Clinical

Examination

John Macleod

(1915–2006)

John Macleod was appointed consultant physician at the Western General Hospital, Edinburgh, in 1950. He had major interests in

rheumatology and medical education. Medical students who attended his clinical teach ing sessions remember him as an inspirational

teacher with the ability to present complex problems with great clarity. He was invariably courteou s to his patients and students alike. He

had an uncanny knack of involving all students equally in clinical discussions and used praise rather than criticism. He paid great

attention to the value of history taking and, from this, expected students to identify what particu lar aspects of the physical examination

should help to narrow the diagnostic options.

His consultant colleagues at the Western welcomed the opportunity of contributing when he suggested writing a textbook on clinical

examination. The book was first published in 1964 and John Macleod edited seven editions. With characteristic modesty he was very

embarrassed when the eighth edition was renamed Macleod’s C linical Examination. This, however, was a small way of recognisin g his

enormous contribution to medical education.

He possessed the essential quality of a successful editor – the skill of changin g disparate contributions from individual contributors into a

uniform style and format without causing offence; everybody acce pted his authority. He avoided being dogm atic or condescending. He

was generous in teaching others his editorial skills and these attributes were recognised w hen he was invited to edit Davidson’s

Principles and Practice of Medicine.

For Elsevier

Content Strategist: Laurence Hunter

Content Development Specialist: Helen Leng Project Manager: Louisa Talbott

Designer/Design Direction: Miles Hitchen Illustration Manager: Jennifer Rose

Graham Douglas BSc(Hons) MBChB FRCPE

Consultant Physician Aberdeen Royal Infirmary Honorary Reader in Medicine Univer sity of Aberdeen

Fiona Nicol BSc(Hons) MBBS FRCGP FRCP(Edin) Formerly GP Principal and Trainer Stock bridge Health Centre, Edinburgh

Honorary Clinical Senior Lecturer University of Edinburgh

Colin Robertson BA(Hons) MBChB FRCPEd FRCSEd FSAScot Honorary Professor of Accident and Emergency Medicine

University of Edinburgh

Illustrations by Robert Britton Ethan Danielson

Edinburgh London New York Oxford Philadelphia St Louis Sydney Toron to 2013

Thirteenth edition

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including

photocopying, recording, or any information storage and retrieval system, without permiss ion in writing from the publisher. Details on

how to seek permission, further information about the publisher’s permissions policies an d our arrangements with organisations such as

the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our w ebsite: www.elsevier.com/permissions.

This book and the individual contributions contained in it are protected under copyright by the publisher (other than as may be noted

herein).

First edition 1964 Second edition 1967 Third edition 1973 Fourth edition 1976 Fifth edi tion 1979 Sixth edition 1983 Seventh edition

1986

ISBN 9780702047282 International ISBN 9780702047299 Eighth edition 1990 Ninth edition 1995 Tenth edition 2000 Eleventh edition

2005 Twelfth edition 2009 Thirteenth edition 2013

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

Notices

Knowledge and best practice in this field are constantly changing. As new research and experien ce broaden our understanding, changes

in research methods, professional practices, or medical treatment may become necessary .

Practitioners and researchers must always rely on their own experience and knowledge in ev aluating and using any information,

methods, compounds, or experiments described herein. In using such information or method s they should be mindful of their own safety

and the safety of others, including parties for whom they have a professional responsibility.

With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on

procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the

method and duration of administration, and contraindications. It is the responsibility of practi tioners, relying on their own experience and

knowledge of their patients, to make diagnoses, to determine dosages and the best tr eatment for each individual patient, and to take all

appropriate safety precautions.

To the fullest extent of the law, neither the publisher nor the authors, contributors, or editors , assume any liability for any injury and/or

damage to persons or property as a matter of products liability, negligence or otherwis e, or from any use or operation of any methods,

products, instructions, or ideas contained in the material herein.

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publisher’s policy is to use www.elsevier.com | www.bookaid.org | www.sabre.org

paper manufactured from sustainable forests Printed in China

Preface

The skills of history taking and physical examination are central to the practice of clinical medicine. This book describes these and is

intended primarily for medical undergraduates. It is also of value to primary care and postgraduate hospital doctors, particularly those

studying for higher clinical examinations or returning to clinical practice. The book is also an essential reference for nurse practitioners

and other paramedical staff who are involved in medical assessment of patients .

This edition has four sections: Section 1 details the principles of history taking and general examination; Section 2 c overs symptoms and

signs in individual system examinations; Section 3 reviews specific situations; and a new Section 4 deals with how to apply these

techniques in an OSCE.

The text has been extensively revised and edited, with two new chapters on the frail elderly and the febrile adult. The number of

illustrations has been increased and many have been updated. Line drawings illustrate surface anatomy and techniques of examination;

over 330 photographs show normal and abnormal clinical appearances.

We recognise the current debate where some decry clinical examination b ecause of the lack of evidence supporting many techniques.

Where evidence exists, however, we highlight this in a new feature for this editio n: evidence-based examination boxes (EBEs). We are

convinced of the need to acquire and hone clinical examination skills to avoid unnecessary expen sive and potentially harmful over-

investigation. Nevertheless, there is a need to evaluate rigorously many clinical symptoms and signs. It is possible to open this book at

almost any page and find a topic which cries out for evidence-based analysis. We continue to hope that the book will stimulate this

enquiry and would encourage these responses and incorporate them in future editions.

This 13th edition of Macleod’s Clinical Examination – full text, illustrations and videos – is availab le in an online version, as part of

Elsevier’s ‘Student Consult’ electronic library. It is closely integrated with Davidson’s Principles and Practice of Medicine, and is best

read in conjunction with that text.

G.D. F.N. C.R.

Edinburgh and Aberdeen 2013 v

Acknowledgements

We are very grateful to all the contributors and editors of previous editions; in pa rticular, we owe an immeasurable debt to Dr John

Munro for his teaching and wisdom.

We greatly appreciate the constructive suggestions and help that we have rece ived from past and present students, colleagues and focus

groups in the design and content of the book.

We are particularly grateful to the following medical students who undertook de tailed reviews of the book and gave us a wealth of ideas

to implement in this latest edition: Alessandro Aldera, University of Cape Town; Sabreen Ali, University of Sheffield; Bernard Ho, St

George’s University of London; Edward Tzu-Yu Huang, University of Birmingh am; Emma Jackson, University of Manchester; Amit

Kaura, University of Bristol; Brian Morrissey, University of Aberd een; Neena Pankhania, University of Leicester; Tom Paterson,

University of Glasgow; Christopher Roughley, University of Warwick; and Chr istopher Saunders, University of Edinburgh.

We wish to thank the many individuals who have provided advice and support: Jackie Fiddes for designing the manikins and fo r her

computer skills; Steven Hill of the Department of Medical Illustration, University of Aberdeen; Jason Powell for his help with

illustrations; Victoria Buchan for her help linking the examination videos w ith the online text; Helen Leng and Laurence Hunter at

Elsevier.

G.D. F.N. C.R.

Picture and box credits

We are grateful to the following individuals and organisations for permission to re produce the figures and boxes listed below:
Chapter 1
Fig. 1.1 WHO Guidelines on Hand Hygiene in Health Care First Global Patient Safety Challenge C lean Care is Safer Care
http://www.who.int/gpsc/clean_hands_ protection/en/ © World Health Organization 2009. All r ights reserved. Box 1.1 Courtesy of the
General Medical Council (UK).
Chapter 2
Box 2.32 Trzepacz PT, Baker RW, The psychiatric mental status examination 1993  by permission of Oxford University Press USA. Box
2.50 Hodkinson HM, Evaluation of a mental test score for assessment of mental im pairment in the elderly Age and Ageing 1972 1(4):
233-8 by permission of Oxford University Press.
Chapter 3
Figs 3.19C and 3.28A–D Forbes CD, Jackson WF. Color Atlas of Clinical M edicine. 3rd edn. Edinburgh: Mosby; 2003.
Chapter 5
Fig. 5.3 Currie G, Douglas G, eds. Flesh and Bones of Medicine. Edinburgh: Mos by; 2011.
Chapter 6
Figs 6.6D, 6.16A–D and 6.38A Forbes CD, Jackson WF.
Color Atlas of Clinical Medicine. 3rd edn. Edinburgh: Mosby; 2003. Fig. 6.6E  Colledge NR, Walker BR, Ralston SH, eds. Davidson’s
Principles and Practice of Medicine. 21st edn. Edinburgh: Churchill Livingstone; 2010. Fig . 6.8C Haslett C, Chilvers ER, Boon NA,
Colledge NR, eds, Davidson’s Principles and Practice of Medicine, 19
th
 edn. Edinburgh: Churchill 
Livingstone; 2002. Box 6.19 Reproduced by kind permission of the British Hypertension S ociety.
Chapter 7
Fig. 7.24D Forbes CD, Jackson WF. Color Atlas of Clinical Medicine. 3rd edn . Edinburgh: Mosby; 2003. Box 7.7 Reproduced from
British Medical Journal Fletcher CM, Elmes PC, Fairbairn AS et al 2(5147):257 1959 w ith permission from BMJ Publishing Group Ltd.
Box 7.11 Reproduced from Murray W. Johns. A new method for measuring da ytime sleepiness: the Epworth Sleepiness Scale, Sleep,
1991; 14(6): 540-545. ESS contact information and permission to use: MAPI  Research Trust, Lyon, France. E-mail:
PROinformation@mapi-trust.org Internet: www.
mapi-trust.org. Box 7.17 Reproduced from Thorax Lim WS 58(5):377 2002 with permissio n from BMJ Publishing Group Ltd. Box 7.23
Reproduced from Wells PS, Anderson DR, Rodger M et al, 2000 
Derivation of a Simple Clinical Model to Categorize Patients Probability of Pulmonary Embo lism: 
Increasing the Models Utility with the SimpliRED D-dimer, Thromb Haemost 83(3) 416-420 wi th 
permission from Schattauer Publishers.
Chapter 8
Fig. 8.10 Reproduced by kind permission of Dr K W Heaton, Reader in Medicine at  the University of 
Bristol. © 2000 Norgine Pharmaceuticals Ltd. 
Figs 8.31A&B and 8.32 Forbes CD, Jackson WF. Color Atlas of Clinical Medicine.  3rd edn. Edinburgh: Mosby; 2003. Box 8.15
Reproduced by kind permission of the Rome Foundation. Box 8.20 Reprod uced from Journal of the British Society of Gastroenterology
Rockall TA et al 38(3):316 1996 with permission from BMJ 
Publishing Group Ltd. Box 8.34 Reproduced from Conn HO, Leevy CM, V lahcevic ZR et al 1977 
Comparison of lactulose and neomycin in the 
treatment of chronic portal-systemic encephalopathy. A double blind controlle d trial, Gastroenterology 72(4): 573 with permission from
Elsevier Inc. 
Box 8.47 Reproduced from Pugh RNH, Murray-Lyon IM, Dawson JL et al Tra nsection of the oesophagus for bleeding oesophageal
varices British Journal of Surgery 646-649 1973 with permission from John Wiley and  Sons.
Chapter 9
Fig. 9.12 Pitkin J, Peattie AB, Magowan BA. Obstetrics and Gynaecology: An Illustrated Colo ur Text. 
Edinburgh: Churchill Livingstone; 2003. Box 9.4
Reproduced from Barry MJ, Fowler FJ Jr, O’Leary MP et al The American Urological Associat ion symptom index for benign prostatic
hyperplasia. The 
Measurement Committee of the American Urological Association. J Urol. 1992 148(5):1549-5 7. ESS contact information and permission
to use: MAPI Research Trust, Lyon, France. E-mail: PROinformation@
mapi-trust.org Internet: www.mapi-trust.org
Chapter 11
Fig. 11.15 Epstein O, Perkin GD, de Bono DP, Cookson J. Clinical Examination. 2nd edn. London:  Mosby; 1997. Box 11.18 Medical
Research Council scale for muscle power. Aids to examination of the peripheral  nervous system. Memorandum no 45 London Her
Majesty’s Stationery Office 1976 © Crown Copyright.
vii

Chapter 12
Figs 12.15A &B Forbes CD, Jackson WF. Color Atlas of Clinical Medicine.  3rd edn. Edinburgh: Mosby; 2003. Fig. 12.16 Nicholl D,
ed. Clinical Neurology. Edinburgh: Churchill Livingstone; 2003. Figs 12.27A–D Ep stein O, Perkin GD, de Bono DP, Cookson J.
Clinical Examination. 2nd edn. London: Mosby; 1997.
Chapter 13
Fig. 13.20 Scully C, Oral and Maxillofacial Medicine. 2
nd
 edn. Edinburgh: Churchill Livingstone; 2008. Figs 13.21A and 13.25B Bull
TR. Color Atlas of ENT Diagnosis. 3rd edn. London: Mosby-Wolfe; 1995.
Chapter 14
Fig. 14.2 Colledge NR, Walker BR, Ralston SH, eds. Davidson’s Principles and Practice o f Medicine. 21st edn. Edinburgh: Churchill
Livingstone; 2010. Fig. 14.9A Forbes CD, Jackson WF. Color Atlas of Clin ical Medicine. 3rd edn. Edinburgh: Mosby; 2003. Box 14.3
Reproduced from Aletaha D, Neogi T, Silman AJ et al 2010 Rheumatoid arthritis c lassification criteria: an American College of
Rheumatology/ European League Against Rheumatism collaborative initiative, Arthritis  & Rheumatism 2569-2581 with permission from
John Wiley and Sons. Box 14.13 Reproduced from Annals of the rheumatic diseases  Beighton P, Solomon L, Soskolne CL 32(5): 413
1973 with permission from BMJ Publishing Group.
Chapter 15
Figs 15.7 , 15.8, 15.11A&B and 15.12 Lissauer T, Clayden G. Illustrated Textbook o f Paediatrics. 2nd edn. Edinburgh: Mosby; 2001.
Fig. 15.17 Child Growth Foundation. Fig. 15.23 Courtesy of Dr Jack Beattie, Royal Ho spital for Sick Children, Glasgow. Box 15.4
Reproduced with permission of International Anesthesia Research Society from Curr ent researches in anesthesia & analgesia Apgar V
32(4) 1953; permission conveyed through Copyright Clearance Center, Inc.
Chapter 16
Fig. 16.2 Reproduced from Clarifying Confusion: The Confusion Assessment Method: A N ew Method for Detection of Delirium Inouye
SK, vanDyck CH, Alessi CA et al Annals of Internal Medicine 113 1990 with permission from the Am erican College of Physicians. Fig
16.3 Reproduced by kind permission of BAPEN.
Chapter 19
Fig. 19.9 Reproduced with the kind permission of the Resuscitation Council (UK).  Box 19.1 Adapted from Hillman K, Parr M, Flabouris
A et al 2001 Redefining in-hospital resuscitation: the concept of the medical emergency  team. Resuscitation 48(2): 105-110 with
permission from Elsevier Ltd. Box 19.14 Reproduced from The Lancet 304(7872 ), Teasdale G, Jennett B, Assessment of coma and
impaired consciousness: a practical scale, 81–84, 1974 with permission from E lsevier Ltd.
viii
How to get the most out of this book
The purpose of this book is to document and explain how to:
• Talk with a patient
• Take the history from a patient
• Examine a patient
• Formulate your findings into differential diagnoses
• Rank these in order of probability
• Use investigations to support or refute your
differential diagnosis.
Initially, when you approach a section, we suggest that you glance through  it quickly, looking at the headings and how it is laid  out. This
will help you to see in your mind’s eye the framework to use.
Learn to speed-read. It is invaluable in medicine and in life generally. Most probably, the  last lesson you had on reading was at primary
school. Most people can dramatically improve their speed of reading and increase their comprehension by using and practisin g simple
techniques.
Try making mind maps of the details to help you recall and retain the inf ormation as you progress through the chapter. Each of the
systems chapters is laid out in the same order:
• Introduction and anatomy
• Symptoms and definitions
• The history: what questions to ask and how to
follow them up
• The physical examination: what and how to examine
• Investigations: those done at the patient’s side
(near-patient tests); laboratory investigations; imaging; and invasive investigations.

Your purchase of the book entitles you to access the

complete text online and to search using key words or

using the index. You can view all the illustratio ns and

use the hypertext-linked page cross-references to navigate quickly through the book.

Return to this book to refresh your technique if you

have been away from a particular field for some time. It

is surprising how quickly your technique deteriorates if

you do not use it regularly. Practise at every available

opportunity so that you become proficient at examination techniques and gain a full understanding of the

range of normality.

Ask a senior colleague to review your examination

technique regularly; there is no substitute for this and

for regular practice. Listen also to what patients say – not

only about themselves but also about other health professionals – and learn from these c omments. You will

pick up good and bad points that you will want to

emulate or avoid.

Finally, enjoy your skills. After all, you are learning to

be able to understand, diagnose and help people. For

most of us, this is the reason we became doctors.

Boxes and tables

Boxes and tables are a popular way of presenting information and are particularly usef ul for revision. They are classified by the type of

information they contain using the following symbols:

Causes

Clinical features

Investigations

Evidence-based examination

Other information

Evidence-based examination

Evidence-based examination applies the best available evidence from scient ific method to clinical decision making and is an increasingly

essential part of modern clinical practice. However, most clinical examination techniques have developed over generations of medical

practice without rigorous scientific assessment. To highlight examples where there is evid ence-based examination we have included 55

EBE boxes. The art of medicine depends on being able to combine scientific rigour with long- established techniques but this area needs

to be re-evaluated and updated constantly as new information comes to light.

Examination sequences

Throughout the book there are outlines of techniques that you s hould follow when examining a patient. These are identified with a red

heading ‘Examination sequence’. The bullet-point list provides the exact order to undertake the examination.

To help your understanding of how to perform these technique s many of the examination sequences have been filmed and those marked

with the symbol above can be viewed as part of the Student Consult

ixonline text.

Glasgow Coma Scale videos

The Glasgow Coma Scale (GCS) is the globally accepted standard means of assessing conscious state. It is validated and reliable.

Included as part of the Student Consult website are two video demonstrations of how the Scale should be performed in clinical

situations:

• using the GCS: how to perform the different

elements of the GCS

• clinical scenarios: using the GCS in a clinical

context.

As well as demonstrating correct techniques, the videos illustrate common pitfalls in using the GCS and give guidance on how to avoid

these.

Video production team

Writer, narrator, director and producer Mr Jacques Ker r

Nurses

Dr Sharon Mulhern

Mr Jacques Kerr

Patient

Stevie Allen

Production

Mirage Television Productions

For more information see www.practicalgcs.com

Clinical skills videos

By logging on to the Student Consult website you will have access to clinical examination video s, custommade for this textbook. Filmed

using qualified doctors, with hands-on guidance from the authors hip team, and narrated by one of the editors, Professor Colin Robertson ,

these videos offer you the chance to watch trained professionals performing many of the e xamination routines described in the book. By

helping you to memorise the essential examination steps required for each major system and by demonstrating the proper clinical

technique, these videos should act as an important bridge between textbook learn ing and bedside teaching. The videos will be available

for you to view again and again as your clinical skills develop and will prove invaluable as you pr epare for your clinical OSCE

examinations.

Each examination routine has a detailed explanatory narrative but for maximum benefit view the videos in conjunction with the book. To

facilitate this, sections of the videos are also linked to the online text, thus allowing yo u to view the relevant examination sequences as

you progress through each chapter.

Video contents

• Examination of the cardiovascular system

• Examination of the respiratory system

• Examination of the gastrointestinal system

• Examination of the neurological system

• Examination of the ear

• Examination of the musculoskeletal system

• Examination of the thyroid gland

Video production team

Director and editor

Dr Iain Hennessey

Producer

Dr Alan Japp

Sound and narrator

Professor Colin Robertson

Dr Nick Morley

Clinical examiners

Dr Amy Robb

Dr Ben Waterson

Patients

Abby Cooke

Omar Ali

Contributors

Elaine Anderson

MD FRCS(Ed)

Clinical Director, Breast and Plastics, NHS Lothian; Consultant Breast Surgeon, Wes tern General Hospital, Edinburgh

John Bevan BSc(Hons) MBChB(Hons) MD FRCPE

Consultant Endocrinologist, Aberdeen Royal Infirmary; Honorary Professor of Endocrinology, University of Aberdeen

Colin Duncan

MD FRCOG

Senior Lecturer in Reproductive Medicine, Consultant Gynaecologist, University of Edinbu rgh

Andrew Elder BSc MBChB FRCPE FRCPSG FRCP Consultant in Acute Medicin e for the Elderly and Honorary Senior Lecturer,

Western General Hospital, Edinburgh and University of Edinburgh

Andrew Bradbury BSc MB ChB(Hons) MD MBA FRCS(Ed) Sampson Gamgee Professor of Vascular Surgery, and Director of

Quality Assurance and Enhancement, College of Medical and Dental Sciences, U niversity of Birmingham; Consultant Vascular and

Endovascular Surgeon, Heart of England NHS Foundation Trust, Birmingham

Rebecca Ford MEd MRCP MRCS(Edin) FRCOphth Consultant Ophthalmologist, Aberdeen Roya l Infirmary

David Gawkrodger DSc MD FRCP FRCPE

Consultant Dermatologist, Royal Hallamshire Hospital, Sheffield; Honorary Professor of Der matology, University of Sheffield

Gareth Clegg MB ChB BSc(Hons) MRCP PhD FCEM Senior Clinical Lecturer, University of Edinb urgh; Honorary Consultant in

Emergency Medicine, Royal Infirmary of Edinburgh

Jane Gibson BSc(Hons) MD FRCPE FSCP(Hon)

Consultant Rheumatologist, Fife Rheumatic Diseases Unit, NHS Fife, Kirkcald y, Fife; Honorary Senior Lecturer, University of St

Andrews

Nicki Colledge

BSc(Hons) FRCPE

Consultant Physician in Medicine for the Elderly, Liberton Hospital and Royal Infirmary of Edinburgh; Honorary Senior Lecturer,

University of Edinburgh

Allan Cumming MBChB MD FRCPE

Dean of Students, College of Medicine and Veterinary Medicine, University of Edinbur gh

Richard Davenport DM FRCPE

Consultant Neurologist, Western General Hospital and Royal Infirmary of Edinburgh ; Honorary Senior Lecturer, University of

Edinburgh

Graham Devereux MA MD PhD FRCPE

Professor of Respiratory Medicine, University of Aberdeen; Honorary Cons ultant Physician, Aberdeen Royal Infirmary, Aberdeen

Graham Douglas BSc(Hons) MBChB FRCPE

Consultant Physician, Aberdeen Royal Infirmary; Honorary Reader in Medic ine, University of Aberdeen

Jamie Douglas BSc MedSci MBChB MRCGP

General Practitioner, Albion Medical Practice, Ashton Under Lyne, Lancashire

xii

Neil Grubb BSc(Hons) MBChB MRCP MD

Consultant Cardiologist and Electrophysiologist, Edinburgh Heart Centre, Royal Inf irmary of Edinburgh; Honorary Senior Lecturer,

University of Edinburgh

Iain Hennessey MBChB(Hons) BSc(Hons) MRCS MMIS Specialty Train ee in Paediatric Surgery, Alder Hey Children’s Hospital,

Liverpool

James Huntley MA MCh DPhil FRCPE FRCS(Glas) FRCS(Edin)(Tr&Orth)

Consultant Orthopaedic Surgeon, Royal Hospital for Sick Children, Yorkhill; Ho norary Clinical Associate Professor, University of

Glasgow

John Iredale DM FRCP FMedSci FRSE

Professor of Medicine, Director MRC Centre for Inflammation Research, Dean of Clinical Medicine, Queen’s Medical Research

Institute, University of Edinburgh

Alan Japp MBChB(Hons) BSc(Hons) MRCP

Cardiology Registrar, Royal Infirmary of Edinburgh

Jacques Kerr BSc MB BS FRCS FCEM

Consultant in Emergency Medicine and Clinical Lead, Department of Emergen cy Medicine, Borders General Hospital, Melrose

Robert Laing

MD FRCPE

Consultant Physician in Infectious Diseases, Aberdeen Royal Infirmary; Honorary Cl inical Senior Lecturer, University of Aberdeen

Andrew Longmate MBChB FRCA FFICM

Consultant Anaesthetist, Forth Valley Royal Hospital, Larbert, Stirlingshire

Stephen Payne

MS FRCS FEB(Urol)

Consultant Urological Surgeon, Central Manchester Foundation Trust, Manches ter

Stephen Potts

MA FRCPsych

Consultant Psychiatrist, Department of Psychological Medicine, Royal Infirmary of Edinburgh: Honorary Senior Clinical Lecturer,

University of Edinburgh

Elizabeth MacDonald FRCPE

Consultant Physician in Medicine of the Elderly, Western General Hospital, Edinburgh

Colin Robertson BA(Hons) MBChB FRCPEd FRCSEd FSAScot Honorary Profe ssor of Accident and Emergency Medicine, University

of Edinburgh

Alastair MacGilchrist MD FRCPE FRCPS(Glas) Consultant Gastroente rologist/Hepatologist, Royal Infirmary of Edinburgh

Laura Robertson BMedSci(Hons) MBBS FRCA

Specialty trainee in Anaesthesia, Western Infirmary of Glasgow

Hadi Manji MA MD FRCP(Lond)

Consultant Neurologist and Honorary Senior Lecturer, National Hospital for Neurology and Neurosurgery, London

David Snadden MBChB MCISc MD FRCGP FRCP(Edin) CCFP Professo r of Family Practice and Executive Associate Dean

Education, Faculty of Medicine, University of British Columbia, Canada

Nicholas Morley MA (Cantab) MBChB MRCSEd FRCR Clinical Lecturer in Radiology, Edinburgh Cancer Research UK Centre,

University of Edinburgh

James C Spratt BSc MBChB MD FRCP FESC FACC Consultant Cardiologist, Forth Valley Royal Hospital, Larbert, Stirlingshire

Dilip Nathwani MBChB FRCP(Ed;Glas;Lond) DTM&H Consultant Physician a nd Honorary Professor of Infection, Ninewells Hospital

and Medical School, Dundee

Ben Stenson MD FRCPCH FRCPE

Consultant Neonatologist, Simpson Centre for Reproductive Health, Royal Infirmary of Edin burgh; Honorary Professor of Neonatology,

University of Edinburgh

Fiona Nicol BSc(Hons) MBBS FRCGP FRCP(Edin)

Formerly GP Principal and Trainer, Stockbridge Health Centre, Edinburgh; Hono rary Clinical Senior Lecturer, University of Edinburgh

Jane Norman MD FRCOG F Med Sci

Professor of Maternal and Fetal Health, Consultant Obstetrician, University of Edinburgh

John Olson MD FRCPE FRCOphth

Consultant Ophthalmic Physician, Aberdeen Royal Infirmary; Honorary Reader, University o f Aberdeen

Paul O’Neill MD FRCP(Lond)

Professor of Medical Education, University of Manchester and Honorary Consul tant Physician, UHSM NHS Foundation Trust,

Manchester

Rowan Parks MD FRCSI FRCS(Edin)

Professor of Surgical Sciences and Honorary Consultant Surgeon, Royal Infirmary of Edinb urgh

Kum Ying Tham MBBS FRCS(Ed) MSc

Consultant, Emergency Department, Tan Tock Seng Hospital; Assistant Dean, Lee Kong Chia n School of Medicine, Singapore

Steve Turner MBBS MD MRCP(UK) FRCPCH

Senior Clinical Lecturer in Child Health, University of Aberdeen; Honorary Consultan t Paediatrician, Royal Hospital for Sick Children,

Aberdeen

Janet Wilson MD FRCS(Ed) FRCS(Eng) FRCSLT(Hon) Profess or of Otolaryngology Head and Neck Surgery, University of

Newcastle; Honorary Consultant Otolaryngologist, Freeman Hospital, Newcastl e upon Tyne

xiii This page intentionally left blank

Advisory board

We are proud that Macleod’s Clinical Examination is regular ly consulted by a range of health professionals and at a variety of levels in

their training. It is our wish that the content is regarded as accurate and appropriate by all our readers. To ensure this aim, this latest

edition has benefited from detailed advice from an Advisory Board comprising students and junior doctors, as well as representatives

from the nursing and ambulance professions, primary care and the academic community. Significant changes have resulted as a direct

result of this invaluable input.

Macleod ’s international reputation has grown with each edition and as editors we rece ive and value the feedback from our global

readership. To ensure we take full account of the variations of international curricula we h ave recruited representatives from key

geographical areas to the Advisory Board whose detailed comments and critical appraisal have been of great help in shaping th e content

of this new edition.

We acknowledge the enthusiasm and support of all our Advisory Board members and thank th em for contributing to this edition. We

have listed their details at the time that they reviewed the book.

Anthea Lints, Professor and Director of Postgraduate General Practice Education , South East Scotland Deanery, Edinburgh

Will Muirhead, Foundation Year 1 Doctor, Queen’s Medical Centre, Nottingham

Sarah Richardson, Medical Student, University of Edinburgh

Laura Robertson, Specialty Registrar in Anaesthetics, Glasgow

Gordon Stewart, Professor, Department of Medicine, University College London

International advisory board

Wael Abdulrahman Almahmeed, Consultant Cardiologist and Head of the Division of Ca rdiology, Shaikh Khalifa Medical City, Abu

Dhabi, United Arab Emirates

UK advisory board

Graeme Finnie, Medical Student, University of Aberdeen

Paul Gowens, Head of Clinical Governance and Quality, Scottish Ambulance Servic e, Dunfermline Maaret Castrén, Professor in

Emergency Medicine, Department of Clinical Science and Education, Karolinska Institute, St ockholm, Sweden

Jyothi Mariam Idiculla, Associate Professor, Department of Internal Medicine, St John’s Medical College, Bangalore, India

Mike Greaves, Professor and Head of School of Medicine and Dentistry, University of Aberde en Shubhangi Kanitkar, Professor of

Medicine, Dr D.Y. Patil Medical College and Hospital, Pune, India

Chris Griffiths, Professor of Primary Care, Barts and The London School of Medicine and Dentistry, London Kar Neng Lai, Yu Chiu

Kwong Chair of Medicine, Department of Medicine, University of Hong Kong, Hong Kong

Kate Haslett, Specialty trainee in Oncology, Glasgow

Jayne Langran, Clinical Educator/Chest Pain Nurse Specialist, Coronary Care Unit, Raigmore Ho spital, Inverness

Kum-Ying Tham, Consultant Emergency Physician, Tan Tock Seng Hospital and Cli nical Associate Professor, Yong Loo Lin School of

Medicine, National University of Singapore, Singapore

Contents

SECTION 1 HISTORY TAKING AND GENERAL EXAMINATION 1 A pproach to the patient . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Colin Robertson, Fiona Nicol, Graham Douglas

2 History taking . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

David Snadden, Robert Laing, Stephen Potts, Fiona Nicol, Nicki Colledge

3 The general examination . . . . . . . . . . . . . . . . . . . . . . . . 41

Graham Douglas, John Bevan

SECTION 2 SYSTEM EXAMINATION

4 The skin, hair and nails . . . . . . . . . . . . . . . . . . . . . . . . . 63

David Gawkrodger

5 The endocrine system . . . . . . . . . . . . . . . . . . . . . . . . . 77

John Bevan

6 The cardiovascular system . . . . . . . . . . . . . . . . . . . . . . . 97

Neil Grubb, James Spratt, Andrew Bradbury

7 The respiratory system . . . . . . . . . . . . . . . . . . . . . . . . .137

Graham Devereux, Graham Douglas

8 The gastrointestinal system . . . . . . . . . . . . . . . . . . . . . . .165

Alastair MacGilchrist, John Iredale, Rowan Parks

9 The renal system . . . . . . . . . . . . . . . . . . . . . . . . . . . .195

Allan Cumming, Stephen Payne

10 The reproductive system . . . . . . . . . . . . . . . . . . . . . . . .211

Elaine Anderson, Colin Duncan, Jane Norman, Stephen Payne

11 The nervous system . . . . . . . . . . . . . . . . . . . . . . . . . .239

Richard Davenport, Hadi Manji

12 The visual system . . . . . . . . . . . . . . . . . . . . . . . . . . .275

John Olson, Rebecca Ford

13 The ear, nose and throat . . . . . . . . . . . . . . . . . . . . . . . .297

Janet Wilson, Fiona Nicol

14 The musculoskeletal system . . . . . . . . . . . . . . . . . . . . . .315

Jane Gibson, James Huntley

xvi

SECTION 3 EXAMINATION IN SPECIFIC SITUATIONS

15 Babies and children . . . . . . . . . . . . . . . . . . . . . . . . . . .355

Ben Stenson, Steve Turner

16 The frail elderly . . . . . . . . . . . . . . . . . . . . . . . . . . . . .379

Andrew Elder, Elizabeth MacDonald

17 The febrile adult . . . . . . . . . . . . . . . . . . . . . . . . . . . .391

Dilip Nathwani, Kum Ying Tham

18 Assessment for anaesthesia and sedation . . . . . . . . . . . . . . .401

Laura Robertson, Andrew Longmate

19 The critically ill . . . . . . . . . . . . . . . . . . . . . . . . . . . . .411

Gareth Clegg, Colin Robertson

20 Confirming death . . . . . . . . . . . . . . . . . . . . . . . . . . . .423

Jamie Douglas, Graham Douglas

SECTION 4 ASSESSING CLINICAL EXAMINATION TECHNIQUE 21 OSCEs and other examination formats . . . . . . . . . . . . . . . .

