion reveals that the upper
palpable just below the right costal margin at the height
border of the liver is depressed and that the liver span is
of inspiration. Repeat the palpation in the midline and
within normal limits.
below the left costal margin where the lower edge of
the middle and left lobes should not be palpable. A Abnormal liver shape The right lobe of the liver may
single-handed technique may also be used (Fig. 7.41). be abnormally shaped, with an elongated tongue-like
The radial surface of the index finger is positioned below projection pointing towards the right iliac crest (Fig.
and parallel to the costal margin and this surface is used 7.45). This anatomical variant, known as a Riedel’s lobe,
to explore for the lower liver edge as it descends during is more common in women and feels like a mobile mass
inspiration. on the right side of the abdomen arising from under the
210
Chapter
Riedel’s lobe
normal
liver
edge
Fig. 7.43 Percussion of the upper border of the liver.
Riedel’s
lobe
Liver pushed down by hyperinflation

Fig. 7.45 A Riedel’s lobe is a normal variant of shape. The
elongated ‘tongue’ is palpable and must be distinguished from a
hyperinflated pathological cancer.
lungs
Hepatomegaly
• Macronodular cirrhosis
• Neoplastic disease (primary and secondary cancer,
myeloproliferative disorders)
• Infections (viral hepatitis, tuberculosis, hydatid
disease)
costal
• Infiltrations (iron, fat, amyloid, Gaucher’s disease)
margin
Fig. 7.44 When the lung fields are markedly hyperinflated, the liver
is pushed down and the lower border may be readily palpable, if the liver edge is not palpable and if, on percussion, the
although the span is normal. dullness of the lower liver margin is detected well above
the costal margin (Fig. 7.47). Atrophy of the liver may be
the result either of severe acute liver damage, perhaps
costal margin and moving with respiration. A Riedel’s caused by fulminant viral hepatitis or hepatotoxic poisons,
lobe is commonly mistaken for an enlarged right kidney or of chronic disease causing fibrosis and micronodular
and if in doubt this can be resolved by ultrasound cirrhosis (e.g. alcoholic cirrhosis).
scanning.
General signs of liver disease
Enlargement of the liver Liver enlargement is usually
described as mild, moderate or massive (Fig. 7.46). If the The liver has considerable functional reserve but as this
liver is enlarged, trace the shape of the liver edge and is exhausted the patient develops characteristic signs of
decide whether it is smooth or irregular, whether the liver failure. Look for jaundice in the sclerae, which are
consistency is soft, firm or hard and whether or not the normally a brilliant white colour. Mild jaundice may be
organ is tender. The presence of a palpable spleen difficult to discern in artificial light and in dark-skinned
suggests cirrhosis with portal hypertension or infiltrating patients the sclerae may be slightly pigmented. With
diseases of the reticuloendothelial and haemopoietic deepening jaundice the skin becomes yellow, and in
systems. chronic, severe obstructive jaundice the skin may appear
almost green in colour.
Small livers The lower margin of the liver may not be In patients with chronic liver disease, localised vascular
palpable because of fibrosis or atrophy of the organ. This dilatation results in the appearance of vascular spiders
may be difficult to detect clinically but should be suspected (spider naevi) (see Fig. 3.11). These consist of a central
211
Chapter
7 The abdomen
Smooth and irregular liver surface
mild
smooth irregular
moderate
enlargement enlargement
massive
Fig. 7.46 Liver enlargement. Enlargement of the liver can be smooth (e.g. fatty liver) or irregular (e.g. macronodular cirrhosis, tumour
infiltration).
Symptoms and signs

Percussion of shrunken liver
Signs of liver disease
General examination
• Nutrition status
• Pallor (blood loss)
• Jaundice
• Breath fetor of liver failure
• Xanthelasmata (chronic cholestasis)
• Parotid swelling (alcohol abuse)
• Bruising (clotting diathesis)
• Spider naevi
• Female distribution of body hair
Mental state
• Wernicke’s or Korsakoff’s psychosis
resonance well
• Flapping tremor of hepatic encephalopathy above costal
• Inability to copy a five-pointed star margin
Hands
• Leuconychia (hypoproteinaemia) Fig. 7.47 Atrophy of the liver may be detected by percussing the
• Liver flap lower border. The area of resonance will extend above the costal
• Palmar erythema margin.
• Dupuytren’s contractures
• Mild finger clubbing
Chest arteriole from which branch a series of smaller vessels, in
• Gynaecomastia a pattern resembling spider legs. Spider naevi are found
• Right-sided pleural effusion in the territory drained by the superior vena cava; common
Abdomen sites include the neck, face and dorsa of the hands. The
• Dilated veins central arteriole can be occluded with a pencil tip and on
• Liver or spleen enlargement release of the pressure the vessels rapidly refill from the
• Ascites centre.
• Testicular atrophy Severe hepatocellular disease associated with porto-
systemic shunting can result in hepatic encephalopathy.
212
Chapter
Risk factors
Cirrhosis
• Alcoholism
• Chronic hepatitis B
• Chronic hepatitis C
• Chronic biliary disease (sclerosing cholangitis, primary
biliary cirrhosis)
• Iron overload
• Autoimmune disease
• Copper overload
Fig. 7.48 To elicit a flapping tremor in hepatic encephalopathy, ask

the patient to outstretch the arms with the hands extended at the
wrist and metacarpophalangeal joints. This position is held for 20
seconds. Differential diagnosis
Hepatic encephalopathy
• Protein load (acute bleed, dietary binge)

• Diuretics and electrolyte abnormalities
Often there are accompanying signs of portal hyperten- • Development of hepatocellular cancer
sion, such as splenomegaly and ascites, but the physical • Toxins or drugs (alcohol binge, sedatives, opiates)
sign characteristic of hepatic encephalopathy is a • Infection
‘flapping tremor’. Ask the patient to stretch out both
arms and hyperextend the wrists with the fingers held
separated (Fig. 7.48). A coarse, involuntary flap occurs
at the wrist and metacarpophalangeal joints. A further
sign is sleepiness and this may progress to coma. Differential diagnosis
Encephalopathic patients often have difficulty copying a Portal hypertension
picture of a five-pointed star and they may struggle to
Presinusoidal
complete a simple ‘dot-to-dot’ diagram.
• Portal vein block
The severity of liver disease is categorised by the
• Schistosomiasis
Child–Pugh classification (see ‘symptoms and signs’
• Cystic fibrosis
box), which assigns points to the clinical and biochemical
findings to reach a score. The score is a guide to Sinusoidal and postsinusoidal
prognosis. • Cirrhosis
• Veno-occlusive disease
• Hepatic vein block (Budd–Chiari syndrome)
Symptoms and signs

Child–Pugh classification of severity of liver disease
PALPATING THE GALLBLADDER
Points assigned
Conclude the liver palpation by feeling for the gallbladder.
Parameter 1 2 3
Imagine the position of the fundus, which lies under the
Ascites Absent Slight Moderate
point where the rectus abdominis muscle intersects the
Albumin (g/l) >35 28–35 <2.8
costal margin. This surface marking coincides with the tip
INR (clotting) <1.7 1.8–2.3 >2.3
of the right 9th rib.
Encephalopathy None Grade 1–2 Grade 3–4
Using gentle but firm pressure palpate the gallbladder
Score area by pointing the tips of the fingers towards the
• 5–6 = Grade A (well-compensated disease) organ while the patient inspires deeply (Fig. 7.49).
• 7–9 = Grade B (significant functional disturbance) When the gallbladder is inflamed (cholecystitis), the
• 10–15 = Grade C (decompensated liver disease) most striking physical sign is tenderness and guarding
Prognosis (%) over the gallbladder region. The patient experiences
1 year 2 year intense pain, winces and interrupts the breath as your
Grade A 100 85 fingers make contact with the descending organ (Murphy’s
Grade B 80 60 sign).
Grade C 45 35 The normal gallbladder is impalpable and only becomes
palpable when obstructed and distended with bile. The
213
Chapter
7 The abdomen
Palpating the gallbladder Courvoisier’s law
gallbladder bed
stone in the
common bile duct
fibrosed gallbladder
with gallstones
stricture of the
Fig. 7.49 Palpating the gallbladder bed. bile duct
(carcinoma)
dilated
distended organ is contiguous with the lower border of gallbladder
the liver and moves with respiration. In the absence of
jaundice, a palpable gallbladder suggests obstruction
of the cystic duct with the formation of a mucocele.
Obstruction of the bile duct by a stone causes jaundice
but the gallbladder is rarely palpable because stone
formation is associated with chronic cholecystitis and the Fig. 7.50 If jaundice is caused by impaction of a gallstone in the
thickened, fibrosed gallbladder wall does not distend. bile duct, the fibrosed, stone-filled gallbladder does not dilate.
However, if jaundice is caused by a bile duct stricture the healthy
Jaundice associated with a palpable gallbladder usually
gallbladder dilates and can be palpated as a soft mass arising from
implies biliary obstruction caused by a carcinoma of behind the 9th right rib anteriorly.
either the head of the pancreas or the common bile duct.
In this case the organ is not diseased and is able to dilate
(Courvoisier’s law) (Fig. 7.50). Remember, however, that
exceptions to this rule do occur.
PALPATING THE SPLEEN

The normal spleen cannot be felt and only becomes
palpable once it has doubled in size. The spleen enlarges
from under the left costal margin towards the right iliac
fossa in a downward and medial direction. Often only the
tip of the spleen can be felt as it enlarges, although in
moderate and massive splenomegaly the organ can be
felt well below the costal margin.
Before palpating for the spleen, wrap the palmar
surface of your left hand around the back and side of the Fig. 7.51 When palpating the spleen use your left hand to support
lower rib cage to provide support and lift the spleen the ribcage posteriorly, while the fingertips of your right hand
explore the leading edge of the organ.
anteriorly. Start the examination from the region of the
umbilicus. Position the fingers of the right hand obliquely
across the abdomen, with the fingertips pointing at the
left costal margin and towards the axilla (Fig. 7.51). The felt passing under the fingers and glancing off at the
general technique is similar to that described for the liver. height of inspiration.
Using a moderate amount of pressure, press the index If the spleen is impalpable at the starting point of the
and middle fingers inwards and upwards and hold this examination, move the fingertips progressively closer to
steady while asking the patient to breathe in deeply. At the left lower rib cage. Make a final pass at the lower
the midpoint of the inspiratory effort, lessen the inward costal margin with the fingers probing just under the rib
pressure but maintain the upward pressure, allowing the cage. Some clinicians prefer to palpate the spleen with
fingers to drift in the direction of the descending spleen. the patient rolled into the right lateral position, with their
The notched leading edge of an enlarged spleen can be knees drawn up to relax the abdominal muscles.
214
Chapter
Percussion of spleen Description of splenomegaly
spleen 1–2 cm (tip enlargement)

Traub’s space 3–7 cm (moderate
(9th intercostal splenomegaly)
space) 7 cm (marked
midaxillary
splenomegaly)
line
anterior
axillary line Fig. 7.53 The different degrees of splenomegaly.
Symptoms and signs

Differentiation between splenomegaly and
palpation of the left kidney
Kidney Enlarged spleen

• Moves late in • Moves early in inspiration
inspiration
• Possible to get above • Impossible to get above
upper pole a spleen
• Smooth shape • Notched leading edge
• Resonant to percussion • Dull to percussion in
Traub’s space
• Enlarges towards
Fig. 7.52 After palpating for the spleen, percuss for the enlarged
organ in the 9th intercostal space anterior to the anterior axillary umbilicus
line.
Splenomegaly
At this point in the examination it is useful to percuss
for splenic dullness. The tip of a normal spleen lies • Portal hypertension
posterior to the anterior axillary line and is bounded • Infections (malaria, subacute bacterial endocarditis,
anteriorly by the gas-filled stomach and colon. Percuss tuberculosis, typhoid)
the 9th intercostal space anterior to the anterior axillary • Chronic lymphatic leukaemia
line (Traub’s space) (Fig. 7.52). This space overlies bowel • Chronic myeloid leukaemia
and is normally tympanitic but as the solid spleen enlarges • Myelofibrosis
this area becomes less resonant, eventually sounding dull • Gaucher’s disease
with more marked splenomegaly. • Haemolytic anaemia
An enlarged spleen is readily distinguished from other
organs in the region, such as the left kidney. Note whether
there is tenderness and assess the degree of enlargement, EXAMINING THE RENAL SYSTEM
using a ruler to measure the distance from the left costal Like the examination of the liver, the kidney examination
margin to the tip of the spleen (Fig. 7.53). Splenomegaly is aided by systemic signs that reflect impaired function
may be caused by stimulation and hypertrophy of the of the organ. In acute renal failure, there is oliguria
reticuloendothelial elements, congestion with blood or (<500 ml/24 h) and signs of fluid overload. The clinical
by infiltration by abnormal cells. syndrome is dominated by a rapidly progressive
215
Chapter
7 The abdomen
deterioration of biochemical tests of function (raised be felt. The right kidney is easier to palpate because it lies
blood urea, creatinine and potassium) occurring over lower than the left. A normal kidney has a firm consistency
hours or days (see ‘differential diagnosis’ box – acute and a smooth surface.
renal failure). When renal failure develops over weeks, When examining the kidneys, position the patient
months or years, systemic signs appear (see ‘differential close to the edge of the bed and examine each kidney
diagnosis’ and ‘symptoms and signs’ boxes – chronic from the patient’s right, bearing in mind the surface
renal failure). anatomy. The kidneys are retroperitoneal organs and
deep bimanual palpation is required to explore for them.
Palpating the kidneys
When examining the left kidney, tuck the palmar surfaces
Pole to pole the kidneys extend from the vertebral level of the left hand posteriorly into the left flank and nestle
of T12 to L3 and the larger right lobe of the liver displaces the fingertips in the renal angle (Fig. 7.55a). Position the
the right kidney 2 cm lower than the left. Viewed from middle three fingers of the right hand below the left
the rear, the kidneys lie in the renal angle formed by the costal margin, lateral to the rectus muscle and at a point
12th rib and the lateral margin of the vertebral column opposite the posterior hand (Fig. 7.55b). To examine the
(Fig. 7.54). The adrenal glands perch on the upper pole right kidney, tuck your left hand behind the right loin and
of each kidney. position the fingers of your right hand below the right
The kidneys are not usually palpable through the costal margin, lateral to rectus abdominis. Palpate for the
thickness of the abdominal wall and abdominal contents, lower pole of each kidney in turn. The aim of the
although in thin individuals a normal-sized kidney may manoeuvre is briefly to trap the lower pole of the kidney
between the fingers of both hands as the organ moves
up and down with deep respiration. The spleen is closely
associated with the diaphragm and thus moves early in
Surface markings of the kidney respiration but the kidneys lie lower down and they only
descend towards the end of inspiration. Ask the patient
to inspire deeply; press the fingers of both hands firmly
together, attempting to capture the lower pole as it slips
through the fingertips. This technique is known as
balloting the kidney (Fig. 7.55b). If the kidney is palpable
the rounded lower pole can be felt slipping between the
opposing fingers as the patient breathes in and out.
Acute renal failure
11th rib
• Shock (hypovolaemic, septic or cardiogenic)
12th rib
• Acute glomerulonephritis
costovertebral kidney • Toxins or drugs (ethylene glycol, carbon
angle tetrachloride)
• Acute haemoglobinuria or myoglobinuria
• Acute renal vein thrombosis
Fig. 7.54 The surface anatomy of the kidneys.
a b
Fig. 7.55 Positioning the hands when palpating (a) the left and (b) the right kidney.
216
Chapter
Symptoms and signs

PALPATING THE AORTA
Signs of chronic renal failure The descending aorta emerges through the aortic hiatus
in the diaphragm and hugs the vertebral bodies until it
• Sallow complexion bifurcates into the common iliac arteries at the level of
• Anaemia (normocytic, normochromic) L4, which approximates to a point just below the
• Uraemic fetor umbilicus. It lies adjacent to the inferior vena cava and
• Deep acidotic breathing (Kussmaul respiration) gives off a number of major tributaries that feed the major
• Hypertension abdominal organs (Fig. 7.57). The aorta can be palpated
• Mental clouding between the thumb and finger of one hand or by
• Uraemic encephalopathy (flapping tremor) positioning the fingers of both hands on either side of the
• Pleural and pericardial effusion midline at a point midway between the xiphisternum and
• Pericardial rub (pericarditis) the umbilicus (Fig. 7.58). Press the fingers posteriorly
• Evidence of fluid overload or depletion and slightly medially and feel for the pulsation of the
• Renal masses (polycystic kidneys) abdominal aorta against your fingertips. This pulsation
• Large bladder (chronic bladder outlet obstruction) can be felt in thin individuals but it is usually impalpable
in muscular or obese patients.
An abdominal aortic aneurysm may be felt as a large
pulsatile mass above the level of the umbilicus. The
Differential diagnosis abdominal aorta may also become abnormally prominent
Chronic renal failure in elderly people when marked curvature of the spine
displaces it anteriorly and laterally.
• Chronic glomerulonephritis
• Diabetes mellitus with nephropathy PERCUSSION OF THE ABDOMEN
• Chronic obstructive uropathy At this stage of the examination you will have percussed
• Polycystic disease of the kidneys the liver and spleen. General percussion of the abdomen
• Analgesic nephropathy is used to establish whether abdominal distension is
caused by gas or fluid. Percussion is also used to detect
an overfilled bladder. The stomach, small bowel and
The kidney may be tender, especially when acutely colon fill the entire anterior abdomen and the percussion
infected (pyelonephritis) or obstructed (hydronephrosis). note of the anterior abdomen wall between the costal
This may be apparent on bimanual palpation, although margins and iliac crests is normally tympanic.
a more specific sign is ‘punch’ tenderness over the renal
angles. To test this response sit the patient forward and
place the palm of the left hand over the renal angle. Then, Branches of the aorta
using moderate force, punch the dorsal surface of the
hand with the ulnar surface of the clenched right fist (Fig.
diaphragm
7.56). Perform this test for each kidney in turn and assess
the patient’s reaction.
coeliac
It is important to distinguish kidney enlargement from
axis
splenomegaly on the left and hepatomegaly on the right.
The principal cause of bilateral enlargement is polycystic spleen
disease of the kidney, whereas unilateral enlargement hepatic
artery splenic
suggests a malignant tumour (e.g. hypernephroma). artery
superior mesenteric
artery
right kidney left kidney
renal
artery
inferior
mesenteric
common iliac
artery
artery
external iliac internal

artery iliac
artery
Fig. 7.56 Assessing the punch tenderness over the renal angles. Fig. 7.57 The abdominal aorta and its branches.
217
Chapter
7 The abdomen
Palpation of aorta
aorta
a
Fig. 7.58 Palpation of the aorta at a point midway between the

umbilicus and the xiphisternum.
Percussion to detect ascites

Abdominal distension is usually caused either by gaseous
dilatation of the bowel or abnormal accumulation of
fluid. In the supine position, gas accumulates more
centrally, whereas fluid gravitates into the flanks. The
gas-filled normal bowel tends to float above ascites, so
the gas–fluid interface characteristic of ascites is detected
by a change in the percussion note from the resonance b
overlying bowel to the dullness of fluid. The presence of
ascites can be confirmed by altering the patient’s posture Fig. 7.59 When percussing for ascites, (a) begin in the midline with
your finger parallel to the lateral wall of the abdomen and (b)
and demonstrating a change in the position of the gas– continue towards the left flank. A change in the percussion note
fluid interface. indicates a gas–fluid interface.
A change in percussion note (shifting dullness) is
easiest to assess by percussing from an area of resonance
to an area of dullness. With the patient supine, percuss Percussion to detect a distended bladder
in the midline at the level of the umbilicus with the If the bladder outlet is obstructed and the detrusor muscle
fingers parallel to the lateral wall of the abdomen (Fig. fails, the organ distends and emerges above the pubic
7.59a). This point overlies gas-filled bowel and the bone from its usual position deep within the pelvis. The
percussion note should be tympanic. Progressively suprapubic area is usually tympanic and a dull sound
reposition your hand approximately 2 cm to the left and on percussion here is a useful clinical sign of bladder
repeat the percussion towards the left flank (Fig. 7.59b). distension.
The note should remain tympanic until you reach the Use the general principle of percussing from resonance
lateral abdominal wall. A distinct transition zone between to dullness to check for bladder enlargement. Percuss
tympany and dullness, a gas–fluid interface, should be from the level of the umbilicus, parallel to the pubis (Fig.
marked lightly with a water-soluble marking pen. Now 7.61) and progress down the midline towards the pubic
ask the patient to roll into the right lateral position. This bone. The note should remain tympanic to the pubic
allows the fluid to gravitate to the right flank and the bone. A level of dullness above this landmark indicates
gas-filled bowel to rise into the left flank (Fig. 7.60). the upper margin of a distended bladder or possibly
Repeat the percussion from the midline towards the left enlargement of the uterus. An enlarged bladder is felt as
flank. The tympany should extend well lateral to the a rounded fullness, whereas an enlarged uterus is felt as
interface marked in supine examination. a more distinct solid structure.
218
Chapter
Shifting dullness of ascites
mark the skin at the

gas–fluid interface
gas
fluid (tympany) fluid
(dullness) (dullness)
Fig. 7.62 If you suspect obstruction of the pyloric outlet, check for
a ‘succussion splash’ by simultaneously listening in the epigastrium
and shaking the upper abdomen from side to side.
tympany extends
lateral to your
original mark
tympany mark AUSCULTATION OF THE ABDOMEN
gas when supine The sounds generated by the abdomen are gurgling
noises caused by the intestinal peristalsis moving gas and
fluid through the bowel lumen. These are best assessed
by auscultation.
fluid dullness
Listening for bowel sounds
Place the diaphragm of the stethoscope on the mid-
abdomen and listen for intermittent gurgling sounds
Fig. 7.60 To confirm the presence of ascites, roll the patient into (borborygma). These peristaltic sounds occur episodically
the right lateral position because this causes fluid to settle in the
dependent right flank, whereas gas-filled bowel floats above to fill
at 5–10s intervals, although longer silent periods may
the left flank. A shift in the positions of dullness and tympany occur. Keep listening for approximately 30s before
indicates free fluid. concluding that bowel sounds are reduced or absent.
The absence of any bowel sounds can indicate intestinal
paralysis (paralytic ileus); this is always associated with
abdominal distension. Rapidly repetitive bowel sounds
(often termed ‘active’ bowel sounds) may be normal but
they may also be an early sign of mechanical obstruction
if they are associated with a colicky abdominal pain. In
progressive bowel obstruction, large amounts of gas and
fluid accumulate and the bowel sounds change in quality
to a higher pitched ‘tinkling’. This is an ominous sign of
impending bowel paralysis.
Auscultation may also be helpful when diagnosing
obstruction of gastric outflow. In pyloric obstruction, the
stomach distends with gas and fluid; this can be detected
by listening for a ‘succussion splash’. Steady the
diaphragm of the stethoscope on the epigastrium and
shake the upper abdomen for the splashing sound
characteristic of gastric outflow obstruction (Fig. 7.62).
Listening for arterial bruits

Fig. 7.61 Percuss for the fundus of the bladder from the level of
the umbilicus. Position the diaphragm of the stethoscope over the
abdominal aorta and apply moderate pressure (Fig.
219
Chapter
7 The abdomen
a b
Fig. 7.63 Position of the stethoscope when listening for bruits in (a) the aorta and (b) the renal artery.
Examining the groin

The spermatic cord, inguinal lymph nodes and femoral
artery occupy the groin. A swelling in the groin is usually
the result of either an inguinal or femoral hernia or due
to enlarged lymph nodes.
INGUINAL CANAL AND FEMORAL SHEATH

During male fetal development the testis and spermatic
cord migrate from the abdomen into the scrotum through
the inguinal canal. This passage occludes after the descent
of the testes but it remains a potential route through
which the bowel can herniate in later life, causing an
Fig. 7.64 Position of the stethoscope when listening for a liver inguinal hernia.
bruit.
The inguinal canal passes downward and medially
from the internal to the external ring, running above and
parallel to the inguinal ligament, which forms its lower
7.63a). The heart sounds may be transmitted to this border (Fig. 7.65). The internal ring lies immediately
area but aortic flow should be silent. A distinct systolic above the point at which the inguinal ligament and
murmur (a bruit) indicates turbulent flow and suggests femoral artery intersect. The femoral artery lies at the
arteriosclerosis or an aneurysm. midfemoral point, which is located midway between the
Listen for renal arterial bruits at a point 2.5 cm above anterior superior iliac spine and the symphysis pubis.
and lateral to the umbilicus (Fig. 7.63b). The presence of The external ring lies immediately above and medial to
a renal bruit suggests congenital or arteriosclerotic renal the pubic tubercle. The femoral artery enters the femoral
artery stenosis or narrowing caused by fibromuscular triangle from behind the inguinal ligament and is enclosed
hyperplasia. in a fascial sheath. This sheath also accommodates the
femoral vein, which lies medial to the artery, and the
femoral canal, which is a small gap immediately adjacent
AUSCULTATION OVER THE LIVER AND SPLEEN and medial to the vein. The femoral canal is plugged with
Conclude the auscultation by listening over the liver (Fig. fat and a lymph node (Cloquet’s gland) and it is a potential
7.64) and spleen. A soft and distant bruit heard over an pathway for the formation of a direct femoral hernia.
enlarged liver is always abnormal, suggesting either
Examining herniae
primary liver cell carcinoma or acute alcoholic hepatitis.
Secondary liver tumours do not transmit bruits. An indirect inguinal hernia forms when bowel or
Occasionally, a creaking ‘rub’ may be heard over the liver omentum protrudes through a lax internal ring and finds
or spleen. This indicates inflammation of the outer capsule its way into the inguinal canal. Bowel may force its way
of the organ and adjacent peritoneum, perhaps caused through the external ring and may even slip into the
by perihepatitis or perisplenitis. More rarely, carcinomatous scrotum (Fig. 7.66).
infiltration of the capsule and surrounding structures may An inguinal hernia usually presents as a lump in the
be the cause. groin or the scrotum that is most prominent when the
220
Chapter
Examining the anus, rectum and prostate 7
Anatomy of the inguinal region
internal oblique inferior epigastric anterior superior

aponeurosis artery iliac spine
external oblique external

transversalis internal inguinal
aponeurosis inguinal
fascia ring
inguinal ring
ligament
external
inguinal femoral
ring artery
femoral
vein
femoral artery
femoral vein fascial
internal inguinal sheath femoral
femoral canal ring canal
spermatic
cord
Fig. 7.65 The anatomy of the inguinal canal and femoral sheath.
seldom force their way into the scrotum and, once

Passage of indirect inguinal hernia reduced, their reappearance is not controlled by pressure
over the internal ring.
When an inguinal hernia extends as far as the external
ring it may be confused with a femoral hernia. The
distinction is made by establishing the relationship of the
internal
hernia to the pubic tubercle: an inguinal hernia lies above
inguinal
ring and medial to the tubercle, whereas a femoral hernia lies
indirect
external below and lateral.
inguinal
inguinal
ring
hernia
hernia may
Examining the anus, rectum
migrate to and prostate
scrotum
RECTUM AND ANUS
The rectum is a curved segment of the bowel, approximately
Fig. 7.66 An indirect hernia enters through the internal ring and 12 cm long, lying in the concavity of the mid- and lower
exits through the external ring.
sacrum (Fig. 7.67). The upper two-thirds of the anterior
rectum but not the posterior surface is covered by
intra-abdominal pressure is raised (e.g. when standing or peritoneum. The anterior rectal peritoneum reflects onto
coughing). The hernia may reduce spontaneously when the bladder base in men, it forms the rectouterine pouch
the patient lies down, so it is best to examine the hernia (known as the pouch of Douglas) in women and is filled
with the patient standing. Place two fingers on the mass with loops of bowel. Anterior to the lower one-third
and ascertain whether or not an impulse is transmitted of the rectum lie the prostate, bladder base and
to your fingertips when the patient coughs. Most herniae seminal vesicles in men and the vagina in women.
can be reduced manually, so attempt this by gently The anus is 3–4 cm long and joins the rectum to the
massaging the mass towards the internal ring. Once the perineum. The anal wall is supported by powerful
hernia is fully reduced, occlude the internal ring with a sphincter muscles, the voluntary external and involuntary
finger pressing over the femoral point. Ask the patient to internal sphincters, which constrict to provide tone and
cough. An indirect inguinal hernia should not reappear continence (Fig. 7.68). The rectal mucosa can be directly
until you release the occlusion of the internal ring. visualised through a proctoscope or sigmoidoscope but
A direct inguinal hernia develops through a weakness a great deal may be learned by palpation of the anus,
in the posterior wall of the inguinal canal. These herniae rectum and prostate.
221
Chapter
7 The abdomen
Anatomical relationships of the rectum in males and females

pouch of
Douglas
peritoneum sacrum
rectum
uterus
rectum
cervix
bladder bladder
pubic prostate vagina
symphysis gland pubic
symphysis anus
anus urethra
urethra
Fig. 7.67 The relationship of the anterior rectum to the prostate gland and bladder base in men (left) and the posterior vaginal wall and
uterine cervix in women (right).
The anal sphincters
Causes of faecal incontinence
Severe constipation with overflow longitudinal internal

muscle sphincter
Diseases of the colon and rectum
• Acute diarrhoeal illness
• Inflammatory bowel disease
• Colorectal cancer levator ani
• Hypotonic sphincter following difficult vaginal
delivery
Neurological disorders
• Dementias and depressive illness deep
• Cerebrovascular disease and stroke external superficial
sphincter
• Spinal cord disease
• Autonomic neuropathy subcutaneous
Fig. 7.68 The internal and external anal sphincters.

Rectal examination should not be unduly painful
and it is important to explain this to the patient, along
with your reasons for performing it. The examination external haemorrhoids or prolapsed rectal mucosa
will promote a feeling of rectal fullness and it may (Fig. 7.72). A bluish discoloration of the perineal skin
stimulate a desire to evacuate. Tell the patient to expect suggests Crohn’s disease. The anal skin is innervated
this. Always work with an assistant and always glove with pain fibres and anal pain and tenderness are
both hands. suggestive of infection (e.g. perianal abscess), fissure
Position the patient in the left lateral position with the and fistula-in-ano or thrombosis of an external
hips and knees well flexed and the buttock positioned haemorrhoid.
at the edge of the bed (Fig. 7.69). The positions around Lubricate your index finger with a clear, water-soluble
the anal opening are described by the positions around gel (e.g. K-Y jelly) and press the fingertip against the anal
the clock face (Fig. 7.70). Gently separate the buttocks verge with the pulp facing the 6 o’clock position (Fig.
to expose the natal cleft and anal verge (Fig. 7.71). 7.71). Slip your finger into the anal canal and then insert
Inspection of the natal cleft and anal verge may reveal it into the rectum, directing the tip posteriorly to follow
skin tags, pilonidal sinuses, warts, fissures, fistulas, the sacral curve (Fig. 7.73). With your finger fully
222
Chapter
introduced, check on anal tone by asking the patient to

squeeze your finger with the anal muscles. Then gently
sweep the finger through 180° using the palmar surface
of the finger to explore the posterior and posterolateral
walls of the rectum. Rotate the finger round to the 12
o’clock position. This is accomplished more easily by
adopting a half-crouched position and simultaneously
pronating your wrist. This position allows you to sweep
the finger across the anterior and anterolateral walls of
the rectum. The normal rectum feels uniformly smooth
and pliable. In men, the prostate can be felt anteriorly
and in women it may be possible to feel the cervix as well
as a retroverted uterus.
On rectal palpation you may feel an intrinsic tumour
caused by a carcinoma or polyp. Perirectal sepsis causes
marked rectal wall tenderness and an abscess may be felt
pointing into the lumen. The anterior rectal peritoneal
Fig. 7.69 The correct position of the patient before a rectal reflection straddles both the anterior rectum itself and the
examination. structures lying in front of it. Consequently, malignant or
inflammatory lesions of the peritoneum may be felt
through the anterior wall of the rectum.
Withdraw your finger from the rectum and anus and
The clock face positions around the anus
check the glove tip for stool. There may be melaena,
blood or pus and you may notice the pale, greasy stools
anterior characteristic of malabsorption.
PROSTATE
The prostate gland is examined during the rectal
12 o’clock examination. The normal prostate measures approximately
3.5 cm from side to side and protrudes 1 cm into the
rectum (Fig. 7.74a). The gland has a rubbery, smooth
9 o’clock 3 o’clock consistency and a shallow longitudinal groove separates
the right and left lobes. It should not be tender to palpation
but the patient may experience the urge to urinate.
6 o’clock
posterior Prostate enlargement
• Asymmetric enlargement
Fig. 7.70 The positions of the clock face are used to describe
positions around the anus. • Stony hard consistency
• Discreet nodularity
Palpation of the prostate aims to assess size, consistency,

nodularity and tenderness. The assessment of prostatic
size is learnt through experience. Benign hypertrophy of
the prostate is common in men over 60 years old. The
enlargement is smooth and symmetrical and the gland
feels rubbery or slightly boggy (Fig. 7.74b). A cancerous
prostate may feel asymmetric, with a stony hard
consistency, and discrete nodules may be palpable (Fig.
7.74c). Marked prostatic tenderness suggests acute
prostatitis, a prostatic abscess or inflammation of the
seminal vesicles. If prostatic infection is suspected,
attempt to massage the organ from within the rectum in
order to squeeze prostatic fluid towards the urethral
meatus, where it can be collected for microscopy and
Fig. 7.71 Exposing the anus. culture.
223
Chapter
7 The abdomen
a b c
Fig. 7.72 Lesions commonly seen on

inspection of the anal verge: (a) multiple
pilonidal sinuses in the natal cleft, (b) viral
warts, (c) thrombosed external
haemorrhoids, (d) rectal mucosal prolapse
e and (e) the bluish discoloration typical of
d
Crohn’s disease.
Fig. 7.73 The rectal examination. (a) Insert

the tip of the index finger into the anus
then (b) introduce your finger to follow the
curve of the sacrum. (c) Rotate the finger
b anteriorly to palpate the anterolateral and
lateral walls and the prostate or cervix.
224
Chapter
Palpating the normal and abnormal prostate
(a) (b) (c)
Fig. 7.74 (a) The normal prostate felt through the anterior rectal wall has a median sulcus separating the two lateral lobes. (b) The median
sulcus may become indistinct in a benign hypertrophied prostate and the gland feels firm and smooth and bulges more than 1 cm into the
lumen. (c) A carcinomatous prostate feels hard and irregular and the median sulcus is obliterated.

Abdominal examination in elderly people
• On inspection of the abdomen there may be • Aortic bruits are more common in the elderly,
asymmetry caused by kyphoscoliosis of the spine reflecting atherosclerosis or aneurysm
• Osteoporosis and deformity of the rib cage causes the • Leaking aneurysm presents as backache; rupture
costal margin to migrate towards the pelvis, making presents as an acute abdominal emergency with
abdominal examination more difficult shock, abdominal distension, poor distal perfusion and
• If the patient is hard of hearing or dyspraxic there may asymmetrical pulses
be difficulty obtaining the cooperation needed to • Benign or malignant prostatic hypertrophy in older men
palpate the liver and spleen predisposes to bladder outlet obstruction, detrusor
• Constipation in the elderly often manifests with the instability and failure, urinary retention and infection
impression of a mass in the left lower quadrant (this • Acute urinary retention is a common cause of acute
can be re-assessed after an enema to induce ‘unexplained’ confusion in the elderly – always examine
evacuation) for an enlarged bladder in elderly patients presenting
• An ectatic aorta is often palpable and scoliosis often with confusion, delirium, incontinence or fever
displaces the aorta, giving a false impression of an • Faecal incontinence may be associated with dementia,
aortic aneurysm chronic constipation with overflow, laxative abuse and
• Consider an aneurysm if the aorta is assessed to be disordered sphincteric function
>5 cm in diameter at its widest (readily confirmed on • A rectal examination and plain abdominal x-ray usually
ultrasound) clarifies faecal impaction in the elderly
Review
Framework for the routine examination of the abdomen
General examination • Liver, spleen, kidneys

• Nutrition and hydration • Bladder, uterus, aorta
• Peripheral oedema (hypoproteinaemia) Percussion
• Leuconychia or koilonychia • Upper and lower liver margins
• Signs of liver disease • Spleen (Traub’s space)
Inspection • Shifting dullness (ascites)
• Shape and symmetry • Suprapubic dullness (bladder)
• Scars and striae Auscultation
• Abdominal wall veins and flow pattern • Bowel sounds
• Visible peristalsis • Aortic and renal bruits
• Hernias (paraumbilical, inguinal) • Hepatic and splenic rubs
Palpation (nine segments) Rectal examination
• Light palpation to assess tenderness • Rectal mucosa
• Deeper palpation for masses • Prostate, uterus
225
8
Female breasts and genitalia
The clinical assessment of the reproductive system is moderately overweight girls tend to enter puberty earlier
often neglected in routine examinations because of than their lean contemporaries. Abnormal weight loss
patients’ discomfort and embarrassment and because of (such as occurs with anorexia nervosa or a debilitating
doctors’ reluctance to conduct the genital examination as illness) causes delay of the menarche or cessation of
a routine procedure. The case history and examination established periods altogether (amenorrhoea).
intrude into patients’ most intimate boundaries, so Adolescent development can be assessed using
careful scripting is necessary to reassure the patient. The pubertal milestones defined by Tanner (Fig. 8.1). For girls
sensitivity associated with the examination is further this is based on breast development and the growth of
heightened when dealing with patients of the opposite pubic hair. Puberty in girls begins between 8 and 13 years
sex. A chaperone should always be close at hand when a of age. The average age of the menarche is 12.5 years
member of the opposite sex is examined. and most girls will have menstruated by the age of
It is reassuring to remember that the majority of 14.5 years.
patients feel reasonably comfortable discussing sexual
problems with their doctor; this stems from a cultural Hormonal changes in puberty
acceptance that doctors deal with all aspects of bodily Puberty is established by the activation of the
function and an understanding that the doctor–patient neuroendocrine axis. The cerebral cortex plays a central
relationship is confidential and professional. It is role in the initial activation of the hypothalamus, which
important to establish trust and competence when stores gonadotrophin-releasing hormone (GnRH). This
assessing the genital tract. Undergraduate courses in hormone is released into the hypothalamo-hypophyseal
gynaecology, obstetrics and genitourinary medicine portal system and is carried to the anterior lobe of the
provide the opportunity to learn the examination pituitary gland where it stimulates the release of
techniques required for a thorough examination. sex hormones. During childhood, GnRH secretion is
inhibited and loss of this inhibition signals the onset of
puberty (Fig. 8.2). Pulsatile release of GnRH provides the
Structure and function signal for the pulsatile release of follicle-stimulating
hormone (FSH) and luteinising hormone (LH) from
PUBERTY the pituitary gland which, in turn, stimulates the gonads.
The transition from childhood to adolescence is regulated The hormonal products of the female gonads then
by hormones secreted by the hypothalamic–pituitary exert their specific influences on the reproductive organs
axis. During puberty there is a rapid spurt in growth, and induce the development of secondary sexual
accounting for approximately 25% of the final adult characteristics. Breast growth (telarche) in women is
height. Secondary sexual characteristics develop and followed by the menarche and the establishment of the
sexual awareness is aroused. menstrual cycle.
The age of puberty varies and parents and teenagers
Breast development
often worry about what they perceive as a delayed growth
spurt. A number of factors determine the onset of puberty. Oestrogen secretion from the developing ovaries is the
Over the past 150 years there has been a progressive fall prime stimulus for breast development. Initially, there is
in the age of the first menstrual period (menarche). This widening of the areola with a small mound of breast
is thought to reflect the effects of improving nutrition and tissue developing beneath it. This is followed by
general health on the onset of puberty. There is evidence progressive enlargement of the breasts until the full adult
that body weight is an important trigger for puberty: size is attained (Fig. 8.1).
226
Chapter
Tanner’s stages of breast development in puberty
1. prepubertal 2. breast budding 3. enlargement 4. secondary mound 5. single contour of

formed by areola breast and areola
Fig. 8.1 Stages of breast development. Development from the preadolescent stage (1) begins initially with a widening of the areola and the
development of subareolar tissue (2). Progressive expansion occurs (3–4) until adult size is attained (5).
The hypothalamic–pituitary–gonadal axis Tanner’s stages of pubic hair development

before and after puberty
1. prepubertal: 2. slight labial (and 3. increased amount
Prepuberty Puberty no hair axillary) hair of hair on mons
pubis (and axilla)
cerebral
cortex
hypothalamus hypothalamus
4. adult amount of sexual 5. adult amount of hair and
hair distributed to pubis distribution with extension
GnRH GnRH to upper thighs
pituitary
portal
system
primordial FSH Graafian Fig. 8.3 Pubic hair development. Development from the
follicles +LH follicles preadolescent (1) begins with the growth of sparse straight hair
along the medial borders of the labia (2). Further growth of darker
ovary
coarser curlier hair continues (3–4) until the typical inverted triangular
distribution of the adult female is seen (5).
oestrogen
Pubic hair growth
In both males and females, growth of the pubic hair is
uterus regulated by adrenal androgens, with an additional
contribution of testicular androgen in the male. In
females, the pattern of pubic hair growth has a
characteristic inverted triangular appearance (Fig. 8.3).
Fig. 8.2 The hypothalmic–pituitary–gonadal axis. In childhood,
gonadotrophin-releasing hormone (GnRH) secretion is inhibited (left). Ovarian and menstrual cycle
Loss of GnRH inhibition induces puberty and provides the signal for
the release of follicle-stimulating hormone (FSH) and luteinising The cyclical release of FSH and LH from the pituitary is
hormone (LH). FSH and LH stimulate the gonads and exert cyclical reflected in serum concentration changes. Ovulation
changes in the uterine endometrium (right). occurs in response to these changes and this in turn
227
Chapter
8 Female breasts and genitalia
Physiology of the menstrual cycle Development of Graafian follicle
pituitary
FSH LH
units/l follicle-stimulating
50 hormone
peritoneal
FSH LH cavity
0
oestradiol progesterone primordial
ovum
(μg/l) (μg/l) follicle
0.4 16
antrum
0.3 progesterone 12
oestradiol granulosa
0.2 8
cells
0.1 4 granulosa
0 0 cells
temperature mature
follicle
rises
0.5°C
37°C
cumulus
ovaricus
ovum development thecal liquor

cells folliculi
immature maturation ovum corpus degenerating

follicle luteum corpus luteum
Graafian
follicle
endometrium
Fig. 8.5 Development of a mature ovarian follicle.
hormone in the second phase of the ovulatory cycle. The

discharge regeneration ischaemia
granulosa cells of the corpus luteum express LH receptors
day 1 7 14 21 28
which are also capable of binding human chorionic
menstrual proliferative secretory menstruation gonadotrophin (HCG), a hormone secreted by the fetal
phase phase phase phase syncytiotrophoblast. In the absence of fertilisation, HCG
does not appear in the circulation, and by about the 23rd
day of the cycle, the corpus luteum starts to atrophy.
Fig. 8.4 Physiological changes associated with the menstrual cycle.
Progesterone levels fall, allowing the re-expression of
FSH secretion and the initiation of another cycle. If
conception has not occurred, menstruation commences.
regulates cyclical changes in the uterine endometrium This is caused by an intense vasospasm in the arterioles
(Fig. 8.4). In each cycle, a few ‘selected’ dormant ovarian feeding the superficial layers of the endometrium, which
follicles become responsive to FSH, with usually only a causes hypoxic necrosis of this tissue. The tissue is then
single dominant follicle maturing to the point of ovulation expelled through the vagina.
(Fig. 8.5). The primordial follicle consists of a large oocyte
Climateric and menopause
surrounded by a flattened follicular epithelium. In the
few responsive follicles, FSH stimulates the proliferation By about the age of 40 years, the number of functional
of granulosa cells which secrete an oestradiol-rich fluid oocytes has fallen to the point where sex hormone
that accumulates in the follicle (the antrum). As the synthesis is reduced. This signals the onset of the
follicle grows, it is surrounded by a specialised layer of climacteric, which over a period of years culminates in
thecal cells which are derived from the ovarian stroma. the cessation of menstruation (the menopause). Initially,
The responsive follicle grows to attain a preovulatory size FSH levels increase in an attempt to stimulate follicular
of 2–3 cm. In midcycle there is a surge of both FSH and ripening; later, anovulatory cycles develop with irregular
LH (Fig.8.4); the LH surge is thought to trigger the events menstrual bleeding; finally, at about the age of 50 years,
leading to the extrusion of the ovum from the ovary. menstruation ceases. Loss of hormonal feedback results
Extrusion of the ovum leaves behind the corpus luteum in high serum levels of FSH and LH (Fig. 8.6). Serum
(Fig. 8.4), which secretes progesterone, the dominant sex levels of these hormones are used as a test for the
228
Chapter
Breast structure and function 8
Physiological changes in the menopause Muscles underlying the breast
uninhibited
LH FSH
++ ++
decreased production
of oestrogens
secondary to
depletion of
developing follicles
scarred atrophic
ovarian stroma
depleted of follicles and
refractory to high
gonadotrophin levels
Fig. 8.6 Loss of hormonal feedback in the menopause. The

hypothalamus tries to compensate for the falling oestrogen level by
increasing production of follicle-stimulating hormone (FSH) and
luteinising hormone (LH). Fig. 8.7 The breast overlies pectoralis major and serratus anterior
muscles.
climacteric and menopause. The decline in oestrogen

production results in atrophy of the breasts, genital Segmental anatomy of the breast
organs and bone. Vasomotor instability may result in hot
flushes.
Breast structure and function

tail of Spence
The breasts overlie the pectoralis major and serratus
anterior muscles and extend from the second to sixth ribs
(Fig. 8.7). It is convenient to divide the breast into four
quadrants by horizontal and vertical lines intersecting at upper inner upper outer
the nipple (Fig. 8.8). A lateral extension of breast tissue
(the axillary tail of Spence) extends from the upper outer
lower outer
quadrant towards the axilla.
lower inner
Each breast is formed from 15–20 glandular lobules
embedded in a supporting bed of fatty and fibrous tissue
that gives shape to the organ (Fig. 8.9). Fibrous
septa known as Cooper’s (suspensory) ligaments separate
the lobules and provide support by attaching between
the subcutaneous tissue and the fascia of the muscles.
Each glandular lobule drains into the nipple through
a lactiferous duct. This duct is surrounded by myoepithelial Fig. 8.8 For descriptive purposes, the breast is divided into four
cells that can contract to eject milk into the nipple. quadrants and a tail (of Spence).
The nipple is infiltrated with smooth muscle that
contracts in response to sensory and tactile stimuli,
causing the nipple to become erect. Surrounding the LYMPHATIC DRAINAGE OF THE BREAST
nipple is the pigmented areola. Sebaceous glands (the As breast cancer spreads to regional lymph nodes, it is
glands of Montgomery) provide local secretion. Extra important to appreciate lymphatic drainage because the
nipples with breast tissue may occur along a primordial discovery of affected nodes implies a more serious
‘milk line’ which extends from the axilla to the groin prognosis and influences the mode of treatment. In
(Fig. 8.10). general, the lymphatics follow the blood supply, yet there
229
Chapter
Structure of the breast The axillary nodes
axillary
pectoralis duct opening vein
major onto nipple
muscle lateral nodes
fatty tissue apical nodes
central deep
lactiferous nodes
duct
posterior
nodes
nipple anterior nodes
nipple
pore internal
mammary
nodes
suspensory
ligaments
palpable nodes
of Cooper
deep nodes
Fig. 8.9 The breast is formed by glands with their ducts opening
individually through the nipple. Fatty tissue shapes the breast and the
fibrous (Cooper’s) ligaments provide support.
Fig. 8.11 Diagrammatic representation illustrating the position of
the axillary lymph nodes.
The milk line

axilla becoming affected. Even the abdominal nodes may
be involved.
FUNCTION OF THE BREAST

During puberty, glandular growth is primarily under
the trophic influence of oestradiol and progesterone.
Throughout pregnancy, the breasts enlarge further under
the influences of rising concentrations of oestrogens,
progesterone, placental lactogen and prolactin secreted
by the anterior pituitary. A darkish ring (secondary areola)
appears around the areola during pregnancy. Suckling by
the newborn child stimulates a neuroendocrine reflex
that causes further release of prolactin as well as oxytocin
(from the posterior pituitary). Oxytocin (which also has
a uterine-contracting action) stimulates contraction of
the myoepithelial cells surrounding the lobules and
lactiferous ducts, causing the expression of milk (Fig.
8.12). The effect of sucking on the nipple sustains
lactation. Feeding mothers produce approximately 1 litre
of milk daily. When the child is weaned, the sucking
Fig. 8.10 Supernumerary nipples and breast tissue may appear reflex is lost and lactation dries up.
along the milk line.
is a free connection between the lymphatics of the one Symptoms of breast disease
breast, and sometimes with the other. Nonetheless, the
lateral part of the breast usually drains towards the axillary PAIN
group of nodes and the medial half towards the internal Throughout the menstrual cycle there are cyclical, trophic
mammary chain. The axillary nodes are arranged into five and involutional changes in the glandular tissue. This
groups, each of which must be examined (Fig. 8.11). dynamic response of the tissue to changes in hormones
The vast interconnection of lymphatics predisposes to may cause breast pain and tenderness which fluctuates
widespread metastatic spread, with nodes in the opposite predictably with the menstrual cycle, usually more
230
Chapter
Examination of the breast 8
The suckling reflex in lactation
prolactin oxytocin
Fig. 8.13 Initially, inspect the breast from the front with the patient
+ + sitting with her arms comfortably resting at her sides.
afferent need to decide whether to include a full breast examination

neural as part of your routine examination. Male doctors must
stimulus
from suckling
always examine in the presence of a female nurse or
nipple chaperone. The aim of examination is to check for breast
lumps and it is reasonable to recommend a formal breast
examination in asymptomatic women over the age of
Fig. 8.12 Sucking sends an afferent stimulus to the anterior and
posterior pituitary, resulting in the release of prolactin and oxytocin.
40 years. Before examining the patient, suggest to her
that the general examination of the chest offers a good
opportunity to check the breasts for lumps. Remember to
towards the end of a cycle. A painful breast in the first inform her of your findings (reassurance is the best of all
few months of lactation is almost always due to a bacterial medicines). Many techniques have been described, yet
infection of the gland and is characterised by fever as well the principles remain similar.
as redness and tenderness over the infected segment.
Ask about local trauma, as fat necrosis may cause pain, INSPECTION
and also consider thrombophlebitis of the veins (Mondor’s
disease). The patient should undress to the waist. Position yourself
in front of the patient, who should be sitting comfortably
with her arms at her side (Fig. 8.13). Note the size,
DISCHARGE symmetry and contour of the breasts, the colour and
Patients may present with an abnormal nipple discharge. venous pattern of the skin. Observe the nipples and note
Determine whether the fluid is clear, opalescent or whether they are symmetrically everted, flat or inverted.
bloodstained. In men, and women who have never If there is unilateral flattening or nipple inversion, ask
conceived, a discharge is always abnormal. However, after whether this is a recent or long-standing appearance. In
childbearing, some women continue to discharge a small fair-skinned women, the areola has a pink colour but
secretion well after lactation has stopped. The inappropriate darkens and becomes permanently pigmented during the
secretion of milk (galactorrhoea) is caused by a deranged first pregnancy. Ask the patient to raise her arms above
prolactin physiology. A blood discharge should always
alert you to the likelihood of an underlying breast cancer.
BREAST LUMPS Breast lumps
A patient may present after discovering a breast lump Benign

by self-examination. This discovery causes great alarm • Fibroadenoma (mobile)
because the patient will usually associate the lump with • Simple cyst
breast cancer. • Fat necrosis
• Fibroadenosis (tender ‘lumpy’ breasts)
• Abscess (painful and tender)
Examination of the breast Malignant
• Glandular
You will usually examine the breast in the course of the • Areolar
chest examination. In asymptomatic women, you will
231
Chapter
Fig. 8.16 Asymmetry of the breast.
Fig. 8.14 To accentuate any asymmetry of the breast ask the

patient to raise her arms above her head.
Fig. 8.17 An obvious breast lump.
Fig. 8.15 Another technique for accentuating the breast contours is

by pressing the hands against the hips.
Signs suggestive of breast cancer
(see also Fig. 8.18)
her head and then press her hands against her hips (Figs
8.14, 8.15). These movements tighten the suspensory • Skin dimpling
ligaments, exaggerating the contours and highlighting • Everted, flat or retracted nipple
any abnormality. In men, the nipple should lie flat on the
pectoralis muscle.
ABNORMALITIES ON INSPECTION BREAST PALPATION

In normal women there may be some asymmetry of the During the chest examination the patient will be lying
breast and nipples, ranging from unilateral hypoplasia to on the examination couch with her arms resting
a mild but obvious asymmetry (Fig. 8.16). You may be comfortably at her side or held above her head. Palpate
struck by an obvious lump (Fig. 8.17), retraction or gross the breast tissue with the palmar surface of the middle
deviation of a nipple (Fig. 8.18), prominent veins or three fingers, using an even rotary movement to compress
oedema of the skin with dimpling like an orange skin the breast tissue gently towards the chest wall (Fig. 8.20).
(peau d’orange). Abnormal reddening, thickening or Examine each breast by following a concentric or parallel
ulceration of the areola should alert you to the possibility trail that creates a systematic path that always begins and
of Paget’s disease of the breast, a specialised form of ends at a constant spot (Fig. 8.21). An obsessive and
breast cancer (Fig. 8.19). Male gynaecomastia is an systematic exploration of all the breast tissue ensures that
important physical sign and may be spotted on inspection small lumps which could be easily missed are not. If the
as a swelling of the areola or, in more florid cases, the breasts are abnormally large or pendulous, use one hand
development of obvious breasts (see Ch. 9). to steady the breast on its lower border while palpating
232
Chapter
Examination of the breast 8
with the other. The texture of normal breast tissue varies

Signs suggestive of breast cancer from smooth to granular, even knotty; only experience
will teach you the spectrum of normality. Texture may
also vary with the menstrual cycle; nodularity and
skin
tenderness often increases towards the end of a cycle and
breast
cancer dimpling during menstruation. Remember that breast texture is
normally symmetrical and a comparison of the two
skin breasts may help you to judge whether an area is abnormal
dimpling or not.
To examine the axillary tail of Spence, ask the patient
to rest her arms above her head. Feel the tail between
your thumb and fingers as it extends from the upper
outer quadrant towards the axilla (Fig. 8.22). If you feel a
breast lump, examine the mass between your fingers and
assess its size, consistency, mobility and whether or not
flattening flattening there is any tenderness.
of nipple of nipple
In men, palpation helps distinguish true from ‘pseudo’
gynaecomastia (obesity with fatty breast). In true
gynaecomastia a disc of breast tissue can be felt under
the areola. Unlike fat, breast tissue has a distinctly lobular
Fig. 8.18 Signs suggestive of breast cancer. Nipples may be everted, texture and may be tender to palpation.
flat or retracted.
Fig. 8.19 Typical Fig. 8.20 Palpate

appearance of the breast with the
Paget’s disease of middle three fingers,
the breast with rotating around the
reddening and point of contract
scaling of the areolar while pressing firmly
skin. but gently towards
the chest wall.
Suggested directions of breast palpation
starting point starting points
Fig. 8.22 Examine the tail of Spence with the patient’s arms resting
Fig. 8.21 Trace a systematic path either by following a concentric above the head. Use your thumb and first two fingers to trace the
circular pattern (left) or examining each half of the breast extension of breast tissue between the upper outer quadrant and the
sequentially from above down (right). axilla.
233
Chapter
NIPPLE PALPATION fold. Finally, palpate along the medial border of the
Hold the nipple between thumb and fingers and gently humerus to check for the lateral group of nodes and
compress and attempt to express any discharge (Fig. inspect the infraclavicular and supraclavicular spaces for
8.23). If fluid appears, note its colour, prepare a smear for lymphadenopathy. If you feel nodes, assess the size,
cytology and send a swab for microbiology. shape, consistency, mobility and tenderness.
LYMPH NODE PALPATION ABNORMAL PALPATION

The axillae can be palpated with the patient lying or Breast lumps
sitting. When examining the left axilla in the sitting
position, the patient may rest her (or his) left hand on Although there are clinical features that may favour a
your right shoulder while you explore the axilla with your benign lesion rather than malignancy, all breast lumps
right hand. Alternatively, there are different techniques should be investigated for possible malignancy. Common
for exposing the axilla. You may choose to abduct the arm benign lumps include fibroadenomas, fibroadenosis,
gently by supporting the patient’s wrist with your right benign breast cysts and fat necrosis. A fibroadenoma is
hand and examining with the other hand (Fig. 8.24). The usually felt as a discreet, firm and smooth lump that is
opposite hands are used to examine the other axilla. mobile in its surrounding tissue (endearingly referred to
Slightly cup your examining hand and palpate into the as a ‘breast mouse’). Fibroadenosis is a bilateral condition
apex of the axilla for the apical group of nodes. Small characterised by ‘lumpiness’ of the breasts, which may be
nodes may be felt only by rotating the exploring fingertips tender, especially in the premenstrual and menstrual
firmly against the chest wall. Next, feel for the anterior phases of the cycle. Cancerous lesions usually feel hard
group of nodes along the posterior border of the anterior and irregular and, unlike benign lesions, may be fixed to
axillary fold, the central group against the lateral chest the skin or the underlying chest wall muscle. Special tests
wall and the posterior group along the posterior axillary such as mammography, needle aspiration and biopsy
may be necessary to differentiate benign from malignant
diseases.
Risk factors
Risk factors for breast cancer
• Family history – (10%)

• Genetic mutations – (5–10% BRCA1, BRCA2
positive)
• Endogenous hormones – oestrogen
• Long-term hormone replacement therapy
• Age at menarche (higher risk with earlier menarche)
• Parity – nulliparous women at higher risk
Fig. 8.23 Inspection of the nipple.

Breast abscess (mastitis)
This usually occurs during lactation and is generally
caused by blockage of a duct. The temperature is raised
and the skin of the infected breasts inflamed (Fig. 8.25).
Palpation may reveal an area of tenderness and induration.
If an abscess forms, you usually feel an extremely tender
fluctuant mass.
Abnormal nipple and areola

A bloodstained nipple discharge suggests an intraductal
carcinoma or benign papilloma. Unilateral retraction or
distortion of a nipple should also alert you to the
possibility of malignancy, especially if the abnormality is
Fig. 8.24 Exposing the axilla by abducting the arm and supporting relatively recent. A unilateral red, crusty and scaling
it at the wrist. areola suggests Paget’s disease of the breast (Fig. 8.19).
234
Chapter
Structure of the genital tract 8
The female genitalia and blood supply
ovarian aorta
vein ovarian
ureter artery
common
ovary
iliac
fallopian artery
tube
external
ovarian iliac
ligament artery
cervix uterus
Fig. 8.25 Erythema overlying an area of mastitis.
vagina uterine
artery
This disorder should alert you to a likely ductal carcinoma

Fig. 8.26 The female pelvis and internal genitalia.
underlying the areola. Blockage of the sebaceous glands
of Montgomery may cause retention cysts.
Symptoms and signs Lateral view of genital anatomy
Breast examination sacral

fallopian promontory ureter
Inspection tube
ovarian
• Symmetry and contour sacrouterine ligament
• Venous pattern of skin ligament
body of
• Nipples (asymmetry, inversion) pouch of uterus
• Areola (chloasma, skin ulceration, thickening) Douglas
fundus
Breast palpation of uterus
• Texture
• Symmetry bladder
• Tenderness symphysis
• Masses (mobility, size) levator ani pubis
muscle
• Tail of Spence urethra
external
Lymph node palpation
anal labium
• Axillary nodes (five groups) sphincter minus
• Contralateral axillary nodes anus fornix of cervix vagina labium
• Infraclavicular and supraclavicular nodes vagina majus
Fig. 8.27 Lateral view of the female internal genitalia showing the
relationship to the rectum and bladder.
Palpable lymph nodes
If you detect axillary lymphadenopathy, suspect
malignancy if the nodes are hard, nontender or fixed. rectum posteriorly and the bladder and ureter anteriorly
Infection of axillary hair follicles or breast tissue may (Fig. 8.27). The female internal genitalia can be inspected
cause tender lymphadenitis. Look carefully for a local through the vagina, the cervix can be palpated directly or
primary site of infection such as an abrasion caused by through the anterior rectal wall, and the uterus, fallopian
shaving the axilla. Occasionally, patients with longstanding tubes and ovaries can be examined using the technique
fibrocystic disease may have mild axillary node of bimanual palpation.
enlargement.
VULVA
Structure of the genital tract The external genitalia in the female is termed the vulva
(Fig. 8.28). This comprises a fat pad that overlies the
The female reproductive organs include the ovaries, symphysis pubis (the mons pubis), a pair of prominent
fallopian tubes, uterus and vagina. These organs lie deep hair-lined skin folds extending on either side from the
in the pelvis (Fig. 8.26), occupying the space between the mons to meet posteriorly in the midline in front of the
235
Chapter
The anatomy of the external genitalia The pelvic floor
(a) bulbo adductor

mons pubic hair cavernous longus
pubis muscle muscle
prepuce
urogenital vagina
frenulum
clitoris diaphragm
of clitoris superficial
pubocervical transverse
external ligament
labium perineal
urethral muscle
minus
orifice ischial
(meatus) tuberosity iliococcygeus
vestibule muscle
labium external
fourchette majus anal gluteus
sphincter maximus
posterior vaginal orifice muscle
anus
commissure
coccyx
perineum hymen part of
levator ani
anus muscles
Fig. 8.28 The external female genitalia. (b)

pubis
pubocervical trigone of
ligament bladder
anal verge (the labia majora), and a pair of hairless, flat
folds lying adjacent and medial to the labia majora (the transverse cervix
labia minora). The labia minora converge anteriorly in cervical
ligament
front of the vaginal orifice, with each splitting into two vaginal
small folds that meet in the midline. The anterior folds rectovaginal vault
from either side merge to form the prepuce; the posterior pouch
rectum
folds form the frenulum. A nub of erectile tissue (the
clitoris) lies tucked between the frenulum and prepuce. uterosacral
Posteriorly, the labia minora fuse to form a distinct ridge ligament
known as the fourchette. The labia minora demarcate the
vestibule, which contains the urethral meatus and vaginal Fig. 8.29 The pelvic floor supports the pelvic organs. (a) Superficial
orifice. Bartholin’s glands are a pair of pea-sized mucous perineal muscles. (b) Fascia and ligaments.
glands that lie deep to the posterior margin of the labia
minora and empty through a duct into the vestibule,
UTERUS
providing lubrication of the introitus. Bartholin’s glands
may become infected if the ducts are obstructed, resulting The uterus is a muscular, pear-shaped organ consisting
in painful swelling and abscess formation. of the cervix, body and fundus (Fig. 8.31). The adult
The vulva rests on the pelvic floor, which is formed by uterus is usually angled forward from the plane of the
a complex arrangement of muscles that support the vagina (anteverted) and bends forward on itself at the
rectum, vagina and urethra (Fig. 8.29). junction of the internal os and the body (anteflexion)
(Fig. 8.32a). In some women the uterus assumes different
positions: an anteverted uterus may lie retroflexed
VAGINA
(Fig. 8.32b) and a retroverted uterus may be anteflexed
The vagina is a tube-shaped passage connecting the (Fig. 8.32c) or retroflexed (Fig. 8.32d).
vulva to the cervix of the uterus. Its opening in the vulva The vaginal surface of the cervix is covered by stratified
(the introitus) lies between the urethra and anus. The squamous epithelium. The uterus is covered with
vagina is inclined in an upward and posterior direction. peritoneum which reflects anteriorly onto the bladder,
A connective tissue septum separates the vagina anteriorly posteriorly onto the rectum and laterally to form the
from the bladder base and urethra and posteriorly from broad ligaments. The peritoneum covering the posterior
the rectum. The uterine cervix pouts through the upper uterus and upper vagina reflects onto the anterior rectal
vault of the vagina and divides the blind end of the vagina wall forming a blind pocket: the Pouch of Douglas. The
into the anterior, posterior and lateral fornices (Fig. 8.30). cuboidal cells lining the uterine cavity (the endometrium)
These thin-walled fornices provide a convenient access respond to the hormonal changes of the menstrual
point for examining the pelvic organs. cycle.
236
Chapter
Structure of the genital tract 8
The fornices of the vagina Different positions of the uterus
(a) normal (anteflexed, (b) retroflexion (uterus still

posterior anteverted) anteverted)
(a)
fornix
(b)
lateral (c) retroversion (uterus still (d) retroversion retroflexion

fornix anteflexed)
rectum anterior
fornix
cervix pouts
into apex
of vagina
Fig. 8.30 The cervix projects into the vagina, creating the anterior,
posterior (a) and lateral fornices (b).
Fig. 8.32 The different anatomical positions of the uterine body
within the pelvis. (a) The normal uterus is angled forward from the
plane of the vagina (anteverted) and bends forward on itself
The uterus (anteflexed). In some women the uterus assumes different positions:
(b) retroflexed, anteverted; (c) retroverted, anteflexed; (d) retroverted,
retroflexed.
fundus fallopian tube
uterine
cavity Ovarian ligaments and adnexal structures
endometrium
interstitial isthmus ampulla
body myometrium ovarian position
ligament
isthmus
internal os
supra
cervical canal uterus
vaginal
cervix
external
vaginal
cervical os suspensory
ligament broad fimbria
vagina of ovary ligament ovarium
cervix
Fig. 8.31 Section through the pear-shaped, muscular uterus vagina

showing the cervix, isthmus, body (corpus) and fundus. The mucosa
is called the endometrium. The cervical canal has an internal and
external os. Fig. 8.33 Coronal section of the uterus and fallopian tubes showing
the ligamentous attachments of the ovary.
ADNEXAE The tubes vary in length from 8 cm to 14 cm and open

The adnexae refers to the fallopian tubes, ovaries and into the peritoneum through the trumpet-shaped
their connective tissue attachments. infundibulum. The entrance to the fallopian tube (the
ostium) is bounded by fringe-like fimbria that overlie the
Fallopian tubes
ovary and help to capture the ovum when it is expelled
The fallopian tubes insert into the upper outer uterus (the in midcycle. The ovum moves along the fallopian tube by
cornu) and project laterally along the free edge of the a combination of peristalsis and the wafting action of the
broad ligaments curving around the ovaries (Fig. 8.33). cilia on the mucosal lining cells.
237
Chapter
Ovaries
Rectocoele and vesicocele
There are two ovaries. Each is oval in shape and usually
rests in a slight depression in the side wall of the pelvis.
The ovary is not lined by peritoneum; it measures 3 cm
long, 2 cm wide and 1 cm thick. The ovarian ligament
connects the ovary to the cornu of the uterus. The
connective tissue stroma of the ovary contains graafian
follicles at various stages of development, the corpus
luteum, which develops after ovulation, and the corpus
albicans, a relic of a degenerating corpus luteum.
Pelvic fascia and ligaments

The connective tissue overlying the muscular floor of bulge of posterior
vaginal wall
the pelvis condenses into ligaments that stabilise and sagittal view:
support the pelvic organs by attachments to the pelvis. prolapsing rectum causes bulging
The cardinal ligaments (Mackenrodt’s ligaments) span of posterior vaginal wall
laterally, connecting the cervix and upper vagina to the urethral
bony pelvis. The uterosacral ligaments pass posteriorly opening
and backwards from the posterolateral cervix, attaching
to the periosteum overlying the sacroiliac joints and the
midsacrum. The pubocervical fascia extends forward from
the cardinal ligament, joining to the pubic bone on either
side of the bladder. These pelvic ligaments and the
muscular floor of the pelvis may become lax and weaken,
allowing the pelvic organs to drop and prolapse (Fig 8.34;
and see Fig. 8.49).
The broad ligament is formed from the peritoneum
bulge of anterior
that suspends from the lateral wall of the uterus to the vaginal wall
sagittal view:
lateral wall of the pelvis. The fallopian tubes, ovarian prolapsing bladder causing bulging
ligament, uterine and ovarian vessels and lymphatics run of anterior vaginal wall
in the broad ligament.
Fig. 8.34 Pelvic floor examination. (a) Prolapsing rectum causes
bulging of posterior vaginal wall. (b) Prolapsing bladder causing
bulging of the anterior wall.
Symptoms of genital tract disease
There may be initial reluctance to discuss genital and MENSTRUAL HISTORY
sexual disorders but with gentle coaxing you should be
Establish the age of the menarche
able to lead the patient towards a frank account of her
sexual history. The degree to which you pursue the history As a result of the wide variation in the age of the
depends on the relevance to the patient’s problems. menarche, parents and children may be unduly concerned
Organic and psychological disorders may affect sexual about delay. Most European and North American girls
function and this may be important, although not central, start menstruating by the age of 14.5 years (range 9–16
to the presenting disease. Cardiac and respiratory disease years). Body weight appears to play a role and
may interfere with normal sexual activity; after a the menarche occurs at an average weight of 48 kg. If
myocardial infarct there is often concern about there is anxiety about delayed menarche or primary
recommencing a normal sex life. Reduction or loss of amenorrhoea, ask whether or not pubic and axillary hair
libido is common in acute and chronic illness. Patients growth and breast development have commenced. By the
with psychological disorders such as anorexia nervosa or age of 14 years, secondary sexual characteristics should
depression may present with a primary complaint of loss have appeared. If the menarche has not occurred and
of libido or a menstrual disorder. In contrast, patients there are no other signs of sexual development, it is
suffering from primary sexual problems may present with reasonable to consider organic causes of primary
physical symptoms, such as abdominal pain, that may amenorrhoea, such as gonadal dysgenesis (Turner’s
camouflage the underlying sexual problem. syndrome), congenital anatomical abnormalities of the
The genital-sexual history commonly follows the genital tract (e.g. absence, uterine hypoplasia, vaginal
urinary history. You may find that asking about previous hypoplasia), polycystic ovaries or pituitary or hypothalamic
pregnancies or the pattern of the menstrual cycle provides tumours in childhood. If secondary sexual characteristics
a suitable platform for more detailed questioning. have appeared, reassure the patient that investigation is
238
Chapter
usually only necessary if the menarche has not occurred

by the age of 16 years. Effect of LH and FSH on ovarian hormone synthesis
Determine the pattern of the menstrual cycle

higher centres
Throughout the childbearing years, women should be – +
encouraged to specify the starting date of each menstrual
period (i.e. the date when bleeding commences). Record hypothalamus
–
the starting date of the most recent period. The duration GnRH +
of the menstrual cycle is calculated from the first day of
bleeding to the first day of bleeding in the next menstrual
cycle. This cycle may vary from 21 to 35 days in normal
women but the average duration is 28 days. Most healthy,
fertile women have regular, predictable cycles that vary –
in duration by 1 or 2 days. Once regular periods are
established, concern is soon aroused if there is deviation LH FSH
from the norm.
theca
Questions to ask androgen
interna cells
The menstrual cycle
arom
a
• Age of menarche? enz tisin
l ym g
• Age of telarche? io e
ad
• Do you use the contraceptive pill or hormone
str
oe
replacement therapy?
gra lls
• Length of cycle?
nulos
ce
• Days of blood loss?
a
• Number of tampons or pads used per day?
• Are there clots? Fig. 8.35 Effect of gonadotrophins on the theca interna and
• Has there been a change in the periodicity of the granulosa cells which produce the ovarian hormones.
cycle?
Blood loss from menstruation averages approximately

Secondary amenorrhoea
70 ml (range 50–200 ml). Attempts to assess menstrual
loss are rather inaccurate, yet there are indicators: women Develop the case history by considering possible causes
with heavy periods saturate rather than stain tampons or of secondary amenorrhoea. Pregnancy and lactation are
pads, whereas the passage of large and frequent clots the most common causes. The patient may suspect a
suggests excessive bleeding. The only accurate method pregnancy: there may be clues such as early morning
for assessing menstrual loss is to weigh absorbent pads nausea and vomiting, urinary frequency and tender
before and after each change. enlarged breasts. Stress, anxiety, depression, bereavement
Attempt to classify any change or abnormality in the and a change of environment may interrupt the
menstrual cycle. First establish whether the cycles are cyclical release of sex hormones by the hypothalamic–
regular and, if so, calculate the cycle length and attempt pituitary axis. Consider fear of pregnancy, which is a
to assess whether the periods are scanty or heavy. Bear common cause of delayed menstruation. Not only do
in mind contraceptive practices because the patient’s patients with excessive weight loss due to anorexia
intrinsic rhythms will be masked if she is taking a cyclical nervosa present with amenorrhoea but highly trained
contraceptive pill or undergoing hormone replacement long-distance athletes may also stop menstruating.
therapy (HRT) (Fig. 8.35). The most common irregularities Enquire about contraceptive practices as ‘post pill’
include failure to menstruate at the expected time amenorrhoea is well recognised. Consider the menopause
(secondary amenorrhoea). Cycles may be infrequent in women entering the climacteric years. This is often
and scanty (oligomenorrhoea), unusually frequent heralded by a change in the cyclical pattern, reduced
(polymenorrhoea), excessively heavy (menorrhagia) or menstrual flow and the onset of menopausal symptoms
frequent and heavy (polymenorrhagia). Bleeding after such as hot flushes and dryness of the introitus and
intercourse is termed postcoital bleeding. If regular cycles vagina. In the absence of an obvious cause for
are interrupted by days of spotting or blood-tinged amenorrhoea, consider diseases of the hypothalamus,
discharge, this is known as intermenstrual bleeding. pituitary and ovary.
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Chapter
with hormone treatment. Diseases of the uterus and cervix
may present with abnormal bleeding, so consider disorders
Secondary amenorrhoea
of the mucosa (e.g. endometritis, carcinoma, endometrial
Physiological polyps) or submucosa (e.g. submucosal leiomyomas,
• Pregnancy fibroids). Postcoital bleeding usually indicates local cervical
• Lactation or uterine disease (carcinoma or a cervical polyp).
Psychological Vaginal discharge
• Anorexia nervosa
• Depression Vaginal discharge is a common complaint during the
• Fear of pregnancy child-bearing years. Many women notice slight soiling of
the underwear at the end of the day; this is a normal
Hormonal
physiological response to the cyclical changes occurring in
• Post contraceptive pill
the glandular epithelium of the genital tract and it is likely
• Pituitary tumours
to become more profuse in pregnancy. A physiological
• Hyperthyroidism
discharge is scanty, mucoid and odourless. Pathological
• Adrenal tumours
discharge is usually trichomonal or candidal vaginitis. The
Ovarian discharge may irritate the vulval skin causing itching
• Polycystic ovaries (pruritus vulvae) or burning. Attempt to assess the severity
• Ovarian tumour of the discharge by ascertaining whether the discharge
• Ovarian tuberculosis merely stains the underwear or is heavier and requires
• Constitutional disease protective pads.
• Severe acute illness
• Chronic infections or illnesses
• Autoimmune diseases Differential diagnosis
Vaginal discharge
Physiological
• Pregnancy
Abnormal patterns of uterine bleeding
• Sexual arousal
Oligomenorrhoea Oligomenorrhoea is the term used to • Menstrual cycle variation
describe infrequent or scanty menstrual periods. This Pathological
pattern may be normal between the menarche and the • Vaginal
establishment of a regular menstrual pattern and is also – candidosis (thrush)
a feature of the climacteric as the menopause approaches. – trichomoniasis
In some women, the oligomenorrhoea of puberty persists – Gardnerella associated
into adult life. Ascertain whether the infrequent, scanty – other bacteria (e.g. caused by a retained tampon)
periods are a change from the normal pattern or a pattern – postmenopausal vaginitis
present from puberty. If oligomenorrhoea presents as a • Cervical
distinct change in the menstrual pattern, consider the – gonorrhoea
same factors implicated in the differential diagnosis of – nonspecific genital infection
secondary amenorrhoea. – herpes
Dysfunctional uterine bleeding This term is used to – cervical ectopy
describe frequent bleeding or excessive menstrual loss – cervical neoplasm (e.g. polyp)
that cannot be ascribed to local pelvic pathology (e.g. – intrauterine contraceptive device
fibroids, pelvic inflammatory disease, carcinoma, polyps).
Establish whether the abnormal cyclical pattern is regular
or irregular. Regular dysfunctional bleeding may present Questions to ask
as menorrhagia, epimenorrhoea or polymenorrhoea. The Vaginal discharge
predictability of these abnormal cycles usually implies
• How long has the discharge been present?
that ovulation is occurring, although this needs to
• Is the discharge scanty or profuse?
be confirmed. Irregular dysfunctional bleeding usually
• Is extra protection necessary or does the discharge
implies that ovulation has ceased; the menstrual rhythm
simply spot or stain?
is lost and the cyclical pattern is replaced by unpredictable
• What is the colour and consistency?
bleeding of varying severity.
• Is there an odour?
Intermenstrual and postmenopausal bleeding Patients • Is the discharge bloodstained?
may complain of vaginal bleeding unexpectedly between • Is there associated lower abdominal pain and fever?
normal periods or after the menopause. Enquire about sex • Is there itching or burning of the vulval area?
hormone therapy, as ‘breakthrough bleeding’ may occur
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Chapter
The nature of the discharge may be helpful. With pelvic congestion; it occurs a day or two before
vaginitis caused by Candida albicans the discharge is white, menstruation or with uterine contraction during the
has a curd-like appearance and consistency (Fig. 8.36) shedding and expulsion of the endometrium. Severe
and causes intense itching. Vaginitis caused by Trichomonas dysmenorrhoea should alert you to the possibility of
vaginalis usually presents with a profuse opaque or cream- endometriosis, a disorder resulting from cyclical changes
coloured, frothy discharge that has a characteristic ‘fishy’ (including withdrawal bleeding) occurring in endometrial
smell (Fig. 8.37). The trichomonal discharge may cause tissue implanted in ectopic sites (e.g. in the fallopian
vulval irritation and is occasionally accompanied by tubes or peritoneum).
burning on micturition: this is caused by inflammation of Ovulation may cause a unilateral iliac fossa or
the urethral meatus. If the patient complains of a profuse, suprapubic pain in midcycle that lasts a few hours
foul-smelling discharge, consider a retained foreign body (mittelschmertz). Severe iliac fossa pain should warn you
(e.g. a tampon). Cervical infection due to gonorrhoea, of the possibility of a haemorrhage into an ovarian
Chlamydia trachomatis or nonspecific cervicitis may cyst or torsion of a cyst. If the pain is preceded by a
present with a discharge but, unlike vaginitis, these rarely missed period, and especially if there is shock, you should
cause itching or burning of the vulva. also consider the possibility of a ruptured ectopic
pregnancy. If the lower abdominal pain is accompanied
Pain
by a vaginal discharge, fever, anorexia and nausea,
Gynaecological disorders should always be considered in consider acute infection of the fallopian tubes (acute
women presenting with lower abdominal pain. If the salpingitis).
pain predictably occurs immediately before and during a
Dyspareunia
period, the likely cause is dysmenorrhoea. This is a
suprapubic, boring or cramp-like pain caused by intense Pain on intercourse (dyspareunia) may be caused by
either psychological or organic disorders. Try to distinguish
vaginal spasm that makes penetration difficult (vaginismus)
from pain occurring once penetration has occurred.
Assess whether the pain is superficial (suggesting a local
vulval cause or a psychological spasm) or deep (suggesting
inflammatory or malignant disease of the cervix, uterus
or adnexae). After the menopause, the vulva and vagina
become dry and atrophic and this may cause discomfort
on intercourse.
PSYCHOSEXUAL HISTORY
A satisfactory sex life is an important component of a
healthy emotional relationship. In an unmarried woman,
ask whether she has had intercourse. Patients may
complain of loss of sex drive (libido), failure to achieve
orgasm, pain or difficulty with intercourse and ambivalence
about sexual preference. These symptoms and personal
Fig. 8.36 Vaginal candidiasis has a curd-like appearance.
problems are often camouflaged behind other symptoms
such as nonspecific abdominal pain, depression, fatigue
or headache. It requires shrewd clinical judgement to
recognise the underlying psychosexual problem. Tactfully
enquire about the sexual history.
Questions to ask
Psychosexual history
• Are you able to develop satisfying emotional

relationships?
• Do you have satisfying physical relationships?
• Are you heterosexual, homosexual or ambivalent?
• Do you use contraception and, if so, what form?
• Do you have problems achieving arousal?
• Do you experience orgasm?
Fig. 8.37 Trichomoniasis.
241
Chapter
OBSTETRIC HISTORY to an endocrine imbalance. Anaemia may occur with