.427

Paul O’Neill

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 441

xvii

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SECTION 1 HISTORY TAKING AND GENERAL EXAMINATION

Being a ‘good’ doctor 2 Confidentiality and consent 2 Personal respons ibilities 3 Dress and demeanour 3

Colin Robertson Fiona Nicol Graham Douglas

Approach to the patient1

Communication skills 3

Expectations and respect 3

Hand washing and cleanliness 3

1 BEING A ‘GOOD’ DOCTOR

From your first day as a student you have professional obligations placed upo n you by the public, the law and your colleagues which

continue throughout your working life. Patients want more than merely intellec tual and technical proficiency. To be a good doctor or

nurse it is much easier if you genuinely like and are in terested in people. Most patients want a doctor who listens to them and over 70

separate qualities have been listed as being important. Fundamentally, though, we all want doctors who:

• are knowledgeable

• respect people, healthy or ill, regardless of who

they are

• support patients and their loved ones when and

where needed

• always ask courteous questions, let people talk and

listen to them carefully

• promote health as well as treat disease

• give unbiased advice, let people participate actively

in all decisions related to their health and

healthcare, assess each situation carefully and help

whatever the situation

• use evidence as a tool, not as a determinant of

practice

• humbly accept death as an important part of life;

and help people make the best possible

arrangements when death is close

• work cooperatively with other members of the

healthcare team

• are proactive advocates for their patients, mentors

for other health professionals and ready to learn

from others, regardless of their age, role or status. Doctors also need a balanced life an d to care for them selves and their families. In

short, we want doctors who are happy and healthy, caring and competent, and who care for p eople throughout their life.

One way to reconcile these expectations with your inexperience and incomple te knowledge or skills is to put yourself in the situation of

the patient and/or rela tives. Consider how you would wish to be cared for in the patient’s situation, acknowledging that you are different

and your preferences may not be the same. Most clinicians approach an d care for patients differ ently once they have their own or a

relative’s experience as a patient. Doctors, nurses and everyone involved in healthcare have a profound influence on how patients

experience illness and their sense of dignity. When you are dealing with patients, alwa ys consider your:

• A: attitude – how would I feel in this patient’s

situation?

• B: behaviour – always treat patients with kindness

and respect

• C: compassion – recognise the human story that

accompanies each illness

• D: dialogue – listen to and acknowledge the patient.

CONFIDENTIALITY AND CONSENT

As a student and as a doctor or nurse you will be given

private and intimate information about patients and

1.1 The duties of a registered doctor

• The care of your patient is your first concern

• Protect and promote the health of patients and the public

• Provide a good standard of practice and care

• Keep your professional knowledge and skills up to date

• Recognise and work within the limits of your competence

• Work with colleagues to serve your patients’ interests best

• Treat patients as individuals and respect their dignity

• Treat patients politely and considerately

• Respect patient confidentiality

• Work in partnership with the patient

• Listen to your patients and respond to their concerns and preferences

• Give information in a way they can understand

• Respect their right to reach decisions with you about their care

• Support patients in caring for themselves to improve and maintain their health

• Be honest and open, and act with integrity

• Act without delay if you have a good reason to believe that you or a colleag ue may be putting patients at risk

• Never discriminate unfairly against patients or colleagues

• Never abuse your patient’s or the public’s trust in you or the profession

Courtesy of the General Medical Council (UK).

their families. This information is confidential, even after a patient’s death. This is a general r ule, although its legal application varies

between countries. In the UK, follow the guidelines issued by the General Medical Council (Box 1.1). There are exceptions to the

general rules gov erning patient confidentiality, where failure to disclose information w ould put the patient or someone else at risk of

death or serious harm, or where disclosure might assist in the preventio n, detection or prosecution of a serious crime. If you find yourself

in this situation, contact the senior doctor in charge of the patient’s care immediately and inform him or h er of the situation.

Take all reasonable steps to ensure that consultation and examination of a patient is private. Never discu ss patients where you can be

overheard or leave patients’ records, either on paper or on screen, where they can be seen by other patients, unauthorised staff or the

public. Always obtain consent or other valid authority before undertaking any examination or investigation, pro viding treatment or

involving patients in teaching or research. Even where you have been given signed consent to disclose information about the patient,

only disclose what is being asked for. If you have any doubts discuss your report with the patient so that he is clear about what

information is going to a third party.

Clearly record your findings in the patient’s case notes immediately after the con sultation. These case notes are confidential and must be

stored securely. They also constitute a legal document that could be used in a court of law. Keeping accurate and uptodate case notes is

an essential part of good patient care (p. 38). Remember that what you write may be seen by the patient, as in many countries, including

the UK, patients can ask for and receive access to their medical records.

Hand washing and cleanliness

PERSONAL RESPONSIBILITIES

Always look after yourself and maintain your own health. Register with a general practitioner (GP). Do n ot selfdiagnose and selftreat. If

you know, or think that you might have, a serious condition you could pass on to patients, o r if your judgement or performance could be

affected by a condition or its treatment, consult your GP and be guided as to the need for secondar y referral. Heed your doctor’s advice

regarding investiga tions, treatment and changes to your working practice. Protec t yourself, your patients and your colleagues by being

immunised against common but serious com municable diseases where vaccines are availab le, e.g. hepatitis B.

Your professional position is a privileged one; do not use it to establish or pursue a sexual or improper emo tional relationship with a

patient or someone close to the patient. Do not give medical care to anyone with whom you have a clos e personal relationship. Do not

express your personal beliefs, including political, religious or moral ones, to your patients in ways that exploit their vulnerability or could

cause them distress.

DRESS AND DEMEANOUR

The way you dress is important in establishing a suc cessful patient–doctor relationship. Y our dress style and demeanour should never

make your patient or col leagues uncomfortable or distract them. Smart, sensitive and mo dest dress is appropriate; expressing your per‐

sonality is not. Exposing your chest, midriff and legs may not only create offence but impede co mmunication. Have short or threequarter‐

length sleeves or roll long sleeves up, away from your wrists, before examining patients or carrying out pr ocedures. This allows you to

clean your hands effectively and reduces the risk of crossinfection. Tie back long hair and keep any jewel lery simple and limited to

allow effective hand washing. Some medical schools and hospitals require students and staff to w ear white coats or ‘scrubs’ for reasons

of professionalism, identification and as a barrier to infec tion. If this is the case, these must be clean and smart and you should a lways

wear a name badge which can be read easily, i.e. not at your waist.

Whenever you see a patient or relative, introduce yourself fully and clearly. A friendly smile h elps to put your patient at ease.

How you speak to, and address, a patient depends upon the patient’s age, background and cu ltural envi ronment. Many older patients

prefer not to be called by their first name, and it is best to ask patients how they would prefer to be addressed.

COMMUNICATION SKILLS

A consultation is a meeting of two experts: you as the clinician and the patient as an expert on his own body and mind. Excellent

communication skills allow you to identify a patient’s problem rapidly and accurately and improv e patient satisfaction (p. 7). Poor

communi cation skills are associated with increased medicolegal vulnerability and clinician burn out. Improve your skills by videoing

yourself consulting with a patient (having obtained informed signed consent) and rev iew this with a senior clinician using one of the

many techniques developed for this. Continually seek to improve your communication skills. These will develop with experi ence but can

always be improved.

Most doctors and nurses work in teams with col leagues in other professions. Working in teams does not change your personal

accountability for your conduct and the care you pro vide. Try to act as a positive role 1

model and motivate and inspire your colleagues. Always

respect the skills and contributions of your colleagues and communicate effectively with them particularly when handing over care.

EXPECTATIONS AND RESPECT

The literary and media stereotypes of doctors frequently involve miraculous intuition, the confirmation of rare and brilliant diagnoses

and the performance of dramatic lifesaving interventions. Reality is different. Medicine often inv olves seeing and treating patients with

common conditions and chronic diseases where we may only be able to provide palliation or simply bear witness to patients’ suffering.

The best doctors are humble and recognise that humans are in finitely more complex, demanding and fascinating than one can imagine.

They understand that much socalled medical ‘wisdom’ is at best incomplete, and often s imply wrong.

If a patient under your care has suffered harm or distress, act immediately to put matters right, if th at is possible. Apologise and explain

fully and promptly to the patient what has happened, and the likely effects. Patien t complaints about their care or treatment are often the

result of a breakdown in communication and they have a right to expect a prompt, ope n, constructive and honest response. Do not allow a

patient’s complaint to affect adversely the care or treatment you provide.

HAND WASHING AND CLEANLINESS

Transmission of microorganisms from the hands of healthcare workers is the main source of crossinfec tion

1.2 Infections that can be transmitted on the hands of healthcare workers

Healthcare-acquired infections

• Meticillin-resistant Staphylococcus aureus (MRSA)

Diarrhoeal infections

• Salmonella

• Escherichia coli 0157:H7

Respiratory infections

• Influenza

• Respiratory syncytial virus (RSV) Other infections

• Hepatitis A

• Clostridium difficile

• Shigella

• Norovirus

• Common cold

How to hand rub with alcohol based hand rub

How to handwash with soap and water

Apply a palmful of the product and cover all hand surfaces Wet hands and apply enou gh soap to cover all hand surfaces

2 3 4

Rub hands palm to palm Right palm over the back of the

other hand with interlaced fingers and vice versa

8 Palm to palm with

fingers interlaced

Rinse hands with water

Backs of fingers to opposing palms with fingers interlocked

Rotational rubbing of left thumb clasped in right palm and vice versa

Rotational rubbing of left thumb clasped in right palm and vice versa
9 Rotational rubbing, backwards
and forwards with clasped
fingers of right hand in left
palm and vice versa
8
 Steps 2–7 should take at least 15 seconds
11 Steps 2–7 should take
at least 15 seconds
10
 Dry thoroughly with towel
Use elbow to turn off tap
Fig. 1.1 How do I clean my hands properly? © World Health Organization 2009. All right s reserved.
in hospitals, primary care surgeries and nursing homes. Healthcareacquired infections co mplicate up to 10% of hospital admissions and
in the UK 5000 people die from them each year (Box 1.2).
Hand washing is the single most effective way to prevent the spread of inf ection. It is your responsibility to prevent the spread of
infection and routinely wash your hands after every clinical examination. Do  not be put off by lack of hand hygiene agents or facilities
for hand washing, or being short of time.
• If your hands are visibly soiled, wash thoroughly
with soap and water.
• If your hands are not obviously dirty, wash with soap and water or use an alcoholbased rub or gel.
• Always wear surgical gloves when you may be in contact with blood, mucou s membranes or non intact skin.
While washing with alcoholbased gels will remove most microorganisms, e.g. meticillinresistant Staph ylococcus aureus (MRSA),
Escherichia coli, Salmonella), when dealing with patients with influenza, norovirus or Clostridium difficile infection, always clean han ds
with liquid soap and water (Fig. 1.1).
SECTION 1 HISTORY TAKING AND GENERAL EXAMINATION
David Snadden Robert Laing Stephen Potts Fiona Nicol Nicki Colledge
History taking2
TALKING WITH PATIENTS 6 Patient-centred medicine 6
Beginning 6
Difficult situations 9
Your patient has communication difficulties 9
Your patient has cognitive difficulties 9
Sensitive situations 9
Gathering information 11
THE PSYCHIATRIC HISTORY 21
The history 21
Sensitive topics 21
The uncooperative patient 21
Mental state examination 21
Appearance 22
Behaviour 22
Speech 22
Mood 22
Thought form 22
Thought content 23
Risk assessment 25
Screening questions for mental illnesses 25
The physical examination 26
MEDICALLY UNEXPLAINED SYMPTOMS (MUS) 27
Symptoms and definitions 27
History 28
Physical examination 29
Investigation 29
Putting it all together 29
DOCUMENTING THE FINDINGS: THE CASE NOTES 30

2 TALKING WITH PATIENTS

Think about the last time you visited your doctor. What prompted your visit? What arrangeme nts did you have to make? Even a

straightforward visit can be a big event. You have to make an appointment, w ork out what you are going to say and possibly arrange time

off work or for child care. People visit doctors for many reasons (Box 2 .1). They may have already spoken to family, friends or other

health professionals, tried various remedies, and trawled the internet for inform ation to explain their illness or problem. Most patients

have some idea of what might be wrong with them and have worries or concerns they wish to discuss.

All patients seek explanation and meaning for their symptoms. You need to work out why the patient has come to see you, what he is

most concerned about, and then agree with him the best course of action.

The first and major part of any consultation is talking with your patient. Comm unication is integral to clinical examination and is most

important both at the start of the interview, to gather information, and at the en d, to find common ground and engage your patient in his

management.

your patients in their healthcare. Poor communication leads to misunderstanding, conflicting messages and patient dis satisfaction, and is

the root cause of complaints and litigation. Over time you will develop your own consulting style; consultation frameworks are usef ul

places to start (Box 2.4).

BEGINNING

Setting up

Preparation

Read your patient’s records and any transfer or admission letters before you see your patient.

Where will you see your patient?

Choose a quiet, private space. This is often difficult in hospital, where privacy may be afforded only by curtains, which means no

privacy at all. Always be sensitive

PATIENT-CENTRED MEDICINE

Patient-centred medicine helps you understand your patient as a whole person. Good communication supports the building of trust

between you and your patient and helps you provide clear and simple informati on (Boxes 2.2 and 2.3). It allows you to understand each

other and agree goals together. Communication means much more than ‘taking a history’; it is about involving

2.1 Reasons why people visit doctors

• They have reached their limits of tolerance

• They have reached their limits of anxiety

• They have problems of daily living presenting as symptoms

• For prevention

• For administrative reasons

2.2 Effective communication skills

Improve patient satisfaction

• Patients understand what is wrong

• They understand what they can do to help

Improve doctor satisfaction

• Patients are more likely to follow advice when they agree

mutual goals with their doctor

Improve health by positive support and empathy

• Improve health outcomes

• Enhance the relationship between doctor and patient

Use time more effectively

• Active listening helps the doctor recognise what is wrong

• Active listening leads to fewer patient complaints

2.3 Tips for effective conversations

• Speak clearly and audibly

• Ask open questions to start with

• Don’t interrupt your patient

• Try and appear unhurried

• Use silence to encourage explanations

• Do not use jargon or emotive words

• Find out about your patient as a person

• Clarify and summarise what you understand – you may need to do th is more than once

• Make sure the story makes sense to you – keep seeking facts until it does

• Acknowledge emotions

• Seek ideas, concerns and expectations

• Negotiate mutual goals

2.4 Consulting with patients (BASICS)

Beginning

• Setting up

• Preparation

• Introduction

Active listening

• The patient’s experience of his illness

Systematic enquiry

• Disease-oriented systematic enquiry

Information gathering

• Clinical examination

Context

• Understanding your patient as a person Sharing

• Information

• Agreeing action and goals

Talking with patients

to privacy and dignity. If your patient is in hospital but is mobile, use a side room or interview room. If there is no alternative to speaking

to patients at their bedside, let them know that you understand your conversation may b e overheard and give them permission not to

answer sensitive questions about which they feel uncomfortable.

How long will you have?

Consultation length varies. In UK general practice the average length is 12 m inutes. This is usually adequate, as the doctor may have

seen the patient on several occasions and is familiar with the family and social background. In hospital 5–10 minutes may be adequate

for returning outpatients, but for new and complex problems 30 minutes or more is usually needed. If you are a student, allow at least 30

minutes.

How will you sit?

Arrange seating in a non-confrontational way. If you use

a desk, arrange the seats at the corner of the desk. This is less formal and helps communication (Fig. 2.1A). If you use a computer, make

sure the screen and keyboard do not get in the way. Face your patient, not the screen (Fig. 2.1B). At a bedside, pull up a chair and sit

level with your patient to see him easily and gain eye contact.

Non-verbal communication

First impressions are important. Your demeanour, attitude and dress influence your patient from the outset. Be professional in dress and

behaviour (p. 3) and show concern for your patient’s situation. Avoid interruptions such as the telephon e (Fig. 2.1B).

Look for non-verbal cues such as distress and mood. Changes in your patient’s demeanour and body language during the consultation can

be clues to difficulties that she cannot express verbally. If the patient ’s body language becomes ‘closed’ – that is, she may cross her arms

and legs and break off eye contact – this may indicate discomfort (Fig. 2.1B).

Starting your consultation

Introduce yourself, and anyone else who is with you. Use your patient’s and your own names to confirm identity. It may be appropriate

to shake hands. If you are a student, inform the patient that you are in training; 2 patients are usually eager to help. Write down facts that

are easily forgotten, e.g. blood pressure readings or family tree, but writing notes should not interfere with the consultation.

Here are some ideas on how to get an interview going, though the words you use will change depending on the situation:

Good morning, Mrs Jones. I have got the right person, haven’t I? I’m Mr Brow n. I’m a fourth-year medical student. I’ve been asked to

come and talk with you and examine you.

It might take me 20–30 minutes, if that’s all right.

I see that you can’t really get out of bed so we’ll need to talk here. I’ll pull the s creens round. I’m sorry it’s not very private. If I ask you a

question that you don’t want to answer in case other people overhear, then just say so.

I’ll need to make a few notes so I don’t forget anything important. Now, if I’m writing thing s down, it doesn’t mean I’m not listening. I

still will be.

Are you happy with all that?

Fig. 2.1 Seating arrangements.

Active listening

Hearing your patient’s story about his illness experience

is vital. Ask open questions to start with (see below). In the community, try ‘How can I help you today?’ or ‘What has brought you along

to see me today?’

Active listening means encouraging the patient to talk by looking interested, making enco uraging comments or noises, e.g. ‘Tell me a bit

more’ or ‘Uhuh’, and giving the impression that you have time for the patient. A ctive listening helps gather information and allows

patients to tell their story in their own words. Clarify anything you do not understand. Tell patients what you think they have said and ask

if your interpretation is correct (reflection).

The way you ask a question is important:

• Open questions encourage the patient to talk. They start with a word like ‘whe re’ or ‘what’, or a phrase like ‘tell me more about …’.

They are most useful initially when you are finding out what is going on and encouraging the patient to talk

• Closed questions, e.g. ‘Have you had a cough today?’ seek specific information as part of a systematic enquiry. They invite ‘yes’ or

‘no’ answers.

Both types of question have their place.

Can we start with you telling me what has happened to bring you into hospital? (Opening)

Well, I’ve been getting this funny feeling in my chest over the

last few months. It’s been getting worse and worse but it was

really awful this morning. I got really breathless and felt someone was crushin g me.

Can you tell me a bit more about the crushing feeling? (Open

questioning)

Well, it was here, across my chest. It was sort of tight.

And did it go anywhere else? (Clarifying)

Well, maybe up here in my neck.

So, you had a tight pain in your chest this morning that went on a

long time and you felt it in your neck? (Summarising)

You’ve had the pain for the last few months. Can you tell me

more? (Reflecting and open questioning)

Well, it was the same but not that bad, though it’s been getting worse recently.

OK. Can you remember when it first started? (Clarifying) Oh, 3 or 4 months ago.

Does anything make it worse? (Open questioning)

Well, if I go up steps or up hills that can bring it on.

What do you do?

Stop and sometimes take my puffer.

Your what? (Clarifying)

This spray the doctor gave me to put in my mouth.

Can you show me it, please?

OK.

And what does it do? (Clarifying)

Well, it takes the pain away, but I get an awful headache with it.

So, for a few months you’ve had a tightness in your chest, which

gets worse going up hills and upstairs and which goes away if you

use your spray. Sometimes you feel the pain in your neck. But

today it came on and lasted longer but felt the same. Have I got

that right? (Summarising)

No, it was much worse this morning.

Once you have established what has happened, find out about your patient’s ICE:

• I: Ideas on what is happening to him

• C: Concerns in terms of the impact on him

• E: Expectations of the illness and of you, the doctor. Patients will hav e feelings and ideas about what has happened to them, and these

may or may not be accurate. A patient with chest pain might think he has indigestion wh ile you are considering angina. Ask: ‘Do you

have any thoughts about what might be happening to you?’ A simple question like: ‘What were y ou thinking I might do today?’ can

avoid unnecessary prescriptions or investigations. Modern medicine may be unable to ‘cure’ a problem, and the important issue is what

you can do to help a patient to function.

her upper jaw. Her wound has healed, but she has a drooping lower eyelid and significant facial swelling. She returns to work. Think how

you would feel and imagine yourself in this situation. Express empathy through questio ns which show you can relate to your patient’s

experience.

So, are you all healed up from your operation now?

Yes, but I still have to put drops in my eye.

And what about the swelling under your eye?

That gets worse during the day, and sometimes by afternoon I

can’t see that well.

And how does that feel at work?

Well, it’s really difficult. You know, with the kids and

everything. It’s all a bit awkward.

I can understand that that must make you feel pretty

uncomfortable and awkward. That must be very difficult. How do you cope? Thinking about it makes me wonder if there are any other

areas that are awkward for you, maybe in other aspects of your life, like the social side …

Understanding your patient’s context

The context of our lives has a major influence on how we deal with illness. Finding out about your patient’s con text is crucial. It is far

more than just a ‘social history’. You should understand your patients’ personal con straints and supports, including where they live, who

they live with, where they work, who they work with, what they actually do, their cultural and religious beliefs, and their relationships

and past experience. It is about your patient as a person. It may not be appropriat e to explore these sensitive areas with everyone, or on

an initial consultation, but they are important in any longterm doctor–patient relationship. Understanding the w hole person modifies the

information you give and the way you give it, the treatment you advise and the d rugs you use.

Enquire about your patient’s job and explore in some depth what this job entails, as this may have a bearing on the illness. A single job

description can cover many tasks, e.g. engineer, so find out what your patient act ually does, whether there are any stresses involved, and

if there are any relationships at work that affect him, for example, a bullying boss or a harassing colleague.

In the following dialogue, Patient A is under stress and Patient B may be suf fering the consequences of exposure to fungal spores which

can cause farmer’s lung. However, their initial answer to the first question is the same.

Empathy

Being empathic helps your relationship with patients and improves their health outcomes (p. 2). What is empathy and how do you

express it? Empathy is not sympathy, the expression of sorrow; it is much more. It is helping your patients feel that you understand what

they are going through. Try to see the problem from their point of view and relate that to them.

Consider a young teacher who has recently had dis

figuring facial surgery to remove a benign tumour from

Doctor: So, tell me what your job is.

Patients A and B: I work on a farm.

Doctor: Yes, but what do you actually do?

Patient A: Well, I own the farm and mostly do the book work and buying and selling of animals.

Patient B: I’m a labourer on the farm.

Doctor: So, what are you doing at the moment?

Patient A: It’s been a terrible year with the drought. The yields are down and I’m trying to get a nother loan from the bank manager.

Difficult situations

Patient B: Well, just now we work in the barn first thing in the mornings, cleaning up and then laying feed for the cattle. It’s very

mouldy this year. After that, we’re in the fields doing the early ploughing.

Find out about your patient’s home circumstances. Try asking, ‘Is there anyone at h ome with you?’ or ‘Is there anyone that can help?’

and be equally tactful enquiring about relationships and the home environment. If a 15-year-old newly diagnosed diabetic is about to go

home, ask about the home circumstances: who is at home and are the relationships supportive? Different arrangements should be made

for a patient in a stable home whose mother is a healthcare worker compared to one f rom a deprived background, who has a lone parent

and poor relationships.

Patients’ beliefs influence healthcare. Religious and cultural beliefs affect how they cope with a disability or a dying relative, and

whether they will accept certain treatments. Be sensitive to, and tolerant of, these issues.

Sometimes the consultation also gives you an opportunity to bring up issues around preventive activities, and a chance to address risk

factors and lifestyle challenges. Examples include smoking cessation, dealing with obesity and drug or alcohol dependency, or illnesses

that run in the family.

Sharing information

and agreeing goals

Clarify and summarise what you say. Use words that the patient will understand and tailor the explanation to your patient.

Explain what you have found and what you think this means. Give important information first an d check what has been understood.

Provide the information in small chunks and warn the patient how many important things are coming: for example, ‘There are two

important things I want to discuss with you. The first is …’.

Use simple language and ensure your patient understands the treatment o ptions and likely prognosis. What you say should be accurate

and unambiguous, and the information should be given sensitively. Imagine yourself in the patient’s position and your response. There is

no place for being abrupt or for brutal honesty.

Engaging your patient

Make sure patients are involved in any decisions. Share

your ideas with them, make suggestions and encourage them to contribute their thoughts. Be sensitive to your patients’ body language. If

they seem unclear about something or disagree with you, reflect this back to them. Use ph rases like ‘Are you comfortable with what I’m

saying?’ or ‘Is there anything that I’ve said that isn’t clear to you or has maybe confused you?’ Whenever possible help decision making

by giving written information to take home or by suggesting other sources of information : for example, self-help groups or the internet.

Check they have understood you and discuss any investigations or treatment you think m ight be needed, including risks or side-effects

(Box 2.3).

In this way, you will be able to negotiate a mutually agreed plan. For example, a patient with cancer may have the choice of surgery or

radiotherapy. By involving him and discussing the pros and cons of treatments, yo u will enable the patient to reach a decision that you

both understand and agree with. The patient will have to live with the consequences of the tre atment, which will be much easier to accept

if he has chosen the treatment himself.

Try to agree realistic goals. These might be areas that your patient needs to work on. For example, if the patient is trying to stop

smoking, then you may set goals together that involve when he is going to stop, what help he will need, e.g. support groups, nicotine

replacement therapy or both, how he will identify risky situations, 2

e.g. socialising, and handle these to avoid being tempted

to have a cigarette.

Finally, arrange for follow-up if necessary or give the patient some idea about when to retur n. This depends on how the patient is feeling

and on any treatment you have suggested. End a complex discussion by b riefly summarising what you have agreed, or ask your patient to

summarise for you (Box 2.4).

DIFFICULT SITUATIONS

Your patient has communication

difficulties

If your patient does not speak your language, or has hearing or speech difficulties such as dysphasia or dysarthria , follow the principles of

good communication, but in addition you can do the following:

• Use an interpreter, but remember to address the

patient, not the interpreter.

• Write things down for your patient if he can read.

• Employ lip reading or sign language.

• Involve someone who is used to communicating

with your patient.

Your patient has cognitive difficulties

Be alert for early signs of dementia. You may have to rely on help from relatives or carers. If you do suspect this, use a memory or

mental status test (Ch. 16).

Sensitive situations

Doctors sometimes need to ask personal or sensitive questions and examine intimate parts. If you are talking to a patient who may have a

sexually transmitted disease, broach the subject sensitively. Indicate that you are going to ask questions in this area, and make sure the

conversation is entirely private. Here are some examples of ques tions that might work.

Because of what you’re telling me, I need to ask you some rather personal questions. Is that OK?

Can you tell me if you’ve had any casual relationships recently? Are you worried that y ou might have picked anything up – I mean, in a

sexual way?

You’ve told me that you think you’re at risk. Can I ask if you have a regular sexua l partner?

Follow this up with: ‘Is your partner male or female?’ If there is no regular partner, ask how many sexual partners there have been in the

past year and how many have been male and how many female.

Ask permission sensitively if you need to examine intimate areas. This is most likely for examin ation of the breasts, genitals or rectum,

but may apply in some circumstances or cultures whenever you need to touch the patien t. First warn your patient; then seek permission

to carry out an examination, explaining what you need to do. Always offer a chaperone , even if you are of the same gender as the p atient.

Record the chaperone’s name and position. If patients decline the offer, respect their wishes and record this in the notes.

Give clear instructions about what clothes they need to remove. If necessary, reschedule an in timate examination until sufficient time,

appropriate facilities or a chaperone are available.

Your patient is emotional

Ill people feel vulnerable and may become angry or distressed. Exploring their reasons for th e emotion often defuses the situation.

Recognise that your patient is angry or sad and ask him to explain w hy. Use phrases such as, ‘You seem angry about something’ or ‘Is

there something that is upsetting you?’ Recognise your patient’s emotion , show empathy and understanding, encourage him to talk and

offer what explanations you can.

Talkative patients or those who want to deal with a lot of things at once may respond to: ‘I only have a short time left with you, so what’s

the most important thing we need to deal with now?’ If patients have a long list of complaints, suggest: ‘Of the six things you’ve raised

today, I can only deal with two, so tell me which are the most important to you and we’ll deal with the rest next time.’

Set professional boundaries if your patient becomes overly familiar: ‘Well, it would be inappr opriate for me to discuss my personal

issues with you. I’m here to help you so let’s focus on your problem.’

Cultural sensitivity

Patients from a culture that is not your own may have different social rules (Bo x 2.5). Ideas around eye contact, touch and personal space

may be different. In some western cultures, it is normal to maintain eye contact for long periods; in most of the world, however, this is

seen as confrontational or rude. Shaking hands with the opposite sex is strictly forbidden in certain cultures. Death may be dealt with

differently in terms of what the family expectations of physicians may be, wh o will expect to have information shared with them and

what rites will be followed. Appreciate and accept differences in your patients’ cultures and beliefs. When in doubt, ask them. This lets

them know that you are aware of, and sensitive to, these issues.

Third-party information

Confidentiality is your first priority ( p. 2). You may need to obtain informa tion about your patient from someone

else: usually a

relative and sometimes a friend or carer.

2.5 Transcultural awareness

• Use appropriate eye contact

• Use appropriate hand gestures

• Respect personal space

• Consider physical contact between sexes, e.g. shaking hands

• Be sensitive to cultures and beliefs surrounding illness

• Ask yourself what should happen as death approaches?

• Ask yourself what should happen after death?

2.6 Talking to patients by telephone

• Listen actively and take a detailed history

• Frequently clarify and paraphrase to ensure that the messages got across in bo th directions

• Listen for cues (such as pace, pauses, change in voice intonation)

• Offer opportunities to ask questions

• Offer patient education

• Safety net – make sure the patient knows what to do if things don’t imp rove

• Document carefully

• As the assessment is based solely on the history, and the management plan canno t be reinforced with non-verbal cues, being systematic

in covering all issues is especially important

Ask your patient’s permission and have the patient present to maintain confiden tiality. If the patient cannot communicate, you will have

to rely on family and carers to understand what has happened to the patient. Third parties may app roach you without your patient’s

knowledge. Find out who they are, what their relationship to the patient is, and whet her your patient knows the third party is talking to

you. Tell third parties that you can listen to them but cannot divulge any clinical inf ormation without the patient’s express permission.

They may tell you about sensitive matters, such as mental illness, sexual abuse, or drug or alco hol addiction. This information needs to

be sensitively explored with your patient to confirm the truth.

Telephone consultation

Consulting with patients using the telephone brings specific challenges as there are no vi sual cues to changes in body language or

demeanour. The principles of good communication apply, but it is even more important to listen actively to your patient and frequently

check your mutual understanding. Do not make assumptions or jump to diagno ses. Much of clinical medicine relies on direct observation

and your intuition as a physician, so err on the side of caution when deciding whether to see a patient or not (Box 2.6).

Breaking bad news

Breaking bad news is one of the most difficult communication tasks you will face. Follow the principles of good communication. Speak

to your patient in a quiet private environment. Ask patients who else they would like to be prese nt – this may be a relative or partner –

and offer a nurse or counsellor. Then find out how much

2.7 Framework for breaking bad news: SPIKES

S etting

• Privacy

• People

• You, be calm and attentive

Perception

• What your patient already knows

Invitation

• What does the patient want to know?

Knowledge

• Warn the patient that you have bad news

Empathy

• Acknowledge and address the patient’s emotions Summary and strategy

• The patient knows and agrees what the next steps are

they know and how much they want to know. Share the information you have. Pl an in advance what you need to share, and prioritise so

that the important information, which may include a diagnosis and the next steps in planning, do not get lost in a lot of detail. Respond to

their feelings, as they may be upset or bewildered, and ensure that they unders tand and agree on the next steps (Box 2.7).

GATHERING INFORMATION

The presenting complaint

Diagnosis

Experienced clinicians make a diagnosis by recognising patterns of symptoms. With e xperience you will refine your questions according

to the presenting complaint; you should then have a list of possible diagnoses (a differe ntial diagnosis), before you examine the patient.

Ensure that patients tell you the problem in their own words and record this. Use your knowledge to direct your questioning. Clarify what

they mean by any term they use. Some terms need to be explored (Box 2 .8). Each answer increases or decreases the probability of a

particular diagnosis, and excludes others.

In the following example, the patient is a 65-year-old male smoker. His age and smoking statu s increase the probability of certain

diagnoses related to smoking. A cough for 2 months increases the likelihood of lung cancer and chronic obstructive pulmonary disease

(COPD). Chest pain does not exclude COPD since he could have pulled a muscle on coughing , but the pain may be pleuritic from

infection or thromboembolism. In turn, infection could be caused by obstruc tion of an airway by lung cancer. Haemoptysis lasting 2

months dramatically increases the chance of lung cancer. If the patien t also has weight loss, the positive predictive value of all these

answers is very high for lung cancer. This will focus your examination and inve stigation plan.

2.8 Examples of terms used by patients that should be clarified

• Allergy

• Angina

• Arthritis

• Diarrhoea

• Dizziness

• Eczema

• Fits

• Heart attack

• Migraine

• Pleurisy

• Vertigo

What is your main problem? ( Open question)

I’ve had a cough that I just can’t seem to get rid of. It started after I’d been ill w ith flu about 2 months ago. I thought it would get better

but it hasn’t and it’s driving me mad.

Can you please tell me more about the cough?

(Open question)

Well, it’s bad all the time. I cough and cough, and bring up some phlegm. I can’t sleep at night sometimes and I wake up feeling rough

because I’ve slept so poorly. Sometimes I get pains in my chest because I’ve been coughing so much.

Follow up by asking key questions to clarify the cough.

Can you tell me about the pains? ( Open question) Well, they’re here on my side when I cough.

Does anything else bring on the pains? (Open and prompting

question)

Taking a deep breath.

Follow this up by asking key questions about the pain (see Box 2.10).

What colour is the phlegm? (Closed question, focusing on the symptom offered)

Clear.

Have you ever coughed up any blood? (Closed question)

Yes, sometimes.

How often? (Closed question)

Oh, most days.

How much? (Closed question, clarifying the symptom)

Just streaks, but sometimes a bit more.

Do you ever get wheezy or feel short of breath with your cough?

A bit.

How has your weight been? (Open question, seeking additional confirmation of serious patholog y)

I’ve lost about 6 kilos.

What sort of pathology does

the patient have?

Think about which pathological process may account for the symptoms. Diseases are either congenital or acquired, and there are only

certain pathological processes that cause acquired disease. The onset, progression, timescale and associated symptoms of the presenting

complaint may guide you to the likely pathology (Box 2.9).

2 2.9 Deciding on the type of pathology Type of pathology Infection

Onset of symptoms Usually hours

Progression of symptoms

Usually fairly rapid over hours or days

Inflammation Often quite sudden Weeks or months

Metabolic Malignant Toxic

Very variable Gradual

Abrupt

Hours to months Weeks to months Rapid

Trauma

Vascular

Degenerative

Abrupt Sudden Gradual Little change from onset Hours

Months to years

Associated symptoms/pattern of symptoms Fevers, localising symptoms, e.g. pleuritic pain and cough

Localising symptoms of variable severity, often coming and going

Steadily progressive in severity with no remission Weight loss, fatigue

Dramatic onset of symptoms; vomiting often a feature

Diagnosis usually clear from history

Rapid development of associated physical signs Gradual worsening interspersed with p eriods of more acute deterioration

What about physical signs?

Some diseases have no physical signs, e.g. migraine or angina. Other conditions almost always p roduce physical signs, e.g. fractured

neck of femur or stroke. The absence of physical signs may simply reflect the early stage of a disease while some diseases have few or

no signs, e.g. Addison’s disease. Experience should help you to r ank the reliability of signs to support your diagnosis, e.g. the patient

with a history suggesting a transient ischaemic attack may have a carotid bruit but its absence would not exclude th is diagnosis. However,

a moderately breathless patient with suspected asthma is likely to have wheeze on chest auscultation. If there is no, or minimal, wheeze

and the patient has an elevated jugular venous pressure (Ch. 6) with peripheral oedema and inspiratory crackles on inspira tion, heart

failure with pulmonary oedema is likely. You should have a clear differential diagn osis before examining the patient. Always reconsider

your diagnosis if you do not find an expected physical sign or find an unexpected one.

Pain

The characteristics of pain suggest the likely cause.

Explore these to make a differential diagnosis. Use the SOCRATES approach (Box 2.10 ), the principles of which can also be helpful for

other symptoms, including dizziness or shortness of breath.

Associated symptoms

Any severe pain can produce nausea, sweating and faintness from the vagal and sympathetic response but some associated s ymptoms

suggest a particular underlying cause; e.g. visual disturbance may p recede migraine; palpitation (suggesting an arrhythmia) might occur

with angina. Pain disturbing sleep suggests a physical cause.

Effects on lifestyle

Ask ‘How do you cope with the pain?’ This helps you

to gain insight into the patient’s coping strategies (ICE:

2.10 Characteristics of pain (SOCRATES) Site

• Somatic pain, often well localised, e.g. sprained ankle

• Visceral pain, more diffuse, e.g. angina pectoris

O nset

• Speed of onset and any associated circumstances Character

• Described by adjectives, e.g. sharp/dull, burning/tingling,

boring/stabbing, crushing/tugging, preferably using the patient’s own description rather than offering suggestions Radiation

• Through local extension

• Referred by a shared neuronal pathway to a distant unaffected site, e.g. diaph ragmatic pain at the shoulder tip via the phrenic nerve

, C

)

Associated symptoms

• Visual aura accompanying migraine with aura

• Numbness in the leg with back pain suggesting nerve root irritation

Timing (duration, course, pattern)

• Since onset

• Episodic or continuous

• If episodic, duration and frequency of attacks

• If continuous, any changes in severity

Exacerbating and relieving factors

• Circumstances in which pain is provoked or exacerbated, e.g. food

• Specific activities or postures, and any avoidance measures that have been taken to prevent onset

• Effects of specific activities or postures, including effects of medication and alternative medical approaches

S everity

• Difficult to assess, as so subjective

• Sometimes helpful to compare with other common pains,

e.g. toothache

• Variation by day or night, during the week or month, e.g.

relating to the menstrual cycle

Work

Have you had to take time off

work?

How does your employer feel about it?

Are you self-employed?

Money

Have you lost money because of illness?

Do you think you are due compensation for your illness? Are you getting any benefits because you can’t work?

Leisure

Have you had to give up any of your hobbies or pastimes

because of your pain? What can you no longer do which you used to enjoy?

Chronic pain

Relationships

How has this affected your relationship with your partner/family?

Do you feel those close to you understand how you feel?

2.12 Questions to ask about common symptoms System

Cardiovascular

Respiratory

Gastrointestinal

Fig. 2.2 The effects of chronic pain: questions you might ask. Note that pain affects sev eral areas of a patient’s life but that these are

interlinked.

2.11 Pain threshold

Increased

• Exercise

• Analgesia

• Positive mental attitude

• Personality

Decreased

• Sleep deprivation

• Depression

• Financial and personal worries

• Anxiety and fear about the cause

• Past experience

p. 8). Areas to consider in relation to chronic pain are shown in Figure 2.2.

Genitourinary

Musculoskeletal

Endocrine

Neurological

Question

Do you ever have chest pain or tightness?

Do you ever wake up during the night

feeling short of breath?

Have you ever noticed your heart racing or thumping?

Are you ever short of breath?

Have you had a cough?

Do you ever cough anything up? 2

Have you ever coughed up blood?

Are you troubled by indigestion or

heartburn?

Have you noticed any change in your bowel habit recently?

Have you ever seen any blood or slime in

your stools?

Do you ever have pain or difficulty passing urine?

Do you have to get up at night to pass

urine? If so, how often?

Have you noticed any dribbling at the end of passing urine?

Have your periods been quite regular?

Do you have any pain, stiffness or swelling in your joints?

Do you have any difficulty walking or

dressing?

Do you tend to feel the heat or cold more

than you used to?

Have you been feeling thirstier or drinking

more than usual?

Have you ever had any fits, faints or

blackouts?

Have you noticed any numbness, weakness or clumsiness in your arms or legs?

Attitudes to illness

Many symptoms, such as pain and fatigue, are subjective and patients with identical conditions can present with dramatically different

histories.

• Pain threshold and tolerance: these vary between

patients and also in the same person in different circumstances. Patients vary i n their willingness to speak about their discomfort (Box

2.11).

• Past experience: personal and family experience influence the response to symptoms. A f amily history of sudden death from heart

disease may affect how a person interprets chest pain.

• Gains: most illness brings some gains to the patient. These vary from attention from family a nd friends to financial allowances and

avoiding work or stress. Patients may not be conscious of these but sometimes deliberate ly exaggerate symptoms (p. 27).

Examples of questions that can be used to ask about common symptoms are shown in Box 2.12.

Past history

Past medical history may be relevant to the presenting complaint: e.g. previous migraine in a patient with

2.13 Past history

• Have you had any serious illness that brought you to see your doctor ?

• Have you had to take time off work because of ill health?

• Have you had any operations?

• Have you attended any hospital clinics?

• Have you ever been in hospital? If so, why was that?

headache; haematemesis and multiple minor injuries in a patient with suspected alcohol abuse.

Ask open questions initially but move to closed questions to obtain relevant, meaningful information (Box 2.13 ).

Drug history

Ask about prescribed drugs and other medications, includi ng over-the-counter remedies, herbal and homeopathic remedies, laxatives,

analgesics and vitamin/ mineral supplements. Note the name of each drug, dose,

2 2.14 Example of a drug history

Drug

Aspirin Atenolol

Dose

75 mg daily

50 mg daily

Duration Indication

5 years Started after myocardial infarction

Cocodamol

(paracetamol + codeine) Salbutamol MDI

Up to 8 tablets daily 4 weeks Back pain

Side-effects, patient concerns Indigestion

Causes cold hands

(? compliance)

Causes constipation

2 puffs as necessary 6 months Asthma Palpitation, agitation

dosage regimen and duration of treatment, along with

2.15 Examples of single-gene inherited disorders

any significant adverse effects. Clarify, if

necessary, with

the general practitioner (GP). For patients being pre

scribed drugs for addiction, e g. methadone, ask the

dispensing community pharmacy to stop dispensing for

the duration of the hospital admission (Box 2.14).

Compliance, concordance

and adherence

Half of all patients do not take prescribed medicines

as directed. Patients who take their medication as pre

scribed are said to be compliant. Concordance implies

that the patient and doctor have negotiated and reached

Autosomal dominant

• Adult polycystic kidney

disease

• Myotonic dystrophy

• Neurofibromatosis

• Huntington’s disease

Autosomal recessive

• Cystic fibrosis

• Sickle cell anaemia

• Alpha-thalassaemia

• Alpha-1-antitrypsin deficiency

X-linked

• Duchenne muscular

dystrophy

• Haemophilia A

• Fragile X syndrome

an agreement on management, and adherence with

therapy is likely (though not guaranteed) to improve.

Ask patients to describe how and when they take their

medication. Check to see if they know the names of the

drugs and what they are for. Give them permission to

admit that they do not take all their medicines by saying:

since this may suggest environmental risks to the patient’s health.

‘That must be difficult to remember’.

Drug allergies/reactions

Ask if your patient has ever had an allergic reaction to

medication, especially before prescribing an antibiotic

(particularly a penicillin or vaccine). Clarify exactly

what patients mean by allergy. Drug allergies are over

reported by patients: only 1 in 7 who report a rash with

penicillin will have a positive penicillin skin test. Note

other allergies, such as foodstuffs or pollen. Record true

allergies prominently in the patient’s case records, drug

chart and computer notes. If the patient has had a severe

or life-threatening allergic reaction advise him to wear

an alert necklace or bracelet (Fig. 3.3).

Family history

Start with open questions, such as: ‘Are there any illnesses that run in your family?’ Follow up the presenting complaint , e.g. ‘Is there

any history of heart disease in your family?’ Many illnesses are associated with a positive family history but ar e not due to a single-gene

disorder (Box 2.15).

Document illness in first-degree relatives, i.e. parents, siblings and children. If you suspect an inh erited disorder such as haemophilia, go

back three generations for details of racial origins and consanguinity (Fig. 2.3). Note whether your patient or any close relative has been

adopted. Record the health of other household members,

Social history

The social history helps you to understand the context of the patient’s life and possib le relevant factors (Box 2.16). Focus on the relevant

issues; for example, ask an elderly woman with a hip fracture if she lives alone, whether she has any friends or relatives nearby , what

support services she receives and how well suited her house is for someone with poor mobility.

The patient’s illness may affect others such as a relative for whom the patient cares; but there may be no one at home to look after the

patient because, although she is married, her husband works abroad. Successful discharge from hospita l to the community requires these

problems to be addressed.

Lifestyle

Exercise

Does your patient undertake sports or regular exercise? What is it, how often does he d o it and how strenuous is it? Has the patient

modified the exercise because of illness?

Diet

Does your patient have any dietary restrictions and how has he decided on these? Some patients believe that they have a food intolerance

and may follow rigid exclusion diets with no medical evidence. Ask about

Normal male Dizygotic twins Affected male

Normal female Monozygotic twins Affected female

Mating Propositus

Consanguineous mating

Parents with son and daughter

(in order of birth)

Female with children by two males Zygosity uncertain ?

Sex unspecified

Number of children

2 3of sex indicated

Number of children

2 3of sex indicated

Heterozygotes for autosomal genes

Carrier X-linked 2

recessive gene

Dead

Abortion or stillbirth of unspecified sex

Identification of

person in pedigree

from the generation II (Roman numerals)

and the location in III the generation.

Proposita is III

Fig. 2.3 Symbols used in constructing a pedigree chart, with an example.

2.16 The social history

Upbringing

• Birth injury or complications

• Early parental attachments and disruptions

• Schooling, academic achievements or difficulties

• Further or higher education and training

• Behaviour problems

Home life

• Emotional, physical or sexual abuse*

• Experiences of death and illness

• Interest and attitude of parents

Occupation

• Current and previous (clarify exactly what a job entails)

• Exposure to hazards, e.g. chemicals, asbestos, foreign travel,

accidents and compensation claims

• Unemployment: reason and duration

• Attitude to job

Finance

• Circumstances, including debts

• Benefits from social security

Relationships and domestic circumstances

• Married or long-term partner

• Quality of relationship

*only ask if relevant to the history

• Problems

• Partner’s health, occupation and attitude to patient’s illness

• Who else is at home? Any problems, e.g. health, violence, bereavement?

• Any trouble with the police?

House

• Type of home, size, owned or rented

• Details of home, including stairs, toilets, heating, cooking facilities, neighbour s

Community support

• Social services involvement, e.g. home help, meals on wheels

• Attitude to needing help

Sexual history*

Leisure activities

• Hobbies and pastimes

• Pets

Exercise

• What, where and when? Substance misuse*

2 2.17 Examples of occupational disorders

Occupation

Shipyard workers, boilermen

Factor

Asbestos

Dairy farmers Leptospira hadjo

Fungus spores on mouldy hay

Divers Surfacing from depth too quickly

Industrial workers

Bakery workers

Healthcare workers

Work involving noisy machinery

Chemical exposure, e.g. chromium

Flour dust

Cuts, needlestick injuries Excessive noise

HIV, human immunodeficiency virus.

Disorder

Pleural plaques

Asbestosis

Mesothelioma

Lymphocytic meningitis

Farmer’s lung (hypersensitivity pneumonitis)

Decompression sickness

Central nervous system, skin, bone and joint symptoms

Dermatitis on hands

Presents

Over 20 years later

Within 1 week

Within 4–18 hours

Immediately and up to 1 week

Variable

Occupational asthma

HIV, hepatitis B and C Sensorineural hearing loss Variable

Incubation period >3 months Develops over months

2.18 Incubation periods of travel-related infections

Disease Incubation period Falciparum malaria 8–25 days Vivax malaria 8–27 days Typhoid fever 10–14 days Dengue fever 3–15

days Schistosomiasis 2–63 days Hepatitis A 28–42 days HIV infection 12–26 weeks

HIV, human immunodeficiency virus.

Travel to presentation Up to 6 weeks

Up to 1 year

Up to 3 weeks

Up to 10 weeks

Up to 6 weeks

Up to ?12 years

Usual symptoms

Fever

Fever, headache

Itch, fever, haematuria, abdominal discomfort Jaundice

Weight loss, pneumonia

the frequency and times of meals and the types of foods eaten.

Occupational history

Work profoundly influences health, while unemployment is associated with increas ed morbidity and mortality. Some occupations are

associated with particular illnesses (Box 2.17).

Take a full occupational history from all patients. ‘Tell me about all the jobs you have done in your working life.’ Clarify what the

patient does at work, in particular, any chemical or dust exposure (p. 8). Symptoms that improve over the weekend or during holidays

suggest an occupational disorder. Hobbies may also be relevant, e.g. psittacosis pneumonia or hypersensitivity pneumonitis in those who

keep birds.

Travel history

Returning travellers commonly present with illness.

They risk unusual or tropical infections, and air travel itself increases certain

conditions, e.g. middle-ear problems or deep vein thrombosis. The incubation period is helpful in deciding on the likelihood of an illness

(Box 2.18).

List the countries visited and the dates they were there. Enquire about the type of accommo dation used and the activities undertaken,

including sexual contacts. Note any travel vaccination or malarial prophylaxis taken.

Sexual history

Only take a full sexual history if this is appropriate (p. 224). Ask questions sensitivel y and objectively. Signal your intentions: ‘As part of

your medical history, I need to ask you some questions about your relationships. Is th is all right?’ (Box 2.19).

Smoking

Ask if your patient has ever smoked; if so, find out for how long, what form (cigarettes, cigars, pipe,

2.19 Taking a sexual history

• Are you currently in a relationship?

• How long have you been with your partner?

• Is it a sexual relationship?

• Have you had any (other) sexual partners in the last 12 months?

• How many were male? How many female?

• When did you last have sex with:

• your partner?

• anyone else?

• Do you use barrier contraception – sometimes, always or never?

• Have you ever had a sexually transmitted infection?

• Are you concerned about any sexual issues?

2.20 Calculating pack years of smoking 20 cigarettes = 1 packet

Number of cigarettes smoked per day ×Number of years smoking 20

For example, a smoker of 10 cigarettes a day who has smoked for 15 years would have s moked:

10 ×15

= 7 5pack years

2.21 An alcohol history

• Quantity and type of drink

• Daily/weekly pattern (especially binge drinking and morning drinking)

• Usual place of drinking

• Alone or accompanied

• Purpose

• Amount of money spent on alcohol

• Attitudes to alcohol

2.22 Calculating units of alcohol Method 1

Standard measure (1unit)=1small glass of wine

1half-pint of beer

1short of spirits

Method 2

Standard measure(1unit)= 25ml of 40% alcohol

=10ml ethanol

x % proof = x units of alcohol per litre

Examples

1 litre of 40% proof spirits contains 400 ml ethanol or 40 units 750 ml (standard b ottle) contains 30 units alcohol

1 litre of 4% beer contains 40 ml ethanol or 4 units 500 ml can contains 2 unit s of alcohol

Alternatively, use an online calculator, e.g. http://

www.drinkaware.co.uk/how-many-units.html.

chewed) and how much. For smokers, use ‘pack years’ (Box 2.20) to estimate th e risk of tobacco-related health problems (Fig. 2.4) (p.

147). Most patients with COPD have tobacco consumption >20 pack years. If appropr iate, enquire about other substances smoked, e.g.

cannabis, heroin. Don’t forget to ask non-smokers about their exposure to environmental t obacco smoke (passive smoking).

Cerebrovascular disease Tobacco amblyopia Oral cancer

Lung cancer

Alcohol

Try asking: ‘Do you ever drink any alcohol?’ Use open questions, giving permission for patients to tell you, and do not judge them.

Follow up with closed questions covering:

• what?

• when?

• how much? (Box 2.21).

Other useful questions are:

• When did you last have a drink?

• What’s the most you ever drink?

The number of units of alcohol consumed each week can be calculated in two ways (Box 2.22).

Alcohol problems

• Hazardous drinking is the regular consumption of more than:

• 24 g of pure ethanol (3 units) per day for men

• 14 g of pure ethanol (2 units) per day for women.

Chronic obstructive pulmonary disease

Ischaemic heart disease

Peptic ulceration

Small babies, and other obstetric problems

Erectile dysfunction

Peripheral vascular disease

Fig. 2.4 Tobacco-related disorders. 17

2 2.23 Features of alcohol dependence

• A strong, often overpowering, desire to take alcohol

• Inability to control starting or stopping drinking and the amount that is drunk

• Tolerance, where increased doses are needed to achieve the effects originally produce d by lower doses

• Withdrawal state when drinking is stopped or reduced, including tremor, sw eating, rapid heart rate, anxiety, insomnia and occasionally

seizures, disorientation or hallucinations (delirium tremens). It is relieved by more a lcohol

• Neglect of other pleasures and interests

• Continuing to drink in spite of being aware of the harmful consequences

2.24 The CAGE questionnaire

• Cut down: Have you ever felt you should cut down on your drinki ng?

• Annoyed: Have people annoyed you by criticising your drinking?

• Guilty: Have you ever felt bad or guilty about your drinking?

• Ever: Do you ever have a drink first thing in the morning to steady you or help a hangover (an eye opener)?

Positive answers to two or more questions suggest problem

drinking; confirm this by asking about the maximum taken.

Cerebellar

degeneration

Wernicke’s

encephalopathy

Pseudo-Cushingoid facies

Cortical atrophy Head injury

Seizures

Delirium tremens

CAGE questionnaire is easy to remember and will identify heavy drinkers but is not ver y sensitive (Box 2.24). The fast alcohol screening

test (FAST) questionnaire is more sensitive but more complex (Box 2.25).

Non-prescribed drug use

Ask all patients who may be using drugs about their use of non-prescribed drugs. In B ritain about 30% of the adult population has used

illegal or non-prescribed drugs (mainly cannabis) at some time (Boxes 2.26 and 2.2 7).

Gastritis

Erectile

dysfunction

Cardiomyopathy Hypertension

Hepatitis and chronic liver

disease

Portal

hypertension

Pancreatitis

Burns and other trauma Proximal myopathy

Fig. 2.5 Alcohol-related disorders. Peripheral neuropathy

• Binge drinking, involving a large amount of alcohol causing acute intoxication, i s more likely to cause problems than if the same

amount is consumed over 4 or 5 days. Everyone should have at least 2 days per week when the y drink no alcohol.

• Harmful drinking results in physical or mental health damage or disruption to social

circumstances.

• Alcohol dependence is when alcohol use takes a

higher priority over other behaviours that

previously had greater value (Box 2.23).

Identifying alcohol problems early is important because of the health risks to patients and their families (Fig. 2.5). It can be difficult and

screening tests can help. The

Systematic enquiry

Systematic enquiry uncovers symptoms that may have been forgotten. Ask: ‘Is there anything else you would like to tell me about?’

Until you are experienced, run through with every patient all of the symptoms i n Box 2.28. Follow up any positive response by asking

questions to increase or decrease the probability of certain diseases.

Some examples of targeted systematic enquiry are as follows:

• The smoker with weight loss: are there any

respiratory symptoms, e.g. unresolving chest infection or haemoptysis to suggest lung cancer?

• The patient with recurrent mouth ulcers: do any alimentary symptoms suggest C rohn’s disease or coeliac disease?

• The patient with palpitation: are there any endocrine symptoms to suggest thyroto xicosis or is there a family history of thyroid disease?

Is the patient anxious or drinking too much coffee?

• If a patient smells of alcohol, ask about related symptoms, such as numbness in the feet due to alcoholic neuropathy.

Putting it all together

With all the relevant information assembled, you should have a list of differential d iagnoses. Before you examine the patient:

• Briefly summarise what the patient has told you.

• Reflect this back to the patient. This allows patients

to correct anything you have misunderstood and add anything they have forgotten.

• Gain the patient’s permission to examine him.

2.25 The fast alcohol screening test (FAST) questionnaire

For the following questions please circle the answer that best

applies

1 drink = 1/2 pint of beer or 1 glass of wine or 1 single

measure of spirits

1. Men: How often do you have eight or more drinks on one occasion?

Women: How often do you have six or more drinks on one occasion?

• Never (0)

• Less than monthly (1)

• Monthly (2)

• Weekly (3)

• Daily or almost daily (4)

2. How often during the last year have you been unable to remember what happened the night before because you had been drinking?

• Never (0)

• Less than monthly (1)

• Monthly (2)

• Weekly (3)

• Daily or almost daily (4)

3. How often during the last year have you failed to do what was normally expected of you because of drinking?

• Never (0)

• Less than monthly (1)

• Monthly (2)

• Weekly (3)

• Daily or almost daily (4)

4. In the last year has a relative or friend, or a doctor or other health worker been c oncerned about your drinking or suggested you cut

down?

• Never (0)

• Yes, on one occasion (2)

• Yes, on more than one occasion (4)

Scoring FAST

First stage

If the answer to question 1 is Never, then the patient is probably not misusing alcohol

If the answer is Weekly or Daily or Almost daily, then the patient is a hazardous, harmful or dependent drinker 50% of people are

classified using this one question Second stage

Only use these questions if the answer is Less than monthly or Monthly

Score questions 1–3: 0, 1, 2, 3, 4

Score question 4: 0, 2, 4

Minimum score is 0

Maximum score is 16

Score for hazardous drinking is 3 or more

2.26 Non-prescribed drug history

• What drugs are you taking?

• How often and how much?

• How long have you been taking drugs?

• Any periods of abstinence? If so, when and why did you start using drugs again?

• What symptoms do you have if you cannot get drugs?

• Do you ever inject? If so, where do you get the needles and syringes?

• Do you ever share needles, syringes or other drug

paraphernalia? 2

• Do you see your drug use as a problem?

• Do you want to make changes in your life or change the way you use drugs?

• Have you been checked for blood-borne viruses?

2.27 Complications of drug misuse Infections

• Hepatitis B and C

• Soft-tissue infection and abscesses

• Necrotising fasciitis

• Septic pulmonary

thromboembolism

• Lung abscesses

• Aspiration pneumonia

Injury

• Thrombophlebitis and deep vein thrombosis

Overdose

• Rhabdomyolysis and renal failure

Chaotic lifestyle leading to

• Poor nutrition

• Poor dental hygiene

• Failure to care for

dependants

HIV, human immunodeficiency virus.

• HIV

• Endocarditis

• Tetanus

• Wound botulism

• Sexually transmitted

disease: many work in the sex industry to finance their habit

• Skin ulceration

• Arterial injury and occlusion

• Respiratory failure

• Debt

• Crime

• Prison

2 2.28 Systematic enquiry: cardinal symptoms

General health

• Well-being

• Appetite

• Weight change

Cardiovascular system

• Chest pain on exertion (angina)

• Breathlessness:

• Lying flat (orthopnoea)

• At night (paroxysmal nocturnal dyspnoea)

• On minimal exertion – record how much

Respiratory system

• Shortness of breath (exercise tolerance)

• Cough

• Wheeze

Gastrointestinal system

• Mouth (oral ulcers, dental problems)

• Difficulty swallowing (dysphagia – distinguish from pain on swallowing , i.e. odynophagia)

• Nausea and vomiting

• Vomiting blood (haematemesis)

• Indigestion

Genitourinary system

• Pain passing urine (dysuria)

• Frequency passing urine (at night, nocturia)

• Blood in the urine (haematuria)

Men

If appropriate:

• Prostatic symptoms, including difficulty starting – hesitancy

• Poor stream or flow

• Terminal dribbling

Women

• Last menstrual period (consider pregnancy)

• Timing and regularity of periods

• Length of periods

• Abnormal bleeding

Nervous system

• Headaches

• Dizziness (vertigo or lightheaded)

• Faints

• Fits

• Altered sensation

Musculoskeletal system

• Joint pain, stiffness or swelling

• Mobility

Endocrine system

• Heat or cold intolerance

• Change in sweating

Other

• Bleeding or bruising

• Energy

• Sleep

• Mood

• Palpitation

• Pain in legs on walking (claudication)

• Ankle swelling

• Sputum production (colour, amount)

• Blood in sputum (haemoptysis)

• Chest pain (due to inspiration or coughing)

• Heartburn

• Abdominal pain

• Change in bowel habit

• Change in colour of stools (pale, dark, tarry black, fresh blood)

• Libido

• Incontinence (stress and urge)

• Sexual partners – unprotected intercourse

• Urethral discharge

• Erectile difficulties

• Vaginal discharge

• Contraception

• If appropriate:

• Pain during intercourse (dyspareunia)

• Weakness

• Visual disturbance

• Hearing problems (deafness, tinnitus)

• Memory and concentration changes

• Falls

• Excessive thirst (polydipsia)

• Skin rash

THE PSYCHIATRIC HISTORY

Mental disorders are very common, frequently coexist with physical disorders, and cause much mortality and morbidity. Psychiatric

assessment has four elements:

• history

• mental state examination (MSE)

• selective physical examination

• collateral information.

THE HISTORY

The distinction between symptoms and signs is less clear in psychiatry than the rest of me dicine. The psychiatric interview, which covers

both, has three purposes:

• to obtain a history (Boxes 2.29 and 2.30)

– symptoms

• to assess the present mental state – signs

• to establish rapport to help further management.

Sensitive topics

In some settings, and for some subjects, use particular skill and tact to obtain a nswers and to maintain rapport. This applies particularly

to:

• sexual issues, e.g. sexual dysfunction, gender

identity

• major traumatic experiences, e.g. rape, childhood

sexual abuse, witnessing a death

• illicit drug use

• crime

• suicidal or homicidal ideas

• non-clinical settings, e.g. police stations, prisons.

2.29 Content of a psychiatric history

• Referral source

• Reason for referral

• History of presenting complaint(s)

• Systematic enquiry into other relevant problems and symptoms

• Past medical/psychiatric history

• Prescribed and non-prescribed medication

• Substance use: illegal drugs, alcohol, tobacco, caffeine

• Family history (including psychiatric disorders)

• Personal history

2.30 Personal history

• Childhood development

• Losses and experiences

• Education

• Occupation(s)

• Financial circumstances

• Relationships

• Partner(s) and children

• Housing

• Leisure activities

• Hobbies and interests

• Forensic history (trouble with the police and courts) You should develop goo d rapport at the first interview, and consolidate it before

raising a sensitive topic, though sometimes you have to cover such material without delay. In these cases, tell t he patient about the nature

of and reason for your sensitive enquiries (Box 2.31).

The uncooperative patient

Adapt your assessment when a patient is mute, agitated, 2

hostile or otherwise uncooperative, and place greater

reliance on observation and collateral information. The safety of the patient, other patients , staff and yourself is paramount so you may

only be able to make a partial assessment of agitated or hostile patients.

Mental state examination

The MSE systematically evaluates the patient’s mental condition at the time of interv iew (Box 2.32). The aim is to establish signs of

disorder that, with the history, enable you to make, suggest or exclude a diagnosis. While making specific enquiries, you should observe,

evaluate, and draw inferences in the light of the history. This is daunting, but with good teaching, practice and experience you will learn

the skills.

MSE involves:

• observation of the patient

• incorporation of relevant elements of the history

• specific questions exploring various mental

phenomena

• short tests of cognitive function.

The focus is determined by the history and potential diagnoses. For examp le, detailed cognitive assessment in an elderly patient

presenting with confusion is crucial; similarly, carefully evaluate mood and suicid e risk when the presenting problem is depression.

2.31 Sensitive topics: what to ask

• You said a few minutes ago that sometimes you wish you had died in your sleep. I need to ask you a bit more about that thought. Have

you ever considered doing something that would make that happen?

• You’ve just told me that you feel your life isn’t worth living. Do you ev er think in the same way about your children’s lives?

• You indicated that something terrible happened to you when you we re a child. Do you want to tell me more about that now?

2.32 Elements of the Mental State

Examination (MSE)

• Appearance

• Behaviour

• Speech

• Mood

• Thought form

• Thought content

• Perceptions

• Cognition

• Insight

• Risk assessment

2 2.33 Behaviour: definitions 2.35 Mood: definitions Term

Agitation

Compulsion

Disinhibition

Motor retardation

Posturing

Definition

A combination of psychic anxiety and excessive, purposeless motor activity An unn ecessary, purposeless action that the patient is unable

to resist performing repeatedly

Loss of control over normal social behaviour

Decreased motor activity, usually a combination of fewer and slower movements

The maintenance of bizarre gait or limb positions for no valid reason

Term

Blunting

Catastrophic reaction

Flattening

Incongruity

Lability

Definition

Loss of normal emotional sensitivity to experiences

An extreme emotional and

behavioural overreaction to a trivial stimulus

Loss of the range of normal

emotional responses

A mismatch between the emotional expression and the associated thought

Superficial, rapidly changing and poorly controlled emotions

2.34 Speech: definitions

Appearance

Observe:

• general elements, e.g. attire, signs of self-neglect

• facial expression

• scars, tattoos, features of injury and/or self-injury

• signs of physical disease, e.g. spider naevi (chronic

alcoholic liver disease), exophthalmos

(thyrotoxicosis).

Term

Clang associations

Mutism

Neologism

Pressure of speech

Word salad

Echolalia

Definition

Thoughts connected by having a similar sound rather than by meaning

Absence of speech without impaired consciousness

An invented word, or a new meaning for an established word

Rapid, excessive, continuous speech (due to pressure of thought)

Meaningless string of words, often with loss of grammatical construction Senseless rep etition of the interviewer’s words.

Behaviour

Observe:

• cooperation, rapport, eye contact

• social behaviour, e.g. aggression, disinhibition

• overactivity, e.g. agitation, compulsions

• underactivity, e.g. stupor, motor retardation

• abnormal activity, e.g. posturing, involuntary

movements (Box 2.33).

Speech

Observe:

• articulation, e.g. stammering, dysarthria

• quantity, e.g. mutism, garrulousness

2.36 Mood: what to ask

• How has your mood been lately?

• Have you noticed any change in your emotions recently?

• Has your family commented recently on your mood?

• Do you still enjoy things that normally give you pleasure?

• rate, e.g. pressured, slowed

• volume, e.g. whispering, shouting

• tone and quality, e.g. accent, emotionality

• fluency, e.g. staccato, monotonous

• abnormal language, e.g. neologisms, dysphasia, clanging (Box 2.34).

Mood

This is the pervasive emotional state. Affect is the observable express ion of emotions, which is more variable over time. A useful

analogy is to think of a patient’s mood as a climate, with affect as the current weather.

Assess mood objectively by observation, and subjectively from the history and sp ecific enquiries (Boxes 2.35 and 2.36). Disturbance of

mood is the most important feature of depression, mania and anxiety, but mood changes commonly occur in other mental disorders such

as schizophrenia and dementia.

Abnormalities of mood consist of:

• problematic pervasive mood, e.g. depressed, elated, anxious, fearful, angry, suspicio us, irritable, perplexed

• abnormal range, e.g. flattened, expanded

• abnormal reactivity, e.g. blunted, labile, catastrophic

• inappropriateness, e.g. incongruous to

circumstances.

Thought form

Loosening of associations is sometimes termed formal thought disorder, and is a core featu re of schizophrenia. Subjectively, patients

may report having difficulty thinking clearly. Hypomania is characterised by pressure o f thoughts and flights of ideas. With depression

these processes are slowed and impoverished; this is also characteristic of dementia (Box 2.37 ).

2.37 Thought form: definitions Term

Circumstantiality

Concrete thinking Flight of ideas

Loosening of associations

Perseveration

Pressure of thought

Definition

Trivia and digressions impairing the flow but not direction of thought Inability to thin k abstractly

Rapid shifts from one idea to another, retaining sequencing

Logical sequence of ideas impaired Subtypes include knight’s move thinking, derailment, thought blocking and, in its extreme form,

word salad Inability to shift from one idea to the next

Increased rate and quantity of

thoughts

2.39 Thought content: what to ask

• What have your main worries been recently?