Enquire whether the patient has ever been pregnant and menstrual disorders and you may recognise syndromes
whether there were fertility problems. Record the number that are commonly associated with menstrual disorders
of completed and unsuccessful pregnancies. If the patient (e.g. thyrotoxicosis, myxoedema, Cushing’s syndrome,
has miscarried, record the maturity of the pregnancy at anorexia nervosa, other serious chronic diseases). You
the time of miscarriage. Ask about complications during will have examined the breasts during the chest
pregnancy (e.g. hypertension, diabetes) and problems examination and assessed the development of secondary
associated with labour and the period after delivery (the sexual characteristics.
puerperium).
Examination of the abdomen

Questions to ask A full abdominal examination precedes the vulval and
Obstetric history vaginal examination. Although the uterus and adnexae
• Have you ever been pregnant and, if so, how often? lie deep within the protective confines of the pelvis,
• Did you have any problems falling pregnant? abnormalities may be apparent above the pubis. Lower
• How many children do you have? abdominal tenderness occurs in pelvic inflammatory
• Have you miscarried and, if so, at what stage of disease and enlargement of the uterus or ovaries may
pregnancy? present with a palpable lower abdominal mass. Large
• Were there any complications in pregnancy (e.g. ovarian cysts may fill the abdomen; this presentation is
high blood pressure or diabetes)? readily mistaken for ascites. Careful abdominal percussion
• Was the labour normal or did you require forceps helps distinguish ascites from a cystic ovarian tumour. A
assistance or a caesarean section? large ovarian cyst displaces the bowel laterally, and on
percussion there is central dullness with resonance in the
flanks (Fig. 8.38). This contrasts with ascites, which is
characterised by central resonance and dullness in the
Examination of the female genital tract flanks.
Examination of the genitalia is intrusive; nonetheless,

most women are psychologically prepared if they are
seeking attention for a gynaecological disorder. In the
course of taking the history you should already have Percussion of pelvic tumour or ascites
established a rapport with your patient and if there are
gynaecological symptoms the examination should follow
naturally.
Before the examination, take the time to explain the
need for the examination and the procedure. If you have
no reason to suspect a painful examination, reassure the
patient that there should be little discomfort. If there is a
suggestion of vaginitis or pelvic inflammatory disease,
explain that there may be a little discomfort and that the
patient should inform you if there is pain. While ensuring
the patient’s comfort and privacy you should always be
accompanied by a nurse who can provide reassurance for
the patient and assist you with the procedure (e.g.
speculum examination, cervical smears).
Before the examination, ask the patient to empty her
bladder. This adds to the comfort of the examination and
excludes a full bladder in the differential diagnosis of
suprapubic and pelvic swellings. Ensure that a clean
gown is available and that there are satisfactory facilities central dullness lateral dullness
for the patient to undress. of a large pelvic tumour of ascites
Fig. 8.38 Careful examination of the abdomen allows

GENERAL EXAMINATION differentiation between large ovarian cysts and ascites. An ovarian
cyst displaces the bowel towards the flanks: the central abdomen is
Before examining the genital tract you should perform a dull, whereas the flanks are more resonant. This contrasts with
general examination. Excessive facial hair (hirsutism) ascites, in which the flanks are dull and the central abdomen
may be normal but if overly excessive may provide a clue tympanitic.
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Chapter
Examining the external genitalia 8
Assessing the height of the fundus in pregnancy Examination of the genitalia
week height of uterus
12 palpable above pubic bone
16 midway between
symphysis and umbilicus
36
40 20 lower border of umbilicus
32
28
24 28 midway between
20 umbilicus and xiphisternum
16
34 just below xiphisternum
12
38–40 height drops as fetal head
engages pelvis Fig. 8.40 The correct position of the patient before examination of
the genitalia.
Fig. 8.39 The maturity of a pregnancy can be assessed by

examining the height of the fundus.
Labial palpation
Abdomen in pregnancy
After the 12th week of the pregnancy, the uterus becomes
palpable above the symphysis pubis, making it possible
to assess the maturity of the fetus from the height of the
fundus (Fig. 8.39).
Examining the external genitalia

This examination is usually performed on a conventional
examination couch. The nurse should prepare and
position the patient for the examination. The patient lies
supine with the hips and knees flexed and the heels close
together. Help the patient to abduct the thighs to allow
adequate access to the external genitalia (Fig. 8.40). Use
a blanket or sheet to cover the abdomen and mons pubis.
Ensure good general lighting; you will also require a Fig. 8.41 Palpating the labia majora between the thumb and index
finger.
direct light source to focus on the vulva. When examining
the vulva and vagina, wear disposable plastic gloves on
both hands.
The labia majora on either side lie in close contact in
the midline. Gently separate the labia with the fingers of
INSPECTION AND PALPATION OF THE VULVA your left hand and inspect the medial aspect, which
Explain that you are going to examine the labia and should be pink and slightly moist. Palpate the length of
the area surrounding the vaginal opening. Maintain the labia majora between index finger and thumb
intermittent eye contact with the patient. Uncover the (Fig. 8.41); the tissue should feel pliant and fleshy. Next,
mons to expose the external genitalia. The pattern of hair examine Bartholin’s glands between the index finger and
distribution over the mons pubis provides a useful thumb (Fig. 8.42). The right index finger palpates from
measure of sexual development. Once puberty is complete the entrance of the vagina while the thumb palpates the
the mons and outer aspects of the labia majora should outer surface of the labia majora posteriorly. A normal
be well covered with hair. Systematically examine the Bartholin’s gland is not palpable.
labia majora, labia minora, the introitus, urethra and To expose the vestibule, separate the labia minora. The
clitoris. vestibular tissue should be supple and slightly moist.
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Chapter
Vulval ulceration has a wide differential diagnosis. The

Palpation for Bartholin’s gland most common ulcerating lesions include carcinoma of
the vulva or macerated, ulcerating herpetic warts. Acute
vulval ulceration occurring with mouth and tongue ulcers
and inflamed red eyes suggests Behçet’s syndrome. A
firm painless labial ulcer suggests the chancre of primary
syphilis, whereas broad, moist ulcerating papules covered
by grey slough suggest secondary syphilis. Suspect
granuloma inguinale (caused by C. trachomatis) in women
from tropical and subtropical regions presenting with
vulval nodules and inguinal lymphadenopathy. The
nodules coalesce and ulcerate, forming a large ulcer with
rolled edges which must be distinguished from carcinoma.
Chancroid, caused by Haemophilus ducreyi, is another
sexually-transmitted ulcerating disease affecting the
vulva.
Leucoplakia is a potentially malignant, hypertrophic
skin lesion affecting the labia, clitoris and perineum. The
skin thickens, feels hard and indurated and is distinguished
Fig. 8.42 Palpating Bartholin’s gland with the index finger just from surrounding tissue by its white colour.
inside the introitus and the thumb on the outer aspect of the labium Bartholin’s glands are palpable if the ducts obstruct.
majus. This results in a painless cystic mass or an acute
(Bartholin’s) abscess: a hot, red, tender swelling in the
posterolateral labia majora deep to the posterior end of
Separation of the labia minora exposes the vaginal orifice the labia minora (Fig. 8.48).
and urethra.
After the menopause the skin and subcutaneous tissue
of the external genitalia become atrophic and the Examination of the vagina
mucosa loses its moist texture. These involutional,
atrophic changes are normal and result from the loss of If the patient has an intact hymen, you may choose to
ovarian hormones. examine the genitalia indirectly through the rectum. If
the woman has an intact hymen but uses vaginal tampons,
Abnormalities of the vulva
it is usually possible to perform a single digit vaginal
A confluent, itchy, red rash on the inner aspects of the examination.
thighs and extending to the labia suggests candidiasis Before proceeding with the internal examination,
(Fig. 8.43). This is often associated with a vaginal discharge separate the labia to expose the vestibule and ask the
and should alert you to the possibility of diabetes or patient to ‘bear down’ and exert a downward force on
recent treatment with broad-spectrum antibiotics. A the vulva. If the pelvic floor is stable and the muscles
vaginal discharge due to candidiasis or a trichomonal intact, bulges and swellings should not appear through
infection may irritate the vulval skin, causing redness and the vaginal walls below the introitus. If there is muscle
tenderness (vulvitis). weakness, the posterior bladder wall may prolapse,
The vulva is a common site for boils (furuncles) to causing a bulge (a cystocele) along the anterior vaginal
appear. These are tender to palpation and should be wall (see Fig. 8.34). If the rectum prolapses, this may
distinguished from sebaceous cysts, which are firm,
rounded, yellowish and nontender, with an apical
punctum indicating the opening of the blocked duct.
Many papular vulval lesions are caused by sexually Differential diagnosis
transmitted infections. Crops of small, painful, vulval and Vulval ulceration
perianal papules and vesicles that ulcerate suggest a
Squamous cell carcinoma
herpes simplex infection (Fig. 8.44). You may notice
multiple genital warts (condylomata acuminata), which Infections
can coalesce to form large irregular tissue masses (Figs • Syphilitic chancre
8.45, 8.46). Most genital warts are caused by a human • Secondary syphilis
papillomavirus. The lesions usually occur on the fourchette • Granuloma inguinale (Chlamydia)
and may extend onto the labia, into the vagina, and • Chancroid (Haemophilus ducreyi)
posteriorly onto the perineum. Flat, round or oval papules • Ulcerating herpetic warts
covered by a grey exudate suggests lesions of secondary Behçet’s syndrome
syphilis (condylomata lata) (Fig. 8.47).
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Chapter
Examination of the vagina 8
Fig. 8.43 Primary cutaneous candidosis of Fig. 8.44 Herpes simplex vesicles in the Fig. 8.45 Multiple perianal warts
the vulva. perianal region, fourchette and inner surface (condylomata acuminata) encroaching onto
of the labia minora. the labia.
Fig. 8.46 Perianal warts. Fig. 8.47 Condylomata lata caused by Fig. 8.48 Swelling of posterolateral
secondary syphilis tend to occur in moist perineum caused by Bartholin’s abscess.
areas of the body and are prevalent in the
vulva and perineum.
cause a bulge (a rectocele) in the posterior vaginal wall. cervical smears. If you anticipate taking samples, use
Uterine prolapse may also occur (Fig. 8.49). water as a lubricant for your gloved fingers and the
A full vaginal examination includes inspection with a speculum because lubricant gels may interfere with the
speculum, followed by a bimanual examination of the processing and analysis of samples.
uterus and adnexae. Before continuing the examination, A bivalve speculum (e.g. Cusco’s) is the instrument
explain that you are about to inspect the vagina and most commonly used to inspect the vagina (Fig. 8.50).
cervix with a speculum. Thoroughly familiarise yourself with its operation before
examining a patient. The instrument is made of either
stainless steel or plastic, and is available in different
SPECULUM EXAMINATION sizes. There are two blunt, rounded, elongated blades
The speculum is designed for inspection of the cervix and hinged at the base. In the closed position, the tips of the
vaginal walls. In addition, the speculum provides access blades appose, allowing the closed blades to slide safely
to the cervix and fornices for bacteriological swabs and into the slit-shaped introitus and into the tubular vagina.
245
Chapter
Uterine prolapse
(a) (b)
Fig. 8.50 A bivalve Cusco’s speculum used for examining the

(c) (d)
vaginal walls and cervix.
Fig. 8.49 Uterine prolapse. (a) Normal uterus. (b) First- and
(c) second-degree prolapse of the uterus. (d) Complete prolapse
of the uterus.
The blades open when the thumbpiece is squeezed (Fig.

8.51) and, once positioned in the vagina, a hinged screw Fig. 8.51 Speculum held in the open position with a lock-nut.
and nut arrangement fixes the blades in the open
position.
Warm the blades under a stream of tepid water. The speculum in a more horizontal plane. Make any minor
most convenient hand position for holding the speculum adjustments necessary to establish the optimal position
is illustrated in Figure 8.50. Explain to the patient that for visualising the cervix, then tighten the thumbscrew to
you are about to insert the instrument and reassure her secure the position.
that the procedure should be painless. Use the index
and middle fingers of the free hand to separate the labia
and expose the introitus (Fig. 8.52a). Position these Examination of the cervix
two fingers just inside the introitus, pressing gently
towards the perineal body. Slide the closed blades The position of the cervix relates to the position of the
obliquely over the fingers into the introitus and introduce uterus (see Fig. 8.32). The cervix usually points posteriorly
the instrument into the vagina, directing it to follow and the uterus lies in an anterior plane (anteversion).
the line of the long axis of the vagina, maintaining a Conversely, the cervix may point anteriorly with the
posterior angulation of approximately 45° (Fig. 8.52b). uterus in a posterior retroverted position. There are also
While inserting the instrument, rotate it in a clockwise intermediate positions between these two. The cervix
direction until the anterior and posterior blades run should lie centrally along the long axis of the vagina
along the length of the anterior and posterior vaginal projecting 1–3 cm into the vagina. The shape of the
walls with the handles pointing towards the anus (Figs external os changes after childbirth. In nulliparous
8.52c,d). Maintain a downward pressure on the speculum women, the os is round, whereas after childbirth, the os
and press on the thumbpiece to hinge the blades may be slit-like or stellate (Fig. 8.53).
open (Fig. 8.52e) to expose the vaginal vault and cervix Inspect the colour of the cervix. The colour varies
(Fig. 8.52f). according to the position of the meeting point, usually in
Adjust the light source to illuminate the vagina. If the the region of the external os, of the squamous epithelium
cervix is not immediately visible, arc the blades anteriorly covering the vaginal surface of the cervix and the mucosal
to bring the cervix into view. If you have difficulty finding lining of the cervical canal. The surface of the cervix is
the cervix, withdraw the blades a little and reposition the pink, smooth and regular, and resembles the epithelium
246
Chapter
Examination of the cervix 8
Speculum examination of the vagina External os
(a) (b)
(c) (d)
Fig. 8.53 In nulliparous women, the external os is round (left);
it becomes slit-shaped (right) after birth of a child.
distinguished from early cervical cancer, so cytology

should always be performed.
ABNORMALITIES OF THE CERVIX

An eccentric cervix suggests disease of the uterus or
the adnexae. Nabothian cysts may develop if there is
(e) (f) obstruction of the endocervical glands. These are seen as
small, round, raised white or yellow lesions which only
assume importance if they become infected. There may
be a cervical discharge. If there is a pungent odour,
suspect an infective cause and swab the area. An inflamed
cervix covered by a mucopurulent discharge or slough is
characteristic of acute and chronic cervicitis; the mucosa
looks red rather than pink and, if the cervicitis follows
pregnancy, you may notice laceration and pouting of the
Fig. 8.52 (a) Expose the vaginal opening, (b) direct the closed endocervical mucosa (ectropion). Cherry-red friable
speculum into the vagina, (c) rotate the speculum as it penetrates polyps may grow from the cervix (a source of vaginal
the long axis. (d) Final position of the fully inserted speculum.
(e) Open the blades. (f) Search for the cervix and os.
bleeding after intercourse). Ulceration and fungating
growths suggest cervical carcinoma.
Cervical smear
of the vagina. In early pregnancy the cervix has a bluish Cytologists can detect premalignant cells or established
colour caused by increased vascularity (Chadwick’s sign). cervical cancer by examining a preparation of cells
During pregnancy, the squamocolumnar junction may scraped from the surface of the cervix. The technique is
migrate beyond the external os and onto the cervix, routine in the course of the speculum examination.
retreating back, a few months after childbirth, into The demonstration of premalignant cells provides
the cervical canal. Periodically, after pregnancy, the the opportunity for cancer prevention: the early detection
squamocolumnar junctions fail to regress into the os, of cancer allows for a higher, successful cure rate.
giving the appearance of an erosion (ectopy). Failure to Before proceeding with the smear, prepare three
regress during fetal development may give rise to a clean glass microscope slides. Accurate labelling of the
congenital erosion. Cervical ‘erosions’ are not ulcerated specimens is critical: slides with frosted glass at one end
surfaces but a term used to describe the appearance of are preferable, for this allows you to write the patient’s
the cervix when the endocervical epithelium extends name and number clearly on the slide. Prepare the slide,
onto the outer surface of the cervix. The columnar mark with the patient’s details, and label ‘cervical smear’.
epithelium appears as a strawberry-red area spreading Explain to the patient that you are about to take a smear.
circumferentially around the os or onto the anterior or The cervical smear is performed after inspecting the
posterior lips. Cervical ectopy cannot be confidently cervix. A specially-designed disposable wooden spatula
247
Chapter
Cervical smear
Fig. 8.54 Spatula with bifid end used for cervical cytology.
Transport medium for microbiology, and swab.
Fig. 8.55 Cervical meatus. The bifid end of the spatula is advanced
to the external os and cervical cells are harvested by rotating the
with a bifid end at one side and a rounded end at the
spatula around the circumference of the os.
other is used (Fig. 8.54). The bifid end is used to harvest
the cervical cells. Introduce the spatula through the
speculum and position the bifid end at the os (Fig. 8.55).
The desquamating cells are collected by rotating the
spatula around the circumference of the os and the lips
of the cervix. Withdraw the spatula and spread the cervical
material onto the labelled glass slide by stroking each
side of the bifid end of the spatula along the glass. The
cervical cells and some mucus should cling to the glass.
Immediately spray the slides with fixative or fix them by
immersion in 95% alcohol.
Taking vaginal swabs

If the patient has a vaginal discharge, use the speculum
examination to take a swab for culture. You can use a
conventional throat swab; insert the cotton wool end into
the secretion (e.g. the region of the cervical os and vaginal Fig. 8.56 The finger position used for performing a vaginal
pool) and allow the tip sufficient time to soak up secretion. examination.
Remove the swab, place it in a suitable transport medium
and send the specimen immediately to the laboratory for
processing. Again, expose the introitus by separating the labia with
the thumb and forefinger of the gloved left hand and
Removing the speculum gently introduce the gloved and lubricated right index
and middle fingers into the vagina, remembering that the
After inspecting the cervix, undo the thumbscrew and
organ is directed backwards in the direction of the sacrum.
simultaneously withdraw the speculum and rotate the
The thumb is abducted to allow maximum use of the
open blades in an anticlockwise direction to ensure that
length of the index and middle fingers; the ring and little
the anterior and posterior walls of the vagina can be
finger are flexed into the palm (Fig. 8.56). Palpate the
inspected. Near the introitus, allow the blades to close,
vaginal wall as you introduce your fingers. The walls are
taking care not to pinch the labia or any hairs while
slightly rugose, supple and moist.
withdrawing the speculum.
CERVIX
Internal examination of the uterus Locate the cervix with the pulps of your fingertips. The
cervix should feel firm, rounded and smooth. Assess
The speculum examination is followed by the vaginal the mobility of the cervix by moving it gently and
examination. Explain that you are about to perform an palpate the fornices. This procedure should be
internal examination of the uterus, tubes and ovaries. painless.
248
Chapter
Bimanual palpation of the uterus Palpating the anterior surface of the uterus
Fig. 8.57 The bimanual technique used to palpate the uterus. The Fig. 8.58 By placing the vaginal fingers in the anterior fornix it is
vaginal fingers lift the cervix, while the other hand dips downwards possible to examine the anterior surface of the uterus.
and inwards to meet the fundus.
Abnormalities of the cervix Abnormalities of the uterus

In pregnancy, the cervix softens (Hegar’s sign). If there If the uterus appears to be uniformly enlarged, consider
is tenderness on movement (known as ‘excitation a pregnancy, fibroid or endometrial tumour. Fibromyomas
tenderness’), suspect infection or inflammation of the (fibroids) are common benign uterine tumours which
uterus or adnexae; or if the patient is shocked, suspect an may be single or multiple and may vary in size. Single,
ectopic pregnancy. You may palpate an ulcer or tumour large uterine fibroids are felt on abdominal examination
already noted on the speculum examination. as a firm, nontender, well-defined rounded mass arising
from the pelvis. On bimanual palpation, the mass appears
contiguous with the cervix: the two structures move
UTERUS together. Multiple fibroids give the uterus a lobulated
Next, palpate the uterus. A bimanual technique is used feel. Occasionally, the fibroid is pedunculated and is felt
to assess the size and position of the organ (Fig. 8.57). as a mobile pelvic mass which is readily confused with a
Position the palmar surface of your free hand on the mass arising from the adnexae.
anterior abdominal wall about 4 cm above the symphysis
pubis. Attempt to ‘capture’ the uterus gently between
your apposing fingers. Use your internal fingers to elevate ADNEXAE
the cervix and uterus in the direction of the external hand Palpate the left and right adnexae in turn. Note, the
while simultaneously pressing the fingertips of the adnexae are difficult to palpate in obese women. Place
external hand in the direction of the internal fingers. the fingers of your abdominal hand over the iliac fossa
Using this displacement technique an anteverted fundus while readjusting the vaginal fingers into the lateral fornix
should be palpable just above the symphysis. Assess its and positioning the finger pulps to face the abdominal
size, consistency and mobility, and note any masses and fingers (Fig. 8.59). Remembering the anatomy of the
tenderness. ovaries and fallopian tubes, gently but firmly appose the
Further exploration may be helped by re-examining fingers of either hand by pressing the abdominal hand
the uterus with your fingers positioned in the anterior inward and downward, and the vaginal fingers upwards
fornix (Fig. 8.58); this permits the vaginal fingers to and laterally. Feel for the adnexal structures as the
examine the anterior surface of the uterus while the interposed tissues slip between your fingers. The
abdominal fingers explore the posterior wall. If the uterus manoeuvre should be relatively painless, although
is retroverted, the fundus is more difficult to feel through palpation of the ovaries might elicit some tenderness.
the abdominal wall; nevertheless, it might become more Yet again, reassure you patient that any discomfort she
readily palpable if the vaginal fingers are positioned in feels is normal. If you feel an adnexal structure, assess
the posterior fornix. its size, shape, mobility and tenderness. Ovaries are firm,
249
Chapter
ovoid, and often palpable. Normal fallopian tubes are

Palpating the adnexae impalpable.
Abnormalities of the adnexal structures
The most common causes of enlarged ovaries include
benign cysts (e.g. follicular or corpus luteal cysts) and
malignant ovarian tumours. Ovarian tumours are either
unilateral or bilateral. Cysts feel smooth and the wall may
be compressible. Occasionally, ovarian tumours are large
enough to be palpable on abdominal examination and
may fill the lower and mid-abdomen, creating the
impression of ascites.
In acute infections of the fallopian tubes (salpingitis),
there is lower abdominal tenderness and guarding, and,
on vaginal examination, marked tenderness of the lateral
fornices and cervix. The acute pain makes palpation
of the adnexae difficult. In chronic salpingitis, the
lower abdomen and lateral fornices are tender, yet the
uterus and adnexae may be amenable to examination.
If the uterus is retroverted and fixed by adhesions, it may
be possible to feel thickening and swelling of the
tubes extending to the ovaries. If the tubes are
blocked, there may be cystic swelling of the tubes
Fig. 8.59 Positioning the vaginal and abdominal fingers to palpate
(hydrosalpinx) or they may become infected and purulent
the adnexal structures.
(pyosalpinx).
After completing the bimanual examination, withdraw
your fingers from the vagina and inspect the glove tips
for blood or discharge. Re-drape the genital area and
reassure the patient that the examination is complete and
that you will discuss the findings in the consulting room
once she is dressed.

Breasts and genital tract
• There is rapid fall in sex hormone synthesis after the • Loss of sex hormones results in altered hair
menopause, resulting in changes in the structure and distribution and androgen dominance may be
function of the genitalia apparent with male pattern facial hair growth, mild to
• There is progressive involution of the breast tissue moderate male pattern baldness and loss of the
and, as the acinar tissue atrophies, the breasts become female pattern labial hairline
more pendulous • Despite involutional changes, many older women
• The risk of breast cancer remains at any age, including maintain libido and remain sexually active into the
the very old later years of life
• After the menopause there is loss of vulval adipose • Atrophy of the vagina and introitus can be prevented
tissue, and reduction in vaginal secretion results in by hormone replacement therapy and topical
drying of the mucosal surface oestrogen application
• The atrophy of tissue of the introitus results in • Vaginal lubrication can be enhanced by using water-
vestibular narrowing, increased susceptibility to urinary soluble lubricant jellies
tract infection and dyspareunia
250
Chapter
Review
Framework for the routine examination of female breasts and genitalia
General examination – fornices

• Endocrine syndrome – pouch of Douglas
• Hirsutism, acne Uterus
• Breast examination • Bimanual palpation
• Routine abdominal examination – body and fundus
• Inguinal lymph nodes – adnexal region
Vulva – ovaries
• Inspection and palpation of the vulva Speculum
• Bartholin’s gland palpation • Inspect cervix and os
Vagina • Take cervical smear
• Digital examination • Bacterial swab for culture
– cervix • Inspect vaginal mucosa as speculum withdrawn
– cervical tenderness
251
9
The male genitalia
Unlike the female genitalia, the male organs are readily for both urine and semen. In fetal development, the testes
accessible for examination. As for women, taking a sexual develop close to the kidneys and slowly migrate caudally,
case history and examining a male is embarrassing and emerging at the external inguinal ring in the eighth month
intrusive, so care must be taken to ensure confidentiality, of development and descending into the scrotum in the
privacy and comfort. An overview of structure and ninth month. The neural, vascular and lymphatic supply
function will help you gain confidence when taking a to the testes also arise from near the kidney and the
history and examining the genitalia and will aid the migrating testes drag these structures through the inguinal
interpretation of symptoms and signs. canal into the scrotum. This has important clinical
implications, as renal pain is often referred to the scrotum
and the natural route for lymphatic spread of testicular
Structure and function cancer is to para-aortic (rather than inguinal) nodes.
The male genitalia include the penis, scrotum, testes, PUBERTY

epididymides, seminal vesicles and prostate gland (Fig.
9.1). The penis provides a common pathway to the exterior In boys, puberty starts 1–2 years later than in girls. The
onset of male puberty is signalled by an increase in
testicular volume and this is followed approximately one
year later by a spurt in linear growth and an increase in
muscle bulk.
Anatomy of the male genitalia
Hormonal changes in puberty
Testosterone feedback to the hypothalamus can inhibit
rectum the hypothalamic–pituitary axis release of luteinising
hormone (LH) and follicle-stimulating hormone (FSH).
seminal In the child, this feedback is especially sensitive and even
vesicle
low levels of circulating gonadal steroids are sufficient to
bladder inhibit the secretion of FSH and LH. Male puberty is
initiated by a fall in the sensitivity of the hypothalamus
symphysis to inhibition at low levels of circulating sex hormones.
pubis
ejaculatory By resetting the sensitivity of the feedback to the
duct prostate hypothalamus, FSH and LH are released, thereby exerting
gland their trophic effects on their target cells in the testes.
levator ani
muscle Throughout male puberty, LH levels increase slowly
urethra
anus
and steadily (Fig. 9.2), whereas FSH levels increase more
sharply in early puberty, with a more gentle increase
glans afterwards. FSH stimulates the Sertoli cells and regulates
bulbocavernosus
the growth of seminiferous tubules and spermatogenesis.
testis
muscle As most of the testis is formed of tubules, the increased
testicular volume in puberty is largely under the control
of FSH. LH stimulates the Leydig (interstitial) cells which
Fig. 9.1 The male genitalia include the external organs, seminal synthesise testosterone from cholesterol (Fig. 9.3).
vesicles and the prostate gland. Testosterone circulates bound to sex hormone-binding
252
Chapter
globulin (SHBG). The linear growth spurt follows closely

behind the surge of testosterone. Some testosterone is Testosterone synthesis
converted to oestradiol in the Leydig cells and other
extragonadal tissue sites. The effects of testosterone are
shown in Table 9.1. The importance of oestrogen in males
remains unclear, although it does regulate the synthesis
A
of SHBG.
cholesterol
Development of secondary sexual characteristics
20–22 desmolase
Tanner described the pubertal development of the male
adrenal and testes

genitalia and pubic hair growth (Fig. 9.4). Initially, the pregnenolone
testes enlarge and the scrotal skin becomes thin and red 1β OH steroid dehydrogenase
(stage 2). The enlargement of the phallus occurs later in
progesterone
the growth spurt and is associated with thickening,
crinkling and pigmentation of the scrotal skin (stage 3). 17 hydrogenase
Increasing levels of gonadal and adrenal androgens
17-OH-progesterone
stimulate the growth of pubic, axillary and facial hair.
Pubic hair begins to develop as sparse, long, slightly curly 17–20 desmolase
hair at the base of the phallus (stage 4). Later, coarser, androstenedione
curlier hair extends to cover the symphysis pubis and
finally extends to the inner thigh and along the linea alba 17β OH steroid dehydrogenase
(this constitutes the male escutcheon) (stage 5).
testes
testosterone
Developmental changes in LH and FSH
LH 60 5α reductase aromatase
peripheral tissues
μg/dl 30
6
4
2
dihydrotestosterone oestradiol
FSH 60
μg/dl 40
20 Fig. 9.3 Biochemical pathway in the synthesis of testosterone from
16 cholesterol.
12
8
4
Genital maturation in puberty
birth
y
od
rty
d
nc
oo
stage 2 stage 3
be
ho
fa
lth
pu
in
ld
u
i
ch
ad
Fig. 9.2 Changes in LH and FSH secretion before, during and after
puberty.
stage 4 stage 5
Table 9.1 Effects of testosterone
• Stimulates the development of secondary sexual characteristics

• Controls libido
• Anabolic effect causes muscle growth and fat deposition
• With growth hormone, stimulates linear growth in adolescence
• With erythropoietin, stimulates red cell production Fig. 9.4 Tanner’s five stages of male genital maturation (Stage 1
preadolescence is not shown).
253
Chapter
9 The male genitalia
Histology of the testis The hypothalamic–pituitary–testicular axis
interstitial spermatogonia and tubule hypothalamus

blood spermatocytes
vessel GnRH
+ –
FSH LH
inhibin
–
(interstitial) cell + +
Leydig
testosterone
Sertoli cell Leydig cells +

spermatids
and
spermatozoa tubular lumen Sertoli cell spermatogenesis virilisation
Fig. 9.5 Histological section through a testis shows seminiferous Fig. 9.6 The hypothalamic–pituitary–gonadal axis. Pulsatile release
tubules, developing sperm, Leydig and Sertoli cells. of GnRH stimulates the anterior pituitary to secrete LH and FSH,
which stimulate the Leydig and Sertoli cells, respectively.
Male fertility
The male testis is composed of a network of tightly coiled
and convoluted seminiferous tubules that drain through
Anatomy of the penis
the rete testis into the epididymis. Spermatozoa develop
from the germinal epithelium of the seminiferous tubules
which lie in close contact with the Leydig and Sertoli cells glans penis
(Fig. 9.5). LH binds to the Leydig cells, stimulating the
production of testosterone from cholesterol. FSH binds urethra
to the Sertoli cells, stimulating the synthesis of inhibin, a
peptide hormone that inhibits FSH production by the corpus cavernosum
pituitary (Fig. 9.6). The development from immature
spermatogonia to mature spermatozoa takes 72 days. The corpus spongiosum
passage of the sperm through the epididymis to the
ejaculatory ducts takes a further 14 days, during which
time the spermatozoa become motile.
Spermatogenesis occurs most efficiently when the
ambient testicular temperature is 36°C. The smooth
muscle of the scrotum and spermatic cord alters the crus penis
position of the testicles in relation to the external inguinal
ring to maintain (under various conditions of heat and
cold) an optimal temperature for spermatogenesis. ischial tuberosity
PENIS
dorsal vein
The penis consists of the two sponge-like cylinders, the
corpora cavernosa, forming the dorsal and lateral surfaces, corpus cavernosum
and the corpus spongiosum, which ends in a bulbous
expansion, the glans penis (Fig. 9.7). The urethra passes corpus spongiosum
through the corpus spongiosum. The skin covering the
corpora extends over the glans to form the prepuce. urethra
Tactile and psychogenic stimuli cause sexual arousal.
An autonomic (parasympathetic) reflex causes increased Fig. 9.7 The shaft and glans penis is formed from the corpus
arterial flow through branches of the pudendal artery to spongiosum and the corpus cavernosum.
254
Chapter
the penis and fills the corpus spongiosum. The organ appendix testis and hydatid of Morgagni, respectively.
assumes the erectile position necessary for vaginal These occasionally twist and can cause severe testicular
penetration. The reflex is completed by a sympathetic pain.
neural outflow that results in contraction of the Lymphatics from the penile and scrotal skin drain to
ejaculatory ducts and the bladder neck, causing the inguinal nodes. Examination of the groin nodes is an
ejaculation of semen and orgasm. This is followed by integral part of the genital examination, especially if there
increased tone in the arterioles and sinusoids of the is an ulcer or discharge.
corpora, diversion of blood away from the penis and,
finally, detumescence.
PROSTATE
The structure of the prostate is described in Chapter 7.
SCROTUM AND ITS CONTENTS The organ envelops the first part of the urethra and
Before attempting to examine the testis and epididymis, the ejaculatory ducts from the seminal vesicles, which
it is important to understand the structure of these organs. open into the prostatic urethra. The prostate secretes
The scrotum is a muscular pouch that holds the testes. A a specialised fluid that provides lubrication before
septum separates the left and right testicles. The scrotal intercourse and serves also to increase the volume of the
skin is thin, pigmented and crinkled and lined by the ejaculate.
dartos muscle. This permits considerable contraction and
relaxation of the scrotum, which helps keep the optimal
temperature for spermatogenesis. Symptoms of genital tract disease
The left testis almost always lies lower than the right.
Each testis is ovoid in shape, measuring approximately 4 Like women, men may choose either to express their
× 3 × 2 cm. A fibrous capsule, the tunica albuginea, invests symptoms openly or to expose the problem in a less
the testis. The seminiferous tubules converge and obvious manner. Moreover, the doctor may feel
anastomose posteriorly to form the efferent tubules which embarrassed to broach the sensitive issues of sexual
converge to form the head of the epididymis (Fig. 9.8). orientation, sexual function, sexually transmitted disease
This, in turn, gives rise to the body and tail which drain and possible exposure to HIV. Learn to ask direct
into the vas deferens. The vas deferens passes through questions with sensitivity while maintaining the firm
the inguinal canal (Fig. 9.9), joining the seminal vesicles, impression that you are both confident and decisive
which, in turn, converge to form the ejaculatory duct. The when talking about what is, after all, another normal
epididymis attaches along the posterior border and upper bodily function.
pole of the testis. Both the testis and the epididymis have At the outset of your history-taking, you will already
vestigial remnants of fetal development known as the have ascertained whether the patient is single or married
Structure of the testes and epididymis The spermatic cord
vas deferens vas deferens
head of
body of penis
epididymis
epididymis
efferent
tubules
spermatic
cord
pampiniform
plexus
tail of testis
seminiferous
epididymis tubules
scrotum
Fig. 9.8 Coronal section through the testis shows the seminiferous Fig. 9.9 The vas deferens passes into the inguinal canal as the
tubules of the testis converging to form the efferent tubules, which spermatic cord, which then converges on the seminal vesicles. The
then give rise to the head, body and tail of the epididymis and the pampiniform vascular plexus surrounds the spermatic cord.
vas deferens.
255
Chapter
and if he has fathered any children. The genital and about the possibility of contact with sexually transmitted
sexual history follows on naturally from the urinary tract disease. Ask about a recent episode of gastroenteritis, for
history (see Ch. 7). Ask about penile discharge, pain or urethritis may follow a few weeks later. Reiter’s syndrome
swelling of the testes and ability to enjoy normal sexual (Fig. 9.10) is the most florid manifestation of this
relations. These questions should provide the cue for a association and is characterised by a urethral discharge,
shy or inhibited patient to talk about sexual or genital balanitis, painful joints (arthritis and tendinitis) and
problems. Depending on the nature of the presenting bilateral conjunctivitis.
symptoms, you may wish to ask about homosexual
contact. You may feel uneasy about phrasing the question
but in societies in which AIDS is acknowledged as a Differential diagnosis
problem, the majority of patients understand the Urethral discharge
importance of the question and most often will not take Physiological
offence to a question like ‘Have you ever had a homosexual • Sexual arousal
partner?’ or ‘Do you practise safe sex?’ If a genital or
Pathological
sexual symptom becomes apparent, assure the patient of
the confidentiality of the interview and attempt to analyse • Gonococcal urethritis (incubation 2–6 days)
the problem in greater depth. • Nongonococcal urethritis
• Idiopathic nonspecific urethritis
• Chlamydia trachomatis
URETHRAL DISCHARGE • Trichomonas vaginalis
A urethral discharge is a common presenting symptom. • Candida albicans
Remember that a discharge of smegma from a normal • Posturinary catheter
prepuce is very different from a discharge caused by • Reiter’s syndrome (may follow gastroenteritis)
urethritis. In urethritis, the patient may notice staining of includes arthritis and conjunctivitis
his underwear and complain of urinary symptoms
such as burning or stinging when passing urine.
Sexually transmitted disease is a common cause of GENITAL ULCERS
urethral discharge and patients concerned about sexually
transmitted disease will usually mention fear of it. If this The appearance of an ulcer or ‘sore’ always raises the
information is not forthcoming, ask the patient directly spectre of sexually transmitted disease. Consequently,
this possibility is likely to alarm your patient even though
ulcers are not always caused by sexual transmission.
Questions to ask
Enquire discreetly about possible contact with sexually
transmitted disease or casual sexual encounters. Ask
Urethral discharge
whether the ulcer is painful and try to assess a possible
• Is there a possibility of recent exposure to a sexually incubation period. Herpetic ulcers tend to recur and may
transmitted disease? be preceded by a prodrome of a prickly sensation or pain
• How long ago might you have had such a contact in the loins. There may be a clear history of contact with
(incubation period)? a partner infected with herpes and sexual transmission
• Does your partner complain of a vaginal discharge? may affect the mouth or anus as well as the penis. Exotic
• Have you experienced joint pains or gritty, red eyes? ulcerating venereal infections occur in the tropics and it
• Have you recently suffered from gastroenteritis? is important to obtain a careful history of foreign travel
and possible sexual contact.
a b
Fig. 9.10 Reiter’s syndrome is characterised by (a) circinate balanitis and (b) conjunctivitis.
256
Chapter
TESTICULAR PAIN prescribed drugs are associated with impotence. An

Inflammation or trauma to the testes causes an intense obvious association with organic disease may be apparent
visceral pain that may radiate towards the groin and in patients presenting with concomitant cardiovascular,
abdomen. Testicular pain has a deep boring quality often respiratory or neurological symptoms.
accompanied by nausea. The pain may be accompanied
by swelling and be aggravated by movement or even light INFERTILITY
palpation. Painless swelling of a testis should alert you to Primary infertility refers to a failure to achieve conception,
the possibility of a cystic lesion or malignancy. whereas secondary infertility refers to a difficulty or a
failure to conceive, although there has been at least one
successful conception in the past. Male infertility accounts
Questions to ask for approximately one-third of childless relationships.
Testicular pain Consequently, both partners are evaluated when couples
present with infertilty. Ask about the duration of infertility
• Was the pain preceded by trauma?
and whether the patient has ever managed to conceive.
• How rapidly did the pain develop?
As many couples have little understanding of the timing
• Was the pain preceded by a fever or swelling of the
of ovulation and conception, you should enquire in some
salivary glands (mumps)?
depth about the frequency and timing of intercourse and
• Was the pain preceded by burning on micturition or
about attempts to time intercourse to coincide with the
a urethral discharge?
female partner’s fertile period. Ask about drugs, as
antimetabolites used in cancer treatment or sulfasalazine
used in colitis may cause subfertility.
Testicular pain
Questions to ask
• Trauma Infertility
• Infection (mumps orchitis)
• Epididymitis • Have you or your partner ever conceived?
• Testicular torsion • Do you have difficulty obtaining or maintaining an
• Torsion of epididymal cyst erection?
• Do you ejaculate?
• Do you understand the timing of ovulation in your
partner?
IMPOTENCE • Are you on any medication that may cause
The term impotence refers to a spectrum of sexual impotence or sperm malfunction (e.g. sulfasalazine)?
dysfunction ranging from loss of libido, failure to • Have you noticed any change in facial hair growth?
obtain or to maintain an erection, to inability to achieve • Have you ever had cancer treatment?
orgasm. Impotence is often a manifestation of emotional
disturbance; therefore, you should try to assess whether
the patient is depressed, anxious about sexual encounters
or troubled by emotional aspects of the relationship. Fear Examination of the male genitalia
of causing pregnancy and concern about a contagious
disease such as AIDS may serve to cause impotence. Take This examination usually follows the abdominal
a careful drug and alcohol history; alcoholism is an examination and you will already have approached the
important cause of impotence and many widely area when examining the groin and hernial offices.
Although a detailed genital examination is usually only
undertaken when the patient complains of appropriate
symptoms, it is advisable to check the testes in the course
of a routine examination as ‘opportunistic screening’ may
Drug-related causes of impotence
occasionally reveal a testicular tumour. Explain that you
• Major tranquillisers (phenothiazines) would like to examine the penis and testes and offer
• Lithium reassurance that the examination will be quick and gentle.
• Sedatives (barbiturates, benzodiazepines) Like any other examination, your confidence, or lack of
• Antihypertensives (methyldopa, clonidine) it, soon becomes apparent to the patient. If you have a
• Alcohol good knowledge of the anatomy and physiology already
• Oestrogens outlined, you will soon master a quick but thorough
• Drug abuse (heroin, methadone) examination. It is advisable for women doctors to examine
the genitalia with a chaperone close at hand.
257
Chapter
Fig. 9.12 Typical appearance of male gynaecomastasia.

Fig. 9.11 Hernias may only become apparent when the patient
stands.
It is usual practice to wear disposable plastic gloves for Male gynaecomastia

hygienic reasons and to emphasise the strictly clinical Physiological
nature of the examination. The genitalia are usually • Puberty
examined with the patient lying but remember that • Old age
varicoceles and scrotal hernias may only be apparent Pathological
when the patient stands; it is advisable to check for scrotal • Hypogonadism
swellings in the standing position if the diagnosis is • Liver cirrhosis
unclear with the patient lying down (Fig. 9.11). Avoid • Drugs (spironolactone, digoxin, oestrogens)
creating a feeling of total nakedness by covering part of • Tumours (bronchogenic carcinoma, adrenal
the thighs. carcinoma, testicular tumours)
• Thyrotoxicosis
GENERAL EXAMINATION
You will already have performed a general examination
and noted the distribution of facial, axillary and abdominal to express the secretion; if not, you may try to express a
hair. In testicular malfunction (hypogonadism), there discharge by ‘milking’ the shaft of the penis from the base
may be loss of axillary hair, the pubic hair distribution towards the glans. If a discharge appears, swab the area
may start to resemble the distinctive female pattern and with a sterile bud and immerse the specimen in a transport
there is a typical facial appearance with wrinkling around medium for quick dispatch to the microbiology
the mouth. You will have also checked the breast laboratory.
and noted whether or not gynaecomastia was evident
(Fig. 9.12). Abnormalities of the penis
Prepuce The prepuce may be too tight to retract over the
EXAMINATION OF THE PENIS glans (phimosis). If the prepuce is tight but retracts and
catches behind the glans, oedema and swelling may
Normal penis
occur, preventing the return of the foreskin (paraphimosis).
The length and thickness of the flaccid penis vary widely If left untreated, the swelling and congestion may result
and bear no relationship either to potency or to fertility. in gangrene.
The dorsal vein of the penis is usually prominent along
Glans Hypospadias (Fig. 9.13) is a developmental
the dorsal midline. Gently retract the foreskin (prepuce)
abnormality causing the urethral meatus to appear on
to expose the glans penis. The foreskin should be supple,
the inferior (ventral) surface of the glans (primary
allowing smooth and painless retraction. There is often a
hypospadias), penis (secondary hypospadias) or even the
trace of odourless, curd-like smegma underlying the
perineum (tertiary hypospadias). Inflammation of the
foreskin. Examine the external urethral meatus, which is
glans is termed balanitis (Fig. 9.10); if there is inflammation
a slit-like orifice extending from the ventral pole of the
of the glans and prepuce, the term balanoposthitis is
tip of the glans. Use your index finger and thumb to
used. Genital (herpetic) warts may be seen on the
squeeze the meatus gently open. This should expose
glans.
healthy, glistening pink mucosa. If the patient has
complained of a urethral discharge, try to elicit this sign. Urethral discharge This is one of the most common
The patient may be able to ‘milk’ the shaft of the penis genital disorders in men and is caused by urethral
258
Chapter
Hypospadias
primary
secondary
tertiary
Fig. 9.13 Hypospadias: a developmental abnormality. The urethral

meatus opens on the ventral surface of the penis.
b
Fig. 9.14 After 4–5 days incubation, a crop of relatively painless
inflammation (urethritis). The cause of a urethral herpetic vesicles appear on the penis (a). Vesicles rupture, with the
discharge cannot be confidently predicted from development of painful superficial erosions with a characteristic
appearance, although gonorrhoea is likely to cause a erythematous halo (b).
profuse purulent discharge. Nongonococcal urethritis
may also be caused by urethral infection or be associated
with Reiter’s syndrome.
Genital ulcers
Infections
• Genital herpes
• Syphilis (chancre, mucous patches, gumma)
• Tropical ulcers
Balanitis
• Severe candidiasis
• Circinate balanitis (Reiter’s syndrome)
Fig. 9.15 The primary chancre of syphilis may occur on the glans,
Drug eruption prepuce or shaft.
• Localised fixed drug eruption
• Generalised (Stevens–Johnson syndrome)
Carcinoma that can become secondarily infected. The urethral meatus
Behçet’s syndrome may be affected causing dysuria. If there is a possible
history of sexually transmitted disease, consider syphilis
(primary chancre) (Fig. 9.15) and in the tropics consider
chancroid, lymphogranuloma venereum and granuloma
Penile ulcers Ulceration of the glans or, more rarely, the
inguinale. Infrequently, fixed drug reactions may cause
shaft of the penis may occur in a number of disorders.
penile ulceration. Squamous cell carcinoma may present
Examine the ulcer and always palpate the groins for
as an ulcer of the penis or the scrotum.
inguinal lymph node involvement because the skin of the
penis drains to this group of nodes. The most common Priapism Occasionally, a patient may present with a
cause is herpetic ulceration. Characteristic painless painful and prolonged erection. This pathological
vesicles occur 4–5 days after sexual contact (Fig. 9.14). erection is termed priapism. Most often there is no
The vesicles often rupture, causing painful superficial obvious cause but predisposing factors such as leukaemia,
erosions with a characteristic erythematous halo. The haemoglobinopathies (e.g. sickle cell anaemia) and drugs
confluence of these erosions may cause discrete ulcers (aphrodisiacs) should be considered.
259
Chapter
EXAMINATION OF THE SCROTUM The epididymis normally feels smooth and is broadest
Inspect the scrotal skin, which is pigmented when superiorly at its head.
compared with body skin. The left testis lies lower than Finally, roll with the finger and thumb the vas deferens,
the right but the impression of both testes is readily which passes from the tail of the epididymis to the
identified (Fig. 9.16). The tone of the dartos muscle is inguinal canal through the external inguinal canal. This
influenced by ambient temperature. Consequently, the structure is smooth and nontender and is felt leading
normal scrotal appearance varies with temperature. from the epididymis to the external inguinal ring.
Ensure that your hands are warm before palpating Abnormalities of the scrotum
the testis. Use gentle pressure, sufficient to explore the
If one-half of the scrotum appears smooth and
bulk of the tissue without causing pain. Throughout the
poorly developed, consider an undescended testis
examination, watch the patient’s facial expression, for
(cryptorchidism). This appearance of the scrotum helps
this should reassure you that the examination is not
to distinguish a maldescent from a retractile testis, in
causing undue discomfort. Compare the left and right
which the testis has descended but retracts vigorously
testes because many testicular disorders are unilateral.
towards the external inguinal ring. The retracted testis
Feel the testicle between your thumb and first two fingers
will be difficult to palpate.
(Fig. 9.17). Note the size and consistency of the testis.
The scrotal skin may be red and inflamed; a common
The organ has a pliant, soft rubbery consistency and there
cause is candidiasis (Fig. 9.19). Small yellowish scrotal
should not be much tenderness. Next, palpate the
lumps or nodules are common and usually represent
epididymis, which is felt as an elongated structure along
sebaceous cysts.
the posterolateral surface of the testicle (Fig. 9.18).
Swellings in the scrotum
Decide whether the swelling arises from an indirect
inguinal hernia or from the scrotal contents. It is possible
to ‘get above’ a testicular swelling but not a scrotal
hernia (Fig. 9.20). An intrinsic swelling may arise from
enlargement of the testis, testicular appendages and
epididymis or by an accumulation of fluid in the tunica
vaginalis, the double membrane that invests the testes.
Palpate the swelling between the thumb and first
two fingers and decide whether the swelling is solid or
cystic.
Cystic swelling Cystic accumulations are caused by
entrapment of fluid in the tunica vaginalis (a hydrocele)
Fig. 9.16 The left testis lies lower than the right. or accumulation of fluid in an epididymal cyst and are
Palpation of the testes Palpation of the epididymis
Fig. 9.17 Palpate the testis between your thumb and first two Fig. 9.18 The epididymis is felt along the posterior pole of the
fingers. testis.
260
Chapter
Testing for scrotal swellings
a fingers can ‘get b fingers cannot

above’ mass ‘get above’ mass
Fig. 9.19 Candida infection of the scrotum often extends to the Fig. 9.20 It is possible to ‘get above’ a true scrotal swelling (a),
groin and thigh. whereas this is not possible if the swelling is caused by an inguinal
hernia that has descended into the scrotum (b).
Fluctuations of the cystic swelling Epididymal cyst
cyst
Fig. 9.21 To distinguish a solid from a cystic mass, fix the swelling Fig. 9.22 An epididymal cyst is felt separately from the testis and
between finger and thumb of one hand and use the index finger of lies posteriorly.
the other hand to invaginate at right angles.
typically fluctuant. Steady the mass between the thumb 9.22). In contrast, a hydrocele surrounds and envelops
and first two fingers of one hand and use the index finger the testis, which becomes impalpable as a discrete organ
of the other hand to invaginate the mass in a second (Fig. 9.23). The distinction between an epididymal cyst
plane (Fig. 9.21). The tense fluid-filled cyst will fluctuate and hydrocele is not always clear and the two may occur
between finger and thumb in response to the pressure together.
change. Cystic lesions usually transilluminate. Darken
the room and place a pen-torch light up against the Varicocele Varicoceles occur in 5–8% of normal adult
swelling. A fluid-filled cyst spreads a bright red glow into males and are almost always left sided (Fig. 9.24). A
the scrotum, whereas this does not occur with solid varicocele results from a varicosity of the veins of the
tumours. Remember that if the cyst wall is abnormally pampiniform plexus, a leash of vessels surrounding
thickened or the effusion is bloodstained, transillumination the spermatic cord, and is caused by abnormality of the
may not occur. Next, try to distinguish between a valve mechanism of the left testicular vein, which drains
hydrocoele and an epididymal cyst. As the epididymis into the left renal vein (the right drains directly into the
lies behind the body of the testis, an epididymal cyst is inferior vena cava). Most varicoceles do not cause
felt as a distinct swelling behind the adjoining testis (Fig. symptoms and are discovered as an incidental finding.
261
Chapter
Varicocele
Hydrocele
swelling
Fig. 9.23 A hydrocele surrounds the entire testis, which cannot, Fig. 9.24 A left-sided varicocele has the texture of a ‘bag of
therefore, be felt as a discrete organ. worms’ when palpated. The mass is separate from the testis and
epididymis.
Swollen testis Discrete testicular tumour Testicle replaced by tumour
a b
Fig. 9.25 In orchitis, the testis is swollen, tense and very tender. Fig. 9.26 Carcinoma may present as a discrete mass within a testis
Usually only one testis is involved. (a) or may expand to replace the entire organ (b).
However, patients may rarely present with scrotal testicular and an epididymal mass. Diffuse, acutely painful
swelling, discomfort or infertility. Examine the patient in swelling usually occurs in acute inflammatory condition
the standing position – the varicocele feels like a ‘bag of such as orchitis (Fig. 9.25) or torsion of the testis. These
worms’. Ask the patient to cough while you palpate the acute emergencies are usually readily distinguishable
varicocele – a characteristic feature is transmission of the from a solid or discrete swelling of the body of the testis.
raised intra-abdominal pressure to the varicocele, which Solid masses may be smooth or craggy, tender or painless
is felt as a discrete cough impulse. The varicocele is but, whatever the character, carcinoma must be the first
separate from the testis. The ipsilateral testis is usually differential diagnosis (Fig. 9.26). Other solid masses
smaller than expected. A varicocele usually empties when include tuberculomas and syphilitic gummas. Solid
the patient lies supine. tumours of the epididymis are due to chronic inflammation
(usually tuberculous epididymitis) and are usually benign.
Solid swellings As with cystic swellings, use your The epididymis feels hard and craggy (Fig. 9.27) and is
knowledge of the anatomy to distinguish between a not unduly tender.
262
Chapter
Thickened appendages in tuberculous epididymitis
Fig. 9.27 In tuberculous epididymitis, the epididymis is firm and

thickened and the cord may feel beaded.
Fig. 9.29 In lymphogranuloma venereum, the inguinal lymph nodes

enlarge.
Torsion of the testes
opposite testis may have an abnormal lie because it is not

uncommon for both testes to be abnormally positioned.
The presentation and findings may be confused with
orchitis and testicular torsion.
Scrotal oedema
Scrotal oedema usually occurs when there is diffuse
oedema (anasarca) caused by severe congestive heart
twisted spermatic failure or hypoproteinaemia such as in nephrotic
cord syndrome. The scrotal tissue becomes stretched and taut
with pitting of the skin.
EXAMINATION OF THE LYMPHATICS

The skin lymphatics of the penis and scrotum drain
towards the inguinal nodes; you should complete
your genital examination by feeling for nodes in the
Fig. 9.28 Torsion of the testicle on the spermatic cord impairs the groin, which are felt deep to the inguinal crease. The
blood supply. The affected testis is swollen, tender and lies higher testicular lymphatics drain to intra-abdominal nodes.
than expected. The overlying scrotal skin is often reddened and Special tests such as computerised tomography or
oedematous. lymphangiography are necessary to evaluate the testicular
lymphatics.
Torsion of the testis Enlarged inguinal nodes
This usually occurs in young boys and presents with Enlarged nodes occur in infective and malignant
severe scrotal pain that usually radiates to the inguinal disorders affecting the skin of the penis and scrotum.
region and lower abdomen. On examination, the scrotal The primary chancre of syphilis is usually associated
skin overlying the affected testis may be reddened, with with lymphadenopathy. The nodes are typically
the affected testis lying higher than the unaffected testis mobile, rubbery and not tender. The most florid forms of
(Fig. 9.28). The testis may be very tender and the spermatic inguinal lymphadenopathy occur in patients with
cord may feel thickened and sensitive to palpation. The lymphogranuloma venereum (Fig. 9.29).
263
Chapter

Genitalia in elderly males Framework for the routine examination of
the male genitalia
• Men remain sexually active well into the later years
of life • Note pattern of hair distribution
• Impotence and loss of libido commonly accompany • Stage sexual development
chronic disease such as heart failure and respiratory • Examine abdomen generally
and renal/prostatic disease • Examine inguinal lymph nodes
• Always consider drugs when elderly patients • Inguinal hernias?
complain of impotence or loss of libido (e.g. • Retract foreskin
antihypertensive medication) • Examine glans penis and meatus
• While women stop ovulating by the sixth decade, • Check for urethral discharge
most men continue to produce sperm well into the • Examine the scrotum
eighth and ninth decades – inspect scrotal skin
• Benign prostatic hypertrophy of its own accord does – check lie of testes (left lower than right)
not affect genital function; prostatectomy may result – palpate the testes and epididymis
in retrograde ejaculation or nerve damage and – check scrotal swellings for fluctuation and
impotence. transillumination
• Hydrocele and varicocele are common causes of – palpate the spermatic cord within the scrotum
testicular swelling in elderly men but testicular
cancer is rare
264
10
Bone, joints and muscle
The skeleton provides protection for the internal organs The tubular arrangement of the long bones achieves
along with a strengthening and support system for the maximal resistance to a bending force while economising
limbs. The presence of joints in the limbs and spine on the amount of material used in its construction. The
permits movement of what would otherwise be rigid lines of the trabeculae in cancellous bone match the lines
structures. The cartilage interposed between the bone of stress encountered at those particular points. The
surfaces of a joint cushions the forces that are generated surface markings and contours of bone are determined
during movement. Joint strength is enhanced by ligaments by external forces and the origins of tendons and
that are either incorporated into the joint capsule or ligaments.
independent of it. Movement at the joint is achieved by Cartilage consists of a collection of rounded cells
contraction of the muscles passing across it. (chondroblasts) embedded in a matrix. There are three

Bone structure
BONE internal
circumferential
Long bones are hollow with an outer layer of compact lamellae
bone arranged, on the surface, into flat layers of lamellae
and, more deeply, as concentric rings traversed by
longitudinal passages (the Haversian canals) (Fig. 10.1). Haversian
The central cavity of a long bone is occupied by bone lamellae
marrow. At the ends of the long bones, a meshwork
external
(cancellous bone) forms with marrow in its interstices. circumferential
The arrangement of the meshwork is determined by the lamellae
stresses to which the bones are exposed. Between adjacent
Haversian
Haversian canals and their surrounding concentric rings, canal
the bony lamellae are arranged more haphazardly. In the
spaces between these bony lamellae lie osteocytes.
Formation of bone is controlled by osteoblasts, and its
destruction by osteoclasts. The osteocytes, derived from
osteoblasts, are concerned with the exchange of calcium
between bone and the extracellular fluid. Collagen,
synthesised by osteoblasts and fibroblasts, forms the
major part of the bone matrix. The calcium content of
bone is mainly composed of crystals of hydroxyapatite.
Approximately 1% of the calcium and phosphate of bone
is in equilibrium with the extracellular fluid. Only
osteoclastic resorption can release the remainder. The
exchange of calcium between bone and extracellular fluid
is controlled by parathormone and calcitriol, a metabolite
of vitamin D. Fig. 10.1 Representation of bone structure.
265
Chapter
10 Bone, joints and muscle
Synovial joint Shoulder joint
coracohumeral coracoacromial
ligament ligament
skin and
bone subcutaneous
tissue
bursa
tendon
capsule
synovium tendon
sheath
fibrocartilage
pad
joint
space ligamentous
thickening
hyaline of capsule
articular Fig. 10.3 The shoulder joint and the attachments of the
cartilage muscle coracohumeral ligament.
bursa
Fig. 10.2 Cross-section of a synovial joint.
main types: hyaline, elastic and fibrocartilage. Hyaline

cartilage is found on the articular surface of joints, in the
costal cartilages and in the larynx, trachea and bronchi.
Hyaline cartilage combines elasticity with a capacity
to resist external forces. With increasing age, cartilage
water content falls, with a consequent deterioration in
tensile stiffness, fracture strength and fatigue resistance.
Fibrocartilage is predominantly composed of fibrous
tissue and is a part of the tendon at the point of its
insertion into bone (Sharpey’s fibres). It is also found in
certain joints. Elastic cartilage has a concentrated network
of elastic fibres that give its structure considerable
flexibility. It is found in the pinna and in some of the Fig. 10.4 Longitudinal section through myofibrils.
laryngeal cartilages.
at one end but are attached to bone at the other

JOINTS (Fig. 10.3) or remain totally independent of the joint
Joints can be classified into those allowing free movement capsule.
(diarthroses), those that are fixed (synarthroses) and The synovial membrane is one cell thick. One type of
those that permit limited movement (amphiarthroses). In cell ingests foreign or autologous material that has
diarthroses (synovial joints), a space exists between the entered the joint; another synthesises and secretes the
bone surfaces, allowing movement of one bone against synovial fluid. Synovial fluid is a dialysate of plasma with
the other (Fig. 10.2). Further classification of these joints the addition of hyaluronate proteoglycan. The ratio of the
can be made according to the type of movement that concentration of a synovial fluid protein to its serum
occurs (e.g. ball and socket, hinge). A synovial joint is concentration is determined by molecular size. The
enclosed by a collagenous capsule attached to the bone synovial fluid provides both nutrition for the articular
at some distance from the joint. The inner surface of the cartilage and lubricates the joint surfaces.
capsule is lined by a fluid-producing membrane. Localised Temporary synarthroses (synchondroses) are found
thickenings of the capsule, the ligaments, connect the at the growing points of long bones in the form of
adjacent bones. Other ligaments blend into the capsule epiphyseal cartilage. The sutures of the skull are
266
Chapter
Symptoms of bone, joint and muscle disorders 10
synarthroses, the bony margins being joined by fibrous Differential diagnosis

tissue.
Bone pain
Amphiarthroses are permanent joints. A good example
is the intervertebral disc of the spine. An outer layer of Focal pain
dense concentric bundles of collagen, the annulus • Fracture or trauma
fibrosus, encloses a core of hydrated compact tissue, the • Infection
nucleus pulposus. • Malignancy
• Paget’s disease
• Osteoid osteoma
MUSCLE
Diffuse pain
A motor neuron innervates 100–1000 skeletal muscle
• Malignancy
fibres. Within the muscle fibre is a recurring anatomical
• Paget’s disease
structure, the sarcomere, consisting of thin filaments that
• Osteomalacia
are composed of actin and thick filaments composed of
• Osteoporosis
myosin (Fig. 10.4). During the contraction and relaxation
• Metabolic bone disease
of muscle, the thin and thick filaments move in relationship
to one another. All the fibres of a particular motor unit
have similar properties. Muscle fibres are divided into fast
and slow twitch (type I and type II) according to their Risk factors
speed of contraction, although in humans a continuum
Age-related osteoporosis
of twitch speed exists.
Slowly contracting motor units are innervated by • Female
slowly conducting nerve fibres with a low threshold and • Premature loss of gonadal function
firing frequency. Rapidly contracting motor units are • Family history of osteoporosis
innervated by axons that conduct rapidly but have a high • Thin body habitus
threshold. The strength of muscle contraction can be • Decreased physical activity
altered either by varying the number of motor units • Low calcium intake
recruited or by altering their firing frequency. The • Smoking
recruitment process begins with small units and progresses • High alcohol intake
to larger. Firing frequency ranges from 10 to 20 Hz • Nulliparity
for slow units and up to 100 Hz for fast units. Slow
twitch muscles have a high myoglobin content, producing
a reddish appearance. Slow twitch fibres use oxidative
mechanisms for energy formation; fast twitch fibres Pain
employ glycolysis. The former are fatigue-resistant, In an arthritic disorder, pain is usually the most prominent
the latter rapidly fatiguable. In general, slow units complaint. Important aspects to determine are the site
provide sustained muscle tension over long periods, and severity of the pain, whether it is acute or chronic,
of the sort required to maintain a particular posture, how it is influenced by rest and activity and whether it
whereas fast units allow short-lived, sudden muscle appears during a particular range of movement.
contraction. Ask the patient to point to the maximal site of pain.
Although irritation of structures close to the skin produces
well-localised pain, disturbance of deeper structures
Symptoms of bone, joint and produces pain that is poorly localised and eventually
segmental in distribution.
muscle disorders
The segments to which the pain is referred (the
BONE sclerotomes) differ somewhat from dermatomal
distributions. Consequently, deep pain can be felt at a
Pain point some distance from the affected structure, that is,
Bone pain has a deep, boring quality. The pain is focal referred pain. Where joint disease exists, misinterpretation
in the presence of a bone tumour or infection but diffuse of the site of the disease process can follow (Fig. 10.5).
in generalised disorders (e.g. osteoporosis). The pain Spinal pain can also be referred. Abnormal function in
of a fracture is sharp and piercing and exacerbated by the upper cervical spine can lead to pain over the occipital
movement but relieved by rest. region, whereas disorders of the lower lumbar spine may
lead to upper lumbar back pain stemming from the fact
that the posterior longitudinal ligament is innervated by
JOINTS the upper lumbar nerves.
Joint symptoms include pain, swelling, crepitus and Severity of joint pain is difficult to judge, depending,
locking. as it does, on the patient’s personality. Osteoarthritis and
267
Chapter
rheumatoid arthritis typically result in chronic pain with

Joint pain periodic exacerbation; septic arthritis or gout produce an
acutely painful joint.
Inflammatory joint disease tends to cause pain on
waking, improving with activity but returning at rest.
Mechanical joint disease (e.g. caused by osteoarthritis)
leads to pain that worsens during the course of the day,
particularly with activity.
a
b For certain joint disorders (e.g. at the shoulder), pain
is apparent only during a specific range of movement. If
confirmed by examination, this selectivity can be valuable
in differential diagnosis.
Swelling and crepitus

If the patient has noticed joint swelling, elicit for how
long it has been present, whether there is associated pain
and whether the swelling fluctuates. A noisy joint is not
necessarily pathological. Introspective individuals are
c
likely to interpret periodic clicking in a joint, in the
d
absence of pain, as having pathological significance. It
does not. Crepitus is a grating noise or sensation; it can
have both auditory and palpable qualities. Fine crepitus
is more readily felt than heard, but crepitus stemming
from advanced degeneration of a large joint (e.g. the hip)
is readily audible.
Locking
A joint locks if ectopic material becomes interposed
between the articular surfaces. It is particularly associated
with damage to the knee cartilages. Ascertain if the
Fig. 10.5 Distribution of pain arising from (a) the acromioclavicular
or sternoclavicular joints, (b) the scapulohumeral joint, (c) the hip
locking occurs at a particular point during movement of
joint and (d) the knee joint. the joint.
Questions to ask MUSCLE

Joint pain Muscle symptoms include pain and stiffness, weakness,
wasting, abnormal spontaneous movements and cramps.
• Where is the maximal site of pain?
• Does the pain change during the course of the day?
Pain and stiffness
• Has the pain been there for a short or long time?
• Does the pain get better or worse with movement? Muscle pain tends to be deep, constant and poorly
localised. If caused by local muscle disease, it is likely to
Differential diagnosis Differential diagnosis

Joint pain Muscle pain
• Inflammatory • Inflammatory
– rheumatoid arthritis – polymyositis
– ankylosing spondylitis – dermatomyositis
• Mechanical • Infective
– osteoarthritis – pyogenic
• Infective – cysticercosis
– pyogenic • Traumatic
– tuberculosis • Polymyalgia rheumatica
– brucellosis • Neuropathic
• Traumatic – e.g. Guillain–Barré syndrome
268
Chapter
be exacerbated by contraction of the muscle and relieved angularity. Is there limb shortening? Look for tenderness
by rest. If the patient complains more of muscle stiffness by gently palpating those parts of the bone close to the
(particularly of the lower limbs) than pain, suspect the skin surface.
possibility of spasticity caused by an upper motor neuron
lesion.
JOINTS
Weakness You need to follow a strict routine with joint examination,
A complaint of global weakness is more likely in neurotic incorporating inspection, palpation and assessment of
individuals than in patients with neurological disorders. the movement of the joint.
Important questions to ask include the distribution of Inspection
the weakness, whether it appears related to any pain in
the limb, whether it fluctuates and whether it is static Things you are looking for include swelling, joint
or progressive. A complaint of predominant proximal deformity, overlying skin changes and the appearance of
weakness suggests the possibility of primary muscle the surrounding structures.
disease (e.g. polymyositis or myopathy). A predominantly Swelling Causes of joint swelling include effusions,
distal weakness is more likely to be neuropathic. If the thickening of the synovial tissues and of the bony margins
weakness is fluctuant, and particularly if it worsens during of the joint. Differentiation of these causes is achieved by
the course of activity, you will need to consider myasthenia palpation. If you suspect joint swelling, compare it with
gravis when you come to examine the patient (see also the joint of the opposite limb. Particularly note if the
Ch. 11). Weakness caused by sudden entrapment of a swelling appears to be of the joint itself or of the adjacent
peripheral nerve (e.g. a traumatic radial nerve palsy) will structures.
be stable or even improving by the time the patient seeks
medical attention. In other conditions the weakness is Deformity Deformity results either from misalignment
progressive (e.g. motor neuron disease). of the bones forming the joint or from alteration of the
relationship between the articular surfaces. If misalignment
exists, a deviation of the part distal to the joint away from
the midline is called a valgus deformity and a deviation
Questions to ask towards the midline a varus deformity (Fig. 10.6). If a
Muscle weakness deformity exists you will need later to determine whether
it is fixed or mobile. Partial loss of contact of the
• Is the weakness global or focal?
articulating surfaces is called subluxation, and complete
• Is the weakness secondary to a painful limb?
loss dislocation. Although these are usually traumatic,
• Does the weakness fluctuate?
they can also be seen in inflammatory joint disease,
• Is the weakness increasing in severity?
particularly rheumatoid arthritis. Swan neck, Boutonnière
and mallet are descriptive terms used for deformities of
Wasting and fasciculation

Both these features form an important part of the
examination, but both may have been noticed by the Knee deformities
patient and volunteered during history-taking. If
the patient describes muscle twitching, ascertain whether
the movement has occurred in several different muscles
or whether it has been confined to one area, most likely
the calf.
Cramps
Cramps are seldom of pathological significance. They are
usually confined to the calves and can be triggered by
forced contraction of the muscle.
General principles of examination

BONE
genu varum genu valgum
Whichever structure is being examined, ensure that it is
completely exposed and that the patient is comfortably
positioned. Determine whether there is any abnormal Fig. 10.6 Genu varum (left) and genu valgum (right).
269
Chapter
Finger deformities
PIP
normal MCP
DIP
swan neck
Fig. 10.8 Acute gout of the first metatarsophalangeal joint.
boutonnière
mallet
Fig. 10.7 Deformities of the finger in rheumatoid arthritis.
the metacarpophalangeal and interphalangeal joints of

the hand (Fig. 10.7).
Fig. 10.9 Osteoarthritis of the DIP joint.
Skin changes You should palpate the skin over a joint
to assess its temperature rather than relying simply on
its colour. Redness of the skin over a joint implies to a joint. Again determine their consistency. Soft
an underlying acute inflammatory reaction (e.g. gout) fluctuant swellings suggest enlarged bursae. Harder
(Fig. 10.8). swellings occur in rheumatoid arthritis and gout.
Changes of adjacent structures The most striking Tenderness Carefully palpate the joint margin and
change adjacent to a diseased joint is wasting of muscle. adjacent bony surfaces together with the surrounding
Assess muscle bulk above and below the affected joint, ligaments and tendons. Your task is to discover whether
making a comparison with the opposite limb if that is any tenderness is within the joint or outside it, and
spared. Wasting of quadriceps is particularly conspicuous whether the tenderness is focal or generalised. In an
in severe disease of the knee joint. acutely inflamed joint, the whole of its palpable contours
will be tender. If there is derangement of a single
Palpation
knee cartilage, tenderness will be confined to the margin
During palpation of a joint, assess the nature of any of that cartilage. In degenerative joint disease, you may
swelling, whether there is tenderness and whether the find tenderness in structures adjacent to the joint.
joint is hot. Tenderness close to the joint may reflect primary
Swelling The method of examining for an effusion will pathology in bone (e.g. osteomyelitis) or in the tendon
be described for the individual joints. Your first step is sheath (e.g. De Quervain’s tenosynovitis) (Figs 10.10,
to determine the consistency of any swelling. Is the 10.11).
swelling hard, suggesting bone deformities secondary to Temperature For a small joint, for example, in the finger,
osteoarthritis? Certain sites are particularly susceptible to assess temperature with the finger tips, using an
osteoarthritic change (e.g. the distal interphalangeal unaffected joint in the same or the other hand for
joints of the hand) (Fig. 10.9). A slightly spongy or boggy comparison. For a larger joint, for example, the knee, rub
swelling suggests synovial thickening and is particularly the back of your hand across the joint then compare with
associated with rheumatoid arthritis. An effusion is the other limb. If the contralateral joint is also affected,
fluctuant, that is, the fluid can be displaced from one part carry your hand above and below the joint margins to
of the joint to another. Swellings may also arise adjacent make the comparison.
270
Chapter
Neutral position
Fig. 10.10 De Quervain’s tenosynovitis of the wrist.
De Quervain’s tenosynovitis
extensor pollicis
longus
Fig. 10.12 The neutral position from which joint measurement is
performed.
Range of joint movement
abductor pollicis extensor pollicis

longus brevis
Fig. 10.11 De Quervain’s tenosynovitis. The tendons of abductor

pollicis longus and extensor pollicis brevis are inflamed.
Joint movement
Next proceed to examine the range of movement of the
joint, whether movement is limited by pain and whether
there is instability.
To define the range of joint movement, start with the Fig. 10.13 Measuring the range of joint movement.
joints in the neutral position, defined as the lower limbs
extended with the feet dorsiflexed to 90°, and the
upper limbs midway between pronation and supination From the neutral position, record the degrees of flexion
with the arms flexed to 90° at the elbows (Fig. 10.12). and extension. If extension does not normally occur at a
For accurate measurement of joint movement you will joint (e.g. the knee) but is present, describe the movement
need a goniometer (Fig. 10.13) but for routine purposes as hyperextension and give its range in degrees.
your eye should allow a reasonably true estimate. Sometimes there is restriction of the range of movement.
Movement of a joint is either active (i.e. induced by the For example, if the knee fails by 30° to reach the extended
patient) or passive (i.e. induced by the examiner). position, describe this as either a 30° flexion deformity or
Sometimes you need to assess both but you will generally as a 30° lack of extension (Fig. 10.14). For the ankle and
assess active movements in the spine but passive wrist, extension is described as dorsiflexion and flexion
movements in the limb joints. Restriction of active as plantar and palmar flexion, respectively. For a ball and
compared with passive movement is usually due to socket joint, you will need to record the range of flexion,
muscle weakness. extension, abduction, adduction and internal and external
271
Chapter
Flexion deformity Types of joint movement
dorsal
palmar
0º
flexion hyperextension
30º
flexion
Fig. 10.14 30° flexion deformity of the knee. rotation
rotation (Fig. 10.15). The range of joint movement varies

between individuals: an excessive range of movement
can be constitutional as well as pathological. Carefully
note if pain occurs during joint movement. In joint external internal
disease, pain is likely to occur throughout the range of adduction abduction
movement. In certain disease processes around the joint
(e.g. in the ligaments or bursae), pain can be restricted to
a particular range or type of movement. Damage of either
the articular surfaces or of the ligaments related to a joint
can lead to instability. You will discover this partly by
finding that the joint can be moved into abnormal
positions and partly, particularly for the knee joint, by Fig. 10.15 Description of joint movement according to the type of
joint.
observing the joint as the patient walks.
GALS
ask the patient to try to place the relevant ear on each
shoulder in turn (lateral neck flexion).
A screening history and examination process for
• Arms – From in front ask the patient to place both
the musculoskeletal system has been devised for
hands behind the head, elbows back.
undergraduate use (GALS – gait, arms, legs and spine).
• Place both hands by the side, elbows straight.
• Place both hands out in front, palms down, fingers
SCREENING HISTORY straight.
• Have you any pain or stiffness in your muscles, joints • Turn both hands over. Make a tight fist with each
or back? hand.
• Can you dress yourself completely without difficulty? • Place the tip of each finger onto the tip of the thumb
• Can you walk up and down stairs without difficulty? in turn.
If the answers to all three questions are negative, • The examiner then squeezes across the second to
significant musculoskeletal abnormality is unlikely. the fifth metacarpals to elicit tenderness.
• Legs – Inspect from in front (with the patient
standing).
SCREENING EXAMINATION • Inspect with the patient lying flat.
• Gait – Inspect the patient walking, turning and walking • Flex each hip and knee while holding the knee
back. (confirming full knee flexion without knee
• Spine – Inspect the patient from three positions from crepitus).
behind, from the side, then ask the patient to bend • Passively internally rotate each hip in flexion
forwards and touch the toes, and finally from in front (checking for pain and restricted movement).
272
Chapter
GALS 10
• Press on each patella for tenderness and palpate for Increased muscle bulk Usually abnormal muscle bulk
an effusion. reflects the patient’s obsession with his own bodily
• Squeeze across the metatarsals for tenderness due strength (it is almost always a man). There are rare
to metatarsophalangeal disease. conditions that lead to muscle hypertrophy. If the
• Inspect both soles for callosities reflecting abnormal enlargement is due to increase in muscle bulk, it is called
weight-bearing. true hypertrophy and is seen, for example, in congenital
myotonia. If the increased bulk is due to fatty infiltration
(and you will then discover the muscle is actually
RECORDING FINDINGS weak), it is called pseudohypertrophy. This finding is
Normal response to the screening questions can be characteristic of certain of the muscular dystrophies (e.g.
recorded as: Duchenne’s).
Pain 0 Spontaneous contractions Completely expose the