• What has been on your mind lately?

• Do you have any particular thoughts you keep coming back to?

2.40 Abnormal beliefs: definitions Term

Delusion

Delusional perception

2.38 Thought content: definitions Magical thinking Term

Hypochondriasis

Morbid thinking

Phobia

Preoccupation

Ruminations

Obsessions

Definition

Unjustified belief of suffering from a particular disease in spite of appropriate exa mination and reassurance

Depressive ideas, e.g. themes of guilt, burden, unworthiness, failure, blame, death, suicide

A senseless avoidance of a situation, object or activity stemming from a belief that has caused an irrational fear

Beliefs that are not inherently abnormal but which have come to dominate the patient’s thinki ng

Repetitive, intrusive, senseless thoughts or preoccupations

Ruminations which persists despite resistance.

Elements of thought form are:

• rate, e.g. pressure of thought, retardation (slowing)

• flow, e.g. flights of ideas, circumstantiality,

perseveration

• sequencing, e.g. loosening of associations

• abstract thinking, e.g. concrete thought.

Record examples of speech from the history to show how a person thinks and expresses thoughts.

Thought content

This is assessed from the history and specific enquiries (Box 2.38). Note though t content from what the patient has discussed during

history taking and then explore it by further questioning. It is divided into preoccupa tions, ruminations and abnormal beliefs:

• Preoccupations are common in normal and

abnormal mood states: an anxious person worries about physical illness, or the morbid thoug hts of depression.

Overvalued ideas

Thought

broadcasting Thought

insertion

Thought

withdrawal

Definition

2An abnormal belief, held with total

conviction, which is maintained in spite of proof or logical argument to the contrary

and is not shared by others from the

same culture

A delusion which arises fully formed from the false interpretation of a real

perception, e.g. a traffic light turning

green confirms that aliens have landed on the rooftop

An irrational belief that certain actions

and outcomes are linked, often culturally determined by folklore or custom, e.g.

fingers crossed for good luck

Beliefs that are held, valued, expressed

and acted on beyond the norm for the

culture to which the person belongs

The belief that the patient’s thoughts are heard by others

The belief that thoughts are being placed in the patient’s head from outside

The belief that thoughts are being

removed from the patient’s head

• Ruminations are preoccupations which are

abnormal because they are so repetitive or

groundless. They occur in hypochondriasis and obsessional disorders (Box 2.39 ).

• Abnormal beliefs fall into two categories: those that are not diagnostic of mental illness, e.g . overvalued ideas, superstitions, magical

thinking, and those that invariably signify mental illness, i.e. delusions. The main d ifference is that delusions either lack a cultural basis

for understanding the belief or have been derived from abnormal processes.

Overvalued ideas are beliefs of great personal significance that are abnormal because of their effects on a person’s behaviour or well-

being. For example, patients with anorexia nervosa may still believe they are fat when they are seriously underweight. They respond to

beliefs about their body image rather than their weight (Box 2.40).

Delusional beliefs matter greatly to the person, resulting in powerful emotional and important behavioural consequences: they are always

of clinical significance. They are classified by their content, such as:

• paranoid

• religious

• grandiose

• hypochondriacal

• guilt

2 2.41 Abnormal beliefs: what to ask

• Have there been times when you’ve thought something strange is going on?

• Do you ever think you’re being followed or watched?

• Do you ever feel other people can interfere with your thoughts or a ctions?

2.43 Perceptions: what to ask

• Do you ever hear voices when nobody is talking?

• What do they say?

• Where do they come from?

• Have you had any visions?

• Have you ever felt that you were not real or that the world around you wasn’t real?

2.42 Perceptions: definitions Term

Depersonalisation

Derealisation

Hallucination

Illusion

Pseudohallucination

Definition

A subjective experience of feeling unreal

A subjective experience that the surrounding environment is unreal A false perception ar ising without a valid stimulus from the external

world A false perception that is an

understandable misinterpretation of a real stimulus in the external world A false perception which is perceived as part of one’s internal

experience

• love

• jealousy

• infestation

• thought interference

• control.

Bizarre delusions are easy to recognise, but not all delusions are weird ideas: a man con vinced that his partner is unfaithful may or may

not be deluded. Even if a partner were unfaithful, it would still amount to a delusiona l jealousy if the belief were held without evidence

or for some unaccountable reason, such as finding a dead bird in the garden.

Delusions can sometimes be understood as the patient’s way of trying to make sense of his experie nce. Their content often gives a clue

that may help type the underlying illness, e.g. delusions of guilt suggest severe depression whereas grandio se delusions typify mania

(Box 2.41). Some delusions are characteristic of schizophrenia, most notably a delusional perception or primary delusion. These include

‘passivity phenomena’: the belief that thoughts, feelings or acts are no longer controlled by the person’s free will.

Perceptions

Assess perceptions using the history and specific enquiries backed up by observation (Box 2.42). People normally distinguish easily

between their inner and outer worlds and know what is real and what reality feels like. This can occasionally be disrupted so that normal

perceptions become unfamiliar while abnormal perceptions seem real. These an omalies fall into several categories:

• depersonalisation, derealisation

• altered perceptions: sensory distortions, illusions

• false perceptions: hallucinations,

pseudohallucinations.

Depersonalisation and derealisation are associated with severe tiredness and inte nse anxiety, but also occur in

most types of mental illness. With altered perceptions there is a real external objec t but its subjective perception has been distorted.

Sensory distortions, such as unpleasant amplification of light (photophobia) or sound (hyperacusis), can occur in physical diseases, but

are also common in anxiety states and drug intoxication or withdrawal. Dim inution of perceptions, including pain, can occur in

depression and schizophrenia.

Illusions commonly occur among people with established impairment of vision or hearing . They are also found in predisposed patients

subjected to sensory deprivation, notably after dark in a patient with clouding of cons ciousness.

True hallucinations arise without external stimuli; they usually indicate severe mental illness, bu t can occur naturally when going to

sleep (hypnagogic) or waking up (hypnopompic). Hallucinations can be:

• auditory

• visual

• olfactory

• gustatory

• tactile.

Any form of hallucination can occur in any severe mental disorder. The most common are auditory and visual hallucinations, the former

are associated with schizophrenia, the latter with delirium. Some auditory hallucin ations are characteristic of schizophrenia, e.g. voices

discussing the patient in the third person, or giving a running commentary on the person’s activities.

Pseudohallucinations are common. The key distinction from a true hallucin ation is that these phenomena occur within the patient, rather

than arising externally. They have an ‘as if’ quality, and lack the vividness and reality o f true hallucinations. Consequently, the affected

person is not usually distressed by them; and does not normally feel the need to respond, as happens with true hallucinations (Box 2.43).

Cognition

This is assessed from the history and observation; evaluate any deficit using standard tests. Use the history, observation, MSE and rating

scales (see below) together to diagnose and distinguish between the ‘three Ds’ (dementia, deliriu m and depression) which are common in

the elderly and hospital patients.

Core cognitive functions include ( Box 2.44):

• level of consciousness

• orientation

• memory

• attention and concentration

• intelligence.

Mental disorders are rarely associated with a reduced level of (or clouded) c onsciousness, except delirium (which is both a physical and a

mental disorder), where it is common.

2.44 Cognition: definitions 2.45 Insight: definitions

Term

Clouding of consciousness Confabulation

Definition

A reduced level of consciousness observed as drowsiness (coma in extreme cases) P lausible but false memories that cover memory gaps

Term

Insight

Definition

Recognising that abnormal mental experiences are in fact abnormal

Accepting that these abnormalities amount to a mental illness

Accepting the need for treatment

Orientation is a key aspect of cognition, being particularly sensitive to impairment. Disorientati on is the hallmark of the ‘organic mental

state’ found in delirium and dementia. Abnormalities may be evident during the interview. Check the patient’s knowledge of the current

time and date, recognition of where he is (place) and identification of familiar people (person).

Memory function is divided into:

• Registration: test by asking the patient to repeat the names of three unrelated objects e.g. ap ple, table,

penny; any mistake is significant. Alternatively, slowly and clearly say several rando m single digits, e.g. 6, 3, 5, 9, 1, 4, 7. Then ask the

patient to repeat them. A person with normal function can repeat at least five digits.

• Short-term memory: test by giving the patient some new information; once this has registered, ch eck retention after 5 minutes (with a

distracting task in between). Do the same with the names of three objects ; any error is significant. Alternatively, use a six-item name and

address, e.g. Mr David Green, 25 Sharp Street. More than one error indicates impairment.

• Long-term memory is assessed mainly from the personal history that the patient provides . Gaps and mistakes are often obvious, but

some patients confabulate (fill in gaps in their memory with unconsciously fabricated facts) s o check the account with a family member

if possible. Failing long-term memory is characteristic of dementia, although th is store of knowledge can be remarkably intact in the

presence of severe impairment of other cognitive functions. Confabulation is a core fe ature of Korsakoff’s syndrome, a complication of

chronic alcoholism.

Impaired attention and concentration occur in many mental di sorders and are not diagnostic. Impaired attention is obs erved as increased

distractibility, with the patient responding inappropriately to extraneous stimuli which may be real, e.g. a noise outside the room, or

unreal, e.g. auditory hallucinations. Concentration is the patient’s ability to stick with a mental tas k. It is tested by using simple,

repetitive sequences, such as asking the patient to repeat the months of the yea r in reverse or to do the ‘serial 7s’ test, in which 7 is

subtracted from 100, then from 93, then 86, etc. Note the finishing point, the number of errors and the time taken.

Estimate intelligence clinically from a combination of the history of educational attainment and occupations, and at interview from

vocabulary, general knowledge, abstract thought, foresight and understanding. If in doubt as to whether the patient has a learning

disability, or if there is a discrepancy between the history and presentation, a psycholog ist should formally test IQ.

2.46 Insight: what to ask 2

• Do you think anything is wrong with you?

• What do you think is the matter with you?

• If you are ill, what do you think needs to happen to make you bette r?

Insight is the degree to which a patient agrees that he is ill and in need of treatment. Insight matters, since absent or incomplete insigh t

leads to non-compliance (Boxes 2.45 and 2.46).

Risk assessment

Risk assessment is a crucial part of every psychiatric assessment. Consider:

• The person(s) at risk.

Usually the patient, but others at risk are likely to be family, or, less commonly, specific individua ls (neighbours, celebrities) or members

of specific groups (defined by age, ethnicity, occupation, etc.).

• Nature of the risk:

There may be direct risk to life and limb (as in suicide, self-harm or violence to oth ers) or indirect risk to health (through refusal of

treatment for physical or mental illness) or welfare (through inability to provide basic care – food, warmth, shelter, hygiene – for oneself

or one’s dependants).

Evaluate risk in all psychiatric assessments ( Box 2.47), but in depth when the:

• presentation includes acts or threats of self-harm or

reports of command hallucinations

• past history includes self-harm or violent behaviour

• social circumstances show a recent, significant loss

• mental disorder is strongly associated with risk, e.g.

depression or a paranoid state.

Screening questions for mental illnesses

A psychiatric diagnosis is made by identifying particular clusters of symptoms and ment al state changes in the patient. Cover certain

areas routinely when you suspect a particular mental illness (Box 2.48). No single que stion clinches the diagnosis for any specific type of

mental disorder, but some features are closely associated with particular mental illnesses, e.g:

• passivity phenomena and schizophrenia

• re-experiencing an ordeal and post-traumatic stress

disorder

• phobia of normal weight and anorexia nervosa.

2 2.47 Risk assessment: what to ask

Suicide/self-harm

• How do you feel about the future?

• Have you thought about ending your life?

• Have you made plans to end your life?

• Have you attempted to end your life?

Homicide/harm to others

• Are there people you know who would be better off dead?

• Have you thought about harming anyone else?

• Have you been told to harm anyone else?

2.49 Personality disorder

Definition

Patterns of experience and behaviour which are:

• Pathological (i.e. outwith social norms)

• Problematic (for the patient and/or others)

• Pervasive (affecting most or all areas of a patient’s life)

• Persistent (adolescent onset, enduring throughout adult life

and resistant to treatment)

2.48 Screening questions for mental illnesses

When you suspect an anxiety disorder

• What physical symptoms have you been experiencing?

• How relaxed have you been feeling recently?

• Have there been any particular concerns or worries on your mind re cently?

When you suspect a depressive disorder

• How has your mood been recently?

• Are you still enjoying things the way you used to?

• How do you view the future just now?

When you suspect schizophrenia

• Have you any beliefs that you think other people might find odd?

• Have you had any unusual experiences recently?

• Have you had any difficulty controlling your thinking?

• Have you heard people’s voices when there’s no one around? (Where do y ou think the voices come from? What do they say?)

2.50 The Abbreviated Mental Test

Each question scores 1 mark; a score of 8/10 or less indicates confusion

• Age

• Date of birth

• Time (to the nearest hour)

• Year

• Hospital name

• Recognition of two people, e.g. doctor, nurse

• Recall address

• Dates of First World War (or other significant event)

• Name of the monarch (or prime minister, president as

appropriate)

• Count backwards from 20 to 1

health professionals. Previous psychiatric assessments are valuable when considering a diagnosis of pers onality disorder, as this depends

on information about behaviour patterns over time rather than deta ils of the current presentation (Box 2.49).

However, these features may occur in other mental disorders.

Some symptoms are non-specific but important. They include:

• sleep disturbance

• impaired concentration

• anxiety.

THE PHYSICAL EXAMINATION

Physical and mental disorders are associated, so always consider the physical dimension in a ny patient presenting with a psychiatric

complaint. The patient’s age, health and mode of presentation will determine the extent of physical assessment required. Usually, general

observation, coupled with basic cardiovascular and neurological examination, is ade quate.

Collateral history

This is important, especially when the patient:

• has a severe learning disability or confusional state

• has a mental disorder that prevents effective

communication

• is very disturbed or uncooperative.

Sources of third-party information include family and

other carers, as well as past and present GPs and other

Psychiatric rating scales

Most of these were developed in research studies to assist diagnosis, or to measure change in severity of illness. Some require special

training; all should be used sensibly. In general, scales are too inflexible and limited in scope to replace a well-conducted standard

psychiatric interview, but they can be useful adjuncts for screening, measuring r esponse to treatment or focusing on particular areas. In

routine practice, scales are most widely used to assess cognitive function when a n organic brain disorder is suspected. They include:

• Abbreviated Mental Test (AMT): takes <5 minutes

( Box 2.50)

• Mini Mental State Examination (MMSE): takes

5–10 minutes.

Well-known instruments assessing areas other than cognition include:

• general morbidity:

• General Health Questionnaire (GHQ)

• mood disorder:

• Hospital Anxiety and Depression Scale (HADS)

• Beck Depression Inventory (BDI)

• alcohol:

• CAGE questionnaire (Box 2.24)

• FAST questionnaire (Box 2.25).

Medically unexplained symptoms (MUS)

MEDICALLY UNEXPLAINED SYMPTOMS (MUS)

Symptoms are not synonymous with disease but are subjective experiences that may arise from many so urces (Box 2.51). There is a

major distinction between disease and illness. Disease is a cluster of symptoms resulting from demonstrable pathological processes, e.g.

coronary artery disease. Illness (or disorder) is a cluster of symptoms where there m ay be no demonstrable pathological process despite

clearly impaired function, e.g. anxiety.

When symptoms impair a patient’s normal function, do not fit characteristic patterns of disease and persist witho ut any abnormalities on

examination and investigation, they are called ‘functional’ or ‘medically unexplained’. Mo re than 30% of patients attending their GP

have MUS (with similar proportions in secondary care, where disease prevalence is much greater) (Fig. 2.6). MUS cause similar levels of

disability to those resulting from disease and are often associated wit h significant emotional distress. If such patients are not managed

effectively, fruitless investigations and harm from unnecessary drugs or procedu res may result. The approach to such patients is

important and may differ between specialists.

MUS raise strong feelings in patients and doctors. Patients may f eel they are not believed, or that their symptoms are being dism issed as

‘all in the mind’. Doctors may feel their competence is being questioned.

A dualistic model of mind and body as separate entities is too simplistic and clinically unh elpful. If you think of physical disorders as

‘real’ and MUS as ‘not real’ because they arise from emotional distress or psych iatric disorder your patients will soon detect this and

react accordingly. Symptoms result from complex interactions

between biological, social and psychological factors; 2

each component is unique to the individual. Many people with severe diseases co pe with

their symptoms, function remarkably well and work in full-time jobs. Others, wit h apparently modest symptoms, cannot function

effectively. There may be little correlation between symptom severity, disease processes, social functioning and response to treatment.

Patients with a proven disease may not improve symptomatically with treatment. For example, therapy for Helicoba cter pylori-

associated gastritis in a patient with a peptic ulcer may cure the ulcer but not the dysp eptic symptoms. We should understand our patients

as individuals and help them to cope with the distress that their symptoms provoke.

2.51 Examples of factors influencing symptoms

Factors Example

Pathological Chest pain from coronary artery disease Physiological Tremor

Psychological Paraesthesia from hyperventilation Behavioural Weakness from excess b ed rest External Compensation and the welfare

state

Symptoms and definitions

Many terms are used to describe MUS and most specialities have a name for the common ones they see (Box 2.52). These include

symptom labels (low back pain), symptom syndromes (chronic fatigue syndrome, irritable bow el syndrome), non-diagnoses (MUS,

functional), psychological causes (psychosomatic), psychological proc esses (somatisation), psychiatric diagnoses (conversion disorder)

and malingering (fictitious symptoms simulated for material gain).

Patients with multiple symptoms are more likely to have MUS. In general, the more symptoms a patient has, the greater the likelihood of

psychiatric illness or distress, e.g. anxiety and depression. Certain symptoms are more likely t o be MUS and are not accompanied by any

Pathological cause 8

2.52 Examples of medically unexplained symptoms and ‘functional’ syndromes in the me dical specialities

Neurology

Gastroenterology 2

Gynaecology

Ear, nose and throat Cardiology

Fig. 2.6

Chest pain

tigue

Dizziness Headache Oedema Back pain Dyspnoea Insomnia

Common symptoms presenting in primary care, showing Abdominal pain Numbness the percentage with an underlyin g pathological cause.

Rheumatology

Infectious disease Immunology/allergy

Functional weakness, tension

headache, non-epileptic attacks, hemisensory symptoms

Irritable bowel syndrome, non-ulcer dyspepsia, chronic abdominal pain

Chronic pelvic pain, urethral syndrome Functional dysphonia, globus

Atypical chest pain, unexplained palpitation, non-cardiac chest pain

Fibromyalgia

(Postviral) chronic fatigue syndrome

Multiple chemical sensitivity syndrome 27

2.53 Symptoms and their relationship to physical disease Sometimes

Chest pain

Breathlessness

Syncope

Abdominal pain

Infrequently Fatigue

Back pain Headache Dizziness

2.55 Misdiagnosis and conversion disorder 24% of people diagnos ed with conversion disorder develop an illness that could have

explained their presenting symptoms. Stone J, Smyth R, Carson A et al. Systematic revie w of misdiagnosis of conversion symptoms and

‘hysteria’. BMJ 2005;331:989.

a positive diagnosis from the history and confirming this by negative findings on physical exam ination allow reassurance and an

explanation tailored to the patient.

2.54 Risk factor for medically unexplained symptoms (MUS)

Women who have experienced parental illness or lack of care

during childhood are predisposed to MUS.

Craig TKJ, Cox AD, Klein K. Intergenerational transmission of somatization behaviou r: a study of chronic somatisers and their children.

Psychol Med 2002;32:805–816.

Physical disease

Learnt illness behaviour Female

MUS

Depression and anxiety Lack of care as

child

Health worries and

stressors

Fig. 2.7 Risk factors for medically unexplained symptoms (MUS).

Presenting complaint

Keep an open mind when talking with all patients; remember that patients with MUS ma y also have or develop disease. Always take a

full history and perform a full clinical examination. Patients will feel that you are taking them seriou sly and you are less likely to miss

any serious physical disease (Box 2.55).

Accept all symptoms at face value and find out about all of them. Explore exac erbating and relieving factors. Find out when it all started;

try asking ‘when did you last feel well?’

Patients’ beliefs in their illness matter; what do they think is wrong? Why have they com e now and what do they hope you can do for

them? How disabling are their symptoms? What do the symptoms now prevent them from doing? Find out what a typical day is like.

What has happened to them with previous doctors? Patients may complain about previous doctors or certain treatment s they have been

offered. Allowing a patient to express dissatisfaction shows that you are inter ested, and helps you avoid suggesting management options

the patient is likely to reject. However, recognise that you are only being shown one side of a complicated situation. Maintain a

professional approach, ensuring that you do not get drawn into criticising othe r healthcare providers or their actions.

Often, there are inconsistencies in the history which you should explore and highlig ht for the patient, e.g. a patient with severe disabling

chest pain without angiographic evidence of coronary artery disease may still fir mly believe he has angina. His records show that this is

not the case and that he has clearly been told this previously. This needs to be explored with him to help demonstrate that his belief is not

based on evidence.

of the usual features that suggest serious physical disease. Some symptoms are par ticularly unlikely to be associated with significant

disease (Box 2.53).

Causes

Certain factors increase the risk of MUS (Fig. 2.7 and Box 2.54).

History

MUS are so common that primary care physicians become adept at spotting this from the history. Making

Past history

Whenever possible, get all the previous notes, or at least summaries of them. Review these care fully, including childhood illnesses. This

can be time-consuming but worth the effort.

Social history

Note any welfare benefits where money is being received for disability, or lega l cases where financial compensation may be pending.

Putting it all together

Psychiatric history

Leave this until last. To gain the patient’s trust you should be empathic and non-judgem ental. Patients will then gain confidence that you

are not going to use their emotional symptoms ‘against them’. Patients are acutely sensitive to questions that sug gest they are making

things up so frame your questions carefully in terms of their symptoms. Ask ‘Do your symptom s ever make you feel down or frustrated?’

rather than ‘Do you ever feel depressed?’

Do not ask about a history of abuse at a first consultation unless the patient volunteers th e information. If the abuse was in the past, do

not feel that you have to do anything other than bear witness to the patient’s past suffering and acknowledge it. Patients need to feel in

control as their past experience has been about being in someone else’s power. Follow local guid elines for any current abuse that may be

revealed.

2.56 Common functional syndromes

In all cases, physical examination and investigation fail to reveal an underlying phys ical cause and symptoms should have lasted more

than 3 months in those marked with an asterisk.

Chronic fatigue syndrome Irritable bowel syndrome

Chronic pain syndrome

Fibromyalgia

Chronic back pain

Physical examination

The physical assessment begins as soon as you see the patient in the waiting room and ends when the patient leaves the consulting room.

Watch carefully for inconsistent signs, though this does not tell you if s ymptoms are consciously or unconsciously produced. The

symptoms dictate the clinical features that you should look for. Usually there are no physical signs of disease but some non-pathologic al

signs are associated with MUS. These do not exclude disease so interpret them with caution. The history has often suggested the

diagnosis and so you are seeking to exclude any unexpected physical findings that warrant further investigation as well as to demonstrate

to patients that you are taking them seriously, e.g. in irritable bowel syndrome you may find evidence of bloating and some tenderness

but otherwise the gastrointestinal examination will be normal (Ch. 8).

Any signs you find may vary between examinations but overall the examination is commonly normal.

Investigation

The main objective of investigation is to reassure the physician and the pati ent. Routine, standard investigations and management to

exclude all physical illness are costly, unhelpful, risk side-effects and do not achieve the longer -term reassurance of patients. Before

proceeding with any investigation, discuss the likelihood and significance of a normal test result w ith the patient. The effect of diagnostic

testing will depend on what the patient thinks a normal result means. Patie nts are more likely to be satisfied when your explanation

makes sense to them, removes blame and helps generate ideas about how they can manage their s ymptoms.

PUTTING IT ALL TOGETHER

Positively identify patients with MUS early by recognising the possibility as you listen to t heir complaints. Some

Urethral syndrome Persistent fatigue

Abdominal pain, altered bowel

habit (diarrhoea or constipation),

and abdominal bloating

*Persistent pain in one or more 2

parts of the body sometimes

following injury but which

outlasts the original trauma

*Pain in the axial skeleton with

trigger points (tender areas in the

muscles)

*Pain, muscle tension, or

stiffness localised below the

costal margin and above the

inferior gluteal folds, with or

without leg pain

Recurrent dysuria and urinary

frequency but absence of

significant bacteriuria

2.57 Examples of possible patients’ concerns for common-functional disorders Sym ptoms

Tired all the time

Abdominal pain – relieved by defecation

Bloating

Low back pain

Rabbit pellet stools

Band-like headache

Coming on during the day Not relieved by analgesics Sharp intermittent

left-sided chest pain

Patient’s

concern

Bowel cancer

Common

diagnosis

Irritable bowel syndrome

Brain tumour Tension headache

Heart attack Musculoskeletal chest pain and anxiety

symptoms are more likely to be medically unexplained than others (Box 2.56). Work with your patient’s ideas an d together plan a way

forward that avoids unnecessary investigations and treatment (Box 2.57). In 75% of primary care patients with no abnormality on

physical examination, symptoms are self-limiting. Reviewing the patient may be more appropriate than performing costly and potentially

confusing investigations.

2 DOCUMENTING THE FINDINGS: THE CASE NOTES

The case notes, or records, are the written record of a patient’s medic al condition. They include your initial findings, proposed

investigations and plan of management, together with information about the patient’s progress. Information is recorded for each episode

of illness over time and shared by all the healthcare staff caring for a patient. Notes should there fore be accurate, legible, dated and

signed. Primary care records contain the whole story of a patient’s health rather than di screte episodes of hospital care, and follow the

patient if he changes practices (Box 2.58).

You may write notes while talking with a patient, but do not let this interrupt the discussion and maintain as much eye contact as

possible. Active listening is difficult if you are writing, so make brief notes to remind yoursel f of the important points, and only write up

the full history and physical findings when the examination is completed. Only reco rd objective findings. Never make any judgemental

or flippant remarks.

Although structured proformas for recording history and examination findings are used in many hospitals, it is not necessary to record

every detail in every patient. Only record negative findings if they are relevant. For example, in a patient with breathlessness, the

negative details of the respiratory enquiry are important but negative responses to the gastroin testinal enquiry can be condensed to a

single entry of ‘none’. You may use abbreviations but they should not be ob scure or ambiguous (Fig. 2.8). The prefix ‘°’ is often used to

signify ‘no’: for example, ‘° tenderness’. Use diagrams to show the site and size of superficial injuries or wounds, and for the abdome n

to illustrate the position of tenderness, masses or scars (Fig. 8.12). Record injuries accurately; you may be asked to give legal evide nce

from the notes many months later (Box 2.59).

Unitary or ‘multidisciplinary’ notes allow the whole team to record their finding s in one document rather than each keeping separate case

records. Unitary records can be cumbersome but encourage shared care, avoid duplication and make it easy to access information.

2.58 Information in the case record

• History and examination findings

• Investigations and results

• Management plan

• Assessments by other health professionals, e.g. dieticians, health visitors

• Information and education provided to patients and their relatives

• Correspondence about the patient

• Patient’s progress

• Advance directives or ‘living wills’

• Contact details for next of kin

2.59 Describing wounds

Position

• Where on the body, including which aspect of a limb Size and orientation

• e.g. 5 cm × 3 mm vertical scratch

Appearance

• e.g. colour, shape

Type of lesion

• Abrasion: loss of the outer skin due to impact with a rough

surface

• Scratch: linear abrasion due to drawing of a sharp point over

the skin

• Bruise: bleeding within the tissues beneath the skin

• Laceration: tearing of the skin due to blunt trauma;

ragged edges

• Incised wound: cut or gash; sharp edges

• Penetrating wound: breaches full skin thickness; depth is

greater than length

Computer records

Records may be held on paper or online. Computers allow easy access t o medical and prescribing information during the consultation.

All electronic data should be stored securely, accessible only to relevant staff and p assword-protected. Paperless general practices hold all

patient information on computer and this can be downloaded on to laptops for domicilia ry use. Some patients carry Smart cards holding

their entire medical record. break confidence if a patient poses a risk to himself or other members of the public.

In the UK, patients have the right to receive a copy of their paper case record an d to see any personal information held on computer,

including their medical records. Remember this when you make your notes or record info rmation about third parties, particularly in cases

of sexual abuse. Some patients already hold their own records, usually when antenatal or diabetic c are is shared between hospital and

community. You can stop patients seeing a part of their record if you think it wou ld seriously harm their physical or mental health or that

of any other individual.

Confidentiality

The case record is confidential and constitutes a legal document that may be used in a court of law. You cannot share details with anyone

who is not involved in a patient’s care, unless the patient gives fully informed written consent. This includes insurance companies,

lawyers, the police and research workers. You may only

Writing letters

Letters must be written when referring a patient to a specialist, and to the GP following an outpatien t consultation or hospital admission.

The hospital discharge letter (or summary) is structured in a standard format, which can be adapted for referral and outpatient letters.

Documenting the findings: the case notes

The text should be brief; concentrate on the main issues but include any unexpected fin dings or complications and relevant investigation

results. Include the reason for referral as well as the diagnosis, along with full d etails of the patient’s past history and current medication.

Ensure copies of letters are sent to the patient’s GP and any other specialist involved in the patient ’s care.

Most letters are dictated and typed, although structured com puterised letters may also be used. When dictating, remember the following:

• State your name and the date of dictation.

• State the patient’s name and date of birth.

• State other important dates, e.g. the patient’s

attendance at an outpatient appointment, or hospital admission.

• Speak slowly and clearly. Spell out unusual medical terms.

• Say ‘full stop’ at the end of a sentence and ‘new paragraph’ as required, and in clude any details of punctuation required. Use paragraph

headings as in Box 2.60.

2.60 Discharge letter headings

• Diagnosis

• Primary or active

• Inactive: list comorbidities or previous illnesses

• Procedures or operations

• History (include important social factors)

• Examination

• Investigations: only give detailed results if abnormal

• Clinical progress: brief description of course during

hospital stay

• Social arrangements where relevant 2

• Drugs on discharge, including doses and duration of course

• Follow-up arrangements

• Information given to patients (and relatives)

In many hospitals, voice-activated recognition is now in use and instructions for this may vary from the above. Letters are always easier

to dictate when you have just seen the patient rather than several days later.

Date : 03.08.13 Time : 14.00

Emergency admission to CCU via GP: Dr Wells, High St., Edinburgh MARY BROWN aged 78 32 Tartan Cresc.

Edinburgh

DOB 12.09.35

History from patient PC Chest pain 2 hours Breathlessness 1 hour Dizziness 30 mins

HPC Severe pain ‘like a band around chest’ while watching TV which has now l asted 2 hours despite using GTN, aspirin and diltiazem.

Radiates to jaw and inner aspect of L arm.

Has gradually become breathless over the last hour and dizzy in last 30 minutes.

First began 6 months ago: episode of lower retrosternal chest pain after walking about 1 /2 mile uphill:

• no associated palpitation or SOB.

Two further episodes over the next 3 months.

3 months ago: increasing frequency of pain

• now brought on by walking 200 yards on the flat or climbing 1 flight of stairs

• worse after heavy meals

• other features of pain as before.

2 months ago: visited GP who diagnosed angina. Prescribed GTN which gave effective relief.

1 week ago: three episodes of chest pain at rest, all immediately relieved by GTN.

°Blackouts °pain in calves on exertion.

PH Tonsillectomy 1952 Perforated peptic ulcer 1977 COPD Since 1990 Hospital X

Hospital Y

General practitioner

°MI, °DM, °J, °HBP, °Stroke, °RF, °TB

DH Salbutamol inhaler

Zopiclone

Senokot (self medication) GTN spray

Aspirin

No allergies

Pit accident

aged 36

DOSE FREQUENCY DURATION

2 puffs As necessary 3 years

7.5mg At night 6 months

2 tabs 2–3 times per week 10 years

1 puff As required 2 months

75mg Once daily 2 months

Heart failure age 83

Breast cancer 79 aged 50

1 aunt died aged 57 of acute MI 1

Fig. 2.8 Case notes: example.

Demographic Details

Always record

• The patient’s name and address, date of birth and age

• Any national health identification number such as CHI in the UK

• Source of referral e.g. from Emergency Department

or General Practitioner

• GP’s name and address

• Source of history e.g. patient, relative, carer

• Date and time of examination

Presenting Complaint (PC)

State the major problem in one or two of the patient’s own words (or give a brief list), f ollowed by the duration of each. Do not use

medical terminology.

History of Presenting Complaint (HPC)

Describe the onset, nature and course of each symptom. Paraphrase the patient’s accou nt and condense it if necessary. Omit irrelevant

details.

Put particularly telling comments in inverted commas. Include other parts of the history i f relevant, such as the smoking history in

patients with cardiac or respiratory presentations, or family history in disorders with a p ossible genetic trait such as

hypercholesterolaemia or diabetes.

Correct grammar is not necessary.

GTN – glyceryl trinitrate

SOB – short of breath

Drug History (DH)

Tabulate these and include any allergies particularly to drugs. Record any previous adv erse drug reactions prominently on the front of the

notes as well as inside.

Past History (PH)

Tabulate in chronological order.

Include important negatives, e.g. in a patient with chest pain ask about previous myocar dial infarction, angina, hypertension or diabetes

mellitus and record whether these are present or absent. Jaundice is important because i t may pose a risk to healthcare workers if due to

hepatitis B or C.

COPD– Chronic obstructive pulmonary disease

MI – Myocardial infarction

DM – Diabetes mellitus

J – Jaundice

HBP – Hypertension

RF – Rheumatic fever

Family History (FH)

Record the age and current health or the causes of or the ages at death of the patient’s parents, siblings and children. Use the symbols

shown in Fig. 2.3 to construct a pedigree chart.

Retired cleaner.

Widow for 3 years. Lives alone in sheltered housing.

Smoked 20/day from age 19.

Teetotal.

HH once a week for cleaning and shopping. Daughter nearby visits regularly.

CVS: See above.

RS: Long-standing cough most days with white sputum on rising in morning only. °Hae moptysis. Wheezy in cold weather.

GI: Weight steady.

Nil else of note.

GUS: PARA 1 + 0. °PMB, °urinary symptoms

CNS: Nil of note.

MSS: Occasional pain and stiffness in right knee on exertion for 5 years.

ES: Nil of note.

O/E

Anxious, frail, cachectic lady.

Weight 45 kg. Height 1.25 m

2 cm craggy mass in upper, outer quadrant L breast. Fixed to underlying tissues. Patien t unaware of this

1 cm node in apex of left axilla.

°Pallor, °cyanosis, °jaundice, °clubbing.

CVS

P90 reg, small volume, normal character.

BP 140/80 JVP + 3 cms normal character, °oedema, AB 5ICS MCL, °thrills. HS I + II + 2/6 ESM at LLSE °radiation.

°Bruits.

PP:

Radial Brachial Carotid Femoral Popliteal Post. Tibial Dorsalis pedis R + + + + +/+/+/L + + + + + + + (Normal +, Reduced +/-, Absent -)

Trachea central. Reduced cricosternal distance and intercostal indrawing on inspiration. Expansion reduced but symmetrical.

PN resonant.

BS vesicular and quiet.

VR normal and symmetrical.

Social History (SH)

Occupation

Marital status

Living circumstances; type of housing and with whom Smoking

Alcohol

Illicit drug use (if appropriate)

Social support in the frail or disabled

HH – home help

Systematic Enquiry (SE)

Document positive responses that do not feature in the HPC.

CVS – Cardiovascular system

RS– Respiratory system

GI– Gastrointestinal system

GUS – Genito-urinary system

PMB– Postmenopausal bleeding

CNS– Central nervous system

MSS– Musculoskeletal system

ES– Endocrine system

General / On examination (OE)

Physical appearance e.g. frail, drowsy, breathless

Mental state e.g. anxious, distressed, confused

Undernourished, cachectic, obese

Abnormal smells e.g. ketones, alcohol, uraemia, fetor hepaticus Record height, weight a nd waist circumference

Skin e.g. cyanosis, pallor, jaundice, any specific lesions or rashes Breasts, normal or describe an y mass

Hands; finger clubbing, or abnormalities of skin and nails Lymph nodes; characteristics and site

Respiratory System (RS)

Any chest wall deformity

Trachea central or deviated

Signs of hyperinflation

Expansion and its symmetry

Percussion note (PN) and site of any abnormality

Breath sounds (BS), any added sounds and site of abnormality Vocal resonance (VR) and site of abnormality

Cardiovascular System (CVS)

Pulse (P) rate, rhythm, character and volume

Blood pressure (BP)

Jugular venous pressure (JVP) height and character Presence or absence of ankle oed ema

Apex beat (AB) position, character, presence of thrills Heart sounds (HS) any added s ounds, murmurs and grade Peripheral pulses (PP)

and bruits

5ICS – 5th intercostal space MCL – Mid clavicular line

ESM – Ejection systolic murmur LLSE – Lower left sternal edge

Abdo. Scar

Normal oral mucosa

Upper midline scar

Hernial orifices intact

°Tenderness or guarding

°Masses

°LKKS or ascites

BS normal

PR not done

PV not performed

CNS

AMT 9/10

Cranial nerves II–XII: PERLA, NAD Speech normal

RIGHT LEFT UL LL UL LL Power 5 5 5 5 Tone normal (n) n n n Light touch n n n n Position n n n n Coordination n n n n

+ ++

Reflexes K A B T S Pl

R ++ + ++ + + flexor

L ++ + ++ + + flexor

(increased +++, normal ++, diminished +, absent -)

MSS

Heberden’s nodes on index and middle fingers bilaterally. Full ROM in all joints.

Crepitus in right knee. No other bony abnormality.

IMPRESSION

Active problems

1 Chest pain suggestive of acute coronary syndrome 2 Left breast lump and axillary no de suspicious of cancer 3 Smoker

Inactive problems

1 Stable COPD

2 Perforated duodenal ulcer 1977

3 Possible osteoarthritis of right knee

Abdominal System (AS)

Mouth

Any abnormality – own teeth or dentures

Abdomen

Scars and site

Shape, distended or scaphoid

Hernial orifices

Tenderness and guarding and site of this

Masses and description of these

Enlargement of liver, kidneys or spleen (shorten to LKKS)

Ascites if present

Bowel sounds (BS); presence and character

Rectal examination (PR) record whether or not it was

performed and your findings. It should not be done in patients

with possible cardiac chest pain, as arrhythmias may be provoked

in acute MI.

In women; vaginal examination (VE) is only carried

out if relevant

In men; external genitalia

Central Nervous System (CNS)

In older patients, record the abbreviated mental test (AMT) score In impaired consciou sness, head injury or possible raised intracranial

pressure record the Glasgow Coma Scale (GCS)

Abnormal speech

Cranial nerves; record abnormalities only

Fundoscopy

Tabulate the remaining examination

If it is relevant record the presence or absence of tremor, gait, abnormality, fasciculatio n, dyspraxia, two point discrimination,

stereognosis or sensory neglect.

PERLA – Pupils equal and react to light and accommodation NAD– No abnormality de tected

UL– Upper limb

LL– Lower limb

K – Knee

A– Ankle

B– Biceps

T– Triceps

S– Supinator

Pl– Plantar

Musculoskeletal System (MSS)

Gait if abnormal

Muscle or soft tissue changes

Swelling, colour, heat, tenderness

Deformities in the bones or joints

Limitation of ranges of movements (ROM) in any affected joint

Clinical Diagnosis or Impression

Record your conclusions and the most likely diagnoses in order of probability.

In patients with multiple pathology make a problem list so the key issues are seen immedi ately.

Diagnosis

ECG performed on admission shows sinus rhythm and deep ST depression in leads II, III and aVF Troponin at 12 hours

Repeat ECG in 1 hour

Chest X-ray

Full blood count

Urea and electrolytes, glucose

Oxygen and cardiac monitor

IV morphine and metoclopramide

Aspirin and clopidogrel

Low molecular weight heparin

Continue aspirin and diltiazem

Discuss beta-blocker with consultant in view of COPD

Advice to stop smoking

When stable

1 Review anti-anginal management

2 Referral for mammography and fine needle aspiration of breast lump

3 Spirometry and assessment of inhaler technique

Information given

Diagnosis and treatment explained to patient and daughter

N.B. Breast lump not mentioned at this stage until discussed with senior staff

A. Doctor (signed) A. DOCTOR (Date and Time) capitals

Progress notes

3.8.13

1800 Ward Round – Dr Consultant

No further chest pain

O/E

P70 BP 100/70

JVP not elevated, °oedema

HS I + II and ESM as above

Chest clear

Breast lump noted

ECG at 4 hours – resolution of inferior ST changes

Impression

Acute coronary syndrome – no ST segment elevation

Plan

Await troponin

Continue LMW heparin

Check lipid profile

For echocardiography in view of murmur then consider ACE inhibitor

Spirometry and assessment of inhaler technique

Consultant to discuss finding of breast lump A. Doctor (signed) with patient and daugh ter A. DOCTOR (Date and Time) capitals

• List the investigations required. When a result is already available, for example of an e lectrocardiograph, record it.

• Record any immediate management instigated

• If uncertain about an investigation or treatment, precede with a ‘?’ and discuss with a more senior member of staff

Information given

Document what you have told the patient and any other family member. It is also impor tant to document any diagnosis that you have not

discussed.

If the patient voices any concerns or fears, document these too.

Progress Notes
Follow the same structure with these additions
• Changes in the patient’s symptoms
• Examination findings
• Results of new investigations
• Clinical impression of the patient’s progress
• Plans for further management, particularly drug changes. Make progress notes regul arly depending on the speed of change in the
patient’s condition; in an intensive therapy setting, this may be several times a day b ut, in a stable situation, daily or alternate days.
Date, time and sign all entries.
Record any unexpected change in the patient’s condition as well as routine prog ress notes.
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SECTION 1 HISTORY TAKING AND GENERAL EXAMINATION
The setting for a physical examination 42 Sequence for performing a physical examination 42
First impressions 42
Gait and posture 42
The handshake 43
Facial expression and general demeanour 43 Clothing 43
Complexion 43
Odours 47
Spot diagnoses 47
Graham Douglas John Bevan
The general examination3
The hands 49
The tongue 51
Lumps or swellings 51
The lymph nodes 53
Weight and height 55
Hydration 58
Temperature 61
3 THE SETTING FOR A PHYSICAL 
EXAMINATION
Privacy is essential when you examine a patient. Pulling the curtains arou nd the bed in a ward obscures vision but not sound. Talk quietly
but ensure good communi cation, which may be difficult with deaf  or elderly patients (Ch. 2). The room should be warm and well lit.
Subtle abnormalities of complexion such as mild jaun dice are easier to detect in natural light. The height of the examination couch or
bed should be adjustable, with a step to enable patients to get on to it easily. An adjust able  backrest is essential, particularly for
breathless patients who cannot lie flat.
Seek permission and sensitively, but adequately, expose the areas of the body to be examined; cover the rest of t he patient with a blanket
or sheet to ensure that he or she does not become cold. Avoid unnecessary exposure and embarrassment.  A female patient will appreciate
the opportunity to replace her bra after her chest examination before you examine her abdomen. Tactfully ask r elatives to leave the room
before the phys ical examination. Sometimes it is appropriate for a rela tive to remain if t he patient is very apprehensive, if you need a
translator or if the patient requests it. Parents should always be present when you e xamine children (Ch. 15).
Always offer a chaperone for any intimate examina tion to prevent misunderstandings and  to provide support and encouragement for the
patient (Ch. 2). Record the chaperone’s name and presence. If patients decline the  offer, respect their wishes and record this in the notes.
Collect together all the equipment you need before starting the examination ( Box 3.1).
correct diagnosis if you are unduly swayed by early clues in the history, overvalue recent or memorable ca ses or lean too heavily towards
diagnoses that seem to match a pattern. Examine the patient, looking for signs that will conf irm or refute your diagnoses.
With experience, you will develop your own style and sequence of physical examin ation (Box 3.2). There is no single correct way of
performing a physical examina tion. A regular routine reduces errors of omission.
The sequence of examination is:
• Inspection
• Palpation
• Percussion
• Auscultation (Fig. 3.1).
Learn to integrate these smoothly into each component of the physical examination.
FIRST IMPRESSIONS
The physical examination starts as soon as you see the patient. Assess patients’ gen eral demeanour and exter nal appearance, and watch

how they rise from their chair and walk into the room.

Gait and posture

Observe the patient as he walks towards you. The gait may suggest an important neurologica l or musculo skeletal disorder or provide

clues to the patient’s emo tions and overall function. Disorders of gait occur because of pain, fixed or immobile jo ints, muscle weak ness

or abnormal limb control (Fig. 3.2). If the patient is in bed, look at his posture.

SEQUENCE FOR PERFORMING

A PHYSICAL EXAMINATION

Keep an open mind as you talk with the patient and formulate a differential diagnosis. You may miss the

3.1 Equipment required for a full examination

• Stethoscope

• Pen torch

• Measuring tape

• Ophthalmoscope

• Otoscope

• Sphygmomanometer

• Tendon hammer

• Tuning fork

• Cotton wool

• Disposable Neurotips

• Wooden spatula

• Thermometer

• Magnifying glass

• Accurate weighing scales and a height-measuring device (preferably a Harpend en stadiometer)

• Disposable gloves may be required

• Facilities for obtaining blood samples and urinalysis

3.2 A personal system for performing a physical examination

• Handshake and introduction

• Note general appearances while talking:

• Does the patient look well?

• Any immediate and obvious clues, e.g. obesity, plethora, breathlessness

• Complexion

• Hands and radial pulse

• Face

• Mouth and ears

• Neck

• Thorax

• Breasts

• Heart

• Lungs

• Abdomen

• Lower limbs

• Oedema

• Circulation

• Locomotor function and neurology

• Upper limbs

• Movement and neurology

• Cranial nerves, including fundoscopy

• Blood pressure

• Temperature

• Height and weight

• Urinalysis

Introduce yourself to the patient including handshake and first impressions

3.3 Information from a handshake

Talk with the patient (History)

1. Presenting complaint

2. Other history

• Past history

• Drug history

• Family history

• Social history

• Occupational history

• Travel history

• Sexual history*

• Tobacco

• Alcohol

3. Systematic enquiry

Diagnosis

Anxiety

Raynaud’s phenomenon

Hyperthyroidism

Acromegaly

Regular water exposure

Manual occupation

Hypothyroidism 3

Myotonic dystrophy

Trauma

Rheumatoid arthritis

Dupuytren’s contracture

Features

Cold, sweaty hands

Cold, dry hands

Hot, sweaty hands

Large, fleshy, sweaty hands Dry, coarse skin

Delayed relaxation of grip Deformed hands/fingers

Differential diagnosis

Examine the patient Use a systematic approach

• Inspection

• Palpation

• Percussion

• Auscultation

Confirm or refute your diagnoses

3.4 Abnormal facial expressions

Features

Poverty of expression

Startled expression

Apathy, with poverty of expression and poor eye contact

Apathy, with pale and puffy skin

Lugubrious expression with bilateral ptosis

Agitated expression

Diagnosis

Parkinsonism Hyperthyroidism Depression

Hypothyroidism

Myotonic dystrophy

Anxiety

Hyperthyroidism Hypomania

* if appropriate

Fig. 3.1 Overall plan of clinical assessment.

The handshake

Introduce yourself and shake hands. This may provide diagnostic clues (Box 3.3). G reet your patient in a friendly but professional

manner. Note if his right hand works; in patients with a right hemiparesis you may need to shake his left hand. Avoid too f irm a grip,

particularly in patients with arthritis.

Facial expression and general demeanour

Ask yourself:

• ‘Does this patient look well?’

Facial expression and eyetoeye contact reflect physical and psychological we llbeing (Box 3.4), but in some cultures direct eyetoeye

contact is impolite. Patients who deliberately selfharm may cover  their face with their hands or bedclothes and be reluctant to communi‐
cate. Actively recognise the features of anxiety, fear, anger or grief, and e xplore the reasons for these. Some patients conceal anxieties
and depression with inappro priate cheerfulness.
Clothing
Clothing gives clues about personality, state of mind and social circumstances. Y oung people wearing dirty clothes may have problems
with alcohol or drug addic tion, or be making a personal statement. Unkempt elderly patients  with faecal or urinary soiling may be unable
to look after themselves because of physical disease, immobility, dementia or other mental illness. Anore ctic patients wear baggy
clothing to cover weight loss. Consider bloodborne viral infections, e.g. hepatitis B  or C, in patients with tattoos. A MedicAlert bracelet
(Fig. 3.3) or necklace highlights important medical con ditions and treatments.
43
3
A) Spastic hemiparesis One arm held immobile and close to the side with elbow, wris t and fingers flexed. Leg extended with plantar
flexion of the foot.
On walking, the foot is dragged, scraping the toe in a circle (circumduction). Caused b y upper motor neurone lesion, stroke.
B) Steppage gait
Foot is dragged or lifted high and slapped onto the floor. Unable to walk on the heels. C aused by foot drop owing to lower motor neurone
lesion.
C) Sensory or cerebellar ataxia Gait is unsteady and wide based. Feet are thrown forward and outwar d and brought down on the heels. 
In sensory ataxia, the patient watches the ground. With eyes closed, he cannot stand stead ily (positive Romberg sign).
In cerebellar ataxia, turns are difficult and patients cannot stand steadily with feet toget her whether eyes open or closed. Caused by
polyneuropathy or posterior column damage, e.g. syphilis.
D) Parkinsonian gait
Posture is stooped with head and neck forwards. Arms are flexed at elbows and wrists. Littl e arm swing. Steps are short and shuffling
and patient is slow in getting started (festinant gait). Caused by lesion in the basal ganglia.
Fig. 3.2  Abnormalities of gait. 
Fig. 3.3  MedicAlert bracelet. 
Complexion
Facial colour depends on oxyhaemoglobin, reduced hae moglobin, melanin and carote ne. Unusual skin colours are due to abnormal
pigments, e.g. the sallow yellow brownish tinge in chronic kidney  disease. A bluish tinge is produced by abnormal haemoglobins,  e.g.
sulphae moglobin or methaemoglobin, or by drugs, e.g. dap sone. Some drug metabolites cause striking abnor mal coloration of the skin,
particularly in areas exposed to light, e.g. mepacrine (yellow), amiodarone (bluishgrey)
44
 and phenothiazines (slategrey) (Fig. 3.4).
Haemoglobin
Untanned European skin is pink due to the red pigment oxyhaemoglobin in the  superficial capillary–venous plexuses. A pale complexion
may be misleading but can suggest anaemia (Box 3.5). The pallor of anaemia is best seen in the mucous membranes  of the conjunctivae,
lips and tongue and in the nail beds (Fig. 3.5). Angular stomatitis (Fig. 3.19B) and koilonychia (spoonsha ped) nails (Fig. 4.15F) can be
features of iron deficiency anaemia. Ask about dyspepsia, chan ge in bowel habit and heavy menstrual periods if you are investigating
anaemia.
Pallor from vasoconstriction occurs during a faint or from fear. Vasodilatation may produce  a pink complex ion, even in anaemia.
Perimenopausal women may have transient pink flushing, particularly of the face, due to  vasodilatation, which may be accompanied by
sweating. Facial plethora is caused by raised haemoglobin concen tration w ith elevated haematocrit (polycythaemia) (Box 3.6). Blue
sclerae are a sensitive indicator of iron defi ciency anaemia.
Cyanosis
Cyanosis is a blue discoloration of the skin and mucous membranes that occurs wh en the absolute concentration of deoxygenated
haemoglobin is increased (Box 3.7). It can be difficult to detect, particularly in  black and Asian patients.
Fig. 3.4  Phenothiazine-induced pigmentation. 
Fig. 3.6  Central cyanosis of the lips. 
3
3.6 Types of polycythaemia
Primary

Primary

• Polycythaemia rubra vera Secondary

• Hypoxia

• Chronic lung disease

• Cyanotic congenital heart disease

• Altitude

• Excess erythropoietin

• Adult polycystic kidney disease

• Renal cancer

• Ovarian cancer

3.7 Central cyanosis

The minimum arterial level of deoxyhaemoglobin required to detect central cyanosis is 2 .38 g/dl. The mean value for detection is 3.48 ±

0.55 g/dl.

Barnett HB, Holland JG, Josenhans WT. When does central cyanosis become d etectable? Clin Invest Med 1982;5:39–43.

McGee S. Evidence based physical diagnosis, 2nd edn. St Louis, MO: Saunder s, Elsevier, 2007, p. 86.

Fig. 3.5 Conjunctival pallor.

3.5 Types of anaemia

Microcytic (MCV < 80 fl)

• Chronic blood loss

• Iron deficiency

• Anaemia of chronic disease

Macrocytic (MCV > 96 fl)

• Megaloblastic marrow due

to vitamin B

or folate deficiency

• Excess alcohol

Normocytic (MCV 80–96 fl)

• Acute blood loss

• Anaemia of chronic disease

• Chronic kidney disease

MCV, mean corpuscular volume.

• Thalassaemia

• Sideroblastic anaemia

• Haemolytic disorders

• Liver disease

• Hypothyroidism

• Connective tissue disorders

• Marrow infiltration

Central cyanosis

This is seen at the lips and tongue ( Fig. 3.6). It corre sponds to an arterial oxygen satur ation (SpO

) of <90% and usually indicates

underlying cardiac or pulmonary disease. Anaemic or hypovolaemic patients rarely have central cyanosis because severe hypoxia is

required to produce the necessary concentration of deoxygen ated haemoglobin. Converse ly patients with polycythae mia can become

cyanosed at normal arterial oxygen saturation.

Peripheral cyanosis

This occurs in the hands, feet or ears, usually when they

are cold. In healthy people it occurs in cold conditions when prolonged peripheral capillary f low allows greater oxygen extraction and

hence increased levels of deoxy haemoglobin. In combination with central cyanosis, it i s most often seen with poor peripheral circulation

due to shock, heart failure, vascular disease and venous obstruction, e.g. deep vein thrombosis.

Fig. 3.7 Vitiligo.

3.8 Causes of abnormal melanin production Condition

Underproduction

Vitiligo (patchy depigmentation)

Albinism

Hypopituitarism

Overproduction

Adrenal insufficiency

(Addison’s disease)

Nelson’s syndrome (may occur after bilateral adrenalectomy for Cushing’s disease)

Cushing’s syndrome due to ectopic adrenocorticotrophic hormone secretion by tumours, e.g. small cell l ung cancer

Pregnancy and oral

contraceptives

Haemochromatosis

Mechanism

Autoimmune destruction of melanocytes

Genetic deficiency of

tyrosinase

Reduced pituitary secretion of melanotrophic peptides, growth hormone and sex steroids

Increased pituitary secretion of melanotrophic peptides Increased pituitary secretion of mela notrophic peptides

Ectopic release of

melanotrophic peptides by dysregulated tumour cells

Increased levels of sex hormones

Iron deposition and

stimulation of melanocytes

Melanin

Skin colour is greatly influenced by the deposition of melanin (Box 3.8).

Vitiligo

This chronic condition produces bilateral symmetrical depigmentation, commonly of the face, neck and ex ten sor aspects of the limbs,

resulting in irregular pale patches of skin. It is associated with autoimmune d is eases, e.g. diabetes mellitus, thyroid and adrenal disor‐

ders, and pernicious anaemia (Fig. 3.7).

Albinism

This is an inherited disorder in which patients have little

or no melanin in their skin or hair. The amount of

Fig. 3.8 Hypercarotenaemia.

3.9 Jaundice

Clinical detection of jaundice depends upon the level of serum bilirubin, ambient lighting a nd colour perception of the examining

clinician: 70–80% of observers will detect jaundice if levels are 43–51 umol/L, 83% at 171 um ol/L and 96% if levels are >256 umol/L.

Hung OL, Kwan NS, Cole AE et al. Evaluation of the physician’s ability to re cognise the presence or absence of anaemia,

fever and jaundice. Acad. Emerg. Med. 2000: 7; 146–156

Ruiz MA, Saab S, Rickman LS. The clinical detection of scleral icterus: Observ ations of multiple examiners. Mil. Med.

1997: 162; 560–563

pigment in the iris varies; some individuals have reddish eyes, but most have blue.

Overproduction of melanin

This can be due to excess of the pituitary hormone,

adrenocorticotrophic hormone, as in adrenal insuffi ciency. It produces brown pigmentation, particularly in skin creases, recent scars,

sites overlying bony promi nences, areas exposed to pressure, e.g. belts and bra straps, and the mucous membranes of the lips and mouth,

where it results in muddy brown patches (Fig. 5.19A–C).

Pregnancy and oral contraceptives

These may produce chloasma (blotchy pigmentation of the face). Pr egnancy increases pigmentation of the areolae, axillae, genital skin

and a linea nigra (dark line in the midline of the lower abdomen).

Carotene

Hypercarotenaemia occurs in people who eat large amounts of raw carrots and tomatoes, and in hypo thyroidism. A yellowish

discoloration is seen on the face, palms and soles, but not the sclerae, and this dis tinguishe s it from jaundice (Fig. 3.8).

Bilirubin

Jaundice is detectable when serum bilirubin concentra tion is elevated and the sclerae, m ucous membranes and skin become yellow (Fig.

8.8 and Box 3.9). In longstand ing jaundice a green colour develops in the sclera e and skin due to biliverdin. Patients with pernicious

anaemia have a lemonyellow complexion due to a combination of mild jaundice and anae mia.

Fig. 3.9 Haemochromatosis with increased skin pigmentation.

Fig. 3.10 Erythema ab igne.

Iron

Haemochromatosis increases skin pigmentation due to iron deposition and increased melanin production (Fig. 3.9). Iron deposition in the

pancreas causes diabetes mellitus and the combination with skin pigmentation is called ‘bronz ed diabetes’.

Haemosiderin, a haemoglobin breakdown product, is deposited in the skin of the low er legs following extrava sation of blood into

subcutaneous tissues from venous insufficiency. Local deposition of haemosiderin (ery thema ab igne or ‘granny’s tartan’) occurs with

heat damage to the skin from sitting too close to a fire or from applying loca l heat, such as a hot water bottle, to the site of pain (Fig.

3.10).

Easy bruising

Approximately 20% of patients complain they bruise easily (Fig. 3.24). It is more co mmon in the elderly because of increased skin and

subcutaneous tissue fra gility and a greater likelihood of increased episodes of minor trauma. A lifelong tendency suggests an inherited

disorder whereas recent onset suggests an acquired dis order. Enquire if there are othe r family members with a similar problem (bleeding

disorder), what drugs the patient is receiving, e.g. anticoag ulants, corticosteroids and ask about recurrent nose bleeds (epistaxis) and

heavy menstrual periods (menorrhagia).

Odours

Everybody has a natural smell, produced by bacteria acting on apocrine sweat; th is may be altered by antiper spirants, deodorants and

perfume. Excessive sweating and poor personal hygiene increase body odour and may be compoun ded by dirty or soiled clothing and

stale urine. Excessive body odour occurs in:

• extreme old age or infirmity

• major mental illness

• alcohol or drug misuse

• physical disability preventing normal hygiene 3

• severe learning difficulties.

Tobacco’s characteristic lingering smell pervades skin, hair and clothing. Marijuana (cannabis) can also be identified by smell. The

smell of alcohol on a patient’s breath, particularly in the morning, may sugge st an alcohol problem.

Halitosis (bad breath) is caused by decomposing food wedged between the teeth, gingivitis, st omatitis, atrophic rhinitis and tumours of

the nasal passages.

Other characteristic odours include:

• fetor hepaticus: stale ‘mousy’ smell of the volatile amine, dimethylsulphide, in p atients with liver

failure

• ketones: a sweet smell (like nail varnish remover)

due to acetone in diabetic ketoacidosis or starvation

• uraemic fetor: fishy or ammoniacal smell on the

breath in uraemia

• putrid or fetid smell of chronic anaerobic

suppuration due to bronchiectasis or lung abscess

• foulsmelling belching in patients with gastric outlet

obstruction

• strong faecal smell in patients with gastrocolic

fistula.

Spot diagnoses

Many disorders have characteristic facial features ( Fig. 3.11). Osteogenesis imperfecta is an autosomal domi nant cond ition causing

fragile and brittle bones in which the sclerae are blue due to abnormal collagen form ation. In systemic sclerosis the skin is thickened and

tight, causing loss of the normal wrinkles and skin folds, ‘beaking’ of the nose, and na rrowing and puckering of the mouth. Hereditary

haemorrhagic telangiectasia is an autosomal dominant condition associated with small d ilated capillaries or terminal arteries

(telangiectasia) on the lips and tongue. Dystrophia myotonica is an auto somal dominant condition with characteristic features of fronta l

balding, bilateral ptosis and delayed relaxation of grip after a handshake.

Major chromosomal abnormalities

There are several genetic or chromosomal syndromes that you should easily recognise on first contact with the patient.

Down’s syndrome (trisomy 21 –

47XX/XY + 21)

Down’s syndrome is characterised by typical physical features, including sh ort stature, a small head with flat

Fig. 3.11 Characteristic facial features of some disorders. (A) Blue sclerae of osteog enesis imperfecta. (B) Telangiectasia

around the mouth typical of hereditary haemorrhagic telangiectasia. (C) Systemic sclerosis with ‘beaking’ of the nose and

taut skin around the mouth. (D) Dystrophia myotonica with frontal balding an d bilateral ptosis.

A B

Fig. 3.12 Down’s syndrome. (A) Brushfield’s spots: grey-white areas of depigmen tation in the iris. (B) Single palmar crease.

occiput, upslanting palpebral fissures, epicanthic folds, a small nose with a poorly developed bridge and small ears. Greywhite areas of

depigmentation are seen in the iris (Brushfield’s spots; Fig. 3.12A). The hands are broad with a single p almar crease (Fig. 3.12B), the

fingers are short and the little finger is curved.

Turner’s syndrome (45XO)

Turner’s syndrome is due to loss of a sex chromosome.

It occurs in 1 : 2500 live female births and is a cause of delayed puberty in

girls. Typical features include short stature, webbing of the neck, small c hin, lowset ears, low hairline, short fourth finger, increased

carrying angle at the elbows and widely spaced nipples (‘shield like chest’).

Achondroplasia

This is an autosomal dominant disease of cartilage caused by mutation of the fibroblast growth factor gen e. Although the trunk is of

normal length, the limbs are

The hands

Fig. 3.13 Dupuytren’s contracture.

very short and broad. The vault of the skull is enlarged, the face is small and the bridge of the n ose is flat.

THE HANDS

Examination sequence

■ Inspect the dorsal and then palmar aspects of both hands. ■ Note changes in the:

■

skin

■

nails

■

soft tissues (evidence of muscle wasting)

■

tendons

■

joints.

■ Feel the temperature.

Abnormal findings

Deformity

Deformity may be diagnostic: for example, the flexed hand and arm of hemiplegia or radial nerve palsy, and ulnar deviation at th e

metacarpophalangeal joints in longstanding rheumatoid arthritis (Fig. 14.34). Dupuytre n’s contracture is a thickening of the palmar

fascia causing fixed flexion deformity and usually affect ing the little and ring fingers ( Fig. 3.13). Arachnodactyly (long thin fingers) are

typical of Marfan’s syndrome (Fig. 3.28B). Trauma is the most common cause of h and deformity.

Colour

Look for cyanosis in the nail bed and tobacco staining of the fingers (Fig. 7.8). Examine the skin creases for pig mentation, although

pigmentation is normal in many nonEuropean races (Fig. 3.14).

Temperature

In a cool climate the temperature of the patient’s hand is a good guide to peripheral perfusion. In chronic obstructive pulmonary disease,

the hands may be

Fig. 3.14 Normal palms. African (left) and European (right). 3

Fig. 3.15 Self-cutting.

cyanosed due to reduced arterial oxygen saturation but warm due to vasodilatation from elevated arterial carbon dioxide levels. In heart

failure the hands are often cold and cyanosed because of vasoconstriction in response to a low cardiac output. If they are warm, heart

failure may be due to a highoutput state, such as hyperthyroidism.

Skin

The dorsum of the hand is smooth and hairless in chil dren and in adult hypogonadism. Manual work  may produce specific callosities
due to pressure at character istic sites. Disuse results in soft, smooth skin, as seen on the so les of the feet in bedbound patients.
Look at the flexor surfaces of the wrists and forearms. Note any venepuncture marks of intra venous drug use and linear (usually
transverse), multiple wounds or scars from deliberate selfharm (Figs 3.15 and 3.16). Look careful ly at the fingernails, which can provide
useful diagnostic clues (Fig. 4.15).
Finger clubbing
Clubbing is painless softtissue swelling of the terminal phalanges. The enlargement increases  convexity of the nail. It may be produced
by growth factors from 
49
3
Fig. 3.16  The linear marks of intravenous injection at the right elbow. 
A
B
Fig. 3.17  Clubbing. (A) Anterior view. (B) Lateral view. 
megakaryocytes and platelets lodged in nail bed capil laries stimulating vascular connecti ve tissue (Fig. 3.17). It is an important sign of
major diseases, although it may be congenital (Box 3.10). It u sually takes weeks or months to develop, and may disappear if the
underlying condition is cured. Clubbing usually affects the fingers symmetrically, but may  involve the toes. Unilateral club bing can be
caused by proximal vascular conditions, e.g. arteriovenous shunts for dialysis. A utoimmune hyper thyroidism may be associated with
thyroid acropachy – clubbing which is more pronounced on the radial side 
50
 of the hand (Fig. 5.3C).
3.10 Causes of clubbing Congenital or familial (5–10%)
Acquired
Thoracic (~70%)
Lung cancer
Chronic suppurative conditions
Bronchiectasis
Lung abscess
Empyema
Cystic fibrosis
Mesothelioma
Fibroma
Pulmonary fibrosis
Cardiovascular
Cyanotic congenital heart disease Infective endocarditis
Arteriovenous shunts and aneurysms Gastrointestinal
Cirrhosis
Inflammatory bowel disease
Coeliac disease
Others
Thyrotoxicosis (thyroid acropatchy)
Examination sequence
■   Look across the nail bed from the side of each finger. Observe  the dis tal phalanges, nail and nail bed.
■  Measure the anteroposterior distance at the level of the  interphalangeal join t. Repeat at the level of the nail bed   (Fig.  
3.18).
■  Measure the nail bed angle (Fig. 3.18B).
■  Place the nails of corresponding fingers back to back and look  for a vi sible gap between the nail beds – Schamroth’s 
window  sign (Fig. 3.18C).
■  Place your thumbs under the pulp of the distal phalanx and  use your in dex fingers alternately to see if you can feel 
movement of the nail on the nail bed. This is fluctuation.   (Fig. 3.18A ).
Abnormal findings
Finger clubbing is present if:
• the interphalangeal depth ratio (B/A in Fig. 3.18) is >1
• the nail bed angle is >190°
• Schamroth’s window sign is absent (Fig. 3.18C).
Increased nail bed fluctuation may be present, but its 
presence is subjective and less discriminatory than the 
above features.
Joints

Arthritis frequently involves the small joints of the hands. R heumatoid arthritis typically affects metacarpo phalangeal and proximal

interphalangeal joints (Fig. 14.34), and osteoarthritis and psoriatic arthropathy affect the distal inter phalangeal joints (Fig. 14.12).