Dress ✓ muscle when looking for evidence of spontaneous
Walk ✓ contraction. Make sure the patient is warm and relaxed.
Shivering brought on by cold can be difficult to distinguish
Results of the physical examination can be recorded if from fasciculation. Spontaneous movements can occur
gait (G) is normal, there are no abnormalities to the with both upper and lower motor neuron lesions. In the
appearance (A) of the areas inspected (i.e. no swelling, former, particularly at the spinal level, you may see either
deformity, wasting, abnormal position or skin change) flexor or extensor spasms of the legs, either at the hips
and no abnormalities of movement (M) of the arms (A), or knees. The movements can occur spontaneously or be
legs (L) or spine (S) as follows: triggered by attempting to move the patient and are often
G ✓ painful. Fasciculation produces episodic muscle twitching
A M that can be subtle in small muscles. It is a feature of lower
A ✓ ✓ motor neuron lesions but can also be seen in normal
L ✓ ✓ individuals. Fasciculation is intermittent. Wait for a few
S ✓ ✓ minutes before deciding it is absent. It is particularly
important to determine whether the fasciculation is
Any abnormality is recorded as an X and described in confined to a single muscle or whether it is more widely
more detail. distributed. The former may reflect the result of cervical
radiculopathy or be physiological (particularly if confined
to the calves); the latter suggests a diagnosis of motor
MUSCLE
neuron disease.
The methods for examining individual muscles will be
given in the section on regional examination. Initially Palpation
your assessment will include inspection, palpation, then Muscle palpation is of limited value. If the muscle is
testing of muscle power. infected or inflamed it is likely to be tender. Most
myopathies are painless but there are exceptions (e.g. the
Inspection acute myopathy occurring in alcoholics). Muscle
Look for evidence of muscle wasting, for signs of abnormal tenderness can also occur in neurogenic disorders (e.g.
muscle bulk and for spontaneous contractions. the peripheral neuropathy of thiamine deficiency can
lead to marked calf tenderness).
Wasting Remember that striking muscle wasting can
Testing muscle power
accompany joint disease (e.g. wasting of the small hand
muscles in rheumatoid arthritis and wasting of the You should follow the UK Medical Research Council
quadriceps in virtually any arthropathy affecting the knee classification (p. 363) when testing and recording muscle
joint). If there is no significant joint disease, wasting power. Remember to make allowance for sex, age and
(other than caused by a profound loss of body weight) the patient’s stature. If the muscle itself, or the joint that
reflects either primary muscle disease or disease of its it moves, is painful then power will be correspondingly
innervating neuron. Make allowances for the age of the limited. Patterns of muscle weakness are particularly
patient and his or her occupation. Some thinning of the important in neurological diagnosis. Is the weakness
hand muscles occurs in elderly people but is not global, does it predominate distally or proximally in the
accompanied by weakness. If you suspect wasting of one limb, does its distribution fit with either a peripheral
limb, measure the circumference of that limb and compare nerve or root distribution? Sometimes muscle power is
it with its fellow. For example, for the thigh, mark the line decidedly fluctuant: there is a sudden give, alternating
of the medial cartilage of the knee joint, measure up, for with more effective contraction. Although this pattern
example, 20 cm, on each thigh and record the circumference can occur in myasthenia gravis, it is usually the reflection
of the legs at that point. of a nonorganic disability. If muscle fatigue is a prominent
273
Chapter
symptom assess it objectively. For example, for the

deltoid, ask the patient to abduct the shoulder to 90°. Test Spinal deformities
power immediately, then after the patient has held that
posture for 60 seconds.
You will need to be selective when deciding which gibbus scoliosis
muscles to test. Your choice will be guided partly by the
patient’s complaints, both in terms of their distribution
and their quality.
REGIONAL STRUCTURE, FUNCTION

AND EXAMINATION
Temporomandibular joints
Ask the patient to open and close the jaw. If the
temporomandibular joints are lax, there may be
considerable side-to-side movement. Now palpate the
joint margins by placing your fingers immediately in
front of and below the tragus. As the patient opens kyphosis
lordosis
the jaw, palpate the head of the mandible as it moves
forwards and downwards. In temporomandibular joint
dysfunction, the joint capsule is tender and chewing is
painful. The generalised arthritic disorders seldom affect Fig. 10.16 Spinal deformities.
this joint.
The spine flexion deformity (Fig. 10.16). Using the position of the
spinous processes tends to underestimate the degree
STRUCTURE AND FUNCTION of scoliosis, as the spines rotate towards the midline.
The scoliosis is accentuated when the patient bends
The primary curvatures of the spine, in the thoracic and
forwards.
sacral regions, are determined by differences in height
For each spinal level, start by inspection and follow by
of the anterior and posterior aspects of the vertebrae
palpation to elicit any tenderness. Finally, assess the
at these levels. The secondary curvatures of the cervical
range of movement and determine whether it is restricted
and lumbar regions depend more on the relative
by pain.
heights of the anterior and posterior aspects of the
intervertebral discs. The nucleus pulposus allows an even
distribution of applied force onto the annulus fibrosus CERVICAL SPINE
and the hyaline laminae covering the opposing vertebral The examination is best achieved with the patient sitting.
bodies. Note any deformity, then palpate the spinous processes.
Forward flexion and extension occur at all levels of the A cervical rib is sometimes palpable in the supraclavicular
spine but are maximal at the junction of the atlas fossa. Obliteration of the radial pulse by downward
with the occiput and in the lumbar and cervical regions. traction of the arm does not reliably predict the presence
Lateral flexion is greatest at the atlanto-occipital junction, of a cervical rib or band.
occurs to some extent in the lumbar and cervical regions, Examine active then passive movements. For flexion,
but minimally in the thoracic region. Rotation other than ask the patient to bring the chin onto the chest and for
at the atlantoaxial joints, is determined by the shape of extension ask them to bend the head backwards as far as
the apophyseal joints and is maximal at the thoracic possible. Observe both these movements from the
level. side. For lateral flexion, stand in front of or behind
the patient and ask the patient to bring the ear towards
Examination of the spine the shoulder first on one side, then the other. For rotation,
stand in front or over the patient asking the patient to
With the patient undressed to the underwear, ask the look over one shoulder then the other (Fig. 10.17).
patient to stand upright. Assess the posture of the whole Note whether any movement triggers pain either locally
spine before examining its component parts. An increased or in the upper limb. Repeating the movements while
flexion is called kyphosis, increased extension, lordosis applying gentle pressure over the vertex of the skull
and a lateral curvature, scoliosis. Gibbus refers to a focal may trigger pain or paraesthesiae in the arm if there is a
274
Chapter
The spine 10
Cervical spine Lumbar flexion
neutral rotation
10+ cm
10 cm
5 cm
5 cm
Fig. 10.19 Measuring lumbar flexion.
LUMBAR SPINE
Having inspected the lumbar spine and tested for
flexion and extension lateral flexion tenderness, assess the range of movement. While
standing at the patient’s side, ask the patient to touch the
Fig. 10.17 Movements of the cervical spine. toes, keeping the knees straight. To assess the contribution
made to flexion by the lumbar spine, mark the spine at
the lumbosacral junction, then 10 cm above and 5 cm
below this point. On forward flexion the distance between
the two upper marks should increase by approximately
Skull compression
4 cm, the distance between the lower two remaining
unaltered (Fig. 10.19). Now assess extension, again from
the side, then lateral flexion. For this, stand behind the
patient and ask the patient to slide the hand down the
outside of the leg, first on one side and then on the other
(Fig. 10.20).
SACROILIAC JOINTS
Palpate the joints, which lie under the dimples found
in the lower lumbar region. To test whether movement
Fig. 10.18 Compression of the vertex of the skull to reproduce at the joint is painful, first press firmly down over
cervical root pain. Compression with the head in the neutral position the midline of the sacrum with the patient prone
(left) or laterally flexed to the right is painless (middle). With the (Fig. 10.21) then, with the patient supine, forcibly flex
head flexed to the left (right), the side of the root compression,
one hip while maintaining the other in an extended
downward pressure is painful.
position.
NERVE STRETCH TESTS

critical degree of narrowing at an intervertebral foramen
(Fig. 10.18). Nerve stretch tests are carried out to determine whether
there is evidence of nerve root irritation, usually as a
consequence of prolapse of a lumbar disc.
THORACIC SPINE
Straight leg raising
Sit the patient with the arms folded across the chest, then
ask the patient to twist as far as possible first to one side With the patient supine, carefully elevate the extended
then to the other. The range of movement is best leg at the hip. Normally, 80–90° of flexion is possible.
appreciated from above. Next measure chest expansion. Restriction of movement can occur with both spinal
A movement of at least 5 cm should occur and provides and hip disease. In the presence of nerve root irritation
an assessment of the mobility of the costovertebral at the L4 level or below, straight leg raising evokes pain
junction. Palpate the spinous processes for any tenderness as the sciatic nerve is stretched (Fig. 10.22). If the foot is
and assess any deformity. now dorsiflexed, the pain increases (Bragard’s test).
275
Chapter
Thoracolumbar spine Sacroiliac joint
flexion extension
Fig. 10.21 Assessing the sacroiliac joint.
Back pain
• Muscle or ligamentous strain

• Degenerative intervertebral disc
• Spondylolisthesis
left right • Arthritis
– osteoarthritis
– rheumatoid arthritis
lateral flexion rotation – ankylosing spondylitis
• Bone infection
Fig. 10.20 Movements of the thoracolumbar spine. – pyogenic
– tuberculous
• Trauma
• Tumour
Return the foot to the neutral position, then flex the knee. • Osteochondritis
The hip can now be flexed further before pain reappears • Metabolic bone disease
but if the knee is then extended, the pain increases
(Lasegue’s test).
Femoral stretch test Questions to ask
Turn the patient into the prone position. First flex the Back pain
knee. If this fails to trigger pain, extend the leg at the hip. • Is the pain confined to the back or does it radiate to
A positive response, with pain in the back extending into the upper or lower limb?
the anterior thigh, suggests irritation of the second, third • Is the pain exacerbated by coughing or sneezing?
or fourth lumbar root on that side (Fig. 10.23). • Did the pain begin suddenly or gradually?
Clinical application
Back pain can arise from disease processes in the PROLAPSED INTERVERTEBRAL DISC
vertebrae, from degenerative changes in the joints A prolapse of disc material is most likely to occur either in
between the vertebrae, from degeneration or actual the cervical (principally at C5/6) or the lumbar (principally
prolapse of the intervertebral disc and from the ligaments at L5/S1) region. Once nerve root irritation occurs, likely
and muscles supporting and moving the spine. symptoms include local and referred pain, with sensory
276
Chapter
The spine 10
Stretch tests
a. neutral position roots slack
b. straight leg raising limited by

tension of root over prolapsed disc
d. pain relieved by knee flexion
c. pain increased by dorsiflexion

of foot (Bragard's test)
e. with knee extension further extension of the

nerve root increases the pain (Lasegue's test)
Fig. 10.22 Stretch tests: (a) neutral position, (b) straight leg raising, (c) Bragard’s test, (d) knee flexion and (e) Lasegue’s test.
and motor symptoms in the limb. The pattern of

Femoral stretch distribution of sensory change, weakness or reflex change
allows prediction of the affected nerve root (Fig. 10.24).
a
OTHER CONDITIONS
Ankylosing spondylitis
In ankylosing spondylitis the patient, usually male,
complains of spinal pain and stiffness, the latter improving
with exercise. The sacroiliac joints are affected initially.
Increasing loss of spinal mobility can lead to a thoracic
b
kyphosis combined with loss of the lumbar lordosis
(Fig. 10.25).
Rheumatoid arthritis
This complaint commonly involves the upper cervical
spine. Synovitis affecting the cruciate ligament allows
posterior subluxation of the odontoid peg. Compression
c of the upper cervical cord is a potential hazard, producing
a tetraparesis (Fig. 10.26).
Spinal tumours
Spinal tumours are usually metastatic from prostate,
Fig. 10.23 (a) Femoral stretch. The pain may be triggered by breast, bronchus or kidney. Initially, there is local severe
(b) knee flexion alone or (c) in combination with hip extension.
rest pain, sometimes with a referred component caused
by spinal root compression. Later, focal neurological
signs appear.
277
Chapter
Root syndromes
muscle
C5 spinati
supinator L1
C3 C3
deltoid
biceps C4 C4 L1
C6 S5 L2
L2 S4
triceps Sensory
finger extensors S3
C7
C8 long finger flexors C5 T2 T2 C5
L4 tibialis anterior
L3
L5 extensor hallucis longus L3
S1 gastrocnemius, soleus S2
T1 T1
C6 C6 L5
reflex L4 L4
L5
C5
biceps C8 C8
supinator
C C
7 7 S1
C6 triceps
C7 S1
front back front back

L4 knee (+L2,3)
L5 no reflex
S1 ankle
Fig. 10.24 Sensory, motor and reflex changes in cervical and lumbar root syndromes.
Posture in advanced long-term ankylosing spondylitis
Fig. 10.26 Axial T2-weighted MRI scan showing atlantoaxial

dislocation.
Tuberculosis
This disease most commonly involves the thoracic or
Fig. 10.25 Posture in advanced long-term ankylosing spondylitis on lumbar spine. The infective process begins in the anterior
the right with control subject on the left. margin of the vertebral body with early involvement of
278
Chapter
The shoulder 10
the disc space. Vertebral collapse with gibbus formation

and paraspinal abscess follow. Symptoms include back Shoulder dislocation
pain and deformity with evidence of spinal cord
compression.
TRAUMATIC LESIONS
Cervical spine injuries include atlantoaxial dislocation,
fractures of the arch of the atlas and compression fractures
of the vertebral bodies. Complications include spinal
instability and neurological damage.
Fractures around the cervicothoracic junction are easily
missed unless the shoulders are well depressed at the
time of the radiograph.
Thoracic and lumbar spine injuries include com-
pression fractures and fractures of the transverse
processes. Pathological fractures commonly occur at this
level. Complications include paraplegia (with thoracic
fractures) and haemorrhage into the retroperitoneal
space.
The shoulder Fig. 10.27 Dislocation of the shoulder.
STRUCTURE AND FUNCTION

Movement of the shoulder takes place both at the Palpate the shoulder and sternoclavicular joints for
glenohumeral and the scapulothoracic joints. For tenderness.
abduction, the first 90° of movement takes place at
the glenohumeral joint. This is achieved by contraction
first of supraspinatus (0–30°) then of deltoid (30–90°). JOINT MOVEMENT
Abduction of the shoulder beyond 90° requires rotation Remember that most movement at the shoulder
of the scapula, which is achieved by contraction of involves both the glenohumeral joint and rotation of
trapezius. Adduction is principally due to pectoralis the scapula across the thorax. You will test flexion
major and latissimus dorsi. Forward flexion depends and extension, internal and external rotation, abduction
mainly on pectoralis major and the anterior fibres and adduction (Fig. 10.28). When testing abduction,
of the deltoid, extension on latissimus dorsi, teres anchor the scapula with your free hand, to ensure
major and the posterior fibres of the deltoid. Lateral that over the first 90° only glenohumeral movement is
rotation is accomplished by contraction of infraspinatus allowed (Fig. 10.29). Test first passive then active
and medial rotation by pectoralis major, latissimus movement. During abduction, note particularly if pain
dorsi and the anterior fibres of the deltoid. Immediately occurs. Is the pain present throughout the movement or
above the glenohumeral joint lies the subacromial only over a particular range? With a frozen shoulder
bursa and the rotator cuff, which is formed by the (attributed to capsulitis of the glenohumeral joint), pain
tendons of the supraspinatus, infraspinatus and is accompanied by restriction of all glenohumeral
subscapularis. movements.
INSPECTION AND PALPATION Painful arc syndrome

Inspect the contour of the shoulder and its surrounding The painful arc syndrome causes pain on shoulder
structures. Small effusions in the shoulder are difficult elevation. As the arm is elevated, elements of the rotator
to detect. Anterior dislocation results in a forward cuff, comprising the tendons of the supraspinatus,
and downward displacement with alteration of the infraspinatus and subscapularis, come into contact with
shoulder contour (Fig. 10.27). Posterior dislocation the undersurface of the acromion. Inflammation of one
is obvious. Fracture of the clavicle and anterior of the muscles, particularly the supraspinatus or of the
dislocation of the sternoclavicular joint are usually readily subacromial bursa, causes pain in the region of the
visible. Look at the deltoid to see if it is wasted. Then shoulder, with a painful arc of movement during
inspect the periscapular muscles. The bulk of the abduction (Fig. 10.30). Pain is absent initially, develops
supraspinatus and infraspinatus is easily assessed. during abduction as elements of the cuff come into
279
Chapter
Shoulder movement Glenohumeral joint
neutral rotation
internal external
flexion and extension
extension flexion
Fig. 10.29 Testing shoulder abduction at the glenohumeral joint.
Rotator cuff
abduction subacromial subscapularis

bursa
180º
subacromial
tendon
90º infraspinatus
tendon
deltoid
muscle
Fig. 10.28 Testing shoulder movement.
deltoid muscle subacromial acromioclavicular

bursa joint
contact with the undersurface of the acromion, then

disappears in the final part of abduction as the tendons
fall away from the acromion.
Bicipital tendonitis
In bicipital tendonitis, tenosynovitis involves the long
head of the biceps. The patient complains of pain in the infraspinatus
anterior aspect of the shoulder and arm. The pain is tendon
reproduced by palpating the tendon or by contracting the subscapularis
muscle.
Traumatic lesions
Fig. 10.30 The rotator cuff apparatus.
These include dislocation, fracture dislocation and
fractures of the neck of the humerus. Dislocations are
usually anterior, less commonly posterior. With the
280
Chapter
The shoulder 10
a b c
d e
Fig. 10.31 Testing the major muscles concerned with shoulder movement. (a) Supraspinatus, (b) deltoid, (c) infraspinatus, (d) latissimus dorsi
and (e) pectoralis major.
former, the contour of the shoulder is flattened and

the arm abducted. Axillary nerve damage can occur
and, less often, trauma to the brachial plexus or the
axillary artery.
MUSCLE FUNCTION
In the presence of any of the above conditions, muscle
power is limited by concomitant pain. If shoulder
movements are free and painless, the individual muscles
concerned with movement around the joint can now be
tested (Fig. 10.31).
Cervical radiculopathy
Fig. 10.32 Wasting of deltoid, infraspinatus and supraspinatus in a
Cervical radiculopathy often affects the fifth nerve root. right C5 root lesion.
Weakness is found in the spinati, deltoid and biceps.
Wasting may follow (Fig. 10.32). The biceps and supinator
reflexes are depressed.
Neuralgic amyotrophy Nerve palsies

In neuralgic amyotrophy, severe pain around the shoulder Nerve palsies affecting the shoulder are rare. A fracture
is followed by patchy weakness and wasting in the of the upper end of the humerus can damage the
shoulder girdle muscles. One form affects the long circumflex nerve, resulting in weakness of deltoid and a
thoracic nerve, with consequent winging of the scapula small patch of numbness over the lateral aspect of the
as the arm is pushed forwards (Fig. 10.33). shoulder.
281
Chapter
Elbow movement
flexion
up to 150º
90º 90º
supination pronation
180º extension
Fig. 10.34 Range of movement at the elbow.
Carrying angle
b
Fig. 10.33 Winging of the scapula on forward pressure.
The elbow
There are two joints at the elbow, one involving the
humerus, radius and ulna, the other joining the upper
ends of the radius and ulna. Flexion or extension
movement occurs at the former through a range of
approximately 150°. The latter joint allows the forearm to
rotate (pronation-supination) through a range of 180°
(Fig. 10.34). In males, the forearm is only slightly abducted
from the axis of the humerus. In females, the abduction
is greater, forming a carrying angle of about 15°
(Fig. 10.35). 15º
The biceps flexes the elbow when the arm is supinated.
Fig. 10.35 Carrying angle of the forearm.
The brachioradialis and brachialis flex the elbow in either
the pronated or supinated position. Extension of the
elbow is achieved by triceps, with a minor contribution
from anconeus (Fig. 10.36). Supination is produced by either side of the olecranon. Swelling of the olecranon
contraction of the supinator and pronation by the bursa can follow trauma or occurs in association with
combined action of pronator teres and pronator rheumatoid arthritis. Now palpate the subcutaneous
quadratus. border of the ulna, a common site for rheumatoid
nodules (Fig. 10.37). Move on to palpate the lateral
and medial epicondyles (Fig. 10.38). Inflammation of
INSPECTION AND PALPATION the extensor and flexor origins at these respective sites
Inspect the joint from behind, comparing its alignment (tennis elbow and golfer’s elbow) leads to pain in the
with the other arm. An effusion produces a swelling on region of the elbow exacerbated by forced wrist extension
282
Chapter
The forearm and wrist 10
Muscles acting at the elbow
biceps
(short head)
biceps
(long head)
triceps
brachialis
a
brachioradialis
anconeus
Fig. 10.36 Flexors and extensors of the elbow.
Fig. 10.38 Eliciting tenderness in a case of lateral (a) and (b) medial
epicondylitis.
in a posterolateral direction. Both ulnar and median

nerve damage can occur. Fractures of the head of
the radius typically follow a fall onto an outstretched
hand.
Fig. 10.37 Olecranon bursitis, rheumatoid nodule.
MUSCLE FUNCTION
for the former and forced wrist flexion for the latter. Test the principal muscles concerned with elbow flexion
Immediately inside the medial epicondyle is the ulnar and extension, together with pronation and supination
groove, within which you can palpate the ulnar nerve. (Fig. 10.39).
The nerve tends to thicken at this site even in normal A lesion of the C6 nerve root is common (Fig. 10.40).
individuals. Muscles that can be affected include the biceps,
brachioradialis, supinator and triceps. In practice, triceps
weakness predominates, with depression or loss of the
JOINT MOVEMENT triceps reflex. Any loss of sensation occupies the thumb
and index finger.
Flexion and extension at the elbow allow a total range
of movement of approximately 150°. Supination and
pronation both occur through a range of approximately
90°. The forearm and wrist
TRAUMATIC LESIONS Movements of the wrist comprise flexion, extension
These include dislocations, fractures of the radial head and ulnar and radial deviation (Fig. 10.41). Flexion–
and of the distal humerus. Dislocation is usually extension movements of the fingers occur at both
283
Chapter
a b c
d e
Fig. 10.39 Examining the muscles acting at or around the elbow joint. (a) Biceps, (b) brachioradialis, (c) triceps, (d) supinator and (e) pronator.
INSPECTION AND PALPATION

C6 root
Compare the size of the forearms, but remember that the
Muscles Dermatomal Reflex dominant forearm tends to be rather larger. Compare the
affected changes changes two wrists for size and for any evidence of swelling or
deviation. Malunion of a distal fracture (Colles’) leads to
extension deformity. If the patient describes a wrist strain,
biceps (biceps) carefully palpate in the region of the anatomical snuff
brachioradialis
supinator triceps box. Localised tenderness suggests a diagnosis of a
triceps fractured scaphoid. In De Quervain’s tenosynovitis,
inflammation of the tendons of the abductor pollicis
longus and extensor pollicis brevis causes wrist pain, with
localised tenderness and crepitus as the tendon moves
through its sheath (see Fig. 10.11).
JOINT MOVEMENT
Fig. 10.40 C6 root syndrome.
From the neutral position test flexion of the wrist
(approximately 90°) then extension (approximately 70°).
the metacarpophalangeal and the interphalangeal A comparison of the degree of dorsiflexion between the
joints. two wrists is best achieved by asking the patient to press
The major flexors of the wrist are flexor carpi radialis the palms together while elevating the elbows so that the
and ulnaris. The major extensors are extensor carpi ulnaris forearms are in a straight line. The range of palmar flexion
and extensor carpi radialis longus and brevis. The long can be similarly compared with the back of the hands
flexors and extensors of the fingers and thumb, by virtue pressed together. Now assess radial and ulnar deviation
of passing over the wrist joint, also exert a minor effect of the wrist. Wrist involvement is common in rheumatoid
there. arthritis. Besides pain and limitation of movement,
284
Chapter
The forearm and wrist 10
stretching of the ulnar collateral ligament allows the head

Wrist movements of the ulna to subluxate upwards (Fig. 10.42).
70º
TRAUMATIC LESIONS
extension
Fractures usually occur through the distal radius or ulna,
typically after a fall on an outstretched hand. Colles’
fracture is sited about 1–2 cm above the distal end of the
0º radius. The fracture is displaced dorsally. Smith’s fracture
is one at this site which is displaced in the opposite
direction.
flexion Deformity is common after a Colles’ fracture leading
90º
to shortening of the radius. Carpal tunnel syndrome can
occur as a late complication.
0º Wrist sprains are commonplace. The wrist may be
20º
painful and swollen but radiographs reveal no bony
radial
ulnar
55º
Fig. 10.41 Wrist movements.
Fig. 10.42 Elevation of the ulnar head in rheumatoid arthritis. The

flexion deformity of the fourth and fifth digits is the result of rupture
of their extensor tendons.
Fig. 10.43 Examining some of the muscles

of the forearm. (a) Flexor carpi radialis,
(b) flexor carpi ulnaris, (c) extensor carpi
ulnaris and (d) extensor carpi radialis longus.
a b
c d
285
Chapter
Fig. 10.44 Examining the long finger

flexors and extensors. (a) Extensor digitorum,
(b) extensor pollicis longus, (c) flexor
digitorum sublimis and (d) flexor digitorum
profundus.
a b
c d
injury. Treatment consists of immobilisation in a

plaster.
MUSCLE FUNCTION
Now test the muscles acting at the wrist (Fig. 10.43)
and the long flexors and extensors of the fingers
(Fig. 10.44).
A C7 root lesion affects the triceps together with wrist
and finger extension. The triceps jerk may be depressed
and sensory loss, if present, occurs over the middle
finger.
A radial palsy most commonly results from damage Fig. 10.45 Wrist and finger drop in a left radial palsy.
to the nerve in the spiral groove. There is weakness
of the supinator, brachioradialis and wrist and finger
extension (Fig. 10.45). The brachioradialis component of The small muscles of the hand control fine movements
the supinator reflex is depressed. of the thumb and fingers. The thenar eminence muscles
Sensory loss is often slight, mainly involving an consist of abductor pollicis brevis, flexor pollicis brevis
area of skin in the region of the anatomical snuff and opponens pollicis. Contained in the hypothenar
box. eminence are abductor digiti minimi, flexor digiti minimi
and opponens digiti minimi. Finally, there are the lumbrical
muscles, the dorsal and palmar interossei and adductor
The hand pollicis. The lumbricals extend the fingers at the
interphalangeal joints (with additional more complex
STRUCTURE AND FUNCTION actions), the interossei principally abduct and adduct the
fingers, whereas the adductor pollicis adducts the
The metacarpophalangeal joints allow abduction and thumb.
adduction movements when the fingers are extended
(Fig. 10.46). Abduction of the thumb carries it away from
the plane of the palm of the hand and adduction towards The hand joints
it. Extension moves the thumb radially in the plane of the
hand, flexion in the ulnar direction. Opposition rotates INSPECTION AND PALPATION
the thumb, bringing its palmar surface into contact with A good way to examine the hands both for joint and
the fifth finger (Fig. 10.47). muscle function is to ask the patient to sit opposite you
286
Chapter
The hand 10
with the hands spread on a flat surface. You are looking Now turn the hands over to look at the palmar aspects.
for signs of joint deformity and whether any deformity is Is there evidence of tendon thickening?
generalised or focal. If the latter, are particular joints Now carefully palpate the joints. Is there joint
affected? While inspecting the joints, remember to look tenderness? Assess the quality of any swelling (Fig.
at the state of the skin and whether the nails are deformed. 10.48). Can you feel any nodules along the tendon
sheaths?
In early rheumatoid arthritis, slight swelling of the
Finger movements proximal interphalangeal joints is accompanied by
tenderness (Fig. 10.49). At a later stage of the condition,
30º substantial deformities occur (see Fig. 10.7) accompanied
hyperextension by wasting of the small hand muscles. If the changes
predominate in the distal interphalangeal joints, carefully
0º inspect the nails for signs suggesting a diagnosis of
psoriasis (Fig. 10.50). In osteoarthritis, nodules (Heberden’s
flexion nodes) typically appear over the distal interphalangeal
joints but are also seen at the proximal interphalangeal
90º joints (Bouchard’s nodes) (Fig. 10.51).
Osteoarthritis commonly affects the carpometarcarpal
joint of the thumb in combination with changes in the
Fig. 10.46 Finger movements at the metacarpophalangeal (left and

right) and at the interphalangeal joints (below).
Thumb movements
extension flexion adduction opposition abduction
Fig. 10.47 Movements of the thumb. Fig. 10.49 The hand in early rheumatoid arthritis.
a b c
Fig. 10.48 Palpating the wrist (a), metacarpophalangeal (b) and interphalangeal (c) joints.
287
Chapter
Trigger finger
Fig. 10.50 Psoriatic arthropathy.
Fig. 10.53 Trigger finger. The thickened area becomes trapped in

an area of narrowing of the tendon sheath (arrow).
Questions to ask
Weakness of the hand
Fig. 10.51 Osteoarthritis at the proximal interphalangeal joints. • Is the weakness associated with joint pain?
• Is the weakness confined to the muscles supplied by
the median or ulnar nerve?
• If the weakness is global, are both hands or just one
hand affected?
• Is there accompanying sensory loss?
TRAUMATIC LESIONS
Hand injuries include tendon damage and fractures.
Severed extensor or flexor tendons require suturing to
facilitate healing.
Fractures include those of the phalanges, with or
without dislocation, and of the carpal and metacarpal
bones. Scaphoid fractures are easily missed on radiography,
Fig. 10.52 The square hand of osteoarthritis. requiring oblique views for their detection. Typically they
produce pain, swelling and tenderness in the region of
the anatomical snuff box, usually after a fall on an
distal interphalangeal joints resulting in the appearance outstretched hand. Avascular necrosis is a recognised
of a ‘square hand’ (Fig. 10.52). complication.
Nodule formation on a flexor tendon can lead to the
tendon being caught in a localised narrowing of the
sheath. The result, trigger finger, is a flexion deformity MOVEMENT
from which the finger can be extended only by force Test the range of movement in the thumb and fingers.
(Fig. 10.53). For abduction and adduction of the fingers, outlining the
288
Chapter
The hand 10
fingers on blank paper gives a quantitative assessment opportunity to assess the bulk of muscles supplied by the
of the degree of their abduction from the neutral median nerve by examining the thenar eminence. By now
position. you have determined whether there is any small muscle
wasting, whether it is bilateral or unilateral and, if
unilateral, whether it is global or confined to the
The hand muscles distribution of the median or ulnar nerve.
Muscle and joint function cannot always be conveniently

separated. A generalised joint disorder (e.g. rheumatoid TESTING POWER
arthritis) may well lead to wasting of the small hand Start with a muscle supplied by the ulnar nerve. A good
muscles caused by disuse, or may lead to focal wasting choice is the first dorsal interosseous (Fig. 10.54). If the
caused by entrapment of a particular nerve (e.g. the muscle is weak, test two other readily accessible muscles
median). supplied by the nerve, the adductor pollicis and abductor
digiti minimi. Now move on to muscles supplied by the
INSPECTION median nerve. Start with abductor pollicis brevis then
proceed to test opponens pollicis (Fig. 10.55).
First inspect the dorsum of the hands. In this position, all
the muscles that are visible are supplied by the ulnar
nerve. In elderly people, muscle bulk in the hand reduces Clinical application
but without accompanying weakness. Wasting produces
guttering between the extensor tendons, hollowing If the weakness is confined to the muscles of the thenar
between the index finger and thumb and loss of the eminence, you are dealing with a distal median nerve
convexity of the hypothenar eminence. Look for lesion, most probably within the carpal tunnel. Weakness
fasciculation. Now turn the hands over and inspect the with or without wasting of the muscles of the thenar
palmar surfaces. For the first time, you have the eminence is accompanied by a characteristic failure of the
a b c
Fig. 10.54 Testing some of the small muscles supplied by the ulnar nerve. (a) First dorsal interosseous. With the fingers flat, the patient is
trying to abduct the index finger against resistance. (b) Adductor pollicis. The patient is forcibly adducting the thumb towards the palmar
surface of the index finger. (c) Abductor digiti minimi. The patient is abducting the little finger against resistance.
a b
Fig. 10.55 Testing the muscles of the thenar eminence. (a) Abductor pollicis brevis. The patient is lifting the thumb vertically from the plane
of the palm of the hand. (b) Opponens pollicis. Against resistance, the patient is trying to touch the base of the little finger with the tip of the
thumb.
289
Chapter
Fig. 10.57 Bilateral ulnar nerve lesions.
digits (Fig. 10.57). In addition, there should theoretically

be weakness of flexor carpi ulnaris and of flexor digitorum
profundus to the fourth and fifth digits. In practice, these
long muscles may be spared, even though the lesion is
proximal. Distal ulnar lesions occur. According to the site,
there may be sparing of the muscles of the hypothenar
eminence and absence of sensory change.
If there is weakness of all the small hand muscles, you
b are probably dealing with a proximal lesion; combined
median and ulnar lesions are uncommon. If the other
Fig. 10.56 Carpal tunnel syndrome. Wasting of the left thenar
hand is normal, suspect a problem at the level of the
eminence (a). Failure of opposition of the left thumb (b).
brachial plexus or of the T1 root. The brachial plexus can
be damaged by trauma or invaded by tumour. Damage
to the upper trunk affects the fifth and sixth cervical
thumb to rotate during attempted opposition (Fig. 10.56). segments, damage to the middle trunk predominantly
The carpal tunnel syndrome predominates in women, affects fibres supplying the radial nerve, and damage to
often triggered by pregnancy. Although usually the lower trunk produces a global weakness of the hand.
idiopathic it can be triggered by other conditions, If the sympathetic fibres in the T1 root are involved, there
including rheumatoid arthritis, acromegaly, myxoedema will be an accompanying Horner’s syndrome (Fig.
and previous wrist fracture. Typically, the patient 10.58).
complains of nocturnal pain and paraesthesiae. The The cervical rib (thoracic outlet) syndrome results from
symptoms are often felt diffusely in the hand and forearm compression of the C8 and T1 roots or the lower trunk
rather than being confined to the digits supplied by the of the plexus by a fibrous band passing from the transverse
nerve. Sensory loss is often not conspicuous. Ask the process of the seventh cervical vertebra to the first rib.
patient to compare touch sensation on the two sides of Curiously, the hand weakness affects the muscles of the
the ring finger. If percussion of the median nerve at the thenar eminence much more than those supplied by the
wrist produces tingling in the digits (Tinel’s sign), ulnar nerve. A typical radiological feature is beaking of
compression at the site of percussion is likely. The test, the C7 transverse process (Fig. 10.59). If you find bilateral
however, is frequently negative even in proven cases. An weakness, with or without wasting, of the small hand
alternative test is to maintain forced flexion of the wrist muscles, you are dealing with a more diffuse process.
for several minutes to see if it triggers paraesthesiae in (Bilateral brachial plexus lesions are rare.) You have to
the fingers (Phalen’s sign). consider a peripheral neuropathy or a lesion of the
If the weakness is confined to the muscles supplied by anterior horn cell (e.g. syringomyelia or motor neuron
the ulnar nerve, you next need to determine the site of disease) (Fig. 10.60).
the lesion. The most common site is in the region of the
ulnar groove at the elbow, usually the consequence of
recurrent trauma and angulation, or in the cubital tunnel The hip
from pressure by the aponeurosis of flexor carpi ulnaris.
The hand muscles affected include the interossei, the STRUCTURE AND FUNCTION
hypothenar muscles and the third and fourth lumbricals. The hip is a ball and socket joint allowing flexion,
A characteristic deformity affects the fourth and fifth extension, abduction, adduction, and both internal and
290
Chapter
The hip 10
Fig. 10.58 Global wasting of the right hand (left and right),
together with a Horner’s syndrome (below left). Malignant invasion
of the lower trunk of the brachial plexus and the T1 root.
Fig. 10.59 Wasting of the small hand muscles of the right hand (left and middle) associated
with beaking of the right C7 transverse process (right).
external rotation. The neck of the femur forms an angle biceps) as extensors of the hip joint and flexors of the
of approximately 130° with the shaft. knee joint.
Muscles acting at the hip joint may have additional
actions on the spine or knee. The psoas major passes
from the lumbar spine to the lesser trochanter of the INSPECTION AND PALPATION
femur. In addition to flexing the hip, it flexes the lumbar The patient should be wearing only underpants if you are
spine. The iliacus passes from the iliac fossa, part of the to examine the hip joints satisfactorily. Begin with the
hip bone, and inserts principally into the lesser trochanter patient standing. Look for evidence of shortening of one
(Fig. 10.61). It acts as a hip flexor. The glutei arise mainly of the legs. Compensation for this is achieved by a scoliotic
from the ileum. The gluteus maximus is a pure hip posture or by flexion of the longer leg. An abduction
extensor; the other glutei principally act as abductors. The deformity is compensated by flexion of the ipsilateral
thigh is externally rotated by the obturator and adducted knee and adduction deformity by flexing the contralateral
by the adductor majoris. Several muscles connect the knee (Fig. 10.63). A flexion deformity is compensated by
pelvis with the tibia and fibula. The hamstrings comprise an exaggerated lordosis.
the biceps femoris, semitendinosus and semimembranosus With the patient still standing, assess the integrity of
(Fig. 10.62). They act (apart from the short head of the each hip joint and its surrounding muscles by asking the
291
Chapter
a b
Fig. 10.60 Bilateral wasting of the small hand muscles in (a) hereditary sensorimotor neuropathy and (b) motor neuron disease.
Hip flexors Hamstrings
psoas
major
gluteus
maximus
semitendinosus
biceps
(long head)
semimembranosus biceps
iliacus (short head)
Fig. 10.61 Origin and insertion of iliacus and psoas muscles.
Fig. 10.62 The hamstring muscles.

patient to stand first on one leg and then the other
(Trendelenburg’s test). Normally, as the foot is lifted the there is any joint tenderness, palpate over the middle of
pelvis tilts upwards on the same side. If there is an the inguinal ligament.
abnormality in the hip joint or weakness of the muscle
activity across it, the pelvis sinks downwards (Fig.
10.64). MEASUREMENT OF LIMB LENGTH
Now lie the patient flat. First determine whether the When measuring limb length, you need to distinguish
iliac crests can be positioned in the same horizontal plane between true and apparent shortening. Make sure that
at right angles to the spine (Fig. 10.65). If this is not the position of the two hip joints is comparable when
possible, there is an abduction or adduction deformity of measuring. The true length is measured from the anterior
one or other hip. Beware of the fact that flexion deformity superior iliac spine to the medial malleolus (Fig. 10.67).
of the hip can be concealed as the patient lies flat by a If one leg is shorter, suspect pathology in or around the
compensatory lumbar lordosis. To check for this, flex the hip joint of that side. Apparent length is measured from
opposite hip to its maximum, thereby eliminating the the umbilicus to the medial malleolus. A difference here,
lordosis. If a flexion deformity exists, the affected leg will without a difference in true lengths, indicates a lateral tilt
flex at the hip (Thomas’ test) (Fig. 10.66). The joint is so of the pelvis, most often due to adduction deformity of
deep that effusions are unlikely to be detected. To see if the hip.
292
Chapter
The hip 10
JOINT MOVEMENT
Compensatory postures
When measuring the range of hip movement, you need
to ensure that the pelvis remains stationary. To do this,
keep your free hand on the anterior superior iliac spine
to detect any movement.
To test flexion, bend the leg, with the knee flexed, into
the abdomen. Extension is best assessed by standing
behind the patient and drawing the leg backwards
until the point at which the pelvis starts to rotate.
Abduction is measured by taking the leg outwards,
again to the point where, by using the opposite hand, the
pelvis is felt to move. Internal and external rotation
are tested with the hip and knee flexed to 90° (Fig.
10.68).
Causes of hip pain vary, in terms of frequency,
according to the age of the patient. Osteoarthritis
frequently involves the hip joint. Pain is either local or
referred. Movements of the joint are both restricted and
painful. In advanced cases, shortening of the limb occurs
with external rotation (Fig. 10.69).
Fig. 10.63 Compensatory postures associated with (a) shortening
of one leg, (b) adduction deformity of the right leg and (c) flexed
deformity of the hips.
a b
Fig. 10.64 Trendelenburg’s sign. When the patient stands on the normal left leg the pelvis Fig. 10.65 Positioning the pelvis.
tilts to the left (a). When she stands on the right leg (where there was osteoarthritis at the
hip) the pelvis fails to tilt to the right (b).
a b
Fig. 10.66 Thomas’ test. The fixed flexion deformity of the right hip can be obscured by a compensatory lumbar lordosis (a). When the
lordosis is overcome by flexing the left hip, the right leg then lifts (b).
293
Chapter
Lower limb length Hip rotation
apparent length
of leg
true length
of leg
Fig. 10.68 Measuring the extent of hip rotation.
Fig. 10.67 True and apparent lengths of the lower limbs.
Risk factors
Osteoarthritis
• Age
• Obesity
• Hereditary
• Trauma
• Congenital joint anomalies
• Previous inflammatory joint disease
Knee pain
• Trauma Fig. 10.69 Advanced osteoarthritis of the left hip. The leg is
– dislocation shortened and externally rotated.
• Arthritis
– osteoarthritis are commonplace in elderly people. The leg may be
– rheumatoid arthritis shortened and externally rotated. The condition carries a
• Slipped femoral epiphysis high morbidity for elderly people and has a capacity to
• Osteochondritis (Perthes’ disease) progress to avascular necrosis of the femoral head.
• Infection Fractures of the femoral shaft are either traumatic or
– e.g. osteomyelitis pathological. Traction is the preferred treatment option
in children but internal fixation is used for adults.
Slip of the upper femoral epiphysis occurs in
adolescents, leading to pain and inability to weight
TRAUMATIC LESIONS bear.
Dislocations are usually posterior and may then be Groin strains are common in people involved in
accompanied by acetabular fractures. The leg is internally sporting activities. The pain is dull, exacerbated by hip
rotated, adducted and flexed. Sciatic nerve palsy is a movement and is likely to be the result of tears in the
potential complication. Fractures of the neck of the femur fibres of the hip flexors.
294
Chapter
The knee 10
a
Fig. 10.71 Right sciatic palsy.
Muscle function
Test the power of hip flexion, extension, abduction and
adduction (Fig. 10.70). Sciatic palsies are associated with
pelvic trauma, injuries to the buttock or thigh or infiltration
by tumour. The muscles supplied by the lateral popliteal
component of the nerve tend to be more affected than
those supplied by the medial popliteal branch (Fig.
10.71).
b The knee
Although principally a hinge joint, a limited range of
rotation is possible at the knee. Anteriorly, the capsule
is formed by the tendon of the quadriceps femoris and
the patella. At the sides, the capsule is strengthened by
the medial and lateral collateral ligaments. Within the
joint are the anterior and posterior cruciate ligaments
passing from the tibia to the lateral and medial
condyles of the femur, respectively (Fig. 10.72). Interposed
between the femoral condyles and the tibia are the
fibrocartilaginous semilunar cartilages. The joint capsule
is lined by synovium that partly surrounds the cruciate
c
ligaments. Communicating with the synovial cavity are
bursae that are related to the insertions or origins of
some of the tendons around the joint (Fig. 10.73).
Flexion-extension occurs between approximately 0°
and 150° (Fig. 10.74). A minor degree of hyperextension
can occur in some normal individuals. As full extension is
reached, the femur rotates medially because of the longer
articular surface of the medial condyle, tightening the
capsular ligaments in the process. Flexion is produced by
the hamstrings and extension by the quadriceps femoris.

With the patient standing, look for a knee deformity,
d either genu valgum (knock-knee) or genu varum (bow
leg). Now continue your inspection with the patient lying
Fig. 10.70 Testing the muscles acting at the hip joint: (a) flexion,
(b) extension, (c) adduction, (d) abduction. supine. The bulk of the quadriceps muscle is a sensitive
295
Chapter
Knee ligaments Knee flexion–extension

patella
anterior
cruciate
ligament
transverse
medial ligament
semilunar
cartilage
lateral
semilunar
medial
cartilage
ligament
tendon of
posterior quadriceps hyperextension
cruciate femoris
ligament 15º
ligament
of patella
lateral posterior
ligament cruciate
flexion 150º
ligament
medial
semilunar
Fig. 10.74 Flexion–extension at the knee joint.
cartilage
Fig. 10.72 The ligaments of the knee joint.
Knee bursa
quadriceps
muscle
gastrocnemius
bursa
suprapatellar
pouch
patella
semimembranosus patellar Fig. 10.75 Effusion in the suprapatellar pouch in a patient with
bursa ligament rheumatoid arthritis.
subpopliteal
recess
effusions are detectable only by palpation. First, try
popliteal
bursa
ballottement: the patellar tap test. Use your left hand to
infrapatellar
bursa
force any fluid out of the suprapatellar pouch and then
gently press the patella into the femur with the second
Fig. 10.73 Bursae related to the knee joint. and third fingers of your right hand. If there is a substantial
effusion the patella will spring back against your fingers
(Fig. 10.76a). For smaller effusions, look for the bulge
guide to the presence of knee joint pathology. If necessary sign. Again, force any fluid out of the suprapatellar pouch
measure the thigh of each leg at a comparable distance but at the same time anchor the patella with the index
from the joint margin. Next look for an effusion. If this is finger of the same hand. Next, gently stroke down
large, the swelling will extend from the suprapatellar between the patella and the femoral condyles, first on
region down either side of the patella (Fig. 10.75). Smaller one side then the other. If an effusion is present, a bulge
296
Chapter
The knee 10
a b
Fig. 10.76 Detection of an effusion. (a) Patellar tap. (b) Bulge sign.
appears on the other side of the knee during the

manoeuvre (Fig. 10.76b).
Palpate the joint and surrounding structures, looking
for any tenderness and also to assess the consistency of
any swelling.
JOINT MOVEMENT
Test the range of movement with the patient lying supine.
As you record the movement, palpate the joint for any
crepitus. In addition, move the patella laterally and
medially across the femoral condyles. Is the movement
painful or does it elicit crepitus? a
STABILITY
There are several important procedures that allow you to
determine the integrity of the collateral and cruciate
ligaments.
To test the collateral ligaments, attempt to abduct and
adduct the lower leg. If there is lateral instability, record its
degree (Fig. 10.77). For the assessment of cruciate ligaments,
bend the knee to a slight angle, sit on the patient’s foot
(better to ask permission first!) then tense the lower leg
first forwards then backwards. If either ligament is lax,
excessive movement will occur (Fig. 10.78). Damage to
b
these ligaments is almost always the consequence of
trauma. If the ligaments rupture, a bloodstained effusion Fig. 10.77 Testing the collateral ligaments of the knee.
results. Damage to the synovial lining will allow the blood
to track outside the joint margin.
ASSESSMENT OF THE SEMILUNAR CARTILAGES

Damage to the cartilages is common. In order to test
their integrity, bend the hip and knee to 90° and grip the
heel with your right hand while pressing on the medial
then lateral cartilage with your left (Fig. 10.79). Now
internally and externally rotate the tibia while extending
the knee. If there is a cartilage tear, its engagement
between the tibia and femur during the manoeuvre leads
to severe pain, a clunking noise and, sometimes, actual
locking of the joint (McMurray’s test).
Fig. 10.78 Testing the cruciate ligaments.
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Chapter
Fig. 10.79 McMurray’s test.
Fig. 10.80 Osteoarthritis of the knee. Bony swellings associated

Questions to ask with quadriceps wasting.
Knee pain
• Is the pain unilateral or bilateral?

• Has the patient noticed swelling of the joint?
• Does the knee lock in certain positions?
Knee pain
• Trauma
– fracture
– dislocation
– ligament damage
– cartilage damage
• Arthritis
– osteoarthritis Fig. 10.81 A Baker’s cyst that has partially ruptured into the calf.
– rheumatoid arthritis
• Osteochondritis dissecans necessitates surgical repair. Meniscal tears tend to occur
• Infection in young people as the consequence of a twisting injury.
– e.g. osteomyelitis The medial meniscus is usually affected. Effusion appears
• Bone tumours and the knee may lock, inhibiting complete extension.
• Referred The torn elements are removed arthroscopically.
– e.g. from the hip Patellar dislocation occurs laterally and tends to be
recurrent. Total knee dislocation is unusual and generally
the consequence of a road traffic accident. Fractures of
In osteoarthritis, periarticular tenderness, particularly the lower femur or upper tibia that involve the knee joint
at the insertion of the capsule and collateral ligaments, is are complicated by joint stiffness and accelerated
an important diagnostic clue. Later, bony swellings degenerative changes.
around the joint and secondary quadriceps wasting are
common (Fig. 10.80). Remember to look at the back of
MUSCLE FUNCTION
the joint: the popliteal fossa. Posterior synovial protrusions
(Baker’s cysts) are visible here. They can complicate Test the muscles responsible for knee extension and
rheumatoid arthritis, in which additional features include flexion, the quadriceps and hamstrings, respectively (Fig.
effusions, synovial swelling and deformity (Fig. 10.81). 10.82). Both quadriceps weakness and wasting can
accompany joint disease. If the knee joint is normal,
unilateral quadriceps weakness suggests either a femoral
TRAUMATIC LESIONS neuropathy or an L3 root syndrome. In the latter, there
Ligament sprains are not associated with detectable laxity is weakness of both quadriceps and the hip adductors,
and are treated with a support bandage or plaster. With associated with a depressed knee jerk and sensory change
ligament rupture, the consequent joint instability over the medial aspect of the thigh and knee (Fig. 10.83).
298
Chapter
The ankle and foot 10
L3 syndrome
Muscle Segmentary sensory Reflex

weakness change depression
quadriceps knee
hip adductors
Fig. 10.83 L3 root syndrome. Motor, sensory and reflex

b abnormalities.
Fig. 10.82 Testing knee extension (above) and flexion (below).
A femoral neuropathy can result from thigh trauma or

haemorrhage into the psoas sheath. In diabetes mellitus,
wasting of the thigh is more often the result of ischaemia
of the lumbar roots rather than being caused by a femoral
neuropathy. Consequently, the thigh adductors are also
affected. Femoral neuropathy leads to weakness and
wasting of the quadriceps, loss of the knee jerk and
sensory change over the anterior thigh and the medial
aspect of the lower leg (Fig. 10.84). If the nerve is damaged
at the level of the psoas sheath, hip flexion is also affected.
An obturator nerve palsy can follow surgery or pelvic
fracture or be secondary to an obturator hernia. Weakness
is confined to the thigh adductors, with altered sensation
over the thigh’s inner aspect.
Meralgia paraesthetica
It is worth mentioning meralgia paraesthetica. The patient
complains of pain, tingling and numbness over the Fig. 10.84 Left femoral neuropathy after profundoplasty.
anterolateral aspect of the thigh. There are no motor
changes. The condition is caused by compression of the
partly by movement at the midtarsal joints (20°). The
lateral cutaneous nerve of the thigh at the level of the
predominant movements of the toes are dorsiflexion and
groin, and is the commonest entrapment neuropathy of
plantar flexion (Fig. 10.85).
the lower limb.
The main muscles of the calf are the soleus and
gastrocnemius. The soleus acts purely as a flexor of the
The ankle and foot ankle, while the gastrocnemius flexes both the ankle and
the knee. Of the other muscles in the posterior
STRUCTURE AND FUNCTION compartment, the tibialis posterior inverts the foot,
Movements of the ankle are essentially confined to whereas flexor digitorum longus and flexor hallucis longus
extension (dorsiflexion) and flexion (plantar flexion). flex the toes and big toe, respectively (Fig. 10.86).
Inversion and eversion of the foot are partly achieved by The anterior compartment muscles include tibialis
movement at the subtalar joint (approximately 5°) and anterior, extensor digitorum longus, extensor hallucis
299
Chapter
Ankle and foot movements Calf muscles
ankle
plantaris
20º dorsiflexion
gastrocnemius
50º plantar flexion 5º eversion
5º inversion
forefoot metatarsophalangeal interphalangeal soleus

joint joint
tendo
calcaneus
60º
flexion Fig. 10.86 Muscles of the calf.
60º extension
Anterior tibial compartment muscles
30º 20º 40º flexion
eversion inversion
Fig. 10.85 Movements of the ankle, foot and big toe.
longus and the peronei (Fig. 10.87). Tibialis anterior

inverts the foot and dorsiflexes the ankle. The two
extensors dorsiflex the toes and big toe, respectively. The peroneus
peronei act as evertors of the foot. longus
tibialis
anterior
To assess the alignment of the feet at the subtalar joints,
look at the ankles from behind with the patient standing.
extensor
In a varus deformity, the foot will be deviated towards digitorum
extensor
the midline, in a valgus deformity away from it. With the hallucis
longus
longus
patient still standing, look for any foot deformity. Is the
arch of the foot exaggerated or absent? Is there deformity
or swelling of the toe joints? Remember to inspect the
sole of the foot as well as its dorsal aspect. Now palpate
the margins of the ankle joint. In an inflammatory
arthropathy, the whole joint is likely to be tender, with
corresponding pain on all movement. In ankle strain, the
tenderness is likely to be confined to one site with pain Fig. 10.87 Muscles in the anterior compartment of the leg.
predominantly occurring when the joint is moved in one
direction. Next palpate the heel and Achilles tendon. The the calf just below its maximal circumference. If the
latter is a fairly common site for rheumatoid nodules. To tendon is intact, the foot plantar flexes; if ruptured, no
detect tenderness in the metatarsophalangeal joints, movement occurs.
compress each one between your thumb and finger (Fig. Deformity of the foot is common. In flat foot, the
10.88). To test the integrity of the Achilles tendon, squeeze longitudinal arch is lost with the consequence that most
300
Chapter
The ankle and foot 10
a b c
Fig. 10.88 Palpating (a) the anterior aspect of the ankle joint and (b) and (c) testing for tenderness of the metatarsophalangeal joints.
or the whole of the sole comes into contact with the

ground (Fig. 10.89a). In pes cavus, the arch of the foot is Foot deformities
exaggerated, with accompanying hyperextension of the
toes (Fig. 10.89b). Hallux valgus predominates in women. a b
It consists of abnormal adduction of the big toe at the
metatarsophalangeal joint, with a bursa at the pressure
point over the head of the first metatarsal (Fig. 10.89c).
A hammer toe is characterised by hyperextension
at the metatarsophalangeal joint with flexion at the
interphalangeal joint. Painful thickenings of the skin c
(corns) are liable to develop at pressure points (e.g. over
the proximal interphalangeal joints) (Fig. 10.89d). d
Questions to ask
Foot deformities
• Has the deformity been present from birth?

• Does it affect both feet?
• Is it associated with joint pain or tenderness? Fig. 10.89 Foot deformities: (a) pes planus, (b) pes cavus, (c) hallux
valgus and (d) hammer toe.
JOINT MOVEMENT
Rupture of the Achilles tendon results in pain in the
The ankle joint proper is concerned with plantar and heel. The calf is swollen with a palpable gap in the tendon.
dorsiflexion. Inversion and eversion of the foot occur both Open operation is called for if the condition is detected
at the subtalar and midtarsal joints. To test this movement, early.
hold the heel firmly with one hand while inverting and Osteoarthritis can affect both the ankle and the foot.
everting the foot with the other hand. You have already In the foot, involvement of the first metatarsophalangeal
looked for tenderness in the metatarsophalangeal joints. joint leads either to deformity (hallux valgus) or fixation
Now test the range of flexion and extension. (hallux rigidus). Gout typically affects the same joint. In
an acute attack, there is intense pain associated
TRAUMATIC LESIONS with swelling and erythema of the overlying skin (see Fig.
Ankle sprains result from an inversion force typically 10.8). The reaction is secondary to deposition of urate
damaging the anterior talofibular ligament. Swelling salts within the connective tissues. If the hyperuricaemia
develops with pain on weight-bearing. The condition is is inadequately treated, urate deposits appear in
treated by a support bandage. periarticular and subcutaneous tissues. Typical sites
Pott’s fracture is a fracture-dislocation of the ankle, include the first metatarsophalangeal joint, the elbow,
sometimes requiring open reduction and fixation. the Achilles tendon and the ear (Fig. 10.90).
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Chapter
Fig. 10.90 Gouty tophi.
a b
c d
Rheumatoid arthritis involves both the ankle and the

foot. When the disease is established, subluxation of the
metatarsophalangeal joint is associated with flexion
deformity at the proximal interphalangeal joints (Fig.
10.91). A variety of other inflammatory reactions can
affect the ligamentous and tendon insertions around the
heel. Causative agents include trauma and the seronegative
arthritides.
MUSCLE FUNCTION
Test the individual muscles concerned with movement at
the ankle and foot. Start with the plantar and dorsiflexors
of the ankle, then of the toes (Fig. 10.92). Specifically
test the extensor of the big toe, extensor hallucis longus
(Fig. 10.93). Finally, test the evertors and invertors of the
foot.
Fig. 10.91 Rheumatoid arthritis of the feet.
a b c
Fig. 10.92 Testing (a) and (b) plantar flexion and dorsiflexion of the ankle and (c) dorsiflexion of the toes.
302
Chapter
Patterns of weakness in muscle disease 10
L5 and S1 syndromes
Muscle Sensory Reflex

weakness change depression
anterior posterior
extensor
hallucis none
L5 longus
eversion
hip extension
a L5
L5
plantar flexion
S1 knee flexion
hip extension ankle
and S1 S1
abduction
Fig. 10.94 L5 and S1 root syndromes.
Lumbar spondylosis commonly affects the L5 and

S1 roots. The motor deficit with the former is often
confined to extensor hallucis longus. There is no reflex
change but there may be sensory change over the medial
aspect of the foot. In an S1 root syndrome, there is
b weakness of plantar flexion of the foot (and potentially
also of the calf and buttock muscles) together with a
depressed or absent ankle jerk and sensory loss over the
lateral border of the dorsal and plantar aspects of the foot
(Fig. 10.94).
In lateral popliteal palsy, there is weakness of
dorsiflexion of the foot and toes and of the foot evertors.
The sensory change is often relatively inconspicuous,
sometimes being confined to a small area of loss over the
dorsum of the foot around the base of the first and second
toes. There are no reflex changes.
c Patterns of weakness in muscle disease

The pattern of weakness found in primary muscle
disease differs from that seen in nerve root or peripheral
nerve disorders. Conditions primarily affecting muscle
include a group of genetically determined disorders
(the muscular dystrophies), a group of inflammatory
disorders (e.g. polymyositis), various biochemical
and endocrinological dysfunctions and, finally, a
further genetically determined group associated with
myotonia.
Certain characteristics support a clinical diagnosis of
primary muscle disease. The weakness, which is usually
symmetrical, tends to predominate proximally. In the
d upper limbs, the periscapular muscles and deltoid are
weak but the hand muscles are spared. In the lower
Fig. 10.93 Testing the (a) long toe flexors, (b) extensor hallucis limbs, weakness of hip flexion and extension is often
longus, (c) peroneus longus and brevis and (d) tibialis posterior. conspicuous. The patient adopts a lordotic posture and
has a waddling gait.
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Chapter
Questions to ask
Patterns of weakness
• Is the weakness associated with sensory symptoms

or signs?
• Is there a family history of muscle disease?
• Is the weakness symmetrical?
• Is the weakness predominantly proximal or distal?
Trendelenburg’s sign is likely to be positive bilaterally

(see Fig. 10.64). There is particular difficulty getting
upright from a lying position. Typically, the patient turns
into the prone position, kneels then climbs up the legs
using the upper limbs in order to extend the trunk
(Gowers’ manoeuvre) (Fig. 10.95). Muscle wasting and
loss of tendon reflexes are late features of the myopathies.
In some of the muscular dystrophies, pseudohypertrophy
of muscle occurs because of infiltration by fat and
connective tissue (Fig. 10.96). Distal weakness sometimes
occurs in primary muscle disease, often then showing a Fig. 10.96 Pseudohypertrophy of the calves.
a b
Fig. 10.95
Gowers’ manoeuvre.
The patient having
reached a flexed
position has to
extend the trunk,
partly by pressing
on the table and
partly by pressing
on her thighs.
c d
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Chapter
Patterns of weakness in muscle disease 10
characteristic distribution. Weakness of the hands is a stiff, with thrusts of the trunk being used to assist
prominent feature of dystrophia myotonica, in which locomotion.
muscle weakness is accompanied by myotonia, particularly
of grip.
FOOT DROP GAIT
You will have noticed how the patient walks when
entering the consulting room. Having completed your Foot drop (Fig. 10.97b) can be either unilateral or bilateral.
limb assessment of joint and muscle you can now examine The former is usually the result of a lateral popliteal palsy,
the gait formally. Remember that disease of the joints of the latter is the consequence of a peripheral neuropathy.
the lower limbs can affect walking. The possibility will Increased flexion at the hip and knee allows the plantar
have been raised by the history and suggested by the flexed foot to clear the ground.
joint examination. If the patient has described a substantial
problem with gait, be ready to provide support when the ATAXIC GAIT
patient starts to walk. Ask the patient to walk for a few
An ataxic gait (Figs 10.97c, d) can reflect either loss of
metres, then turn and walk back towards you. You should
sensory information from the feet or a disorder of
observe both the pattern of leg movement and the posture
cerebellar function. In the former case, the patient stamps
of the arms together with control of the trunk. If gait
the feet down in order to overcome the instability.
appears normal, ask the patient to walk heel–toe, that is,
Consequently, patients with this problem are much more
‘as if on a tightrope’. If the patient appears nervous, walk
alongside them.
SPASTIC GAIT Questions to ask

Gait
In a hemiplegia (Fig. 10.97a), the arm is held flexed and
adducted while the leg is extended. In order to move • Does the patient trip?
the leg, the patient tilts the pelvis, which produces an • Is one shoe worn out more readily than the other?
outward and forward loop of the leg (circumduction). • Does the patient stagger to one particular side?
Failure to dorsiflex the foot leads to it scraping along • Does the patient, despite apparently severe ataxia,
the ground. If both legs are spastic, for example, seldom sustain injury?
because of spinal cord disease, the whole movement is
Gait disorders
a b c d e
Fig. 10.97 Gait disorders: (a) hemiplegic, (b) unilateral foot drop, (c) sensory ataxia, (d) cerebellar ataxia and (e) parkinsonism.
305
Chapter
unstable in the dark or with the eyes closed (positive one or both arms fail to swing. There may be a problem
Romberg’s test). initiating or arresting gait. Turning is difficult and requires
Cerebellar disease leads to a broad-based gait that is an exaggerated number of steps.
unaffected by the presence or absence of visual
information. Loss of truncal control produces erratic body
APRAXIC GAIT
movement. With unilateral cerebellar disease the patient
staggers to the affected side. In certain conditions (e.g. normal pressure hydrocephalus)
there is a particular problem with the organisation of gait
even though other skilled lower limb movements are
WADDLING GAIT spared. The patient is liable to freeze to the ground,
Patients with substantial proximal lower limb weakness unable to initiate movement.
waddle from side to side as they walk, from a failure to
tilt the pelvis when one leg is raised from the ground.
HYSTERICAL GAIT
There is usually an exaggerated lumbar lordosis. The
findings suggest a proximal myopathy. Here, walking is erratic and unpredictable. The patient
staggers wildly, often with an exaggerated movement of
the arms. Falls and injuries do not exclude the possibility
PARKINSONIAN GAIT of a hysterical conversion reaction. There is often a violently
Patients with Parkinson’s disease develop an increasingly positive Romberg’s test which the patient self-corrects.
flexed posture (Fig. 10.97e). Stride length diminishes and

Bones, muscles and joints Framework for the routine examination of
the musculoskeletal system
• Muscle strength declines with age; for example, grip
strength falls by approximately 50% between the • Use GALS as a screening history and examination
ages of 25 and 80 years process
• Muscle bulk declines with age, for example, in the • Screening history enquires about pain or stiffness,
small hand muscles dressing difficulty and any walking difficulty
• Some degree of ulnar deviation at the wrists can • The screening examination assesses four areas: gait,
occur with ageing spine, arms and legs (GALS)
• The range of joint movement lessens with age • For individual joints, during a more detailed
• Gait becomes less certain in elderly people, with a examination, a routine is followed of inspection,
tendency for the steps to shorten palpation and assessment of joint movement
• Elderly people tend to stand with slightly flexed hips • For individual muscles, the process incorporates
and knees inspection, palpation then formal testing of muscle
power, using the MRC scale of 0–5
• In the lower limbs, additional stretch tests are
available (straight leg raising and femoral stretch) to
test for nerve root irritation in the lumbosacral
region
306
11
The nervous system
Medical students often approach the neurological to one another. Surrounding the primary cortical areas
examination with trepidation, no doubt partly because of for movement, sensation and vision are the cortical
the complexities of the nervous system and partly because association areas. For example, the lateral geniculate
of the difficulties sometimes experienced in attempting body projects not just to the visual cortex (area 17) but
anatomical localisation on the basis of abnormal physical also to areas 18 and 19, parts of the visual association
signs. The problem for the student, however, often begins cortex (Fig. 11.1).
with a failure to acquire the skills necessary to elicit those The frontal lobe is separated from the parietal lobe
signs. If they are not identified correctly, mistakes in posteriorly by the central (rolandic) sulcus, while the
interpretation and diagnosis inevitably follow. temporal lobe lies below the lateral (sylvian) sulcus. The
This chapter summarises the examination of the central
and peripheral nervous systems, although it will seldom
be necessary to examine all the areas covered. Selection
is influenced partly by the patient’s history but also by Brodmann's cortical areas
cooperation, conscious state and level of fatigue. Certain
examination techniques demand a good deal of both
patient and examiner and if responses become erratic it 4
is better to return to the examination later. Students, and 6
sometimes doctors, are prone to examine only those
areas immediately accessible with the patient supine.
Remember to turn the patient over in order to assess the 39
spine and the muscles of the shoulder and pelvic girdles. 44 19 18
Always record your findings in full, avoiding irritating 17
acronyms (e.g. PERLA for pupils equal, reacting to light
and accommodation) and, if your examination has been
limited, state exactly what you have done (rather than
just ‘CNS’ followed by a tick). Remember that physical
signs can alter, sometimes rapidly, and repeating your
examination can give you useful insight into the 6 4
mechanisms of certain disorders.
19
The cortex 18
17
18
19
On the basis of differences in histological structure,
distinct areas can be identified within the cerebral cortex
(Fig. 11.1). Tracts within the cortex comprise efferent
pathways such as the pyramidal system, afferent pathways
such as the thalamocortical projections, association
fibres passing from regions within the hemisphere Fig. 11.1 Lateral and medial aspects of the cerebral hemisphere
and commissural fibres connecting regions contralateral showing some of Brodmann’s cortical areas.
307
Chapter
11 The nervous system
the arachnoid villae. The rate of CSF production is

Lobar boundaries approximately 120 ml/24 h.
Acquisition of memory requires a number of stages.
sulci central sulcus All data, whether visual or verbal, are recorded temporarily
in a short-term pool. A selective and active process then
passes some of the data into a long-term memory store.
Finally, an active process of retrieval restores the memory
to consciousness. Conventionally, memory is divided
into immediate, recent and remote components, although
these divisions are not absolute. Immediate or short-term
memory lasts a few seconds; recent memory relates to
activities or events occurring within a few hours or days
lateral sulcus superior
and remote memory to events of the past, for example,
temporal sulcus
the individual’s youth. Structures particularly associated
precentral gyri postcentral
with learning storage include the hippocampi, the
mamillary bodies and the dorsomedial nuclei of the
superior supramarginal thalami – the limbic system. Remote memory, however,
frontal can be retrieved even if these structures are damaged,
suggesting that it is stored predominantly in the
middle association cortex appropriate to the memory modality.
frontal Visuospatial ability is dependent mainly on
nondominant parietal lobe function. Language function
inferior is located in the left hemisphere in around 99% of right-
frontal
angular handed individuals. For left-handed individuals, some
60% have language dominance in the left hemisphere,
superior middle inferior
temporal temporal temporal with 40% in the right hemisphere. Something like 80%
of all left-handed individuals have mixed dominance,
Fig. 11.2 Lateral surface of the cerebral hemisphere. with language represented in both hemispheres. Within
the hemisphere, a posteriorly placed area (Wernicke) is
concerned with the comprehension of spoken language
and an anterior area (Broca) with language output. The
boundaries of the parietal, temporal and occipital lobes two are connected by the arcuate fasciculus (Fig. 11.5).
are not defined by a specific sulcus (Fig. 11.2). The integration of the auditory and visual data required
The brain is supplied by paired internal carotid and for reading and writing is achieved by the angular gyrus
vertebral arteries. The former terminate in the anterior (area 39) (Fig. 11.1).
and middle cerebral arteries, the latter in the basilar
artery, which ends by forming the posterior cerebral
arteries (Fig. 11.3). An anastomotic system at the base of Questions to ask
the brain (the circle of Willis) connects these various Higher cortical function
components. The lateral surface of the cortex is supplied
• Has there been a change in your mood?
predominantly by the middle cerebral artery. The anterior
• Has your memory deteriorated?
cerebral artery supplies a strip of cortex spanning its
• Do you have difficulty finding the right word in
superior margin, while the posterior cerebral artery
conversation?
supplies the occipital lobe and the inferior aspect of the
• Have you ever become lost while travelling a familiar
temporal lobe (Fig. 11.4). Normal cerebral blood flow, at
route?
approximately 55 ml/100 g/min, represents approximately
• Do you have difficulty dressing?
15% of cardiac output. The level of blood flow is largely
dependent on the PCO2 of arterial blood. Vasodilatation
and increased flow occur as PCO2 rises. During a specific
task orientated to speech, vision, hearing or motor activity, Although certain functions can be localised to specific
a focal increase in flow occurs in the appropriate part of cortical areas, other aspects of higher cortical function are
the cortex. represented more diffusely.
The ventricular system contains cerebrospinal fluid
(CSF) which originates predominantly in the choroid
plexuses of the lateral ventricles, then circulates through SYMPTOMS
the third ventricle and aqueduct before reaching the Many of the symptoms arising from a disorder of higher
fourth ventricle. The CSF exits through the foramina of cortical function will be more evident to a close friend or
the fourth ventricle and is eventually reabsorbed through relative than to the patient. Areas to cover, although
308
Chapter
The cortex 11
Cerebral arteries
anterior communicating artery

internal carotid artery
posterior anterior cerebral artery

communicating artery
middle cerebral artery

posterior
cerebral artery
superior
cerebellar artery
basilar artery
anterior
inferior
cerebellar artery
posterior
inferior
cerebellar artery
anterior spinal artery vertebral artery
Fig. 11.3 Arteries at the base of the brain.
some will be more evident during formal examination, history-taking from the patient becomes impossible.
are the following. Listening to the history allows estimation of the degree
of fluency in speech production, an assessment that will
Mood
continue during the course of the examination. Patients
This can be assessed by direct questioning but also are likely to volunteer any associated difficulty with
by observation of the patient’s behaviour. Is the mood reading (dyslexia) or writing (dysgraphia).
appropriate to the setting of the interview? Is the patient
passive, apparently disinterested or even denying disability?
Geographical orientation
Is there evident anxiety or a heightened state of arousal,
accompanied by restlessness and pressure of talk? Does The first sign of geographical disorientation may be the
the history suggest delusions or hallucinations? inability to follow a familiar route. If the impairment is
severe, patients can become lost in their own home but
Memory
at this level of disability the problem will be volunteered
The demented patient often denies loss of memory, by relatives rather than by the patient.
particularly once the condition is established. In the early
stages, however, patients can retain awareness of their
Dressing
difficulty, and sometimes volunteer that remote memory
is partly spared. Ask patients if they have encountered any problems
while dressing. Mistakes will usually have been rectified
Speech
by a relative but sometimes it is evident that the patient
Aphasic patients usually retain insight into their word- has lost understanding of the order and arrangement for
finding difficulty. At times the defect is so substantial that items of dress.
309
Chapter
Cerebral artery distribution Speech areas
Broca’s area Wernicke’s area
anterior cerebral arcuate fasciculus

middle cerebral
posterior cerebral
Fig. 11.4 The arterial supply of the lateral surface of the cerebral Fig. 11.5 Broca’s and Wernicke’s areas and their connecting arcuate
hemisphere. fasciculus.
comprehension. Start with two or three figures at 1s

Examination intervals, avoiding recognisable sequences. Normal
individuals can repeat a 5–7 digit sequence. Reverse
Assessment of the mental state begins as soon as the repetition of a set of digits is a more difficult process
patient enters the consulting room. During the history- not solely dependent on memory. Normal individuals
taking it will become apparent if there is an alteration can achieve a 4–5 figure sequence. The performance of
of mood, whether there is any disturbance in the serial sevens (subtracting seven serially from 100) is
comprehension or production of speech and whether the dependent on many factors. An abnormal response to
patient has retained insight. The physical appearance can this test does not specifically identify the patient with
be helpful. Demented patients often have a bemused dementia.
look, wondering why they are seeing a doctor. Evidence
Recent memory (new learning ability)
of self-neglect is usually concealed by the attentions of
friends or relatives. The way in which the patient responds The examination begins by asking the patient about
to questioning is of value in diagnosis. Demented patients recent events, although interpretation of the responses
tend to be inert and apathetic but a similar impression must take account of the patient’s premorbid intelligence
can be given by depressed individuals. and level of culture. Next ask the patient to memorise
three objects or, alternatively, a name, an address and
ORIENTATION a flower. Repeat the objects immediately and ask the
patient to repeat them, so that they have clearly been
Begin by assessing the patient’s orientation in time and registered. Over the next 10 min distract the patient
space. Establish the patient’s age and ask the time, date so that there is no opportunity for mental rehearsal,
and the name of the hospital or clinic in which the then ask the patient to repeat the data. Most normal
interview is taking place. Ask either how long the patient individuals can recall all the data at 10 min and 75% at
has been in hospital or the duration of the interview. 30 min. For further testing of verbal recall, give the patient
a short story containing a standard number of items and,
MEMORY as soon as the story has been told, ask the patient to
recount it.
Immediate recall
Visual memory can be tested by displaying drawings
For testing recall, use digit repetition, although a normal for a 5 s period then asking the patient to reproduce the
response also requires intact attention and adequate design 10 s later. Patients with visuospatial disorders will
310
Chapter
The cortex 11
Level of information
Visual memory test
Ask the patient to give an account of recent events and
a their understanding of them.
Calculation
Give the patient simple addition, subtraction, multi-
plication, and division sums. Assessment of the results
must take account of the patient’s education.
Proverb interpretation
Interpretation of proverbs tests both general knowledge
and capacity for abstract thinking. Proverbs of increasing
b
complexity are read out to the patient and their
interpretation recorded. A simple proverb to interpret
would be ‘A bird in the hand is worth two in the bush’;
more difficult would be ‘People in glass houses should
not throw stones’. Concrete responses, typically seen in
demented individuals, fail to see beyond the immediate
implications of the proverb. For example, a concrete
score: 0 score: 1 response to the second example would be that the glass
would get broken.
Constructional ability
Constructional ability can be tested by asking the patient
to copy designs of increasing complexity (Fig. 11.7). A
scoring system can be devised, low values for which
correlate well with the presence of brain damage. When
assessing the patient’s drawing, look for evidence
of unilateral neglect, suggesting the probability of a
score: 2 score: 3 contralateral parietal lobe syndrome.
Fig. 11.6 (a) Standard design and (b) reproductions scored from 0 GEOGRAPHICAL ORIENTATION
to 3.
Evidence concerning this may have been forthcoming
during history-taking but to test it specifically ask the
patient to draw an outline of their native country,
have problems with the task even if their visual memory placing within it a few of the principal cities. From the
is intact. The copies can be graded on a four-point scale, figure it should be apparent whether or not the patient
with a score of two, for example, indicating a recognisable has an overall defect of geographical localisation or
design containing minor flaws and three a near-perfect one based on neglect of one-half of the visual field
or perfect reproduction. Average individuals score two or (Fig. 11.8).
three on each test item (Fig. 11.6).
Remote memory SPEECH AND SPEECH DEFECTS
Ask the patient about schooling, childhood, work Determine the patient’s handedness. Asking which hand
history, marriage and, if relevant, the ages of any is used for writing is insufficient because some left-
children. The accuracy of the responses will need handed individuals have been taught to write with their
verification by a relative. Remote memory is spared right hand. Ask which hand is used for holding a knife,
in individuals with minor degrees of brain damage but using a hair brush, using a screwdriver or for playing
will inevitably be eroded in people suffering from racket sports. Check on the family history of
dementia. handedness.
Dysarthria
INTELLIGENCE This is a defect of articulation without any disturbance of
Testing a patient’s knowledge and abstract thinking must language function. Dysarthric patients have a normal
be performed in the light of their social background. speech content and, if they are able to write, their script
Inherent in all assessments of intelligence is an estimate will be free of dysphasic errors. Production of certain
of the patient’s premorbid ability. consonants depends on specific parts of the vocal
311
Chapter
Construction test Defect of geographical localisation
a
Seattle
New York
Los Angeles Chicago
Miami
Seattle
New York
c Chicago
Los Angeles
Miami
Fig. 11.7 Drawings of increasing complexity to be reproduced by Fig. 11.8 Control (above); patient with left-sided neglect (below).
the patient.
apparatus; P and B are labial sounds, D and T are Questions to ask

lingual.
Assessment of dysphasia
Dysphonia
• What is the patient’s handedness?
Dysphonia is a defect of speech volume and is usually the • Is the speech fluent or not?
result of a disorder limiting the excursion either of the • What is the level of comprehension?
muscles of respiration or of the vocal cords. • Can the patient repeat words or phrases?
Dysphasia (aphasia) • Can the patient name objects?
This is a defect of language function in which there is

either abnormal comprehension or production of speech
or both. Much of the patient’s language function will
Fluency
have been tested, although not deliberately, while taking
the history. Seldom is there no spontaneous speech, Fluency may be defined as the amount of speech produced
although in certain types of dysphasia, the patient may in a given period of time. Nonfluent speech, therefore,
be reduced to uttering short, meaningless phrases. contains a limited number of words. Typically, the patient
Dysphasic speech lacks grammatical content, displays makes a greater effort in speech production, the output
word-finding difficulty and contains word substitutions is often dysarthric and the phrase length limited. The
(paraphasias). Paraphasias are either whole word overall result is a loss of rhythm and melody (dysprosody).
substitutions (verbal, e.g. bread for table), syllable Fluent dysphasia is near or even above normal in terms
substitutions (literal, e.g. speed for feed) or complete of output. Melody tends to be retained and phrase length
nonsense words (neologisms, e.g. tersh). is normal. Despite this, the patient fails to produce critical,
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Chapter
The cortex 11
meaningful words and output is incoherent. Verbal premotor areas. Here conception of the action is spared
fluency can be formally tested by asking the patient to but not the ability to perform it. The nomenclature of
name as many objects as possible in a particular category apraxia has become much more complex, along with the
(e.g. fruits and vegetables) in a set length of time. recognition that ideational apraxia is a less definable
entity.
Comprehension Start by asking the patient to carry out a particular task
In testing comprehension, increasingly complex questions (e.g. ‘pretend to use a screwdriver’). If the patient is
can be asked but all should be answerable by a simple unable to perform the task, do it yourself and then
yes or no response. A substantial number of questions ask the patient to copy your movement. If a response is
requiring randomly distributed yes or no responses are still not forthcoming, provide the object in question
needed to avoid errors in interpretation. Avoid asking the and ask the patient to demonstrate its use. These three
patient to perform a skilled task; those individuals with tiers of command are in descending order of difficulty
apraxia will fail even if their comprehension is intact. for the apraxic patient. Instructions that will test
relevant movements include ‘put out your tongue’,
Repetition ‘pretend to whistle’, ‘salute’ and ‘show how you would
Start by asking the patient to repeat simple words, then use a toothbrush’. For whole body movements, ask the
give sentences of increasing complexity. Patients with patient to stand to attention or stand as if about to start
repetition difficulty often have a particular problem dancing. A more complex motor sequence is tested by
repeating ‘no, ifs, ands or buts’. asking the patient to go through a series of related
movements. For example, taking the cap off a toothpaste
Naming tube, squeezing the toothpaste onto a brush, then
A naming defect is found in virtually all dysphasic replacing the cap.
patients. Point to a succession of items, and ask the Right–left orientation
patient to name each one. Use objects commonly and less
commonly encountered and mix the categories rather A proportion of normal individuals have some problem
than restrict the test to, say, parts of the body. with right–left orientation. Patients who are dysphasic
can have problems understanding your commands. Start
testing with simple tasks (e.g. ‘show me your right hand’)
READING then gradually increase their complexity (e.g. ‘put your
Reading assessment must take account of educational left hand on your right ear’).
background. Ask the patient to read aloud, then test
comprehension by asking questions requiring simple yes Agnosia
or no responses. Patients with visual agnosia are unable to recognise
objects they see, despite intact visual pathways and
WRITING speech capacity. Show objects to the patient, asking the
patient to name each one and then allow the patient to
Dysgraphia is an inevitable accompaniment of dysphasia.
manipulate the object to see if this improves recognition.
Begin testing writing ability by asking the patient to write
Other forms of agnosia that can be tested include the
single words, then sentences, initially writing them
ability to name and recognise individual fingers (finger
spontaneously and then in response to dictation. After
agnosia) and colours (colour agnosia).
checking word content, note whether the writing is
crammed into one side of the page, suggesting the Conclusion
possibility of unilateral neglect.
It is clearly not appropriate to go through such an
extensive testing of higher cortical function in every
PRAXIS patient. Screening tests have been devised that allow
Apraxia is a disorder of skilled movement not attributable a rapid assessment of function. Such tests, for example,
to weakness, incoordination, sensory loss or a failure the mini mental-state test (Fig. 11.9) are useful,
of comprehension. The problem in movement may although their limitations need to be remembered
be confined to the limbs, to the trunk or even to when using them for screening purposes. A score of 20
the buccofacial musculature. Historically, apraxia was or less suggests the possibility of a cognitive disorder,
separated into two main categories. In ideational apraxia, particularly dementia.
destruction of the motor programming area in the
supramarginal gyrus impairs the conception of an
action, leading to defecits in using tools or performing PRIMITIVE REFLEXES
actions to verbal commands, though sparing the ability At this stage it is worth testing a number of primitive
to mimic. Ideomotor apraxia results from separation of reflexes (Fig. 11.10) before passing on to the cranial nerve
the motor programming area from the motor and examination.
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Chapter
Mini mental-state examination
Orientation
1. What is the year, season, date, month, day? (One point for
each correct answer.)
2. Where are we? Country, county, town, hospital, floor? (One
point for each correct answer.)
Registration
3. Name three objects taking 1 s to say each. Then ask the
patient to repeat them. One point for each correct answer.
Repeat the questions until the patient learns all three.
Attention and calculation

4. Serial sevens. One point for each correct answer. Stop after
Fig. 11.10 Primitive reflexes (hand and foot grasp).
five answers. Alternatively, spell ’world’ backwards.
Recall Grasp reflex

5. Ask for the names of the three objects asked in Question 3.
One point for each correct answer.
Stroke firmly across the palmar surface of the hand from
the radial to the ulnar aspect. In a positive response, the
Language examiner’s hand is gripped by the patient’s fingers,
6. Point to a pencil and a watch. Have the patient name them making release difficult. A foot grasp reflex is elicited by
for you. One point for each correct answer.
stroking the sole of the foot towards the toes with the
7. Have the patient repeat ’No, ifs, ands or buts.’ One point.
handle of the patella hammer. A positive response leads
8. Have the patient follow a three-stage command: 'Take the
paper in your right hand, fold the paper in half, put the
to plantar flexion of the toes.
paper on the floor.' Three points.
9. Have the patient read and obey the following: Close Clinical application
your eyes. (Write this in large letters.) One point.
10. Have the patient write a sentence of his or her own choice.
(The sentence must contain a subject and an object and DEMENTIA
make some sense.) Ignore spelling errors when scoring. Dementia is defined as a disorder or progressive memory
One point.
impairment coupled with at least one other cognitive
11. Have the patient draw two intersecting pentagons with
equal sides. Give one point if all the sides and angles are deficit (aphasia, apraxia, agnosia or a defect of executive
preserved and if the intersecting sides form a quadrangle. function), though in, for example, Alzheimer’s disease
the memory impairment may antedate the other features
Maximum score = 30 points
by some years. The majority of patients with dementia
have Alzheimer’s disease. Most of the remainder has
Fig. 11.9 The mini mental-state test. either cerebrovascular disease or a mixed pathology. In
the early stages of dementia, the most prominent
symptoms are apathy and lack of concentration, together
with defects in memory, and performance. Later, word-
The glabellar tap finding difficulty appears, with impaired comprehension
and paraphasic substitutions. The patient becomes
Tap repetitively with the tip of your index finger on the apraxic. There is a surprisingly poor correlation between
glabella. The blinking response should inhibit after three the presence of dementia and the size of the cortical
to four taps. In dementia and Parkinson’s disease, the sulci as demonstrated on computerised tomography (CT).
response persists. Ventricular size provides a better correlate (Fig. 11.11).
The palmomental reflex
Apply firm and fairly sharp pressure to the palm of the
hand alongside the thenar eminence. If the response is
positive, contraction of the ipsilateral mentalis causes a
puckering of the chin.
Pout and suckling reflexes
A positive pout response results in protrusion of the
lips when they are lightly tapped by the index finger.
A positive suckling reflex consists of a suckling
movement of the lips when the angle of the mouth is
stimulated. Fig. 11.11 CT scan of a patient with dementia.
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Chapter
The cortex 11
Examples of differential diagnosis

Vocal cord paralysis
Higher cortical function and speech With unilateral paresis, speech is hoarse and of reduced
volume. With bilateral paresis speech is virtually lost. If
• Dementia
the vocal cords are adducted, there will be inspiratory
– Alzheimer’s disease
stridor.
• Amnesia
– postherpes simplex encephalitis Cerebellar lesions
• Dysarthria
There is loss of speech rhythm with fluctuation in volume
– brainstem stroke
and inflexion. Slurring and staccato elements are found.
• Dysphonia
– myasthenia gravis Dysphonia
• Dysphasia Many patients who lose their voice do not have organic
– Broca type, Wernicke type disease. In spastic dysphonia, a form of dystonia,
• Apraxia inappropriate muscle contraction produces strained and
– corpus callosum lesions strangulated speech.
• Grasp reflex
– frontal lobe tumours
APHASIA
Nonfluent speech is associated with anterior hemisphere
lesions and fluent speech with posterior hemisphere
AMNESIA lesions. Further differentiation is based on the results
Damage to the limbic system results in a failure to learn of testing comprehension, repetition and naming
new memories (antegrade amnesia) associated with a (Fig. 11.12).
defect of memory for the more recent past (retrograde Broca’s aphasia
amnesia). In some instances, the patient confabulates
responses, particularly soon after the onset. Immediate The output is nonfluent and usually dysarthric,
memory remains intact. Conditions causing this picture comprehension is intact except for complex phrases and
include herpes simplex encephalitis and alcoholism. there are naming errors. The lesion lies in and around
Unilateral temporal lobe lesions can have a selective area 44 (Fig. 11.1) of the frontal lobe and may be vascular
effect on verbal or visual memory, according to whether or neoplastic.
the dominant or nondominant hemisphere is affected. Transcortical motor aphasia
This is similar to Broca’s aphasia except that repetition is
DYSCALCULIA retained. The pathological process (again, usually vascular
Dyscalculia can occur with bilateral or unilateral lesions.
Generally, the dyscalculia is greater when the dominant
hemisphere is affected.
Localisation of aphasia
CONSTRUCTIONAL APRAXIA AND
GEOGRAPHICAL DISORIENTATION
Constructional difficulty is particularly associated with
parietal lobe lesions of the nondominant hemisphere. It
appears relatively early in the course of Alzheimer’s
disease. Geographical disorientation has a similar
topographical significance.
DYSARTHRIA
Bulbar palsy
Combined weakness of the lips, tongue and palate. With
palatal weakness the speech is nasal. One cause is
myasthenia gravis. transcortical motor Broca
transcortical sensory Wernicke
Pseudobulbar palsy
conduction
Speech is hesitant and has an explosive, strangulated
quality. When severe, diction is almost impossible Fig. 11.12 Anatomical sites associated with the various aphasic
(anarthria). Motor neuron disease can cause this picture. syndromes.
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Chapter
or neoplastic) is located above or anterior to Broca’s with lesions affecting both the left occipital cortex and the
area. splenium of the corpus callosum and is most commonly
the result of an occlusion of the posterior cerebral
Wernicke’s aphasia
artery.
Here the patient has fluent, easily articulated speech but
there are frequent paraphasias and meaning is largely AGRAPHIA
absent. Comprehension and repetition are severely
impaired and attempts at naming produce paraphasic Although virtually all aphasic patients have agraphia,
errors. The patient is often described as confused. many patients with agraphia are not aphasic. Writing
skill is also affected by motor disability, involuntary
Conduction aphasia movements and visuospatial disorders.
Conduction aphasia is fluent but not to the degree seen
in Wernicke’s aphasia. Interruptions to the speech rhythm
are frequent but there is no dysarthria. Naming Review
is imperfect but comprehension good. Despite this, Assessment of higher cortical function
repetition is severely abnormal. Reading, at least out
loud, and writing are impaired. The condition occurs with • Orientation
disruption of the arcuate fasciculus connecting the – time, place and person
posterior temporal lobe to the motor association cortex • Memory
(Fig. 11.12). Cerebrovascular disease is the most common – immediate, short-term, remote
cause. • Level of information
• Calculation
Transcortical sensory aphasia • Proverb interpretation
Transcortical sensory aphasia is fluent but frequently • Constructional ability
interrupted by repetition of words or phrases initiated • Geographical orientation
by the examiner (echolalia). Despite the readiness and • Speech
accuracy of the patient’s repetition, comprehension – articulation, volume, fluency, comprehension,
is severely impaired. Naming is poor and reading repetition, naming
comprehension defective. The responsible anatomical • Reading and writing
site is less well localised than for some of the other forms • Praxis
of aphasia but lies in the borderlands of the temporal and • Right–left orientation
parietal lobes of the dominant hemisphere. • Gnosis
Anomic aphasia
Anomic aphasia is fluent and interrupted more by pauses
than by paraphasic substitutions. Comprehension is APRAXIA
relatively preserved, repetition is good and naming is The pathway involved in performing a skilled task to
affected but to a varying degree. There is no specific command begins in the auditory association cortex of
anatomical location. Anomic aphasia can be the final the dominant hemisphere then passes to the parietal
stage of recovery from other forms of aphasia and is seen association cortex, subsequently travelling forwards to
with both structural and metabolic brain disease. the premotor cortex and finally the motor cortex itself.
Interruption of this pathway at any point results in an
Global aphasia
ideomotor apraxia affecting both the dominant and
Global aphasia affects all aspects of speech function. nondominant hands (Fig. 11.13). The pathway from the
Output is nonfluent and comprehension, repetition, dominant to the nondominant premotor cortex (D–D)
naming, reading and writing are all affected, often to a passes through the anterior corpus callosum. A lesion
severe degree. The causative pathology occupies a there will produce an apraxia confined to the left hand.
substantial part of the language area of the dominant Whole body movements tend to be relatively spared even
hemisphere and is usually an extensive infarct in middle when limb ideomotor apraxia is substantial. Ideational
cerebral artery territory. apraxia is usually the consequence of bilateral hemisphere
lesions or predominant left hemisphere dysfunction.
DYSLEXIA AND ALEXIA
Dyslexia refers to developmental disorders of reading, RIGHT–LEFT DISORIENTATION
and alexia to disorders secondary to acquired brain Right–left disorientation is usually the result of a
damage. Alexia with agraphia is found with lesions of the posteriorly placed dominant hemisphere lesion.
angular gyrus of the dominant hemisphere. Alexia Gerstmann’s syndrome comprises right–left dis-
without agraphia in right-handed individuals is associated orientation, finger agnosia, dysgraphia and dyscalculia.
316
Chapter
The psychiatric assessment 11
lobe. A foot grasp or tonic plantar reflex can be one of

The pathway for a skilled motor task
the earliest signs of a frontal lobe lesion.
The psychiatric assessment

C Make sure that the patient understands who you are, and
D B the purpose of the interview. Privacy is particularly
E important when sensitive issues are being explored. To
A
begin with, avoid making notes, as this can detract from
the relationship you are trying to establish with the
patient. During this preliminary phase, observation of the
patient’s posture, gestures and facial expression may
D
provide information regarding mood and feeling. The
D
depressed patient appears apathetic, has little expressivity
and may well be reluctant to discuss the history. The
E E agitated patient is restless.
A C HISTORY OF PRESENT CONDITION

This proceeds in much the same way as history-taking
from a patient with a physical complaint. Indeed, physical
B symptoms often predominate in those individuals with a
primary psychiatric illness. Try to establish when the
patient last felt well, as a means of determining the overall
length of the history and as a means then of establishing
the chronological order of subsequent symptoms. If
necessary, interrupt the patient if there is digression into
Fig. 11.13 Pathway involved in the formulation and performance of
a skilled motor task.
other areas, for example current social issues, through
making clear that you are interested in those issues, and
will wish to return to them later. Sometimes directive
questions are needed to focus the patient’s attention on
If all four components are present, the causative pathology a particular symptom, for example headache, in order to
is likely to lie in the dominant parietal lobe, though doubt explore that symptom in greater detail. As the history
has been expressed regarding its specificity. proceeds, open questions will be partly replaced by closed
questions, answerable by a simple yes or no response.
VISUAL AGNOSIA Sometimes signs of emotional distress may appear as
certain issues are raised. Rather than ignoring these,
One form of visual agnosia is caused by a disconnection
gently probe them, even if this temporarily diverts the
between the visual cortex and the speech area. Patients
course of the history.
can recognise objects and demonstrate their use but are
Quite often, patients only indirectly refer to stressful
unable to name them. Bilateral temporo-occipital lesions
issues by giving oblique reference to them in the course
are the usual cause. In the other form of visual agnosia,
of describing their physical symptoms. Try to pick up
recognition of objects fails but their use can be
these cues and develop the relevant issue. Failure to
demonstrated if the object is placed in the hand. In other
detect them will deter the patient from discussing them
words, sensory information can bypass the defect of
further.
visual recognition, which is a consequence of damage to
Many symptoms are common to both physical and
the visual association cortex in both hemispheres, usually
psychiatric illness but others are more specifically within
vascular in nature.
the territory of psychiatry.
PRIMITIVE REFLEXES
SPECIFIC SYMPTOMS
The palmomental reflex is found bilaterally in some
Mood
normal individuals but a unilateral palmomental reflex
suggests a contralateral frontal lobe lesion. Snout and Enquire whether the patient, or a relative, has noticed
suckling reflexes are elicited in patients with diffuse any mood change. A particularly valuable question when
bilateral hemisphere disease. Bilateral grasp reflexes are screening for depression is whether the individual has
of limited localising value but a unilateral response is lost pleasure in their normal activities (anhedonia).
associated with pathology in the contralateral frontal Supplementary to this will be enquiries regarding sleep
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Chapter
pattern, loss of libido and suicidal ideation. Sometimes Symptoms and signs
the patient denies flattening of mood, when that is all too
Somatic and psychic symptoms of anxiety
evident from the interview. Such discrepancies should be and depression
carefully recorded.
Patients will usually complain of anxiety but sometimes Anxiety Depression
its somatic manifestations, for example palpitations, Somatic Palpitations Altered appetite
sweating and tremulousness, predominate. The anxiety Tremor Constipation
may be chronic and spontaneous or be triggered acutely Breathlessness Headache
by a specific stimulus – phobic anxiety. Fatigue Bodily fatigue
Patients seldom complain of euphoria – a feeling of Diarrhoea Tiredness
limitless physical and mental energy. There is likely to be Sweating
a pressurised manic quality to the patient’s conversation, Psychic Feelings of tension Apathy
coupled with physical restlessness. Irritability Poor concentration
Difficulty sleeping Early morning waking
Abnormal thoughts
Fear Diurnal mood swing
These will be elicited only by sensitive questioning. Depersonalisation Retardation
The patient can be understandably reluctant to reveal Guilt
certain abnormal thoughts. It may be apparent from
the interview that the patient’s thought pattern is
difficult to follow or that abnormal thoughts have
pervaded the conversation. Ask patients about paranoid
ideas, in other words, whether they feel people are against Abnormal perceptions
them. Ask whether certain thoughts or ideas regularly These are auditory or visual phenomena that other
intrude into their thinking, or whether they believe their individuals are not aware of.
thoughts are being interfered with or influenced Hallucinations are experiences that have no objective
by external agencies. Thought disorders include the equivalent to explain them. They are predominantly
following. visual or auditory but can occur in other forms, for
Delusions These are beliefs which can be demonstrated example of smell or taste in patients with complex partial
to be incorrect but to which the individual still adheres. seizures. Visual hallucinations can be unformed, for
Members of the Flat Earth Society are deluded. Often example an ill-defined pattern of lights, or formed, the
there is an element of reference, in other words that individual then describing people or animals, often of a
actions or words are directed specifically at that individual frightening aspect. Visual hallucinations are more often
even if they appear on a global platform, for example a feature of an organic brain syndrome, e.g. delirium
television. Paranoid delusions contain a persecutory tremens or adverse drug reaction, than a functional
element. Delusions of worthlessness are particularly psychosis, e.g. schizophrenia. Auditory hallucinations are
associated with depressive illness. also either unformed or formed. They are found more
often in the functional psychoses than in organic brain
Obsessions These are recurrent thoughts which often disease. The voices can take on a persecutory quality in
result in the performance of repetitive acts (compulsions). schizophrenia and an accusatory element in depression.
The patient is aware that they are inappropriate but In déja and jamais vu, intense feelings of a relived
cannot resist returning to them or acting upon them. experience or a sensation of strangeness in familiar
Examples of obsessional thought include convictions that surroundings occur, respectively. Both can be a feature of
a particular individual is antagonistic or that a spouse is everyday life but when pathological are usually epileptic.
unfaithful. Illusions are misinterpretations of an external reality: all
of us have this when watching a magician at work. In
depersonalisation, the individual feels a detachment from
the normal sense of self; in derealisation, the individual
feels a detachment from the external world. Both occur
Questions to ask in neurotic illnesses but also, periodically, in normal
individuals.
Psychiatric assessment
• Do you feel unduly anxious or depressed?

Cognition
• Do you repeat certain tasks over and over again? The assessment of higher cortical function has already
• Do you feel people are against you? been discussed. It is necessary to distinguish cognitive
• Have you heard or seen things that are not there? impairment due to dementia from cognitive impairment
• Do you ever lose the sense of yourself or your due to delirium. In the latter there is clouding of
environment? consciousness, usually manifested as reduced awareness
of, or response to, the environment.
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Chapter
The psychiatric assessment 11
THE FAMILY HISTORY DRUG HISTORY

Begin by obtaining details of the patient’s father and Determine alcohol consumption, but be aware of the
mother, in terms of their current age (or age at death), possibility that the figure does not correspond to actual
their own quality of health, whether they had any history intake. Features suggesting alcohol dependency include
of psychiatric disorder and the quality of the patient’s early morning drinking, morning vomiting, taking a drink
relationship with them. Ask similar questions about the before an interview, erratic work attendance and drinking
patient’s siblings. Questions regarding the patient’s own in isolation. Ask about narcotic exposure, the use of softer
children are usually included in the personal history. drugs such as cannabis and exposure to tranquillisers. If
Genetic factors are particularly strong in schizophrenia the patient is using codeine derivatives, ascertain for
and manic-depressive psychosis. what purpose and the dosage.
THE PERSONAL HISTORY PERSONALITY PROFILE

Childhood Evidence suggesting changing personality and mood is
It is unlikely patients will have accurate details of their often better provided by colleagues, relatives or friends
birth or early development unless there was a particular than by the patient. Questionnaires exist for the
problem with them. A direct question to the patient assessment of personality, but even without them the
regarding whether they were happy or unhappy in patient’s attitude and behaviour, in terms of work and
childhood is useful. Some ‘happy’ responses turn out to social relationships, personal drive, level of dependence,
be rather less so with further delving. If there is an ambition and authority and response to stress will indicate
expression of remembered unhappiness, explore it further the nature of the patient’s personality.
in terms of relationships with parents and any physical
illness.
Examination
Schooling and further education
Establishing the details of this is helpful in forming an The concept of the psychiatric examination needs to be
assessment of the patient’s premorbid intelligence. At the interpreted broadly. A physical examination is necessary
same time, enquire about friendships or a tendency to but the most telling diagnostic details will be revealed by
isolation, and about teasing or bullying. an exploration of the patient’s mental state, emerging as
much from the history as from the answers to specific
Sexual development questions.
For female patients, enquire about the age of the
menarche and how they attuned to adolescence in terms
of menstruation and sexuality. For men, discussion should
include whether their sexuality could be discussed in the
ORGANIC MENTAL STATES
home and how they acquired their sexual experience.
Further issues relating to sexual development, for example In organic mental states, a specific pathological basis for
homosexual experiences, are best left, at this stage, for the mental disorder has been established. Acute forms
the patient to raise. include the toxic confusional states, characterised by
alteration of the conscious level, disordered perceptions
Marital history (e.g. visual hallucinations), restlessness and thought
An overall outline includes the age of the spouse when disorder. Almost any structural or metabolic disorder can
the marriage occurred, the overall quality of the trigger the reaction. Examples include encephalitis, head
relationship, the state of the sexual relationship and injury and alcohol withdrawal. The principal chronic
details of any unease. organic mental state is dementia.
Occupational history
FUNCTIONAL MENTAL STATES
Ask how many jobs the patient has had, reasons for
leaving previous posts, the quality of relationships in the In functional mental states, a specific underlying
workplace and the level of job satisfaction. If there has pathological or metabolic cause has not been identified.
been one or more periods of unemployment, explore Psychotic states are those in which the individual
what effect this has had on the patient’s overall welfare. has lost insight and neurotic states are those in
which insight is preserved. The distinction is not
absolute, however, and the terms are best avoided. In
PAST MEDICAL HISTORY affective disorders, for example, anxiety, depression and
This follows the usual pattern, and includes history of mania, an alteration of mood is a major feature of the
both physical and mental illness if these have occurred. illness.
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Chapter
disorders. Thought disorder leads to irrational
conversation, in which the development of ideas is
Organic and functional mental states
either blocked or moves suddenly into unconnected
• Acute anxiety state channels. The emotions are blunted and the patient
• Chronic anxiety state becomes increasingly withdrawn. Delusions are
• Endogenous depression prominent and frequently contain paranoid elements.
• Reactive depression Auditory hallucinations are particularly characteristic of
• Manic depression schizophrenia.
• Schizophrenia
• Obsessional states OBSESSIONAL STATES
• Conversion hysteria
• Drug- and alcohol-related disorders In obsessional states, a preoccupation with mental or
• Toxic confusional state physical acts predominates. An obsessional personality
• Dementia displays these characteristics but not to the point where
they interfere with the normal activities of life. In
obsessional states, however, the relevant thought or
action takes on a compulsive quality, ineffectively
Questions to ask countered by the patient. Obsessional symptoms can
Mental state
feature in other psychiatric illnesses.
• For anxiety
– Are the symptoms provoked by particular
Symptoms and signs
environments?
• For depression The psychiatric patient
– Are there suicidal thoughts? A full examination is performed to exclude any physical
• For schizophrenia disorder that may contribute to the patient’s condition
– Has the patient had auditory hallucinations?
– Does the patient believe his or her thoughts are
controlled by others?
HYSTERIA (CONVERSION HYSTERIA)
Hysteria is a disorder in which physical symptoms or
signs exist for which there is no objective counterpart and
PHOBIAS
which require, in the case of signs, an elaboration on the
Phobias are a particular form of anxiety triggered by a part of the patient of which he or she is unaware. Many
specific environment or circumstance. Agoraphobia, for of the symptoms are referred to the nervous system, for
example, results in a fear of leaving the home, particularly example, memory loss, paralysis, unsteadiness and visual
if this involves entering crowded places. impairment. Malingerers, on the other hand, consciously
elaborate their disability.
DEPRESSIVE ILLNESS
Depressive illnesses include those triggered primarily by HYSTERICAL PERSONALITY
genetic or constitutional factors (endogenous) and those Hysterical personality is distinct from hysteria, although
precipitated by adverse external events (reactive). individuals with this personality trait may develop
Increasingly, the distinction is felt to be artificial. conversion reactions. The hysterical personality is
characterised by superficiality and shallow emotional
MANIA AND HYPOMANIA responsiveness combined with a histrionic overwrought
reaction to events.
In mania and hypomania (its lesser form), there is pressure
of talk and physical activity. Patients lack insight and
react adversely if their grandiose schemes are questioned.
Headache and facial pain
In manic-depressive illness, the mood fluctuates between
two extremes.
HEADACHE
Headache is a common complaint. Often the history
SCHIZOPHRENIA suffices to separate the more serious causes. The length
Schizophrenia has been classified into a number of types, of history is particularly important, rather then necessarily
although the entities defined are not absolutely distinct. the severity of the pain. Critical issues are whether the
It is characterised by thought disorder, blunting of pain is continuous or intermittent and, if the latter, what
emotional responses, paranoid tendencies and perceptual is the duration of individual attacks. There may be
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Chapter
The olfactory (first) nerve 11
particular precipitants for attacks, e.g. alcohol triggering causes will generally be associated with revealing local
an attack of cluster headache. Accompanying symptoms symptomatology, e.g. focal facial tenderness. Some facial
should be sought, e.g. nausea or vomiting. As for any pain is more or less continuous, but an important cause
pain, it is important to determine whether there are of severe, but episodic, facial pain is trigeminal neuralgia.
relieving factors. Patients often find it difficult to describe Again seek the quality of the pain, its duration, if it is
the quality of their pain – it may be helpful to provide episodic, and its severity. Ask for specific triggers, e.g.
them with a list of alternatives. particular trigger zones on the face, palpation of which
can precipitate an attack of trigeminal neuralgia. In some
Examination
instances facial pain is referred from the ear.
With recent onset headache, careful fundoscopy is
Examination
essential to exclude the presence of papilloedema.
Patients will seldom be seen during a migraine attack; Determine if the patient has any trigger zones. Patients
between attacks their physical examination will be experiencing trigeminal neuralgia are unlikely to allow
normal. Patients with tension (muscle contraction) you to examine the face.
headaches often show focal or diffuse scalp tenderness.
Patients with cranial arteritis have tenderness of the scalp
vessels which are more likely to show reduced rather Questions to ask
than absent pulsation. Facial pain
• Are there accompanying dental or sinus symptoms?

Questions to ask • What is the quality of the pain?
Headache • If paroxysmal, does the pain have any triggers?
• Are there accompanying symptoms suggesting a
• How long has the headache been present?
psychological problem?
• Is the headache continuous or episodic?
• If continuous, how long do the attacks last?
• What is the quality and severity of the pain?
• Are there any triggering or relieving factors? THE CRANIAL NERVES
• Are there any accompanying symptoms?
The olfactory (first) nerve
Differential diagnosis STRUCTURE AND FUNCTION
Headache The olfactory epithelium contains specialised receptor
• Migraine cells and free nerve endings, the latter derived from
• Tension headache the first and second divisions of the trigeminal nerve.
• Cluster headache Unmyelinated axons from the receptor cells traverse the
• Analgesic abuse headache cribriform plate before synapsing in the olfactory bulb.
• Cranial arteritis From here, the olfactory tract passes backwards, dividing
• Intracranial mass lesion into lateral and medial roots in the region of the anterior
perforated substance. The more important lateral root
projects predominantly to the uncus of the ipsilateral
temporal lobe.
Red flag – urgent referral Molecules derived from particular odours are absorbed
Recent onset of headache into the mucus covering the olfactory epithelium. From
here they diffuse via ciliary processes to the terminal
If accompanied by:
processes of the receptor cells where they bind reversibly
• scalp arterial tenderness – consider cranial arteritis
to receptor sites. This initiates an action potential in the
• motor, sensory or speech disorder – consider a
olfactory nerve with a firing frequency related to the
space-occupying lesion of some sort
intensity of the stimulus.
• papilloedema – consider space-occupying lesion or
Women have a more sensitive sense of smell than
benign intracranial hypertension
men. In both sexes, smell sensitivity declines with age.
Many healthy individuals have difficulty naming or
describing the quality of a particular odour even though
FACIAL PAIN they can distinguish it from others. The value of a
Facial pain is commonly of psychological rather than particular odour for the testing of olfactory nerve function
neurological origin. The first step in analysing facial is determined principally by how selectively it stimulates
pain is to determine whether it might be related to local the specialised receptor cells rather than the free
causes, e.g. a dental abscess or focal sinus infection. Such trigeminal endings. Odours stimulating the latter include
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Chapter
peppermint, camphor, ammonia, menthol and anisol.

Retinal nerve fibres
Highly selective stimulants of olfactory nerve endings
include β-phenyl ethyl alcohol, methyl cyclopentenolone
and isovaleric acid. Coffee, cinnamon and chocolate are
useful everyday odours for the bedside testing of smell.
optic
disc
Symptoms and signs
nasal fovea temporal
Disturbance of smell
• Hyposmia-partial loss
• Anosmia-total loss
• Hyperosmia-exaggerated sensitivity
• Dyosmia-distorted sense
Fig. 11.14 Representation of the course of the retinal nerve fibres.
Disturbances of olfaction almost directly but fibres from the temporal border
pass almost vertically, both superiorly and inferiorly,
• Post-traumatic anosmia
before arching around the other foveal fibres on their way
• Postinfective anosmia
to the optic disc (Fig. 11.14). Axons in the papillomacular
• Olfactory hallucinations in complex partial seizures
bundle originate in the cones of the fovea and occupy a
substantial proportion of the temporal aspect of the optic
disc. Fibres from the superior and inferior parts of the
periphery of the retina occupy corresponding areas in
SYMPTOMS
the optic nerve. As the papillomacular bundle approaches
The disturbances of smell that occur are defined in the the chiasm, it moves centrally. The crossing, nasal,
‘symptoms and signs’ box. For loss of smell, determine macular fibres occupy the central and posterior part of
whether it is bilateral or unilateral. the chiasm.
The superior peripheral nasal fibres cross more
Examination posteriorly than the ventral fibres, which loop slightly
into the terminal part of the opposite optic nerve
The most convenient method for testing smell uses (Fig. 11.15). Crossed and uncrossed fibres are arranged
squeeze bottles bearing a nozzle that can be inserted into in alternate layers in the lateral geniculate body. The
each nostril in turn. The patient is asked either to identify optic radiation extends from the lateral geniculate body
the smell or to describe its quality. to the visual (striate) cortex, area 17 (Fig. 11.1). The
ventral fibres of the radiation loop forward towards the
tip of the temporal lobe. The visual cortex is situated
Clinical application along the superior and inferior margins of the calcarine
fissure, extending approximately 1.5 cm around the
Olfaction is commonly disturbed by upper respiratory
posterior pole. The macular representation lies posteriorly,
tract infection or local nasal pathology. Hyposmia can
with dorsal and ventral retina above and below the
persist after an apparently banal viral illness and also
fissure, respectively. The unpaired outer 30° of the
after head injury. Smell sensitivity is diminished in
temporal field is represented in the contralateral
dementia. Unilateral hyposmia is rarely the presenting
hemisphere at the anterior limit of the striate cortex
symptom of a subfrontal meningioma. Olfactory
(Fig. 11.16).
hallucinations occur in complex partial seizures.
Conditions of high (photopic) illumination activate
cone photoreceptors, providing high spatial resolution
and colour vision sense. Colour appreciation depends on
The optic (second) nerve three types of cone with spectral sensitivities spanning
the range of colour vision. Low-illumination (scotopic)
responses are mediated by rods.
Two types of retinal photoreceptor, rods and cones, have
been identified in humans. At the fovea only cones are
SYMPTOMS
found, with rods predominating in the periphery. Fibres
from the nasal aspect of the fovea pass directly to the A number of questions are appropriate when assessing
optic disc. Fibres from above and below the fovea pass the patient’s complaint of vision loss or alteration.
322
Chapter
The optic (second) nerve 11
Crossed and uncrossed fibres
decussating fibres
nondecussating fibres
optic nerve
optic tract
Fig. 11.15 Crossed and uncrossed fibres from the macula and the peripheral retina.
Representation of right visual field
90 90
105 75 105 75
left right
120 80 60 120 80 60
70 70
135 45 135 45
60 60
50 50
150 30 150 30
40 40
30 30
165 15 165 15
20 20
10 10
90 80 70 60 50 40 30 20 10 10 20 30 40 50 60 70 8090 0 90 80 70 60 50 40 30 20 10 10 20 30 40 50 60 70 8090 0
180 180
10 10
20 345 20 345
195 195
30 30
40 40
210 330 210 330
50 50
60 60
225 315 225 315
70 70
240 80 300 240 80 300
255 285 255 285
270 270
posterior pole splenium of the
of left occipital lobe corpus callosum
Fig. 11.16 The right visual field in the left occipital cortex.
The visual acuity is then expressed as the ratio of the

Examination distance between the patient and the card (usually 6 m),
to the figure on the chart immediately above the smallest
VISUAL ACUITY visible line. An acuity of 6/18, therefore, indicates that, at
Visual acuity is tested in conditions of high illumination, 6 m from the chart, the patient is able to read down only
producing a measure of cone function. The Snellen chart to the 18 m line. Make sure the patient wears glasses if
is used for testing distance vision. With the patient at the they contain a distance correction. If the patient’s glasses
distance shown above a particular line, the visual angle are not available, reading through a pinhole will partly
subtended by a letter in that line is 5' and by individual correct for any myopia. If unable to read the 60 m line at
components of the letter, 1' (Fig. 11.17). 6 m, the patient can move nearer the test type, say to 3 m.
Seat or stand the patient 6 m from the card. Ask the If the patient can then just read the 60 m line, the visual
patient to cover each eye in turn and find which is acuity, for that particular eye, is 3/60. A visual acuity of
the smallest line of print that can be read comfortably. less than 1/60 can be recorded as counting fingers (CF),
323
Chapter
Visual acuity
5' 1'
60 metres
0 20 40 60 80 100 200 feet

distance
Fig. 11.17 The angles subtended by standard Snellen type.
hand movements (HM), perception of light (PL) or no

perception of light (NPL). Near vision is tested using I am glad to say
reading test types, such as that produced by the UK
Faculty of Ophthalmologists (Fig. 11.18). Near visual
that I have never
acuity does not necessarily correlate well with distance seen a spade.
acuity.
vows mice immune
Questions to ask
N. 48
Visual disturbances
• Is the vision loss unilateral or bilateral? A poet can

• Is it confined to one area of the visual field?
• Are there positive as well as negative visual survive every-
phenomena?
• Do colours appear different? thing but a
misprint.
COLOUR VISION
Tests of colour vision are designed principally to detect
verse ransom
congenital defects. In the Farnsworth Munsell test the Fig. 11.18 Page from standard reading type.
patient grades the shading of 84 coloured tiles. Red-
green deficiency can be assessed more rapidly using
the Ishihara test plates (Fig. 11.19). With the plates at temporally for about 100°, and inferiorly for approximately
about 75 cm from the eyes, which are covered in turn, 75°. The blind spot, situated approximately 15° from
ask the patient to read plates 1 to 15. If 13 or more plates fixation in the temporal field, marks the position of the
are read correctly, colour vision can be regarded as optic disc. The field of vision to a coloured object, reflecting
normal. cone function, is more restricted than the field of a white
object of the same size. Only the central portions of the
two visual fields are binocular, the temporal margins
VISUAL FIELDS being monocular (Fig. 11.20). Static perimetry involves
Retinal sensitivity diminishes with increasing distance the detection of a stationary target of varying brightness,
from the fovea. Visual field mapping defines points in the while kinetic perimetry involves the detection of a moving
visual field at which an object of a particular size or target.
illumination is detected. The visual field is not symmetrical. To test the visual field sit approximately 1 m from
It extends superiorly and medially for approximately 60°, the patient. In infants or poorly cooperating adults, a
324
Chapter
Visual field test
Fig. 11.21 Testing visual fields by confrontation.

Fig. 11.19 Two plates from the Ishihara series. A patient with
normal vision reads both (a) and (c) without difficulty; however,
a patient with red–green deficiency is unable to read the figure 6 the right hand, while you cover or close your left eye (Fig.
(b) but is able to read the figure 12 (d) correctly. 11.21). Ensure that the patient’s left eye remains fixed on
your right eye throughout the examination. The limits of
the peripheral field can be determined by bringing the
Visual fields moving fingers of your right hand into the four quadrants
of the patient’s field. If individual half fields are full, then
the target object, usually your moving fingers, should be
90 presented in both peripheral fields simultaneously. In
parietal lobe lesions, particularly of the nondominant
60 hemisphere, a visual target presented in isolation in the
contralateral field is perceived but is missed (visual
30
10 Symptoms and signs

180 180
Types of field defect
• Absolute central scotoma

– area around fixation in which there is no
appreciation of the visual stimulus
• Relative central scotoma
– area in which object is detected but its colour is
diminished or desaturated (Fig. 11.23)
• Centrocaecal scotoma
– extends from fixation towards the blind spot
Fig. 11.20 Superimposed fields indicating binocular and monocular • Bitemporal hemianopia
components.
– temporal halves of both fields are affected
• Homonymous hemianopia
meaningful response may be impossible to elicit or may – a field defect in which the left or right half field is
be obtained only by using visual threat, in other words, affected; in a complete right homonymous
a sudden, unexpected hand movement. For cooperative hemianopia, therefore, the temporal field of the
adults and older children, either finger movements or right eye and the nasal field of the left eye
coloured objects can be used. For testing the left visual are lost
field, ask the patient to close or cover the right eye with
325
Chapter
the temporal field along the horizontal meridian. First

Visual inattention explain to the patient that the object will disappear briefly
then reappear and that the patient should indicate when
this happens. Once you have found the position of the
blind spot its shape can be mapped. Seldom will the blind
spots of the patient and yourself completely coincide.
Having identified the blind spot, assess the central visual
field.
FUNDOSCOPY
Normally it is not necessary to dilate the pupils in order
to examine the central fundus but if the patient has small
pupils, or the background illumination is high, take the
patient into a darkened room for the examination. If this
fails to dilate the pupils sufficiently, then a mydriatic, for
example, Mydrilate (1% cyclopentolate), can be instilled.
This should never be done in the unconscious patient and
must always be recorded in the patient’s notes. Do not
use mydriatics in a patient with glaucoma. Remember to
reverse the effects of the mydriatic at the end of the
examination by instilling 2% pilocarpine.
Ask the patient to fixate on a distant target (Fig. 11.24).
Fig. 11.22 Simultaneous presentation of finger movements in the
two half fields.
If the patient wears glasses with a substantial correction,
it sometimes facilitates the examination to perform it
with the patient’s glasses in place.
The optic disc is examined first to assess its shape,
colour and clarity. The temporal margin of the disc is
Central scotoma slightly paler than the nasal margin. The physiological
cup varies in size but seldom extends to the temporal,
and never to the nasal margins of the disc. The blood
vessels are not obscured as they cross the disc margin,
nor are they elevated (Fig. 11.25).
Retinal and visual pathway disorders
• Anterior ischaemic optic neuropathy

• Optic neuritis
• Optic nerve compression
Fig. 11.23 Comparison of colour sensitivity between central and • Papilloedema
peripheral field. In this patient with a central scotoma, the red object • Hypertensive retinopathy
appears brown in the central field. • Diabetic retinopathy
• Glaucoma
• Chiasmatic compression due to pituitary tumour
suppression or inattention) when a comparable target • Optic tract, radiation or visual cortex lesions due to
is presented simultaneously in the ipsilateral half-field vascular disease
(Fig. 11.22). Peripheral field defects are often detected
only if a small target object (e.g. a 10 mm red pin) is used
rather than moving fingers.
Hand or finger movements are too crude a stimulus The vessels are examined next. The arteries are
for assessing central field defects and here a small narrower than the veins and a brighter colour. They
coloured object is used. It is useful to outline the blind possess a longitudinal pale streak as a consequence of
spot first, partly because its successful identification light reflecting from their walls. The retinal veins should
increases confidence in one’s own technique and partly be closely inspected where they enter the optic disc. In
because it indicates good fixation on the part of the approximately 80% of normal individuals the veins
patient. Move a red pin of some 10 mm in diameter into pulsate. This pulsation ceases when CSF pressure exceeds
326
Chapter
Fig. 11.24 Direct fundoscopy.
Fig. 11.26 Optic atrophy.
is examined for the presence of haemorrhages and

exudates, the positions of which are best shown by a
small diagram in the patient’s notes, or by a description
that uses the optic disc as a clock face for localisation
purposes, for example, ‘one large haemorrhage at 6
o’clock, one disc diameter from the disc’.
OPTIC ATROPHY
Optic atrophy follows any process that damages the
ganglion cells or the axons between the retinal nerve fibre
layer and the lateral geniculate body. It is associated with
Fig. 11.25 The normal fundus. loss of bulk of the nerve and pallor of the disc (Fig. 11.26).
The pallor may be diffuse or segmental. Temporal pallor
200 mm of water. Therefore the presence of retinal venous is the most common form of segmental atrophy,
pulsation is a very sensitive index of normal intracranial attributable to the susceptibility of the papillomacular
pressure. Learn to identify this physical sign. It will save bundle to degenerate after optic nerve damage by
countless references to ‘swollen optic discs?’. The fundus compression or metabolic disturbance.
The colour of the normal optic disc is variable and the
ophthalmoscopic diagnosis of optic atrophy notoriously
Emergency
subjective. Additional features that may help the diagnosis
Acute visual failure include the number of capillaries visible on the optic disc,
• Unilateral – consider and the presence of retinal nerve fibre atrophy. The
• cranial arteritis former criterion has not been substantiated and detection
• optic neuritis of the latter requires considerable experience. Inspection
• retinal detachment of the retinal vessels is worthwhile. The presence of
• central retinal artery occlusion sheathing or attenuation of the retinal arterioles suggests
• acute glaucoma that the optic atrophy is secondary to ischaemic optic
• vitreous haemorrhage neuropathy or central retinal artery occlusion.
• Bilateral – consider
• cranial arteritis PAPILLOEDEMA
• optic neuritis Patients with papilloedema often have no visual com-
plaints, although some describe transient obscurations
327
Chapter
of vision either occurring spontaneously or triggered which haemorrhages are visible. The disc becomes
by postural change. Papilloedema is usually bilateral, hyperaemic (as a result of capillary dilatation) with a
although sometimes asymmetrical. Its pathogenesis loss of definition of its margins, and retinal venous
remains unsettled. The term papilloedema is best reserved pulsation disappears (Fig. 11.27). In fully developed
for patients in whom the disc swelling is secondary to papilloedema there is engorgement of retinal veins,
raised intracranial pressure. Transmission of the raised obscuration of the disc margin, flame haemorrhages
intracranial pressure, via the subarachnoid space of the and cotton wool spots (the consequence of retinal
optic nerve, results in venous stasis and also interrupts infarction). The vessels are tortuous (Fig. 11.28). Often
both fast and slow axoplasmic flow in the optic nerve. the only visual field change at this stage is an enlargement
As papilloedema develops, swelling of the nerve fibre of the blind spot (Fig. 11.29). In the later stages of
layer appears (best seen with a red-free light), within papilloedema, hard exudates appear on the disc, which
Fig. 11.28 Chronic papilloedema. Swollen optic discs, dilated

Fig. 11.27 Early papilloedema. Dilated nerve fibre bundles,
capillaries, haemorrhages and cotton wool spots.
superficial haemorrhages and disc hyperaemia.
Enlarged blind spots
90 90
105 75 105 75
120 80 60 120 80 60
70 70
135 45 135 45
60 60
50 50
150 30 150 30
40 40
30 30
165 15 165 15
20 20
10 10
90 80 70 60 50 40 30 10 20 30 40 50 60 70 80 90 0 90 80 70 60 50 40 30 20 10 30 40 50 60 70 80 90 0
180 180
10 10
20 345 20 345
195 195
30 30
40 40
210 330 210 330
50 50
60 60
225 315 225 315
Relat Intens
70 70
240 300 240 300
80 80
255 285 255 285
Object
270 270
Fig. 11.29 Papilloedema. Visual fields showing bilaterally enlarged blind spots.
328
Chapter
becomes atrophic, and other visual field abnormalities where they appear as yellow excrescences, often distorting
appear, including arcuate fibre defects and peripheral the disc margin. They do not usually produce visual
constriction. symptoms (Fig. 11.31).
Papilloedema can probably appear within 4–5 h of the
development of intracranial hypertension and may not
resolve for some weeks after its reduction. RETINAL VASCULAR DISEASE
Retinal artery and vein occlusion
OTHER FUNDUS ABNORMALITIES After occlusion of the central retinal artery, the retina
Myelinated nerve fibres becomes pale and opaque with a cherry-red spot at the
macula. The optic disc, initially swollen, becomes atrophic
A congenital anomaly in which myelinated and therefore (Fig. 11.32). The presence of microemboli, containing
visible nerve fibres are found at, or adjacent to, the disc either cholesterol or a fibrin–platelet mixture, establishes
margin (Fig. 11.30). that the occlusion is embolic (Fig. 11.33). A branch
occlusion produces a corresponding sector-shaped visual
Drusen (hyaline bodies)
defect. In central retinal vein occlusion there is swelling
Drusen are thought to be derived from axonal debris and of the optic disc, dilatation of the retinal veins and fundal
are situated in the disc anterior to the lamina cribrosa, haemorrhages (Fig. 11.34).
Fig. 11.30 Myelinated nerve fibres. Fig. 11.31 Bilateral drusen (associated with peripapillary
haemorrhage on right).
Fig. 11.32 Central retinal artery occlusion. Fig. 11.33 Cholesterol embolus. Fig. 11.34 Central retinal vein occlusion.
329
Chapter
Fig. 11.35 Hypertensive retinopathy with

haemorrhages, cotton wool spots and
variation in arteriolar calibre.
Fig. 11.36 Diabetic retinopathy. Fig. 11.37 Diabetic retinopathy. Hard

Microaneurysms, haemorrhages, exudates exudates at the macula.
and cotton wool spots.
Hypertensive retinopathy
In hypertensive retinopathy, the light reflex from
the arteriolar wall is abnormal and constriction of
the venous wall appears at sites of arteriovenous
crossing. Both the former (silver or copper-wiring) and
the latter (arteriovenous nipping) are encountered in
normal older individuals. A more reliable sign of
hypertensive retinopathy is variation in the calibre of the
retinal arterioles. As the retinopathy advances,
haemorrhages and cotton wool spots appear (Fig. 11.35)
and in malignant or accelerated hypertension disc
swelling occurs.
Diabetic retinopathy
Diabetic retinopathy in its early stages principally affects
the retinal microcirculation, producing the characteristic,
although not pathognomonic, microaneurysm (Fig.
11.36). Subsequently small haemorrhages, exudates and
cotton wool spots appear. Visual failure is usually due
either to macular disease, in the form of oedema, Fig. 11.38 Vitreous haemorrhage with evidence of new vessel
infarction or lipid deposition (Fig.11.37), or to the formation at the disc margin.
appearance of new vessel formation (proliferative diabetic
retinopathy), leading to vitreous haemorrhage and of cup size to vertical disc diameter beyond 0.6 and retinal
retinal detachment caused by traction of fibrous tissue nerve fibre atrophy. Arcuate field defects accompany
(Fig. 11.38). these changes. With advanced glaucoma there is marked
undermining of the disc margins and bowing of the blood
vessels (Fig. 11.39).
GLAUCOMA
Glaucoma, characterised by raised intraocular pressure,
can occur either secondarily to various ocular pathologies OPTIC NERVE DISEASE
(e.g. uveitis) or in a primary form. The latter is far In lesions of the optic nerve, the visual defect is
more common. Resulting changes in the optic disc monocular. Visual acuity is usually reduced and colour
include enlargement of the physiological cup (particularly perception is disturbed (particularly for red–green). There
significant if in the vertical axis), an increase in the ratio is a relative afferent pupillary defect (see p. 341). The
330
Chapter
most likely visual field defect is a central scotoma (Fig. across the vertical meridian (Fig. 11.42). Patients
11.40). Optic atrophy is a relatively late development in frequently complain of blurred or double vision, a
optic nerve compression. Proptosis is likely if the lesion consequence of lost integration between independent
is within the orbit. nasal fields.
CHIASMATIC LESIONS
OPTIC TRACT AND LATERAL GENICULATE
Most chiasmatic syndromes are the result of compression BODY LESIONS
by pituitary tumour, meningioma or craniopharyngioma.
The result is a bitemporal hemianopia, although the type These are uncommon. A lesion in the anterior part of the
of defect relates to the position of the growth and its optic tract, before the homonymous fibres have joined,
relation to the chiasm. Typically, the visual defect is produces an incongruous homonymous hemianopia,
asymmetrical (Fig. 11.41). In its earliest stages, the field that is, one in which the two half field losses are not equal
defect can be detected only by moving a coloured target (Fig. 11.43).
OPTIC RADIATION AND OCCIPITAL

CORTEX LESIONS
The type of visual field loss from lesions of the optic
radiation depends on their localisation. All the defects are
homonymous but not necessarily congruous. In lesions
affecting the temporal radiation, the superior quadrantic
field is more affected than the inferior. If the defect is
incongruous, the nasal loss in the ipsilateral eye is more
extensive than the temporal loss in the contralateral eye
(Fig. 11.44).
With parietal lobe lesions, the defect is often complete
but, rarely, principally affects the inferior quadrants.
Occipital lobe pathology produces congruous defects
that can be total, quadrantic or scotomatous. In some
instances there is macular sparing, probably because
of a dual vascular supply to the macular area of the
occipital cortex (Fig. 11.45). An isolated homonymous
hemianopia is usually occipital in origin and almost
always due to vascular disease. Temporal or parietal
Fig. 11.39 Advanced chronic simple glaucoma. lobe pathology associated with visual field defects will
Central scotoma
90 90
105 75 105 75
120 80 60 120 80 60
70 70
135 45 135 45
60 60
50 50
150 30 150 30
40 40
30 30
165 15 165 15
20
10
90 80 70 60 50 40 30 20 10 10 20 30 40 50 60 70 80 90 0 90 80 70 60 50 40 30 40 50 60 70 80 90 0
180 180
195 20 345 195 345

30 30
40 40
210 330 210 330
50 50
Relat Intens
60 60
225 315 225 315
70 70
Object
240 80 300 240 80 300

255 285 255 285
270 270
Fig. 11.40 Large right central scotoma.
331
Chapter
Chiasmatic compression
90 90
105 75 105 75
optic chiasm
120 80 60 120 80 60 optic nerve
70 70
135 45 135 45
60 60
optic tract
150
50
30 150
50
30
lateral
40 40
30 30
geniculate
165
20
15 165
20
15
body
10 10
50 40 30 20 10 10 20 30 40 50 60 70 80 90 0
18090 8070 60 10 20 30 40 50 60 708090 0 80 50 40 30 20 10
18090 70 60
10 10
195 20 345 195 20 345

30 30
40 40
210 330 210 330
50 50
60 60
225 315 225 315
70 70
240 80 300 240 80 300
255 285 255 285
270 270
geniculocalcarine
tract calcarine fissure
Fig. 11.41 Visual pathways (right) with field defect produced by chiasmatic compression (left).
there is denial of visual disability and confabulation of

Colour comparison visual detail (Anton’s syndrome).
The oculomotor, trochlear and abducens

(third, fourth and sixth) nerves
Pupillary light response pathway
The pupillary light response pathway originates in the
same rods and cones that register visual stimuli. Fibres
from the receptors partly decussate in the chiasm, then
leave the optic tract before the lateral geniculate body
on their way to the brachium of the superior colliculus
and, hence, the Edinger–Westphal nucleus, via the
pretectal nuclear complex (Fig. 11.46). A light stimulus
to one eye triggers a bilateral, symmetrical, pupillary
response. The pupillomotor fibres lie superficially
in the oculomotor nerve before joining the inferior
division of the nerve on their way to the ciliary
ganglion. After synapsing, the fibres enter the short
Fig. 11.42 Comparison of coloured targets in nasal and temporal ciliary nerve.
fields. There is red desaturation in the temporal field of the left eye.
Near reaction
usually produce additional symptoms and signs. The near reaction comprises pupillary constriction,
Furthermore, the pathology is often neoplastic rather ocular convergence and increased accommodation of
than vascular. the lens. The accommodation reaction is controlled
Bilateral occipital infarction results in cortical blindness. by the rostral and midportion of the Edinger–Westphal
The pupillary responses are normal. In some instances nucleus. The efferent pathway passes through the
332
Chapter
The oculomotor, trochlear and abducens (third, fourth and sixth) nerves 11
Hemianopia due to optic tract lesion
90 90
105 75 105 75
120 80 60 120 80 60
70 70
135 45 135 45
60 60
50 50
150 30 150 30
40 40
30 30
165 15 165 15
20 20
10 10
90 80 70 60 50 40 30 20 10 10 20 30 40 50 60 70 80 90 0 90 80 70 60 50 40 30 20 10 10 20 30 40 50 60 70 80 90
0
180 180
10 10
20 345 20 345
195 195
30 30
40 40
210 330 210 330
50 50
60 60
225 315 225 315
70 Relat Intens 70 Relat Intens
240 80 300 240 80 300
255 285 255 285
Object
Object
270 270
Fig. 11.43 Incongruous right homonymous hemianopia associated with a left optic tract lesion.
Superior quadrantic homonymous hemianopia
90 90
105 75 105 75
120 80 60 120 80 60
70 70
135 45 135 45
60 60
50 50
150 30 150 30
40 40
30 30
165 15 165 15
20 20
10 10
90 80 70 60 50 40 30 20 10 10 20 30 40 50 60 70 80 90 0 90 80 70 60 50 40 30 10 10 20 30 40 50 60 70 80 90 0
180 180
10 10
20 345 195 20 345

195
30 30
40 40
210 330 210 330
50 50
60 60
225 315 225 315
70 70
240 300 Relat Intens 240 300
Relat Intens
80 80
255 285 255 285
270 270
Object
Object
Fig. 11.44 Incongruous left superior quadrantic homonymous hemianopia associated with a lesion of the temporal part of the right optic
radiation.
oculomotor nerve, ciliary ganglion and short ciliary segments of C8 and T2. Second-order neurons exit
nerve. from the cord, principally in the first ventral thoracic
root, and pass through the inferior and middle cervical
Ocular sympathetic fibres
ganglia before terminating in the superior cervical
The ocular sympathetic fibres originate in the ganglion (Fig. 11.47). Sudomotor and vasoconstrictor
hypothalamus and remain uncrossed. The first-order fibres to the face, except for those to a small area on
neurons terminate in the spinal cord in the the forehead, run with branches of the external carotid
intermediolateral cell column between the spinal artery. Fibres accompanying the internal carotid artery
333
Chapter
Right homonymous hemianopia
90 90
105 75 105 75
120 80 60 120 80 60
70 70
135 45 135 45
60 60
50 50
150 30 150 30
40 40
30 30
165 15 165 15
20 20
10 10
90 80 70 60 50 40 30 20 10 10 20 30 40 50 60 70 80 90 0 90 80 70 60 50 40 30 20 10 10 20 30 40 50 60 70 80 90 0
180 180
10 10
20 345 20 345
195 195
30 30
40 40
210 330 210 330
50 50
60 60
225 315 225 315
70 70
240 300 Relat Intens 240 Relat Intens
80 80 300
255 285 255 285
270 270
Object
Object
Fig. 11.45 A right homonymous hemianopia, sparing the macula and the peripheral temporal crescent of the right eye.
Horizontal and vertical saccades

Pupillary light pathway
There are supranuclear, internuclear and infranuclear
components in the anatomical pathways for eye
pretectal nucleus superior colliculus
movements, with different supranuclear pathways for
saccadic (refixation) movements and pursuit (following)
movements. Horizontal saccades originate in both the
lateral frontal and parietal lobes. Certain types of eye movement
geniculate
are also probably initiated in the temporal lobe. From the
body
frontal eye fields, the principal descending pathway
passes through the anterior limb of the internal capsule,
continues along the ventrolateral aspect of the thalamus,
decussates in the lower midbrain, then passes in the
Edinger–Westphal paramedian pontine reticular formation to end at the
ciliary ganglion nucleus excitatory burst neurons in the pontine gaze centre (Fig.
11.48). From here, neurons project to the ipsilateral
abducens nucleus and through it, via the medial
longitudinal fasciculus, to the medial rectus component
of the contralateral third nerve nucleus. The pathway for
vertical saccades has been less clearly defined but it
projects eventually to the rostral interstitial nucleus of the
medial longitudinal fasciculus (Fig. 11.49), which is
located at the junction of midbrain and thalamus. The
nucleus receives additional ascending inputs through
the medial longitudinal fasciculus and, directly, from the
Fig. 11.46 Pupillary light pathway. The input from the left eye paramedian pontine reticular formation. From this
decussates at the chiasm and reaches both third nerve nuclei.
nucleus, the pathway for downward saccades passes
caudally to the third and fourth cranial nerve nuclei;
that for upward saccades traverses the posterior
reach the pupil via branches of the ophthalmic division commissure.
of the trigeminal nerve and the eyelids via branches of Pursuit movements in both the horizontal and vertical
the ophthalmic artery. The fibres supply the dilator planes originate in the parieto-occipital cortex, then
muscle of the iris and smooth muscle in the upper and descend in an uncrossed pathway whose exact location
lower lids. remains undetermined. The path for horizontal pursuit is
334
Chapter
Ocular sympathetic pathway
lacrimal gland hypothalamus

ophthalmic
artery
nasociliary trigeminal
pupil nerve nerve
long
dilator ciliary
nerve
Müller‘s muscles internal
of the eyelids carotid
artery
sudomotor and superior

vasoconstrictor fibres to face cervical
ganglion
subclavian
artery
external
carotid C8
artery T1
T2
lung
Fig. 11.47 The ocular sympathetic pathway.
known to pass through the paramedian pontine reticular Third nerve

formation and that for vertical pursuit is controlled, at
The third nerve nucleus is located in the midbrain at
least in part, by fibres passing rostrally through the medial
the level of the superior colliculus. All its neurons
longitudinal fasciculus.
project ipsilaterally, apart from those passing to the
The globe has an innate tendency to return to the
contralateral superior rectus muscle. The levators of the
primary position of gaze after ocular deviation, so the
upper lids are supplied by a single midline nucleus.
stimulus for a sudden horizontal or vertical movement
The third nerve emerges from the anterior aspect of the
needs to be followed by a sustained neuronal discharge
midbrain and lies close to the posterior communicating
to the relevant muscles if ocular deviation is to be
artery before entering the cavernous sinus, in which it
sustained. Burst neurons trigger the initial saccade; at
runs superiorly (Fig. 11.50). It terminates in superior and
other times their output is suppressed by pause neurons.
inferior divisions, the latter containing pupillomotor
Simultaneously, there is inhibition of the nucleus
fibres.
supplying the contralateral antagonist muscle. For
sustained deviation, a tonic neuronal discharge occurs
that uses the same final common pathway as the burst Fourth nerve
neurons but which is influenced by other structures, The fourth nerve decussates before exiting from the
including the cerebellum and the medial vestibular dorsal aspect of the midbrain, eventually innervating
nucleus. A similar tonic mechanism exists for other forms the contralateral superior oblique muscle. It lies
of eye movement. immediately below the third nerve in the cavernous
Saccadic movements with a velocity of up to 700°/s sinus and enters the orbit through the superior orbital
permit a rapid refixation of gaze from one object to fissure, along with the other nerves supplying the eye
another, while pursuit movements allow tracking of a muscles.
slowly moving target at velocities up to 50°/s. Vestibular
movements are initiated in the semicircular canals by
Sixth nerve
head movement or, reflexly, by caloric stimulation. These
movements maintain a stable perception of the The sixth nerve emerges from the lower border of the
environment during bodily movement. pons, runs beneath the petroclinoid ligament, then lies
335
Chapter
Horizontal gaze Vertical gaze
brainstem
PC riMLF
A
LR MR
INC
III brain stem

III
EBN
PN MLF
MLF IV
VI
VN PRF
IBN
EBN excitatory burst neurons LR lateral rectus riMLF rostral interstitial nucleus PRF pontine reticular formation
of the medial
IBN inhibitory burst neurons MR medial rectus longitudinal fasciculus A aqueduct
PN pause neurons excitatory neurons INC interstitial nucleus of PC posterior commisure

Cahal
inhibitory neurons VN vestibular nucleus
Fig. 11.48 Organisation of horizontal gaze. Fig. 11.49 Organisation of vertical gaze.
close to the internal carotid artery in the medial aspect tonic discharge of neuronal activity during eccentric
of the cavernous sinus. It supplies the lateral rectus gaze.
muscle.
Nystagmus SYMPTOMS
Nystagmus is a repetitive to-and-fro movement of the If the patient complains of ptosis, find out whether the
eyes. In pendular nystagmus, the phases are of equal problem is bilateral or unilateral and whether it fluctuates.
velocity, in phasic (jerk) nystagmus they differ. The slow If necessary obtain old photographs to make a
phase of jerk nystagmus may show a linear or nonlinear comparison.
time course. Vestibular dysfunction, either centrally or For diplopia, a number of questions may help to
peripherally, is the usual cause of a jerk nystagmus in suggest the underlying mechanism. Weakness of the
which the slow-phase is linear. In gaze- evoked nystagmus lateral or medial rectus muscles produces a horizontal
the eyes drift back from an eccentric position with a diplopia. Weakness of the other eye muscles produces a
nonlinear velocity, followed by a saccadic correction. This vertical or oblique diplopia. The diplopia increases as the
type of nystagmus is thought to result from dysfunction patient looks in the direction of action of the paralysed
of the neural integrator, the mechanism that sustains a muscle.
336
Chapter
Cavernous sinuses
optic tract
III nerve pituitary gland

IV nerve
V nerve
VI nerve internal carotid artery
sphenoidal sinus
Fig. 11.50 Transverse section of cavernous sinuses.
Questions to ask
defect of the afferent pupillary pathway is best appreciated
by swinging the torch from one eye to the other. As the
Diplopia
torch swings from, say, the right eye to the left, the pupil
• Is the diplopia relieved by covering one or other eye? of the latter, which has just started to dilate because
• Is the diplopia horizontal or vertical/oblique? of the loss of its consensual reaction, immediately
• Does the diplopia increase in one particular direction constricts.
of gaze?
Near reaction
• Does the diplopia fluctuate or is it constant?
If the light response is normal there is little point in
testing the near reaction. If the light response is depressed,
test the near reaction by asking the patient to fixate on a
target (e.g. your forefinger) as it approaches the eyes.
Examination Many patients, especially elderly people, have difficulty
sustaining convergence. If there is no immediate reaction,
INSPECTION OF THE EYELIDS AND PUPILS maintain convergence for a minute or so to see if a
Note the position of the eyelids. If there is a ptosis, assess delayed reaction appears. The near reaction is additive to
its fatiguability by asking the patient to sustain upward the pupillary light response, in other words, it can be
gaze. Next examine the pupils, which normally are tested in bright light.
circular and symmetrical, although a slight difference in
size (anisocoria) of up to 2 mm is seen in some 20% of INSPECTION OF EYE MOVEMENTS
the population. If there is a slight size difference, take the
Conjugate eye movements
patient into a darkened room. A physiological anisocoria
will remain unchanged. An irregular pupil is most Next assess conjugate eye movements. To test pursuit,
commonly the consequence of iris disease. Ask the ask the patient to follow a slowly moving target, first in
patient about previous ocular trauma or infection. If the horizontal then in the vertical plane. If pursuit
the pupils are markedly different in size, make sure that movements are slowed, brief saccades must be
the patient is not using a mydriatic or meiotic in one eye superimposed to allow the eyes to catch their target. The
alone. resulting movement is jerky rather than smooth. The
slowing may be in one or more directions. To assess
Pupillary light response
saccadic movements, ask the patient to rapidly fixate
Now examine the pupillary light response using a bright between two targets, for example, two fingers in the same
pencil torch. The background illumination should be low, plane. Saccades may be abnormal in terms of their
and to prevent a near reaction the patient should fixate velocity, accuracy or persistence. An overshoot or
on a distant object. Observe the direct (ipsilateral) and undershoot is readily detected during refixation
consensual (contralateral) responses. A unilateral movements. Slowing, in either initiation or performance,
depression of the light response may be obvious but a can occur in the horizontal or vertical plane. Inappropriate
337
Chapter
saccades will disrupt fixation. When continuous, they are and incomitant if the angle of deviation varies. The latter
described as ocular flutter if confined to the horizontal is usually caused by paresis of one or more of the
plane or opsoclonus if multidirectional. extraocular muscles. Now perform a cover test. In the
presence of a concomitant squint, covering the fixating
Doll’s head manoeuvre (oculocephalic reflex) eye produces a movement in the squinting eye that allows
If the eyes fail to respond to a saccadic or pursuit stimulus, it to take up fixation (unless the vision in that eye is
perform the doll’s head manoeuvre. Ask the patient to severely depressed) (Fig. 11.52). Most patients with
fixate on your eyes, grasp the head and rotate it, first in concomitant squint do not complain of diplopia, a
the horizontal then in the vertical plane. An intact symptom that suggests a disorder of one or more of the
response (a measure of vestibular eye function) allows extraocular muscles or their nerve supply. After a
the patient’s eyes to remain fixed on your own (Fig. recent oculomotor nerve paresis, altered patterns of
11.51). contraction in the yoke and antagonist muscles produce
characteristic deviations when alternate cover testing
is performed. In the presence of a right lateral rectus
TESTING THE ACTION OF INDIVIDUAL weakness, the patient fixates with the left eye, the right
EYE MUSCLES eye tending to turn inwards because of the unopposed
The action of the individual eye muscles can now be action of medial rectus (the primary deviation). If the left
assessed. This is particularly relevant if the patient eye is now covered, increased innervation attempts are
complains of double vision (diplopia). made in order to achieve fixation with the paretic eye.
In a strabismus, or squint, the axes of the eyes are no This abnormal stimulus spills over to the yoke muscle,
longer parallel. Esodeviation indicates that the axes are the medial rectus of the left eye, which accordingly over-
convergent and exodeviation that they are divergent. The adducts that eye (secondary deviation). In a paralytic
strabismus is concomitant if the angle of deviation strabismus, secondary deviation is greater than primary
remains constant throughout the range of eye movement (Fig. 11.53).
Doll‘s head manoeuvre
Fig. 11.51 Performing the doll’s head manoeuvre in the horizontal plane.
Fig. 11.52 Cover testing. There is a right esotropia that corrects temporarily when the left eye is covered.
338
Chapter
Right abducens palsy
right left right left

lateral medial medial lateral lateral medial medial lateral
rectus rectus rectus rectus rectus rectus rectus rectus
Fig. 11.53 Right abducens palsy. The right eye tends to converge, particularly when the left eye is used for fixation. When the right eye tries
to fixate, overaction of the left medial rectus occurs.
Muscles responsible for eye movements
The pupil and eye movements
right
superior eye inferior Pupillary syndromes
rectus oblique • Horner’s
• Tonic pupil
• Argyll Robertson pupil
• Relative afferent pupillary defect
Eye movement disorders
lateral medial • Gaze paresis
rectus rectus • Internuclear ophthalmoplegia
• One-and-a-half syndrome
• Abducens, trochlear and oculomotor nerve palsies
Nystagmus
• Congenital
• Vestibular
inferior superior • Gaze-evoked
rectus oblique • Downbeat
• Convergence-retractory
Fig. 11.54 The muscles responsible for eye movements in particular
directions.
Having confirmed that the diplopia is binocular (in is longstanding, examine old photographs. Finally,
other words, that it disappears when one or other eye is remember that a pattern of diplopia that is variable and
covered) ask the patient to look in the six directions difficult to interpret suggests the possibility of myasthenia
illustrated in Figure 11.54. The false image (which often gravis.
appears indistinct or blurred) is peripheral to the true
Nystagmus
image and belongs to the affected eye. Having elicited
the diplopia, cover first one eye, then the other, to Note the presence of nystagmus and whether it is
establish to which eye the false image belongs. Observe pendular or jerk. Record the amplitude (fine, medium or
if the patient has an abnormal head tilt as a compensation coarse), persistence and the direction of gaze in which it
for the diplopia. To establish whether the head tilt occurs. Additionally, indicate whether the movement is
339
Chapter
horizontal, vertical, rotary or a mixture of several types.

First-degree nystagmus to the left is a fast beating Clinical application
nystagmus to the left on left lateral gaze. In second- and
third-degree nystagmus to the left, the same nystagmus THE PUPIL
is present on forward and right lateral gaze, Horner’s syndrome
respectively.
Horner’s syndrome results from interruption of the
Optokinetic nystagmus sympathetic fibres to the eye. The pupil is miosed and
Optokinetic responses are assessed using a drum painted the palpebral fissure is narrowed because of mild ptosis
with vertical lines, which is rotated first in the horizontal of the upper lid and elevation of the lower lid. The
and then in the vertical plane. As the patient looks at the pupillary asymmetry is often slight but can be accentuated
drum a pursuit movement is seen in the direction of its by taking the patient into a darkened room. Although
rotation, followed by a saccade returning the eyes to the enophthalmos is suggested by the appearance of the eye,
midposition. As an alternative, the patient can be asked this is not confirmed by formal measurement. The
to look at a tape measure as it is drawn across the field distribution of sweating loss on the ipsilateral face
of gaze (Fig. 11.55). Both movements are generated by depends on the site of the lesion. If there is uncertainty
the hemisphere towards which the drum is rotating. regarding the diagnosis, instil 4% cocaine into each eye
Thus, with the drum rotating to the right, or the tape – the normal pupil dilates, the affected pupil fails to do
being drawn to the right, pursuit is controlled by the right so (Fig. 11.56), irrespective of the site of the lesion.
parieto-occipital cortex and the correcting saccade by the
right frontal cortex. Tonic pupil syndrome
The tonic pupil syndrome is usually unilateral. The
affected pupil is dilated, although in longstanding cases
it becomes progressively smaller. The light response is
absent or markedly depressed and, consequently, in a
darkened room, the affected pupil becomes smaller than
its fellow because of a failure of reflex dilatation. The near
reaction is delayed but sometimes is then more marked
than that of the normal pupil. On relaxing the near effort,
dilatation is delayed so that for a period the previously
larger pupil is the smaller one (Fig. 11.57). The
accommodation reaction is often sustained, resulting in
blurred vision when switching from a distant to a near
target or vice versa. The iris contains areas of focal atrophy
and, characteristically, the pupils are hypersensitive
to dilute parasympathomimetic agents (e.g. 0.125%
pilocarpine). Tonic pupil syndrome is sometimes
Fig. 11.55 Testing optokinetic nystagmus. associated with depression of the deep tendon reflexes
Fig. 11.56 Horner’s syndrome. Before (a) and after (b) instillation of cocaine.
340
Chapter
Fig. 11.57 Tonic pupil syndrome. (a) Left pupil is dilated. (b) After 1 min near effort. (c) Partial dilatation 15 s after release. (d) Virtually
complete at 60 s.
found with disease of the lens or vitreous. The conducting

systems of the two optic nerves are best compared by
performing the swinging light test. In the presence of a
unilateral optic nerve lesion, for example caused by optic
neuritis, the affected pupil dilates as the torch is swung
onto it from the sound eye.
DISORDERS OF EYE MOVEMENTS

Gaze paresis
In an acute frontal lobe lesion, contralateral saccadic eye
movements in the horizontal plane are depressed or
absent and there is limb paresis ipsilateral to the gaze
palsy (Fig. 11.59). Both pursuit movements and the
oculocephalic responses are spared. Saccades return later
but now initiated by the contralateral frontal lobe.
Fig. 11.58 Argyll Robertson pupil. Subsequent damage to that frontal lobe will result in a
complete horizontal saccadic palsy. A lesion at the level
of the paramedian pontine reticular formation produces
(Holmes–Adie syndrome) and may occur in association
an ipsilateral gaze paresis for both saccadic and pursuit
with various dysautonomias.
movement (Fig. 11.60). The limb paresis is contralateral.
Argyll robertson pupil An ipsilateral pursuit paresis occurs with posterior
The Argyll Robertson pupil is miosed, with a light hemisphere disease and is associated with a contralateral
response that is diminished compared with the near homonymous field defect.
reaction (light-near dissociation). When the defect is fully A paresis of upward saccades, initially with relative
developed, the pupil is fixed to light and fails to dilate in preservation of pursuit, is a feature of the dorsal-midbrain
the dark. The pupil is often irregular with evidence of iris (Parinaud’s) syndrome (Fig. 11.61). Other findings
atrophy (Fig. 11.58). When complete, the syndrome is include impaired convergence and dilated, light-near
pathognomonic of neurosyphilis. The lesion responsible dissociated pupils. At a later stage upward pursuit and
is thought to lie in the midbrain immediately above the down gaze become affected. Causes include vascular
Edinger–Westphal nucleus. A pupil of normal size with disease and pinealoma.
light-near dissociation can occur in other circumstances
(e.g. in a blind eye).
OTHER SACCADIC AND PURSUIT
Relative afferent pupillary defect MOVEMENT DISORDERS
This results from a lesion of the afferent light reflex Saccadic slowing, accompanied by disorganised pursuit
pathway between the retina and the optic tract. It is not movements, is found in both Huntington’s and
341
Chapter
Eye movements in frontal, pontine and dorsal-midbrain lesions

Fig 11.59 Fig 11.60
Fig 11.61
Fig. 11.59 Left frontal lobe lesion. Absent saccades to right, intact to left, preserved doll’s head manoeuvre, right hemiparesis.
Fig. 11.60 Left pontine lesion. Absent saccades, pursuit and doll’s head movements to the left. Right hemiparesis.
Fig. 11.61 Dorsal-midbrain syndrome. Full horizontal and downward saccades, absent upward saccades. Light-near dissociation.
Parkinson’s disease. In progressive supranuclear palsy, undershooting saccades (hypermetria and hypometria,
downward saccades and pursuit fail first, followed by respectively) occur with cerebellar disease. Large or small
involvement of upward and, finally, horizontal movements. inappropriate saccades can interrupt fixation. Causes
Doll’s head movements are spared, at least initially include multiple sclerosis and cerebellar disease. Slowing
(Fig. 11.62). A delay in the initiation of saccades occurs of pursuit movement is most commonly caused by
in many extrapyramidal disorders. Overshooting or sedative medication.
342
Chapter
Fig. 11.62 Progressive supranuclear palsy. Failure of down gaze

(a) is improved by the doll’s head manoeuvre (b).
Fig. 11.63 Left internuclear ophthalmoplegia. Failure of adduction

of the left eye on right lateral gaze. Fig. 11.64 ‘One-and-a-half’ syndrome. Right gaze paresis with right
internuclear ophthalmoplegia.
INTERNUCLEAR OPHTHALMOPLEGIA
A lesion of the medial longitudinal fasciculus leads to The latter is usually due to a lesion of the central
slowing, or total failure, of medial rectus contraction or peripheral course of the sixth nerve but it can be
during lateral gaze (Fig. 11.63). The slowing affects all caused by myasthenia or orbital disease. The eye fails
movement, whether saccadic, pursuit or reflex. To assess to abduct. When the defect is complete, there may
subtle slowing, observe the relative velocity of the two be a convergent strabismus because of unopposed
eyes while the patient rapidly fixates between two targets. action of the ipsilateral medial rectus (Fig. 11.65).
There is usually an accompanying nystagmus in the Unilateral or bilateral sixth nerve palsies sometimes
abducting eye. Bilateral internuclear ophthalmoplegia is result from the effects of raised intracranial pressure
accompanied by upbeat vertical nystagmus and subtle (Fig. 11.66).
abnormalities of vertical eye movement. Multiple sclerosis
is the most common cause in younger patients, vascular TROCHLEAR PALSY
disease in elderly patients.
Although normally a result of trochlear nerve palsy,
weakness of the superior oblique muscle can occur with
THE ‘ONE-AND-A-HALF’ SYNDROME myasthenia or dysthyroid eye disease. An isolated
If the lesion responsible for a unilateral internuclear trochlear nerve palsy sometimes follows a closed head
ophthalmoplegia spreads into the pontine gaze centre, a injury. The head tilts to the side opposite the affected eye
more profound loss of ocular motility results. The only and the patient complains of diplopia, particularly on
normal horizontal movement possible is abduction of the downward gaze. There is defective depression of the
opposite eye (Fig. 11.64). The finding is usually the adducted eye (Fig. 11.67).
consequence of vascular disease.
OCULOMOTOR PALSY
ABDUCENS PALSY Nuclear oculomotor palsies tend to be either incomplete
A lesion of the sixth nerve nucleus produces a gaze or complete but with pupillary sparing. A complete
paresis rather than an isolated lateral rectus weakness. third nerve palsy cannot be nuclear unless there is
343
Chapter
involvement of the contralateral superior rectus muscle.