Nail-fold angles

Normal

B A

Normal

Schamroth’s window absent Clubbed

B A

A B

Fig. 3.18 Examining for finger clubbing. (A) Testing for fluctuation of the nail bed. (B) Nail fold angles. (C) Schamroth’s

window sign. 3

Schamroth’s window present

Lumps or swellings

Clubbed

Fig. 3.19 The tongue as a diagnostic aid. (A) Large tongue (macroglossia) of acrome galy. (B) Smooth red tongue and angular

stomatitis of iron deficiency. (C) Leukoplakia.

Muscles

Small muscle wasting of the hands is common in rheu matoid arthritis, producing ‘dors al guttering’ of the hands. In carpal tunnel

syndrome, median nerve com pression leads to wasting of the thenar mu scles (Fig. 14.29), and cervical spondylosis with nerve root

entrap ment causes small muscle wasting.

THE TONGUE

Examination sequence

■ Ask the patient to put out his tongue.

■ Look at the size, shape, movements, colour and surface (F ig. 3.19).

Normal findings

Tongue furring is normal and common in heavy smokers

Geographic tongue describes red rings and lines which change over days or weeks on the su rface of the tongue. It is usually not

significant but can be due to riboflavin (vitamin B

) deficiency

Abnormal findings

• Tremor can be due to anxiety, thyrotoxicosis, delirium tremens or parkinsonism.

• Fasciculation (irregular ripples or twitching of the tongue) occurs in lower motor neurone d isorders, e.g. motor neurone disease.

• Macroglossia (enlargement of the tongue) may occur in acromegaly, amyloidosis or tumour infiltration.

• White patches that may be scraped off the tongue are due to the fungal yeast, Candida ( oral thrush). Common causes include inhaled

steroids, immune deficiency, e.g. HIV and terminal illness.

• Glossitis is a smooth reddened tongue due to atrophy of the papillae. It is common in alc oholics, in nutritional deficiencies of iron,

folate and vitamin B

, and in 30% of patients with coeliac disease. Glossitis may cause a burning sensati on over the tongue but usually a

painful tongue is a symptom of anxiety or depression.

• Leukoplakia is a thickened white patch that cannot be scraped off the tongue . It may be premalignant.

LUMPS OR SWELLINGS

Patients often present with a lump they have just found. This does not necessarily mean that it has developed recently. Ask about any

changes since they noticed it and whether there are any associa ted features, e.g. pain, tenderness or colour change. During examination

you may find a lump the patient is unaware of.

3 Size

Accurately measure the size of any lump (preferably using callipers), so that with time yo u can detect signifi cant change.

Position

The origin of some lumps may be obvious, e.g. in the breast, thyroid or parotid gland; in other sites, e.g. the abdomen, this is less clear.

Multiple lumps may occur in neurofibromatosis (Fig. 3.20A), skin meta stases, lipoma tosis and lymphomas.

Attachments

Lymphatic obstruction causes fixation of the skin with fine dimpling at the opening of hair follicles that resembles orange peel (peau

d’orange) (Fig. 10.6). This is common in malignant disease when attach ment to deeper structures, e.g. underlying muscle, may occur.

Consistency

The consistency of a lump can vary from soft to ‘stony’ hard. Very hard swellings are usu ally malignant, calci fied or dense fibrous

tissue. Fluctuation indicates the presence of fluid, e.g. abscess, cyst, blister or so ft encap sulated tumours, e.g. lipoma.

Edge

The edge or margin may be well delineated or ill defined, regular or irregular, sharp or r ounded. The margins of enlarged organs, e.g.

thyroid gland, liver, spleen or kidney, can usually be defined more clearly than those of inflammatory or malignant masses. An indefinite

margin suggests infiltrating malignancy, in contrast to the clearly defined edge of a benign tumour.

Fig. 3.20 Lumps and swellings. (A) Neurofibromatosis. (B) Blister

on leg.

Surface and shape

The surface and shape of a swelling can be characteristic. In the abdomen exa mples include an enlarged spleen or liver, a distended

bladder or the fundus of the uterus in pregnancy. The surface may be smooth or irregular, e.g. the surface of the liver is smooth in acute

hepatitis but is often nodular in metastatic disease.

Pulsations, thrills and bruits

Arterial swellings (aneurysms) and highly vascular tumours are pulsatile (they move in time with the arte rial pulse). Other swellings

may transmit pulsation if they lie over a major blood vessel. If the blood flow through a l ump is increased, a systolic murmur (bruit) may

be auscultated and, if loud enough, a thrill may be palpable. Bruits are also heard over arte rial aneurysms and arteriovenous

malformations.

Inflammation

Redness, tenderness and warmth suggest inflam mation.

• Redness (erythema): the skin over acute

inflammatory lesions is usually red due to vasodilatation. In haematomas the pigment from e xtravasated blood may produce the range of

colours in a bruise (ecchymosis).

• Tenderness: inflammatory lumps, e.g. boil or abscess, are usually tender or painful, while noninflamed swellings are not: lipomas, skin

metastases and neurofibromas are characteristically painless.

• Warmth: inflammatory lumps and some tumours, especially if rapidly growing, ma y feel warm due to increased blood flow.

The lymph nodes

Transillumination

In a darkened room, press the lighted end of a pen torch on to one side of the swelling. A cystic swelling, e.g. testicular hydrocoele, will

light up if the fluid is translu cent, providing the covering tissues a re not too thick (Fig. 15.5 and Box 3.11).

Examination sequence

■ Inspect the lump, noting any change in colour or texture of the overlyin g skin.

■ Define the site and shape of the lump.

■ Measure its size and record the findings diagrammatically.

■ Gently palpate for tenderness or change in skin temperature.

■ Feel the lump for a few seconds to determine if it is pulsatile.

■ Assess the consistency, surface texture and margins of the lump.

■ Try to pick up an overlying fold of skin to assess whether the lump is fixed to the skin.

■ Try to move the lump in different planes relative to the surrounding tissu es to see if it is fixed to deeper structures.

■ Compress the lump on one side; see and feel if a bulge occurs on the o pposite side (fluctuation). Confirm the

fluctuation in two Lymph nodes may be palpable in normal people, espe cially in the subm andibular, axilla and groin regions (Fig.

3.21). Distinguish between normal and pathological nodes. Pathological lymphadenopathy may be local or generalised, and is of

diagnostic and prognostic signifi cance in the staging of lymphoproliferative and other malignancies.

Preauricular Posterior auricular Occipital

Tonsillar Superior cervical Posterior cervical

Deep cervical chain (deep to the sternocleidomastoid)

Supraclavicular Submaxillary Submental

From lower abdomen below umbilicus Epitrochlear

Posterior view of knee From buttock and back

Horizontal group Popliteal

Vertical group

From lower limb

From skin of penis, scrotum,

perineum, lower vagina,

vulva, anus

Fig. 3.21 Distribution of palpable lymph glands.

planes. Fluctuation usually indicates that the lump contains fluid, although some s oft lipomas can feel fluctuant. ■

Auscultate for vascular bruits.

■ Transilluminate.

3.11 Features to note in any lump or swelling (SPACESPIT)

• Size

• Position

• Attachments

• Consistency

• Edge

• Surface and shape

• Pulsation, thrills and bruits

• Inflammation

• Redness

• Tenderness 3

• Warmth

• Transillumination

THE LYMPH NODES

Axillary

3 Size

Normal nodes in adults are <0.5 cm in diameter.

Attachments

Lymph nodes fixed to deep structures or skin suggest malignancy.

Consistency

Normal nodes feel soft. In Hodgkin’s disease they are characteristical ly ‘rubbery’, in tuberculosis they may be ‘matted’, and in metastatic

cancer they feel hard.

Tenderness

Acute viral or bacterial infection, including infectious mononucleosis, dental sepsis and tonsillitis, causes tender, variably enlarged

lymph nodes.

Examination sequence

General principles

■ Inspect for visible lymphadenopathy.

■ Palpate one side at a time using the fingers of each hand

in turn.

■ Compare with the nodes on the contralateral side.

■ Assess:

■

site

■

size.

■ Determine whether the node is fixed to:

■

surrounding and deep structures

■

skin.

■ Check consistency.

■ Check for tenderness.

Cervical nodes

■ Examine the cervical and axillary nodes with the patient sitting. ■ From behind, examine the submental, submandibular,

preauricular, tonsillar, supraclavicular and deep cervical nodes in the anterior tri angle of the neck (Fig. 3.22A).

■ Palpate for the scalene nodes by placing your index finger between the sternocleidomastoid muscle and clavicle. Ask the

patient to tilt his head to the same side and press firmly down towards the first rib (Fig. 3.22B).

■ From the front of the patient, palpate the posterior triangles, up the back of the neck and the posterior auricular and

occipital nodes (Fig. 3.22C).

Axillary nodes

■ From the patient’s front or side, palpate the right axilla with your left ha nd and vice versa (Fig. 3.23A).

■ Gently place your fingertips into the apex of the axilla and then draw th em downwards, feeling the medial, anterior and

posterior axillary walls in turn.

A B C

Fig. 3.22 Palpation of the cervical glands. (A) Examine the glands of the anterior tria ngle from behind, using both hands. (B)

Examine for the scalene nodes from behind with your index finger in the ang le between the sternocleidomastoid muscle and

the clavicle. (C) Examine glands in the posterior triangle from the front.

A B C

Fig. 3.23 Palpation of the axillary, epitrochlear and inguinal glands. (A) Examination for right axillary lymphadenopathy. (B)

Examination of the left

epitrochlear glands. (C) Examination of the left inguinal glands.

Epitrochlear nodes

■ Support the patient’s right wrist with your left hand, hold his partially flex ed elbow with your right hand and use your

thumb to feel for the epitrochlear node. Examine the left epitrochlear node wit h your left thumb (Fig. 3.23B).

Inguinal nodes

■ Examine for the inguinal and popliteal nodes with the patient lying down.

■ Palpate over the horizontal chain, which lies just below the inguinal ligame nt, and then over the vertical chain along the

line of the saphenous vein (Fig. 3.23C).

Abnormal findings

If you find localised lymphadenopathy, examine the are as which drain to that site. Infection commonly causes lymphadenitis (localised

tender lymphadeno pathy); e.g. in acute tonsillitis the submandibular nodes are involved. If the lymphadenopathy is nontender , look for a

malignant cause, tuberculosis or features of HIV infection. Generalised lymphadenopa thy occurs in a number of conditions (Box 3.12).

Examine for enlarge ment of the liver and spleen, and for other haematologi cal feature s, such as purpura (bruising under the skin),

which can be large (ecchymoses) or pinpoint (petechiae; Fig. 3.24).

WEIGHT AND HEIGHT

Weight is an important indicator of general health and nutrition. Serial weight measurements are useful in monitoring acutely ill patients

and those with chronic disease. Serial height is helpful in monitoring growth in children and osteoporotic vertebral collapse in the elderly.

Record the body mass index (BMI), rather than weight alone, as it is independent of the patient’ s height. BMI is calculated from the

formula: weight/height

(using metric units, kg/m

). Obesity is defined by BMI and race 3

(Box 3.13).

BMI, however, does not describe body fat distribution and excess intraabdominal fa t is an independent predic tor of hypertension, insulin

resistance, type 2 diabetes mellitus and coronary artery disease. Waist circumfer ence correlates bette r with visceral fat and indirectly

measures central adiposity. Health risk is increased when waist circumference exceeds 94 cm (37 inches) for men and 80 cm (32 inches)

for women. Waist : hip ratio is strongly related to risk of coronary artery disease. ‘Pear shape’ and a waist : hip ratio of ≤0.8 in females or

<0.9 in males have a good prognosis, whereas ‘apple shaped’ subjects with a greater waist : hip ratio have an increased risk o f coronary

artery disease and the ‘meta bolic syndrome’ (Fig. 3.25).

3.12 Important common causes

of lymphadenopathy

Generalised

• Viral: Epstein–Barr virus (glandular fever or Burkitt’s lymphoma), cytomegalovirus, human immunodeficiency virus

• Bacterial: brucellosis, syphilis

• Protozoal: toxoplasmosis

• Malignancy: lymphoma, acute or chronic lymphocytic leukaemia

• Inflammatory: rheumatoid arthritis, systemic lupus erythematosus, sa rcoidosis

Localised

• Infective: acute or chronic, bacterial or viral

• Malignancy: lymphoma

3.13 The relationship between body mass index (BMI), nutritional status and ethnic gro up

Severe malnutrition Underweight

Normal

Overweight

Obese

Morbidly obese

BMI non-Asian BMI Asian <16 <16 <18.5 <18.5 18.5–24.9 18.5–22.9 25–29.9 23–24.9 30–39.9 25–29.9 ≥40 ≥30

Fig. 3.24 Petechiae.

B Fig. 3.25 Abdominal obesity and generalised obesity. (A) Abdominal

obesity (apple shape). (B) Generalised obesity, where fat deposition is mainly o n the hips and thighs (pear shape).

3 Examination sequence

■ Note any abnormalities in stature or body proportions, ■ Measure height usi ng a vertical scale with a rigid, adjustable

arm piece. In the serial assessment of growth in children and teenagers, measu re height to the nearest millimetre using a

calibrated stadiometer (Fig. 15.20).

■ The patient should stand erect and be weighed in his indoor clothing with out shoes. Calculate and record BMI.

■ Look for abnormal fat distribution.

■ Measure the waist with the patient standing at the level equidistant between the costal margin and iliac crest. The

measurement should record the maximum diameter, so measure over any abdom inal fat and not under it.

■ Look for any evidence of malnutrition or specific vitamin deficiencies.

Nutritional status

Illness may produce profound changes in an individu al’s nutritional requirements, app etite and ability to eat. Malnutrition delays

recovery from illness and surgery, and delays wound healing. Record BMI initially and repeat this at least weekly in an acute setting, and

monthly in outpatients or in the community, to monitor nutritional status.

Vitamin deficiencies

Vitamins are organic substances that have key roles in certain metabolic pathways. They are fatsol uble (vita mins A, D, E and K) or

watersoluble (vitamins of the Bcomplex group and vitamin C).

Vitamin deficiencies occur in older people and alco holic patients, and are common in develo ping countries. Folate deficiency is usually

due to poor intake and causes macrocytic anaemia and glossitis. Vitamin B

deficiency is usually caused by the autoimmune disor der

pernicious anaemia but can occur in vegans, small bowel overgrowth, or ileal disease o r resection. Vitamin C deficiency (scurvy) is less

common and produces extensive bruising, particularly in the elderly living alone without access to fresh fru it and vegetables (Fig. 3.26).

Those with alcohol dependency may eat poorly and also become deficient in vitamin B

(thiamine). Smallbowel malabsorption and liver

and biliary tract disease can lead to deficiency of fatsoluble vitamins (Box 3.14).

Abnormal findings

Obesity

Obesity is a major worldwide health problem, largely as a result of changes in lifestyle. It is caused by excess calorie intake associated

with inadequate exercise. Rarely, it is secondary to hypothyroidism, Cushing’s syndrome, Prader–W illi syndrome or drugs (Box 3.15). It

is associated with hypertension, hyperlipidaemia, type 2 diabete s mellitus, gallbladder disease and sleep apnoea (Fig. 3.27). Increased

BMI is associated

with several malignancies, particularly oesophageal and

Fig. 3.26 Scurvy. (A) Bleeding gums. (B) Bruising and perifollicular haemorrhage s.

Benign intracranial hypertension Female hirsutism Sleep apnoea

Exertional breathlessness

Gastro-oesophageal reflux symptoms

Increased blood pressure Non-alcoholic steatohepatitis

Gallstones

Abdominal striae

Impaired fertility

Stress incontinence

Osteoarthritis

Varicose veins

Dependent oedema

Fig. 3.27 Complications of obesity.

renal cancer in both sexes, thyroid and colon cancer in men and endometrial and gallblad der cancer in women. Obesity reduces life

expectancy by about 7 years, about the same as a lifetime of heavy smoking.

Weight loss

Weight loss is important and may be due to:

• reduced food intake from a poor appetite (anorexia)

3.14 Vitamins and deficiencies

Vitamin

Fat-soluble

Vitamin A (retinol)

Source Deficiency

Liver, milk, butter, cheese, fish oils

Vitamin D (cholecalciferol) Manufactured in skin under influence of sunlight

Vitamin E (α-tocopherol) Vegetables, seed oils

Vitamin K

Water-soluble

Vitamin B

(thiamine) Green vegetables, dairy products

Cereals, grains, beans, pork

Vitamin B

(riboflavin) Vitamin B

(nicotinic acid) Vitamin B

(pyridoxine) Biotin

Folate

Vitamin B

(cobalamin) Milk

Meat, cereals

Meat, fish, potatoes, bananas Liver, egg yolk, cereals, yeast Green vegetables

Animal products

Vitamin C (ascorbic acid) Fresh fruit and vegetables Xerophthalmia – night blindness

Keratomalacia

Rickets in children

Osteomalacia

Haemolytic anaemia

Ataxia

Bleeding disorder 3

Beri-beri – neuropathy (dry) or heart failure (wet) Wernicke–Korsakoff syndrome

Glossitis, stomatitis

Pellagra – dermatitis, diarrhoea and dementia

Polyneuropathy

Dermatitis, alopecia, paraesthesiae

Megaloblastic anaemia

Neurological disorders

Scurvy – extensive bleeding, bruising and

perifollicular haemorrhages

3.15 Drugs associated with weight gain Class

Anticonvulsants

Antidepressants Antipsychotics

Beta-blockers

Oral corticosteroids

Migraine prophylaxis

Sulphonylureas/

hypoglycaemic agents Insulin

Protease inhibitors for HIV infection

Examples

Sodium valproate, phenytoin, gabapentin

Citalopram, mirtazapine Chlorpromazine, risperidone, olanzapine, lithium

Atenolol

Prednisolone, dexamethasone Pizotifen

Gliclazide, pioglitazone

All formulations

Indinavir, ritonavir, lopinavir

• malabsorption or loss of nutrients, e.g. in prolonged diarrhoea

• metastatic cancer, e.g. of the lung, breast or gastrointestinal tract

• serious and prolonged infection, e.g. tuberculosis

• untreated advanced HIV infection

• chronic inflammation, e.g. inflammatory bowel disease.

In most of these systemic disorders, weight loss is associ

ated with anorexia. Occasionally, weight loss is associ

ated with a normal or increased appetite (thyrotoxicosis,

coeliac disease or type 1 diabetes mellitus). The patient’s

complaint of weight loss does not always correlate

with true weight loss. Temporary weight loss is most commonly associate d with anxiety, depression or a deliberate attempt to lose

weight.

Malnutrition and starvation are major problems worldwide, even in the d eveloped world. Malnutrition is found in up to 40% of UK

hospital admissions, par ticularly the elderly, usually due to poverty or illness. Weight loss due to malnutrition also occurs in anorexia

nervosa, alcohol abuse and drug addiction.

Short stature

Short stature is usually familial, so ask about the height of the patient’s parents and siblings (p. 368). A ny signifi cant childhood illness

will reduce the rate of growth and may limit final height. Identify causes of short stature from associated features. Other disorders, such

as renal tubular acidosis, intestinal malabsorption and hypo thyroidism, may be less obviou s in young people and delay the diagnosis.

Loss of height is part of normal ageing but is accentuated by compression fractures of the spine due to os teoporosis, particularly in

women. In postmenopausal women loss of >5 cm height is an indi cation to investigate for osteo porosis.

Tall stature

Tall stature is less common than short stature an d is usually familial. Most individuals with heights above the 95th centile are not

abnormal so ask about the height of close relatives. Abnormal causes of increased heig ht include:

• Marfan’s syndrome

• hypogonadism

• pituitary gigantism.

In Marfan’s syndrome, the limbs are long in relation to the length of the trunk, an d the arm span exceeds height

Fig. 3.28 Marfan’s syndrome, an autosomal dominant condition. (A) Tall stature and r educed upper segment to lower segment

ratio (note surgery for aortic dissection). (B) Long fingers. (C) High-arched p alate. (D) Dislocation of the lens in the eye.

( Fig. 3.28A). Additional features include long slender fingers (arachnodactyly) (Fig. 3.28B), narrow feet, a higharched palate (Fig.

3.28C), upward dislocation of the lenses of the eyes (Fig. 3.28D), cardiovascular abnor malities s uch as mitral valve prolapse, and

dilatation of the aortic root with aortic regurgitation.

During puberty, the epiphyses close in response to stimulation from the sex hormones, so in som e patients with hypogonadism the limbs

continue to grow for longer than usual.

Pituitary gigantism is a very rare cause of tall stature due to excessive growth hormone secretion before epi physeal fusion has occurred.

HYDRATION

In adults 60–65% of body mass is water. A male weigh ing 70 kg has 42 litres of wate r, of which twothirds is intracellular (28 litres),

12% interstitial fluid (9.4 litres) and the remainder circulating blood plasma (4.6 litres). Women have a small er percentage of total body

water than men, although they may have cyclical fluctuations in weight due to perimen strual fluid retention.

Dehydration

It is easy to underestimate the severity of dehydration. Assess hydration in all patients, especially those with excess fluid loss, e.g.

vomiting, diarrhoea, sweating, burns and polyuria, and when ambient temperature is raised. If you know the patient’s usual weight,

useful information is obtained by weighing him.

Tachycardia is a common feature. Loss of skin turgor occurs in severe dehydration but adul ts can lose 4–6 litres before the skin becomes

dry and loose. Blood pressure may be low and postural hypotension may ind icate intravascular volume depletion. A dry tongue is an

unreliable indicator of dehydration since it often occurs in mouth breathing.

Oedema

Oedema is tissue swelling due to an increase in intersti tial fluid. The capillary wall separates the interstitial fluid and plasma

compartments. The distribution of water between the vascular and inte rstitial spaces is

Hydration

determined by the balance between hydrostatic pressure forcing water out of the ca pillary, and colloid osmotic (oncotic) pressure,

drawing fluid into the vascular space (Starling’s forces). Oncotic pressure depend s largely on circulating protein concentration,

particularly serum albumin.

Oedema can be generalised, localised or postural. The cardinal sign of subcutaneous oedema is pitting of superficial tissues. Pitting on

pressure may not be demonstrable until body weight has increased by 10– 15%. Daytoday alterations in bo dy weight are usually the most

reliable index of changes in body water.

Hypothyroidism is characterised by mucinous infil tration of tissues (myxoedema). In contrast to oedema, myxoedema and chronic

lymphoedema do not pit on pressure.

• Renal disease, e.g. acute glomerulonephritis, may reduce urine volume, with increased c irculating and extracellular fluid volume and

increased tubular reabsorption of sodium.

• Iatrogenic causes include excess fluid replacement, especially intravenously, producing flu id overload.

Hypoproteinaemia

Hypoproteinaemia, particularly hypoalbuminaemia,

reduces oncotic pressure and encourages fluid to move to the interstitial space, c ausing oedema. 3

Generalised oedema

There are two principal causes of generalised oedema (Box 3.16):

• fluid overload

• hypoproteinaemia.

Distinguish them by assessing the jugular venous pres sure (p. 114). The jugular venous pressure is u sually elevated in fluid overload but

not in hypoproteinaemia (Box 3.17).

Fluid overload

Fluid overload may be due to heart failure or renal

disease, or be iatrogenic (result from medical intervention).

• Heart failure causes oedema in the following ways:

• Renal underperfusion activates the renin– angiotensin–aldosterone system (se condary hyperaldosteronism) and releases vasopressin,

leading to salt and water retention.

• Renal blood flow is reduced, causing increased salt and water reab sorption.

• When the patient lies flat, blood redistributes from the legs into the torso, increasin g venous return to the heart. In the failing heart this

results in increased enddiastolic pressure within the left ventricle, leading to pulmonary oedema. The patient therefore experiences

orthopnoea (breathlessness on lying flat).

3.16 Causes of oedema

Low plasma oncotic pressure

Low serum albumin due to:

• Increased loss – nephrotic syndrome

• Decreased synthesis – chronic liver disease

• Malabsorption – protein-losing enteropathy, e.g. Crohn’s disease and coeliac d isease

• Malnutrition – kwashiorkor

Increased hydrostatic pressure

High venous pressure/obstruction due to:

• Deep vein thrombosis

• Venous insufficiency

• Pregnancy

• Pelvic tumour

• Heart failure

• Intravascular volume expansion, e.g. excess intravenous

fluid, renal failure

Increased capillary permeability

• Local – soft-tissue infection/inflammation

• Systemic – severe septicaemia

• Drugs, e.g. calcium channel blockers

• Acute allergy

Lymphatic obstruction (lymphoedema) – non-pitting

• Malignant infiltration

• Congenital abnormality – Milroy’s disease

• Radiation injury

• Elephantiasis – tropical (filarial) worm infestation

3.17 Features suggesting different causes of oedema

Heart failure

Pitting

JVP raised

Gallop rhythm (third heart sound)

Hypoproteinaemia Pitting

JVP not raised

DVT or ruptured Baker’s cyst * Pitting

Warm

Calf tenderness

Lymphoedema

Non-pitting

Not worse at the end of the day

*On examination is not possible to distinguish a deep venous thrombosis (DVT) from a ruptured Baker’s cyst. JVP, jugular

venous pressure.

Fat

Non-pitting

Spares the feet Patient obese

3 Periorbital oedema

Jugular venous pressure Heart size/apex beat Gynaecomastia

Hepatomegaly Blood pressure

Pleural effusion Splenomegaly Ascites

Abdominal veins

Clubbing, leukonychia Genital oedema Body hair distribution

Ankle swelling

Fig. 3.29 Features to look for in oedema.

Nephrotic syndrome causes heavy proteinuria and most patients with a hepatic cause will have features of chronic liver disease (Fig.

8.11).

The distribution of generalised oedema ( Fig. 3.29) is determined by gravity. In semirecu mbent patients it is usually found in the ankles,

backs of the thighs and the lumbosacral area. If the patient lies flat, it may involve the face and hands, as in nephrotic syndrome.

Localised oedema

This may be caused by venous, lymphatic, inflammatory or allergic disorders.

Venous causes

Increased venous pressure increases hydrostatic pres sure within capillaries, producing oe dema in the area drained by that vein. Venous

causes include deep vein thrombosis, external pressure from a tumour or preg nancy, or venous valvular inc ompetence from previous

thrombosis or surgery. Conditions which impair the normal muscle pumping action, e.g. hemipares is and forced immobility, increase

venous pressure by impair ing venous return. As a result oedema may occur in immobile, bedridden patients, in a paralysed limb, or in a

healthy person sitting for long periods, e.g. during travel (Fig. 3.30).

Lymphatic causes

Normally, interstitial fluid returns to the central circula

tion via the lymphatic system. Any cause of impaired lym phatic flow, e.g. intraluminal or extraluminal obstruction, may produce

localised oedema (lymph oedema) (Fig. 3.31). If the condition persists, fibrous tissues proliferate in t he interstitial space and the affected

area becomes hard and no longer pits on pressure. In

the UK, the commonest cause of leg lymphoedem a is

Fig. 3.30 Swollen right leg, suggesting deep vein thrombosis or inflammation, e.g. s oft-tissue infection or ruptured Baker’s cyst.

Fig. 3.31 Lymphoedema of the right arm following right-sided mastectomy and radiotherapy.

congenital hypoplasia of leg lymphatics (Milroy’s disease), and in the arm after radical mast ectomy and/ or irradiation for breast cancer.

Lymphoedema is common in some tropical countries because of lym phatic obstruction by filarial worms (elephantiasis).

Inflammatory causes

Any cause of tissue inflammation, including infection or injury, liberates mediators, e.g. histamine, bradykinin and cyt okines, which

cause vasodilatation and increase capillary permeability. Inflammatory oedema is accom panied by the other features of inflammation

(redness, tenderness and warmth) and is therefore painful.

Temperature

Fig. 3.32 Angio-oedema following a wasp sting.

Allergic causes

Increased capillary permeability occurs in acute allergic conditions. The affected ar ea is usually red and pruritic (itchy) because of local

release of histamine and other inflammatory mediators but, in contrast to inflamma tion, is not painful.

Angiooedema is a specific form of allergic oedema affecting the face, lips and mouth (Fig. 3.32). Swelling may develop rapidly and may

be lifethreatening if the upper airway is involved.

Postural oedema

This is due to failure of muscle movement and is common in the lower limbs of inactive pati ents.

Examination sequence

■ Apply firm pressure with your fingers or thumb for at least 15 seconds (Fig. 3.33). Pitting may persist for several

minutes until it is obliterated by the slow return of the displaced fluid.

■ Assess the state of hydration by looking for sunken orbits and dry muc ous membranes. Gently pinch a fold of skin on

the neck or anterior chest wall, hold it for a few seconds and then release. W ell-hydrated skin springs back into position

immediately, in severe dehydration skin subsides abnormally slowly.

■ Record weight and urine output.

■ Record the pulse rate and supine/erect blood pressures. Look for tachyca rdia >100 bpm and postural hypotension (a fall

> 15 mmHg in systolic pressure on standing).

■ Check for oedema in the ankles and legs. In bed-bound

patients, check for sacral oedema.

■ Examine the jugular venous pressure (p. 114).

20°C

Fig. 3.33 Demonstration of pitting oedema.

3.18 Clinical features of hypothermia

Clinical features

Increased metabolic rate,

vasoconstriction

Shivering maximal, impaired judgement Uncooperative

Depressed conscious level

Progressive depression of conscious level, muscle stiffness

Failure of vasoconstrictor response and shivering

Bradycardia, hypotension, J waves present on electrocardiogram, risk of arrhythmias

Coma, patient may appear dead, absent pupillary and tendon reflexes

Spontaneous ventricular fibrillation Asystole/profound bradyarrhythmias

TEMPERATURE

The ‘normal’ oral or ear temperature is 37°C but may range betwee n 35.8°C and 37.2°C (98–99°F) (Box 17.2). There is a circadian

variation, with the lowest readings

Core temperature 36°C

35°C (hypothermia)

34°C

33°C

28–32°C (severe hypothermia)

28°C

occurring in the early morning. Rectal temperature is about 0.5°C higher than oral. The axill a is an unreliable site for measuring

temperature. Use a digital thermo meter under the tongue, or in the rectum or the external audi tory meatus. Mercury thermometers have

been replaced by electronic devices, which are safer and more accurate (Fi g. 3.34).

Fig. 3.34 Electronic thermometer.

Fever
Fever is an increase in body temperature usually caused by a cellular response to infection,  immunological dis turbance or malignancy
(Ch. 17).
Hypothermia
Hypothermia is a core temperature <35°C and is easily missed unless rectal temperature is  measured. As body temperature falls,
conscious level is progressively impaired. Altered consciousness is  common with core temperatures <28°C (Box 3.18), and may mimic
death (Box 20.2). If you suspect hypothermia, measure tem perature at more  than one site, e.g. external auditory meatus and rectum.
Hypothermia occurs in:
• elderly immobile patients living alone, particularly during the winter
• water immersion and neardrowning
• prolonged unconsciousness in low ambient temperatures, especially combined with 
alcohol intoxication (which causes peripheral vasodilatation), drug overdosage, stroke or  head injury
• severe hypothyroidism.
SECTION 2 SYSTEM EXAMINATION
David Gawkrodger
EXAMINATION OF THE SKIN, HAIR AND NAILS 64
Anatomy 65
Hair cycle 66
Nails 66
Common patterns of hair disease 71 Nail abnormalities 72
Mucous membranes and other sites 73
The skin, hair and nails4
The history 73
The physical examination 75
Putting it all together 75
Investigations 75
EXAMINATION OF THE SKIN, HAIR AND NAILS
Face and scalp 3
• Hair loss
• Scalp changes, e.g. psoriasis
• ‘Butterfly’ rash, e.g. SLE
• Central or hairline distribution
• Conjunctivitis/blepharitis
in rosacea
4 Mouth
• Lichen planus
• Herpes simplex
• Pemphigus
Hands and fingernails 2
• Pitting in psoriasis and alopecia areata
• Ridging in eczema
• Fungal infection
• Finger web burrows in scabies 5 Genitalia
• Psoriasis
• Intertrigo
• Infestation
• Lichen sclerosus
General observation 1
• Distribution of rash
Symmetrical — extensor, e.g. psoriasis — flexor, e.g. eczema
Asymmetrical, e.g. granuloma annulare
Facial, e.g. rosacea, seborrhoeic

dermatitis

Localized, e.g. morphoea

Widespread, e.g. drug eruption

Dermatomal, e.g. herpes zoster

Truncal, e.g. guttate psoriasis

Sun-exposed, e.g. drugs or SLE

• Morphology of lesions, e.g. macules,

papules, vesicles, pustules, bullae,

nodules, plaques

• Configuration of lesions, e.g. discrete,

confluent, linear, grouped, annular

6 Feet and nails

• Pedal pulses

• Tinea pedis

• Toenail changes, e.g. fungal

infection, psoriasis

7 Joints

• Psoriatic arthritis

• Connective tissue disease

ANATOMY

The skin is the largest organ in the body, making up 16% o f body weight. It protects the body from external factors and keeps the

internal organs intact (Fig. 4.1 and Box 4.1).

Skin has three layers:

• epidermis

• dermis

• subcutis.

The epidermis is stratified squamous epithelium with four layers (basal, prickle, granular and horny), representing the stages of keratin

maturation. The main cell, the keratinocyte, produces keratin. Keratinocytes lose their nuclei in the granular layer and, as flat plates, form

the horny layer. Melanocytes (5–10% of the cell population) originate from the neural crest. They synthesise melanin and are most

numerous on the face and other exposed sites. Langerhans cells are dendritic, immunologic ally active antigen-presenting cells that form a

network throughout the epidermis.

The dermis is a supportive connective tissue matrix containing speci alised structures. It is thin (0.6 mm) on the eyelids and thicker (3

mm or more) on the back, palms and soles. It contains fibroblasts, dendritic cells, mast cells, macro phages and lymphocytes. Collagen

fibres make up 70% of the dermis and give strength and toughness. Elastin fibres prov ide the skin with elasticity. Glycosaminoglycans

form a semisolid matrix that allows some movement of dermal structures, such as hair follicles, sweat glands, blood and lymphatic

vessels, and nerves.