Peripheral third nerve lesions are commonly caused
by diabetes. The paresis is typically painful and pupil-
sparing in about 50% of patients (Fig. 11.68). In a
complete third nerve palsy there is a substantial ptosis
and the eye is deviated laterally and slightly downwards.
Compression of the oculomotor nerve, for example by
a posterior communicating aneurysm, almost always
results in pupillary dilatation (Fig. 11.69). To assess
whether the fourth nerve is intact in the presence
of a complete third nerve palsy, ask the patient to
look down. If the superior oblique muscle is still
functioning, the abducted eye shows an inwardly rotating
twitch.
COMBINED PALSIES
A lesion within the cavernous sinus, for example a
cavernous aneurysm, is liable to affect the oculomotor
nerves in combination rather than individually. At risk
are the third, fourth and sixth nerves, the first and second
Fig. 11.65 Left sixth nerve palsy. Left esotropia on forward gaze
(a). Failure of abduction of left eye (b).
divisions of the trigeminal nerve and the ocular
Fig. 11.66 Bilateral sixth nerve palsies. There is a tendency for the eyes to converge on forward gaze (a), with partial failure of abduction to
right (b) and to left (c).
Fig. 11.67 Right superior oblique palsy. Fig. 11.68 Pupil-sparing right oculomotor Fig. 11.69 Left third nerve paresis. The pupil
palsy caused by diabetes. is dilated.
344
Chapter
Trigeminal nuclei
IV nerve
III nerve mesencephalic

nucleus
motor
nucleus
principal
sensory
nucleus
VI nerve
nucleus
nerves IX X of spinal
tract
Fig. 11.70 Dysthyroid eye disease. Failure of laevoelevation of the Fig. 11.71 Organisation of trigeminal nuclei within the brainstem.
left eye.
sympathetic fibres. A complex, mixed ophthalmoplegia

The trigeminal (fifth) nerve
without pupillary involvement raises the possibility of
myasthenia or dysthyroid eye disease (Fig. 11.70). STRUCTURE AND FUNCTION
The motor nucleus of the nerve lies in the floor
of the upper part of the fourth ventricle and receives
NYSTAGMUS fibres from both hemispheres, but principally the
Certain types of nystagmus suggest disease at particular contralateral one. It also receives afferents from the
sites of the nervous system. sensory nuclei. Initially, the motor root remains separate,
• Pendular – usually congenital but sometimes found in running below the gasserian ganglion before joining the
brainstem vascular disease or multiple sclerosis. mandibular division of the nerve to emerge through
• Vestibular – if peripheral, usually both horizontal the foramen ovale. The principal muscles supplied
and rotary components and is suppressed by by the nerve are the medial and lateral pterygoids,
visual fixation. The slow phase is to the side of temporalis and masseter. Smaller muscles supplied
the lesion. If central, more variable and unaffected include tensor tympani and tensor palati. Jaw closure is
by fixation. achieved by contraction of temporalis and masseter. Jaw
• Gaze-evoked – often drug-induced but also seen with opening and lateral movements are performed by the
disease of the cerebellum or brainstem. Vertical pterygoids.
components indicate brainstem or cerebellar disease. There are three sensory nuclei: the main nucleus, the
• Down-beat – when present on down and out gaze, very mesencephalic nucleus and the nucleus of the spinal tract
suggestive of a lesion at the foramen magnum, for (Fig. 11.71). Tactile stimuli are relayed through the main
example Chiari malformation. nucleus. From here, ascending fibres, most of which
• Convergence-retractory – occurs in the dorsal-midbrain decussate, terminate in the thalamus. The spinal
syndrome. Attempts at upwards saccades produce nucleus, continuous above with the main nucleus, extends
retractory movements of the globes. caudally to the second cervical segment where it lies in
• End-point – physiological. Occurs at extremes of the posterior horn continuous with the substantia
lateral gaze and can affect one eye more than the gelatinosa. A rostrocaudal organisation of fibres from
other. concentric segments over the face and head has been
345
Chapter
suggested, based on the pattern of facial sensory loss which pass to the mesencephalic nucleus in the motor
sometimes seen with lesions of the spinal tract (Fig. rather than the sensory root. Collaterals from the
11.72). Terminating in close proximity to the nucleus of axons of the unipolar mesencephalic neurons synapse
the spinal tract are fibres from the seventh, ninth and with cells in the motor nucleus, producing a monosynaptic
tenth cranial nerves that supply cutaneous fibres to reflex arc, the efferent pathway being within the motor
the region of the ear. The nucleus contains fibres root.
concerned principally with pain and temperature
sensation. Fibres from the nucleus decussate then ascend
to the thalamus. The mesencephalic nucleus receives
proprioceptive fibres from the muscles of mastication. Course of the trigeminal nerve
Collaterals from the afferent fibres synapse on cells in the
motor nucleus.
The sensory root accompanies the motor root through superior sagittal
the pontine cistern before entering the gasserian ganglion, sinus
which is situated in a depression in the petrous temporal
bone (Fig. 11.73). From here the ophthalmic division infratrochlear nerve
enters the orbit through the superior orbital fissure and lacrimal nerve
the maxillary and mandibular divisions leave the skull
through the foramina rotundum and ovale, respectively. optic nerve
The facial and scalp innervation of the three divisions is
shown in Figure 11.74. In addition, the trigeminal nerve
ophthalmic nerve
innervates the mucous membranes of the nose and
maxillary nerve
mouth, certain sinuses, part of the external auditory
mandibular nerve
meatus and most of the dura.
trigeminal ganglion
The jaw jerk
The afferent part of this reflex is formed by large
afferents from muscle spindles in masseter and temporalis, Fig. 11.73 The peripheral course of the trigeminal nerve.
Organisation of spinal trigeminal tract
ventral gracile nucleus
cuneate nucleus
nucleus of spinal
trigeminal tract
A
fibres from
A VII IX X
BB
B
C
C
Fig. 11.72 Suggested organisation of concentric segments of facial cutaneous innervation within the spinal tract.
346
Chapter
Divisions of the trigeminal nerve
C2
III
II
Fig. 11.75 A depressed left corneal response.
ophthalmic
maxillary Now test pinprick sensation at the same sites. If there
mandibular is sensory loss confined to the trigeminal nerve
distribution, the response to this stimulus becomes
Fig. 11.74 Cutaneous distribution of the three divisions of the normal at the level of the vertex but well above the
trigeminal nerve. angle of the jaw (Fig. 11.74). Again, variations in the
response at different sites should be noted. As it is difficult
to repeat the stimulus with equal force, minor differences
of sensitivity should be ignored unless they are
The corneal reflex consistent.
The afferent limb of the corneal reflex is contained in
the ophthalmic division of the trigeminal nerve. The
efferent pathway is within the seventh nerve. Stimulation THE CORNEAL RESPONSE
of the cornea produces both an ipsilateral and
The corneal response is elicited by lightly touching the
a contralateral blink response, the latter being
cornea with cotton wool. Carefully explain the procedure
approximately 5 ms slower than the former. The central
to the patient before proceeding. The patient’s subjective
conduction time for the reflex, approximately 40 ms,
reaction is assessed and the ipsilateral and contralateral
indicates it is polysynaptic. Scleral, rather than corneal,
blink reaction noted. Corneal sensitivity varies
stimulation results in a reflex with a considerably longer
considerably. Patients who wear contact lenses will need
latency.
to remove them first; even then dulling of the response
is likely but will be symmetrical. If the response is
substantially depressed, the cotton wool can be held
against the cornea without provoking a reaction (Fig.
Examination
11.75). Testing the response in an unconscious patient
must be done with great care. Repeated stimulation can
SENSORY
easily traumatise the cornea.
Details of the techniques for sensory examination are
given on pp 377–380. Convenient sites for testing are the
forehead, the medial aspect of the cheek and the chin.
Normally, it suffices to test light touch and pinprick alone MOTOR
but occasionally it is necessary to assess temperature Look for muscle wasting before testing the muscles of
appreciation. mastication. Wasting of temporalis produces hollowing
With the patient’s eyes closed, test light touch by above the zygoma (Fig. 11.76). Wasting of the masseter
touching the appropriate areas of the face with a wisp of is more difficult to detect but both masseter and temporalis
cotton wool. Avoid dragging the stimulus across the skin. can be palpated while the teeth are clenched (Fig. 11.77).
A partial loss of sensation is more likely than total The power of pterygoids and of masseter and temporalis
anaesthesia, so ask the patient to compare the stimulus can be assessed by resisting the patient’s attempts at
with sites in other divisions of the nerve on that side, then opening and closing the jaw, respectively. Ask the patient
with comparable areas on the other side of the face. to open the jaw first without, then with, resistance. In a
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Chapter
Fig. 11.76 Wasting of the temporalis producing hollowing above

the zygoma.
Fig. 11.78 Left trigeminal nerve lesion. Jaw deviation to the left.
The jaw jerk
Fig. 11.77 Palpating the masseter muscles.
unilateral trigeminal lesion, the jaw deviates to the

paralysed side (Fig. 11.78).
THE JAW JERK

Ask the patient to open the mouth slightly. Rest your
index finger on the apex of the jaw and tap it with the
patella hammer (Fig. 11.79). The response, a contraction
of the pterygoid muscles, varies widely in normal
individuals. Fig. 11.79 Testing the jaw jerk.
348
Chapter
MOTOR INVOLVEMENT
In a unilateral upper motor neuron syndrome, motor
involvement of the trigeminal distribution is not usually
clinically detectable. In a bilateral upper motor neuron
syndrome, the jaw jerk is exaggerated.
Facial numbness
• Malignant invasion of the trigeminal nerve

• Isolated trigeminal neuropathy
• Involvement in the lateral medullary syndrome Fig. 11.80 Tissue necrosis consequent to loss of nasal sensation.
• Involvement with cerebellopontine angle tumours
• Sensory involvement with thalamic, capsular or
cortical infarction
Facial nerve pathway
nervus intermedius greater superficial lacrimal

SENSORY INVOLVEMENT petrosal nerve gland
Malignant invasion of the nerve or its ganglion results in motor root
both sensory and motor deficit, although the latter is geniculate
spared initially if the ganglion is invaded. In isolated ganglion
trigeminal neuropathy, motor function is spared but there
is progressive loss of facial sensation. Inadvertent self-
sphenopalatine
injury can result in tissue necrosis (Fig. 11.80). In spinal ganglion
lesions above C2, selective loss of facial pain and
temperature sense is possible, sometimes with an ‘onion
ring’ distribution (Fig. 11.72). Loss of facial pain and lingual
nerve
temperature sense occurs ipsilaterally in the lateral chorda
medullary syndrome. Depression of light touch alone tympani
occurs with damage to the main sensory nucleus, while
sublingual
thalamic infarction is liable to affect all facial sensory gland
modalities. submandibular
gland
ALTERED CORNEAL RESPONSE

Fig. 11.81 Pathway of the facial nerve.
Loss of the corneal response may be the first or an early
sign of trigeminal compression and should be carefully
assessed in patients with unilateral facial pain or deafness.
The response is depressed in a patient with a unilateral and the internal auditory artery and vein. Shortly
lower motor neuron facial paresis but the contralateral afterwards, the facial nerve enters its own canal, passing
response is preserved. forwards above the cochlea before bending sharply
backwards, at which point the nerve expands to form the
geniculate ganglion. Here, the greater superficial petrosal
nerve leaves, eventually to reach the lacrimal gland via
The facial (seventh) nerve the sphenopalatine ganglion (Fig. 11.81). The nerve
to stapedius and the chorda tympani leave the facial
STRUCTURE AND FUNCTION nerve before its exit from the stylomastoid foramen.
Fibres from the seventh nerve nucleus loop around the Parasympathetic fibres in the chorda tympani supply the
lower end of the abducens nucleus before leaving the submandibular and sublingual glands. Special afferent
pons in close proximity to the acoustic nerve. Having fibres in the nerve supply taste sensation to the anterior
crossed the cerebellopontine angle, the nerve enters the two-thirds of the tongue. After leaving the stylomastoid
internal auditory meatus along with the acoustic nerve foramen, the nerve courses through the parotid gland on
349
Chapter
its way to the muscles of facial expression. Of these, small area of skin behind the ear. The taste fibres, having
frontalis elevates the eyebrow, orbicularis oculi closes the entered the pons, terminate in the nucleus of the tractus
eye and orbicularis oris the mouth, while platysma solitarius. From here, fibres project to the thalamus and
depresses the angle of the mouth. The buccinator muscle, hence the cortical gustatory area.
also supplied by the facial nerve, assists in mastication. The intensity of a taste experience is determined by the
Frontalis receives an innervation from both cortices size of the neural response. Taste buds are found in the
but the muscles of the lower face are innervated solely by tongue, soft palate, pharynx, larynx and oesophagus. A
the contralateral hemisphere. Emotional movements particular taste represents an amalgam of four primary
receive an additional supply from other sources, including taste functions, sweet, sour, bitter and salt, combined
the thalamus and globus pallidus. with any olfactory stimulating effect that the food or
The sensory component of the nerve innervates the beverage possesses. There is some decline in taste acuity
external auditory meatus, the tympanic membrane and a with age but to a lesser extent than occurs with
olfaction.
Questions to ask SYMPTOMS

Facial weakness of lower motor neuron type In a patient with a lower motor neuron facial weakness,
• Have you noticed any loss of taste on the front part certain questions may help to define the site of the
of the tongue? lesion.
• Have you noticed that noises appear excessively loud
in the ear on the same side?
• Does the eye on that side still water? Examination
Facial asymmetry is common, as is an asymmetry of
movement of the lower face during conversation.
Differential diagnosis Carefully observe the movements of the patient’s face
Facial weakness
while you are taking the history. An asymmetry of
blinking is a useful indicator of mild weakness of
Upper motor neuron facial weakness orbicularis oculi. Decide whether the nasolabial folds are
• Cerebrovascular disease equally well defined. Note any difference in the position
• Tumour of the angles of the mouth but remember that in a long-
Lower motor neuron facial weakness standing facial weakness fibrotic contracture of the
• Bell’s palsy muscles can elevate the angle of the mouth, suggesting
• Ramsay Hunt syndrome that the facial weakness is on the other side. Bilateral
• Trauma facial weakness is easily overlooked. The face lacks
• Parotid tumour expression and appears to sag (Fig. 11.82).
• Sarcoid Ask the patient to elevate the eyebrows (Fig. 11.83)
• Multiple sclerosis then close the eyes tightly. Normally, the eyelashes
virtually disappear. A useful sign of a mild weakness is a
Fig. 11.82 Bilateral facial weakness. Fig. 11.83 The patient has been asked to elevate the eyebrows, then to close the eyes
tightly.
350
Chapter
more marked protrusion of the eyelashes on the affected (sugar), salt, bitter (quinine) and sour (vinegar) solutions
side (Fig. 11.84). Try to open the eyes by pressing the are applied in turn, the mouth being washed out with
eyelids apart with your thumbs. If there is no weakness, distilled water between testing. Taste assessment is
the patient can prevent the eyelids separating. Now ask seldom justified for routine diagnostic purposes. Ask the
the patient to blow out the cheeks, then purse the lips patient if there has been any loss of lacrimation.
tightly together (Fig. 11.85). Finally, ask the patient to The area of skin around the ear that is supplied by the
tighten the neck muscles in order to assess platysma. seventh nerve receives overlapping innervation from the
Weakness of stapedius is suggested if the patient fifth and ninth nerves. Nothing is gained, therefore, by
complains of an undue sensitivity (hyperacusis) to noise testing sensation in this area.
in the affected ear.
Many patients who complain of an altered sensation
of taste are found to have a disturbance of olfaction. Taste Clinical application
is difficult to test. Simply applying drops of a test solution
on the protruded tongue seldom produces a consistent UPPER MOTOR NEURON FACIAL WEAKNESS
response. For assessing seventh nerve function, the
An upper motor neuron facial weakness results from
stimulus should be confined to the anterior two-thirds of
interruption of descending fibres passing from the
the tongue, each side of which is tested separately. Sweet
contralateral motor cortex to the ipsilateral facial nerve
nucleus. There is minimal asymmetry of frontalis
contraction on the two sides but substantial asymmetry
of the lower face (Fig. 11.86). Causes include
cerebrovascular disease, tumour and head injury.
LOWER MOTOR NEURON FACIAL WEAKNESS

In a lower motor neuron facial weakness, all the facial
muscles are equally affected unless the lesion lies so
distally that it involves individual branches of the nerve.
The site of the lesion can be deduced from the presence
or absence of certain symptoms and signs. If it lies at or
beyond the stylomastoid foramen, there will be no
disturbance of taste, hearing or lacrimation. Involvement
of the nerve immediately proximal to the origin of chorda
tympani will result in loss of taste over the anterior two-
thirds of the tongue; involvement proximal to the
departure of the nerve to stapedius will result in
Fig. 11.84 The patient has been asked to close the eyes tightly. hyperacusis. Loss of lacrimation is added to these other
The eyelashes on the right are slightly more prominent than those on symptoms if the nerve is damaged at or proximal to the
the left. gasserian ganglion.
Fig. 11.85 The patient is blowing out the cheeks, pursing his lips and baring his teeth.
351
Chapter
BELL’S PALSY fibres may extend to muscles not originally part of their
Bell’s palsy is an idiopathic paralysis of the facial nerve. innervation (aberrant reinnervation). In such patients
When the resulting facial weakness is substantial, there blinking can result in synkinetic contraction of muscles
is loss of forehead furrowing, eye closure and mouth in the lower face (Fig. 11.88) and misdirection to the
elevation (Fig. 11.87). If denervation occurs, regrowth of lacrimal gland of fibres originally destined for the salivary
glands results in eye watering when a food stimulus
appears (crocodile tears).
RAMSAY HUNT SYNDROME

The Ramsay Hunt syndrome is the consequence of
herpetic involvement of the geniculate ganglion. A
vesicular eruption can occur at a number of sites, including
the pinna (Fig. 11.89).
FACIAL MOVEMENT DISORDERS

• Fasciculation – virtually confined to patients with motor
neuron disease.
• Myokymia – produces a fine, more or less continuous,
shimmering contraction of some or all of the muscles
supplied by the facial nerve. Multiple sclerosis is the
most common cause.
• Hemifacial spasm – involuntary, haphazard contraction
of facial muscle, often initially confined to orbicularis
Fig. 11.86 Upper motor neuron facial weakness. The patient has oculi (Fig. 11.90). Eventually a mild facial weakness
been asked to bare her teeth. appears.
Fig. 11.87 A right Bell’s palsy in a girl aged

11 years.
Fig. 11.88 Aberrant reinnervation. The Fig. 11.89 Vesicular eruption in a case of Fig. 11.90 Left hemifacial spasm. The left
right angle of the mouth elevates during eye the Ramsay Hunt syndrome. palpebral fissure has narrowed during the
closure. Previous right Bell’s palsy. contraction.
352
Chapter
The acoustic (eighth) nerve 11
• Blepharospasm – forced involuntary repetitive The inferior part of the bony labyrinth contains the
blinking. osseous canal of the cochlea. A bony spur, the osseous
• Tics – stereotyped repetitive movements, at least in spiral lamina, projects into the canal, dividing it into two
part under voluntary control. corridors: the scala vestibuli and the scala tympani (Fig.
• Orofacial dyskinesia – involuntary semirepetitive 11.92). In the wall of the cochlear duct, resting on the
contraction of muscles round the mouth, often with basilar membrane, is the spiral organ of Corti, which is
abnormal movements of the tongue. Occurs innervated by the cochlear component of the auditory
spontaneously and with certain drugs, particularly nerve. The vestibular component innervates the specialised
phenothiazines. receptor areas of the utricle and the semicircular canals.
The saccule and part of the posterior semicircular canal
receive fibres from the cochlear division.
The acoustic (eighth) nerve The vestibular and cochlear components unite within
the internal auditory canal. The nerve then crosses the
STRUCTURE AND FUNCTION subarachnoid space and enters the brainstem at the
Vibration of the tympanic membrane, triggered by a junction of pons and medulla, lateral to the facial nerve.
sound stimulus, is transmitted through a chain of three In the brainstem the acoustic nerve projects predominantly
ossicles (the malleus, incus and stapes) situated in the to the contralateral inferior colliculus. From here, fibres
middle ear (Fig. 11.91). The movements of the ossicles pass to the medial geniculate body and then in the
are also influenced by the tensor tympani and stapedius auditory radiation to the auditory cortex in the upper
muscles. The base of the stapes is attached to the oval aspect of the temporal lobe (Heschl’s gyrus). The fibres
window. Vibration of the oval window sets up movement of the vestibular nerve terminate in four separate nuclei.
in the perilymph which occupies the bony labyrinth, A projection from the lateral vestibular nucleus forms the
comprising the cochlea, the vestibule and the semicircular vestibulospinal tract, which descends, mainly ipsilaterally,
canals. Lying within the bony labyrinth and containing to the cervical and lumbar motor neurons. The medial
endolymph is the membranous labyrinth comprising the vestibular nucleus has connections to the contralateral
cochlear duct, the saccule, the utricle and three semicircular abducens nucleus and the cerebellum. These pathways
ducts. The semicircular canals, each surrounding a are important in gaze-holding and for the control of
semicircular duct, are arranged in planes roughly at right smooth pursuit eye movements.
angles to each other. The canals open into the vestibule Sound waves, transmitted through the perilymph,
which contains the saccule and utricle. Specialised reach the organ of Corti via the ossicular chain, by
receptor areas (maculae) are found in the saccule and vibration of the round window or by bony transmission.
utricle. At one end of each semicircular canal is a receptor High-frequency waves produce a maximal response in
organ (crista ampullaris). the basal part of the cochlea; low-frequency waves at its
apex. Activity in the components of the auditory brainstem
Middle and inner ear

Cochlea
semicircular crista ampularis

duct osseous spiral
perilymphatic ductus lamina
space endolymphaticus
utricular macula scala
saccular macula vestibuli
dura vestibular
mater membrane
incus
malleus cochlear
aqueduct of
duct
cochlea
external auditory
scala spiral basilar
meatus
vestibuli ganglion membrane
stapes
osseus cochlear organ of
fenestra cochleae spiral nerve Corti
(round window) lamina
scala
pharyngotympanic cochlear duct tympani
tube scala tympani
Fig. 11.91 Organisation of the middle and inner ear. The

endolymphatic system is coloured purple. Fig. 11.92 The cochlea.
353
Chapter
pathway is reflected in a succession of negative potentials

recorded from mastoid and scalp electrodes following a Glossopharyngeal nerve
click stimulus. Seven potentials occurring within the first
tractus dorsal
10 ms of the stimulus are thought to relate to specific
solitarius vagoglossopharyngeal
anatomical sites. nucleus
spinal tract hypoglossal
The nerve endings in the cristae and maculae are of trigeminal nucleus
triggered by movements of the endolymph, either from nerve
stimulation of the hair processes of the cristae or
by movements of small calcific particles (the otoliths)
embedded in a membrane of the maculae of the utricle
and saccule. Head position is coded by the receptors of
the utricle and saccule. Head tilt shifts the otoliths,
displaces the hair cells and initiates an action potential in
the fibres of the vestibular nerve. The semicircular canals
are responsible for the detection of rotational head
movements, via patterns of flow produced in the
endolymphatic system. hypoglossal
nerve
Overall, the vestibular system provides information on
head posture and movement, integrated with visual data
vagus and olivary spinothalamic nucleus
and proprioceptive information arising from neck muscle glossopharyngeal nucleus tract ambiguus
receptors. nerves
SYMPTOMS Fig. 11.93 Relationship of the central components of the

Deafness glossopharyngeal nerve.
If the patient complains of deafness, determine the mode

of onset, whether progressive or static, and whether oesophagus (Fig. 11.93). Corticobulbar fibres destined for
unilateral or bilateral. Other important factors include the each nucleus ambiguus originate in both cerebral
family history and noise exposure. hemispheres. The glossopharyngeal nerve emerges from
the upper part of the medulla, bounded above and below
Vertigo
by the facial nerve and the vagus respectively. It leaves
If the patient has vertigo, ascertain whether symptoms the skull through the jugular foramen in company
can be induced by certain postures or movements. with the vagus and the accessory nerves. The general
visceral efferent and special visceral afferent fibres are not
Questions to ask readily testable. Somatic afferent components in the
glossopharyngeal nerve supply a number of structures,
Dizziness
including the tonsillar fossa and parts of the pharynx.
• Does the patient describe dizziness or giddiness or is Arterial baroreceptors in the carotid sinus are innervated
there an experience of rotation, either of the patient by the glossopharyngeal nerve, while those in the aortic
or of the environment (vertigo)? arch are innervated by the vagus.
• Is the dizziness accompanied by an unsteadiness
when walking?
• Is any vertigo triggered only by a certain movement
or head posture? Ninth cranial nerve disorders
• Jugular foramen syndrome

• Chiari malformation
• Lateral medullary syndrome
Examination and clinical application • Glossopharyngeal neuralgia
See Chapter 4.
The gag reflex

The glossopharyngeal (ninth) nerve The gag reflex is triggered by applying a stimulus to the
tonsillar fossa. The end-result is midline elevation of
STRUCTURE AND FUNCTION the palate. The afferent arc probably travels in the
The ninth, tenth and eleventh cranial nerves share a glossopharyngeal nerve only if the stimulus is painful.
motor nucleus (nucleus ambiguus) that innervates the The efferent arc, supplying levator palati, passes in the
striated muscle of the pharynx, larynx and upper vagus.
354
Chapter
The vagus (tenth) nerve 11
the painful paroxysms or triggered independently by

The gag reflex
swallowing.
The vagus (tenth) nerve

The roots of the vagus leave the medulla immediately
below the glossopharyngeal nerve. Both nerves pass
through the jugular foramen alongside the accessory
nerve. The components of the vagus mirror those of
the glossopharyngeal nerve. The special efferent fibres
innervate the striated muscle of the pharynx, larynx and
upper oesophagus. The recurrent laryngeal branch of the
vagus supplies all the intrinsic muscles of the larynx
except for cricothyroid, which is supplied by the external
branch of the nerve.
In the heart, fibres from the right vagus end principally
around the sinoatrial node, while fibres from the left end
principally around the atrioventricular node. Vagal fibres
innervating the aortic arch are concerned with the
Fig. 11.94 The gag reflex. The orange stick is pressed into the base baroreceptor reflex.
of the tonsillar fossa.
Tenth cranial nerve disorders
Examination
Bilateral supranuclear palsy (pseudobulbar palsy)
The motor innervation of the ninth nerve cannot be • Stroke
tested, nor can the cutaneous distribution in the region • Motor neuron disease
of the pinna be separated from the overlapping Unilateral nuclear lesions
contributions of the seventh and tenth nerves. • Lateral medullary syndrome
Testing the gag reflex is an uncomfortable experience Bilateral nuclear lesions (bulbar palsy)
and should be performed only if there is a suspicion of a • Motor neuron disease
disturbance of the lower cranial nerves. Clearly indicate
Recurrent laryngeal palsy
to the patient what is involved. Press the end of an orange
• Aortic aneurysm
stick first into one tonsillar fossa then the other (Fig.
• Malignancy
11.94). Besides confirming that the palate rises in the
• Post-thyroid surgery
midline, ask the patient if the sensation is comparable on
the two sides. In the presence of a glossopharyngeal
lesion, the gag reflex is depressed or absent on that
side.
Examination
Evaluation is confined to assessment of spontaneous and
Clinical application reflex movements of the uvula and posterior pharyngeal
wall. A unilateral lesion of the vagus produces paralysis
Isolated lesions of the ninth nerve are almost unknown. of the ipsilateral soft palate. At rest, the palate lies slightly
A destructive process in the region of the jugular lower on the affected side then deviates to the intact side
foramen, most commonly a nasopharyngeal carcinoma, during phonation or on testing the gag reflex (Fig. 11.95).
disrupts the ninth, tenth and eleventh cranial nerves. In An accompanying deviation of the median raphe of the
the Chiari malformation, stretching of the ninth nerve posterior pharyngeal wall is more characteristic of a
can lead to depression of the gag reflex on one or both glossopharyngeal, rather than a vagal, lesion. Minor
sides. Glossopharyngeal neuralgia usually results from deviations of the uvula, particularly if not consistent,
distortion of the nerve by a tumour or a vascular anomaly. should be ignored. The accompanying unilateral vocal
Paroxysms of pain in the tongue, soft palate or tonsil are cord paralysis, leading to hoarseness, is not confirmable
triggered by swallowing, chewing or protruding the by bedside examination.
tongue. Involvement of fibres from the carotid sinus can Bilateral palsies of the vagus produce severe palatal
result in syncopal attacks occurring at the time of palsy, with nasal regurgitation and aphonia.
355
Chapter
Accessory nerve
accessory
nerve
medulla
vagus oblongata
nerve
spinal accessory
nerve spinal cord
C2
nerves to
sternomastoid C3
C4
nerves to C5
trapezius
muscle
Fig. 11.96 Distribution of the components of the accessory nerve.
combined nerve leaves the skull through the jugular

foramen.
Fig. 11.95 Palsy of the left vagus. The palate deviates to the right The cranial root joins the vagus, while the spinal root
on phonation (b). receives contributions from the second, third and fourth
cervical roots (Fig. 11.96) before innervating sternomastoid
and the upper fibres of trapezius. The fibres from the
second and third cervical roots passing to the sternomastoid
Clinical application are probably proprioceptive, while the fibres from the
third and fourth roots to the lower part of trapezius are
A unilateral disturbance of the corticobulbar projection purely motor.
to the nucleus ambiguus is usually without consequence. The spinal accessory nucleus receives innervation from
However, bilateral supranuclear lesions, for example both cerebral hemispheres. The fibres concerned with the
caused by cerebrovascular disease, are symptomatic. innervation of sternomastoid possibly undergo a double
Nuclear vagal lesions occur in polio and after lateral decussation within the brainstem.
medullary infarction. The main branch of the vagus is
seldom affected in isolation. Recurrent laryngeal palsies
are more common and are usually left-sided because of
the longer course of the nerve on that side. Causes include Differential diagnosis
aortic aneurysm, thyroid surgery and malignant invasion Accessory nerve disorders
of the mediastinum. Isolated laryngeal palsies are often
• Involvement in jugular foramen tumours
of unknown aetiology.
• Accessory palsy of unknown cause
The accessory (eleventh) nerve

Examination
The accessory nerve has both cranial and spinal There is no way of assessing the innervation of the cranial
components. The cranial part originates from the nucleus component of the accessory nerve but that of the spinal
ambiguus and exits from the medulla in line with the component can be assessed by examining trapezius and
ninth and tenth cranial nerves (Fig. 11.96). The spinal sternomastoid. The function of trapezius is assessed by
part is formed by a series of rootlets that emerge from asking the patient to elevate the shoulder, first without,
the lateral aspect of the cervical spinal cord down to the then with, resistance (Fig. 11.97). The strength of
fifth segment. The rootlets form a single trunk that contraction of sternomastoid can be gauged by asking the
ascends alongside the cord, passes through the foramen patient to rotate the head to the relevant side against
magnum and unites with the cranial component. The resistance (Fig. 11.98).
356
Chapter
The hypoglossal (twelfth) nerve 11
Fig. 11.99 Right accessory nerve lesion.
of the head and neck, which lead to hypertrophy of the

relevant muscles in longstanding cases (Fig. 11.100).
Fig. 11.97 Testing the trapezius muscles. The shoulders are
elevated first without, then with, resistance.
The hypoglossal (twelfth) nerve
The hypoglossal nucleus lies close to the midline in the
floor of the fourth ventricle and receives supranuclear
fibres from both but principally the contralateral
hemisphere. The hypoglossal nerve leaves the skull
through the anterior condylar canal and supplies all the
intrinsic muscles of the tongue, and all its extrinsic
muscles except palatoglossus.
Tongue paralysis
• Malignant invasion of the skull base

• Chiari malformation
• Pseudobulbar palsy with cerebrovascular disease or
motor neuron disease
Fig. 11.98 Testing head rotation.
Examination
First inspect the tongue as it lies in the base of the oral
Isolated lesions of the eleventh cranial nerve are rare. cavity. In many patients there are tremulous movements
Tumours in the region of the jugular foramen are likely that are often hard to distinguish from fasciculation
to produce a combined palsy of the ninth, tenth and or true involuntary movements. Fasciculation imparts
eleventh nerves (Fig. 11.99). In the presence of a a shimmering motion to the surface of the tongue.
hemiplegia, the trapezius muscle on the hemiplegic side Involuntary movements include a coarse tremor, for
is affected. A delay in shoulder shrug may be an early example in Parkinson’s disease, and complex,
sign. The same hemiplegia, however, will affect the unpredictable movements found in such conditions as
contralateral sternomastoid, that is the muscle rotating Huntington’s disease and orofacial dyskinesia. While
the neck towards the hemiplegic limbs. The weakness in assessing the tongue for spontaneous contractions,
such patients is incomplete. Spasmodic torticollis is a observe its bulk. As the tongue wastes it becomes thinner
focal dystonia particularly affecting the sternomastoid and more wrinkled. Now ask the patient to protrude the
muscle. Typically, there are repetitive rotatory movements tongue. Minor deviations from the midline are sometimes
357
Chapter
Fig. 11.102 Left hypoglossal nerve lesion.
brainstem motor nuclei, resulting in dysphagia and

dysarthria. The tongue is wasted and immobile.
Fig. 11.100 Spasmodic torticollis associated with contraction of the
left sternomastoid. UNILATERAL UPPER MOTOR NEURON LESION
A unilateral upper motor neuron lesion has little effect
on tongue function, although it may protrude slightly to
the side of the hemiparesis.
BILATERAL UPPER MOTOR NEURON LESION

Bilateral involvement of the pyramidal projections to the
brainstem nuclei, usually the consequence of
cerebrovascular disease, results in a pseudobulbar palsy.
There is dysphagia, dysarthria and emotional lability. The
tongue is stiff and immobile and there is weakness of
palatal elevation combined with a brisk gag reflex and
jaw jerk.
Review
Fig. 11.101 Examination of the tongue. Protrusion (a) and lateral
movements (b). Cranial nerve examination
I Examine smell in each nostril

II Examine visual acuity, visual field, fundus
seen in normal individuals. Finally, ask the patient to and pupillary light response
move the tongue rapidly from side to side and assess its III, IV, VI Examine eye movements and near reaction.
power by instructing the patient to push the tongue Check for nystagmus
against the side of the cheek (Fig. 11.101). A disturbance V Examine motor and sensory innervation
of the speed of tongue movement occurs in extrapyramidal plus the jaw jerk and the corneal response
diseases, including Parkinson’s disease. VII Examine the muscles of facial expression
(plus buccinator) and taste over the anterior
two-thirds of the tongue
Clinical application VIII Examine hearing and perform Rinne’s and
Weber’s tests
UNILATERAL AND BILATERAL LOWER IX Examine pain sensation in the tonsillar
MOTOR NEURON LESIONS fossae
In a unilateral hypoglossal nerve lesion, there is focal X Examine palatal movement plus the gag
atrophy, fasciculation and deviation to the paralysed side reflex
(Fig. 11.102). Such a lesion can occur in isolation or as XI Examine sternomastoid and the upper
the consequence of malignant invasion of the skull base. fibres of trapezius
Bilateral involvement of the lower motor neuron XII Examine tongue movements and
projections to the tongue is usually part of a bulbar palsy. appearance
There is additional involvement of the other lower
358
Chapter
The motor system 11

the contralateral half of the body are represented
inversely, with a large area responsible for the hand,
Cranial nerve symptoms
thumb and fingers, and a much smaller area, on the
• Visual obscuration with posture change. Suggests medial aspect of the hemisphere, responsible for the
papilloedema. If confirmed – urgent referral. lower limb (Fig. 11.103). Corticospinal neurons originate
• Diplopia. Numerous causes, but all require in the premotor association area (6), the motor area (4),
neurological or ophthalmological appraisal. the sensory area and part of the sensory association area.
• Facial numbness. In isolation, may be the first sign of The medial aspect of area 6 is called the supplementary
an isolated trigeminal neuropathy, but skull base motor area.
metastases need to be considered. The motor cortex sends approximately a million
• Lower motor neuron facial paresis. Usually due to a pyramidal tract axons to the medulla. Less than 50% of
Bell’s palsy. If so, may benefit from steroids and the neurons providing the fibres traversing the medullary
aciclovir. pyramids are located in the precentral primary and
• Dysarthria. In isolation, may be part of a cranial supplementary motor areas, with the rest coming from
neuropathy, but not uncommonly the presenting the postcentral cortex. The fibres from the cortex pass
feature of motor neuron disease. through the corona radiata and internal capsule before
traversing the midbrain and pons on their way to the
medulla (Fig. 11.104). Approximately 75% of the fibres
The motor system reaching the medulla continue into the spinal cord,
forming the lateral and ventral corticospinal tracts.
STRUCTURE AND FUNCTION Approximately three-quarters of the fibres decussate.
The major supraspinal influences on motor activity are Some pyramidal fibres terminate directly on anterior
the sensorimotor cortex (exerting its role primarily horn cells but most synapse with internuncial neurons in
through the pyramidal system), the basal ganglia, a the spinal grey matter, which, in turn, transmit to the
number of tracts descending from the brainstem and the anterior horn cells.
cerebellum. The upper motor neuron defines that part of The motor cortex is particularly concerned with skilled
the motor pathway between the cerebral cortex and the activities requiring finely tuned movements of the hand
anterior horn cell. The lower motor neuron consists of and fingers. Less than 25% of the corticospinal neurons
the anterior horn cell and its motor axon. conduct at a velocity exceeding 25 m/s. The majority are
small and slowly conducting, influencing fine gradations
The pyramidal tract of force by being recruited early in the performance of a
The motor cortex is situated in the precentral convolution, motor task. The larger, more rapidly conducting neurons
anterior to the rolandic fissure (area 4). Movements of are recruited late when larger movements are required.
Motor cortex
wrist elbow
hand shoulder
little finger trunk
ring finger hip
middle finger knee
index finger ankle
thumb toes
neck
brow
eyelid and eyeball
face
lips
jaw
tongue vocalisation
swallowing salivation
pyramidal tract
mastication
Fig. 11.103 Organisation of the motor cortex.
359
Chapter
thalamus and the reticular formation. Major outputs pass

Pyramidal system
from the globus pallidus to the thalamus and pons and
from the substantia nigra to the thalamus, superior
colliculus and reticular formation. Finally, there are
multiple interconnections between the various
components of the system. The pigmented structures of
the basal ganglia give rise to dopaminergic driven
pathways passing from the pars compacta of the substantia
nigra to the striatum (caudate nucleus and putamen) and
from the ventral tegmentum to the nucleus accumbens
and the frontal cortex.
The basal ganglia integrate the individual components
of skilled motor tasks and are important in the control of
heavily learned motor activity.
The tracts descending from the brainstem

Vestibulospinal tract The vestibulospinal tract descends
level of uncrossed from the lateral vestibular nucleus. Its principal
V motor nucleus projection is to the cervical cord.
Reticulospinal tracts Inhibitory and facilitatory
reticulospinal tracts descend from the region of the
midbrain and pons (Fig. 11.105). There are four
level of inhibitory pathways, two of which are monoaminergic.
VII motor nucleus The pathways of the monoaminergic tracts are
uncertain. A dorsal reticulospinal system passes from the
pontomedullary reticular formation to the dorsolateral
column of the spinal cord. The fourth inhibitory pathway
level of originates in the medulla and descends ventral to the
nucleus ambiguus lateral corticospinal tract. The facilitatory reticulospinal
tract passes from the pons and runs in the anterior column
level of of the cord close to the ventral sulcus.
pyramidal The initiating signals for locomotion are largely the
decussation responsibility of the reticulospinal and vestibulospinal
tracts. The two monoaminergic inhibitory reticulospinal
pathways alter the effects of the flexor reflex afferents.
The dorsal reticulospinal tract inhibits segmentally active
flexor reflex afferents and Ib polysynaptic paths. By doing
so, it allows the activation of coordinated stepping
movements. The ventral reticulospinal pathway inhibits
the monosynaptic reflex arc, particularly of extensors,
Fig. 11.104 Pathway of the pyramidal system. again in preparation for the release of spinal cord
structures from their antigravity function. Interruption
of this pathway results in hypertonicity and increased
Discharge rates in the neurons relate to the force being
reflexes. The antigravity reflexes for standing are promoted
exerted and its rate of change.
by the facilitatory reticulospinal tract. Stimulation of this
Activity within the corticospinal system also releases
pathway tonically augments flexors in the upper limbs
limbs from the postures imposed by gravity. In the
and extensors in the lower limbs. The vestibulospinal
upper limbs, this results in inhibition of flexors and
pathway has similar properties. The cerebellum has major
facilitation of extensors, with the reverse effects in the
inputs to the lateral vestibular nucleus and hence its
lower limbs.
descending pathway.
The extrapyramidal system The spinal cord and lower motor neuron
The basal ganglia are located in the basal forebrain and The anterior horn cell contains alpha, beta and gamma
the midbrain. They include the nucleus accumbens, the motor neurons. The alpha axons are of large diameter,
putamen, globus pallidus and caudate nucleus, the conducting at approximately 45 m/s in the lower limb
substantia nigra and the subthalamic nucleus. Major and 55 m/s in the upper limb. A motor unit comprises
inputs to the basal ganglia come from the cortex, the the anterior horn cell, its axon and the muscle fibres
360
Chapter
The motor system 11
it innervates, which may range from 10 to several organ have an inhibitory effect on the stretch reflex via
hundred. interneurons (Fig. 11.106).
The stretch reflex The afferent limb of the stretch reflex Other reflexes Flexor reflex afferents (FRA), contained
arc is contained in Ia fibres innervating the muscle spindle. in small fibres, are excited by painful stimulation of the
The fibres synapse with anterior horn cells that supply skin and deeper structures. They reach the motor neurons
alpha motor neurons to the skeletal muscle containing by polysynaptic pathways through interneurons within
that spindle. The muscle spindle is innervated by gamma the spinal cord. For the lower limb, these polysynaptic
fibres. Ib afferent fibres, originating from the Golgi tendon pathways innervate the segments needed to evoke
a flexor withdrawal reaction to a painful stimulus.
Connections to the other side of the cord facilitate
extensor tone there.
Descending pathways
Muscle The fibres of skeletal muscle consist of myofibrils
neocortex pontine reticular
bounded by a sarcolemmal membrane. There are at least
(frontal and formation two types of muscle fibre with differing histochemical
parietal (central nuclei) characteristics. Type 1 fibres are slow contracting, type 2
lobes)
fast contracting.
lateral
vestibular The reflexes and abnormal muscle tone The stretch
nucleus
reflex has phasic and tonic components. The tendon
medullary dorsal reflexes are phasic. Tonic stretch reflexes result in a
reticular reticulospinal sustained muscle contraction that has both dynamic
formation tract
(central nuclei)
(velocity-dependent) and static (length-dependent)
(inhibitory)
components. Patients who relax poorly are activating
tonic stretch reflexes that then hinder displacement of the
lateral limb.
corticospinal
pontine tract Spasticity Spasticity is a feature of an upper motor
reticulospinal neuron lesion, although its appearance owes more to
tract
(facilitatory) disruption of the ventral reticulospinal pathway than to
altered pyramidal tract function. Indeed, selective damage
ventral vestibulospinal medullary of the latter results in hypotonia rather than spasticity.
corticospinal tract reticulospinal In spasticity the increase in muscle tone is velocity-
tract tract (inhibitory)
dependent. As the speed of displacement is increased, a
critical velocity is reached at which muscle tone suddenly
Fig. 11.105 Descending pathways from the brainstem concerned increases and resistance appears. After a pyramidal tract
with movement. lesion, the development of increased tone in antigravity
Stretch reflex arch
tendon Golgi tendon organs
muscle fibre
muscle spindle
primary ending
nuclear-bag fibre
chain fibre
vestibulospinal tract
Fig. 11.106 The stretch reflex arc.
361
Chapter
muscles results in extension of the lower limbs. At a

certain point of flexion of the extended limb, the
hypertonicity suddenly resolves because of a length-
dependent inhibition of the quadriceps stretch reflex: the
clasp-knife effect. The phenomenon is less evident in the
upper limbs and is particularly evident in spinal lesions.
The inhibition of lower limb extensors at a critical level
of stretch results from facilitation of the flexor reflex
afferent system due to loss of its inhibition by interruption
of the dorsal reticulospinal tract. The degree of loss of
flexor inhibition determines the likelihood of flexor
spasms emerging.
Rigidity The rigidity of Parkinson’s disease and
other extrapyramidal disorders is more uniformly
distributed between flexors and extensors and is not
velocity-dependent. Furthermore, a clasp-knife effect
does not occur. In some cases, the rigidity is fluctuant,
producing a cogwheel effect. The frequency of the
Fig. 11.107 Focal wasting of the right thenar eminence secondary
cogwheeling is more closely linked to the frequency of to median nerve compression.
the action than to the resting tremor found in parkinsonian
patients.
more likely to be the result of impaired nutrition or

malignancy rather than neurological disease. Focal muscle
Questions to ask
wasting can rapidly follow injury of a joint with consequent
Muscle weakness immobilisation. If you suspect a discrepancy in size
• Is the weakness confined to one limb or to one side between two limbs, use a tape measure to record the limb
of the body? cirumference. Choose a suitable landmark, for instance
• Is the weakness static, progressive or fluctuant? the joint margin of the knee, then measure the
• Is the weakness accompanied by a feeling of circumference of the limb at a specified distance from
stiffness or is the affected limb floppy? the landmark. Remember that the circumference of the
dominant limb is likely to be slightly greater. The pattern
of wasting often suggests a particular peripheral nerve or
root disorder (Fig. 11.107).
SYMPTOMS While inspecting the muscle, look for spontaneous
contractions. Fasciculation is caused by spontaneous
When recording a complaint of weakness, determine its contraction of the fibres belonging to a single motor unit.
mode of onset, it distribution, whether it fluctuates in Depending on the size of the motor unit, the fasciculation
severity and whether it is associated with feelings of appears either as a fine flicker (e.g. in a hand muscle) or
stiffness in the affected part. as a coarse twitch (e.g. in the thigh). Fasciculation often
appears in short bursts before disappearing for several
minutes. Muscles may hypertrophy as well as atrophy.
Examination Pseudohypertrophic muscles are infiltrated by fat and
connective tissue and are weak on formal testing (Fig.
A detailed outline of the limb muscles and their 11.108). Muscle palpation provides little information,
examination is contained in Chapter 10. This section although ischaemic, fibrotic muscle feels harder than
concentrates on an overview of patterns of weakness and normal and acutely inflamed muscle is tender.
how that pattern is helpful in diagnosis.
TONE
APPEARANCE Assessment of muscle tone requires both skill on the part
Some thinning of the small hand muscles is common in of the examiner and relaxation on the part of the patient.
elderly people but is not associated with weakness. When Ensure that the patient is comfortable and warm. First
assessing muscle wasting, do not neglect areas hidden observe the limb posture, as this may indicate the
when the patient lies in the supine position. Sit the distribution of altered tone between the flexors and
patient forward to look at the periscapular muscles and extensors of the limb. For screening purposes, assess
turn the patient over to assess the bulk of the glutei, flexion and extension at the elbow, pronation and
hamstrings and calves. A global loss of muscle bulk is supination of the forearm and flexion and extension at
362
Chapter
The motor system 11
Many tense, nervous patients will appear to have a

fluctuant increase in tone but the variability should
suggest there is no significant pathology.
Gegenhalten
A more diffuse increase in tone, Gegenhalten, can be
found in patients with an altered level of consciousness
and in individuals with frontal lobe lesions.
Hypotonia
Reduced tone is more difficult to detect. The limb is
floppy and is liable to show abnormal excursions when
moved passively. Hypotonia occurs in the presence of a
lower motor neuron lesion and in cerebellar disease.
MUSCLE POWER
Muscle weakness is often suggested by lack of spontaneous
movement in the affected part during conversation or
Fig. 11.108 Pseudohypertrophy of the calf muscles.
when the patient walks. In Parkinson’s disease, however,
certain automatic movements can disappear even in the
absence of weakness. The UK Medical Research Council
system of classification is recommended for grading
the knee, using a range of speeds rather than a fixed
muscle weakness. To apply this system to a muscle, test
velocity. Remember to take account of any painful limb
its strength as shown for biceps in Figure 11.109.
or joint.
Remember to take account of the patient’s age, occupation
and your own physical development. In practice grades
Spastic limbs
4 and 5 are separated by a wide range of strength but as
In spastic limbs, at a critical velocity a catch appears that you gain experience you can overcome this problem by
is absent during slower displacements. Subsequently, the using the grades 4+, 4++ and 5−.
hypertonus fades away as stretch continues. Spasticity is
selectively distributed. In the upper limbs it predominates
Symptoms and signs
in flexors and is more evident when the forearm is
supinated than when it is pronated. In the lower limb it Definitions of paralysis
is greater in quadriceps than in the hamstrings. This Paresis Partial paralysis
selectivity may vary, particularly in spinal cord disease Plegia Complete paralysis
but the finding is highly suggestive of a disorder affecting Monoplegia Involvement of a single limb
the upper motor neuron. In spinal cord disease, release Hemiplegia Involvement of one-half of the body
of flexor reflex afferents may be so prominent that mild Paraplegia Paralysis of the legs
stimulation of the lower limb produces a flexor reaction Tetraplegia Paralysis of all four limbs
at the hip and knee. In longstanding spasticity, you may
find that the limb can no longer be fully displaced at the
affected joint. For example, in the leg, persistent
hypertonia in the plantar flexors can lead to shortening Symptoms and signs
of the tendo Achilles. MRC classification of muscle power
0 Total paralysis
Rigidity
1 Flicker of contraction
Rigidity is more uniformly distributed in the limb. It may 2 Movement with gravity eliminated
begin unilaterally and is sometimes easier to detect in 3 Movement against gravity
one joint than another. The resistance is felt at low speeds 4 Movement against resistance but incomplete
of displacement and does not ‘melt away’. Rigidity is 5 Normal power
activated by contraction of muscle in an unaffected limb.
If you have doubts regarding an increase in tone, ask the
patient either to clench the teeth or grip the hand not A description of the methods of assessing individual
being tested. In patients with rigidity, the increased tone muscles is given in Chapter 10. Looking at a limited
becomes more evident during this procedure. At times number can screen for many neurological disorders. In
rigidity is not uniform but fluctuates in a phasic manner, the upper limbs, first ask the patient to shrug the
aptly described as cogwheeling. shoulders. In an early pyramidal lesion above the level of
363
Chapter
Testing biceps Early pyramidal lesion
grade 5
grade 4
grade 3 Fig. 11.110 Delayed right shoulder shrug in a patient with an early
pyramidal lesion.
abducted to 90°. Then ask the patient to maintain this

posture for a minute and retest. In the lower limb, hip
flexion can be tested in a similar fashion. Remember that
a fluctuating performance is also often prominent in
nonorganic weakness.
grade 2 Myotonia results in impaired relaxation of skeletal
muscle after contraction. Ask the patient to clench the
fists tightly then release them; if the patient has myotonia,
there is a significant delay before the fingers can be fully
extended. There is likely to be abnormal dimpling of
muscle after percussion. Tap the thenar eminence with
the patella hammer. In the presence of myotonia, the
muscle dimples and stays dimpled for several seconds.
The same sign can be elicited in the tongue (Fig.
11.111).
Fig. 11.109 The application of the MRC system of grading muscle
power to the examination of biceps.
Emergency
Rapidly developing limb weakness
C2 (but also in unilateral Parkinson’s disease), the affected
Consider: Guillain–Barre syndrome, cord compression
shoulder lags behind its fellow (Fig. 11.110). Next, test
deltoid, biceps, triceps, then the first dorsal interosseous
and abductor pollicis brevis. Score each muscle on the
MRC scale. Test one arm at a time rather than trying to Emergency
test both arms together. In the lower limb, look at hip
Acute hemiplegia
flexion and extension, knee flexion and extension and
dorsiflexion and plantar flexion of the feet. Consider: most likely CVA (cerebrovascular accident),
If the degree of muscle weakness fluctuates during the but other possibilities include abscess, cerebral tumour
course of the examination, test for fatiguability. In the and encephalitis
upper limb first attempt to depress the arms when
364
Chapter
The motor system 11
Fig. 11.112 Posture of the upper limbs for testing the biceps and
Fig. 11.111 Percussion myotonia of the tongue. supinator reflexes.
DEEP TENDON REFLEXES

Testing the reflexes assesses the reflex arc and the
supraspinal influences that operate on it. Each reflex is
graded according to strength of response, as shown in
the ‘symptoms and signs’ box.
Reflexes are remarkably variable in normal individuals.
Some patients have very brisk reflexes, although
unaccompanied by clonus. Others have very depressed
responses that often appear better preserved at the ankle
than elsewhere, the opposite of what one would find if a
neuropathy was the cause of the hyporeflexia.
Symptoms and signs

Grading reflexes
Grade Definition Fig. 11.113 Testing the right biceps reflex.

0 Absent
± Present only with reinforcement
+ Just present contraction of the biceps muscle. If there is no response,
++ Brisk normal ask the patient to clench the teeth or grip the fingers of
+++ Exaggerated response the other hand shortly before testing (Jendrassik
manoeuvre). Now examine the reflex in the left arm.
Lean over and use your inverted thumb to mark the
position of the tendon.
THE UPPER LIMB
Supinator (C5/6)
The reflexes of the upper limb routinely tested are the
biceps, triceps and supinator (the roots subserving each With the patient’s arm in the semipronated position,
reflex are shown in brackets). The biceps and supinator strike the radial margin of the forearm approximately
reflexes are tested first, with the patient in the posture 5 cm above the wrist (Fig. 11.114). You can if you
shown in Figure 11.112. wish interpose your finger. The response is a contraction
of brachioradialis and biceps. When eliciting the
Biceps (C5/6)
biceps and supinator reflexes, observe also the fingers of
The whole arm must be exposed when testing this reflex. the hand. A brisk reflex is accompanied by finger flexion.
Place the thumb or index finger of your left hand on the In certain instances, despite a depression of the direct
biceps tendon then strike it with the patella hammer reflex, flexion of the fingers still occurs (inversion). This
using a pendular motion by extending then flexing your physical finding, usually due to cervical spondylosis,
wrist. Grasp the hammer at the end rather than halfway suggests the combination of a depression of the reflex arc
down the shaft (Fig. 11.113). The response consists of at the C5/C6 level, together with an exaggeration of
365
Chapter
Fig. 11.114 Testing the right supinator reflex. Fig. 11.116 Eliciting a finger jerk.
Fig. 11.117 Eliciting the knee reflexes.

Fig. 11.115 Testing the left triceps reflex.
LOWER LIMB
reflexes at a lower level due to a coexistent pyramidal Knee (L2/3/4)

tract disorder. To test the knee jerks insert your left arm underneath the
Triceps (C6/7) patient’s knees and flex them to approximately 60° (Fig.
11.117). If the patient is properly relaxed, the legs will sag
To test the right triceps jerk, bring the patient’s right arm when you remove your arm. Tap first the right patella
well across the body, with the elbow flexed at approximately tendon and then the left. If one or both reflexes is
90° so that the triceps tendon is adequately exposed (Fig. particularly brisk, test for knee clonus by fitting your
11.115). Strike the tendon with the patella hammer. A thumb and index finger along the upper border of the
normal response is contraction of the triceps. Having patella with the knee extended (Fig. 11.118). Exert a
tested the reflex on the right, bring the left arm over and sudden, downward stretch and maintain it. Any repetitive
test the reflex on that side. contraction of the quadriceps (i.e. clonus) even if only
Finger (C8) two or three beats, is strongly suggestive of a pyramidal
tract disorder.
The finger jerk is usually present only when there is a
pathological exaggeration of the reflexes. With the
patient’s arm pronated, exert slight pressure on the flexed ANKLE (S1)
fingers with the fingers of your left hand. Now strike the The patient’s leg is abducted and externally rotated at the
back of your own fingers with the hammer. A positive hip, flexed at the knee and flexed at the ankle. If hip
response leads to a brief flexion of the fingertips (Fig. abduction is limited, rest the leg on its fellow to allow
11.116). adequate access to the Achilles tendon (Fig. 11.119). If
366
Chapter
The motor system 11
Fig. 11.120 Testing for ankle clonus.

Fig. 11.118 Testing for knee clonus.
Fig. 11.121 Testing the abdominal responses.

Fig. 11.119 Eliciting the ankle reflex.
Cremasteric reflex
the reflex is brisk, look for clonus. With the limb in the The cremasteric reflex is elicited by stroking the upper
same position, forcibly dorsiflex the ankle and maintain inner aspect of the thigh. It is mediated through segments
that position (Fig. 11.120). Three to four beats of L1 and L2 and leads to retraction of the ipsilateral
symmetrical ankle clonus is acceptable in normal testicle.
individuals but asymmetric or more sustained clonus is Plantar response
pathological.
The plantar response is elicited by applying firm pressure
(use an orange stick) to the lateral aspect of the sole of
OTHER REFLEXES the foot, moving from the heel to the base of the fifth toe,
then, if necessary, across the base of the toes (Fig. 11.122).
Abdominal responses
While you do this observe the metatarsophalangeal joint
The abdominal responses diminish with age and are of the big toe. In the normal adult, the toe plantar flexes.
more difficult to elicit in the obese or in women who have In the presence of a pyramidal tract lesion, the toe
had children. They are cutaneous reflexes whose latency dorsiflexes. The same dorsiflexion appears in normal
suggests mediation through a spinal reflex arc. Before you individuals if a sharp stimulus is applied to the big toe
can assess the abdominal reflexes, the patient must be and in infants if the stimulus is applied over a wider area.
relaxed and lying flat. Lightly draw the end of an orange The reflex is considered to be part of a flexor withdrawal
stick across the four segments of the abdomen around response to a noxious stimulus. With the development of
the umbilicus (Fig. 11.121). Normally there is a reflex the upright posture, descending pathways, one of which
contraction in each segment. To summarise the findings is the pyramidal tract, inhibit the reaction except when
in your notes draw a cross with an o, ± or + in each stimulation is applied directly to the big toe. Damage
segment according to response. to descending pathways, particularly the corticospinal
367
Chapter
with bradykinesia the movement will again fade away.

There are many ways of assessing bradykinesia without
recourse to formal examination. Watch the patient
dressing or using a knife and fork. Ask them to write and
examine the size of the script and its legibility. See how
easily they stand from a sitting posture and time how
long they take to walk a set distance.
Involuntary movement
Begin by detailing the characteristics of the movement. Is
it present at rest, with the limb completely supported or
when the limb takes up a particular posture or only when
the patient carries out a skilled activity? Ascertain the
frequency of the movement and its distribution. Is the
Fig. 11.122 Testing the plantar response. problem mainly proximal or distal? Are the movements
brief or sufficiently prolonged to cause an abnormal
posture?
system, releases the inhibition and allows the appearance Tremor
of the pathological response. In certain spinal cord
Tremor is a rhythmic movement that, at a particular joint,
disorders, in which the flexor withdrawal response is
is usually confined to a single plane. Physiological tremor
totally disinhibited, minor stimulation of the foot or other
is a normal finding, usually detectable only with
part of the leg results in flexion at hip, knee, ankle
electromyography. Enhanced physiological tremor is
and toe. There is no point in testing the plantar
triggered by agitation, the use of sympathomimetic agents
response if the big toe is immobile or if there is severe
and thyrotoxicosis. Its frequency is around 9 Hz in
loss of S1 cutaneous innervation. Summarise your
younger people. Stimulation of β2-adrenergic receptors
findings with arrows: for flexor ↓, for extensor ↑ and for
in muscle accounts for enhanced physiological tremor.
equivocal ↓↑.
Anal reflex
The anal reflex is assessed by pricking the skin at the anal Questions to ask
margin. Normally, there is a brisk contraction of the anal Tremor
sphincter. The tone of the anal sphincter can be assessed
• Is the tremor mainly present at rest, when the hands
by inserting a finger into the anus and asking the patient
are held out, or when they are used?
to bear down.
• Is the tremor relieved by alcohol?
• Is there a family history of tremor?
THE EXTRAPYRAMIDAL SYSTEM
Examination of tone has already been considered and the
interpretation of abnormal movements including tremor
Myoclonus
will be considered later.
Myoclonus is characterised by rapid, recurring muscle
Bradykinesia
jerks. The movement is similar to the startle reaction
Bradykinesia is particularly associated with Parkinson’s described as ‘jumping out of one’s skin’. The movements
disease. The problem may be confined to one limb, at are either generalised or confined to one part of the body.
least initially, or it may be generalised. Initiation of In some patients they appear only when the limb is
movement is delayed, the actual movement slowed and activated.
its adjustment insensitive. Muscle power remains intact.
Chorea
To look for bradykinesia in the upper limbs, ask the
patient to tap repetitively the back of one hand with the Patients with chorea appear to fidget. They show brief,
other. Ask the patient to use such force that the tapping random movements that do not have the shock-like
is audible. Typically, if the movement is bradykinetic, quality of myoclonus. Typical movements include
its sound diminishes and falters. Now ask the patient furrowing of the eyebrows, pursing of the lips, elevation
to ‘polish’ the back of one hand with the other. In of a shoulder and random contraction of the fingers. Both
bradykinesia, a movement of reduced amplitude is seen proximal and distal limb muscles can be affected. As the
that eventually may cease completely. To assess movements are short-lived, sustained postures do not
bradykinesia in the lower limbs, ask the patient to tap occur. Ask the patient to grip your hand: you will find
your hand repetitively, first with one foot, then the other. that the grip waxes and wanes with the fluctuations of
Many individuals find it difficult to sustain a rhythm but the chorea. The tendon reflexes may be prolonged
368
Chapter
The motor system 11
because of the superimposition of a late, sustained younger people. Typical examples are head nodding and
contraction on the phasic reflex. The choreiform jerking. The movement is easily mimicked.
movements tend to be accentuated by a skilled action.
Dyskinesia
Athetosis
Brief, involuntary movements around the mouth and
Athetoid movements are slower still than chorea and face are relatively common in elderly people
become prominent during the performance of voluntary (orofacial dyskinesia). Similar movements can be induced
activity. The distal parts of the limbs are predominantly by long-term phenothiazine therapy and in patients on
affected. In the hand, the posture oscillates between L-dopa. The former problem tends to persist whatever
hyperextension of the fingers and thumb, usually with adjustment is made to the medication but the latter is
pronation of the forearm and flexion of the digits dose-dependent.
associated with supination (Fig. 11.123). In some patients,
the movements are superimposed on more sustained
postures. In the hand, this combines flexion of the wrist Differential diagnosis
with extension of the fingers and, in the foot, flexion Movement disorders
of the toes associated with inversion at the ankle.
In progressive disease states, the abnormal sustained • Parkinson’s disease
postures become dominant. Assessment of the plantar • Multisystem atrophy
response is difficult if athetosis is affecting the foot. • Huntington’s disease
Stimulation of the sole is liable to produce extension of • Essential tremor
the toes whether or not there is a pyramidal tract disorder. • Palatal myoclonus
A combination of choreiform and athetoid movements is • Hemiballismus
called choreoathetosis. • Generalised torsion dystonia
• Focal dystonia
Hemiballismus • Facial myokymia
Hemiballismus results in violent swinging movements of
the contralateral arm and leg. The movements, in which
rotation is prominent, are of maximal amplitude at the Myokymia
shoulder and hip. The affected limbs are relatively
flaccid. Myokymia confined to the eyelid is a common experience
in normal individuals and is felt as a fine twitching. In
Dystonia pathological myokymia, this fine movement extends to
In dystonia, abnormal postures result from contraction of other parts of the facial musculature. The movements are
antagonistic muscle groups. It is exacerbated by attempts easily missed but on examination a continuous, fine
at voluntary movement. The dystonia may be generalised flickering motion can be seen. If the movements are
or localised to one area. extensive, the eye may close slightly and the mouth
retract (Fig. 11.124).
Tics
Tics are repetitive movements that appear, at least briefly,
to be under voluntary control. They predominate in
Fig. 11.123 Athetoid hand posture. Fig. 11.124 Facial myokymia. The right eye is slightly narrowed.
369
Chapter
Asterixis prominent when the anterior horn cells or cranial nerve

motor nuclei are disrupted. If the lesion is at the anterior
In certain metabolic disorders, particularly hepatic and
horn cell level, for example in motor neuron disease,
renal failure, there is a defect of limb posture control. If
there will be no sensory signs. If the lesion affects the
the patient is asked to extend the arms and hold the
combined nerve root or the peripheral nerve, sensory
fingers in the horizontal plane, a downward drift of the
signs will almost certainly accompany the motor deficit.
fingers and hands is interrupted by a sudden, upward,
corrective jerk.
Symptoms and signs
Clinical application Features of lower motor neuron lesion
UPPER MOTOR NEURON LESION • Muscle weakness

• Depressed deep tendon reflexes
An upper motor neuron lesion results from disruption of
• Fasciculation
the pyramidal pathway at any point between the motor
• Wasting
cortex and the anterior horn cell. Its characteristic features
• Flaccidity
are shown in the ‘symptoms and signs’ box.
The pattern of weakness is influenced by the site of
the lesion but generally it predominates in the upper limb
extensors and the lower limb flexors. Nerve root disorders are commonly the result of
degenerative disease of the spine. Lesions of a single
peripheral nerve are usually the consequence of abnormal
Differential diagnosis angulation, stretch or compression. A diffuse disorder of
The motor system peripheral nerves (although the pattern of distribution
can vary) is called a peripheral neuropathy. In most
Upper motor neuron syndrome
instances, both sensory and motor components of the
• Cerebrovascular disease
nerves are affected, resulting in weakness, distal sensory
• Head or spinal injury
loss and reflex depression.
• Tumour
Lower motor neuron syndrome Myasthenia gravis
• Motor neuron disease In myasthenia gravis, deposition of antibody on the
• Spinal root or peripheral nerve disorder postsynaptic acetylcholine receptor site interrupts the
Fluctuating weakness function of the neuromuscular junction. Fatiguable
• Myasthenia gravis weakness can affect any skeletal muscle. Diplopia and
Myotonia ptosis are particularly common (Fig. 11.125). Muscle
• Dystrophia myotonica wasting is a late and inconsistent feature. The tendon
reflexes are preserved.
Symptoms and signs

Features of upper motor neuron lesion
• Muscle weakness
• Increased deep tendon reflexes
• Depressed abdominal responses
• An extensor plantar response
• Spasticity
LOWER MOTOR NEURON LESION

The characteristic findings in a lower motor neuron lesion
secondary to disruption of the pathway between the
motor nucleus and the neuromuscular junction are shown
in the ‘symptoms and signs’ box.
The weakness is found in all the muscles supplied by
the affected motor neuron. Wasting results from
interruption of the nerve axon or its parent cell but can
take several weeks to emerge. Fasciculation is particularly Fig. 11.125 Myasthenia gravis.
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Chapter
EXTRAPYRAMIDAL DISORDERS Hemiballismus

A combination of tremor, rigidity and bradykinesia occurs • Usually due to a vascular lesion in the contralateral
in Parkinson’s disease. The distribution can sometimes subthalamic nucleus.
be disconcertingly focal and often a patient with unilateral
Parkinsonism is believed to have a hemiplegia. Postural Dystonia
problems are common; the neck and trunk become • Torsion dystonia – familial, generalised dystonia
flexed. When walking, arm swing is reduced on one or predominating in either axial or limb muscles.
both sides and turning is difficult, the patient taking more • Drug-induced – e.g. dopa.
steps than usual. Eye movements are slowed and • Focal dystonia – e.g. blepharospasm, spasmodic
convergence and upward gaze tend to be diminished in torticollis and writer’s cramp.
range. Some patients have an associated dementia. An
Myokymia
identical clinical (and pathological) pattern can coexist
with degeneration of the intermediolateral columns of • Facial myokymia is associated with brainstem tumours
the spinal cord, producing profound autonomic failure. and multiple sclerosis.
Multisystem atrophy causes extrapyramidal features but
also affects pyramidal, cerebellar and autonomic pathways.
Many patients with rigidity and bradykinesia have had Review
their symptoms induced by drugs affecting the release of Examination of the motor system
dopamine or its receptor sites, for example, a phenothiazine.
Another disorder affecting the extrapyramidal pathways • Inspect muscle bulk and assess any fasciculation
disrupts first the supranuclear, then the nuclear, • Examine muscle tone
gaze pathways: progressive supranuclear palsy (Steele– • Examine power using MRC classification
Richardson–Olsczewski syndrome). • Perform the deep tendon reflexes, along with the
abdominal and plantar responses
• Assess any involuntary movement
MOVEMENT DISORDERS
Tremor
• Essential (familial tremor) – absent at rest. Can affect Red flag – urgent referral
the head, neck and voice as well as the upper and
Motor or sensory symptoms
lower limbs. Inherited as an autosomal dominant.
Alcohol responsive in 50%. • Fatiguable muscle weakness – may indicate
• Parkinsonian tremor – classically a resting tremor myasthenia gravis, but often not linked to
at 4–5 Hz, with flexion–extension movements at the neurological disease
wrist and fingers, together with pronation–supination • Fasciculation – if isolated, particularly to the calves, is
of the forearm. Inhibited briefly by a skilled activity. usually benign; if more diffuse, suspect motor
Sometimes an action or postural tremor is also neuron disease
found. • Rest tremor – highly suggestive of Parkinson’s
disease
Myoclonus • Exercise-induced sensory or motor symptoms – very
• Palatal myoclonus – affects the palate, larynx and face. suggestive of multiple sclerosis
Frequency is 2–3 Hz. Associated with brainstem • Lhermitte’s phenomenon – shock-like sensations in
pathology, usually vascular. the spine triggered by neck flexion indicate a cervical
• Segmental myoclonus – occurs with spinal cord cord lesion
disease.
• Generalised myoclonus – many causes, including
familial cases, subacute sclerosing panencephalitis
and Creutzfeldt–Jakob disease. The cerebellar system
Chorea STRUCTURE AND FUNCTION
• Sydenham’s (rheumatic) chorea – rare. Sometimes The cerebellum comprises two hemispheres and a midline
reappears in adult life, either spontaneously or during structure, the vermis. Between the vermis and each
pregnancy. hemisphere lies the paravermis (intermediate zone).
• Huntington’s disease – usually a prominent feature, From above downwards, the cerebellar cortex is divided
although not in juvenile-onset cases. into the anterior and posterior lobes and the flocculonodular
• Other causes – thyrotoxicosis, systemic lupus lobe. Phylogenetically, there are three components: the
erythematosus, polycythaemia and the oral archicerebellum, palaeocerebellum and neocerebellum.
contraceptive. The archicerebellum (principally the flocculonodular
371
Chapter
lobe) receives its major input from the vestibular nuclei. effect on the vestibulo-ocular reflex via the fastigial
The palaeocerebellum (predominantly the vermis) nucleus.
receives projections from the spinal cord, while the
neocerebellum, located mainly in the cerebellar
SYMPTOMS
hemispheres, lies on a circuit incorporating the cerebral
cortex and the pons. The fibres projecting in and out of The symptoms of a disruption of the cerebellar system
the cerebellum pass through the superior, middle or include dysarthria, limb clumsiness and gait ataxia.
inferior cerebellar peduncles. Dysarthria
Embedded in the white matter of each cerebellar
hemisphere is the dentate (lateral) nucleus. The fastigial Patients with dysarthria have a defect of pronunciation,
nucleus lies medially, beneath the vermis. Lateral to the although speech content remains normal.
fastigial nucleus is the nucleus interpositus. Limb clumsiness
A unilateral cerebellar disorder results in an ipsilateral
Risk factors
limb ataxia. If the dominant limb is affected, the patient
may well have noticed an alteration in writing. Sometimes
Cerebral haemorrhage
the patient may refer to an ataxic limb as being weak
• Hypertension rather than clumsy.
• Vascular malformations Gait ataxia
• Bleeding disorders
• Sympathomimetic agents If the cerebellar problem is confined to one hemisphere,
• Cerebral amyloid angiopathy the patient often complains of deviating to that side when
• Intracranial tumours walking. With disruption of midline cerebellar structures,
however, unsteadiness when walking is the main
complaint rather than a tendency to deviate to a particular
side. In such cases, the limbs are relatively spared.
Risk factors
Cerebral infarction Examination
• Hypertension
SPEECH
• Diabetes mellitus
• Cardiac disease Dysarthria will be apparent while you take the history.
• Atrial fibrillation Remember to take account of accent. There is no need to
• Cigarette smoking give the patient set phrases to pronounce, a brief
• Oral contraceptives conversation suffices. In cerebellar dysarthria, speech
• Lipoprotein abnormalities volume and pitch are typically erratic, so that the rhythm
• Haematological abnormalities of speech is lost, with pauses then accelerations. If the
disorder is severe, speech is shot out in a staccato
fashion.
The cerebellar cortex is supplied by three vessels: the
upper surface is supplied by the superior cerebellar EYE MOVEMENTS
arteries and the lower surface is supplied by the anterior In patients suspected of having cerebellar disease, you
inferior cerebellar arteries, with a contribution from the need to look for nystagmus and for abnormalities of
posterior inferior cerebellar arteries. The first two pairs of either saccadic or pursuit movements. The assessment of
vessels arise from the basilar artery, the last pair from the eye movement has been discussed on pages 337–340.
vertebral artery.
Dentate neurons discharge before the onset of motor
activity and even before the relevant motor cortical
Symptoms and signs
discharge. The nucleus interpositus is active during the
control of movement and at its termination. Both nuclei Eye signs in cerebellar disease
are concerned with posture control but activity in the Location Sites
interpositus nucleus appears more closely related to the Flocculus Abnormal smooth pursuit
force of muscle contraction and its velocity. Discharge in Gaze-evoked nystagmus
fastigial neurons relates partly to velocity and partly to Flocculus/nodulus Down-beat nystagmus
force. Vermis/fastigial nucleus Ocular dysmetria
The cerebellum exerts an influence on muscle tone Lateral zones Ocular dysmetria
through an effect on motor neuron output to the muscle Gaze-evoked nystagmus
spindle. Efferents from the flocculus exert an inhibitory
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Chapter
LIMB EXAMINATION Now assess alternating movements in the upper limbs.