The subcutis is a loose layer of connective tissue and fat of variable thickness (up to 3 cm thic k on the abdomen).

The hair and nails are specialised epidermal structures.

4.1 Functions of skin Barrier

• Against chemicals, particles, microbes, ultraviolet

radiation

Homeostasis

• Regulation of body

temperature

Sensation

• Touch

• Temperature

Mobility

• Provides a surface for grip Metabolism

• Role in vitamin D production Immunity

• Outpost for immune

surveillance

Psychology

• Sexual attraction

• Against mechanical injury

• Against loss of body fluids 4

• Pressure

• Pain

• Self-image

Shaft of hair

Opening of sweat duct Epidermis

Sweat duct Subpapillary vascular plexus

Sebaceous gland Arrector pili muscle Sweat gland Hair follicle Subcutaneous adipose tis sue

Deep cutaneous vascular plexus Subcutis

Muscle layer

Fig. 4.1 Structure of the skin. Dermis

Hair has a protective and sexual function and hairs cover the surface of the skin, except for the glabrous skin of the palms and soles, the

glans penis and the vulval introitus. The follicle density is greatest on the face. The hair shaft has an outer cuticle enclosing a cortex of

packed keratinocytes.

There are three types of hair:

• lanugo: fine and long; found in the fetus

• vellus hairs: short, fine and light in colour; cover

most body surfaces

• terminal hairs: long, thick and dark; found on the

scalp, eyebrows, eyelashes, pubic, axillary and

beard areas.

Amount and type of hair vary and are influenced by racial and genetic factors. Typically, Europeans h ave straight hair, black Africans

have curly hair and East Asians have sparse facial and body hair. People fro m the Mediterranean area have more body hair than northern

Europeans.

Lateral nail fold Distal edge of nail plate

Lunula Nail plate

Cuticle

Eponychium

Hyponychium Nail plate Proximal nail fold

Nail bed Cuticle Matrix

Hair cycle

Regular cycles of growth (anagen), resting (telogen) and shedding (c atagen) occur. The cycle lasts up to 5 years for scalp hair, but less

for eyebrow, axillary and pubic hair. Adjacent hairs are not in the same phase b ut illness or childbirth can synchronise the hair cycle and

cause an alarming loss of large amounts of hair (telogen effluvium).

Puberty

Body hair develops with sexual maturity, with wide normal variation in its pattern (Fig. 15.19). At puberty, andr ogens induce vellus hairs

of the pubic region to develop into terminal hairs. Gonadotrophins are not involved in this process, so patients with gonadotrophin

deficiency have pubic hair but no other pubertal development. Axillary hair appear s 2 years after pubic hair and coincides with the onset

of facial hair in boys (p. 369).

Nails

The nail is a plate of hardened, densely packed keratin protecting the finger tip. It facilitates grasp and tactile sensitivity in the finger

pulp (Fig. 4.2). The nail matrix contains dividing cells that mature, keratinise and move f orward to form the nail plate, which in the finger

is 0.3–0.5 mm thick and grows at 0.1 mm/24 hours (Fig. 4.2). Toenails grow mor e slowly. Adjacent dermal capillaries produce the pin k

colour of the nail; the white lunula is the visible distal part of the matrix.

Symptoms and definitions

Symptoms include:

• a rash

• itch (pruritus) and sleep disturbance (Box 4.2)

• a growth or lump

• discharge, crusting and smell

• scales falling from the skin or scalp

• disfigurement and psychological distress

Distal phalanx

Fig. 4.2 Structure of the nail.

4.2 Causes of severe pruritus

Condition

Scabies

Dermatitis herpetiformis Urticaria

Eczema

Insect bites

Lichen planus Generalised itch

Look for:

Burrows on hands or feet

Small blisters on extensor sites Intermittent wheals on limbs or trunk

Scaly, crusted, excoriated or lichenified patches

Linear or grouped patterns of recent onset

Typical purplish papules on wrists If no rash, check blood tests for renal, haematological or he patic diseases

• inability to work or pursue leisure activities, e.g. swimming.

Rashes

The distribution on the body, morphology (shape) of individual lesions and their grouping (configuration)

4.3 Some examples of skin lesions and systemic disease Skin lesions

Erythema

nodosum

Pyoderma

gangrenosum

Dermatitis herpetiformis

Associations

Sarcoidosis,

tuberculosis,

poststreptococcal infection, connective tissue diseases,

drugs

Ulcerative colitis, rheumatoid arthritis, leukaemia

Gluten enteropathy

Generalised purpura

Dermatitis artefacta

Idiopathic

thrombocytopenic purpura and other haematological

disorders

Personality disorders

Ask about

Cough and sputum, breathlessness, sore throat, drugs

Rectal bleeding, joint symptoms

Family history, change in bowel habit

Family history, haematuria, fever and weight loss

Stresses or anxieties

can be diagnostic. The history of a lesion and systemic features can also be helpful.

Distribution patterns

• Symmetrical or universal eruptions suggest systemic or constitutional causes.

• Asymmetrical rashes that spread from one focus are more likely to be due to fungal, bac terial or viral infection (Box 4.3).

The time and evolution of the spread and change in

morphology help diagnosis.

• An itchy rash typically involving the flexures of the popliteal fossa, antecubital fossa , neck and face occurs in atopic eczema (Fig. 4.3).

• Extensor plaques on elbows and knees, the scalp and the sacrum suggest psoriasis (Fig. 4.4).

• Facial:

• Seborrhoeic dermatitis, an inflammatory reaction to a yeast, Malassezia, that form s part of normal skin flora, affects the forehead,

nasolabial folds and scalp.

• Acne vulgaris produces comedones (blackheads), pustules and cysts and also affects the chest and back. Rosacea causes telangiectasia

together with the above features.

• Sun damage and malignant tumours, such as basal cell cancer, are relatively common (Fig. 4.5).

• Psoriasis is uncommon.

• Truncal:

• Guttate psoriasis, following a streptococcal throat infection

• Pityriasis rosea, which usually starts with one lesion, the ‘herald patch’

• Tinea versicolor, caused by Pityrosporum yeast

• Urticaria, producing itchy wheals that clear within 24 hours (Fig. 4.5E).

Fig. 4.3 Distribution: flexural. Atopic eczema in the popliteal fossae and ankles.

Fig. 4.4 Distribution: extensor. Psoriasis on the knees.

• Peripheral:

• Wrist lesions suggest lichen planus (Fig. 4.6). Look at the buccal mucosa for the white lacy lesions of Wickham’s striae to confirm

this.

• Lower leg lesions include necrobiosis lipoidica (associated with diab etes mellitus and

occasionally rheumatoid arthritis: Fig. 4.5F), erythema nodosum (due to sarcoidosis or

poststreptococcal infection) and vasculitis caused by circulating immune complexes damag ing dermal blood vessels (Fig. 4.5G).

• Hands or feet can be affected by fungal infection, typically ‘athlete’ s foot’ (caused by Trichophyton) (Fig. 4.5H).

Fig. 4.5 Anatomical distribution of lesions. Facial: (A) Seborrhoeic dermatitis. (B) Basa l cell cancer showing pearly papules

and telangiectasia. Facial

and truncal: (C) Acne vulgaris. Truncal: (D) Pityriasis rosea. (E) Urticaria. Peri pheral: (F)

Necrobiosis lipoidica. (G) Vasculitis. (H) Fungal infection.

Fig. 4.6 Diagnostic sequence, lichen planus. (A) Discrete flat-topped papules on the wrist. (B) Wickham’s striae visible on

close inspection. (C) White lacy network of striae on buccal mucosa.

Fig. 4.7 Distribution: dermatomal. This distribution suggests shingles.

Fig. 4.8 Nodule. (A) Seborrhoeic wart. (B) Squamous cell cancer.

Fig. 4.9 Macule. Macules can be pigmented (a freckle), erythematous (haemangiom a) or hypopigmented, as shown here in

vitiligo.

69 B

Fig. 4.10 Plaque. (A) Lupus vulgaris (tuberculosis of the skin). (B) Tuberculoid le prosy.

4 4.4 Terms used to describe skin lesions

Term

Abscess Atrophy

Bulla

Definition

A localised collection of pus

Loss of epidermis, dermis or both, thin, translucent and wrinkled skin, visible blood vesse ls

A fluid-filled blister >5 mm in diameter

Term

Milium Nodule

Definition

A small white cyst that contains keratin A solid elevation of skin >5 mm in diameter

Papilloma

Burrow

Callus

Comedo

Crust

Cyst

Ecchymosis

Erosion

Erythema

A tunnel in epidermis caused by a parasite, e.g. Acarus in scabies

Local hyperplasia of horny layer on palm or sole, due to pressure

A plug of sebum and keratin wedged in a dilated pilosebaceous orifice on the face Dried exudate, e.g. serum, blood or pus, on the skin

surface

A nodule consisting of an epithelial-lined cavity filled with fluid or semisolid material

A macular red or purple haemorrhage, >2 mm in diameter, in skin or mucous membrane

A superficial break in the epidermis, not extending into dermis, heals without scarring R edness of the skin due to vascular dilatation

Papule

A nipple-like projection from the surface of the skin

A solid elevation of skin <5 mm in diameter

Petechia

Plaque

Purpura

Pustule

A haemorrhagic punctate spot 1–2 mm in diameter

A palpable elevation of skin >2 cm diameter and <5 mm in height

Extravasation of blood resulting in redness of skin or mucous membranes

A visible collection of pus in a blister

Scale Accumulation of easily detached fragments of thickened keratin

Scar

Stria

Excoriation

Fissure

Freckle

Lichenification

A superficial abrasion, often linear, due to scratching

A linear split in epidermis, often just

extending into dermis

A macular area showing increased pigment formation by melanocytes

Chronic thickening of skin with increased skin markings, from rubbing or scratching

Telangiectasia

Ulcer

Vesicle

Replacement of normal tissue by fibrous connective tissue at the site of an injury At rophic linear band in skin, white, pink or purple, from

connective tissue changes Dilated dermal blood vessels resulting in a visible lesion

A circumscribed area of skin loss extending into the dermis

A clear, fluid-filled blister <5 mm in diameter

Wheal A transitory, compressible papule or plaque of dermal oedema, red or white, indicating urticaria

Macule A localised area of colour or textural change in the skin

Fig. 4.11 Bulla from an insect bite.

• Sun-exposed, on the face (sparing areas beneath the eyes and lower lip), the V of the neck or the posterior neck and exposed areas of

the arms and legs. Causes include connective tissue diseases, e.g. systemic lupus eryth ematosus (SLE),

photosensitising drugs, e.g. thiazide diuretics or non-steroidal anti-inflammator y drugs, cutaneous porphyrias or a primary sun

sensitivity condition, e.g. polymorphic light eruption or a photosensitive eczema.

• Dermatomal, e.g. herpes zoster (shingles) (Fig. 4.7).

Morphology is the shape and pattern of the skin lesions

(Box 4.4 and Figs 4.8–4.11). Lesions may be:

• Monomorphic (all have the same appearance), as in guttate psoriasis

• Pleomorphic (of differing appearance), as in chickenpox.

Configuration is the pattern in which lesions are

arranged and include linear, grouped, annular (in a

ring), or the Koebner phenomenon (an eruption in an

area of local trauma) (Fig. 4.12). Secondary changes of

crusting, erosion and excoriation complicate primary

lesions.

Fig. 4.12 Configuration. (A) Dermatitis herpetiformis: grouped. (B) Granuloma ann ulare: annular. (C) Insect bites: linear.

(D) Psoriasis: showing the Koebner phenomenon – lesions in an area of traum a. (E) Viral warts: Koebner phenomenon.

Duration

Anatomy

Actinic keratoses ( Fig. 4.13) are typically present for several years and slowly increase in number. Bas al cell cancers commonly develop

over 1–2 years and may show ulceration. Squamous cell cancers fo rm more rapidly over weeks or months.

Associated features

In a patient with a hand eruption, look for skin lesions

elsewhere, e.g. atopic eczema affecting the antecubital or popliteal fossae or psoriasis on the elbows, knees or scalp, and for burrows of

scabies between the fingers or genitalia. The vulva and penis can be affected by psoriasis but only rarely by eczema. Asym metrical

arthritis of large joints and of distal interphalangeal joints is found in up to 30% of patients with psoriasis (Fig. 14.3B).

Common patterns of hair disease

Hair loss (alopecia) can be total or partial ( Fig. 4.14):

• Diffuse alopecia. In common male-pattern hair loss terminal scalp hairs under go miniaturisation to

Fig. 4.13 Actinic keratoses on the scalp. A skin graft from the removal of a previou s squamous cell carcinoma is evident.

vellus hairs. This ageing phenomenon is strongly inherited and depends on androgens. Age-related hair loss in women is more diffuse.

Non-scarring diffuse hair loss occurs in hypothyroidism, hypopituitarism and iron defi ciency, connective tissue diseases, e.g. SLE,

postpartum or postmenopausal or may be drug-induced, e.g. cytotoxic agents.

• Localised non-scarring alopecia. In alopecia areata there is circumscribed lo ss of scalp, beard or eyebrow hair. Alopecia areata may

involve the whole scalp (alopecia totalis) or all body hair. (alopecia universalis ). Localised hair loss can be caused by fungal infection,

hair pulling, traction from braiding and secondary syphilis.

4.5 Causes of hirsutism

Type

Pituitary Adrenal

Ovarian

Drugs

Idiopathic

Example

Acromegaly

Cushing’s syndrome, virilising tumours, congenital adrenal hyperplasia

Polycystic ovary syndrome, virilising tumours Androgens, progestogens

End-organ hypersensitivity to androgens

• Scarring alopecia. Burns, severe infections, e.g.

herpes zoster, lichen planus and SLE, may permanently scar the scalp with perman ent hair loss.

• Loss of secondary sexual hair. In old age, cirrhosis and hypopituitarism, axillar y and pubic hair is lost. Excess hair growth takes two

forms:

• Hirsutism: in females with male-pattern growth of terminal hair, including facial and pub ic hair extending towards the umbilicus (male

escutcheon). It is a racial trait but may be idiopathic, and is rarely caused by an androgen-secreting tumo ur (Box 4.5). In these cases there

are other features of virilisation, e.g. male-pattern hair loss,

clitoromegaly or a deep voice.

• Hypertrichosis: in males or females with excess

terminal hair growth in a non-androgenic

distribution. It is uncommon and usually due to a

systemic disorder, e.g. porphyria cutanea tarda,

malignancy, anorexia nervosa, malnutrition or

drugs, e.g. ciclosporin, minoxidil and phenytoin.

Nail abnormalities

Nail changes are useful in diagnosing internal conditions and skin diseases (Box 4.6). In chronic iron

Fig. 4.14 Hair disorders. (A) Male-pattern baldness with hair loss from the temples and vertex of the scalp. (B) Alopecia

areata with ‘exclamation mark’ hairs, which taper as they approach the skin. (C ) Scalp ringworm with secondary bacterial

infection and localised hair loss.

4.6 Nail changes in systemic disease and skin disorders Change

Beau’s lines

Description of nail Transverse grooves

Brittle nails Nails break easily, usually at distal margin

Clubbing

Colour changes

Loss of angle between nail fold and nail plate. Finger tip bulbous. Nail matrix feels s pongy

Blue

Blue-green

Brown

Brown longitudinal streak

Differential diagnosis

Any severe systemic illness which affects growth of the nail matrix

Effect of water and detergent, iron deficiency, hypothyroidism, digital ischaemia

Familial or may signify serious cardiac or respiratory disease

Cyanosis, antimalarials, haematoma

Pseudomonas infection

Fungal infection, staining from cigarettes,

chlorpromazine, gold, Addison’s disease

Melanocytic naevus, malignant melanoma, Addison’s disease, racial variant

The history

4.6 Nail changes in systemic disease and skin disorders – cont’d Change Description of nail

Red streaks (splinter haemorrhages) White spots

White/brown ‘half and half’ nails White (leukonychia)

Yellow

Yellow nail syndrome

Combination changes

Koilonychia

Longitudinal ridges and triangular nicks at the distal nail

Spoon-shaped depression of nail plate

Nail fold erythema and telangiectasia

Onycholysis

Dilated capillaries and erythema at nail fold

Nail separates from nail bed

Onychomycosis

Pitting

Thimble pitting

Coarse pitting Ridging

Splinter haemorrhages

Thickening of the nail plate with colour change, usually whitening or brown

discoloration

Fine or coarse pits in the nail

A particular type of fine regular pitting, as seen on a thimble

Larger irregular pits in the nail plate

Transverse (across nail)

Longitudinal (up/down)

Small red streaks that lie longitudinally in the nail plate

Differential diagnosis

Infective endocarditis, trauma

Trauma to nail matrix (not calcium deficiency) Chronic kidney disease

Hypoalbuminaemia, e.g. associated with cirrhosis Psoriasis, fungal infection, jaundice, te tracycline Defective lymphatic drainage –

pleural effusions may occur

Darier’s disease

Iron deficiency anaemia, lichen planus, repeated

exposure to detergents

Connective tissue disorders, including systemic

sclerosis, SLE, dermatomyositis

Psoriasis, fungal infection, trauma, thyrotoxicosis,

tetracyclines (photo-onycholysis)

Fungal infection

Psoriasis, eczema, alopecia areata, lichen planus Alopecia areata

Eczema

Beau’s lines (see above), eczema, psoriasis, tic dystrophy, chronic paronychia

Lichen planus, Darier’s disease

Trauma, but can signify infective endocarditis

4.7 Causes of hypoalbuminaemia and leukonychia

Reduced albumin synthesis

• Chronic liver disease

Urinary protein loss

• Nephrotic syndrome

Protein-losing enteropathy

• Crohn’s disease

• Ulcerative colitis

• Ménétrier’s disease of the

stomach

• Coeliac disease

Protein malnutrition

• Kwashiorkor

• Intestinal lymphoma

• Bacterial overgrowth

• Radiation damage in psoriasis. Dilated capillaries in the proximal nail fold occur in vasculitic conditions, such as SLE (Fig. 4.15 and

Box 4.6).

Mucous membranes and other sites

Changes in the mucous membranes of the mouth and genitalia accompany , and may be characteristic of, certain skin conditions, e.g. oral

Wickham’s striae in lichen planus, oral lesions in Kaposi’s sarcoma (Fig. 4.16), vulval involvement with lichen sclerosus. Fully examine

patients with skin lymphoma for lymphadenopathy and hepatosplenomegaly. In patients with leg ulcers, feel the leg an d foot pulses to

assess the arterial supply (Fig. 6.40).

deficiency the nails become brittle, flat and eventually spoon-shaped (k oilonychia) (Box 4.7). White nails (leukonychia) are a sign of

hypoalbuminaemia. Beau’s lines, due to arrest of nail growth, are transverse white groove s that appear on all nails shortly after a severe

illness and which move out to the free margins as the nail grows. Altho ugh one or two splinter haemorrhages are commonly seen under

the nails of manual workers, multiple lesions raise the possibility of bacterial endocarditis . Distal nail separation (onycholysis) is

common

THE HISTORY

Presenting complaint

Ask when, where and how the eruption or lesions began, about the initial appearance and what changes have occurred with time. Note

associated features, such as itch and systemic upset, together with aggravating and relievi ng factors. Use SOCRATES to remember what

to ask (Box 2.10).

Onycholysis with pitting in psoriasis. (C) Beau’s lines. (D) Leukonychia. Fig. 4.15 The nail as a diagnostic aid. (A)

Splinter haemorrhages. (B)

(E) Dilated proximal nail fold capillaries in systemic lupus erythematosus. (F) Ko ilonychia.

Fig. 4.16 Kaposi’s sarcoma. (A) In the mouth and (B) on the skin.

Past and drug histories

Ask about previous skin disease, atopic symptoms (hay

fever, asthma, childhood eczema), medical disorders

Fig. 4.17 Stevens–Johnson syndrome. (A) Facial and oral lesions. (B) ‘Target lesion s’ on hands.

that may involve the skin, e.g. Stevens–Johnson syndrome caused by drugs (Fig. 4.17) or have cutaneous features, and prescribed or self-

medicated drugs, including creams and cosmetics.

Investigations

Social, family and genetic histories

Foreign travel gives exposure to tropical infections or sunlight that could cause a photosensitive eruption. Does the patient have a fair

skin type, i.e. does he burn easily and tan poorly or not at all? Skin cancers are commoner with a pale s kin. Is there a family history of

malignant melanoma or other skin cancer? A family his tory is found in 10% of patients with malignant melanoma. Psoriasis and atopic

eczema also have strongly inherited traits.

Occupational and environmental histories

■ shape

■ colour

■ border changes

■ spatial interrelationships: are lesions confluent or separate?

Palpate with your finger tips to establish its consistency, putting on gloves if the skin is broken.

If any pigmented lesion (mole) has recently changed, note the distribution of pigment with in it and whether it is inflamed or ulcerated.

Malignant melanoma commonly shows variation in pigmentation and has an irregular or diffuse edge. Re member ‘ABCDE’ –

Asymmetry, Border irregular, Colour irregular and D iameter 4

>6 mm, Enlargement (

Fig. 4.19 and Box 4.8). Examine

the entire skin as abnormal moles are more common in patients with a malignant melanoma.

Chemicals encountered at work or leisure may cause contact dermatiti s. Suspect industrial dermatitis if the eruption improves when the

patient is away from work.

THE PHYSICAL EXAMINATION

General examination

Examining the skin is part of the general examination. When y ou examine the hands or face, note any abnormalities of the skin.

Ensure a warm, well-lit, private place is available. Offer a chaperone; record the chaperone’s nam e or if the patient declines the offer.

For widespread lesions ask the patient to undress to his underclothes. Use a hand lens to examine individual lesi ons. A dermoscope,

using a ×10 magnification illuminated lens system, is helpful for pigmented lesions (Fig. 4.18).

The skin, hair and nails

Look at:

■ nails on hands and feet

■ different areas of the scalp (ask the patient to point to the

problem to localise, then part the patient’s hair to see) ■ mucous me mbranes.

Examine local lymph nodes in any patient with a potential squamous cell cancer, malignant melanoma or cutaneous T-cell lymphoma

(Fig. 3.21).

Take a skin scraping for microscopy and culture if you suspect fungal infection.

PUTTING IT ALL TOGETHER

In order to diagnose skin disease familiarise yourself with the patterns of skin conditions and then mentally test multiple hypotheses for

the best fit against the facts of the history and examination. Not all historic or physical findings match the classic descriptions.

Investigations, such as a skin biopsy, are sometimes required to establish a diagn osis.

Examination sequence

Stand back and look at the skin in its entirety: is it abnormal? Note the distributio n of lesions.

Pick a typical individual lesion and check:

■ size (with a tape measure if need be)

INVESTIGATIONS

See Box 4.9.

Fig. 4.18   A dermoscope. This is helpful when looking at suspicious  pigmented lesio ns. 
Fig. 4.19   Malignant melanoma. A darkly pigmented nodule, with  irregular margins  and variability of pigmentation. 
75
4
Fig. 4.20  Patch testing. Known allergens are applied to the patient’s back and rea d at 2 and 4 days. 
4.8 An enlarging mole
In a patient with an enlarging mole, use the ABCDE checklist. Any single positiv e finding justifies a biopsy or referral for specialist
advice.
Whited JD, Grichnik JM. Does this patient have a mole or a melanoma?  JAMA  1998;279:696-701.
4.9 Investigations in skin disease Investigation Wood’s light
Blood tests, including 
haematology and biochemistry
Serology
Microscopy and fungal culture
Surgical biopsy
Doppler studies
Photography
Patch tests
Prick tests
Indication/comment Vitiligo, fungal infection Hand-held ultraviolet lamp shows  vitiligo not apparent in ordinary light, or fluorescence
in fungal infection
Systemic disease
Anaemia, kidney, liver and thyroid function may confirm systemic disease. Monitor blo od parameters in patients on systemic drugs
Autoimmune disease and eczema
SLE and rheumatic disease. Serum IgE or allergen-specific IgE in some patients with ato pic eczema
Rashes
Use a disposable scalpel to scrape the active margin of the rash, dislodging scales on to  a piece of black paper
Rashes or nodules
Histology or direct immunofluorescence (vasculitis)
Leg ulcers
An index of the dorsalis pedis blood pressure over brachial blood pressure of <0.8 he lps suggests arterial disease
Pigmented lesions
Compare the development of the lesion over time
Delayed-type contact allergy, e.g. to fragrances
Prepared allergens on small aluminium discs are applied to the upper back and the skin  reviewed 2 and 4 days later (Fig. 4.20)
Immediate allergy, e.g. to latex
Prepared allergen solutions are pricked into the dermis and reviewed 15 minutes later. H istamine and saline solutions are used as
positive and negative controls
SECTION 2 SYSTEM EXAMINATION John Bevan
The endocrine system5
ENDOCRINE EXAMINATION 78
Anatomy 79
Symptoms and definitions 79
The history 80
The thyroid 80
The parathyroids 84
The pancreas 85
The pituitary 87
The adrenals 90
The gonads 92
Other endocrine disorders 94
Putting it all together 94
Investigations 95
ENDOCRINE EXAMINATION
Eyes 4
• Exophthalmos
• Ophthalmoplegia

• Visual field defect

5 Face

• Features of

Cushing’s syndrome Addison’s disease Acromegaly

6 Neck

• Goitre – smooth/nodular

7 Breasts

• Gynaecomastia

• Galactorrhoea

Pulse and blood pressure 3

• Tachycardia/AF – hyperthyroidism

• Hypertension – Cushing’s and

Conn’s syndromes

• Postural hypotension – Addison’s

disease

8 Bones

• Osteoporosis in hyperthyroidism, Cushing’s syndrome and

hypogonadism (loss of height, thoracic kyphosis)

Hands 2

• Skin crease pigmentation –

Addison’s disease

• Large, sweaty, fleshy – acromegaly

• Tremor – hyperthyroidism

• Carpal tunnel syndrome

• Palmar erythema

General observation 1

• Demeanour, mental state,

e.g. agitated – hyperthyroidism

slow – hypothyroidism

• Appearance, e.g. central obesity

in Cushing’s syndrome

• Pallor

• Hair distribution,

e.g. absent axillary,

pubic – hypopituitarism

• Vitiligo

• Hirsutism

9 Genitalia

• Virilisation

• Pubertal development

• Testicular volume

10 Legs

• Proximal myopathy

• Pretibial myxoedema

• Necrobiosis lipoidica

11 Height, weight, BMI

12 Urinalysis

Psychological/psychiatric assessment

Symptoms and definitions

ANATOMY

The main endocrine glands are the pituitary, thyroid, parathyroids, pancreas, adrenals and gonads: testes and ovaries (Fig. 5.1). These

glands synthesise hormones which are released into the circulation and act at d istant sites. Disease may result from excessive or

inadequate production of hormones, or target organ hypersensitivity or resistance to the hor mone. Although some endocrine glands, e.g.

parathyroid glands and pancreas, respond directly to metabolic signals, most are controlled by hormones released from the pituitary

gland. A wide variety of molecules act as hormones:

• peptides, e.g. insulin

• glycoproteins, e.g. thyroid-stimulating hormone

• amines, e.g. adrenaline (epinephrine)

• steroid hormones, e.g. cortisol, aldosterone,

oestradiol, testosterone

• thyroid hormones, e.g. levothyroxine (T

) and

tri-iodothyronine (T

Nevertheless, diagnosis often depends upon careful observation of a patient with non-specific symp toms prompting the recognition of

specific features. Apart from diabetes mellitus, thyroid disease and some reproductive conditions, endocrine disorders are uncommon.

Most patients with tiredness, excessive sweating or sexual dysfunction, for example, do not have an underlying endocrine cause (Box

5.2).

Weight loss

Short stature

SYMPTOMS AND DEFINITIONS

Symptoms of endocrine disturbance are frequently nonspecific and affect many body systems (Box 5.1). Endocrine conditions may be

detected by chance, e.g. glycosuria on screening, or if the clinician sees a patient after a significant time interval and notice s diagnostic

facial features, e.g. in acromegaly or hypothyroidism.

Hypothalamus/pituitary Hirsutism

Thyroid

Parathyroids ‘Funny turns’

Adrenals Sweating Pancreas Flushing Ovaries

Testes

Fig. 5.1 The principal endocrine glands.

5.1 Common clinical features

in endocrine disease

Symptom, sign or problem Differential diagnoses

Weight gain

Hypothyroidism, polycystic ovary syndrome (PCOS), Cushing’s

syndrome

Hyperthyroidism, diabetes

mellitus, adrenal insufficiency

Constitutional, non-endocrine systemic disease (e.g. coeliac disease), growth horm one

deficiency

Delayed puberty Constitutional, non-endocrine systemic disease,

hypothyroidism, hypopituitarism, primary gonadal failure

Menstrual disturbance PCOS, hyperprolactinaemia,

thyroid dysfunction

Diffuse neck swelling Simple goitre, Graves’ disease, Hashimoto’s thyroiditis

Excessive thirst Diabetes mellitus or insipidus, hyperparathyroidism, Conn’s

syndrome

Idiopathic, PCOS, Cushing’s

syndrome, congenital adrenal hyperplasia

Hypoglycaemia,

phaeochromocytoma,

neuroendocrine tumour

Hyperthyroidism, hypogonadism, acromegaly, phaeochromocytoma Hypogonadism (especially

menopause), carcinoid syndrome

Resistant hypertension Conn’s syndrome, Cushing’s

syndrome, phaeochromocytoma, acromegaly, renal artery stenosis

Erectile dysfunction Primary or secondary

hypogonadism, diabetes mellitus, non-endocrine systemic disease, medication-induced (e.g.

beta-blockers, opiates)

Muscle weakness Cushing’s syndrome,

hyperthyroidism,

hyperparathyroidism,

osteomalacia

Bone fragility and

fractures

Altered facial appearance

Hypogonadism, hyperthyroidism, Cushing’s syndrome

Hypothyroidism, Cushing’s

syndrome, acromegaly, PCOS

5.2 Prevalence and incidence of endocrine conditions Condition

Common

Type 2 diabetes mellitus

Primary hypothyroidism

Polycystic ovary syndrome

Moderately common Hyperthyroidism

Type 1 diabetes mellitus

Male hypogonadism

Uncommon

Hypopituitarism Addison’s disease

Differentiated thyroid cancer

Rare

Carcinoid tumour

Pituitary-dependent Cushing’s disease Acromegaly

Incidence/prevalence

4–8% prevalence (increasing with obesity)

2% prevalence (5% including subclinical disease); mostly women

6–8% prevalence, depending on definition

• change in sexual function:

• erectile dysfunction or loss of libido in hypogonadism

• gynaecomastia (breast tissue enlargement in men)

• galactorrhoea (breast milk production in men, or in women outwith pregnancy or bre astfeeding) in pituitary adenomas producing

hyperprolactinaemia

• primary or secondary amenorrhoea (p. 221) in pituitary or hypothalamic disease

• tiredness: can be a non-specific feature of diabetes

mellitus, hypothyroidism or Addison’s disease.

1% prevalence (80% Graves’ disease, 80% in women)

0.5% prevalence (increasing in children)

1–2% prevalence, depending on definition

Prevalence: 50–100 per million

Prevalence: 50 per million (western countries, mostly autoimmune)

Incidence: 5 new cases per 100 000 per year

Incidence: 20 new cases per million per year

Incidence: 5 new cases per million per year

Incidence: 4 new cases per million per year

THE HISTORY

General points

Past history

Tuberculosis and HIV infection are associated with adrenal insufficiency.

Drug history

Excessive corticosteroid exposure causes cushingoid features and dopamine antagonist drugs such as haloperidol and domperidone cause

hyperprolactinaemia.