The reduced limb tone associated with a cerebellar lesion Ask the patient to hold one hand steady, in the horizontal
is difficult to detect. If the problem is unilateral, ask the plane, with the fingers closed. Next ask the patient to tap
patient to hold the arms in the position shown in Figure first the dorsal then the palmar surface of one hand with
11.126. If the limb is hypotonic, the hand tends to sag the fingers of the other, pronating and supinating the
below the horizontal. If there is a severe cerebellar forearm in the process. The patient with cerebellar ataxia
disturbance, the outstretched hands may oscillate. More is clumsy and there are fluctuations in both the speed and
likely, however, is the presence of an intention tremor. amplitude of the movement (dysdiadokokinesis) that are
To test this ask the patient to touch first his or her nose, both visible and audible.
then your finger held approximately 0.5 m away (Fig. Ask the patient to raise the arms rapidly from the sides
11.127). In a cerebellar ataxia, a tremor emerges that but stop them abruptly in the horizontal plane. In
becomes more apparent as the target is approached. If cerebellar disease, the affected arm oscillates about its
you are undecided, continue but now move your target intended resting place because of a failure of the damping
finger in a random fashion. A mild ataxia may then mechanism. You will already have examined the limb
become more evident. reflexes as part of the motor system examination. They
Occasionally, in disease of the cerebellar pathway, a may be unusually sustained in cerebellar disease (‘hung
severe swinging tremor appears as a result of interruption up’ reflexes).
of the corticocerebellar circuit at the level of the red To assess lower limb coordination, ask the patient to
nucleus (rubral tremor). While testing for intention slide the heel of one foot in a straight line down the shin
tremor, observe whether the patient’s finger reaches the of the other leg: the heel–knee–shin test (Fig. 11.128). In
target accurately. It may reach beyond the target the presence of cerebellar ataxia the heel wavers around
(hypermetria), fall short (hypometria) or even bounce the intended pathway. When the heel has reached the
against it in an uncontrolled fashion. bottom of the shin, ask the patient to flex the leg then
bring the heel back down on to the shin just below the
knee. If there is cerebellar incoordination, the heel may
fall short of its target or thump into the shin rather than
landing gently. Finally, ask the patient to tap your hand
repetitively using first one foot then the other. Be aware,
however, that the performance of this test is variable in
normal individuals and tends to be less smooth in the
nondominant limb.
Cerebellar disorders
Hemisphere lesions
• Stroke
Fig. 11.126 Hypotonia of the left hand in a left cerebellar lesion.
• Primary and secondary tumours
• Multiple sclerosis
• Degenerative disorders
Vermis lesions
Finger–nose test
• Alcohol-related
• Hypothyroidism
Review
Examination of the cerebellar system
• Assess articulation
• Examine pursuit and saccadic eye movements and
analyse any nystagmus
• Examine the finger–nose and heel–knee–shin tests
• Assess gait
Fig. 11.127 The finger–nose test.
373
Chapter
Heel–knee–shin test
Fig. 11.130 Left cerebellar infarct. T2-weighted MRI.
Fig. 11.128 Performing the heel–knee–shin test with the right leg.
Heel–toe walking
LESIONS OF THE CEREBELLAR HEMISPHERE
The lesions most commonly affecting the cerebellar
hemisphere are infarcts (Fig. 11.130), haemorrhage and
tumour. In adults, a tumour involving the cerebellum is
usually metastatic. Characteristic symptoms include an
ipsilateral limb ataxia, a gait which tends to deviate to the
affected side and ocular dysmetria.
MIDLINE CEREBELLAR LESIONS

The predominant complaint in patients with lesions of
the vermis or paravermis is a gait ataxia. Tumours are
sometimes confined to this area but more often the
syndrome is due to selective atrophy secondary, for
example, to alcohol. The familial cerebellar atrophies
tend to produce a more diffuse atrophy readily detectable
Fig. 11.129 Heel–toe walking. by scanning (Fig. 11.131).
Cerebellar signs are very common in patients with
established multiple sclerosis but the triad of tremor,
GAIT dysarthria, and nystagmus, described by Charcot, is rare
as an isolated clinical feature. More often it is accompanied
Unless there is a substantial disturbance of midline
by other features of the disease.
cerebellar structures, patients do not display any instability
of the trunk while sitting but, on standing, oscillations of
the body may occur even before gait is initiated. When The sensory system
walking, the patient will use a wide-based gait and is
likely to show caution when turning. Attempts to turn STRUCTURE AND FUNCTION
quickly will result in problems with posture control. Be
The sensory nerve endings
prepared to support ataxic patients when you ask them
to walk independently. If the patient has a lesion of one The majority of the sensory nerve endings in the skin are
cerebellar hemisphere, then deviation to that side occurs located in the epidermis. They are more numerous in the
on walking. To detect a more subtle disturbance of face, hands and feet than in the trunk. The individual
cerebellar function, ask the patient to walk heel–toe (Fig. cutaneous receptors do not respond solely to a specific
11.129). Again you need to appreciate how variably stimulus but their sensitivity for one usually far exceeds
normal individuals perform this test. People lacking that for the others. Cutaneous receptors include those
confidence in walking, for any reason, are likely to responding to a deformity of the skin (mechanoreceptors),
perform badly. those responding to temperature (thermoreceptors),
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Chapter
Distribution of spinal nerve
posterior posterior posterior root

primary ramus primary ramus
(lateral branch) (medial branch)
sympathetic
ganglion
anterior
root
Fig. 11.131 Cerebellar atrophy. T2-weighted MRI.
and those responding to pain (nociceptors). Light touch

responses are perceived principally by the pacinian
corpuscle and the hair follicle receptors. Pacinian
corpuscles also identify a vibrating stimulus when applied
to the skin. Information about the position and posture
of the limbs (proprioception) is derived from lateral anterior
end organs in muscle, the muscle spindle and the Golgi cutaneous cutaneous
branch
tendon organ. The nerve fibres issuing from these various branch
receptors are either myelinated or nonmyelinated.
The spinal roots Fig. 11.132 Distribution of a spinal nerve.
At each segmental level, the dorsal root (purely sensory)

and the ventral root (predominantly motor) join to form displaced medially. Immediately above the gracile nucleus
a mixed spinal nerve that produces two branches: the is nucleus Z, believed to receive proprioceptive information
posterior primary ramus and the anterior primary ramus. from the ipsilateral lower limb. Second-order neurons
The brachial and lumbosacral plexuses, responsible for from the gracile and cuneate nuclei and from nucleus Z
the nerve supply of the upper and lower limbs, are each decussate to form the medial lemniscus, which in turn
supplied by the relevant anterior primary rami. In the projects to the ventroposterior nucleus of the thalamus.
trunk, the anterior and posterior primary rami are Vibration sense is principally conveyed in the posterior
distributed to the hypaxial (ventral) and epaxial (dorsal) columns but also in the spinothalamic system.
musculature, respectively, and to the corresponding
The spinothalamic tract
overlying skin (Fig. 11.132). The areas of skin supplied by
the branches of the dorsal roots are called dermatomes. Another group of fibres enters the spinal cord and
The arrangement of dermatomes is straightforward in the terminates in the posterior horn. The majority of the
trunk but more complicated in the limbs (Fig. 11.133). axons within the spinothalamic tract originate from layer
The cutaneous distribution of some of the peripheral V (Fig. 11.134). The fibres then pass ventral to the spinal
nerves is summarised in Figure 11.133. Considerable canal before ascending in the anterolateral quadrant.
overlap of distribution exists both for adjacent dermatomes Here the fibres from the sacral segments come to lie
and peripheral nerves. laterally and superficially as they are displaced by fibres
from higher segmental levels. There is no firm evidence
The posterior columns
that the ascending spinothalamic tract is divided into
All sensory fibres have their first cell station in the dorsal discrete ventral and dorsal components. Fibres conveying
root ganglion. Proprioceptive fibres tend to run the whole temperature sense and pain travel in the spinothalamic
length of the cuneate fasciculus but fibres in the gracile tract.
fasciculus leave in the upper lumbar segments of the
The spinocervical tract
cord, synapsing in Clarke’s column before passing into
the dorsal spinocerebellar tract. Above this level, the The third ascending pathway begins with cells from
fasciculus gracilis is occupied by fibres solely concerned laminae IV and V of the dorsal horn that send fibres
with cutaneous sensation. Initially, as successive fibres ipsilaterally in the spinocervical tract to the lateral cervical
enter the dorsal columns, distal segmental fibres are nucleus, which is situated lateral to the dorsal horn of the
375
Chapter
C3 C3
C4 C4
T2
3
T2 T2 4
C5 C5
Radial Radial 5
Ulnar 6
7
Median Median
8
T1 T1
9
C6 C6 10
11
12
C C8 C8
7 C L1
7
Lateral cutaneous L1
L1
nerve of thigh
front back
S5
Medial and L2
S3 S4
intermediate L2
cutaneous
nerve of thigh
S2
L3 L3
Saphenous nerve
S2
L5 L4 L4 L5
Superficial peroneal
Deep peroneal
Sural Sural S1
S1 L5
back front
Fig. 11.133 Sensory examination. Distribution of (a) some peripheral nerves, (b) limb dermatomes and (c) thoracic dermatomes.
upper segments of the cervical cord (Fig. 11.134). From The cortex
here fibres decussate and join the medial lemniscus. The
Areas of the cortex concerned with the processing of
spinocervical tract contains axons that respond principally
ascending sensory information include the primary
to light pressure but also contains fibres responding to
somatic area (S1), the secondary somatic area and the
noxious thermal and mechanical stimuli.
adjacent cortex. Most of the afferent fibres to S1 arise
The thalamus from the ventroposterior nucleus of the thalamus.
Representation is parallel to that of the motor cortex.
In simplified terms, the medial part of the ventroposterior
nucleus of the thalamus receives information from the
Pain
face and the lateral portion from the medial lemniscus
and the spinothalamic tract. According to the gate control theory of pain perception,
the activity level of certain cells in the substantia gelatinosa
Symptoms and signs (lamina II and III) can inhibit conduction of impulses in
the central pain pathways. These inhibitory cells are
Sensory disturbances
activated by impulses in large diameter peripheral afferent
Light touch Pain fibres and switched off by impulses in small diameter
Reduced Hypaesthesia Hypalgesia myelinated and unmyelinated fibres.
Lost Anaesthesia Analgesia Visceral pain is transmitted by sympathetic or
Exaggerated Hyperaesthesia Hyperpathia parasympathetic fibres. Impulses emanating from free
Exaggerated — Hyperalgesia nerve endings in the gut pass into the posterior root via
(at normal the splanchnic nerves. Their central connections are
threshold) similar to those of the spinothalamic fibres. In some
instances pain from a viscus is interpreted as arising from
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Chapter
Questions to ask
Spinal sensory pathways
Sensory disturbances
• When numbness is described, does that mean actual

medial lemniscus loss of cutaneous sensation?
to thalamus
• Does the distribution of any numbness or tingling
and bulbar brainstem
follow the distribution of a peripheral nerve or nerve
to thalamus root?
and bulbar
brainstem
• Does any loss or altered sensation ascend onto the
lateral cervical gracile and abdomen or thorax?
nucleus cuneate nuclei
anterolateral
pathways
numbness to describe a lack of use of a limb, rather than
a defect of sensation.
Pain
Only rarely does the particular quality of a pain serve to
identify its likely source. In peripheral nerve injury, signs
of nerve damage may be accompanied by a distressing,
spinocervical
pathway persistent burning sensation known as causalgia. Pain
related to peripheral nerve disease usually localises to the
distribution of the affected nerve. In nerve root disorders,
the pain is not referred in a dermatomal distribution but
follows a distribution corresponding to the muscles
(myotome) or to other deep structures (sclerotome)
dorsal root supplied by that root. A particular type of pain can emerge
ganglion after damage to the spinothalamic tract or the thalamus
I
itself (thalamic pain). It is persistent, with a very
II II
unpleasant burning or scalding quality and is exacerbated
III by painful or tactile contact.
IV IV
V
III
Paraesthesiae and numbness
VI V
VI Patients often struggle when describing the nature of
sensory disturbances. They tend to resort to a previous
VII experience to assist their description (e.g. the recovery of
VII sensation after a dental anaesthetic).
IX
VIII
Examination
Sensory examination is difficult. There are few objective
criteria, assessment being largely dependent on the
patient’s subjective responses, which may well falter as
the patient fatigues. It is seldom necessary to test all
substantia gelatinosa sensory modalities and even then certainly not in all parts
Fig. 11.134 Sensory pathways in the spinal cord.

Conditions affecting sensation
a superficial body part possessing the same segmental • Mononeuropathies, e.g. carpal tunnel syndrome
innervation (referred pain). • Radiculopathies, e.g. cervical spondylosis
• Transverse myelitis
• Brown–Séquard syndrome
SYMPTOMS • Syringomyelia
Sensory symptoms include pain, paraesthesiae (tingling) • Multiple sclerosis
and numbness. Frequently the patient’s understanding • Spinal cord compression
and use of these terms differ from that of the physician. • Cerebrovascular disease of the cerebral hemisphere
Clearly establish what the patient means. Many use
377
Chapter
Review
TWO-POINT DISCRIMINATION
Sensory examination Two-point discrimination is tested with a pair of
compasses specifically designed for this purpose, with
• Light touch gradations in centimetres indicating the separation of the
• Two-point discrimination tips, which are blunt rather than pointed. Apply the tips
• Proprioception with equal, gentle pressure (Fig. 11.136) while the
• Vibration sense patient’s eyes are closed and establish the minimum
• Pain and temperature separation at which two points are confidently identified.
• Cortical sensory function As an approximate guide, a young adult will detect a
• Sensory suppression separation of approximately 3 mm on the finger tips,
1 cm on the palm of the hand and 3 cm on the sole of
the foot. The sensation is conducted in large myelinated
of the body. The areas tested and the modalities used fibres via the posterior columns to the cortex.
should be influenced by the type of sensory disturbance
suggested by the history. If the patient has an area of
reduced cutaneous sensation, start testing within that PROPRIOCEPTION
area, moving out gradually to determine the zone of While assessing joint position sense ensure that the
transition to normal sensation. patient’s eyes remain closed. Begin by testing the patient’s
Avoid being overpersuasive when attempting to ability to appreciate passive movements of the joints. It
confirm a preconceived area of sensory deficit. is rare to find a loss of proximal joint position sense; more
often the problem is confined to the digits. During testing
avoid pressing on the digit in such a way that the patient
LIGHT TOUCH
appreciates the direction of movement. To test the
Use a wisp of cotton wool to test light touch sensation terminal interphalangeal joint of the index finger grip the
(Fig. 11.135). The distal parts of the limb are more sensitive sides of the phalanx with the thumb and forefinger of
than the proximal and hair-containing skin is more your right hand using your left to stabilise the proximal
sensitive than smooth skin. Do not drag the cotton wool joints of the finger (Fig. 11.137). The movement
along the surface of the skin but apply it at a single point. appreciated will be barely perceptible to the naked eye.
Ask the patient to keep the eyes closed and to respond If the responses are inaccurate, move proximally until the
when contact is made. movements are accurately perceived. Indicate your
If the patient complains of unilateral sensory change, findings in the notes as ‘JPS – intact to movement of the
compare equivalent parts on the two sides of the body. distal interphalangeal joint of 10°’ or whatever range you
If the history suggests a cortical lesion but cutaneous have chosen.
sensation appears intact, assess the effect of simultaneous
stimulation of equivalent body parts. In parietal lesions,
the half-body supplied by the damaged cortex may fail
to register a stimulus when there is competition from the Two-point discrimination
intact opposite side, even though a stimulus, applied
in isolation, is appreciated (sensory suppression or
extinction). In hemisensory loss, the change to normal
appreciation will occur strictly at the midline.
Light touch
Fig. 11.135 Testing light touch with a wisp of cotton wool. Fig. 11.136 Testing two-point discrimination.
378
Chapter
Joint position sense Vibration sense
Fig. 11.137 Testing joint position sense.
Fig. 11.139 Testing vibration sense in the right index finger.
VIBRATION SENSE
Vibration sense is tested using a 128 Hz tuning fork. To
test in the finger, apply the gently vibrating base of the
fork to the pulp of the finger or the knuckle of the distal
interphalangeal joint (Fig. 11.139). For the foot, start with
the pad of the big toe or the dorsum of the interphalangeal
joint. If vibration sense is absent there, test more
proximally. The chest wall acts as a resonator and a more
accurate level of vibration loss on the trunk is obtained
by applying the fork to a fold of skin pulled away from
the underlying rib. In practice, this is seldom necessary.
Semiquantitative testing is achieved by waiting until the
perception of vibration has ceased on one limb then
transferring the tuning fork to the other limb.
Fig. 11.138 Pseudoathetoid posturing.
PAIN
Pain is best tested using a sharp pin or needle (Fig.
You can test active proprioception by asking the 11.140). Venepuncture needles are unsuitable as they
patient, with the eyes closed, to locate a digit of one hand readily puncture the skin, particularly in elderly people.
with the index finger of the other limb. Alternatively, Purpose made ‘sharps’ are now available and should be
move the limb with intact sensation into a certain posture discarded using standard safety procedures after use.
and then ask the patient to mimic that position with the Remember that you are testing the painful quality of
affected limb. Finally, ask the patient to hold the hands the stimulus, rather than merely an appreciation of
outstretched while the eyes are closed. With severe loss contact. Either ask the patient to close the eyes and
of distal proprioception, the fingers move in an irregular, identify if the contact is painful or present the sharp and
purposeless fashion, as if exploring their environment blunt ends of the pin in a random fashion, asking the
(pseudoathetosis) (Fig. 11.138). patient to distinguish one stimulus from another. In some
To test the quality of the proprioceptive information pathological states, diffuse pain radiates out from the site
coming from the lower limbs, ask the patient to stand of contact. Remember that certain areas, for instance
with the feet together and the eyes closed. Where there callouses, are liable to show diminished sensitivity to
is loss of proprioception, the patient immediately loses pain. Deep pain sense can be tested by applying pressure
stability (positive Romberg’s test). Be ready to support to deeper structures, for example, by pinching the
the patient. tendoachilles.
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Chapter
Pin-prick
Fig. 11.141 Charcot joint – right ankle.
or agnosic. Such patients will face difficulties in describing

the object, even in the absence of any sensory loss. Coins
can also be used for testing size recognition. You can use
materials of different form (velvet, wool, linen and so on)
to test the patient’s appreciation of texture.
Fig. 11.140 Testing pin-prick sensation.
TEMPERATURE NERVE AND ROOT DISORDERS
A reduced or exaggerated response to a thermal stimulus Considerable anatomical variation exists in the classical
can exist over a fairly narrow band of temperature but to cutaneous distributions. For example, the median nerve
test temperature sense it generally suffices to use two can supply three or four digits, rather than three and a
metal tubes, one containing water mixed with ice chips, half. Within an affected nerve or root distribution all
the other containing hot water. Test the tubes on yourself sensory modalities will be equally affected, with a
before testing the patient. Ask the patient to distinguish boundary zone of partial loss in which appreciation of
hot from cold on comparable parts of the two sides of the light touch is more disturbed than that of pain and
body. You will need to renew the tubes if the examination temperature. In a peripheral neuropathy affecting sensory
is protracted. fibres, there will be a distal disturbance of sensory function
which gradually merges into normality. A large-fibre
neuropathy will tend to spare pain and temperature
WEIGHT, SHAPE, SIZE AND TEXTURE
sensitivity. A small-fibre neuropathy, predominantly
Certain sensory modalities are worth testing if a affecting pain and temperature, is rare. If pain fibres to
disturbance of cortical function is suspected. To test the skin and joints are affected, consequences include
weight appreciation put an object in the patient’s palm, painless skin ulceration, sometimes leading to amputation
allowing the hand to move up and down so that the or a severe derangement of joint function which remains
patient appreciates both the pressure exerted by the painless – Charcot joint (Fig. 11.141).
weight and the resistance experienced when the hand is
moved against gravity. Compare the effect of the same
weight in the other hand or alternate differing weights SPINAL CORD DISORDERS
between the two hands and ask the patient to distinguish • Transverse cord lesion – sensory level around the site of
them. the lesion, often with a small zone in which cutaneous
Shape recognition is also heavily dependent on cortical stimulation can evoke a painful reaction. Causes
function. Ask the patient to assess the shape of a coin include transverse myelitis and trauma.
and also (although this involves other sensory modalities) • Unilateral cord lesion (Brown–Séquard) – produces
whether it possesses a milled edge. If the hand is paretic, contralateral loss of pain and temperature to a level
the patient will experience great difficulty in manipulating slightly below the lesion, with ipsilateral weakness and
the object but in this case you can guide the patient’s depression of vibration and joint position sense (Fig.
finger over the surface and edge of the coin. Watching 11.142). Causes include trauma and multiple sclerosis.
the patient manipulate the coin gives you valuable • Central cord lesion – disrupts crossing spinothalamic
information about both the motor and sensory status of fibres, leading to bilateral, selective loss of pain and
the digits. Another problem arises if the patient is aphasic temperature over the affected segments (Fig. 11.143).
380
Chapter
Central cord lesion

Brown – Séquard lesion
zone of
altered
sensitivity
to pin prick
loss of
proprioception
loss of pain
and
temperature
Fig. 11.142 Distribution of sensory and motor deficit in Brown– Fig. 11.143 ‘Cape’ of selective pain and temperature loss due to a
Séquard lesion. central cord lesion extending from approximately C3 to D10.
Causes include central cord tumours and CORTICAL LESIONS

syringomyelia. The cortex is concerned principally with the finer aspects
• Dorsal column lesion – interferes with vibration sense, of sensory appreciation. It allows definition of object size,
proprioception and two-point discrimination. A cervical shape, weight and texture. Loss of this facility is called
cord lesion will predominantly affect upper limb joint astereognosis. The cortex allows both accurate definition
position sense. Some patients with cervical dorsal of the site of contact and discrimination of single or
column lesions describe a shock-like sensation radiating multiple stimulation. It is closely concerned with the
down the spine when the neck is flexed (Lhermitte’s appreciation of joint position. Sensory suppression is a
sign). particular feature of cortical lesions. In nondominant
• External compression – tends to spare the deeper fibres parietal lobe lesions, neglect of the contralateral limbs
in the spinothalamic tract coming from the segments can be so profound that the patient denies their existence
immediately below the level of compression. Conversely, and tries to remove them as if belonging to another
a tumour spreading from the centre of the cord is likely person.
to spare the superficial fibres emanating from the sacral
segments.
• Brainstem and thalamic disorders – in the medulla,
lateral lesions predominantly affect contralateral pain Risk factors
and temperature sensation, while medial lesions
Epilepsy
disrupt sensation served by the dorsal columns. Above
this level, pathological processes usually disturb all • Genetic factors
sensory modalities in the contralateral half of the body • Head injury
and cause ipsilateral facial sensory loss if the relevant • Intracranial tumours
part of the trigeminal nucleus is involved. Thalamic • Stroke
lesions affect all aspects of sensation on the opposite • Abscess
side of the body. In some cases, spontaneous pains • Alzheimer’s disease
occur, accompanied by intense burning sensations • Alcohol
when certain cutaneous stimuli are applied (thalamic • Drugs
syndrome). The cause is almost always vascular.
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Chapter
NONORGANIC SENSORY LOSS either of extensive bilateral hemisphere disease, a

The most common pattern of nonorganic sensory loss is unilateral hemisphere mass lesion or a more discrete
one in which cutaneous sensation to all modalities is pathology confined to certain parts of the brainstem.
affected, with little or no change in proprioception. Mass lesions in one cerebral hemisphere affect the
Typically, a single limb is involved but sometimes the conscious level by causing downward herniation of brain
problem occupies one side or the lower half of the body tissue through the tentorial notch, with secondary
(Fig. 11.144). compression of the brainstem (Fig. 11.145). Two types of
Many patients with nonorganic sensory loss perceive herniation are described: a central form, usually associated
it as confined strictly to the limb. Consequently, sensation with slowly expanding, medially placed masses, and an
returns to normal at the shoulder or above an approximately uncal form, in which masses in the middle cranial fossa,
horizontal line at the level of the groin. Typically, the
transition is sudden with the patient reacting adversely if
a painful stimulus is being used. Rarely, the patient will
respond to a stimulus in the intact limb by saying yes and
in the defective limb by saying no. Sometimes, when the
patient turns into a prone position, the previously numb
leg regains sensation on its extensor surface, having been
transposed, so to speak, to the other side of the bed.
Levels of nonorganic loss can fluctuate, even within the
course of a single examination. Hemisensory loss virtually
never ceases at the midline, either straying beyond or
falling short. Facial sensory loss, when not organically
determined, has a tendency to be purely facial, following
the hair line superiorly and the jaw line inferiorly.
The unconscious patient

SYMPTOMS
Lesions confined to one cerebral hemisphere seldom Fig. 11.145 CT scan showing herniation of a right temporal mass
interfere with consciousness. Coma is the consequence with distortion of the upper brainstem.
Nonorganic sensory loss
Fig. 11.144 Patterns of nonorganic sensory loss (shaded blue).
382
Chapter
particularly of the temporal lobe, cause displacement of trauma and inspect the external auditory meati for signs
the medial aspect of the uncus over the free edge of the of bleeding, suggesting the possibility of a basal skull
tentorium. Pathological consequences of this herniation fracture.
include ipsilateral third nerve compression, distortion of
the contralateral cerebral peduncle, and paramedian
CARDIOVASCULAR SYSTEM
brainstem haemorrhages.
Perform a routine cardiovascular assessment, looking
particularly for hypotension or hypertension, pulse
Examination abnormality and abnormal heart sounds or murmurs.
Many aspects of the general examination can be

RESPIRATORY SYSTEM
performed in the unconscious patient. The posture may
be of value in diagnosis. Carefully examine the skin for Assess respiratory rhythm and rate. Sometimes the
signs of injury, petechial haemorrhages or evidence of patient’s fetor, for example of alcohol, gives a clue to the
drug abuse. diagnosis but remember that in an individual who has
been drinking the coma may have another cause (e.g. a
head injury).
Symptoms and signs
Some aspects of clinical examination in
GASTROINTESTINAL SYSTEM
the unconscious patient Palpate the abdomen. Is there hepatomegaly, suggesting
• Boggy scalp swelling
primary liver disease, perhaps resulting in gastrointestinal
• Alcoholic fetor
haemorrhage from oesophageal varices? Look for other
• Spider naevi
markers of liver disease, such as spider naevi.
• Venepuncture marks
• Hepatomegaly LEVEL OF CONSCIOUSNESS
• Hypotension Do not use terms such as stupor or coma to describe the
patient’s conscious state. Record the best level of response
of which the patient is capable (Fig. 11.146). Having
performed other aspects of the examination, you can
SKELETAL SYSTEM then proceed to grade the conscious level using the
Palpate the long bones for evidence of fracture. Note the Glasgow Coma Scale (Fig. 11.147). Note that this scale
presence of any localised scalp swelling indicating focal assesses neither eye movements nor the pupils.
Grading of coma Glasgow coma scale
1. Alert
Patient's response Score 08.00 10.00 12.00
2. Drowsy but responds to verbal
stimulation Eye opening spontaneous 4
to speech 3
to pain 2
3. Unconscious – no response to none 1
verbal stimulation, but
withdrawal response to pain
Best verbal responses orientated 5
confused 4
4. Unconscious – decorticate inappropriate 3
responses to pain (flexion of incomprehensible 2
upper limb and extension of none 1
lower limb)
Best motor responses obeying 6

5. Unconscious – decerebrate
localising 5
responses to pain
withdrawing 4
(hyperextension of both upper
flexing 3
and lower limbs)
extending 2
none 1
6. Unconscious – no response to
pain
Fig. 11.146 Grading of coma. Fig. 11.147 Glasgow coma scale.
383
Chapter
Testing for Kernig's sign and neck stiffness
a b
Fig. 11.148 Eliciting Kernig’s sign (a) and testing for neck stiffness (b).
Pupillary responses
right left right left right left

L R
1. lesion of left
optic tract
2. lesion of
1
pretectal part of
2 midbrain
3. lesion of
3
oculomotor
nuclei
4. lesion of
4 left oculomotor
nerve
Fig. 11.149 Pupillary responses in the presence of lesions of the left optic tract, the pretectal part of the midbrain, the oculomotor nuclei and
the left oculomotor nerve.
SIGNS OF MENINGEAL IRRITATION THE PUPILS

Flex the neck to see whether there is any abnormal Examine the pupils for symmetry and size then test the
resistance to the movement or a reaction on the part of direct light response using a bright pencil torch (Fig.
the patient (Fig. 11.148). Neck stiffness suggests meningeal 11.149). The presence of an optic tract lesion can
irritation. Kernig’s test is performed by flexing the leg at sometimes be confirmed by finding a lack of response
the hip with the knee flexed, then extending the leg at when light is shone into the eyes from the affected half
the knee. The patient may react as the leg is extended or field. A pathological process in the region of the pretectum
there may be an obvious reflex spasm in the hamstring will interrupt the pupillary light response. The pupils are
muscles. With deepening levels of coma, these signs of midposition in size and fixed to light. Lesions of the
meningeal irritation disappear. oculomotor complex itself are likely to produce slightly
384
Chapter
irregular pupils fixed to all forms of stimulation. Disruption the tendoachilles. Always test bilaterally; an absent
of the third nerve beyond the nucleus produces a response from one side alone suggests the likelihood of
characteristic eye position associated with a fixed dilated an interruption of the pyramidal tract supplying that side
pupil. of the body. An appropriate response is one that
In metabolic coma, the pupils remain reactive and withdraws the limb from the stimulus. The two principal
symmetric, although often relatively small. Only in inappropriate responses are decorticate and decerebrate
profound metabolic coma do the pupils become fixed. posturing. In the former, the upper limbs flex and adduct,
Certain drugs can influence pupil size or reactivity. the lower limbs extend and plantar flex. This response
Atropine will cause pupillary dilatation, as will overdosage typically follows an acute vascular event affecting the
of amphetamines or tricyclic antidepressants. Morphine cerebral hemisphere or internal capsule. In decerebrate
derivatives, in excessive dosage, result in pinpoint pupils rigidity, the upper limbs are extended, adducted and
that retain their reactivity. hyperpronated, with the lower limbs fully extended. This
pattern appears with lesions in the region of the pons
OCULAR MOVEMENTS that separate lower brainstem structures from descending
pathways but it can also occur in some of the metabolic
First note any spontaneous eye movements. In many
comas.
unconscious patients the eyes roam from side-to-side.
The movements are usually conjugate but may occasionally
become disconjugate. At other times the eyes should Differential diagnosis
remain in the midposition. Any deviation of one or both
Coma
eyes implies a defect of oculomotor function unless there
is a pre-existing strabismus. Metabolic coma
Now assess eye movements. Having gently elevated • Hypoglycaemia
the upper lids, firmly rotate the head laterally, then • Hyperglycaemia
vertically (doll’s head manoeuvre). If reflex eye movements • Uraemia
are intact, the eyes move so as to leave them directed • Hepatic encephalopathy
forwards. A more potent stimulus for reflex eye movement • Hypercapnoea
is achieved by caloric stimulation. Clear the external • Drugs
auditory meatus of any wax then inspect the tympanic Structural coma
membrane to ensure it is intact. Position the patient so • Hemisphere mass lesions: tumour, extradural
that the head is elevated to approximately 30° above the haematoma, subdural haematoma
horizontal and, using a soft rubber catheter, gently instil • Brainstem stroke
ice-cold water into the external auditory meatus. A total
volume of about 50 ml suffices. If the brainstem reflexes
are intact the eyes will tonically deviate to the side of the
irrigated ear. It is usually not necessary to test reflex RESPIRATORY STATUS
vertical movements. In order to do so, both ears have to A number of abnormal respiratory patterns in the
be simultaneously irrigated with cold water (for down unconscious patient may allow localisation of the lesion
gaze) or warm water (for up gaze). Nystagmus is an responsible for the coma (Fig. 11.150).
unlikely finding in the comatose patient but a variety of In Cheyne–Stokes respiration the respiratory rate
vertical movements can occur. Commonly a rapid waxes and wanes, with intervening periods of apnoea.
downward or upward conjugate movement followed by The pattern is seen in metabolic coma but also with
a gradual return to the midposition (ocular bobbing and bilateral deep hemisphere lesions. Central neurogenic
reverse bobbing respectively) is observed. hyperventilation consists of a persistently increased
Sustained horizontal ocular deviation indicates a rate of relatively deep breathing. It is triggered by lesions
frontal or brainstem lesion. In the former, the eyes deviate lying between the lower midbrain and the lower pons.
away from the side of the accompanying hemiplegia. Apneustic breathing results in short periods of respiratory
In a brainstem lesion below the decussation of the arrest on inspiration. Pontine infarction is the usual cause.
supranuclear pathway for horizontal gaze, the eyes Ataxic respiration is erratic in timing and depth and is
deviate to the opposite side and hence to the side of an triggered by disturbances of the respiratory centres of the
accompanying hemiparesis. Failure of upgaze occurs in medulla.
the early stages of central transtentorial herniation.
MOTOR RESPONSES
Motor function in the limbs can be assessed partly by There are significant differences between the neurological
observing the patient’s posture and partly by assessing findings in patients whose coma has a metabolic basis
the response to pressure over the sternum or, for assessing and the findings in patients who have a structural lesion
the limb response by squeezing the nail bed of a digit or affecting the cerebral hemispheres or brainstem.
385
Chapter
With central herniation, as the conscious state alters,

Respiratory patterns in the unconscious patient the first eye movement abnormality observed is
impairment of reflex upward gaze. The pupils remain
reactive. As a hemisphere lesion is present, there is likely
to be a contralateral hemiplegia. The ipsilateral limbs may
A Cheyne–Stokes respiration show a diffuse increase in tone and the most likely
respiratory arrhythmia is Cheyne–Stokes respiration
(Fig. 11.151). Further signs appear as the transtentorial
herniation proceeds. Horizontal eye movements become
increasingly difficult to elicit, even using caloric
B central neurogenic hyperventilation stimulation. The pupils become fixed to light but remain
midposition in size. Decorticate posturing of the
unaffected side becomes decerebrate and the most likely
breathing pattern to emerge is central neurogenic
C apneustic breathing hyperventilation.
Uncal herniation produces a different picture, at least
initially. The pupil of the eye ipsilateral to the lesion
becomes dilated and this is followed by the development
D ataxic breathing
of an ophthalmoplegia. Initially, the contralateral pupil
remains reactive and the eye moves fully with reflex
stimulation but subsequently reflex movements are lost.
The limbs ipsilateral to the lesion can develop a hemiplegic
one minute
posture relatively early, due to compression of the
contralateral cerebral peduncle against the tentorial edge
(Fig. 11.152). Later bilateral decerebrate posturing
Fig. 11.150 Respiratory patterns. appears. Central neurogenic hyperventilation is the most
likely respiratory dysrhythmia.
The final stages of the two types of herniation are
similar. Respiration becomes erratic and signs of
METABOLIC COMA cardiovascular instability emerge. Pupillary dilatation is a
Patients in metabolic coma usually pass through phases terminal event.
of waning consciousness during which they become less Supratentorial masses producing coma are usually
alert, apathetic and disorientated. The pupils remain vascular rather than neoplastic. Causes include extradural,
reactive until the late stages of metabolic coma. The eyes subdural and primary intracerebral haemorrhage. The
remain central but reflex movement, even that elicited by
caloric stimulation, may eventually be lost. The visual
axes remain parallel and undeviated. Both generalised Symptoms and signs
and focal motor seizures can occur. Decorticate or Assessment of coma
decerebrate posturing are seen and some patients (e.g.
• Take history if possible
those with hypoglycaemia or hepatic coma) will display
• Assess level of consciousness – use Glasgow coma
a hemiplegia that recovers when the metabolic abnormality
scale but remember its limitations
is corrected. Myoclonic jerks occur in uraemia and
• Look for signs of meningeal irritation
in patients with hypercapnoea. In Wernicke’s
• Assess pupils
encephalopathy, the altered mental state is accompanied
• Assess ocular movements, if necessary using doll’s
by ophthalmoplegia, nystagmus and ataxia. Papilloedema
head manoeuvre
with intense retinal venous congestion is found in a small
• Assess motor responses
proportion of patients with respiratory failure. In drug-
• Assess respiration
induced coma, although the doll’s head and cold caloric
• Perform a general physical examination, including
responses are eventually lost, the pupils usually remain
the heart, the abdomen and the skull
reactive until the very late stages.
STRUCTURAL CAUSES OF COMA

Emergency
When supratentorial lesions cause coma, the pattern of
Coma
development of physical signs allows differentiation
between central and uncal herniation. The pattern may Consider myriad causes but specialist appraisal is
alter according to the speed with which the size of a mandatory
supratentorial mass increases.
386
Chapter
Central transtentorial herniation
Early Late
intact doll's head and cold calorics Cheyne–Stokes respiration absent doll's head and cold calorics erratic respiration
intact pupillary response fixed pupils
0°C
hemiplegia flaccid limbs with

on left side occasional flexor
responses
Fig. 11.151 Central transtentorial herniation.
Right uncal herniation
Early Late
intact or depressed medial no specific respiratory intact responses in central neurogenic
rectus action arrhythmia unaffected eye hyperventilation
dilated pupil on affected side fixed dilated right pupil
or
hemiplegic posture hemiplegia develops
and response ipsilaterally
Fig. 11.152 Right uncal herniation.
spectrum of pathological processes in the brainstem maintains circulatory function providing that respiration
producing coma is considerably wider and includes is supported by artificial means. There is good evidence
infarction, tumour and haemorrhage. to suggest that if brainstem function can be shown to
have ceased in such patients, there is no prospect for
recovery (Fig. 11.153). Criteria of brainstem death have
BRAIN DEATH been devised to appraise this state, in order to identify
The end point of many structural and metabolic insults patients in whom further attempts at life-support are of
to the brain is a state in which a deeply comatose patient no value (Fig. 11.154).
387
Chapter
Brainstem reflexes
A pupillary light response
B testing the corneal response
C C injection of ice-cold water to

test the vestibulo-ocular reflex
B
A D stimulating the glabella with
the knuckle
E E stimulating the trachea with a

suction catheter
Fig. 11.153 Testing brainstem reflexes.
Criteria for brain death
1. Pupillary response 4. Motor response in cranial nerve distribution

Use a bright torch (not an ophthalmoscope) to This is most readily assessed by applying a painful
confirm that the pupils fail to respond. stimulus to the glabella. The patient fails to respond.
2. Corneal response 5. Gag or tracheal response

Gently apply a wisp of cotton wool to the cornea. Either stimulate the palate or pass a suction
There should be no response. Note that repeated catheter into the trachea. The patient fails to
testing can readily traumatise the cornea. show any response.
3. Vestibulo-ocular reflex 6. Respiratory reaction to hypercapnia

Inspect the tympanic membrane to ensure that it is First administer a combination of 95% O2 and
intact and not obscured by compacted wax. Insert 5% CO2 via the respirator until the Pco2 has risen
a soft rubber catheter into the external auditory above 6.0 kPa (40 mmHg). Disconnect the
meatus and slowly inject approximately 50 ml of respirator but administer 100% oxygen through a
ice-cold water. Repeat the test in the other ear. tracheal catheter at around 6 l/min. Observe if any
There should be no ocular deviation. respiratory reponse occurs when the Pco2
exceeds 6.7 kPa (50 mmHg).
Fig. 11.154 Criteria for diagnosing brain death.
The first essential, when applying these criteria, is reversible factors. The responses to testing of brainstem
to ensure that the coma is not the consequence of function are likely to be depressed in the presence of
a metabolic or drug-induced state that is potentially hypothermia. The patient’s body temperature must be
reversible. Usually retesting is performed after a period above 35°C before testing is carried out. It must be
of at least 24 h. This allows confirmation of the clinical clearly established that the patient’s respiratory failure is
diagnosis by another doctor and the positive exclusion of not the consequence of neuromuscular blocking agents.
388
Chapter
Stimulation of a peripheral nerve can be carried out to reflexes, plantar responses or withdrawal and flexion of the
confirm that neuromuscular conduction is intact. Finally, upper or lower limb triggered by neck flexion. The United
a specific cause for the patient’s coma must be identified. Kingdom criteria for brain death no longer include the
For most neurological disorders this will be evident from presence of an isoelectric electroencephalogram recording,
the patient’s history or imaging. Identification of drug- although this criterion still receives support in other
induced or metabolic coma is likely to take longer. countries, for instance the United States of America.
There are certain spinal reflexes that can persist in the
presence of brainstem death. These include the stretch

The nervous system
Primitive reflexes • Taste

• Glabellar tap – sensitivity declines with age, with a higher threshold
– found with increasing frequency with age • Hearing
• Palmomental reflex – declines with age
– bilateral responses found with increasing frequency Motor system
with age • Reflexes
• Snout and suckling reflexes – contrary to established teaching, the ankle jerks are
– seldom, particularly the latter, found in normal, preserved in old age
elderly, individuals – the abdominal responses diminish and their latency
• Grasp reflex increases with age
– the presence of grasp reflexes correlates with • Movements
evidence of cognitive impairment – lingual–facial–buccal dyskinesias are found in elderly
Cranial nerve function people without a history of neuroleptic drug
• Smell exposure
– sensitivity declines after the age of Sensation
65 years • Vibration
• Eyes – threshold for appreciation increases with age
– mild ptosis common in elderly people • Two-point discrimination
– upgaze declines with age – threshold increases with age
– the light and accommodation responses
Gait
decline with age and the pupils become more
• Becomes increasingly cautious with increasing age
miosed
Review
Framework for the routine examination of the nervous system
• Assess higher cortical function including orientation, • Assess cerebellar function – speech, eye movements,
memory, intelligence, speech and praxis, together with limb coordination and gait
appraisal of the primitive reflexes • Assess sensory function – as appropriate, testing light
• Assess the patient’s psychiatric status if that appears touch, two-point discrimination, proprioception,
relevant vibration sense, pain and temperature, and cortical
• Assess cranial nerve function (see p. 358) sensory function
• Assess motor function – appearance, tone, power, • Where relevant, carry out a standard protocol for
reflexes and involuntary movements assessing the unconscious patient
389
12
Infants and children
One of the challenges of paediatric medicine and child confirming or refuting the working diagnosis revealed
health is dealing with a range of patients, from the during the history. In previous chapters, advice was given
preterm newborn weighing less than 1 kg to the on how to approach patients who provide their own
postpubertal 15-year-old weighing 55 kg. The younger histories of complaints and symptoms; children come to
the child, the more often he or she is brought to see the the doctor with their parents and it is the parents who
doctor, and the more different the consultation is from usually supply these details, although older children will
that described in previous chapters. often make important contributions.
Listen to the parents: they know their child best and,
‘Children are not just small adults – their needs are
generally, if they describe a problem then there is a
different and have to be recognised.’
diagnosis to be made. The younger the child the more
Professor James Spence, 1943
reliant you will be on the parents’ account of the problem.
When examining children, the general principles of Sometimes acute anxiety about a child’s well-being,
history-taking and examination also apply, although the coupled with parental exhaustion, leads to difficulties in
manner and order in which they are approached differ: effective communication between parent and doctor but
the convention of taking a history, inspecting, palpating, if you can empathise with the parents’ perspective it will
percussing and auscultating remain the cornerstones help you to be a more understanding and compassionate
of all consultations but the emphasis is different in doctor.
children. The older the children, the more you can communicate
Trainee doctors need basic skills to begin to feel with them. The challenges lie in communicating effectively
confident in dealing with the child patient and their with children of different ages and abilities. This skill
families. takes time to acquire; some will acquire it faster than
For convenience, this chapter divides the child patient others.
into five age categories, although these groups tend to It is important to establish a rapport with the child and
merge into one another: his or her parents and siblings. Introduce yourself to the
child and other family members as you welcome them
• Newborn and very young baby (0–8 weeks)
into the consulting area. Try and allow the children
• Older baby and toddler (2–24 months)
(including the siblings) to feel relaxed and comfortable
• Preschool child (2–5 years)
during the consultation; this is more likely if there are a
• School child (5–10+ years)
variety of toys and games lying about the room. Children
• Adolescent (10+ to approximately 16 years).
up to and including school age may well prefer to be on
In each section of this chapter, the discussion of a parent’s lap, eventually feeling confident enough to
growth, development, history-taking and examination of explore the room during the history-taking.
systems will take into account important age-related After the presenting complaint has been defined,
differences. information about the child’s previous well-being and
that of the family and their circumstances need to be
recorded.
Taking a history In the very young child, history-taking should include
information about the pregnancy, labour and delivery as
History-taking is the key part of an assessment of a well as the condition at birth and early feeding progress,
child’s condition. The diagnosis is often revealed by a details of immunisations and a developmental history.
well-taken history, with the examination findings These details may become less relevant in the older child.
390
Chapter
Taking a history 12
Previous illnesses, hospital or doctor attendances as well

as recent and previous medications are required in any Pedigrees and family trees
child’s history.
The family history is important and can be clearly
The pedigree chart is preferred by geneticists and
presented by using a two- or three-generation family
uses specific symbols to demonstrate information
tree. Include details about parents’ and siblings’ medical about that family. This pedigree demonstrates an
histories and make direct queries in line with the X-linked condition (e.g. G6PD deficiency)
presenting problems. Include history of previous and an autosomal recessive inheritance
pregnancies and relevant pregnancy and prenatal
problems (Fig. 12.1). If an autosomally recessive condition
is being considered, it may be necessary to ask if the
parents are consanguineously related. Although a large
proportion of the world’s families involve cousin
marriages, this is a delicate subject that should be dealt G6PD CF
with in a tactful way. One approach is to enquire if the
parents have any relatives in common (e.g. grandparents
or cousins) (Fig. 12.2).
G6PD
At first it can seem intrusive to ask about the child’s
family and any surrounding issues. One approach is to
tell the child and family that you are going to ask a Male Female (X-linked) carrier
number of routine questions about the child’s background
after hearing about the presenting complaints. The initial Female Dead
history-taking is the most ‘natural’ opportunity to collect Sex unknown Monozygous twins
this information, as having to go back and ask more
questions out of the context of history-taking is more Abortion/miscarriage Dizygous twins
awkward.
Affected Index patient or
The social history is separate from but allied to the propositus
family history. It is important to understand the Carrier
composition of the household in which the child lives. Consanguineous marriage
The two-generation family tree can be further annotated
with names, occupations and other details, helping to fill
in details of the child’s social history. It should include
More social details about the family can be added.
details about the parents’ occupations and whoever else
Some colleagues find this addition of information
is helping with child care. Children old enough to be ‘graffiti’, others find it helpful as a ‘map’ of the child’s
family, helping the doctor to understand how
the family and the diseases have interacted
Both parents alive Died Died

and well age 65 1979 1989
MI CVA
Uncle Uncle Maria Len Susan Uncle Bill

Fred Bill 32 34 28 died age 23
42 G6PD 3 children CF and
Age 36 aneurysm and
varices
1994
Alice Emily
61/2 8/40
(Asthma) Miscarriage
Bobby Current
1993
G6PD age 9 pregnancy
eczema 18/40
Fig. 12.2 The three-generation family tree.

Fig. 12.1 These identical twins have myotonic dystrophy, as does
their mother. This picture shows the phenomenon of ‘anticipation’,
in which the condition is worse in each successive affected
generation.
391
Chapter
12 Infants and children
attending nursery or school should be asked the name of lap or on a bed or couch, when you are within 1 metre
the establishment as well as how they are getting on. of the patient the child should see you are coming down
Child abuse is a common problem. Children can be to eye level. This is especially important when several
harmed by adults in a number of different ways: doctors congregate around a bed, for example, on ward
emotionally, physically, neglected, sexually or, rarely, by rounds. Always remember what it is like from the child’s
induced illnesses and poisoning. The nature of any injury perspective, especially when being surrounded by a group
or illness in any child, from any background, must be of unfamiliar adults.
explained satisfactorily in the history and be a plausible It may take some time to win the confidence of young
cause of the findings seen on examination. If you have children. Sometimes the pyrexial, irritable child may not
any such concerns about a child or family you must share allow you any physical contact without crying and, despite
them with colleagues and social services. a friendly approach, it may also be impossible to observe
the child at rest. Once a child starts crying it may be
difficult to continue with the examination.
The examination Palpation and auscultation may be important parts of
the physical assessment. The order in which you perform
Inspection and observation are the most important skills them depends on where the problem is, what the problem
to be developed if you are going to arrive at the right is likely to be and how ill and how cooperative your
diagnosis. The younger the child, the more important young patient is. Whenever possible start peripherally
it is to be able to observe the child’s well-being and with the hands or feet, making it clear to the child that
any physical signs from a distance. This process should you are a friendly doctor. Percussion is rarely a rewarding
start from the moment the child and family appear process in the very young.
in front of you. Do not wake up sleeping children to Young patients should think the examination is fun.
examine them until you have observed them carefully If you present yourself as playing a game, they will be
first (Fig. 12.3). relaxed and you will gain more information; if a child is
How one approaches a child to be examined is frightened or in pain, then this can be impossible to
determined by the child’s age, level of development and achieve. Make the child comfortable first. Ensure your
understanding. The younger the child (except in the hands are clean and warm and that your stethoscope will
youngest of infants), the more imaginative one may have not be too cold on the child’s skin.
to be to ensure a satisfactory consultation but remember Avoid unpleasant procedures if at all possible (e.g.
it is easy to make older children and adolescents feel rectal examinations). Think of what implications your
patronised. actions may have in the future: if your examination and
Whenever possible try not to allow your eye level to care of a child does not cause upset, and you relieve pain
be higher than that of your patient. If necessary, get down and discomfort effectively, that child is more likely to
on the floor; this may be very basic psychology but it tolerate future examinations. It is better to have a limited
works. If you are approaching a child seated on its parent’s but tolerable examination than to try and complete a full
Figs 12.3 Swollen wrists (a) and rib ends (b) seen in rickets. Observation may be all that is needed to notice these signs of rickets. Sometimes
these findings are coincidental to the presenting problem.
392
Chapter
examination that results in an inconsolable child because a child in the first year of life is extrapolated into the
the child is more likely to be uncooperative next time. volume of brain growth, it is clear why humans cannot
have more developed newborns – this is the price Homo
sapiens pays for being bipedal with a narrow pelvis and
Growth and development large brain.
The continuum of growth from baby to adult has been
Growth involves an increase in size and concludes when described by three main phases (Fig. 12.5):
an individual has acquired full size and reproductive
• Infant phase: a continuation of the exponential fetal
capabilities. Development parallels growth and leads to
growth rate that slows down in the second year of life.
individuals acquiring all the skills and attributes that
Critical factors are nutrition and hormones controlling
enable them to achieve full independence from their
metabolism (e.g. insulin-like growth factors such as
parents and to raise their own children.
IGF1).
• Childhood phase: this extends from the second to
GROWTH beyond the 10th year. Critical factors are the pituitary
Compared with other mammals and primates, human hormones (especially growth hormone).
offspring are very immature and dependent. A human • Adolescent (pubertal) phase: this extends from the
newborn is completely dependent for most of its first year onset of puberty until the achievement of final adult
until weaned and walking. Our newborns have a head stature and fully mature reproductive capabilities.
that is only just small enough to be delivered through the Critical factors are the sex steroids (androgens and
average woman’s pelvis. The cerebral neuronal network oestrogens).
is almost complete at birth, but is more or less devoid of Each of the phases is interdependent on a large number
myelin, whereas most other species have completed this of factors such as genetics, nutrition, hormones and the
essential ‘wiring’ before the end of gestation, hence the environment (including love and affection) (Fig. 12.6).
more advanced abilities of their newborns. If the growth
in head (or occipital frontal) circumference (Fig. 12.4) of
The three phases of growth in childhood

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
60
58 infant childhood puberty

160
95
56 90
75
50 140
54 25
10
3
52 120
50
100
48
size (cm)
46 80
44
60
42
40 40
38 20
36
0
34
Age, years -1 2 4 6 8 10 12 14 16
32 birth
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
age (years)
Fig. 12.4 Head circumference chart. The phenomenal growth in Fig. 12.5 Three phases of growth in childhood (after Professor J.
head circumference seen during the first years of life is as a result of Karlberg). The growth velocity varies at different ages – this is as
brain myelination, without which the infant’s development cannot result of many variable influences. Karlberg summarised the
advance. (© Child Growth Foundation, adapted with permission.) continuum into three phases, each with their own principal factors.
393
Chapter
6'9"
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
205 205
6'6" 200 200
195 195
6'3" 190 GIRLS 0-20yrs Height 190
6'0" 185 185
180 99.6th
180
5'9" 175 98th
91st
175
5'6" 170 75th
170
165 FOSTERED FOSTERED AND ADOPTED
50th 165
5'3" 160 25th
160
9th
5'0" 155 155

WITH PARENTS PARENTS 2nd
150 0.4th
150
4'9" 145
140 110
4'6" 105
135
4'3" 130 X 100
125 95
4'0" 120 99.6th 90
3'9" 115 85
110 98th 80
3'6" 105 75
3'3" 100 X
91st
70
95 75th 65
3'0" 90 60
50th
2'9" 85 25th 55
80 X 9th 50
2'6" 75 2nd
45
0.4th
2'3" 70 40
65 35
2'0" 60 30
1'9" 55 25
50 20
1'6" 45 15
10 10
5 5
0 0
Age, Years
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Fig. 12.6 Nonorganic failure to thrive. For some children who are not growing as well as expected, no organic cause can be identified. If they
are removed from their home environment, their growth velocities may accelerate. The importance of an affectionate and loving environment
for normal growth and development cannot be over estimated. (© Child Growth Foundation, adapted with permission.)
Measuring length accurately in infants Measuring height accurately in children
Callibration
checked
Head straight, eyes and
ears level
Gentle upward
traction on
mastoid process
Fig. 12.7 Measurement of supine length.
Any examination of a child is incomplete without

an assessment of growth and development. It is usual to
assess weight in all ages, supine length (Fig. 12.7) and
head circumference in infants (<2 years), and standing Knees straight
height in older children (Fig. 12.8). The measurement of
length or height can be misleading and inaccurate unless Barefoot with feet
done correctly, especially in infants. flat on floor
Growth charts are used to help determine the expected heels touching
range at any given age; there are standards derived for back of board
most developed nations and by the World Health
Organization. Either the standard deviation scores either Fig. 12.8 Measurement of standing height.
394
Chapter
side of the mean, or centiles are used to recognise the the more certain one can be about whether the pattern
different normal variations in growth and growth velocity. of growth falls within an expected range (Figs 12.9,
The more serial measurements there are available to plot, 12.10).
6'9"
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
205 205
6'6" 200 200
195 195
6'3" 190 GIRLS 0-20yrs Height 190
6'0" 185 185
180 99.6th
180
5'9" 175 98th
91st
175
5'6" 170 75th
170
165 50th 165
5'3" 160 25th
160
9th
5'0" 155 2nd

155
150 0.4th
150
4'9" 145
140 110
4'6" 105
135
4'3" 130 100
125 95
4'0" 120 99.6th 90
3'9" 115 85
110 98th 80
3'6" 105 75
3'3" 100 91st
70
95 75th 65
3'0" 90 60
50th
2'9" 85 25th 55
80 9th 50
2'6" 75 2nd
45
0.4th
2'3" 70 40
65 35
2'0" 60 30
1'9" 55 25
50 20
1'6" 45 15
10 Breast
4+ 10
3+
5 stage
2+
99.6th 98th 91st 75th 50th 25th 9th 2nd 0.4th
5
0 0
Pubic hair 4+
3+
stage
2+
Age, Years Menarche
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Fig. 12.9 Childhood Growth Foundation (UK) growth charts for girls. (© Child Growth Foundation, adapted with permission.) For pubertal
stages see Figs 8.1, 8.3 and 12.44.
6'9"
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
205 205
6'6" 200 200
195 99.6th
195
6'3" 190 BOYS 0-20yrs Height 98th
190
91st
6'0" 185 75th

185
180 50th
180
5'9" 175 25th 175
5'6" 170 9th 170
165 2nd
165
5'3" 160 0.4th 160
5'0" 155 155
150 150
4'9" 145
140 110
4'6" 105
135 99.6th
4'3" 130 100
125 95
4'0" 120
98th
90
3'9" 115 91st 85
110 80
3'6" 105 75th 75
3'3" 100 50th 70
95 25th 65
3'0" 90 9th 60
2'9" 85 2nd 55
80 0.4th 50
2'6" 75 45
2'3" 70 40
65 35
2'0" 60 30
1'9" 55 25
50 20
1'6" 45 15
4+
10 Penis
stage 3+ 10
2+
5 99.6th 98th 91st 75th 50th 25th 9th 2nd 0.4th 5
0 4+
Pubic hair 3+ 0
stage 2+
Age, Years Testes

volume
12ml
4ml
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Fig. 12.10 Childhood Growth Foundation (UK) growth charts for boys. The charts for boys and girls are British standards derived from
longitudinal data observed in cohorts of British children with cross-sectional observations used in updating them. (© Child Growth Foundation,
adapted with permission.) For pubertal stages see Figs 9.4 and 12.44.
395
Chapter
DEVELOPMENT
The eight areas of child development
Evaluation of a child’s development is more complicated
than assessment of growth because of the large variation
in the normal patterns of development. Furthermore, an
individual child’s rate of development can vary, and there Behaviour Social skills
are also confounding transcultural and transracial
differences. Gross Expressive
motor language
Although newborn babies are dependent, they can
hear, smell, taste, feel and see. By the end of their Fine Comprehension
motor of language
development they will be able to think and solve
problems, be mobile and agile, develop innumerable Vision Hearing
skills and be capable of rearing their own children.
For convenience, development is usually considered
under eight main headings, which can be easily
remembered as four sets of pairs:
• Gross motor Motor skills
Fig. 12.11 Child development. The eight areas are closely
• Fine motor Motor skills interdependent. To reflect this, some group hearing with speech and
• Vision Special senses vision with fine motor.
• Hearing Special senses
• Expressive language Communication
puts on clothes
speech half recognisable

combines words
runs
six words
walks alone
stands alone personal/social
single words speech
thumb/finger grasp fine motor
pulls to stand gross motor
drinks from a cup
waves bye-bye
mama/dada specific
mama/dada-non specific
sits unsupported
rolls over
puts hands together
looks at hands
vocalises
smiles in response to face
looks at faces
birth 2 4 6 8 10 1 yr 14 16 18 20 22 2 yrs 26 28 30 32 34 3 yrs

months
Fig. 12.12 Outline of some important common developmental milestones. The bar represents the typical age of acquisition, the right-hand
end representing when >90% of healthy normal children should have acquired these skills.
396
Chapter
• Comprehension Communication Newborns and young babies are examined routinely

• Social skills Psychosocial at birth, at approximately 6–8 weeks of age and when
• Behaviour Psychosocial receiving immunisations. They are usually seen by doctors
(e.g. general practitioners, paediatric resident staff or
Various schemes have been elaborated to help health
specially trained midwives) trained in their care. They are
professionals determine whether a child is developing
also seen if they are acutely ill by doctors unaccustomed
along an expected pattern of ‘normality’. Some of these
to young babies (e.g. accident department staff).
schemes are merely screening devices; others are more
Specific aspects about the ‘routine neonatal
elaborate and describe an infant or an infant’s abilities
examination’ are discussed at the end of this section.
more thoroughly (Figs 12.11, 12.12).
GROWTH
The newborn and very young baby Newborns appear on the steepest part of the infant
growth curve. They tend to lose 5–10% of their birth
Only babies born at term are discussed here; preterm weight in the first week but then steadily gain an average
newborns have characteristics of their own. Newborns of 25–30 g/day over the next 6 months. The length
(called neonates when <4 weeks old) are extraordinary measurement of newborns and infants is likely to be
patients to be involved with. At birth they are ‘untried’ unacceptably inaccurate unless a supine stadiometer is
in terms of most homeostatic processes. They have used (see Fig. 12.7). The head circumference is a valuable
recently completed the transition from the relatively measurement during this period. Care needs to be taken
hypoxic environment of the uterus, where they were when measuring the true head circumference: use a
dependent on the placental circulation (Fig. 12.13), and nonstretchable tape, applied closely around the scalp and
have had to cope with the stress of delivery, including take the largest circumference obtained around the
huge adaptations in their cardiorespiratory physiology to occiput and forehead. With correct technique a reliable
enable them to breathe air. interobserver measurement to within ±0.1 cm can be
obtained (Fig. 12.14).
DEVELOPMENT
The fetoplacental circulation At birth, the newborn can hear, smell, taste, feel and see
(but only up to approximately 30 cm). The social smile
(smiling in response to smiling and cooing parents) is a
left ventricle very important milestone of higher cortical function.
receives pulmonary return and
inferior vena caval return which has
Most behaviour observed in newborns before this event
passed through the foramen ovale is the result of responses initiated by the brainstem and
superior vena spinal cord, for example, startling to sound and the
caval return primitive reflexes.
right ventricle
output:
i) passes to lungs,
ii) through the
ductus arteriosus
Measurement of head circumference
ductus
arteriosus
inferior vena
caval return: X
i) combines with
descending
superior caval return, X
aorta
ii) passes through
the foramen ovale
to the left atrium 5
6
31
4
0 1 2 3 41
32 40
33
Occipital 34 35 36 37
38 39
Frontal
oxygenated blood
deoxygenated blood
to inferior vena cava
to the placenta via the
via the ductus venosus
umbilical arteries
oxygenation in
the placenta
Fig. 12.13 The fetoplacental circulation. The fetal cardiorespiratory

blood flow is in parallel rather than in series after birth with the Fig. 12.14 Measurement of head circumference. The simplest
closure of the foramen ovale and the ductus arteriosus. ‘investigation’ in paediatric neurology.
397
Chapter
HISTORY vasoconstriction and relative polycythaemia (haemoglobin

The feeding history is important because feeding is the range 14.9–23.7 g/dl at birth): capillary refill time may
most strenuous action the newborn has to do. Any therefore be more sluggish. Central cyanosis is best
compromise in cardiorespiratory function is revealed in observed in the tongue and mucous membranes; these
difficulty in taking or completing feeds. In breastfed may be the only sites that are noticeably blue in cyanosed
babies, it is difficult to be certain how well the feeding is nonwhite babies. On inspection, the only signs of
progressing because the quantities of feed are unknown. congenital heart disease may be respiratory distress at
Mothers breastfeeding for the first time may not be sure rest. A pale baby may be anaemic or even hypoxic.
how well they (both) are doing. Ask the mother how The rate, rhythm and character of the brachial and
often and for how long her baby breastfeeds, how she femoral pulses (Fig. 12.15) need to be assessed. Weak or
feels the feeds are progressing, and whether she has any absent femoral pulses may suggest coarctation of the
subjective feelings of let down of milk. Documented aorta, as would four-limb blood pressure measurements
weight gain in the baby and the mother feeling that her demonstrating an upper limb to lower limb gradient in
breasts empty are helpful indicators. With bottle-fed blood pressure. Large volume pulses are found with a
babies it should be easy to ask about quantities of infant patent ductus arteriosus. The precordium should be
formula taken. palpated and the presence of an apex beat (usually on the
Details about maternal health, the pregnancy and left) and heaves or thrills noted (Fig. 12.16).
delivery, as well as the baby’s condition and birth weight, The separation of the two components of the second
are important to record. Apart from any parental concerns, heart sound on auscultation may be difficult because
ask about vitamin K administration, jaundice, stools and of the baby’s fast heart rate (Fig. 12.17). A single second
how the baby responds to handling. Pay close attention heart sound may indicate pulmonary outflow obstruction.
to what an experienced mother’s observations have to Innocent (non-pathological) systolic murmurs are
say about her baby: she will have spent a great deal of
time observing the baby closely; if she perceives something
different about this baby then it may be an important
diagnostic clue.
EXAMINATION
Newborns and young babies are examined when they
are acutely ill or, more commonly, during routine checks.
The observation and skills used are common to both
the acute and routine situations. You should plot the
progress of weight and head circumference on a centile
chart. The baby must be undressed to be fully
examined.
The very young (like the very old) often have nonspecific
symptoms and signs even when they are seriously ill. Fig. 12.15 Palpating femoral pulses. The femoral pulse can be
Doctors in training need to know the most important difficult to feel; use a point halfway from pubic tubercle to anterior
superior iliac spine as a guide and do not press so firmly as to
signs and symptoms of serious ill health in the very occlude the pulsation.
young. To help less experienced carers of newborns, a
scoring system for symptoms and signs was developed
(see ‘symptoms and signs’ box).
Newborns and young babies can become very sick
quickly. Infections should be included in the differential
diagnosis of any sick baby. These infections can often be
bacterial and serious. It is good practice to think of the
likely infection and how it was acquired and to complete
a full septic screen and give broad-spectrum parenteral
antibiotics until the culture results are known.
Circulation and cardiovascular
The order of examination will depend on the condition
of the baby. Auscultation of the heart sounds and listening
for murmurs may be the priority before the baby cries.
Inspection of the newborn’s colour and perfusion is Fig. 12.16 Palpating the apex beat. Palpate the whole precordium,
crucial. Peripheral cyanosis is common in the first days left and right. The apex beat is usually palpated in the left fifth
of the newborn period (acrocyanosis) because of intercostal space in the midclavicular line.
398
Chapter
Fig. 12.17 Auscultating the heart sounds and listening for

murmurs. Even when the baby is asleep, it can be hard at first to
differentiate the first and second heart sound; palpating a brachial or
femoral pulse simultaneously may help you.
Symptoms and signs

The baby check
Baby check* is a system to help parents, health professionals and carers assess the seriousness of a baby’s illness. It
uses 19 signs and symptoms with scores which, when added together, give a total score which correlates with the
seriousness of the baby’s illness. The scoring system has been validated for use by parents, doctors and nurses in
babies under 1 year old.
Signs Symptoms Score
1. Unusual cry e.g. high-pitched, weak, moaning or painful 2
2. Fluids taken in previous 24 h Less than normal 2
Half normal 4
Very little 9
3. Vomiting Vomiting at least half of a feed in the three previous feeds 4
4. Vomiting bile Any green bile in vomit 13
5. Wet nappies (urine output) Less urine than normal 3
6. Blood in nappy Large amount of blood in nappy 11
7. Drowsiness Occasionally drowsy 3
Drowsy most of the time 5
8. Floppiness Baby seems more floppy than normal 4
9. Watching Baby less watchful than normal 2
10. Awareness Baby responding less than normally to the surroundings 2
11. Breathing difficulties Minimal recession visible 4
Obvious recession visible 15
12. Looking pale Baby more pale than normal, or been pale in last 24 h 3
13. Wheezing Baby has wheezing breath sounds 2
14. Blue nails Apparent blue nails 3
15. Circulation Baby’s toes are white, or stay white for 3 s after squeezing 3
16. Rash Rash over body, or raw weeping area >5 cm × 5 cm 4
17. Hernia Obvious bulge in scrotum or groin 13
18. Temperature (rectal) Temperature >38.3°C by rectal thermometer 4
19. Crying during checks If baby has cried during checks (more than a grizzle) 4
Total scores
0–7 Baby is only a little unwell, medical attention is not necessary
8–12 Baby is unwell but not seriously; seek advice from doctor, health visitor or midwife
13–19 Baby is ill; contact your doctor and arrange to be seen
>20 Baby is seriously ill and needs to be seen by a doctor immediately
If the baby appears to be worse after a low score, re-examine the baby and re-score.
*Adapted from the ‘BabyCheck’ booklet with permission.
399
Chapter
Review Questions to ask

Normal range for newborns Jaundice in young babies
• Heart rate: 110–160 beats/min (>180 tachycardia) • Was the baby jaundiced in the first 24 hours of life?
• Systolic blood pressure: 50–85 mmHg (very variable, • Was the baby still jaundiced during the third week
depending on age, gestation and weight) of life?
• Respiratory rate: 30–50 breaths/min (>60 • Is the baby well, thriving and gaining weight?
tachypnoea) • What is the colour of the stools and the urine?
Symptoms and signs The presence of jaundice is very common. When seen
Respiratory distress
in the first 24 hours of life it is usually due to a pathological
haemolytic process. A physiological jaundice is extremely
• Tachypnoea (normal upper limit varies with age) common after the second day, continuing into the second
• Recession (includes subcostal, intercostals or tracheal week. It is usually related to breastfeeding. If jaundice is
tug) in association with pale stools, dark urine or failure to
• Grunting (an end-expiratory groaning noise, thrive, then pathological hepatic or obstructive cause is
breathing out against partially adducted vocal cords much more likely. Bilirubin in the urine requires
and providing self-positive end expiratory pressure) investigation.
• Flaring of nostrils (the alae nasi are accessory The gastrointestinal tract starts at the mouth and ends
muscles of respiration) at the anus. Both ends need to be looked at. The palate
• Cyanosis (may be subclinical, so check oxygen must be inspected for clefts and palpated for clefts (Fig.
saturation with pulse oximeter) 12.18). The position and patency of the anus needs to be
• Apnoea (may be how a very young baby presents checked (Fig. 12.19). While viewing the perineum, the
with a respiratory disorder, associated with a colour external genitalia should be inspected. In boys, both
change – pallor or cyanosis)
• A periodic breathing pattern may be noted in
preterm or very young babies and is physiological,
often with pauses of 3–5 seconds being observed
(especially during sleep) without a change in colour
being seen
common in the newborn and may be heard on day 1

in over 20% babies who have structurally normal
hearts. Pansystolic and continuous murmurs are
suspicious, as are ejection systolic murmurs that radiate
to the back or neck. Many babies with structural congenital
heart disease may not have a murmur, although they may
have symptoms and other signs of cardiovascular Fig. 12.18 Palpation of palate. The palate needs inspection by
disease. direct vision and palpation.
Breathing and respiration

The presence of respiratory distress is the most important
observation to be made. Auscultatory signs are usually
far less significant than the observation one makes as a
baby is undressed.
Remember that all babies are obligate nose-breathers
during feeding and nasal obstruction may manifest as a
feeding problem. The presence of audible inspiratory
stridor or a hoarse cry warrants further evaluation.
Abdomen
Observing a feed and inspection of stools can be important
parts of the evaluation. The vomiting or ‘posseting’ of
small quantities of milk is common but bile-stained Fig. 12.19 Inspecting the anus. Ask if meconium has been passed
vomiting warrants urgent assessment. during the first 24 hours.
400
Chapter
Fig. 12.20 Palpation of male genitalia. At term both testes should

be well in the scrotum. Hydroceles are common. If the testes are not Fig. 12.22 Palpation of liver edge. Most babies and infants have a
in the scrotum, can you feel them in the inguinal canal? 1 cm palpable liver edge.
Fig. 12.21 Umbilical hernia. Umbilical hernias are very common Fig. 12.23 Examining the hips (abduction). Ortolani manoeuvre
may detect relocation of dislocated hips.
(especially in some racial groups). They do not obstruct, they resolve
spontaneously and need no treatment. Paraumbilical hernias,
however, will require surgery.
testes should be in the scrotum (Fig. 12.20). Small

hydroceles are common and need no action. If hernias
are suspected then make a prompt referral to a paediatric
surgeon. The penis should have a normally sited urethral
orifice with a foreskin adherent to the glans (this
adherence is physiological and should not be interfered
with). In girls there should be an introitus and a normally
sized clitoris. Any ambiguity in the genitalia requires
urgent assessment by a paediatric endocrinologist before
sex is assigned.
The abdomen should not be distended. Divarication of
the rectus abdominis muscles is common, as are umbilical Fig. 12.24 Examining the hips (adduction). Barlow’s manoeuvre
may detect dislocatable hips.
hernias (Fig. 12.21); neither require any treatment. The
umbilical stump has usually separated by the 10th day.
A liver edge is usually palpable (approximately 1 cm with apparent shortening of the thigh. This might be
below the costal margin) (Fig. 12.22) and the lower pole confirmed when abduction is restricted and when anterior
of the right kidney and a spleen tip are sometimes pressure on the greater trochanter (Fig. 12.23) results in
palpable. feeling a ‘clunk’ as the femoral head relocates in the
Examine the hips while the nappy is off. The Ortolani acetabulum (Ortolani’s test). With the hip flexed and the
and Barlow manoeuvres are used to detect abnormalities thigh adducted and with pushing posteriorly in the line
in the hip joint. These manoeuvres must be done very of the femur, a posterior dislocation of the femoral head
gently and should not cause the baby distress. A unilateral will ‘clunk’ back out of the acetabulum as the thigh is
dislocated (subluxed) hip may be found on inspection, abducted (Barlow’s manoeuvre) (Fig. 12.24). Do not
401
Chapter
Fig. 12.25 Palpation on the fontanelle. Note the tone and size of Fig. 12.27 Ophthalmoscopy of the red reflex. Never omit this
anterior and posterior fontanelles. check; if eyes are closed, come back later.
tone or movement must only be considered if the baby’s

head is in the neutral position in the midline. The
asymmetric tonic neck reflex is a strong influence on
posture and movement. The rest of the primitive reflexes
may then be helpful if there are concerns about movement.
The Moro (startle) reflex is an unpleasant stimulus to the
baby and should not be done without a good reason (e.g.
in evaluating a potential Erb’s palsy).
The baby should be able to fix on and follow an object
through 90°. Using an ophthalmoscope, look for the
presence of a red reflex in each eye (Fig. 12.27). Any
absent red reflex may be due to a cataract and warrants
an urgent expert ophthalmological assessment. Squints
Fig. 12.26 Measuring the head circumference. Be accurate because can be normal when under 8 weeks old but should
this measurement may need to be referred to at a future date. diminish with age.
Young babies should startle to loud noises (e.g.
telephone ringing or door slamming) and should quieten
to sounds that are loud and constant (e.g. vacuum
attempt this examination unless you have been trained cleaners).
in it.
Neurology and development
A feel of the anterior fontanelle (Fig. 12.25) is part of the Review
ritual of a paediatrician’s assessment of a newborn baby.
Low birth weight (LBW) babies
Fontanelle size is very variable and its tone is altered by
crying. Bulging fontanelles indicate raised intracranial • Important because of the increased morbidity and
pressure, as in hydrocephalus, meningitis or other causes mortality seen in the affected infants
of space-occupying lesions. A cranial ultrasound scan will • You must differentiate between babies who are
quickly and easily demonstrate enlarged ventricles and preterm, normal for gestation or small for gestational
may show other causes of bulging fontanelles. age
Inspection and palpation of the baby’s head is always • LBW defined as <2.5 kg birth weight; about 7% of
warranted. Moulding or caput is common in the first 24 UK births
hours, as is a ‘chignon’ after a ventouse delivery. Swelling • Babies >2.5 kg birth weight may be at risk of similar
over either parietal bones is usually caused by complications because of antenatal growth
cephalohaematomas (subperiosteal bleeds), which are retardation such babies appear emaciated.
bounded by suture lines and which may persist for • Very low birth weight (VLBW) defined as <1.5 kg;
weeks. The head circumference should be measured about 1% of UK births (mostly all preterm)
(Fig. 12.26). • Extreme low birth weight (ELBW) defined as <1.0 kg;
The best way to assess a newborn’s nervous system about 0.5% of UK births (almost exclusively very
is to observe the baby. Eliciting all the primitive reflexes preterm)
is less helpful than observation. Any asymmetry of
402
Chapter
Review
THE ROUTINE NEONATAL EXAMINATION
Gestation and weight at gestation Most developed countries have a policy of examining all
neonates in the first few days of life. This examination
• Term – born 37–42 completed weeks gestation from has a number of objectives. It is a form of screening,
last menstrual period (LMP) attempting to identify congenital abnormalities that may
• Preterm – born before 37 completed weeks (259 benefit from intervention. It also provides an opportunity
days) gestation from LMP – note that a preterm to answer whatever questions the parents may have
baby’s age can be expressed as either a about their new baby.
chronological (uncorrected) age or an age This examination is best performed at or beyond 24
postconception (corrected); the latter is important hours of age. This is often not possible with earlier
when considering growth and development in the discharge from delivery units. The older the baby, the
first 2 years more confident one can be in diagnosing ‘normality’.
• Post-term – born after 42 completed weeks (294 Examine neonates in front of the parents. The examiner
days) gestation from LMP can review the mother’s notes and take a history of
• Small for gestational age or ‘small for dates’ – birth maternal and family health, the progress during
weight below 10th centile for gestational age pregnancy, the results of antenatal tests (such as
• Large for gestational age or ‘large for dates’ – birth ultrasound anomaly scans) and an account of the delivery
weight greater than 90th centile for gestational age and condition of the newborn at birth. Subsequent
feeding history and whether the baby has passed
meconium and urine normally are important.
Dysmorphology terms
outer
canthus
palpebral
occiput
pinna fissure
outer
canthus X Y
philtrum Y
inner
canthus
normal set
ears
The proportions of a baby’s face when viewed from the front, with a line through the eyes is about half way from vertex to chin (x),
the palpebral fissures (the slits through which your eyes look) should be of equal length (y) measured from inner to outer canthus.
There is usually a very mild slant to the palpebral fissures, if this slant is exaggerated then it is described as upward slanting (as may
be seen in Trisomy 21, Down syndrome). Alternatively, the slant may be in the opposite direction and is described as downward
slanting (as may be seen in many syndromes).
The distance between the eyes is approximately that of the palpebral fissures (y).
Hypotelorism is when this distance is too short and hypertelorism is when this distance is too long and the eyes appear too far apart.
The philtrum leads from the nostrils to the edge of the upper lip.
A line from the outer canthus towards the occiput should cross the attachment of the upper helix of the pinna (ear lobe) to the side
of the head. Where this does not occur then the ear is described as low set and may appear simple (poorly formed helix) and
rotated as well.
upward slanting palpebral fissures downward slanting palpebral fissures low set and rotated ear
Fig. 12.28 Facial dysmorphology vocabulary explained. A few of the commonly referred to anatomical terms used in describing facial features
are demonstrated.
403
Chapter
Fig. 12.29 Scheme for

Neonatal examination examining newborns. By
‘circumnavigating’ the baby in a
systematic way, most visible
Here is an approach to help you remain systematic in your approach to congenital abnormalities will
examining newborns. The more important congenital anomalies tend to
be detected.
occur on or near the midline, so using a constant point of origin (e.g. the
mouth) start examining the neonate along the midline, circumnavigating
the entire baby and arriving back at your point of origin. At some points
you may stray from the midline (e.g. to look at the eyes, or auscultate
the heart). At the end do not forget the hands, feet and hips need
checking.
Eyes Fontanelles
Face
Start at mouth
Neck
Chin
Heart Back
Anterior
abdominal wall
Genitalia
Perineum
Anus
As neonates are ‘new and untested’, this examination,

more than any other at a later date, is more likely to
reveal congenital abnormalities. Single minor congenital
abnormalities occur with a frequency of up to 14% of live
births. The greater the number of congenital abnormalities,
the greater the possibility that there may be more serious
congenital abnormalities present. Severe and lethal
congenital abnormalities are seen in about 1.5% of live
births. It is worth understanding the descriptive terms
used to describe dysmorphic signs (Fig. 12.28). The
examiner needs to develop a systematic method of
looking for and excluding dysmorphic features and
congenital abnormalities. You must examine the
undressed baby in a warm environment (Fig. 12.29).
There are a great number of minor findings that may Fig. 12.30a Cleft palate. Inspect the palate and palpate for
be found on examination that are remarkable because any clefts.
they either are present at birth and resolve on their own
or because they appear after birth but need further
attention (Fig. 12.30).
404
Chapter
Fig. 12.30b Low hairline. Examine the scalp and hair and
hairline. This may be indicative of a syndrome, a low hairline is
seen in Turner’s syndrome.
Fig. 12.30c Cavernous haemangioma. Fig. 12.30d Preauricular tags.
Cavernous haemangiomas (‘strawberry Preauricular tags are common and
naevus’) can occur anywhere and are often there is a family history. They
more common in preterm babies; they may represent a cosmetic problem
get bigger during the first year and requiring plastic surgery or they may
eventually regress. Treatment is only be associated with other otological
indicated if the naevus interferes with abnormalities.
breathing, feeding or vision or if
otherwise problematic.
Fig. 12.30e Thoracic

myelocele. Neural tube
defects are now less
prevalent in developed
countries. Examine the
back carefully by
inspection and palpation
from occiput to coccyx. If
a neural tube defect is
detected, remember to
examine for signs of
hydrocephalus and
bladder and bowel
function as well as
dislocated hips.
Fig. 12.30f Blue spots. These ‘Mongolian’ blue spots are common
in all racial groups (except those of Northern White European origin).
They are present from birth and may persist beyond the third year.
Fig. 12.30g Lumbar meningomyelocele. Lumbosacral neural tube Fig. 12.30h Imperforate anus. Anogenital abnormalities need to be
defects are the most common. Folic acid supplements before excluded by careful history and inspection. Meconium can be passed
conception and in early pregnancy have helped to reduce the via a fistula into any other cloacal structure (e.g. the vagina). These
incidence of these serious malformations. abnormalities are seen associated with other congenital abnormalities.
405
Chapter
Fig. 12.30i Hypospadias. Check that the foreskin has fused Fig. 12.30j Neonatal breast development. The influence of
normally on the ventral surface of the glans. If it has not, then note maternal hormones may result in palpable breast tissue of babies of
where the external urethral meatus is sited. Hypospadias occurs either sex. No action is required and this resolves spontaneously.
when the urethral meatus is not at the tip of the glans; commonly it
is mild and on the glans, or rarely, more severe and on the shaft of
the penis or perineum. Check for fixed flexion of the penis (chordee).
Fig. 12.30k Micrognathia. A small mandible with a normal-sized Fig. 12.30l Single palmar crease. A single palmar crease can be a
tongue represents a potential hazard to this baby’s airway. A cleft normal finding. However, it can be part of a series of minor
palate can be associated. Breathing and feeding may need some observations which can add up to a more important diagnosis, such
assistance. as Down’s syndrome.
n
Fig. 12.30m Syndactyly of the second and third toes. Minor Fig. 12.30n Postaxial extra digit. Also very common and often
congenital abnormalities like this, when isolated, are common and familial. Refer for a plastic surgery consultation, rather than having
often familial. Noticing one minor finding should prompt you to them ‘tied off’.
ensure there is not another to be observed.
406
Chapter
Baby rashes
• Newborns have to adapt from an aqueous,

thermally-regulated environment to the outside
world. They have to keep their skin moist and stay
warm. There are a variety of cutaneous phenomena
that are benign and self-limiting.
• Confusion can occur when trying to differentiate
between staphylococcal septic spots (not common
but serious) (Fig. 12.31) and erythema toxicum, a
transient eosinophilic infiltration of the skin (very
common and completely benign) (Fig. 12.32). The
former spots are often in skin creases and get bigger
and ‘more angry’, the latter look red but are Fig. 12.31 Staphylococcal skin infection. The appearance of
transient and appear anywhere on the baby. pustules in moist skin creases that do not spontaneously go away
may herald the collapse of the baby with staphylococcal sepsis.
Review
Examination of newborns and young babies
• Babies are routinely seen by doctors for checks at

birth and at 6–8 weeks old
• All newly qualified doctors should be able to
perform a routine neonatal examination and define a
baby as normal or otherwise
• Babies can become ill at an alarming rate and all
healthcare professionals seeing them can benefit
from scoring systems to help them to evaluate
symptoms and signs
• Observation is the most important skill that Fig. 12.32 Erythema toxicum. These spots can look a lot like
paediatricians and children’s nurses use to assess staphylococcal pustules except that they spontaneously disappear
and reappear in another area of skin. The rash is caused by
babies
eosinophilic infiltrates that are of no serious significance.
progresses from being primarily supine and unable to

By the time of qualification, students should be
move around, to becoming a toddler who is able to run
confident in examining babies and diagnosing
and talk.
‘normality’.
At the beginning of this period the effects of
passively acquired maternal immunity (transplacental
immunoglobulin G) mean that babies are not as prone
Older babies and toddlers to intercurrent viral illnesses as they will be later (Fig.
12.33). From the age of 3 or 4 months this passive
The term ‘infant’ has been used previously to describe immunity is diminishing and immunologically the baby
children under 2 years of age. We prefer to think of ‘older is now on his or her own. On average, the healthy older
babies’ as being infants that are not yet walking and baby and toddler will have to deal with eight self-limiting
‘toddlers’ as babies who have only recently acquired this viral illnesses per year. Sometimes two or three of these
skill. These children are frequently brought to their illnesses will occur ‘back to back’, causing a great deal of
doctor. They attend for routine immunisations and anxiety in the parents, and the infant may temporarily
developmental checks and are most likely to be seen by fail to thrive. This acquisition of active immunity to the
doctors in various settings (e.g. primary care, accident common viruses prevalent in the child’s community is a
and emergency departments, community clinics, part of normal growth and development.
paediatric departments). In many developed countries, a comprehensive
This period involves very rapid changes in growth and immunisation programme from birth to 2 years aims to
especially in development. During this period, the child prevent up to nine or more important infectious diseases
407
Chapter
Serum immunoglobulin levels Palmar and pincer grip

Serum
immunoglobulin levels
(% adult values)
100
IgM
IgG
maternally
transferred
IgG 50 IgA
total
IgG
20 30 birth 1 10 Fig. 12.34 Palmar and pincer grasp. The development of palmar
and then pincer grasp represents a great step forward in fine motor
Gestation Age (years)
skills and relies heavily on visual feedback.
(weeks)
Fig. 12.33 Immunoglobulin levels vary with age. At birth babies

have had a transplacental transfusion of maternal IgG that wears off occasionally do parents seem truly unaware of their
by the end of the first 6 months. This provides passive immunity to child’s significant developmental problem.
the newborn baby; afterwards the child must develop his or her own
The first areas to develop rapidly are vision and the
active immunity after infection or immunisation.
control of hand movements and the next are the gross
locomotor skills needed to roll over and sit without
support. During this time visual acuity and hand dexterity
(e.g. diphtheria, tetanus, pertussis, polio, Haemophilus are continuing to improve. Fine and gross motor
type B infections, pneumoccal infections, meningococcal development rely heavily on the progression of visual
group C infections, measles, mumps and rubella). Visits development. The child listens to adults and siblings
for primary immunisation provide an opportunity for the intently. He or she starts to babble and to understand
infant’s primary care physician to observe an infant’s more and more of what is said. Once confidence is gained
growth, development and general health. when prone with hips flexed, the baby finds him- or
herself teetering on hands and knees and then begins to
crawl. Soon after that, the toddler is pulling up to stand
GROWTH and cruising around the furniture: the prelude to solo
walking. Fine motor skills include the continued
Babies in this phase are still growing rapidly. There
refinement of grasp until the pincer grip (Fig. 12.34) is
is a distinct deceleration in their growth velocity in the
achieved. At around the same time, vocalisations have
latter part of the first year and into the second year. The
become more and more specific and ‘dada’ and ‘mama’
‘average infant’ will have doubled birth weight by
are said with meaning. Comprehension of language now
approximately 5 months and trebled it by just after a
includes following some instructions and commands.
year.
This is all usually achieved in the first year.
The most dramatic changes are seen in head growth.
In the following year, continued improvements in
This is as a result of myelination of cortical tracts
walking (with the feet less far apart) are followed by
and pathways leading to rapid brain growth, which
running at speed, kicking a ball and rapid changes in
are crucial in enabling developmental advances in this
direction. Fine motor skills are seen in manual dexterity
period.
(tower of six cubes) and improved self-help abilities
(feeding with a spoon, drinking from a cup and beginning
to undress themselves). Communication continues to
DEVELOPMENT
advance with the increase in vocabulary and the
At the beginning of this phase, a baby’s cortical function combination of words to make short phrases.
has only recently demonstrated the important milestone Comprehension of language is still greater than expressive
of social smiling (6–8 weeks age). By the end of this phase language abilities.
(aged 2 years) the child will be walking, communicating
wants and needs verbally and nonverbally, and will
have developed sophisticated hand function and HISTORY-TAKING
coordination. During a consultation the parents are the usual historians.
The key question in this age group is: Are the parents The baby or toddler will often arrive with siblings in tow.
concerned about their child’s developmental progress? Only By involving the whole family in the consultation, the
408
Chapter
child may be put at ease and a more satisfactory result Nearly one-third of children will have a murmur heard
obtained. at some point of their lives. Less than 1% of children will
The history should cover the same areas as with the have a structural heart lesion. Innocent murmurs have
newborn and very young baby and include points particular characteristics: ejection systolic flow murmurs
particularly relevant to this period, for example, current are either ‘short and buzzing’ (caused by turbulent aortic
feeding, weaning, developmental abilities, immunisations flow) or ‘soft and blowing’ (caused by turbulent pulmonary
received. flow); venous hums are low pitched and more noticeable
after exertion or inspiration and they are abolished by
lying supine.
EXAMINATION True pathological murmurs are usually louder, harsher
and longer and may radiate or have a diastolic component
During the history it is often best to keep the child on the
to them. Look for other symptoms and signs of
parent’s lap and play with them. Depending on how well
cardiovascular disease.
you are getting on, you may be able to start examining
the child. If the child is wary, it may be necessary to
demonstrate your intentions by examining an elder
sibling, teddy or parent. Try and show the child that Review
whatever you are going to do is more of a game, rather
Measuring children’s blood pressure
than anything threatening to them.
It is important, as with newborns, to examine the most Children’s blood pressure measurements can be
relevant system indicated by the history first because this obtained using:
may be your only chance. Make sure that you have • Oscillometry (dynamap)
examined the whole child undressed by the end of your • Sphygmomanometry (using a stethoscope or Doppler
examination. This should be done in stages. Save the probe or by palpation)
more unpleasant parts of the examination (e.g. looking • Direct (invasive) measurement (in intensive care)
at the ears and throat) until last. Remember the two-thirds rule:
• Cuff width must be at least two-thirds of the
Circulation and cardiovascular system distance from shoulder to elbow
• Cuff (bladder) length must be at least two-thirds of
Look at the child’s colour and ask if there have been any
the limb circumference
dramatic changes in this. Infants are now no longer
polycythaemic; indeed they are likely to be ‘physiologically’
anaemic (lower end of expected range for haemoglobin
is 9.4 g/dl at 2 months and 11.1 g/dl at 6 months). Central
cyanosis can be missed if a ‘dummy’ (or pacifier) is not Review
removed from the mouth.
Normal cardiovascular and respiratory ranges for
Capillary refill time is a very sensitive sign and should older babies and toddlers
be the same as for adults (less than 2–3 s). Environmental
cold stress can prolong the capillary refill time in otherwise • Heart rate: 110–150 beats/min (>160 tachycardia)
well babies. As in newborns, the cardiac output is mostly • Systolic blood pressure: 80–95 mmHg (depends on
regulated by rate rather than stroke volume. Tachycardia age and height)
is an important physical sign that needs evaluation, e.g. • Respiratory rate: 25–35 breaths/min (>40
febrile, unwell, upset and crying? tachypnoea)
Blood pressure should be measured in any sick infant
or when cardiovascular, renal, endocrine or neurological
diagnoses are being considered. The interpretation of a
single blood pressure measurement requires knowledge
Breathing and respiration
of three factors: what size of cuff was used relative to
the child’s upper arm; the size of the child; and what Watching and listening to the child’s respiratory pattern
emotional state the child was in at the time of is the most useful part of the examination of the respiratory
measurement. The cuff size is critical, as blood pressure system. Auscultation may add some more information,
measurements may be spuriously high if too small a cuff but is frequently ‘drowned’ by loud transmitted upper
is used or the infant is crying. Normal ranges are published respiratory tract breath sounds.
according to size and age. Look at the upper respiratory tract (in the ears, nose
Palpation of the apex beat is helpful because some and throat) at the end of the examination. Coryza (profuse
murmurs may be palpable as heaves or thrills. During discharge) and pink inflamed mucous membranes in the
auscultation of the heart sounds, normal splitting of the throat and ears are most likely to be caused by a viral
second heart sound may be difficult to hear in a tachycardic upper respiratory infection. Antibiotics are not required
child. unless a true secondary bacterial infection is suspected.
409
Chapter
Differential diagnosis Red flag – urgent referral

Childhood rashes Nonblanching (purpuric) rashes
• Rashes in childhood are very common and all you • Meningococcal septicaemia (Fig. 12.35)
need is a simple and logical approach to make a • Idiopathic thrombocytopenic purpura (Fig. 12.36)
diagnosis most of the time. • Fingertip bruises in non-accidental injury (Fig. 12.37)
• The most clinically important rashes to recognise • Henoch–Schönlein purpura (Fig. 12.38)
promptly are ones that are purpuric (nonblanching)
• If the rash is erythematous (blanching) and is
associated with an intercurrent illness, then it is most
probably related to an infection: often viral and
self-limiting
• Any chronically itchy rash is likely to be eczema and
should be treated with emollients
Fig. 12.35 Meningococcal septicaemia. All purpuric rashes in

childhood need careful evaluation. The lives of patients with
meningococcal disease depend on their doctor recognising this
purpuric rash as early as possible. Note that the rash may start off as
erythematous and then progress to nonblanching purpura. It is the
speed of the rash’s progression and the patient’s degree of illness Fig. 12.36 Idiopathic thrombocytopenic purpura (ITP). ITP in
that are the hallmark of this infection. Treat immediately with an childhood differs from the adult condition by being more benign and
appropriate parenteral antibiotic. is self-limiting. Acute leukaemia is a very important differential
diagnosis to be rapidly excluded by a full blood count and blood
film.
Fig. 12.37 Fingertip bruising; nonaccidental injury. All children have

falls and minor injuries that result in bruises. Most bruises occur in Fig. 12.38 Henoch–Schönlein purpura (HSP). HSP is an ‘allergic’
areas of likely accidental impact (e.g. shins and elbows). Any bruise vasculitis that has a characteristic distribution along the back of the
in a usually protected site is a worry. Ask how it happened. Is the legs, extending up to the buttocks. It is associated with many
injury consistent with the history? If you are worried, discuss systemic symptoms, such as joint swelling and (uncommonly) may
immediately with senior staff. result in permanent renal impairment.
410
Chapter
Lymphadenopathy (localised or generalised) is movement, gait and coordination by observation while

common in association with frequent upper respiratory the child plays.
tract infections and viral illnesses. It may appear to persist Observation of gross motor skills will enable posture,
if there is little or no interval between these infections. power and, when the child is picked up, tone to be
Acutely tender lymphadenopathy can be associated assessed. In younger babies antigravity power should be
with bacterial infections. Persisting, asymmetrical large demonstrable by lifting the limbs or, when prone, the
and nontender lymphadenopathy in association with head off the bed. Assessment of truncal tone is important
constitutional symptoms needs accurate diagnosis in the youngest of babies upwards. The limbs can be
and prompt treatment. inspected and palpated in play to ascertain tone, muscle
bulk, power and sensation (by gently tickling). Deep
Abdomen tendon reflexes can be elicited with patience. In an easily
distracted child, reinforcement can be employed in play
Bile-stained vomiting, pallor, excessive inconsolable
(squeeze the toy) if necessary. Coordination is hard to
crying, a distended abdomen, lumps in the groin and
test formally in this age group and the observation of fine
blood in the stool are all indicators of an acute abdominal
motor skills and gait are the most one can rely on.
problem. Children with peritonitis will lie very still, with
The cranial nerves can be assessed by observation of
their knees flexed, and breathe without moving the
behaviour and facial expression.
diaphragm. A diagnosis needs to be established and the
child treated promptly. The olfactory (first) nerve This is rarely tested but smell
After careful inspection, palpation can be attempted can be assessed by asking the toddler to find a mint
with warm hands. This will be a fruitless exercise if the hidden in a handkerchief.
infant is crying. Patience is needed and more than one
The optic (second) nerve In babies and toddlers visual
attempt at palpation may be required, perhaps when the
acuity can be checked formally by a variety of techniques
child is sleeping on a parent’s lap.
in a visual laboratory. Examining the visual fields and
Examine the anogenital area. In boys, always check
employing fundoscopy is often difficult in this age group.
that the testes are in the scrotum (a visual check will do,
However, in the older (preschool age) child this is more
if they are obviously present). Do not attempt to retract
straightforward and acuity can be checked beyond the
the foreskin (it is physiologically adherent to the glans).
age of 2 years with shape or letter matching.
In girls the external genitalia are less visible than when
they are newborn. The labia majora are fleshy and obscure The oculomotor, trochlear and abducens (third, fourth
the introitus, clitoris and urethral opening. The vulval and sixth) nerves For assessing these nerves, eye
area in young girls is consequently infrequently observed movements can be observed when the child follows a toy
by doctors. It is often preferable to ask someone more or light in the vertical and horizontal plane. Nystagmus
used to examining girls’ perineums when this area is the is normally seen in extremes of lateral gaze or may be
focus of the presenting problem in young girls. pendular in a severely visually impaired child.
The hip joint is a frequent cause for concern (in many
The trigeminal (fifth) and facial (seventh) nerves The
age groups) because of an acquired limp. As in abdominal
trigeminal nerve can be tested when the jaws are clenched
palpation, if the child is not relaxed then the chances of
on a bottle or biscuit, and the facial nerve by encouraging
a meaningful examination are limited. With the child
the child to smile or shut their eyes.
on the parent’s lap, gently explore the passive range of
movements the child will tolerate. Look at the child’s The acoustic (eighth) nerve In some places hearing is
expression, to know when to stop. Internal and external still routinely screened in children from 7 to 8 months of
rotation of the hip (with the hip and knee both in 90° of age. Many places have now introduced universal Oto-
flexion) is one of the most reproducible and sensitive Acoustic Emission (OAE) Hearing Screening in the
ways to pick up hip joint pathology. neonatal period.
The glossopharyngeal (ninth), vagus (tenth) accessory
Neurology and development
(eleventh) and hypoglossal (twelfth) nerves Testing the
The neurological assessment of infants relies heavily function of these nerves is slightly more difficult in this
on history (for developmental skills) and inspection and age group, a history of regurgitation or choking on feeds
observation for confirmation of the reported abilities and may be relevant.
the presence of any focal signs. The history is the key in When inspecting the throat, at the end of your
many neurological diagnoses. When dealing with possible examination, you may be lucky and notice the following:
fits or ‘funny turns’, a first-hand account is best of all; a movement of the uvula as you inspect the throat
parent’s video of the episode may be most valuable. (ninth nerve intact); no hoarseness in the cry (tenth nerve
Observation is more important than testing reflexes. intact); shrugging of the shoulders and turning of the
Flexibility and improvisation are needed to extract head using the sternomastoid (eleventh nerve intact);
whatever physical sign you are trying to elicit. Save the waggling of the tongue as the spatula is used (twelfth
cranial nerve examination until last and check behaviour, nerve intact).
411
Chapter
Differential diagnosis Review

Cranial nerve lesions in children Examination of older babies and toddlers
Cranial nerve lesions are not very common. Here are • Young children are frequently brought to see their
three important ones: doctor
• Young children are undergoing the most rapid
• Probably the most common cranial nerve to
changes in development
malfunction is the eighth nerve. Sensorineural
• From the age of 4 months, a child is immunologically
hearing impairment occurs in approximately 0.1%
‘solo’ and is prone to have frequent viral illnesses
live births and has a variety of congenital and
(average 8–10 per year)
acquired causes
• When examining this age group, it is important to
• A lower motor seventh nerve lesion, as seen in a
engage the child in play if you are to be successful
Bell’s palsy, or after birth injury (forceps), is
reasonably common. Remember that there are a
number of causes, some more benign than others.
With Bell’s palsy check blood pressure and perform
an audiogram mingles with peers at playgroup and nursery. Their
• A sixth nerve palsy may be a sign of raised cooperation with your examination can be extremely
intracranial pressure (the affected eye looks medially variable and if you can make their visits to you fun, then
or convergently.) Most childhood squints are all the better.
convergent (or alternating) and are due to refraction
differences or ocular muscle imbalances
GROWTH
Growth during this phase appears almost linear on the
growth chart. In fact, the growth rate is decelerating by
approximately 30% over this period. It should be possible
Review
now to estimate the midparental height centile and
Child development
compare it with that of the child’s height centile.
This is a difficult subject to summarise because of the
large degree of normal variation in acquisition of skills
(milestones). Always correct age for prematurity. Some
warning signs in the first year of life include: Review
• Any child whose parent expresses specific concerns Midparental height
about his or her development
• This calculation enables a prediction of the child’s
• The loss of any acquired skills (developmental
adult target height range
regression)
• The mean difference in final adult height is 14 cm
• Persistence of adducted thumbs from the neonatal
between men and women
period
• For boys add 14 cm to mother’s height
• No social smile by age 8 weeks
• For girls subtract 14 cm from father’s height
• No startling to sound or responding to nearby voices
• The midpoint between the parents’ corrected heights
by 8 weeks
is the midparental height
• Not visually fixing and following from before 8
weeks
• Definite asymmetry of tone and movement (with
head in midline) during the first year
• Not sitting unsupported by 8 months
DEVELOPMENT
• No polysyllabic babbling by 8 months
This period is characterised by advances in communication
and the use and understanding of language and involves
the transition from a mobile toddler, who communicates
only a little verbally, to the chattering 4-year-old, using
The preschool child sentences and telling long, involved stories. Social and
behavioural landmarks include the general behaviour
The preschool age group, 2–5 years of age, are the next of the child in relation to other adults and children, as
most frequent attenders of their doctors. In common with well as specific abilities, for example, potty training. The
younger children they will have a similar frequency of advances in language, speech and communication mean
viral illnesses and potential for accidental self-poisoning. that certain tests and facets of the clinical examination
These viral illnesses will be more frequent as the child are approaching those used in adults.
412
Chapter
The preschool child 12
HISTORY Abdomen
Most of this age group start off on their parent’s lap. Ask All of the points made previously about acute abdominal
the siblings questions as well during your history-taking. problems can occur but now much less commonly. If
The confident and relaxed child will begin to explore the the child is on a bed or couch it is important to make
room before too long and will be happy to supply small sure that a parent is near the head end. It is
pieces of the history (e.g. siblings’ names). The history worthwhile kneeling down, making sure the child’s
may need to contain all of the details noted for a younger eye level is above yours and looking at the child’s face,
child but details about the pregnancy and so on are not the belly.
becoming less relevant. It is likely that an abdominal examination will be
The history should include details about developmental successful as long as one does not mention whether the
skills acquired and whether the parents or health visitor child is ticklish, otherwise it can all become hopelessly
have any concerns. Other specific points include diet ‘giggly’. Sometimes this can be avoided by allowing the
(peak age for incidence of dietary iron-deficiency child to palpate his or her own tummy, with your hand
anaemia), exercise tolerance and coughing (asthma is on top.
commonly underdiagnosed). Leg posture and gait are a frequent source of parental
anxiety as the toddler gains confidence on his or her feet.
Genu varus (bow legs) is normal early on and there is
EXAMINATION then a tendency to genu valgus (knock knees) before
Generally this is best done on the parent’s lap. Even a more straight leg grows in school-age children
the most apparently confident child may become (Fig. 12.39).
upset when placed alone on an examination couch. Again the hip joint may be a focus of concern because
Focus on the area of interest first and save the less of a limp or leg, thigh or knee pain. The limits of external
pleasant parts until last. Make a game of it all and and internal rotation can help decide what needs further
satisfy any curiosity expressed by the child (e.g. by evaluation.
letting them listen to mummy’s heart or look in daddy’s Neurology and development
ear).
Gait and gross motor abilities are assessed as the child is
Circulation and cardiovascular system playing in the room. Fine motor abilities can now be
readily assessed with a pencil and paper, by asking the
An opportunity to auscultate the heart is now less of a child to copy various shapes: a circle by age 3 years, a
priority and checking the perfusion (capillary refill time) cross by 4 years, a square by 4 years 6 months and
pulse and blood pressure (if indicated) can be done before triangles by 5 years. Language and speech can be harder
then. to assess. Hearing can be checked using free field
The fall in heart rate means that the first and second audiometry. Vision can be tested with shape- or letter-
heart sounds can be more carefully assessed. Innocent, matching by the age of approximately 3 years. Social and
benign flow-related murmurs are also common in this behavioural skills are either observed or enquired about
age group. with the history.
The neurological examination is now somewhere
Breathing and respiration between what was described for toddlers and a more
Observation of the chest shape and respiratory pattern adult format. Reflexes, fundoscopy, visual fields and
are again invaluable. Auscultation is seldom rewarding
in the absence of observed respiratory distress. Peak
flow measurements are not reproducible until age 4–5
years.
Review
preschool children
• Heart rate: 110–160 beats/min (>160 tachycardia)

• Systolic blood pressure: 80–100 mmHg (depends on
age and height) Fig. 12.39 Three boys’ legs – which legs are normal? These three
brothers all have normal legs. The youngest has mild genu varus
• Respiratory rate: 25–30 breaths/min (>30 (bow legs), which is physiological in the toddler. The middle brother
tachypnoea) has genu valgus (knock knees), which is physiological in the
preschool-aged child. The eldest brother has ‘straight’ legs.
413
Chapter
specific motor and coordination tasks are all possible, as the midparental centile. Accelerations in height velocity
long as the child perceives your examination as fun. may be attributed to an excessive weight gain (not
uncommon) or more importantly (and rarely) to endocrine
causes (e.g. precocious puberty). Decelerations may be
Review
due to inadequately managed or unrecognised chronic
Examination of preschool children illness (e.g. asthma or coeliac disease) or endocrine
• The preschool child is usually very healthy problems (Figs 12.40, 12.41).
• Thoughtful examination is needed, assessing the
most relevant system first DEVELOPMENT
• The examination should be fun for both patient and
These children are spending the majority of the day away
doctor
from home, at school. They will become more independent
from their parents and carers but more dependent on
their peer group. Social and behavioural aspects of
The school-aged child development are now more important. Language and
cognitive skills, literacy and numeracy are further
The school-age group, 5–10+ years of age (until the onset developed in class and at home. Vision, hearing and
of puberty), are seen less often by their doctors. It is also motor skills are approaching adult abilities.
the age at which psychological factors are beginning to
play a bigger role in how and what the child may complain HISTORY
of to their parents and doctors.
It is a good idea to invite the child to be the historian and
rely on the parent for back-up. Some will want their
GROWTH parents to give all the history, whereas others may be
The growth in this age group is steady but slowly very capable historians. This will depend on the child’s
decelerating. The height will usually be following near character, previous (good or bad) experience of a doctor
6'9"
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
205 205 Mid parental height (MPH)
6'6" 200 200
195 195
6'3" 190 GIRLS 0-20yrs Height 190 Father (F) = 175 cm
6'0" 185 185 Mother (M) = 170 cm
180 99.6th
180
5'9" 175 98th
91st
175 F+ M
170 170 MPH = – 7 cm =
5'6" 75th
2
165 50th 165
5'3" 160 25th
160 345
9th – 7 cm = 165.5 cm
5'0" 155 2nd
155 2
150 0.4th
150
4'9" 145
110 Target height is on 50th
4'6" 140 X
135 105 centile ± 10 cm
4'3" 130 100
125 95 Note: subtract 7 cm for
4'0" 120 99.6th 90
Start 85 estimate of girls' height
3'9" 115
110 thyroxine 98th 80
3'6" 105 75
3'3" 100 91st
70
95 75th 65
3'0" 90 60
50th
2'9" 85 25th 55
80 9th 50
2'6" 75 2nd
45
0.4th
2'3" 70 40
65 35
2'0" 60 30
1'9" 55 25
50 20
1'6" 45 15
10 Breast 4+ 10
3+
5 stage 2+
5
0 0
Pubic hair 4+
3+
stage 2+
Age, Years Menarche
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Fig. 12.40 Growth failure: juvenile hypothyroidism. These growth charts demonstrate an 11-year-old girl diagnosed with hypothyroidism.
Note how her height velocity has decelerated with a retarded bone age. After starting thyroxine she loses weight, her height catches up and
her puberty progresses rapidly (see Figs 12.43 and 12.44). (© Child Growth Foundation, adapted with permission.)
414
Chapter
The school-aged child 12
6'9"
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
6'6" 200 200
195 99.6th
195 Father (F) = 172 cm
190
185
91st
185 Mother (M) = 169 cm
6'0" 75th
180 50th
180
5'9" 175 25th 175 F+ M
170 170 MPH = + 7 cm =
5'6" 9th
2
165 2nd
165
5'3" 160 160 341
0.4th + 7 cm = 177.5 cm
155 155 2
5'0"
150 150
4'9" 145 Target height is on 50th
140 110
4'6" 105 centile ± 10 cm
135 99.6th
4'3" 130 100
125 95 Note: add 7 cm for
4'0" 120
98th
90
X estimate of boys' height
3'9" 115 91st 85
110 80
3'6" 105 75th 75
3'3" 100 50th 70
95 X 25th 65
3'0" 90 9th 60
2'9" 85 2nd 55
80 STARTS 0.4th 50
2'6" 75 GROWTH 45
2'3" 70 HORMONE 40
65 35
2'0" 60 30
1'9" 55 25
50 20
1'6" 45 15
4+
10 Penis
stage 3+ 10
2+
0 Pubic hair 4+
3+
0
stage 2+
Age, Years Testes

volume
12ml
4ml
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Fig. 12.41 Growth failure: early idiopathic growth hormone deficiency. This boy’s infant growth appears reasonably normal, although
perhaps less than his midparental height may suggest. His height velocity decelerates drastically by the age of 5 years and the diagnosis
is made. Growth hormone supplementation through the rest of childhood and adolescence provides catch-up growth and a reasonable
final adult height. His puberty is a little later than average (see Fig. 12.44 for pubertal stages). (© Child Growth Foundation, adapted with
permission.)
and how ill they are. Children with chronic diseases are Review
often poor at the long-term history but more reliable with
the acute story. It is important to pitch the questions in school-age children
terms the child understands and which are not patronising
(e.g. using the family’s terms for faeces, penis, bottom • Heart rate: 80–120 beats/min (>120 tachycardia)
and so on). • Systolic blood pressure: 90–110 mmHg (depends on
Background information about the home and especially age and height)
school is important. Establish how much the presenting • Respiratory rate: 20–25 breaths/min (>25
complaint affects the child’s life at school and at home. tachypnoea)
If only school time is affected then the problem may not
be an organic one. Hobbies, sports and pastimes give
other clues to the seriousness of the illness and its impact
on the child’s life.
Review
Examination of school-age children
EXAMINATION • School-age children are usually very healthy and do
The sequence of the examination is now more or less not see their doctors much
dictated by you. There are very few differences in • Examination is in a manner similar to adults, as long
technique from examining adults, except that the as everything is explained adequately
examination should continue to be fun. Peak flow can • Psychological factors are becoming increasingly
be used as a reproducible way of monitoring asthma relevant
(Fig. 12.42).
415
Chapter
Peak expiratory flow rate: normal paediatric values

Male and female height velocity
height height predicted EU
(m) (ft) 24
PEFR (l /min) 23
22
0.85 2'9" 87 21
0.90 2'11" 95 20
19
0.95 3'1" 104 18
1.00 3'3" 115 17
Height gain (cm/year)

16
1.05 3'5" 127 15
1.10 3'7" 141 14
13
1.15 3'9" 157 12
1.20 3'11" 174 11
1.25 4'1" 192 10 males
9
1.30 4'3" 212 8
1.35 4'5" 233 7
6 females
1.40 4'7" 254 5
1.45 4'9" 276 4
3
1.50 4'11" 299 2
1.55 5'1" 323 1
1.60 5'3" 346
1.65 5'5" 370 1 3 5 7 9 11 13 15 17 19
1.70 5'7" 393 Age (years)
Fig. 12.42 Normal peak expiratory flow (PEF) values in children Fig. 12.43 Height velocity in girls and boys. Note how before the
pubertal growth spurt there is little difference in girls’ and boys’
correlate best with height; with increasing age, larger differences
height velocities. Also note that girls’ pubertal height velocity peaks
occur between the sexes. These predicted values are based on the
are earlier and less tall than those for boys. These are thought to be
formulae given in: Cotes J. E. 1979 Lung function, 4th edn. Blackwell
the main factors determining the difference in adult male and female
Scientific, London. Adapted for EU scale Mini-Wright peak flow
height.
meters by C. Clarke.
• Deliberate self-harm (overdoses especially) in

Adolescents adolescents is becoming more prevalent. Understanding
the reasons for this behaviour can be challenging.
The adolescent group of patients is not usually very well • Confidentiality and consent are sometimes a source of
served by the medical profession, particularly in the latter conflict between patient, parent and doctor.
half of adolescence.
Paediatricians and general practitioners usually feel The adolescent’s doctor needs to be aware of, and
confident with the initial part of adolescence but this open-minded about, the nature and cause of the
wanes towards the middle and end of adolescence. There complaint and sensitive to the patient’s need to be seen
are many reasons for this: with (or without) a parent. Adolescents are usually able
to give informed consent for examination and treatment
• Adolescents seldom consult their doctor, so neither is if the reasons are explained to them in a way they can
very familiar with each other. understand. They are still their parent’s (or carer’s) legal
• Adolescents are in the transition from childhood to responsibility and problems can arise when there is a
adulthood and are uncertain as to how to behave as disagreement. It is good practice to communicate
adults, but do not want to behave as children. effectively with both the adolescent and parents.
• Doctors need to allow them to be adolescent and
accept that the adolescent is easily embarrassed and
often anxious. GROWTH
• The presenting problems can have a psychological During the first 10 years there is remarkably little
basis. difference between the height and weight velocity in the
• Adolescents with a chronic illness (e.g. diabetes, cystic growth of girls and boys. Both have a slowly decelerating
fibrosis, sickle cell disease) will demonstrate normal growth until puberty, then there is a growth spurt that
adolescent rebellion, which can have serious long- lasts for 2–3 years. This will complete the child’s physical
term health consequences. transformation into a young adult (Figs 12.43, 12.44 and
• Risk-taking behaviour (cigarettes, alcohol, drugs, sex, see Figs 8.1, 8.3 and 9.4).
etc.) is normal and when it does go wrong, in health The adolescent phase of growth is initiated by sex
terms, it is hard not to appear judgemental and steroids that are produced by the gonads, stimulated by
authoritative as the doctor. gonadotrophins from the anterior pituitary. Along with
416
Chapter
Adolescents 12
the dramatic increase in size and growth, these sex

Pubertal development steroids will promote the development of secondary
sexual characteristics and fertility.
Female Male PUBERTY

height growth spurt height growth spurt
The onset of puberty is less than 1 year apart in girls
12 14
(mean age 11.4 years) and boys (mean age 12.0 years)
but the pubertal growth spurt occurs in girls approximately
age at menarche penis size 2 years before boys. The first physical sign of puberty in
13 13.5 a girl is the development of breast tissue under the nipples
(mean age 11 years); the first physical sign in boys is the
breast stage testicular volume enlargement of the testes from their prepubertal volume
V
IV
12cc of less than 2 ml to an endocrinologically active volume
II
III
4cc of greater than 4 ml (mean age 12 years). However, a
pubic hair stage pubic hair stage boy’s growth spurt does not occur until the testicular
IV
IV volume is approximately 10 ml.
III
II
III
II A delay in growth and puberty can be a source of great
unhappiness for the adolescent who is endocrinologically
8 10 12 14 16 18 20 8 10 12 14 16 18 20 normal but, because of an inherited tendency, develops
Age (years) Age (years) and matures more slowly than peers (Fig. 12.45).
A constitutional delay in growth and puberty is more
Fig. 12.44 Pubertal staging in males and females. These standard of a problem for boys than girls because boys have their
puberty stagings are important to note whenever you plot children’s pubertal growth spurt 2 years later than girls and because
growth in the second decade (see Figs 8.1, 8.3 and 9.4).
boys’ growth spurts are larger than girls’, so its absence
is more apparent.
6'9"
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
6'6" 200 200
195 99.6th
195
190 Father (F) = 170 cm
6'0" 185
91st
75th
185 Mother (M) = 165 cm
180 50th
180
5'9" 175 25th 175 F+ M
5'6" 170 9th 170 MPH = + 7 cm =
165 165 2
2nd
5'3" 160 160 335
X
0.4th
+ 7 cm = 174.5 cm
5'0" 155 155 2
150 150
4'9" 145 X
140 110 Target height is between
4'6" 105 25th and 50th centile ±
135 99.6th
4'3" 130 100 10 cm
125 95
4'0" 120
98th
90
3'9" 115 85 Note: add 7 cm for
91st
110 80 estmate of boys' height

3'6" X
105 75th 75
3'3" 100 50th 70
95 25th 65
3'0" 90 9th 60
2'9" 85 2nd 55
80 0.4th 50
2'6" 75 45
2'3" 70 40
65 35
2'0" 60 30
1'9" 55 25
50 20
1'6" 45 15
4+
10 Penis
stage 3+ 10
2+
0 Pubic hair 4+
3+
0
stage 2+
Age, Years Testes

volume
12ml
4ml
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Fig. 12.45 Constitutional delay in growth and puberty. Note how final adult height is near the tenth centile as predicted by the growth
velocity observed between age 4 and 10 years. He was most psychologically stressed in his 16th year (see Figs 12.43 and 12.44). (© Child
Growth Foundation, adapted with permission.)
417
Chapter
important to direct your questions primarily to the patient,
and only when necessary to the parent or carer.
Constitutional delay in growth and puberty
Details about the family and relationships between
• This condition is most common in boys members of the household are important. Details about
• Patients usually have a history of growing in the school, progress with school work, hobbies, sports,
lower quartile of the normal range but by the middle pastimes and friendships can all help give an indication
teenage years are very much shorter than their peers of how the adolescent is coping with the increasing
(at this time they present to a specialist clinic) stresses of the real world. Again, it is easier to take a quick
• Severe psychological stress may result from this trip through this part of the history at the beginning
genetic and physiological delay in puberty because, if problems of psychosocial issues arise later, it
• Pharmacologically inducing puberty is an effective can seem awkward to ‘go back’ and ask the straightforward
way of relieving the stress suffered by these patients questions.
EXAMINATION
Over the next 2 years in girls, and 3 years in boys, there Most adolescents are very self-conscious of their
are changes in body shape and composition (lean mass appearance, so make sure they have suitable facilities to
and distribution of body fat) along with growth of pubic prevent undue embarrassment (e.g. blankets and screens
hair (and facial and body hair in boys). around the examination couch). The examining doctor
In girls, when the growth spurt (height velocity) will need to decide during the history-taking whether the
decelerates to less than 4 cm per year, the menarche can parent is to be invited alongside the patient. Which side
occur; height continues to increase for 1.5–2 years after of the screens should the parent stay? This can be difficult
the menarche. Final adult height is achieved when the to get right every time. When an adolescent is seen alone
bony epiphyses fuse in the vertebrae and along the long during the physical examination, it is advisable to include
bones of the leg. It is impossible to evaluate an adolescent’s a chaperone in the examination room.
growth without knowledge of what stage of pubertal Apart from the assessment of growth and puberty and
development they have reached. attention to the adolescent and parent relationship, the
rest of the examination will be similar to that for an adult
DEVELOPMENT patient.
Development continues long after growth has finished.

It is mostly in the spheres of social and behavioural Review
development that adolescents are still progressing. This Normal cardiovascular and respiratory ranges for
age group is requesting and gaining more independence adolescents
from their parents and carers. They have completed their
• Heart rate: 60–100 beats/min (>160 tachycardia)
primary education and will be completing their secondary
• Systolic blood pressure: 100–120 mmHg (depends on
education by the end of this phase. Interests will change
age and height)
and relationships with peers are crucial to the adolescent’s
• Respiratory rate: 15–20 breaths/min (>25
self-image.
tachypnoea)
The gap between the end of growth and the end of
development into a fully independent adult is apparently
widening. The mean age for pubertal milestones appears
to have come down from that of a century ago. In the Review
developed world, there is a decreased need for unskilled Examination of adolescents
workers and an increased need for skills and higher
education to be a successful provider. Thus the end of • Adolescents are usually very healthy and do not see
‘development’ is often only complete after the age of their doctors much
20 years. • They are generally not well served by their doctors
• Psychological factors are important
• Risk-taking is normal but hazardous (sex, drugs and
HISTORY so on)
Depending on the presenting problem, it may be • Deliberate self-harm is increasingly common and
necessary to agree who remains in the consulting room. must be properly assessed by a trained counsellor on
This is one area in which confidentiality and consent may a case by case basis
become a point of conflict. When taking the history, it is
418
Chapter
Adolescents 12

Presentations, symptoms and signs in paediatric medicine
There are so many presentations, symptoms and signs to • At 6–8 months (corrected) old, act if any of the
take a special note of in paediatric medicine. The following is present/absent:
contents of this chapter and this list are no substitute for • obvious hand preference
a standard text in clinical paediatrics and the clinical • fisting of hands
experience gained in the clinic, emergency department • squint (strabismus).
or on the wards. The following are some that are • Persistence of primitive reflexes. Requires expert
considered to be important. developmental examination.
History • At 12 months (corrected) old, expert developmental
• When the parents express grave concern about the examination is required if any of the following is
rapidity of their child’s illness. This is a finding in present/absent:
children with evolving bacterial septicaemia • unable to sit or bear weight
• Any child with any injury where the history is not • persistence of hand regard
consistent with the examination findings. This could • absence of babbling and cooing
be a child protection problem; refer to senior • absence of saving reactions.
colleagues. • At 18 months (corrected) age, expert developmental
• Jaundice in babies under 48 hours old. This is a examination is required if any of the following is
haemolytic neonatal jaundice until proven otherwise. present/absent:
• Persisting jaundice in neonates who have pale stools • inability to stand without support
and dark urine. This is caused by biliary/liver disease • inability to understand simple commands
until proven otherwise. • no spontaneous vocalisation
• Vomiting that is bile stained. This is a surgical cause • no pincer grip
(obstruction/intussusception/ appendicitis) until proven • casting (throwing) still present.
otherwise. Examination
• Passage of blood per rectum. Cause may be surgical • Young children who appear ‘too good/quiet’ (e.g. not
or infective, but can also be due to local causes. crying/complaining) may be more ill than at first
• Persisting and ongoing fever for more than 5 days. appears, as may children who are ‘inconsolable’ (i.e.
Diagnosis of Kawasaki’s disease needs to be too irritable) to their parent’s attempts at soothing
considered. them. The seriously ill child can easily be overlooked
Growth because of their lack of interaction.
• Children whose plotted height, weight or head • Nonblanching (purpuric) spots in a child with fever.
circumference are crossing centiles in a dramatic way Meningococcal bacteraemia can be easily overlooked
(deviation may be upwards but more often in the early stages of the illness.
downwards). Deviation in previous growth patterns • Bulging fontanelle. May suggest raised intracranial
require evaluation of accurate longitudinal data. pressure (ICP) or even meningitis.
• Development of secondary sexual characteristics • Abnormal posture (e.g. opisthotonus, or tripod
before age 8 years in girls and age 10 years in boys. stance). Children will always adopt positions of
Suggests precocious puberty. comfort; if they appear not to, ask yourself why, what
is the discomfort due to?
Development
• Children whose heart rate and/or respiratory rate is
• Any history suggestive of regression (i.e. loss of
sustained and above the normal range for age (out of
previously acquired skills). Indicates possible
proportion to their fever). Refer to age-specific normal
neurodegenerative condition.
ranges. Persistent tachycardia suggests bacteraemia
• At 8 weeks (corrected) old, act if any of the following
and tachypnoea suggests lower respiratory tract
is present/absent:
infection (LRTI).
• failure to fix and follow a visual stimulus
• Any child with central cyanosis (look at the tongue)
• failure to startle to sound
and any child with oxygen saturation <92% in air.
• failure to smile responsively.
Always look at central mucous membrane colour
• Any obvious asymmetry of neonatal reflexes or
(remove the pacifier), use pulse oximeter if available.
persistence of head lag. Requires expert
developmental examination.
419
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Index
Note: Page numbers in bold refer to figures.
A perinephric, 21
peritonsillar, 102, 104
Adrenocorticotrophic hormone (ACTH), 35,
36, 38
Abdomen, 186–225 Abstract thinking, 311 failure, 40, 41
auscultation, 219–20 Acanthosis nigricans, 80 Aerophagy, 199
contours, 205–6, 206 Accessory auricles, 87, 87 Afferent pathways, 307
disorders symptoms, 193–203 Accessory (eleventh) nerve, 356, 356–7, Afterload, heart, 143
distension, 126, 205–6 357, 411 Agnosia, 313
examination, 56, 204, 204–20 Accessory muscles of respiration, 127, 135, Agraphia, 316
cardiovascular disease, 173–4 400 AIDS (acquired immunodeficiency
gynaecological disorders, 242–3 Achalasia of the cardia, 194 syndrome), 120
infants, 411 Achilles tendon, 300–1 Kaposi’s sarcoma, 78
newborns, 400–2 jerk, 32, 33 skin lesions, 60
preschool children, 413 rupture, 301 Air bronchogram, 133, 134
inspection, 205–7, 206 Acid-base balance, 112 Air conduction, 91, 92
pain, 196–9, 197, 198 Acidophil tumours, 39 Airflow limitation, chronic, 135, 136
systems review, 8 Acidosis, 126 see also Asthma; Bronchitis; Emphysema
palpation, 207–9, 208, 209 Acne rosacea, 96 Airways obstruction, 114–15
percussion, 217–18 Acne vulgaris, 64, 64 Albinism, 23, 25, 25, 61
quadrants, 204, 205 Acoustic (eighth) nerve, 353, 353–4, 411 Albumin, 47
responses, 367, 367 Acoustic neuroma, 85 Alcohol consumption
segments, 204–5, 205 Acquired immunodeficiency syndrome see history, 6
structure and function, 186–93, 186–93 AIDS (acquired immunodeficiency pseudo-Cushing’s syndrome, 36
Abdominal aorta, 208 syndrome) Aldosterone, 35–6
aneurysm, 174, 174, 209, 217 Acrocyanosis, 398 Alexia, 316
branches of, 217 Acromegaly, 21, 39, 39, 40, 40 Alkalosis, 112
palpation, 209, 209, 217, 217, 218 ACTH see Adrenocorticotrophic hormone Allergic contact dermatitis, 68
Abdominal paradox, 126 (ACTH) Allergic rhinitis, 98
Abdominal wall, bony landmarks, 204, 204 Acute coronary syndrome, 154–5, 177–8 Alopecia, 60, 60, 80
Abducens (sixth) nerve, 332–45, 411 Adam’s apple, 100 Alveolar macrophage, 106
palsy, 338, 339, 343, 344 Addison’s disease, 37, 37–8 Alzheimer’s disease, 314
Abduction, 271, 272 pigmentation in, 46 history taking, 10
elbow, 282 skin colour, 61 Ambulatory ECG, 145
hand, 286, 287, 288–9 Adduction, 271, 272 Amenorrhoea, 39, 195, 226, 238
hip, 290–1, 293, 295, 295 hand, 286, 287, 288–9 secondary, 239–40
shoulder, 279, 280 hip, 290–1, 292, 292, 295, 295, 401 Amino acids, 189
Abductor digiti minimi, 286, 289, 289 shoulder, 279, 280 Amnesia, 315
Abductor pollicis brevis, 286, 289, 289 Adductor majoris, 291 Amphiarthroses, 266–7
Abductor pollicis longus, 284 Adductor pollicis, 286, 289, 289 Ampicillin, skin reactions to, 64, 65
Aberrant reinnervation, 352 Adenohypophysis, 38 Ampulla of Vater, 189
Abnormal thoughts and perceptions, 318 Adenoids, 51, 51, 99 Amylase, 187
Abscess ADH see Antidiuretic hormone (ADH) Amyotrophy, neuralgic, 281, 282
Bartholin’s, 244, 245 Adnexae of uterus, 237, 237–8 Anaemia, 113
breast, 234, 235 palpation, 249–50, 250 menstrual disorders, 242
cerebral, 89 see also Ovaries pallor, 45
dental, 96 Adolescents, 416–18 Anagen hair growth, 58
fever, 50 Adrenal glands, 35–8 Anarthria, 315
lung, 116, 131 position of, 27 Anasarca, 47, 49, 175, 263
421
Index
Anconeus, 282, 283 Arcus senilis, 26, 26 Automaticity, 145–6

Androgens, 35–6 Areola, 230 Axilla
Aneroid manometers, 161 abnormal, 234–5 hair, failure to develop, 60
Aneurysm, abdominal aorta, 174, 174 hyperpigmentation, 37, 37 temperature, 50
Anger, 10 Argyll Robertson pupil, 341, 341 Axillary lymph nodes
Angina, 154, 154–5, 176, 176, 177 Argyria, 46 breast lymphatic drainage, 230, 230
mesenteric, 199 Arms, GALS, 272 examination, 54, 124, 124
Angio-oedema, 65 see also Upper limb hand and arm lymphatic drainage, 52, 53
Angiotensins, 36 Arrectores pilorum muscles, 58 palpation, 234, 234, 235
Angle of His, 187, 188 Arrhythmias, 145–8, 156 Axillary nerve damage, 281
Angular stomatitis, 42 Arteries, 151–2, 152
Anhedonia, 317
Anisocoria, 337
insufficiency, 178
obstruction, 178
B
Ankle, 299–303, 300, 301, 302 Arterioles, 152 B lymphocytes, 51, 105–6, 106–8
clonus, 367, 367 Artificial heart valve sounds, 170, 170 Babies
reflexes, 32, 33, 366–7, 367 Arytenoid cartilages, 100, 100 baby check, 399
swelling, 7, 47, 117 Asbestosis, 119–20 gestation and weight at gestation, 403
Ankylosing spondylitis, 277, 278 Ascites, 47, 49, 127, 174, 201, 206 growth, 393
Annulus fibrosus, 274 percussion, 218, 219, 242, 242 older, 407–12
Anomic aphasia, 316 Aspergillosis, 116 see also Infants; Newborns
Anorexia, 195 Aspiration into the lungs, 115 Back pain, 276
Anorexia nervosa, 239 Aspirin overdose, 126 Background information, 5–6
Anosmia, 94 Astereognosis, 381 Bacterial conjunctivitis, 23
Anotia, 84, 87 Asterixis, 370 Bacterial endocarditis, 79
Anterior horn cell, 360–1 Asthma, 105, 114, 115 Bacterial infections
Anterior pituitary, 38 blood pressure in, 123 skin, 71–2
Anterior superior iliac spine, 204, 221 chest auscultation, 130 travel-related, 6
Antibiotics, skin reactions to, 64 family history, 120 Bagassosis, 120
Anticipation, 391 lung volumes in, 111 Baker’s cyst, 180, 298, 298
Antidiuretic hormone (ADH), 38–9, 193 occupational, 120 Balanitis, 256, 256, 258
failure, 41 signs of, 126 Balanoposthitis, 258
impaired secretion, 40 sputum production, 116 Balding, 60, 60
Antireflux mechanisms, 187, 188, 194 wheezing, 132 Balloting
Anton’s syndrome, 332 Ataxia, 20 kidney, 216, 216
Anuria, 203 cerebellar, 373 patella, 296
Anus gait, 305, 305–6 Barlow’s manoeuvre, 401, 401
examination, 221–3, 223, 224 respiration, 385, 386 Baroreceptors, 354
imperforate, 405 Atheroma, 149 Barrel chest, 125, 125
pain, 199–200 Athetosis, 369, 369 Bartholin’s abscess, 244, 245
reflex, 368 Athlete’s foot, 74 Bartholin’s glands, 236, 243, 244
sphincters, 221, 222 Atlanto-occipital junction, 274 Basal cell carcinoma
Anxiety, 9, 154, 318 Atlantoaxial dislocation, 278, 279 ears, 87
Aorta, abdominal, 208 Atlas, fractures, 279 skin, 77, 77
branches of, 217 Atopic eczema, 67–8 Basal ganglia, 360
palpation, 209, 209, 217, 217, 218 Atria, 141–2, 144 Basilar artery, 309
Aortic aneurysm, 174, 174, 209, 217 Atrial fibrillation, 148 Bat ears, 87
dissecting, 155 jugular venous pressure, 165 BCG vaccination, 118
ruptured, 197 Atrial natriuretic hormone (ANP), 156 Beau’s lines, 79, 79
Aortic coarctation, 159, 159 Atrial septal defect, 144, 150, 150, 172 Behçet’s syndrome, 244
Aortic valve, 142, 143 Atrioventricular node, 144 Bell’s palsy, 352, 352, 359, 412
incompetence, 172 Atrophic glossitis, 42, 42 Benign positional vertigo, 9, 86, 92–3
regurgitation, 172, 172, 173, 173 Atrophic rhinitis, 98 Beta-blockers, 146
stenosis, 142, 144, 154, 160, 160, 168, Atypical pneumonia, 133 Beta-haemolytic streptococci, 182
171 Audiometry, 91, 92 Bicarbonate, 192
Apex beat, 128, 166, 166–7, 182, 398, 398 Audit, problem-orientated medical records, Biceps brachii, 282, 283, 284, 364
infants, 409 16–17 reflexes, 365, 365
Aphasia, 312, 315, 315–16 Auditory (eighth) nerve, 83, 85 tendonitis, 280
Aphthous ulcers, 101 Auditory hallucinations, 318 Biceps femoris, 292
Apneustic breathing, 385, 386 Auditory ossicles, 82, 83 Bilateral occipital infarction, 332
Apocrine glands, 58 Auricular lymph nodes, 52, 52 Bile, 189, 191
Appearance, doctors, 2–3 Auroscope, 86–7, 87, 96 Bile ducts, 191
Appendicitis pain, 197, 199 Auscultation Biliary colic, 197
Appendix testis, 255 abdomen, 219–20 Biliary diseases, 196
Appetite, loss of, 195 chest, 130, 130, 130–3 Biliary obstruction, 201, 202, 214, 214
Apraxia, 313, 316, 317 heart, 167, 167–73, 398, 399 Bilirubin, 46, 191, 191
constructional, 315 liver, 220 Bimanual palpation
gait, 306 spleen, 220 female genital tract, 235, 249, 249
Archicerebellum, 371–2 thyroid gland, 29, 30 kidneys, 216, 217
Arcuate fasciculus, 310 Austin Flint murmur, 172–3 Biomedical perspective questions, 4
422
Index
Birds, allergy to, 119 inspection, 231, 231–2, 232 Caloric test, 92
Bivalve speculum, 245 lumps, 231, 232, 234 Cancellous bone, 265
Biventricular heart failure, 176, 176 lymphatic drainage, 229–30 Cancer, skin manifestations of, 80
Blackheads, 64 muscles underlying, 229 see also specific cancer
Blackouts, 156–7 pain, 230–1 Candida albicans, 74, 241, 241
Bladder palpation, 232–3, 233 Candidiasis, 59, 74
control, altered, 8 segmental anatomy, 229 oral, 102
cystocele, 244 structure and function, 229, 229–30, 230 scrotal, 260, 261
disease, 202–3 symptoms of disease, 230–1 vaginal, 244, 245
pain, 203 Breasts, neonatal development, 406 Capillary pulmonary hypertension, 181
percussion in distended, 218, 219 Breath sounds, 130, 131, 133 Capillary refill time, 44
prolapsing, 238, 238 Breathing, 108 infants, 409
Blepharospasm, 353 bronchial, 130–1, 131, 132 Carbohydrate digestion, 187, 189
Blind spots, 324, 328 infants, 409–11 Carbon dioxide, 108, 109
Blistering lesions, 75–6 newborns, 400 dissociation curve, 112, 112
Blocked nose, 95 patterns, 126–7 retention, 122–3, 127
Blood preschool children, 413 Carbuncle, 72
in the mouth, 100 Breathlessness see Dyspnoea Cardiac enzymes, 177
in stools, 200 Broad ligament, 238 Cardiac syncope, 156
Blood gases, 109, 111–12 Broca’s aphasia, 315 Cardiac tamponade, 183–4, 184
Blood pressure Broca’s area, 308, 310 Cardinal ligaments, 238
assessment for dehydration, 44 Brodmann’s cortical areas, 307, 307 Cardiogenic shock, 45
assessment for shock, 44–5 Bronchi, 108 Cardiomyopathy, 182, 182
infants, 409 Bronchial breathing, 130–1, 131, 132 dilated, 169, 182
measuring, 161–4, 162 Bronchial carcinoma, 117, 124 hypertrophic, 160, 160, 182, 182
in respiratory disease, 123 clubbing, 121 restrictive, 182
see also Hypertension; Hypotension lung collapse, 135 Cardiovascular system, 139–85
Blue bloaters, 45, 127, 127 Bronchial secretions, 106 and abdominal examination, 173–4
Blue spots, 405 see also Sputum and chest examination, 173
Body attitude, 20 Bronchial tree, 108 clinical history, 152–7
Body language, 3, 20–1 Bronchiectasis examination, 56, 157–64
Body lice, 75 crackles, 132 infants, 409
Body mass index (BMI), 41 haemoptysis, 117 newborns, 398–400
Body temperature see Temperature, body lung collapse, 136 preschool children, 413
Boil see Furuncle sputum production, 116 review, 7
Bone Bronchioloalveolar cell carcinoma, 116 structure and function, 139, 139–44
disease symptoms, 267 Bronchitis, 110 in the unconscious patient, 383
examination, 269 lung volumes in, 111 see also Arteries; Heart; Veins
pain, 267 sputum production, 116 Carey Coombs murmur, 183
structure and function, 265, 265–6 wheezing, 132 Carotenaemia, 46, 61
Bone conduction, 91, 92 Bronchopneumonia, 133 Carotid arteries, 308, 309
Bornholm disease, 117 Bronchospasm, 132 Carotid pulse, 160, 160, 164, 168, 168
Bouchard’s nodes, 287 Brown-Séquard lesion, 380, 381 Carpal tunnel syndrome, 285, 290, 290
Boutonnière deformity, 269–70, 270 Bruises, 62, 410 Carpometacarpal joint, 287
Bow legs see Genu varum Bruits Carpopedal spasm, 35
Bowel habit change, 8, 199–201, 200 femoral artery, 178 Carrying angle, 282, 282
Bowel paralysis, 219 listening for, 219–20, 220 Cartilage, 265–6
Bowel sounds, 219 renal artery, 174 Catagen hair growth, 58
Boyle’s law, 110 thyroid gland, 29 Cauliflower ears, 87
Brachial lymph nodes, 52 Buccal mucosa, 101–2 Causalgia, 377
Brachial plexus, 290, 291, 375 Buccinator, 350 Cavernous haemangioma, 405
Brachial pulse, 159, 159 Budd–Chiari syndrome, 213 Cavernous sinuses, 335, 337, 344
Brachialis, 282, 283 Buffalo hump, 37 Cellular naevus, 77
Brachioradialis, 282, 283, 284 Bulbar palsy, 315 Cellulitis, 72, 72
Bradycardia, 145, 146, 146 Bulge sign, 297 Central cyanosis, 46
Bradykinesia, 368 Bullous pemphigoid, 75, 75, 76 cardiovascular disease, 158
Bragard’s test, 275–6, 277 Bundle of His, 146 infants, 409
Brain death, 387–9, 388 Burst neurons, 335 respiratory disease, 122, 123
Brainstem Butterfly rash, 80 right to left shunts, 151, 151
disorders, 381, 382, 382 Central neurogenic hyperventilation, 385,
reflexes, 387, 388
Breakthrough bleeding, 240
C 386, 386, 387
Central venous pressure, 47
Breastfeeding history, 398 Café-au-lait patches, 62, 62, 76 Central vertigo, 86
Breasts, female, 226–51 Calcium content of bone, 265 Cephalohaematomas, 402
abscess, 234, 235 Calculation, intelligence, 311 Cerebellar arteries, 309, 372
cancer, 233, 234 Calculi, renal, 34 Cerebellum, 371–4
development, 226, 227 Calf muscles, 299, 300 ataxia, 373
discharge, 231, 234 pseudohypertrophy, 304, 304, 363 disease, 306
examination, 56, 231–5, 232 Calgary-Cambridge consultation model, 1 lesions, 315, 374, 374, 375
423
Index
Cerebral abscess, 89 Chondrodermatitis nodularis helicis, 87 Congestive heart failure, 176, 176
Cerebral arteries, 308, 309, 310 Chondroitin sulphate, 57 ankle swelling, 47
Cerebral cortex see Cortex Chondromata, ears, 87–8 jugular venous pulse, 165–6
Cerebral haemorrhage, 372 Chorda tympani, 82 Conjugate eye movements, 337–8
Cerebral hypoperfusion, 45 Chordae tendineae, 142, 142 Conjunctival oedema, 31
Cerebral infarction, 372, 374 Chordee, 406 Conjunctival pallor, 45, 45
Cerebrospinal fluid (CSF), 84, 308 Chorea, 368–9, 371 Conjunctivitis, 23, 256, 256
Cervical rib syndrome, 290 Chronic obstructive pulmonary disease Conn’s syndrome, 36
Cervical spine, 274–5, 275, 278 (COPD), 109, 133 Consciousness, loss of, 8
lymph nodes, 52, 52, 54, 54, 100, 123 Chronic pulmonary thromboembolic disease, see also Syncope; Unconscious patient
nerve roots, 283, 284, 286 181 Consolidation, 131, 133, 134
radiculopathy, 281, 281 Chvostek’s sign, 34, 35 Constipation, 8, 199–200, 222
Cervicitis, 241 Chylomicrons, 189 Constrictive pericarditis, 123, 165, 184,
Cervicothoracic junction fractures, 279 Cigarette smoking see Tobacco smoking 184–5
Cervix, uterine, 222, 224, 236, 237 Cilia syndromes, 106 Constructional ability, 311, 312
abnormalities, 247–8, 249 Ciliary flush, 23 Constructional apraxia, 315
cancer, 247 Circadian rhythm, adrenal cortex hormones, Consultation, 1–3, 2, 10–19
ectopy, 247 35 Contact dermatitis, 68, 68
erosions, 247 Circle of Willis, 308 Contact lens abrasion, 23
examination, 246–8, 247, 248, 248–9 Cirrhosis, 201, 201, 213 Contours, abdominal, 205–6
smear, 247–8, 248 Clarke’s column, 375 Contraceptive pill, 239
Chadwick’s sign, 247 Clasp-knife effect, 362 Conversion hysteria, 320
Chancre, 72, 72, 73 Claudication, 157 Cooper’s ligaments, 229, 230
Chancroid, 244 Clavicles, percussion, 129, 129 Coordination, loss of, 9
Charcot joint, 380, 380 Cleft palate, 404 Cor pulmonale, 117, 123, 127
Charcot’s triad, 374 Climateric, 228–9 Coracohumeral ligament, 266
Cheilosis, 186 Clitoris, 236 Cornea
Chemosis, 31 Clonus, 366, 367, 367 abrasion, 23
Chest Cloquet’s gland, 220 disease, 23
auscultation, 130, 130–3 Closed questions, 3, 4 reflex, 347, 347, 349, 388
examination, 125, 125–33, 126, 173 Clubbing, 80, 80, 121, 121–2, 133, 151, Corns, 301
expansion, 128–9, 129 151, 158 Coronary arteries, 148–9, 149
palpation, 127–8 Coarctation of the aorta, 159, 159 disease, 176, 176–8, 177
percussion, 129, 129–30 Cochlea, 82–3, 85, 353, 353 stenosis, 154
Chest pain Coeliac disease, 76 Corpora cavernosa, 254, 254
cardiovascular system, 154, 154–5 Cognition, 318 Corpus albicans, 238
musculoskeletal, 155 see also Mental state Corpus luteum, 228, 228, 238
red flags, 155 Cogwheel effect, 362, 363 Corpus spongiosum, 254, 254
symptoms, 4 Colic, 198 Cortex, 307–17, 376
systems review, 7 biliary, 197 areas, 307
see also Chest wall, pain; Pleuritic chest pain renal, 197, 203 clinical application, 314–17
Chest wall Collagen, 57, 265 disorder symptoms, 308–9
inspection, 125, 125–6 Collapsing pulse, 151, 159, 172 examination, 310–14
pain, 117 Collateral ligaments, 295, 297, 297 lesions, 381
symptoms, 4 Collateral veins, 201, 201, 207 structure and function, 307–8
systems review, 7 Collecting ducts, 193 Corticospinal neurons, 359
palpation, 128 Colles’ fracture, 284, 285 Corticosteroids, 35
paradox, 126 Colon, 188, 190 Corticotrophin releasing hormone (CRH), 35,
Cheyne-Stokes respiration, 126, 385, 386, abdominal palpitation, 208 36
386, 387 Colour of patient, 45, 45–6, 174 Cortisol, 35, 36
Chiari malformation, 355 see also Cyanosis Coryza, 409
Chiasmatic lesions, 331, 332 Colour vision, 324, 325 Costal margin, 204, 211
Chicken pox, 74 Columella, 93 Costochondritis, 155
Chief cells, 187 Coma see Unconscious patient Cough, 7, 115
Child-Pugh classification of liver disease, 213 Comedones, 64 Cough reflex, 106
Children, 390–419 Communicating arteries, 309 Cough syncope, 156
abuse, 392, 410 Communication skills, 1, 3 Courvoisier’s law, 214, 214
red flags, 419 Compensatory postures, 293 Cover testing, 338, 338
see also specific age range Compound naevus, 76 Crab louse, 75
Chills, 50 Comprehension testing, 313 Crackles, 47, 132, 173
Chlamydia trachomatis, 241, 244 Compulsions, 318 Cramps, muscle, 269
Chloasma, 61 Computerised tomography (CT), 105, 107 Cranial arteritis, 321
Cholecystitis, 197, 213 Conduction aphasia, 316 Cranial diabetes insipidus, 40
Cholecystokinin, 189, 191, 192 Conductive deafness, 85, 91 Cranial nerves, 321–59
Cholestasis, 201 Condylomata acuminata, 72, 73, 244, 245, examination, 358, 411–12
chronic, 46, 46 258 lesions in infants, 412
fat-soluble vitamin deficiency, 43 Condylomata lata see Syphilis symptoms, 9, 359
Cholesteryl embolus, 329, 329 Confidentiality, 17 see also specific nerve
Chondroblasts, 265–6 Congenital abnormalities, 87, 404, 404–6 Cremasteric reflex, 367
424
Index
Crepitus, 268 newborns, 397 illicit, history taking, 7

Cricopharyngeus, 187 preschool children, 412 photosensitive rashes, 66–7
Cricothyroid membrane, 100 school-aged children, 414 porphyria of, 60
Crocodile tears, 352 Di-iodotyrosine (DIT), 28, 28 skin reactions to, 64, 66, 67
Crohn’s disease Diabetes insipidus, 41, 193 Drusen, 329, 329
anus in, 222, 224 cranial, 40 Duodenum, 187
skin manifestations of, 80 nephrogenic, 40 Dynamic lung volumes, 110, 110
Croup, 103 Diabetes mellitus Dysarthria, 311–12, 315, 359, 372
Cruciate ligaments, 295, 297, 297 characteristics, 9–10 Dyscalculia, 315
Cryptogenic fibrosing alveolitis, 111, 137 ketoacidosis, 126 Dysdiadokokinesis, 373
Cryptorchidism, 260 and peripheral vascular disease, 178–9 Dysfunctional uterine bleeding, 240
Cullen’s sign, 207 retinopathy, 330, 330 Dysgraphia, 309, 313
Cushing’s syndrome, 36, 37 skin manifestations of, 80 Dyskinesia, 369
abdomen appearance in, 206–7 Diagnostic tests, problem-orientated medical Dyslexia, 309, 316
skin manifestations of, 80 records, 14 Dysmenorrhoea, 8, 241
Cutis anserina, 58 Diaphragm Dysmorphology, facial, 403, 404
Cutis laxa, 58 movement assessment, 130 Dysmotility syndromes, 194
Cyanosis, 46, 46, 122, 122, 123, 157–8 pain, 198 Dysosmia, 94
infants, 409 paralysis, 126 Dyspareunia, 241
newborns, 398 Diarrhoea, 190, 200 Dyspepsia, 195
Cystitis, 203 dehydration, 44 Dysphagia, 7, 9, 101, 187, 193–4
Cystocele, 244 spurious, 200 Dysphasia, 312, 315, 315–16
Diarthroses, 266 Dysphonia, 312, 315
D Diastolic murmurs, 172, 172–3, 173
Digestion, 186–9, 189
Dyspnoea
causes of, 113–14
Dandruff, 68, 75 Digestive enzymes, 187 duration of, 113, 114
De Quervain’s tenosynovitis, 270, 271, 284 Digestive organs, 186, 186–93 in heart disease, 153–4
Deafness, 85, 354 Digits see Fingers and hypoxia, 115
cranial nerve symptoms, 9 Dilatation, heart, 142 paroxysmal nocturnal, 114–15
in elderly people, 18 Dilated cardiomyopathy, 169, 182 in respiratory disease, 113–15
tests for, 90–2 Diplopia, 9, 336, 337, 338, 359 severity of, 114
Death, brain, 387–9, 388 in Graves’ disease, 31 systems review, 7
Decerebrate posturing, 385 Discharge variability of, 114
Deciduous teeth, 99 breast, 231, 234 Dysprosody, 312
Decision-making, 16–17 ear, 84–5 Dysthyroid eye disease, 345, 345
Decorticate posturing, 385 nose, 95 Dystonia, 369, 371
Decubitus ulcers, 81 Discoid eczema, 67 Dysuria, 203
Deep tendon reflexes, 365–7, 365–7 Discoid lupus, 80
Deep vein thrombosis, 179–80
Defibrillation, 148, 148
Dislocation, 269
Dissecting aortic aneurysm, 155
E
Deformity Distributive shock, 45 Ear, 82–93
finger, 269–70, 270 Divarication hernia, 206, 206 disease symptoms, 83–6
joint, 269–70 Dix-Hallpike test, 92–3 elderly people, 103
knee, 269 Dizziness see Vertigo examination, 56, 86–93
Dehydration, 44, 44, 63 Doctor-patient relationship, 1 external see External ear
Déjà vu, 318 Documentation inner see Inner ear
Delirium, 318 history taking, 11 middle see Middle ear
Deltoid muscles, 42 medical interview, 10–19 structure of the, 82–3, 83
Delusions, 318 systems review, 10 Early diastolic murmurs, 172, 172
Dementia, 310, 314, 314 see also Recording Ecchymoses, 62, 410
in elderly people, 18 Dog-in-the-night-time syndrome, 123 Eccrine glands, 58
history taking, 10 Doll’s head manoeuvre, 338, 338, 385 Echolalia, 316
Dentate nucleus, 372 Dopamine, 38, 39 Ectopic beats, 146, 147, 156
Dependent oedema, 175 Doppler ultrasound, 179 Ectopic pregnancy, 197, 241
Depersonalisation, 318 Dorsal column lesion, 381 Eczema, 67–8, 67–8
Depression, 318, 320 Dorsal interosseus, 286, 289, 289 ear signs, 87
general demeanour, 20 Dorsalis pedis pulse, 161, 161 varicose, 68, 179
history taking, 10 Dorsiflexion, 271, 299, 302 Edinger-Westphal nucleus, 332, 341
Derealisation, 318 Down’s syndrome (trisomy 21), 23, 24, 24 Education, 5, 14–15
Dermal naevus, 76, 77 Dress code, 2–3 Efferent pathways, 307
Dermatitis, 65, 68, 68 Dressing, 309 Effusions, 269, 270
Dermatitis herpetiformis, 76, 76 Drug history, 6–7 elbow, 282
Dermatomes, 375, 376 psychiatric assessment, 319 hip, 292
Dermatomyositis, 80 respiratory disease, 120 knee, 296, 297, 298
Dermatophytes, 74, 74 Drug-induced coma, 386 middle ear, 89
Dermis, 57–8, 58 Drugs pericardial, 123, 183–4, 184
Development, 396, 396–7 associated with tinnitus, 86 pleural, 47, 131, 133, 134, 135
adolescents, 418 causing impotence, 257 shoulder, 279
infants, 408 causing nausea, 196 Eisenmenger’s syndrome, 150, 151
425
Index
Ejaculatory duct, 255 Erythema, 62 Eye contact, 3

Ejection clicks, 169–70, 170 in bullous pemphigoid, 75, 75 Eyelid
Ejection systolic murmur, 171, 172 cellulitis-associated, 72 inspection, 337
Elastic cartilage, 266 toxic, 65, 65 retraction, 31, 31
Elastin, 57–8 Erythema marginatum, 182
Elbow, 282, 282–3, 283, 284
Elderly people
Erythema multiforme, 66, 66
Erythema nodosum, 59, 65, 65, 66, 80, 125
F
abdominal examination, 225 in respiratory disease, 124, 124 Face
bones, muscles and joints, 306 Erythema toxicum, 407, 407 asymmetry, 350
cardiovascular examination, 185 Erythroderma, 65 dysmorphology, 403, 404
ear, nose and throat examination, 103 Erythropoietin, 45, 192 expression, 3, 20
female breasts and genital tract, 250 Euphoria, 318 movement disorders, 352, 352–3
history taking, 18 Eustachian tube, 82, 86, 89 numbness, 9, 359
male genitalia and genital tract, 264 dysfunction, 89 pain, 95, 321
nervous system examination, 389 Examination palsy, 74
nutrition, 55 children, 392–3 paresis, 359
respiratory examination, 137 formal, 21–2 plethora, 45
skin changes in, 81 general, 20–1, 56 weakness, 350, 350, 351, 352
Electrical activity of the heart, 144, 144–5 patient position, 22, 22 Facial (seventh) nerve, 82, 349, 349–53,
Electrocardiogram (ECG), 144–5, 145, 146 recording, 13 350, 411
Electrolyte balance, 44, 192 setting, 22 Facies, 22–7, 158
Emphysema, 110 Exertional dyspnoea, 153 Faecal incontinence, 8
chest auscultation, 130 Exfoliative dermatitis, 65 Failure to thrive, 394
chest percussion, 129–30 Exophthalmos, 31 Fainting, 8, 156–7
lung volumes in, 111 Expiration, 126 Fallopian tubes, 237, 237
surgical, 126 Exploration, 109 Fallot’s tetralogy, 150, 151
Employment history see Occupational Extension, 271 Familial hypercholesterolaemia, 23, 26, 26,
history ankle and foot, 299, 300 27
Encephalopathy, hepatic, 201, 212–13, cervical spine, 275 Family history, 5
213 elbow, 282, 282, 283 cardiovascular disease, 157
Endocarditis fingers, 283, 286 children, 391
acute, 181 forearm and wrist, 283, 284, 285 psychiatric assessment, 319
infective, 158, 181–2 hip, 293, 295, 295 respiratory disease, 120
postoperative, 182 knee, 296, 298, 299 Family trees, 5, 5, 391, 391
subacute, 158, 181 lumbar spine, 275 Farmer’s lung, 120
Endocrine system shoulder, 279, 280 Farnsworth Munsell test, 324
disorders, 23–7, 61 thoracolumbar spine, 276 Fasciculation, 269, 273, 352, 362
history, 9–10 thumb, 287 Fast twitch fibres, 267
organs, 27, 27 (see also specific organ) Extensor carpi radialis brevis, 284 Fastigial nucleus, 372
syndromes, 27 Extensor carpi radialis longus, 284, 285 Fat digestion, 189, 189
Endocytosis, 28, 28 Extensor carpi ulnaris, 284, 285 Fat-soluble vitamin deficiency, 43
Endolymph, 354 Extensor digitorum, 286 Female genitalia and genital tract, 226–51
Endometriosis, 241 Extensor digitorum longus, 299, 300 anatomy, 235
Endometrium, 236 Extensor hallucis longus, 299–300, 300, blood supply, 235
Endophthalmitis, 23 303, 303 disease symptoms, 238–42
Enophthalmos, 124 Extensor pollicis brevis, 284 examination, 56
Enterocytes, 187, 188 Extensor pollicis longus, 286 abdominal, 242, 242–3
Enteroglucagon, 189 External ear cervical, 246–8
Enterokinase, 192 examination, 87, 87–8, 88 external genitalia, 243, 243–4, 244
Enzymes pain, 84 general, 242
cardiac, 177 structure of the, 82 uterine, 248–50
digestive, 187 Extrahepatic cholestasis, 201 vaginal, 244–6
pancreatic, 192 Extraocular muscles, 338 external, 236, 243, 243–4, 244
Eosinophils, 116 Extrapyramidal system, 360, 368–70 in infants, 411
Epicondylitis, 283 disorders, 371 newborns, 400–1
Epidermal cells, 57 Extrasystoles, 146, 147, 155 structure and function, 226–9, 235–8
Epidermis, 57, 58 Extrinsic allergic alveolitis, 120 symptoms of disease, 238–42
Epididymal cysts, 261, 261 Eye Femoral artery, 220
Epididymis, 252, 255, 255 assessment for dehydration, 44 Femoral epiphysis, slipped, 294
palpation, 260, 260 examination, 22–3 Femoral hernia, 220, 221
Epididymitis, 262, 263 in Graves’ disease, 30–1, 31, 32 Femoral neuropathy, 299, 299
Epiglottis, 100, 100 movements, 339, 372 Femoral pulse, 159, 160–1, 161, 178, 398,
Epiglottitis, 103 disorders, 339, 341, 342 398
Epilepsy, 8, 156, 381 inspection, 337 Femoral sheath examination, 220–1, 221
Epistaxis, 94–5, 98 saccadic, 334–5 Femoral stretch test, 276, 277
Epitrochlear lymph nodes, 52, 53, 54, 55 in the unconscious patient, 385 Femur fractures, 294
Eponychium, 59 muscle testing, 338, 338–40, 339 Fenestrae, 190
Erection, prolonged, 259 newborns, 402, 402 Fertility, male, 254
Erysipelas, 72, 72 in respiratory disease, 124–5 Fetal circulation, 149, 149–50, 397, 397
426
Index
Fever, 50 Foot drop gait, 305, 305 Gastrin, 187, 189

dehydration, 44 Forced expiratory volume in 1 second (FEV1), Gastro-oesophageal reflux
in lung disease, 118 110 cough, 115
Fever blister, 73, 73–4 Forced vital capacity (FVC), 110 pain, symptoms, 4
Fibrillation, 148 Forearm, 283–6 Gastrocnemius, 180, 299, 300
Fibroadenoma, 234 Forearm carrying angle, 282, 282 Gastrointestinal system, 186–93, 186–93
Fibroadenosis, 234 Foregut pain, 198, 198 bleeding, 196, 201
Fibrocartilage, 266 Foreign body diseases, 193–9
Fibrocartilaginous semilunar cartilages, 295 in the eye, 23 hormones, 189
Fibromyomas (fibroids), 249 lung collapse, 135 newborns, 400, 400
Fibrosing alveolitis vaginal, 241 review, 7–8
crackles, 132 Foreign travel, history, 6 in the unconscious patient, 383
cryptogenic, 137 Foreskin see Prepuce Gate control theory, 376
Fibrosis, lung, 110, 128, 131, 136, 137 Formal examination, 21–2 Gathering information see History-taking
lung volumes in, 111 Fourchette, 236 Gaze, 334–5, 336
Finger drop, 286, 286 Fourth heart sound, 169, 169 in infants, 411
Finger jerk, 366, 366 Fractures paresis, 341
Fingernails see Nails atlas, 279 Gegenhalten, 363
Fingers cervicothoracic junction, 279 Geniculate body lesions, lateral, 331
clubbing, 31, 80, 80 Colles’, 284, 285 Geniculate ganglion, 74, 349, 349, 352
deformities, 269–70, 270 femur, 294 Genital ulcers, 256, 259
extra, 406 humerus, 280 Genital warts see Condylomata acuminata
movements, 287 Pott’s, 301 Genitalia see Female genitalia; Male
reflexes, 366, 366 scaphoid, 288 genitalia
Fingertip bruising, 410 Smith’s, 285 Genu valgum, 269, 269, 295, 413, 413
First heart sound, 168–9 vertebral body, 279 Genu varum, 269, 269, 295, 413, 413
First impressions, 20–1 Fragile X syndrome, 23 Geographical orientation/disorientation, 309,
Fissured tongue, 102 Frequency of micturition, 8, 202–3 311, 312, 315
Fixed drug eruption, 66, 67 Frontal lobe, 307, 308 Geographical tongue, 102
Flapping tremor, 213, 213 Frontal sinusitis, 98 Gerstmann’s syndrome, 316–17
Flatulence, 7, 199 Frontalis, 350 Gestation and weight at gestation, 403
Flexion Frozen shoulder, 279 Ghrelin, 189
ankle, 300 Functional mental states, 319–20 Gibbus, 274, 274
cervical spine, 275 Functional residual capacity (FRC), 110 Gigantism, 39
deformity, 271, 272 Fundoscopy, 326–7, 327 Gingivitis, 116
elbow, 282, 282, 283 Fungal infections Glabellar tap, 314
fingers, 283–4, 287 ear, 84 Glands of Montgomery, 229, 235
foot, 300 nails, 79 Glandular fever, 102
knee, 295, 296 skin, 74 Glans penis, 254, 254, 258
lumbar spine, 275 Funnel chest, 125, 125 Glasgow coma scale, 383, 383
shoulder, 280 Furuncle, 72 Glaucoma, 23, 330, 331
thoracolumbar spine, 276 ear, 88 Glenohumeral joint, 279, 280
thumb, 287 vulval, 244 Global aphasia, 316
wrist, 285 Furunculosis, 88 Globe, 335
Flexor carpi radialis, 284, 285 Globus pallidus, 350, 360
Flexor carpi ulnaris, 284, 285
Flexor digiti minimi, 286
G Globus syndrome, 103
Glomerular filtration, 193
Flexor digitorum longus, 299 G-cells, 187 Glomerulus, 192
Flexor digitorum profundus, 286 Gag reflex, 354, 355, 355, 388 Glossopharyngeal (ninth) nerve, 186, 187,
Flexor digitorum sublimis, 286 Gait 354, 354–5, 411
Flexor hallucis longus, 299 ataxia, 372 neuralgia, 355
Flexor pollicis brevis, 286 in cerebellar disorders, 374, 374 Glucagon, 189, 192
Flexor reflex afferents (FRA), 361 disorders, 305, 305–6 Glucocorticoids, 35–6
Flow charts, problem-orientated medical first impressions, 20 Gluconeogenesis, 36
record, 15–16, 17, 18 GALS, 272 Glue ear, 89–90, 90
Flow meters, 110, 110 Galactorrhoea, 39, 231 Gluteus maximus, 291, 292
Fluency of speech, 312–13 Gallbladder, 191, 191 Glycosaminoglycans, 57
Fluid balance, 44, 192 pain, 198 Goitre, 29, 29, 30, 30, 31
Focal tachycardia, 147 palpation, 213–14, 214 Golfer’s elbow, 282
Folic acid deficiency, 43 Gallop rhythm, 169 Gonadotrophin-releasing hormone (GnRH),
Follicle-stimulating hormone (FSH), 38, 226, Gallstones, 202, 214, 214 226, 227
227, 228, 252, 253, 254 GALS, 272–4 Goniometer, 271, 271
failure, 40, 41 Gangrene, 178, 178 Gonorrhoea, 241, 259
Follicles Gas exchange, 110–11 Goose pimples, 58
ovarian, 228, 228 Gasserian ganglion, 346 Gout, 301, 302
thyroid, 28 Gastric acid, 187 pain, 268
Fontanelle, 402, 402 Gastric inhibitory polypeptide, 189 swelling, 270
Foot, 299–303, 300, 303 Gastric outflow obstruction, 219, 219 Gowers’ manoeuvre, 304, 304
deformities, 301 Gastric secretions, 187 Graafian follicle, 228, 228
427
Index
Granuloma inguinale, 244 Head circumference measurement, 393, Hiatus hernia, 194, 194
Grasp reflex, 314, 314, 317 393, 397, 402, 402 Hilar lymph nodes, 52
Graves’ disease, 30–2, 31, 32 Head lice, 75 Hindgut pain, 198, 198
bruits, 29 Head position, 354 Hip joint, 290–5, 292, 293, 294, 295
Grey Turner’s sign, 207 Head rotation, 356, 357 in infants, 411
Grip, 21 Headache, 8, 320–1 in newborns, 401, 401–2
Groin Hearing, 82–3 Hirsutism, 60–1, 242
examination, 220–1, 221 loss see Deafness History-taking, 1, 3–7
strains, 294 Heart, 139–85 adolescents, 418
Grommets, 90, 90 auscultation, 167, 167–73, 398, 399 background information, 5–6
Growth autonomic effects on the, 145 biomedical perspective, 4
adolescents, 416, 416–17, 417 blood supply, 148–51 children, 390–2
failure, 21, 394, 414, 415 chambers, 139, 140 elderly people, 18
in general, 393–5 disease, 117–18, 158, 158 exploration of patient’s problems, 3–4
infants, 408 electrical activity of the, 144, 144–5 infants, 408–9
newborns, 397 enlargement, 142, 142 newborns, 398
phases of, 393 muscle, 141, 141–2 past medical history, 6–7
preschool children, 412 structure and function, 139, 139–44, 140 preschool children, 413
school-aged children, 414 valves, 142, 142, 170, 170 psychosocial perspective, 4–5
Growth charts, 394–5, 395 Heart block, 146, 146 recording, 11, 12–13
Growth hormone (GH), 38 Heart failure, 175–6 school-aged children, 414–15
deficiency, 415 acute, 175, 175 skin, 59
excess, 21, 39 chronic, 175–6, 176 see also specific system
failure, 40, 41 oedema, 174–5 Hoarseness, 100–1
Grunting, 400 Heart sounds, 142–4, 143–4, 168–70, Hobbies and respiratory disease, 119
Guarding, 198 168–73 Hodgkin’s disease, 50
Gummas, 72, 262 newborns, 398, 399 Holmes-Adie syndrome, 341
Gut bacteria, 201 Heartburn, 7, 194 Holocrine secretion, 58
Guttate psoriasis, 59, 69, 69 Heberden’s nodes, 287 Holosystolic murmur, 171
Gynaecomastia, male, 232, 233, 258, Heel-knee-shin test, 373, 374 Holter monitoring, 145
258 Heel-toe walking, 374, 374 Homan’s sign, 49, 180
Hegar’s sign, 249 Home circumstances, history, 6
H Height
measurement, 394, 394, 412, 414,
Hordeolum, 72
Horizontal saccades, 334–5, 336
Haematemesis, 7, 100, 116, 196 414–17 Hormones
Haematuria, 203 midparental, 412 gastrointestinal, 189
Haemochromatosis, 46, 61 norms in adults, 41, 41 in puberty, 226, 252–3, 253
skin colour, 61 Hemianopia, 325, 331, 333, 334 Horner’s syndrome, 124, 291, 340, 340
Haemoglobin, 122, 157–8 Hemiballismus, 369, 371 Hospital wards, consultation in, 2
Haemoptysis, 7, 100, 116–17, 133 Hemidesmosomes, 57 Hospitalised patients, posture, 21
Haemorrhage Hemifacial spasm, 352, 352 Hostile patients, 10
cerebral, 372 Hemiplegia, 357, 363 House dust mites, 114
splinter, 79, 158, 158 acute, 364 Human chorionic gonadotrophin (HCG), 228
subconjunctival, 23 gait, 305, 305 Humerus, 282
Haemorrhagic pancreatitis, 207 Henoch-Schönlein purpura (HSP), 410 fracture, 280
Haemorrhoids, 201, 224 Hepatic encephalopathy, 201, 212–13, 213 Hung up reflexes, 373
Haemosiderosis, 61 Hepatitis, 196, 201 Huntington’s disease, 341–2, 371
Hair Hepatocellular disease, 201, 212–13 Hyaline bodies, 329, 329
dermatophytes, 74 Hepatocytes, 190–1, 191 Hyaline cartilage, 266
disease, 60, 60–1 damage, 201 Hyaline laminae, 274
pubic see Pubic hair Hepatomegaly, 211, 212 Hyaluronic acid, 57
structure and function, 58 Herald patch, 70 Hydatid of Morgagni, 255
Hairline, low, 405 Herniae Hydration, clinical assessment of, 44, 44
Hairy tongue, 102 divarication, 206, 206 Hydrocele, 260–1, 262, 401
Halitosis, 98 femoral, 220, 221 Hydrochloric acid, 187
Hallpike (Dix-Hallpike) test, 92–3 hiatus, 194, 194 Hydronephrosis, 217
Hallucinations, 318, 322 incisional, 206, 206 Hydrosalpinx, 250
Hallux rigidus, 301 inguinal, 206, 206, 220–1, 260 Hydrostatic pressure, 47, 47
Hallux valgus, 301, 301 linea alba, 206 Hydrothorax, 47
Hammer toe, 301, 301 paraumbilical, 206, 206 Hydroxyapatite, 265
Hamstrings, 291, 292, 298 scrotal, 258, 258, 260 Hyperacusis, 351
Handedness, 9, 311 transtentorial, 386, 387 Hyperadrenalism see Cushing’s syndrome
Hands, 286, 286–90 umbilical, 401, 401 Hyperbilirubinaemia, 61
in heart disease, 158, 158 uncal, 386, 387 Hypercalcaemia, 34
muscle wasting, 362, 362 Herpes simplex, 73, 73–4, 244, 245 Hypercapnia, 388
Handshake, 21, 21 Herpes zoster, 62, 74, 74, 117 Hypercholesterolaemia, familial, 23, 26, 26,
Haversian canals, 265 Hertel exophthalmometer, 31 27
Hay fever, 98 Heschl’s gyrus, 353 Hyperextension, 271
Head and neck lymph nodes, 53–4, 54 Hesitancy, urinary, 203 Hyperinflation, 136, 211
428
Index
Hyperlipidaemia, 177 Hysterical gait, 306 Internuclear ophthalmoplegia, 343, 343

skin manifestations of, 80 Hysterical personality, 320 Interosseus, dorsal, 286, 289, 289
Hypermetria, 342, 373 Interphalangeal joints, 287, 287, 288
Hyperparathyroidism, 34, 34
Hyperpigmentation, 46
I Interstitial fluid, 47
Intervertebral discs, 274
of the areola, 37, 37 Ichthyosis, 50, 80 prolapsed, 276–7
in dermatitis herpetiformis, 76 Idiopathic guttate hypomelanosis, 62 Interview see Consultation
Hyperprolactinaemia, 39, 40 Idiopathic thrombocytopenic purpura (ITP), Intestinal obstruction, 200
Hypertelorism, 403 410 abdominal pain, 197
Hypertension, 163 Ileocaecal valve, 190 Intracardiac shunting, 149, 149–51
heart sounds, 169 Ileum, 187, 189 Intracranial pressure, raised, 328
pulmonary, 181 Iliac crest, 205, 205 Intrahepatic cholestasis, 201
retinopathy, 330, 330 Iliacus, 291, 292 Intravascular fluid, 47
Hyperthyroidism, 30, 31, 32 Illicit drugs, history taking, 7 Intrinsic factor, 187, 187
onycholysis in, 79 Illusions, 318 Introitus, 236
skin manifestations of, 80 Immunisation, 407–8 Involuntary movement, 368
Hypertrophic cardiomyopathy, 160, 160, Immunity, 407 Iodine, 28, 28
182, 182 Immunoglobulin A, 105–6 Iridocyclitis, 124
Hypertrophic obstructive cardiomyopathy Immunoglobulins, 407, 408 Iritis, 23
(HOCM), 144, 154, 182 Imperforate anus, 405 Iron deficiency, 42
Hypertrophic pulmonary osteoarthropathy, Impetigo, 71–2, 72 anaemia, 201
121, 122 Impotence, 39, 257 nails in, 79, 80
Hypertrophy Incisional hernia, 206, 206 Iron overload see Haemochromatosis;
heart, 142 Incisions, surgical, 158, 158 Haemosiderosis
muscle, 273 Incontinence Ishihara test plates, 324, 325
Hyperventilation, 112, 126 faecal, 8, 222 Islets of Langerhans, 192
central neurogenic, 385, 386, 386, 387 urinary, 8, 203 Isthmus, 82
dizziness with, 9 Incus, 82, 353 Itching see Pruritus
in shock, 45 Indigestion, 195
in the unconscious patient, 385, 386
Hyperventilation syndrome, 115
Infants, 407–12
development, 408
J
Hyphaema, 23 examination, 409–12 J receptors, 114
Hypoadrenalism, 37 growth, 393, 393, 394, 394, 408 Jamais vu, 318
Hypoalbuminaemia, 42, 47 history-taking, 408–9 Janeway lesions, 181
leukonychia in, 79 rashes, 410, 410 Jaundice, 46, 46, 201, 202
Hypodermis, 58, 58 Infections in liver disease, 211
Hypoglossal (twelfth) nerve, 357–9, 358, ear, 87 newborns, 400
411 skin, 71–8 skin colour, 61
Hypogonadism, 258 see also Bacterial infections; Fungal Jaw jerk, 346, 348, 348
Hypomania, 320 infections; Viral infections Jaw opening and closing, 345
Hypometria, 342, 373 Infectious keratitis, 23 Jejunum, 187, 189
Hyponychium, 59 Infectious mononucleosis, 102 Jendrassik manoeuvre, 365
Hypoparathyroidism, 34 Infective endocarditis, 158, 181–2 Jerky carotid pulse, 160, 160
Hypopharynx, 100 Inferior vena caval obstruction, 207 Jobson Horne probe, 88, 88
Hypopituitarism, 40, 41 Infertility, male, 257 Joint position sense, 378–9, 379
skin colour, 61 Infestations, skin, 75, 75 Joints
Hypopyon, 23 Inflammation crepitus, 268
Hyposmia, 94, 322 ear, 87 disease symptoms, 267–8
Hypospadias, 258, 259, 406 oedema, 47 examination, 269, 269–72
Hypotelorism, 403 skin lesions, 63 locking, 268
Hypotension, 163–4 Inflammatory joint disease, 268, 300 movement, 271, 271–2, 272
in acute heart failure, 175 Infraclavicular lymph nodes, 52, 53 pain, 267–8, 268
postural see Postural hypotension Infraspinatus, 279, 280, 281 palpation, 270
Hypothalamic-anterior pituitary endocrine Inguinal canal examination, 220–1, 221 structure and function, 266, 266–7
axis, 38, 38 Inguinal hernia, 206, 206, 220–1, 260 swelling, 268, 269, 270
Hypothalamic-pituitary-gonadal axis, 227, Inguinal ligament, 220 temperature, 270, 271
254 Inguinal lymph nodes, 52, 53, 55, 55 tenderness, 270
Hypothalamus, 28, 38, 38, 252 enlarged, 263 see also specific joint
position of, 27 Inherited disorders, 5 Jugular foramen tumours, 357
tumours, 21 Injuries see Traumatic lesions Jugular venous pressure, 183, 184
Hypothenar eminence, 286 Inner ear, 353, 353 Jugular venous pulse, 123, 164, 164–6, 165
Hypothermia, 50 examination, 90–3 Junctional naevus, 76, 76, 77
Hypothyroidism, 32–3 structure of the, 82–3 Juvenile hypothyroidism, 414
juvenile, 414 Innocent murmurs, 172
Hypotonia, 363, 373, 373
Hypoventilation, 112
Inspiration, 126
Insulin, 189
K
Hypovolaemic shock, 45 Intelligence, 311, 312 Kaposi’s sarcoma, 78, 78, 101
Hypoxia, 113, 115 Intermenstrual bleeding, 239, 240 Keratitis, infectious, 23
Hysteria, 320 Intermittent claudication, 157, 178 Keratosis, senile, 81
429
Index
Kernig’s sign, 384, 384 Leydig cells, 252, 254 defence and histology, 105–8
Kidneys, 192–3, 193 Lhermitte’s phenomenon, 371, 381 effect of disease on other structures, 117–18
disease, 202–3 Libido, 8, 241 fibrosis see Fibrosis, lung
examination, 215–17 loss of, 238 (see also Impotence) function, 108–9
pain, 203 Lice, 75 lobes see Lobes, lung
palpation, 216, 216–17 Lichen planus, 70–1, 71, 102 volume, 109, 109–10, 110
polycystic disease, 174, 217 Lid lag, 31, 31, 32 in disease, 111
stones, 34 Light reflex, 82, 89, 89 Lunule, 59
surface markings, 216 Light touch, 378, 378 Lupus pernio, 80, 124
see also entries beginning with Renal Limbs Luteinising hormone (LH), 38, 226, 227,
Knee, 295–9, 296, 298, 299 in cerebellar disorders, 373, 373 252, 253, 254
clonus, 366, 367 clumsiness, 372 failure, 40, 41
deformities, 269, 269 cranial nerve symptoms, 9 Lymph, 47
pain, 294, 298 length measurement, 292, 294 Lymph nodes, 51, 51, 52, 52
reflexes, 366, 366 lower see Lower limb enlargement see Lymphadenopathy
Knock-knees see Genu valgum spastic, 363 examination of, 53–5
Koebner phenomenon, 69, 71, 71 thin in hyperadrenalism, 36, 37 inguinal, 220
Koilonychia, 42, 79, 80 upper see Upper limb malignant, 53
Korotkoff sounds, 162, 162 weakness, 364 (see also Muscle(s), thyroid carcinoma, 29
Kremer, 368 weakness) tuberculous, 124
Kupffer cells, 190 Linea alba hernia, 206 Lymphadenitis, 53
Kussmaul breathing, 126 Lipase, 189 Lymphadenopathy, 51, 52
Kyphoscoliosis, 126, 126 Lipid storage diseases, 51 in infants, 411
Kyphosis, 20, 126, 274, 274 Lipids, 189 in respiratory disease, 123–4
Lips, central cyanosis, 122 Lymphangitis, 53
L Liver, 190, 190–1, 191
abnormal shape, 210–11, 211
Lymphatic ducts, 51, 51
Lymphatic oedema, 49
L-dopa, 369 auscultation, 220 Lymphatic system, 50–5
Labia majora, 235–6, 243, 243 disease, 201, 201–2 drainage, 51, 52, 53
Labia minora, 236, 243–4 general signs of, 211–13, 213 breasts, 229–30
Labyrinth, ear, 82, 353 malnutrition in, 42, 42 examination, 50–1
dysfunction, 86, 92 oedema, 47, 48 lymph nodes see Lymph nodes
Lacrimation, loss of, 351 downward displacement of, 210, 211 male genitalia, 255, 263
Lactation, 230, 231, 239 enlargement, 211, 212 organs, 51
Lactiferous duct, 229, 230 examination, 204, 204, 209, 209–13, 210 structure and function of, 51–2
Langerhans cells, 57 palpation, 209–11, 210 Lymphoedema, 49
Language function, 308 percussion, 210, 211 Lymphogranuloma venereum, 263, 263
see also Speech small, 211, 212 Lymphoid tissue, 99
Lanugo hair, 58 Liver cell damage, 201, 202 Lymphoma of the tonsil, 102
Laryngeal nerves, 27 Lobes, lung, 105, 106, 107
palsy, 115
Laryngitis, 103, 115
collapsed, 135–6, 136
pneumonia, 133
M
Laryngopharynx, 100 Long bones, 265 Mackenrodt’s ligaments, 238
Laryngoscopy, 101, 101, 102 Long saphenous vein, 179 Macrophage, alveolar, 106
Laryngotracheobronchitis, 103 Loop of Henle, 193 Macules, 62, 65, 65
Larynx, 99–100, 100 Lordosis, 274, 274 Malar erythema, 80
examination, 103 Low birth weight, 402 Malassezia furfur, 74
tumours of the, 103 Lower limb, deep tendon reflexes, 366, Maldigestion, 192
Lasegue’s test, 276, 277 366–7 Male genitalia and genital tract, 252–64, 253
Lateral epicondyle, 282, 283 Lower motor neuron, 359, 360–2 disease symptoms, 255–7
Lateral geniculate body lesions, 331 facial weakness, 351 examination, 56, 257–63, 258
Latissimus dorsi, 279, 281 lesions, 358, 370, 370 in infants, 411
Learning ability, new, 310–11 Lower oesophageal sphincter, 187 newborns, 400–1, 401
Left bundle branch block, 144 Lumbar meningomyelocele, 405 structure and function, 252, 252–5
Left to right shunt, 150, 150 Lumbar nerve roots, 299, 299, 303, 303 Malignant lymph nodes, 53
Left ventricle, 139, 140, 140, 141 Lumbar spine, 275, 275, 276, 278, 279 Malignant melanoma, 77–8, 78
hypertrophy, 167, 169 Lumbosacral plexus, 375 Malignant vasovagal syncope, 156
impairment, 169 Lumbrical muscles, 286 Mallet deformity, 269–70, 270
Left ventricular failure, 114–15 Lumps Malleus, 82, 89, 353
dyspnoea, 153 breast, 231, 232, 234 Mallory-Weiss tear, 196
oedema, 47 neck, 100 Malnutrition, 21, 40, 42, 42
posture, 21 Lung cancer, 105 Mania, 320
Legs chest pain, 117 Manometers, 161, 162
GALS, 272–3 risk factors, 119 Marfan’s syndrome, 23, 24, 24
lymph nodes, 55 weight loss in, 118 arm span, 42
see also Lower limb Lungs Masseter, 346, 347, 348
Leucocytes in sputum, 116 abscess, 116, 131 Mastitis, 234, 235
Leukonychia, 42, 79, 79 collapsed, 128, 130, 133, 135–6, 136 Mastoid air cells, 82
Leukoplakia, 77, 77, 102, 244 breath sounds, 131 Mastoiditis, 89
430
Index
Maxillary sinusitis, 98 Midgut pain, 198, 198 tone, 362–3

McMurray’s test, 297, 298 Midparental height, 412 abnormal, 361
Mechanical joint disease, 268 Midtarsal joints, 299, 301 wasting, 42, 42, 269, 270, 273, 281, 281
Mechanoreceptors, 374–5 Migraine, 8 general examination, 42
Medial epicondyle, 282, 283 Miliary tuberculosis, 124 hands, 289, 291, 292, 362, 362
Medial lemniscus, 375, 376, 377 Milk line, 229, 230 weakness, 20, 269, 362
Medial longitudinal fasciculus, 334 Mineralocorticoids, 35–6 patterns of in disease, 303–6
Median nerve, 289, 289 Mini mental-state examination, 313, 314 Muscular dystrophies, 303, 304
Mediastinum Miosis, 124 Musculoskeletal system
crunch, 126 Mitral facies, 158 chest pain, 155
displacement, 128, 128 Mitral valve, 142 examination, 56
palpation, 127–8 incompetence, 168 review, 10
Medical audit, problem-orientated medical prolapse, 171 Myasthenia gravis, 345, 370, 370
records, 16–17 regurgitation, 142, 170 muscle power, 273
Medical records see Recording stenosis, 167, 168–9, 172, 172, 173, 173 Mydriatics, 326
Medical Research Council classification of Mittelschmertz, 241 Myelinated nerve fibres, 329, 329
muscle power, 363, 364 Mixed heart failure, 176, 176 Myelocele, thoracic, 405
Medical students, 10 Molluscum contagiosum, 73 Myocardial infarction, 154–5, 167, 177–8
Melaena, 8, 201 Mondor’s disease, 231 heart sounds, 169
Melanin, 57, 61 Mongolian blue spots, 405 Myocardial ischaemia, 154–5, 194
Melanocytes, 57, 61 Monitoring tests, problem-orientated symptoms, 4
Melanoma, malignant, 77–8, 78 medical records, 14 Myocarditis, 182
Melasma, 61 Mono-iodotyrosine (MIT), 28, 28 Myocardium see Heart, muscle
Melena, 196 Monoaminergic pathways, 360 Myoclonus, 368, 371
Memory, 9, 309, 310–11, 311 Monoplegia, 363 Myofibrils, 266
acquisition, 308 Mons pubis, 235–6 Myokymia, 352, 369, 369, 371
see also Amnesia Mood, 309, 317–18 Myomalacia, 178
Menarche, 226, 238–9 Moon-shaped face, 36, 37 Myopathies, 304
Ménière’s disease, 86, 92 Moro reflex, 402 Myosin, 266, 267
Meningeal irritation, 384, 384 Motilin, 189 Myotomes, 377
Meningitis, 89 Motility disorders, 194 Myotonia, 303, 364, 365
Meningococcal septicaemia, 410 Motion sickness, 195 Myotonia dystrophica, 21, 305
Meningomyelocele, lumbar, 405 Motor neurons, 267 Myringitis bullosa, 88
Meniscal tears, 298 disease, 292 Myxoedema, 31, 32, 33
Menopause, 228–9, 229 see also Lower motor neuron; Upper
Menorrhagia, 8, 239
Menstruation, 227–8, 228
motor neuron
Motor responses in the unconscious patient,
N
history-taking, 238–41 385 Nabothian cysts, 247
pattern, 239 Motor system, 359, 359–71 Naevi, 76, 76, 77
systems review, 8 Motor units, 267, 360–1 Nails
Mental state, 310–14, 319–20 Mouth see Oral cavity dermatophytes, 74
Meralgia paraesthetica, 299 Movement disorders, 371 disease, 61
Mercury manometers, 161 see also specific disorder disorders, 79–80, 79–80
Mesangium, 192 Mucociliary escalator, 106 in psoriasis, 70
Mesencephalic nucleus of the trigeminal Multisystem atrophy, 371 structure and function, 58–9, 59
nerve, 345–6 Murmurs, heart, 170, 170–3, 171, 172, Naming defect, 313
Mesenteric angina, 199 173 Nasal cavity, 93–4, 96
Metabolic acidosis, 45, 112 in endocarditis, 181 Nasal deformity, 95, 96
Metabolic alkalosis, 112 infants, 409 Nasal obstruction, 95
Metabolic coma, 385, 386 newborns, 400 Nasendoscope, 96, 97, 102
Metacarpophalangeal joints, 286, 287 in rheumatic fever, 183 Nasolacrimal duct, 93–4
Metatarsophalangeal joints, 301 Murphy’s sign, 213 Nasopharyngeal carcinoma, 355
Micelles, 189 Muscle pump mechanism, 179 Nasopharynx, 100
Michelin man, 126 Muscle(s) Nausea, 195–6, 196
Micrognathia, 406 atrophy, 42, 362 Near reaction, 332–3, 337
Microtia, 84 cramps, 269 Neck
Micturition disease symptoms, 268–9 lump in the, 100
frequency, 8, 202–3 eye, 338–40, 339 stiffness, 384, 384
hesitancy, 203 fasciculation, 269 see also entries starting with Cervical;
pain, 8 fibres, 267, 361 Head and neck lymph nodes
syncope, 156 GALS, 273–4 Necrobiosis lipoidica, 80
urgency, 202–3 hypertrophy, 362 Nelson’s syndrome
Mid-diastolic murmurs, 172, 172 increased bulk of, 273 pigmentation in, 46
Mid-systolic click, 170, 170 pain and stiffness, 268–9 skin colour, 61
Midarm muscle circumference, 42–3, 43 palpation, 273 Neocerebellum, 372
Middle ear, 353, 353 power, 363–4 Neonates see Babies; Newborns
examination, 89, 89–90 testing, 273–4, 289, 289, 364 Nephrogenic diabetes insipidus, 40
pain, 84 spontaneous contractions, 273 Nephrons, 192, 193
structure of the, 82 structure and function, 267 Nephrotic syndrome, 47, 48, 135, 263
431
Index
Nerve disorders, 380, 380 Obstetric history, 242 Organ of Corti, 353
Nerve palsies, 281 Obturator nerve palsy, 299 Organic mental state, 319–20
Nerve root disorders, 370, 380 Occipital cortex lesions, 331–2 Orientation, 310
pain in, 377 Occipital infarction, bilateral, 332 see also Geographical orientation/
Nerve stretch tests, 275–6, 277 Occipital lobe, 331 disorientation; Right-left orientation/
Nervous system, 8–9, 307–89 Occipital lymph nodes, 52, 52, 53, 54 disorientation
Neural tube defects, 405 Occult rectal bleeding, 200–1 Orofacial dyskinesia, 353
Neuralgia Occupational history, 5–6 Oropharynx, 100
glossopharyngeal, 355 cardiovascular disease, 157 dysphagia, 9
trigeminal, 321 lung disease, 119–20 examination, 102
Neuralgic amyotrophy, 281, 282 psychiatric assessment, 319 Orthopnoea, 21, 114–15, 153, 154
Neurofibromas, 76 Ocular sympathetic fibres, 333–4, 335 Ortolani manoeuvre, 401
Neurofibromatosis, 23 Oculocephalic reflex, 338, 338, 385 Osler’s nodes, 181
Neurohypophysis, 38 Oculocutaneous albinism, 25 Osseous spiral lamina, 353
Neurological examination, 56 Oculomotor nuclei, 384 Ossicles, auditory, 82, 83, 353
infants, 411–12 Oculomotor (third) nerve, 332–45, 411 Osteoarthritis, 287–8, 288
newborns, 402 compression, 344 ankle and foot, 301
preschool children, 413–14 palsy, 343–4, 344 hip, 293, 294
New York Heart Association (NYHA) Odours, 321–2 knee, 298, 298
classification of heart failure, 153, 154 Odynophagia, 195 pain, 267–8
Newborns, 397–407 Oedema, 46–9, 47, 48 Osteoblasts, 265
baby check, 399 cellulitis-associated, 72 Osteoclasts, 265
congenital abnormalities, 404, 404–6 chronic venous insufficiency, 179 Osteocytes, 265
development, 397 peripheral vascular disease, 174, 174–5 Osteoporosis
growth, 393, 397, 397 signs of, 48–9, 49 first impressions, 20
low birth weight, 402 symptoms of, 47 height in, 41
rashes, 407 see also specific site; specific type Otalgia, 84
routine neonatal examination, 403–7, 404 Oesophagus, 186, 186–7 Otitis externa, 68, 87, 88
Niacin, 43 cancer, 194 Otitis media, 89–90
Nikolsky’s sign, 75 nutcracker, 195 Oto-acoustic emissions test, 92
Nipple, 229 stricture, 194 Otoliths, 354
abnormal, 234–5 varices, 196, 201 Otorrhoea, 84–5
discharge, 231 Oestrogen, 226 Otoscope, 20
palpation, 234, 234 Olecranon, 282, 283 Ovaries, 237, 238
Nits, 75 Olfaction, 321–2 abnormalities, 250
Nociceptors, 375 Olfactory (first) nerve, 321–2, 411 cyst, 242, 242, 250
Nocturia, 203 Olfactory hallucinations, 322 follicles, 228, 228
Nocturnal asthma, 114 Oligomenorrhoea, 39, 239, 240 ligaments, 237
Nodules, 62, 65, 65 Oliguria, 45, 203 palpation, 249–50, 250
Non-refractive visual disturbances, 23 Oncotic pressure, 47, 47 position of, 27
Non-ST segment elevation myocardial One-and-a-half syndrome, 343, 343 tumours, 250
infarction (NSTEMI), 177–8 Onycholysis, 70, 79, 79 Overflow incontinence, 203
Non-steroidal anti-inflammatory drugs in Graves’ disease, 31 Ovulation, 227–8, 241
(NSAIDs), 6 Open-ended questions, 3, 4 Oxygen, 108, 109
Nonaccidental injury, 410 Opening snap, 170, 170 Oxygen dissociation curve, 111–12, 112
Nonorganic sensory loss, 382, 382 Ophthalmoplegia, 31 Oxytocin, 38, 39, 230, 231
Nose, 93–8 Ophthalmoscope, 20
disease symptoms, 94–6
elderly people, 103
Opponens digiti minimi, 286
Opponens pollicis, 286, 289, 289
P
examination, 56, 96–7, 96–8 Opposition, thumb, 286, 287 P wave, 145, 145
structure of the, 93, 93–4 Optic atrophy, 327, 327 Pacemaker, cardiac, 144
Nose bleed, 94–5, 98 Optic disc, 326 Pacinian corpuscles, 375
Nucleus ambiguus, 354 Optic radiation, 331–2 Paget’s disease of the breast, 232, 233, 234
Nucleus interpositus, 372 Optic (second) nerve, 322, 322–32, 323, 411 Pain
Nucleus pulposus, 274 clinical application, 327–32 abdomen see Abdomen, pain
Nucleus Z, 375 disease, 330–1, 331 anal, 199–200
Numbness, 377 examination, 323–7 assessment, 4
Nummular eczema, 67 structure and function, 322 back, 276
Nutcracker oesophagus, 195 symptoms, 322 bone, 267
Nutritional status assessment, 40–3, 55 Optic tract lesions, 331, 333 breasts, female, 230–1
Nystagmus, 92, 336, 339–40, 340 Opticokinetic nystagmus, 340, 340 chest see Chest pain
in infants, 411 Oral cavity, 98, 99, 186–7 ear, 84
types of, 345 blood in, 100 facial, 95
in the unconscious patient, 385 carcinoma, 101 in general, 376–7, 377
Oral temperature, 49–50 gynaecological disorders, 241
O Orbicularis oculi, 350
Orbicularis oris, 350
joint, 267–8, 268
knee, 294, 298
Obesity, 21, 36, 37, 40 Orchitis, 262, 262 micturition, 8
Obsessions, 318, 320 Organ failure, major, 27 muscle, 268–9
432
Index
nasal, 95 Passive immunity, 407 Peripheral vascular system, 174–8

referred, 377 Patella, 295, 298 disease, 178, 178–85
on swallowing, 195 Patellar tap, 297 Peripheral vertigo, 86
testicular, 257 Patent ductus arteriosus, 398 Peristalsis, visible, 206
testing, 379, 380 Pathophysiological abnormalities, Peritoneum, 221
thalamic, 377 consultation, 1–2 Peritonitis, 126
urinary tract, 203 Patients perspective, 2 abdominal palpitation, 208
visceral, 376–7 Pause neurons, 335 in infants, 411
see also specific location Pavement epithelium, 89 posture, 21
Painful arc syndrome, 279–80 Peak expiratory flow rate (PEFR), 110, 110, Peritonsillar abscess, 102, 104
Palaeocerebellum, 372 111 Permanent teeth, 99
Pallor, 45, 45 in children, 415, 416 Peronei, 300, 300, 303
Palmar crease, single, 406 Peau d’orange skin, 232 Persistent ductus arteriosus, 150, 150
Palmar grip, 408, 408 Pectoralis major, 229 Personal history, 5
Palmar interosseus, 286 Pectus carinatum, 125 Personal hygiene, doctors, 2–3
Palmomental reflex, 314, 317 Pectus excavatum, 125, 125 Personality profile, 319
Palpebral fissure, 403 Pedal oedema, 42, 48, 49 Pes cavus, 301, 301
Palpitations, 7, 155–6 Pediculosis, 75 Pes planus, 300–1, 301
Pampiniform plexus, 255 Pedigrees, 391, 391 Petechiae, 62, 62
Pancarditis, 183 Peer review, 16–17 Pets and respiratory disease, 119
Pancreas, 191–2, 192 Pel-Ebstein fever, 50 Peutz-Jeghers syndrome, 23, 25, 25
disease, 202 Pellagra, 42, 42 Peyer’s patches, 51, 51
enzymes, 192 Pelvic fascia and ligaments, 238, 238 Phalen’s sign, 290
position of, 27 Pelvic floor, 236, 236, 238, 238 Pharyngeal pouch, 115
Pancreatic ducts, 191, 192 Pelvic tumour, 242, 242 Pharyngitis, 102
Pancreatic glucagon, 189 Pemphigus, 75, 76 Pharynx, 99–100
Pancreatic juice, 189 Penicillin, skin reactions to, 64 Phenothiazines, 353
Pancreatic polypeptide, 189 Penis, 252, 252, 254–5 Philtrum, 403
Pancreatitis, 202 abnormalities of, 258–9, 259 Phimosis, 258
abdominal pain, 197, 197 anatomy, 254 Phlegm, 115–16
hemorrhagic, 207 examination, 258–9 Phobias, 320
posture, 21 normal, 258 Phobic anxiety, 318
weight loss, 195 ulcers, 259, 259 Phonocardiography, 168, 169
Pansystolic murmur, 170, 171 Penlight inspection of red eye, 23 Photophobia, 23
Papillary muscles, 142, 142 Pepsin, 187, 187, 189 Photoreceptors, 322
Papilloedema, 124–5, 321, 327–9, 328, 359 Pepsinogen, 187, 187 Photosensitive drug rashes, 66–7
Papules, 62, 64, 64 Peptic stricture, 194 Physical stature, 21
Paradoxical splitting of the second heart Peptic ulcer, perforated, 197 Pigeon chest, 125
sound, 144 Perceptions, abnormal, 318 Pigmentation, 46, 46, 57, 61–2
Paralysis, 363 Percussion in chronic cholestasis, 46, 46
Paralytic ileus, 219 abdomen, 217–18, 219, 242, 242 malignant melanoma, 77–8
Paranasal sinuses, 93, 94, 94 bladder, 218, 219 see also Hyperpigmentation
examination, 98 chest, 129, 129–30 Pill rolling, 20
pain, 95 clavicles, 129, 129 Pilonidal sinuses, 222, 224
Paraphasias, 312 liver, 210, 211 Pincer grip, 408, 408
Paraphimosis, 258 spleen, 215, 215 Pinhole test, 23
Paraplegia, 363 Percussion myotonia, 364, 365 Pink puffers, 127, 127
Parasites, travel-related, 6 Perforating veins, 179 Pinna, 82, 83, 84, 87–8, 403
Parathyroid glands, 27, 33–4 Perfusion, 111, 111 Pitting oedema, 63, 175
Parathyroid hormone (PTH), 33–4, 34 Perianal warts, 245 Pituitary gland, 38, 38–40
Paraumbilical hernia, 206, 206 Pericarditis, 155 hormone overproduction syndromes, 39,
Parents, 390 acute, 183 39–40, 40
Paresis, 363 constrictive, 123, 165, 184, 184–5 hypofunction syndromes, 40
Paresthesia, 377 jugular venous pulse, 165 position of, 27
Parietal abdominal pain, 198 posture, 21 structure and function, 38–9
Parietal cells, 187, 187 Pericardium tumours, 39
Parietal lobe, 307, 308, 331 disease, 183–5 (see also specific disease) Pityriasis rosea, 70, 70, 71
Parinaud’s syndrome, 341 effusion, 123, 183–4, 184 Pityriasis versicolor, 62, 74
Parkinsonism, 305, 306, 371 rub, 183, 185 Placental circulation, 397, 397
Parkinson’s disease, 20, 342, 368, 371 Perilymph, 353 Plantar flexion, 299, 302
Paronychia, 79, 79 Perinephric abscess, 21 Plantar response, 367–8, 368
Paronychium, 59 Periostitis Plantaris, 300
Parotid duct, 98 clubbing, 80 Plaque, 62, 69
Parotid glands, 98, 186 in Graves’ disease, 31 Plateau pulse, 160
Paroxysmal nocturnal dyspnoea, 114–15, Peripartum cardiomyopathy, 182 Platysma, 350
153, 154 Peripheral cyanosis, 46, 46, 122, 157–8 Plegia, 363
Paroxysmal tachycardia, 156 Peripheral nerve injury, 377 Plethora, 45
Pars flaccida, 89 Peripheral neuropathy, 370 Pleural effusion, 47, 133, 134, 135
Pars tensa, 89 Peripheral oedema, 174–5 breath sounds, 131
433
Index
Pleural rub, 117, 132–3 Preauricular tags, 405 Psychosocial concerns of patients, 1–2, 4–5
Pleurisy, 115, 128 Precapillary pulmonary hypertension, 181 Pterygoids, 347
Pleuritic chest pain, 4, 117 Precordial catch syndrome, 155 Ptosis, 124, 336, 337
Plummer’s nails, 79 Precordium palpation, 166, 166–7 Puberty, 393, 393, 417, 417–18
Pneumoconiosis, 120 Pregnancy delay in, 417–18
Pneumonia abdomen in, 243, 243 female, 226–9, 227
atypical, 133 cervix during, 247 male, 252–4, 253
bronchial breathing, 131 height of fundus in, 243, 243 Pubic hair
causes of, 133 and nausea, 196 failure to develop, 60
crackles, 132 secondary amenorrhoea, 239 growth, 227, 227, 253, 253
lobar, 133 skin colour during, 61 lice, 75
pleuritic chest pain, 117 Prepuce, 254, 258 Pubic tubercle, 204
sputum in, 116 Presbyacusis, 85 Pubocervical fascia, 238
Pneumothorax, 126, 128, 135, 135 Preschool children, 412–14 Pulmonary embolism, 113, 114
chest percussion, 130 Preshock, 44 acute massive, 180–1
pleuritic chest pain, 117 Pressure load, heart, 142, 143 breathing pattern, 126
Podocytes, 192–3 Pressure sores, 81 deep vein thrombosis, 180
Polycystic kidney disease, 174, 217 Presystolic accentuation, 172 haemoptysis, 117
Polycythaemia, 45, 122 Preterm babies, 403 heart sounds, 169
Polycythaemia rubra vera, 45 Pretibial myxoedema, 80 pleuritic chest pain, 117
Polydipsia, 8, 10 in Graves’ disease, 31 Pulmonary hypertension, 181
Polymenorrhagia, 239 Priapism, 259 Pulmonary infarction, acute, 180
Polymenorrhoea, 239 Primary chancre, 72, 72, 73 Pulmonary oedema, 115
Polyuria, 8, 193, 203 Primitive reflexes, 313–14, 314, 317, 402, 402 in acute heart failure, 175, 175
cranial diabetes insipidus, 40 Primordial follicle, 228 breathing patterns, 127
diabetes mellitus, 10 Prinzmetal’s angina, 154 crackles, 132
Pompholyx, 68, 69 Problem-orientated medical record (POMR), in heart disease, 117
Popliteal lymph nodes, 52, 55 12, 13 sputum in, 116
Popliteal palsy, 303 advantages of, 16–17 wheezing, 132
Popliteal pulse, 161, 161 confidentiality, 17 Pulmonary thromboembolic disease, chronic,
Porphyria of drugs, 60 flow charts, 15–16, 17, 18 181
Portal hypertension, 201 initial problem-related plans, 14–15, 16 Pulmonary valve, 142, 143
fluid retention, 47 problem list, 13–14, 14, 15 incompetence, 172
in hepatic encephalopathy, 213 progress notes, 15, 17 stenosis, 144, 171
venous collaterals in, 201 Progesterone, 228 Pulses, 151–2, 152
venous return in, 207 Progress notes, 15, 17 character, 159
Portal venous system, 190, 190 Progressive supranuclear palsy, 342, 343 palpation, 159–61, 159–61
Portosystemic shunting, 201 Prolactin, 38, 39, 230, 231 rate assessment, 44
Positional dyspnoea, 153 overproduction, 39, 40 Pulsus paradoxus, 123, 183, 184, 184
Posseting, 400 Pronator, 284 Punch tenderness, kidneys, 217, 217
Post pill amenorrhoea, 239 Proprioception, 375, 378–9, 379 Pupillomotor fibres, 332
Post-term babies, 403 Prostate gland, 252, 255 Pupils, 340–1
Postauricular lymph nodes, 53 anatomy, 222 inspection, 337
Postcapillary pulmonary hypertension, 181 examination, 223, 224, 225 light response pathway, 332, 334, 337
Postcoital bleeding, 239, 240 Prosthetic heart valve sounds, 170, 170 responses, 384, 384–5, 388
Posterior columns, 375 Protein digestion, 189, 189 syndromes, 339
Posterior pituitary, 38 Proteolysis, 189 Purpura, 62
Postmenopausal bleeding, 240 Protozoan diseases, travel-related, 6 Pustular psoriasis, 69, 70
Postnasal mirror, 101 Proverb interpretation, 311 Pustules, 64, 64
Postoperative endocarditis, 182 Pruritus, 59, 60, 202 Pyelonephritis, 21, 203, 217
Postural hypotension, 9, 157, 163 Pseudo-Cushing’s syndrome, 36 Pyloric obstruction, 219, 219
in dehydrated patients, 44 Pseudoathetosis, 379, 379 Pyoderma gangrenosum, 80
in hypoadrenalism, 37 Pseudobulbar palsy, 315 Pyosalpinx, 250
in shock, 44–5 Pseudohypertrophic muscles, 273, 304, 304, Pyramidal tract, 359–60, 360, 364, 364
Posture 362, 363 Pyrexia see Fever
abnormal, 20 Pseudomonas ear infection, 84 Pyridoxine deficiency, 43
compensatory, 293 Psoas major, 291, 292
hospitalised patients, 21
Potassium
Psoriasis, 57, 68–70, 69, 287, 288
ear signs, 87
Q
in hypoadrenalism, 37 guttate, 59, 69, 69 QRS complex, 145, 145
loss, 36 nail symptoms, 79, 79 Quadriceps femoris, 295, 298
Pott’s fracture, 301 Psoriatic arthropathy, 70, 70 Questioning patients, 3, 4
Pouch of Douglas, 221, 236 Psychiatric assessment, 317–20 see also Consultation; History-taking
Pout, 314 clinical application, 319–20 Quinsy, 102
PR interval, 145 examination, 319
Praxis, 313
Pre-pro-PTH, 33–4, 34
history, 319
history of present condition, 317
R
Preauricular lymph nodes, 52, 52, 53 specific symptoms, 317–18 Radial nerve palsy, 286, 286
Preauricular sinus, 87, 87 Psychosexual history, 241 Radial pulse, 159, 159, 274
434
Index
Radiography of respiratory system, 105, Refractive visual disturbances, 23 Rigors, 50

106, 118 Reiter’s syndrome, 256, 256, 259 Ringworm, 74, 74
Radius, 282 Relationship, doctor-patient, 1 Rinne test, 90–1, 91, 92
Raised intracranial pressure, 328 Relative afferent pupillary defect, 341 Risk-taking behaviour, 416
Ramsay Hunt syndrome, 74, 352, 352 Remote memory, 311 Rodent ulcer, 77, 77
Rapport, establishing a, 3 Renal artery bruit, 174 Romberg’s test, 306, 379
Rashes, 59–60 Renal colic, 197, 203 Root syndromes
babies, 407 Renal failure cervical, 278, 284
infants, 410, 410 acute, 215–16 lumbar, 278, 298, 299, 303
nutritional deficiency, 42, 42 chronic, 34, 217 sacral, 303, 303
skin examination, 10 Renal hypoperfusion, 47 Rosacea, 64, 64
Raynaud’s phenomenon, 122 Renin, 192 Rotation, 271–2
Re-entry phenomenon, 145–6, 147, 147, Renin-angiotensin system, 35–6, 36, 47, Rotator cuff, 279–80, 280
148 176 Roth spots, 181
Reading, 313 Repetition, 313 Runny nose, 95
Rebound tenderness, 198 Residual volume (RV), 110
Recall memory, 310
Recent memory, 310–11
Respiration, 108, 385, 386
Respiratory acidosis, 45, 112
S
Recording Respiratory alkalosis, 112 Saccadic eye movements, 334–5
examination, 13 Respiratory rate, 126 Sacral oedema, 175
history, 11, 12–13 adolescents, 418 Sacroiliac joints, 275, 276
medical interview, 10–19 in Cheyne–Stokes respiration, 385 Salivary fluid, 186
see also Problem-orientated medical record newborns, 400 Salivary glands, 98
(POMR) older babies and toddlers, 409 Salpingitis, 241, 250
Rectocoele, 238, 244–5 preschool children, 413 Saphenofemoral junction, 179
Rectum, 188 school-age children, 415 Sarcoidosis, 124
anatomy, 222 Respiratory system, 105–38 skin manifestations of, 80
bleeding, 199, 200, 200–1 chest examination, 125–33 Sarcomere, 267
examination, 221–3, 223, 224 common patterns of abnormality, 133–7 Sarcoptes scabei, 75
prolapsing, 238, 238 disease, 133, 400 Scabies, 75, 75
rectocoele, 238, 244–5 symptoms, 112–20 Scaphoid fractures, 288
temperature, 50 examination, 56, 120–5 Scapula, winging of the, 281, 282
Rectus muscles, 208 failure, bedside assessment, 137 Scapulothoracic joint, 279
Recurrent laryngeal nerve, 27 infants, 409–11 Scarlet fever, 59
palsy, 115, 355, 356 preschool children, 413 Scarring, 64, 64
Red eye, 22–3 review, 7 Schizophrenia, 320
Red nucleus, 373 structure and function, 105–12, 106, 107, School-aged children, 414–16
Red reflex, 402, 402 108, 109–11 Sciatic nerve, 275–6
Referred pain, 377 in the unconscious patient, 383 palsy, 294, 295, 295
Reflex(es) see also Lungs Sclera
and abnormal muscle tone, 361 Restrictive cardiomyopathy, 182 jaundice, 46, 61, 211
ankle, 32, 33, 366–7, 367 Reticuloendothelial cells, 192 reflex, 347
anus, 368 Reticulospinal tracts, 360, 361 Scleroderma, skin manifestations of, 80
biceps brachii, 365, 365 Retinal artery occlusion, 329, 329 Sclerosants, 179
brainstem, 387, 388 Retinal nerve fibres, 322, 322, 323 Sclerotomes, 267, 377
cornea, 347, 347, 349, 388 Retinal vascular disease, 329, 329–30, 330 Scoliosis, 126, 274, 274
cough, 106 Retinal vein occlusion, 329, 329 Scotomas, 325, 326, 331, 331
cremasteric, 367 Rheumatic fever, acute, 182–3 Scrotum, 252, 253, 255, 255
deep tendon, 365–7, 365–7 Rheumatoid arthritis, 277, 278 abnormalities, 260, 261
fingers, 366, 366 foot, 302, 302 examination, 260–3
gag, 354, 355, 355, 388 interphalangeal joints, 287, 287 hernia, 258, 258, 260
grasp, 314, 314, 317 pain, 268 oedema, 263
hung up, 373 swelling, 270 swellings, 260–2, 261
knee, 366, 366 Rheumatoid nodules, 282, 300 Sebaceous cysts, 244, 260
light, 82, 89, 89 Rhinitis, 115 Sebaceous glands, 58
Moro, 402 Rhinitis medicamentosa, 98 Seborrheic dermatitis, 68, 68, 96
newborn, 402, 402 Rhinophyma, 96 Sebum, 58
oculocephalic, 338, 338, 385 Rhinorrhoea, 95 Second heart sound, 168–9
palmomental, 314, 317 Rhinoscopy, 101 Secretin, 189, 192
primitive, 313–14, 314, 317, 402, 402 Riboflavin deficiency, 43 Secretory otitis media, 89–90, 90
red, 402, 402 Riedel’s lobe, 210–11, 211 Self-harm, deliberate, 416
sclera, 347 Right bundle branch block, 144 Semicircular canals, 82–3, 353
startle, 402 Right-left orientation/disorientation, 313, Semilunar cartilages, 295, 297–8
stretch, 361, 361 316–17 Semilunar valves, 142, 143
suckling, 314, 317 Right to left shunt, 150–1, 151 Semimembranosus, 292
supinator, 365–6, 366 Right ventricle, 139, 139, 140 Seminal vesicles, 252, 255, 255
triceps, 366, 366 failure, 173–4 Seminiferous tubules, 252, 254, 254, 255
vestibulo-ocular, 388 hypertrophy, 123, 165, 167 Semitendinosus, 292
Reflux, 194 Rigidity, 362, 363 Senile keratosis, 81
435
Index
Sensorimotor neuropathy, hereditary, 292 Smell, 321–2 Squamous cell carcinoma

Sensorineural deafness, 85 loss of, 94 ears, 87
Sensory system, 374–82 Smith’s fracture, 285 skin, 77, 77
clinical application, 380–2 Smoking see Tobacco smoking Square hand, 288, 288
disturbances, 376, 377 Snail-track ulcers, 72 Squint, 338, 412
examination, 377–80, 378 Snellen chart, 323, 324 ST segment elevation myocardial infarction
Septic arthritis, 268 Snoring, 118 (STEMI), 177
Septum, nasal, 93 Snout reflex, 317, 389 Stapedius, 351
perforation, 96–8 Social history, 5 Stapes, 82, 353
Serratus anterior, 229 children, 391 Staphylococcal skin infection, 407, 407
Sertoli cells, 252, 254 respiratory disease, 118–20 Staphylococcus aureus, 181
Setting for examination, 22 Sodium retention, 36, 47 furuncle, 72
Sex hormone-binding globulin (SHBG), Soleus, 299, 300 impetigo, 72
252–3 Somatostatin, 38, 189 Starling forces, 47, 47
Sexual activity, 8 Sore throat, 100 Startle reflex, 402
Sexual arousal, 254–5 Sound waves, 353 Stasis oedema, 175
Shape recognition, 380 Space of Disse, 190, 191 Static lung volumes, 109–10
Sharpey’s fibres, 266 Spasmodic torticollis, 357, 358 Static perimetry, 324
Sheehan’s syndrome, 40 Spastic gait, 305, 305 Stature, 21
Shingles, 62, 74 Spastic limbs, 363 Steatorrhoea, 8, 43, 192, 200
Shivering, 50 Spasticity, 361–2 Steele-Richardson-Olsczewski syndrome, 371
Shock, 164 Speculum examination, vaginal, 245–6, 246, Sternoclavicular joint, 279
clinical assessment of, 44–5 247 Sternomastoid, 356
Short stature, 21 Speech, 309, 310, 311–13, 315, 372 Steroid hormones, 35–6
Shotty lymph nodes, 53 development, 408 Stethoscope, 20, 130, 130, 167–8
Shoulder, 266, 279–81 impediment, 9 Stevens-Johnson syndrome, 66, 66
dislocation, 279, 279, 280–1 see also Dysarthria Stoke-Adams attack, 156
inspection and palpation, 279 Spermatic cord, 220, 255 Stomach, 187, 187
movement, 279–81, 280 Spermatogenesis, 254 Stomatitis, angular, 42
muscle function, 281, 281 Spermatozoa, 254 Stones
structure and function, 279 Sphenopalatine ganglion, 349 kidney, 34
Shunting, intracardiac, 149, 149–51 Sphygmomanometer, 161, 162 ureteric, 197
Sigmoid colon, 188 Spider naevi, 62, 63, 211–12 Stool output, 190
abdominal palpitation, 208 Spinal cord, 360–2 Strabismus, 338
Silent chest, 130 disorders, 380–1, 381 Straight leg raising, 275–6
Silver poisoning, 46 Spinal roots, 375, 375, 376 Strawberry naevus, 405
Sinoatrial node, 144, 144 see also Nerve root disorders; Root Streptococcal infection, 59
Sinuses, paranasal see Paranasal sinuses syndromes beta-haemolytic, 182
Sinusitis, 98 Spinal trigeminal tract, 345–6, 346 Streptococcus pneumoniae, 181
Sinusoids, hepatic, 190, 190, 191 Spine Streptococcus pyogenes, 72
Size recognition, 380 cervical, 274–5, 275 Streptococcus viridans, 181
Skeletal system in the unconscious patient, conditions, 277–9, 278 Stress incontinence, 203
383 deformities, 274, 274 Stretch marks, 206, 206
Skin disease, 117 Stretch reflex, 361, 361
abdominal examination, 206, 206–7 examination, 274 Stretch tests, 275–6, 277
appendages, 58 GALS, 272 Striae gravidum, 206, 206
assessment for dehydration, 44, 44, 63 lumbar, 275, 275, 276 Stridor, 100, 117, 127, 132, 133
changes nerve stretch tests, 275–6, 277 Structural coma, 385, 386–7, 387
ear, 87–8 pain, 267 Students, medical, 10
in elderly people, 81 prolapsed intervertebral disc, 276–7 Stye, 72
colour, 45, 45–6, 57, 61–2 sacroiliac joints, 275, 276 Subclavian vein, 51, 51
in peripheral vascular disease, 174 structure and function, 274 Subconjunctival haemorrhage, 23
disease, 59–60 thoracic, 275, 276 Subcostal plane, 205, 205
examination, 56, 61–71, 63 traumatic lesions, 279 Subluxation, 269
infections, 71–8 tumours, 277 Submandibular glands, 98
joint examination, 270 Spinocervical tract, 375–6, 377 Submandibular lymph nodes, 52, 52, 53, 54
manifestations of systemic disease, 78, 80 Spinothalamic tract, 375, 377 Submaxillary lymph nodes, 52, 52
pigmentation see Pigmentation Spirometry, 105, 109 Submental lymph nodes, 52, 52
in respiratory disease, 124, 124 Spleen, 51, 51, 192 Substantia gelatinosa, 376, 377
review, 10 auscultation, 220 Subtalar joint, 299, 300, 301
staphylococcal infection, 407, 407 enlarged, 174, 215, 215 Succussion splash, 219, 219
structure and function, 57–8, 58 examination, 204, 204 Suckling, 230, 231
temperature in peripheral vascular disease, palpation, 214, 214–15, 215 Suckling reflex, 314, 317
174 percussion, 215, 215 Sulphonamides, skin reactions to, 64, 65
Skinfold thickness, triceps, 43, 43 Splenomegaly, 174, 215, 215 Sunburn, 46, 60
Skull compression, 274–5, 275 Splinter haemorrhages, 79, 158, 158 Superior laryngeal nerve, 27
Sleep apnoea syndrome, 118 Spondylosis, 303 Superior mesenteric vessels, 187
Slow twitch fibres, 267 Spurious diarrhoea, 200 Superior vena cava obstruction, 123, 123,
Small intestine, 187–9, 188, 189 Sputum, 115–16 133, 166
436
Index
Supinator, 284 response to, 380 overactive, 10

reflexes, 365–6, 366 skin, 174 palpation, 29, 30
Suppurative otitis media, 89 Temporal lobe, 307, 308, 331 position of, 27
Supraclavicular lymph nodes, 54, 54, 123, 124 Temporalis, 346, 347, 348 structure and function, 27
Supraglottitis, 103 Temporomandibular joints, 274 thyroxine synthesis and secretion, 27–8
Supranuclear palsy, 371 Tendocalcaneus, 300 underactive, 10
Supraspinatus, 279, 281 Tendon reflexes, deep, 365–7, 365–7 see also Graves’ disease; Hyperthyroidism;
Supratentorial masses, 386–7 Tendonitis, bicipital, 280 Hypothyroidism
Surface markings Tenesmus, 199 Thyroid releasing hormone (TRH), 28
bone, 265 Tennis elbow, 282 Thyroid stimulating hormone (TSH), 27–8,
kidneys, 216 Tenosynovitis, 280 28, 38
lungs, 105, 107 De Quervain’s, 270, 271, 284 failure, 40, 41
Surgical emphysema, 126 Tension headaches, 321 Thyroid storm, 31–2
Surgical incisions, 158, 158 Tension pneumothorax, 135 Thyrotoxicosis, 30, 31
Surgical scars, 207, 207 Terminal dribbling, 8 Thyroxine (T4), 27–8, 28, 29
Swallowing, 187 Terminal hair, 58 Tibialis anterior, 299, 300
difficulty see Dysphagia Terminal ileum, 189 Tibialis posterior, 299, 303
pain on see Odynophagia Testes, 252, 254, 255, 255 Tibialis posterior pulse, 161, 161
thyroid examination, 29 examination, 260, 260 Tics, 353, 369
Swan neck deformity, 269–70, 270 histology of the, 254 Tidal percussion, 130
Sweat glands, 58 in infants, 411 Tietze’s syndrome, 117, 128, 155
Sweating, 50, 58, 124 pain in, 257 Time management, consultation, 2, 10
dehydration, 44 palpation, 260, 260 Tinea, 74, 74
Swinging light test, 341 position of, 27 Tinea versicolor, 62, 74
Sydenham’s chorea, 371 swollen, 262 Tinel’s sign, 290
Sympathetic tone, 145 torsion of the, 263, 263 Tinnitus, 9, 86
Symphysis pubis, 235–6 tumour, 262 Tissue pressure, 47
Symptoms, establishing, 4 Testosterone, 252–3, 253 Tobacco smoking, 119
Synarthroses, 266–7 Tetraplegia, 126, 363 history taking, 6
Syncope, 8, 156–7 Texture, appreciation of, 380 respiratory disease, 118
Syndactyly, 406 Thalamic pain, 377 Toddlers, 407–12
Syndrome X, 154 Thalamus, 376 see also Infants
Syndromes, 22–7 disorders, 381 Tongue, 99
Synovial fluid, 266 Thenar eminence muscles, 286, 289, 289 assessment for dehydration, 44
Synovial joint, 266, 266 Thermocouple, 50 examination, 102, 357–8, 358
Synovial membrane, 266 Thermometers, 49, 50 paralysis, 357
Syphilis, 72, 72, 73, 244, 245, 259, 259 Thermoreceptors, 374–5 percussion myotonia, 364, 365
oral ulceration, 101 Thiamine, 43 Tonic pupil syndrome, 340–1, 341
Syringing, ear, 88 Third heart sound, 169 Tonsillar lymph nodes, 52, 52, 53
Systemic disease, skin manifestations of, 78, Thomas’ test, 292, 293 Tonsillitis, 102
80 Thoracic duct, 51, 51 Tonsils, 51, 51, 99
Systemic lupus erythematosus, 60, 80 Thoracic myelocele, 405 examination, 102
Systemic veins, 152 Thoracic outlet syndrome, 290 unilateral enlargement of, 102
Systems review, 7–10 Thoracic spine, 275, 276, 279 Topical steroids, 60
see also specific system Thoracoplasty, 125, 125 Torticollis, spasmodic, 357, 358
Systolic murmurs, 170, 171–2 Thoughts, abnormal, 318 Total lung capacity (TLC), 109–10
Thrills, 167 Toxic adenoma, 30
T Throat, 98–103
disease symptoms, 100–1
Toxic erythema, 65, 65
Trachea palpation, 127, 127–8
T lymphocytes, 51, 106–8 elderly people, 103 Tracheitis, 115
T wave, 145 examination, 56, 101–2, 101–3 chest pain, 117
Tachycardia, 145, 146–8, 148, 156 sore, 100 Transcortical motor aphasia, 315–16
in acute heart failure, 175 structure of the, 98–100 Transcortical sensory aphasia, 316
heart sounds, 169 Thromboembolic disease, chronic Transfer factor (TF), 110–11
sustained, 147–8 pulmonary, 181 Transient ischaemic attack (TIA), 86
Tachypnoea, 115 Thrombophilia, 180 Transpyloric plane, 205, 205
Tail of Spence, 229, 229, 233, 233 Thrombophlebitis, 49, 179 Transtentorial herniation, 386, 387
Tall stature, 21 Thudicum speculum, 96, 97 Trapezius, 356, 357
Tamponade, cardiac, 183–4, 184 Thumb movements, 287 Traub’s space, 215
Tanner’s pubertal milestones, 226, 227, Thymus gland, 51, 51 Traumatic lesions
253, 253 Thyroglobulin, 28, 28 ankle, 301–2
Taste, 350, 351 Thyroglossal cyst, 27 elbow, 283
Teeth, 98, 99 Thyroid binding globulin (TBG), 28, 28 forearm and wrist, 285–6
Telangiectasia, 62, 62, 80 Thyroid gland, 27–33 hands, 288
Telarche, 226 anatomy and surrounding structures, 28 hip, 294–5
Telogen hair growth, 58 auscultation, 29, 30 knee, 298
Temperature cancer, 27, 29 shoulder, 280–1
body, 49–50, 50 clinical assessment of function, 29 spine, 279
joint, 270, 271 clinical examination and function, 28–9 Travel-related risks, 6
437
Index
Treatment, problem-orientated medical rodent, 77, 77 Vasoactive intestinal polypeptide (VIP), 189
records, 14 snail-track, 72 Vasodilatation, 49
Tremor, 122–3, 371, 373 varicose, 174, 179, 180 Vasomotor rhinitis, 98
flapping, 213, 213 vulva, 244 Vasovagal syncope, 156
thyrotoxicosis, 30, 31 Ulna, 282 Veins, 152, 153
Trendelenburg’s sign, 292, 293, 304 Ulnar nerve, 289, 289 chronic insufficiency, 179
Tri-iodothyronine (T3), 28, 29 lesions, 290, 290 diseases of peripheral, 179–81, 180
Triceps, 284 Ultrasound varicose, 174, 179
reflexes, 366, 366 abdominal, 174 visible abdominal wall, 207, 207
skinfold thickness, 43, 43 Doppler, 179 Vellus hair, 58
Trichomonas vaginalis, 241, 241 Umbilical hernia, 401, 401 Ventilation, 109, 111, 111
Tricuspid valve, 142 Umbo, 82, 89 Ventricles, 139, 139–40, 140, 141, 144
incompetence, 174 Uncal herniation, 386, 387 hypertrophy, 142
regurgitation, 165, 166 Unconscious patient, 382, 382–9 see also Left ventricle; Right ventricle
Trigeminal (fifth) nerve, 345–8, 345–9, 411 coma grading, 383, 383 Ventricular fibrillation, 148, 178
neuralgia, 321 Unilateral deafness, 85 Ventricular septal defect, 150, 150, 170
Trigger finger, 288, 288 Unstable angina, 154–5, 177–8 Verdoperoxidase, 116
Triglyceride, 51, 189 Upper limb deep tendon reflexes, 365–6, Vermis, 371
Trisomy 21, 23, 24, 24 365–6 Vernix caseosa, 58
Trochlear (fourth) nerve, 332–45, 411 Upper motor neuron, 359 Vertebrae see Intervertebral discs; Spine
palsy, 343, 344 facial weakness, 351, 352 Vertebral arteries, 308, 309
Trousseau’s sign, 34, 35 lesions, 358, 370 Vertebral body fractures, 279
Trypsin, 189 syndrome, 349 Vertebrobasilar insufficiency, 157
Tuberculosis, 105, 124, 278–9 Upper pharyngeal sphincter, 187 Vertebrobasilar ischaemia, 86
family history, 120 Ureteric pain, 198 Vertical saccades, 334–5, 336
haemoptysis, 117 Ureteric stones, 197, 203 Vertigo, 9, 86, 354
lung collapse, 136 Urethra, male, 254, 254 Vesicocele, 238
oral ulceration, 101 discharge, 256, 256, 258–9 Vesicular breath sounds, 130, 131
radiographic deformity, 118 Urethral meatus, external, 258 Vestibule, 353
Tuberculous epididymitis, 262, 263 Urethritis, 256, 259 see also Inner ear
Tuberculous lymph nodes, 124 Urgency of micturition, 202–3 Vestibulitis, 98
Tuberculous lymphadenitis, 53 Urinary incontinence, 8 Vestibulo-ocular reflex, 388
Tuberculous pericarditis, 184 Urination see Micturition Vestibulospinal tract, 360
Tuberous sclerosis, 23, 24, 25, 25 Urine Vibration sense, 379, 379
Tumours appearance, 8 Villous atrophy, 76
acidophil, 39 assessment for dehydration, 44 Vincent’s angina, 101
hypothalamic, 21 Urticaria, 65, 65 Viral infections
jugular foramen, 357 Uterosacral ligaments, 236, 238 skin, 72–4
laryngeal, 103 Uterus, 236, 237 travel-related, 6
ovarian, 250 abnormal bleeding, 240 Viral pericarditis, 184
pelvic, 242, 242 abnormalities, 249 Virchow’s node, 54
skin, 62, 77–8, 77–8 examination, 248–50 Visceral pain, 197–8, 198, 376–7
spinal, 277 palpation, 218, 249, 249 Vision
testicular, 262 prolapse, 245, 246 cranial nerve symptoms, 9
Tunica albuginea, 255 double see Diplopia
Tuning forks tests, 90–1, 91
Turbinates, 93
V in elderly people, 18
red eye, 23
Turner’s syndrome, 23, 24, 24, 238, 405 Vagal tone, 145 Visual acuity, 323–4, 324
Two-point discrimination, 378, 378 Vagina, 236, 237 test, 23
Tylosis, 80 discharge, 240–1 Visual agnosia, 317
Tympanic membrane, 82, 83, 88, 89, 89, examination, 244–6, 246, 247, 248 Visual cortex, 322
353 swabs, 248 Visual fields, 324–6, 325, 326
perforation, 90, 90 Vaginismus, 241 Visual hallucinations, 318
Tympanometry, 89, 90 Vaginitis, 241 Visual memory, 310–11, 311
Tympanosclerosis, 89 Vagus (tenth) nerve, 186, 187, 187, 355–6, Visuospatial ability, 308
Typhoid fever, 50 411 Vital capacity (VC), 110
damage, 194 Vitamin deficiencies, 43
U palsy, 355, 356
Valsalva manoeuvre, 156
Vitamin status, 43–4
Vitiligo, 62, 62
Ulcerative colitis, skin manifestations of, Valves, heart, 142, 142 in Addison’s disease, 37
80 Varicella-zoster virus, 74 Vocal cords, 100, 100
Ulcers Varicoceles, 258, 261–2, 262 paralysis, 315
aphthous, 101 Varicose eczema, 68, 179 Vocal fremitus, 128
buccal mucosa, 101–2 Varicose ulcers, 174, 179, 180 Vocal resonance, 131–2
decubitus, 81 Varicose veins, 174, 179 Voice
genital, 256, 259 Vas deferens, 255, 255 hoarse, 100–1
oral, 101 Vasculitis in hypothyroidism, 32
penis, 259, 259 erythema nodosum, 65 tone of, 20
peptic, 197 splinter haemorrhages in, 79 Volume load, heart, 142, 142
438
Index
Vomiting, 196, 196 Water-soluble vitamin deficiency, 43 Wheals, 62, 65, 65

dehydration, 44 Waterbrash, 7, 194 Wheezing, 117, 127, 132, 133
in infants, 411 Wax, ear, 82, 84, 88, 88 systems review, 7
newborns, 400 Weakness, muscle see Muscle(s), Whispering pectoriloquy, 131–2
systems review, 8 weakness White coat hypertension, 163
Von Recklinghausen’s disease, 76 Weber test, 90–1, 91 White lesions, buccal mucosa, 102
Vulva, 235–6 Weed, Lawrence, 12 Wickham’s striae, 70–1
abnormalities, 244 Weight Wind, 199
examination, 243, 243–4, 244 appreciation, 380 Wolff-Parkinson-White syndrome, 147
ulceration, 244 change, 7 Wood’s lamp, 61
Vulvitis, 244 at gestation, 403 Wrist, 283–6, 285, 286
loss Wrist drop, 286, 286
W diabetes mellitus, 10
gastrointestinal disease, 195
Writing, 313
Waardenburg’s syndrome, 23, 26, 26 general examination, 42

Waddling gait, 306
Warts, 72–3, 73
lung cancer, 118
norms in adults, 41, 41
X
Wasting, muscle see Muscle(s), wasting Wernicke’s aphasia, 316 Xanthelasmata, 80
Water drinking, compulsive, 40 Wernicke’s area, 308, 310 Xanthomas, 26, 27
Water retention, 47 Wernicke’s encephalopathy, 386 Xiphisternum, 204–5
ERRNVPHGLFRVRUJ
439

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Clinical Examination

June, Daniel, Marc, Morris and Nancy

Commissioning Editor: Laurence Hunter

G. David Perkin BA MB MRCP

John Cookson MD FRCP

Ian S. Watt BSc MB ChB MPH FFPH

Roby Rakhit BSc MD MRCP

Andrew Robins MB MSc MRCP FRCPCH

Graham A. W. Hornett MA MB BChir FRCGP

First edition 1992

British Library Cataloguing in Publication Data

Library of Congress Cataloging in Publication Data

Working together to grow

1. Consultation, medical history 4. Ear, nose and throat 82

12. Infants and children 390

Examination of elderly people

Symptoms and signs

1 Consultation, medical history and record taking

your headaches stop you from doing?’, and ‘What do you

Gathering information: the history 1

Initial rapport H.M., aged 57, housewife

1 Consultation, medical history and record taking

• What concerns you most about the headaches?

• Myocardial ischaemia – pressure, crushing, pressing

Gathering information: the history 1

of an illness for each individual. Combining information

1 Consultation, medical history and record taking

CARDIOVASCULAR SYSTEM Pain

Chest pain If the patient complains of localised chest pain, ask

1 Consultation, medical history and record taking

Abdominal pain incontinence without warning? Does coughing or

Dizziness and vertigo Diplopia

1 Consultation, medical history and record taking

Recording the medical interview 1

Mrs G. W. 76-year-old female Allergies: None known

Social history: Cardiovascular system:

1 Consultation, medical history and record taking

PROBLEM-ORIENTATED MEDICAL RECORD

Recording the medical interview 1

The structure of problem-orientated medical record

Progress notes Problem-related plans Flow chart

Fig. 1.7 Structure of the problem-orientated medical record (POMR).

1 Consultation, medical history and record taking

Initial problem list

Patient’s name: Hospital no:

No. Active problems Date Inactive problems Date

jaundice (Jan ‘07) 9/1/07

anorexia (Dec ‘06) 9/1/07

weight loss 9/1/07

recurrent rectal bleeding 9/1/07

smoking (since 1980) 9/1/07

unemployed (Nov ‘06) 9/1/07

brother died of colon cancer – patient concerned he may 9/1/07

duodenal ulcer (1996) 9/1/07

Fig. 1.8 Problem list entered on 9 January 2007.

Recording the medical interview 1

Updated problem list

Patient’s name: Hospital no:

No. Active problems Date Inactive problems Date