Family history
Thyroid disease and diabetes mellitus may run in families. Multiple endocrine neoplasia syndromes are r are autosomal dominant
conditions characterised by hyperplasia, adenoma formation and malignant  change in multiple endocrine glands.
Common presenting symptoms are:
• appetite and/or weight change – in hyper/ hypothyroidism, diabetes mellitus, Cushing’ s syndrome
• polydipsia (excessive thirst) and/or polyuria (passing >3 litres urine/day) – in diabetes me llitus, diabetes insipidus or
hyperparathyroidism
• change in facial/body hair growth and distribution – in hypogonadism, hypopituitarism, ad renal insufficiency, androgen excess.
Hirsutism is the excessive growth of thick terminal hair in an androgen-dependent  distribution (upper lip, chin, chest, back, lower
abdomen, thighs) in women
• change in skin and mucosal pigmentation and character: coarse dry skin in hypoth yroidism; excessive pigmentation and/or vitiligo
(areas of depigmented skin) in Addison’s disease (Fig. 5.17D); soft-tissue overgrowth and skin tag s in acromegaly; acanthosis nigricans
(velvety thickening and pigmentation of the major flexures, especially the axillae and gro ins: Fig. 5.11A) in obesity, and type 2 diabetes
• increased sweating in acromegaly and
phaeochromocytoma
• temperature intolerance – in hyperthyroidism (heat) 
80
 and hypothyroidism (cold)
THE THYROID
Anatomy
The thyroid is butterfly-shaped with two symmetrical lobes joined by a central isthmus th at normally covers the second and third tracheal
rings (Fig. 5.2A). The gland may extend into the superior mediastinum, or may occas ionally be entirely retrosternal. Rarely, it is located
higher in the neck along the line of the thyroglossal duct. If situated  at the back of the tongue (lingual goitre),  it may be visible through
the open mouth.
Symptoms and definitions
Goitre is enlargement of the thyroid gland. It is not necessarily associated with thyroid dysfunc tion and most patients with a goitre are
euthyroid (Fig. 5.5).
Hyperthyroidism (thyrotoxicosis) is a clinical state caused by increased levels of circulating levels of the thyroid hormone s, T
3
 and T
4
.
Graves’ disease is the commonest cause of hyperthyroidism. It is an autoimmune  disease with a familial component, which is 5–10 times
more common in women and usually presents between
Hyoid bone
Sternocleidomastoid muscle Thyroid cartilage
Cricoid cartilage Lobe of thyroid gland Parathyroid Isthmus of thyroid gland
Trachea Manubrium of the sternum
5
A B Fig. 5.2  The thyroid gland. (A) Anatomy of the gland and surrounding structures.  (B) Palpating the thyroid gland from 
behind. 
20 and 50 years of age. It has specific extrathyroid features (Fig. 5.3):
• Exophthalmos (proptosis) is increased protrusion
of the eyeball from the orbit. It is caused by an inflammatory infiltration of the orbita l contents (the soft tissues and extraocular muscles,
not the globe). It is usually bilateral. Exophthalmos may lead to diplopia (Fig. 5 .4A&B) and other features of Graves’ ophthalmopathy:
conjunctival oedema, conjunctivitis, corneal ulceration, ophthalmoplegia and optic atrophy (Ch. 1 2).
• Pretibial myxoedema is a raised, discoloured (usually pink or brown) indurated appearance  over the lower legs (Fig. 5.4D). Note that,
despite the name, it is associated with Graves’ disease, not hypothyroidism.
• Thyroid acropachy is a periosteal hypertrophy of the distal phalanges which looks l ike finger clubbing (Fig. 5.4C).
Hypothyroidism ( Fig. 5.3) is caused by reduced levels of thyroid hormones and is usually due to  autoimmune Hashimoto’s thyroiditis.
Women are affected approximately six times more commonly than  men. Many clinical features of hypothyroidism are produced by
myxoedema (non-pitting oedema caused by tissue infiltration by mucopolysaccharides, cho ndroitin and hyaluronic acid) (Box 5.3 and
Figs 5.3 and 5.7).
History
Presenting complaint
Ask about:
• recent weight loss/gain, appetite change, diarrhoea or constipation
• irritability, difficulty sleeping, hyperactivity or excessive fatigue
• heat or cold intolerance
• tremor, palpitation or excessive sweating

• skin or hair changes (excessive dryness or sweating, coarse dry hair or alo pecia)

• eye symptoms: diplopia, pain, irritation or ‘grittiness’.

Hyperthyroidism Hypothyroidism

Exophthalmos, ophthalmoplegia (in Graves’ disease) Periorbital oedema

Goitre (with bruit in Graves’ disease) Husky voice

Tachycardia, angina, atrial fibrillation Goitre

Systolic hypertension Bradycardia Oligomenorrhoea Diarrhoea Carpal tunnel syndrom e

Sweaty, tremulous, warm hands Menorrhagia Proximal myopathy Pretibial myxoedema (in Graves’ disease) Ankle swelling

(in heart failure)

General

• Weight loss despite

increased appetite

• Heat intolerance

• Anxiety, irritability

• Fast, fine tremor

Fig. 5.3 Features of hyper- and hypothyroidism. Constipation

General

• Low metabolic rate, weight gain

• Sensitivity to cold

• Lethargy, mental impairment,

depression

5.3 Hypothyroidism

The diagnosis of hypothyroidism is commonly delayed or missed because symptoms an d signs develop insidiously over years.

Vaidya B, Pearce SHS. Management of hypothyroidism in adults. BMJ 2008;33 7:284–289.

Fig. 5.4 Graves’ hyperthyroidism. (A) Typical facies. (B) Severe inflammatory thyro id eye disease. (C) Thyroid acropachy.

(D) Pretibial myxoedema.

Past drug, family

and social history

Ask about:

• drug therapy (amiodarone and lithium are associated with hypothyroidism), antithyroid drugs

• family history of thyroid or autoimmune disease

• living in areas of iodine deficiency, e.g. the Andes, Himalayas, Central Afric a, can cause goitre and, rarely, hypothyroidism.

■ the eyes for:

■

exophthalmos, diplopia, conjunctival oedema or conjunctivitis, corneal ulceration

■

lid retraction: this is present if the sclera is visible above the iris ( Fig. 5.4A)

■

lid lag: ask the patient to follow your index finger as you move it from the upper to the lower part of his visual field

(Fig. 12.13). Delay between the descent of the upper eyelid in relation to that of the eyeball is lid lag .

Examination sequence

General

Look for:

■ signs of weight loss or gain

■ agitation, restlessness or apathy and lethargy

■ the facial appearance and expression.

Examine:

■ hands

■ pulse and blood pressure (BP)

■ arms and legs for: skin abnormalities, muscle power and the

deep tendon reflexes (p. 263)

The thyroid gland

Examination sequence

■ Inspect the neck from the front. Give the patient a glass of water and a sk him to take a sip. Look for a swelling

while he swallows.

■ Ask the patient to sit with the neck muscles relaxed and stand behind him . Place your hands gently on the front of the

neck, with your index fingers just touching (Fig. 5.2B). Ask him to swallow a sip of wate r and feel the gland as it moves

upwards. Some patients find neck palpation uncomfortable, so be alert for any signs of distress.

Fig. 5.5 Goitres. (A and B) Diffuse – Graves’ disease. (C) Uninodular – toxic nod ule. (D) Multinodular.

■ Note the size, shape and consistency of any goitre and feel for any thr ill.

■ Measure any discrete nodules with callipers.

■ Record the maximum neck circumference of a large goitre using a tape measure (objective measurements are useful for

long-term follow-up).

■ Auscultate with your stethoscope for a thyroid bruit. A thyroid bruit may be confused with other sounds: bruits from the

carotid artery or transmitted from the aorta are louder along the line of the ar tery. Transient gentle pressure over the root

of the neck will interrupt a venous hum from the internal jugular vein.

Normal findings

The normal thyroid gland is palpable in ~50% of women and 25% of men. P rominent skin folds may give a false impression of goitre.

The thyroid (or a thyroglossal cyst) moves upwards on swallowing since it is enveloped in the pre-tracheal fascia, which is attached to

the cricoid cartilage.

Abnormal findings

Shape, surface and consistency Simple goitres are relatively symmetrical in their earlier stages but often become nodular with time.

In Graves’ disease the surface of the thyroid gland is usually smooth and diffuse; i t is irregular in uninodular or multinodular goitre (Fig.

5.5). Nodules in the substance of the gland may be large or small, and single or multiple, and are usually benign. A very hard consistency

suggests malignancy. Large,

Fig. 5.6 Thyroid cancer. Papillary thyroid cancer with regional cervical lymphadeno pathy.

firm lymph nodes near a goitre suggest thyroid cancer (Fig. 5.6). Diffuse tenderness is typ ical of viral thyroiditis. Localised tenderness

may follow bleeding into a thyroid cyst.

Mobility Most goitres move upwards on swallowing. Very larg e goitres may be immobile, and invasive thyroid cancer may fix the

gland to surrounding structures.

Thyroid bruit This may occur in hyperthyroidism and indicates abnormally high blood f low. There can be an associated palpable

thrill.

Fig. 5.7 Hypothyroidism. (A) Before treatment. (B) After levothyroxine replaceme nt.

THE PARATHYROIDS

Anatomy

There are usually four parathyroid glands which lie posterior to the thyroid (Fig. 5.2A). Each is about the size of a pea and produces

parathyroid hormone, a peptide which increases the level of calcium in the blood.

Symptoms and definitions

Parathyroid disease is commonly asymptomatic. In hyperparathyroidism, the commo nest symptoms relate to hypercalcaemia: polyuria,

polydipsia, renal stones, peptic ulceration, tender areas of bone fracture defor mity (‘Brown tumours’: Fig. 5.8A), and confusion or

psychiatric symptoms.

In hypoparathyroidism, hypocalcaemia may cause hyperreflexia or tetany (invo luntary muscle contraction), most commonly in the hands

or feet. Paraesthesiae of the hands and feet or around the mouth may occur. Hypoparathyroidism is mo st often caused by inadvertent

damage to the glands during thyroid surgery.

Patients with the autosomal dominant condition pseudohypoparathyroidism have end-organ r esistance to parathyroid hormone and

typically have short stature, round face and shortening of some metacarpal bones .

History

Ask about:

• recent thyroid or neck surgery or irradiation

• polyuria, polydipsia or renal stones

• fractures

• abdominal pain or constipation

• muscle cramps

• confusion or psychiatric symptoms.

Examination sequence

■ Look at the neck for scars of previous surgery.

■ Assess mental state (p. 21).

■ Take the BP and assess the state of hydration (p. 58). ■ Look at the hands . Ask the patient to make a fist and assess

the length of the metacarpals.

■ Test for muscle weakness (p. 261) and hyperreflexia

(p. 263).

■ Test for latent tetany: place a BP cuff on the upper arm and

inflate above systolic pressure for 3 minutes. In the hand,

carpal muscle contraction produces a typical picture with the

thumb adducted, the proximal interphalangeal and distal

interphalangeal joints extended and the metacarpophalangeal

joints flexed (‘main d’accoucheur’ (hand of the obstetrician) or

Trousseau’s sign: Fig 5.9).

■ Look for evidence of recent fractures and bone tenderness. ■ Use a slit l amp to look for corneal calcification.

■ Perform urinalysis.

Abnormal findings

Parathyroid tumours are very rarely palpable.

Findings in hyperparathyroidism may include altered mental state, dehydration , proximal muscle weakness, fractures and bony

tenderness. In long-standing hypercalcaemia, corneal calcification (band keratopathy) may be present (Fig. 5.8B). Renal stones may

produce haematuria on stix testing.

In moderate/severe hypocalcaemia, hyperreflexia and a positive Trousseau’s sign may be pr esent. In pseudohypoparathyroidism the

metacarpals of the ring and little fingers are shortened (Fig. 5.8C and D).

The pancreas

Fig. 5.8 Parathyroid disease. (A) ‘Brown tumour’ of the phalanx (middle finger) in hyperparathyroidism. (B) Corneal

calcification in hyperparathyroidism. (C) Pseudohypoparathyroidism: short metaca rpals. (D) These are best seen when the

patient makes a fist.

Fig. 5.9 Trousseau’s sign.

THE PANCREAS

Anatomy

The pancreas lies behind the stomach on the posterior abdom inal wall. Its endocrine functions include the production of insulin,

glucagon, gastrin, somatostatin and vasoactive intestinal peptide. Its exo crine function is to produce alkaline secretions containing

digestive enzymes.

Symptoms and definitions

Diabetes mellitus

This is characterised by hyperglycaemia due to absolute or relative insulin deficiency. Insulin-d ependent patients are particularly

susceptible to acute metabolic decompensation due to hypoglycaemia or ketoacidosis, both of which require prompt clinical and

biochemical recognition and treatment.

There are two main subtypes:

• Type 1: severe insulin deficiency due to

autoimmune destruction of the pancreatic islets.

• Type 2: commonly affects people who are obese and insulin-resistant, although impaire d β-cell function is also important.

Diabetes mellitus may present with a classical triad of

symptoms:

• Polyuria (and nocturia): due to osmotic diuresis caused by glycosuria.

• Thirst: due to the resulting loss of fluid and electrolytes.

• Weight loss: due to fluid depletion and breakdown of fat and muscle secondary to insulin def iciency.

Other common symptoms are tiredness, mood changes

and blurred vision (due to glucose-induced changes

in lens refraction). Bacterial and fungal skin infections are common because of the combination of hyperglycaemia, impaired immune

resistance and tissue ischaemia. Itching of the genitalia (pruritus vulvae in women, balanitis in men) is du e to Candida yeast infection

(thrush).

Fig. 5.10 Diabetic retinopathy. Note presence of yellow exudate due to leakage of plasma from abnormal retinal capillaries

and multiple dot and blot haemorrhages indicating widespread capillary occlusion – a precursor of new vessel formation.

Examination sequence

■ Look for evidence of weight loss and dehydration (p. 58). ■ Smell the patient’s breath for the sweet smell of ketones

(diabetic ketoacidosis).

■ Examine the skin: look for signs of infection and rashes. Look

for xanthelasma and xanthomata (Fig. 6.8A and B). Examine

insulin injection sites for evidence of lipohypertrophy (which

may cause unpredictable insulin release), lipoatrophy (rare) or

signs of infection (very rare).

■ Measure pulse and BP and examine the cardiovascular and

peripheral vascular systems.

■ Examine the respiratory and gastrointestinal systems. ■ Examine the central nervous system.

■ Test visual acuity and examine the eyes and optic fundi

(p. 287) (Fig. 5.10).

■ Perform urinalysis.

Abnormal findings

Dehydration and Kussmaul respiration (hyperventilation with a deep, sighing respiratory pattern) are co mmon in ketoacidosis.

Bacterial skin infections, e.g. cellulitis, boils, abscesses and fungal infections, may be seen. Acanthosis nigricans (Fig. 5.11A) occurs in

hyperinsulinism and is seen frequently in patients with insulin-resistant type 2 diabetes.

MACROVASCULAR MICROVASCULAR

TIA, stroke

Myocardial ischaemia/ infarction Retinopathy

Impaired vision

Cataract

Nephropathy

• protein loss

• renal failure

Claudication Gangrene Amputation

INFECTION RISK C

NEUROPATHY

Autonomic

Postural hypotension

Gastroparesis

Diarrhoea

Atonic bladder

Erectile dysfunction

Somatic

Peripheral neuropathy

(sensory loss,

motor weakness)

‘Diabetic’ foot

86
 Fig. 5.11  Diabetes and the skin. (A) Acanthosis nigricans. (B) Necrobiosis lipoidica.  (C) Eruptive xanthomata.  5.4 Diabetic
complications
Up to 40% of patients with diabetes have peripheral neuropathy and 40% have peripher al vascular disease. 5% develop foot ulceration
each year and up to 66% are associated with infection or osteomyelitis.
Cheer K, Shearman C, Jude EB. Managing complications of the diabetic  foot.  BMJ 2009;339:1304–1307.
Necrobiosis lipoidica (a yellow indurated or ulcerated area surrounded by a red margin: Fig. 5.11B ), due to collagen degeneration, may
occur on the shins of some type 1 diabetic patients and often causes chronic ulceration.  Xanthelasmata and xanthomata indicate
significant hyperlipidaemia (Fig. 5.11C and Fig. 6.8).
Microvascular, neuropathic and macrovascular complications of hyperglycaemia (Fig. 5.11) can occur in patients with any type of
diabetes mellitus, and may be present at diagnosis in patients with slow-onset typ e 2 disease. Careful examination of the eyes,
cardiovascular, neurological and renal systems, and feet is essential.
Glycosuria suggests hyperglycaemia and, if accompanied by ketonuria (and Kussmaul respiratio n: Ch. 7) indicates ketoacidosis.
Proteinuria occurs in diabetic nephropathy. Detection of nitrite ± haematuria sugges ts (often occult) urinary infection (Box 5.4).
The diabetic foot
Examination sequence
Diabetic patients have a 15% lifetime risk of foot ulcers, which are  highly susc eptible to infection. Early recognition of 
the ‘at-risk’  diabetic foot is essential. There are two main presentations: ■   Neuropathic: where neuropathy predominates but 
the major 
arterial supply is intact.
■  Neuro-ischaemic: where reduced arterial supply 
produces ischaemia and exacerbates neuropathy  
(Fig. 5.13).
Infection complicates both presentations.
■  Inspection:
■
  Look for hair loss and nail dystrophy.
■
  Examine the skin (including the interdigital clefts) for  excessive callus, infection s and ulcers.
■
  Ask the patient to stand and assess the foot arch.
■
  Look for deformation of the joints of the feet.
■  Palpation:
■
  Feel the temperature of the feet.
■
  Examine the dorsalis pedis and posterior tibial pulses. If  absent, arrange Dopp ler studies to evaluate ankle : brachial 
pressure index (Ch. 6).
■  Test for peripheral neuropathy: use a nylon monofilament 
which buckles at a force of 10 g to apply a standard, 
reproducible stimulus. The technique and best sites to test  
are shown in Figure 5.12. Avoid areas of untreated callus.
A B
Fig. 5.12  Monofilament sensory testing of the diabetic foot.  5
(A) Technique. (B) Sites at highest risk (toes and metatarsal heads). 
excessive in neuropathy or collapsed (rocker-bottom sole). Both conditions cause abnormal pressures  and increase risk of plantar
ulceration.
Warm feet occur in neuropathy and cold feet in ischaemia.
Sensory neuropathy is present if the patient cann ot feel the monofilament in any of the sites. This means loss of protective pain  sensation
and is a good predictor of future ulceration.
Charcot’s arthropathy is disorganised foot architecture, acute inflammatio n, fracture and bone thinning, usually in a patient with
neuropathy but relatively good vascular supply to the lower limb. It presents acute ly as a hot, red, swollen foot often impossible to
distinguish clinically from infection.
Risk assessment
• Low – no risk factors (no sensation loss, peripheral vascular disease or other risk fa ctors).
• Moderate – one risk factor present.
• High – previous ulceration or amputation, or more than one risk factor present.
• Active – ulceration, spreading infection, critical ischaemia, unexplained red, hot, swollen foot.
THE PITUITARY
Anatomy
The pituitary gland is enclosed in the sella turcica in the base of the skull beneath the h ypothalamus. It is bridged over by a fold of dura

mater (diaphragma sellae) with sphenoidal air spaces below and the optic chiasm above. The p ituitary has two lobes:

• Anterior: which secretes several hormones

(adrenocorticotrophic hormone (ACTH), prolactin, growth hormone (GH), thyroid-stimulating hormone and gonadotrophins (luteinising

hormone (LH) and follicle-stimulating hormone (FSH)).

• Posterior: an extension of the hypothalamus, which secretes vasopressin (antidiure tic hormone) and oxytocin.

Abnormal findings

Hair loss and nail dystrophy occur with ischaemia, causing nutritional changes. There may be skin fissures or tinea infection (‘athlete’s

foot’). The foot arch may be

Acromegaly

Some pituitary tumours secrete excess GH. Before puberty, when long bone epiphyses close, this pro duces gigantism; after puberty, it

causes acromegaly. GH

Fig. 5.13 Diabetic foot complications. (A) Infected foot ulcer with cellulitis and ascen ding lymphangitis. (B) Ischaemic foot –

digital gangrene. (C) Charcot arthropathy with plantar ulcer. (D) Neuropathic u lcer (pressure ulcer below metatarsal head.

stimulates excessive insulin-like growth factor-1 production by the liver which is responsib le for the clinical manifestations.

History

Ask about the most common symptoms – headache and excessive sweating.

Has the patient (or more often a relative or friend) noticed changes in his facial features? Photographs taken years earlier can be helpful

to identify changes and the onset of the condition.

Has the patient noticed an increase in shoe, ring or

glove size (Box 5.5)?

5.5 Acromegaly

Clinical presentations, such as carpal tunnel syndrome, sleep apnoea, with asso ciated coarse facial features and symptoms, such as

headache, sweating, an increase in ring or shoe size, should raise the possibility of acromegaly.

Reddy R, Hope S, Wass J. Acromegaly: easily missed? BMJ 2010;341:400–401 .

Fig. 5.14 Acromegaly. (A) Typical facies. (B) Separation of lower teeth. (C) Lar ge fleshy hands. (D) Widening of the feet.

Examination sequence

■ Look at the face for coarsening of features, thick greasy skin, enlargem ent of the nose, prognathism (protrusion of the

mandible) and separation of the lower teeth (Fig. 5.14A, B).

■ Examine the hands and feet. Look for soft-tissue enlargement and comp lications arising from this, e.g. tight-fitting rings

or shoes, carpal tunnel syndrome (Fig. 5.14C, D).

■ Assess the visual fields: expansion of the tumour can cause pressure on the optic chiasm, resulting in visual field

defects, especially bitemporal hemianopia (Fig. 12.3).

■ Check the BP and perform urinalysis. Hypertension and diabetes mellitus are common associations.

Hypopituitarism

Anterior hypopituitarism is due to compression of the pituitary by a macroadenoma, infarction after childbirth (Sheehan’s syndrome),

severe head trauma or cranial radiotherapy.

Apart from headache due to stretching of the diaphragma sellae and visual abnormalities, clinical presentation depends upon the

deficiency of the specific anterior pituitary hormones involved. Indi vidual or multiple hormones may be involved, so questioning in

relation to the thyroid, adrenocortical and sexual function is needed.

Examination sequence

Look for:

■ extreme skin pallor (a combination of mild anaemia

and melanocyte-stimulating hormone deficiency)

■ absent axillary hair

■ reduced/absent secondary sexual hair (caused by

gonadotrophin deficiency) (Fig. 5.15)

■ testicular atrophy.

■ Examine the eyes for: visual field defects (most often

bitemporal hemianopia); optic atrophy or cranial nerve defects (III, IV and VI ) caused by a tumour compressing the optic

chiasm, optic nerve or cavernous sinus.

Fig. 5.15 Hypopituitarism. (A) Hypopituitarism due to a pituitary adenoma (note the fine pale skin). (B) Absent axillary

hair.

THE ADRENALS

Anatomy

The adrenals are small pyramidal organs lying immediately above the kidneys on their p osteromedial surface. The adrenal medulla is

part of the sympathetic nervous system and secretes catecholamines. The adren al cortex secretes cortisol, mineralocorticoids and

androgens.

Symptoms and definitions

Cushing’s syndrome

Cushing’s syndrome is caused by excess exogenous or endogenous corticosteroid e xposure. Most cases are iatrogenic due to side-effects

of corticosteroid therapy. ‘Endogenous’ Cushing’s usually results from an ACTH-se creting pituitary microadenoma. Other causes

include a primary adrenal tumour or ‘ectopic’ ACTH secretion.

The catabolic effects of steroids cause widespread tissue breakdown (particularly in skin, muscle and bone) with central accumulation of

body fat. Proximal myopathy, fragility fractures, spontaneous pu rpura, skin thinning and susceptibility to infection are common (Fig.

5.16). Patients may be hypertensive.

Examination sequence

■ Look at the face and general appearance for central obesity

and a round face (Fig. 5.16).

5.6 Cushing’s syndrome

Easy bruising, facial plethora, proximal myopathy and broad purple striae best discriminate Cushing’s syndrome but these findings do

not have high sensitivity. Furthermore, many features of Cushing’s syndrome are common i n the general population and are less

discriminatory, e.g. obesity, dorsocervical fat pad, oedema, acne and hirsutism .

Nieman LK, Biller BMK, Findling JW et al. The diagnosis of Cushing’s syndro me: an Endocrine Society clinical practice

guideline. J Clin Endocrinol Metab 2008;93:1526–1540.

■ Examine the skin for thinning, hyperpigmentation, acne, hirsutism, bruising , striae (especially abdominal) and signs of

infection or poor wound healing.

■ Check the BP.

■ Examine the legs for evidence of proximal muscle weakness and oedema .

■ Examine the eyes for cataracts, and hypertensive changes ( Fig. 6.16).

■ Perform urinalysis (Box 5.6).

Addison’s disease

Addison’s disease is due to inadequate secretion of cortisol, usually secondary to autoimmune destructi on of the adrenal cortex.

Symptoms are usually non-specific, but weakness, muscle cramps, nausea, vomiting, diarrhoea or c onstipation may occur.

The adrenals

Fig. 5.16 Cushing’s syndrome. (A) Cushingoid facies. (B) After curative pituitary s urgery. (C) Typical features: facial

rounding, central obesity, proximal muscle wasting and skin striae. (D) Skin thin ning: purpura caused by wristwatch

pressure.

Examination sequence

■ Look for signs of weight loss.

■ Examine the entire skin surface for abnormal or excessive pigmentation: t his is most prominent in sun-exposed areas or

epithelia subject to trauma or pressure – skin creases, buccal mucosa and recen t scars (Fig. 5.17A–C). Excess pigmentation

is produced by melanocyte-stimulating hormone in primary adrenal insufficiency . It is most striking in white Europeans.

Vitiligo (depigmentation of areas of skin) occurs in 10–20% of Addison’s dis ease cases (Fig. 5.17D).

■ Check the BP and test for postural hypotension (p. 1 14). Hypotension and postural hypotension result from reduced

mineralocorticoid effects.

Fig. 5.17 Addison’s disease. (A) Facial pigmentation. (B) Buccal pigmentation. (C) Skin crease pigmentation. (D) Vitiligo –

particularly striking due to addisonian pigmentation of the ‘normal’ skin.

THE GONADS

These glands secrete sex hormones (oestrogen and testosterone) in response to gonadotrophin (FSH a nd LH) release by the pituitary.

They also contain the germ cells.

Symptoms and definitions

Klinefelter’s syndrome (47XYY) is the most common 92 cause of primary hypogonadism in men (1 : 600 live male

births). Diagnosis may be delayed until later life, by which time features of prolonged tes tosterone deficiency can be seen. Look for soft,

finely wrinkled, hairless facial skin and gynaecomastia and examine the genitalia (pubic hair is often reduced/absent and the testes <3 ml

in volume; Fig. 5.18).

Hirsutism is common in women with polycystic ovary syndrome (Fig. 5.19). Virilisation is tem poral recession of the scalp hair,

deepening of the voice, breast atrophy, increased muscle bulk and clitoromegaly (Fig. 5.20). If present in women with a short history of

severe hirsutism, it suggests a possible testosterone-secreting tumour.

The gonads

Fig. 5.18 Klinefelter’s syndrome. (A) Hypogonadal facial skin. (B) Gynaecomastia, reduced pubic hair and small testes.

Fig. 5.19 Polycystic ovary syndrome. (A) Facial hirsutism. (B) Ultrasound showing polycystic ovary (arrow).

Fig. 5.20 Testosterone-secreting ovarian tumour. Clitoromegaly.

Fig. 5.21 Carcinoid syndrome. (A) Acute carcinoid flush. (B) Chronic telangiectasia .

OTHER ENDOCRINE DISORDERS

Carcinoid syndrome

Liver metastases from mid-gut carcinoid tumour release vasoactive chemicals into t he systemic circulation which cause flushing,

diarrhoea and bronchospasm. Bending, exercise or even palpation of the enlarged liver may induce typical skin flushing. Permanent

facial telangiectasia occurs after many years of carcinoid flushing (Fig. 5.21).

PUTTING IT ALL TOGETHER

Because of their wide diversity of clinical features, keep alert to the possibility of endocrine disea se in nonspecific presentations. Perhaps

more than in any other

area of medicine, pattern recognition is important.

A structured approach to the general endocrine examination

Examination sequence

Carefully observe the patient’s overall appearance, manner and  habitus for diag nostic clues:
■  Is he restless and agitated (hyperthyroidism) or slow and 
lethargic (hypothyroidism)?
■  Measure the height and weight and calculate the body 
mass index (p. 55). Use a stadiometer in children and 
adolescents (Fig. 15.20). If the patient is obese, is the 
adiposity centrally distributed, e.g. Cushing’s syndrome or GH 
deficiency.
■  Look for a thoracic kyphosis, which may be a sign of 
osteoporotic vertebral collapse.
■  Inspect the face and eyes for a ‘spot’ endocrine diagnosis 
(Figs 5.4A, 5.7A, 5.14A, 5.16A, 5.17A, 5.18A ).
■  Look at the mouth for overgrowth of the chin and tongue 
(acromegaly) and for buccal pigmentation (Addison’s disease). ■  Exam ine the hands: the initial handshake may suggest a 
diagnosis, e.g. tremor and palmar sweating in hyperthyroidism. 
Look for soft-tissue overgrowth (acromegaly) or dysmorphism 
(abnormal metacarpal length in pseudohypoparathyroidism); 
skin crease pigmentation (Addison’s disease); wasting of the 
thenar muscles due to carpal tunnel syndrome (hypothyroidism, 
acromegaly) (Fig. 14.29B).
■  Examine the entire skin surface: look for abnormal pallor 
(hypopituitarism), vitiligo, skin or scar pigmentation (Addison’s 
disease), plethora (Cushing’s or carcinoid syndrome). Patients 
with Cushing’s syndrome often have thin, fragile skin with 
bruising after trivial trauma (Fig. 5.16D). Inspect the axillae  
and groins for acanthosis nigricans (obesity, diabetes mellitus) 
(Fig. 5.11A).
■  Is the body hair normal in quality and amount? Look for 
hirsutism in females (polycystic ovary syndrome: Fig. 5.19)  
and for loss of hair in the axillae and groins (hypopituitarism) 
(Fig. 5.15B).
■  Assess the pulse rate, rhythm and volume. Tachycardia and 
atrial fibrillation may suggest thyrotoxicosis.
■  Record the BP. Hypertension is a feature of several endocrine 
conditions, e.g. Cushing’s syndrome, phaeochromocytoma, 
Conn’s syndrome (primary hyperaldosteronism) (Box 5.1). 
Postural hypotension (p. 114) occurs in adrenal insufficiency. ■  Examine the eyes: look for fe atures of thyroid disease. 
Assess 
visual acuity and perform fundoscopy in patients with diabetes 
mellitus. Assess visual acuities and fields (p. 288) in patients 
with suspected pituitary tumours (to detect bitemporal 
hemianopia due to compression of the optic chiasm). Look for 
optic atrophy in patients with longstanding optic pathway 
compression (Fig. 12.31A).
■  Examine the neck for goitre. If present, record its size, surface 
and consistency.
■  Look for gynaecomastia (common in Klinefelter’s syndrome: 
Fig. 5.18) and galactorrhoea: Gently massage the breast  
tissue towards the nipple to see if milk is expressed.  
Explain beforehand why you are performing this examination 
and watch the patient carefully since this may be 
uncomfortable.
Investigations
■   Examine the abdomen: look for purple striae (Cushing’s  syndrome). Car cinoid syndrome is associated with a palpable, 
nodular liver, which is sometimes massively enlarged. Adrenal  tumours may occ asionally be palpable, but be cautious if you 
suspect phaeochromocytoma, as palpation may precipitate a  hypertensive paroxysm .
■   Inspect the legs for pretibial myxoedema (Graves’ disease:   Fig. 5.4D), proximal muscle wasting or weakness (Cushing’s 
syndrome and hyperthyroidism) and delayed tendon reflexes  (hypothyroidism).
■   Examine the feet for signs of diabetic neuropathy, ischaemia  and ulcers.
■  Examine the external genitalia (p. 225). Inspect the amount of  pubic hair and  make a pubertal staging of all adolescents 
using  Tanner gradings (Ch. 10). In men, record testicular size and  consistency  (p. 238). In women, look for virilising 
features. ■  Test the urine for glucose, ketones, protein and nitrite.
■  Formal psychological evaluation (p. 25) may be appropriate in  selected  patients (Cushing’s syndrome, hyperparathyroidism).

INVESTIGATIONS

Measure serum hormone levels to assess over- or underactivity. Suppression tests can determine whether hormonal secretion is

autonomous. Stimulation tests assess hormonal reserve (or lack of it in deficiency states). Modern imaging enables visualisation of small

endocrine tumours, sometimes only millimetres in diameter (Box 5.7 and Fig. 5.22). 5

5.7 Investigations in endocrine disease

Investigation Bedside

Urinalysis

Capillary blood glucose Blood

Calcium

Free thyroxine

Thyroxine-stimulating hormone

Serum cortisol

Gonadotrophins

Imaging

Ultrasound

Magnetic resonance imaging Computed tomography

Radionuclide

Positron emission tomography (PET)

Invasive

Fine-needle aspiration cytology

Inferior petrosal sinus sampling for adrenocorticotrophic hormone (ACTH)

Indication/comment

Glycosuria in diabetes mellitus

Proteinuria in hypertensive renal damage High in diabetes mellitus

High in hyperparathyroidism

High in hyperthyroidism

Low in hypothyroidism

Undetectable in hyperthyroidism

High in primary hypothyroidism

Low in hypoadrenalism, usually with reduced Synacthen response Loss of diurnal rhyt hm in Cushing’s

Reduced dexamethasone suppressibility in Cushing’s

High in primary hypogonadism in both sexes

Thyroid, parathyroid, ovary, testis

Pituitary, pancreas

Pancreas, adrenal

Thyroid (

123

I), parathyroid (

99m

Tc-sesta-MIBI), adrenal (

123

I-mIBG), neuroendocrine tumours (

123

I-octreotide)

Thyroid and neuroendocrine tumours

Thyroid nodule

ACTH-dependent Cushing’s

The endocrine sysTem

B C

Fig. 5.22 Endocrine imaging. (A) Magnetic resonance imaging showing pituitary ma croadenoma (arrow). (B) Positron

emission tomography-computed tomography scan showing an adrenal cancer (a rrow). (C)

99m

Technetium radionuclide scan

confirming unilateral toxic thyroid adenoma (arrowed) – dotted line shows outli ne of thyroid.

SECTION 2 SYSTEM EXAMINATION

Neil Grubb James Spratt Andrew Bradbury

The cardiovascular system6

CARDIOVASCULAR EXAMINATION 98 PERIPHERAL VASCULAR SY STEM 127

THE HEART 99

Anatomy 99

Symptoms and definitions 99
Chest pain and discomfort 99
Dyspnoea (breathlessness) 101
Palpitation 102
Syncope 103
Oedema 104
Other symptoms 105
The history 105
The physical examination 106
General examination 106
Blood pressure 112
Jugular venous pressure and waveform 114
The precordium 116
Putting it all together 124
Investigations 124
Peripheral arterial system 127
Clinical presentation 127
Lower limb 127
Stroke 129
Abdominal symptoms 130
The history 131
The physical examination 131
Peripheral venous system 134
Clinical presentation 134
Pain 134
Swelling 134
Discoloration 134
Chronic venous ulceration 135
Deep vein thrombosis 135
Superficial venous thrombophlebitis 136
CARDIOVASCULAR EXAMINATION
5 Face
• Pallor
• Central cyanosis
• Malar flush
• Corneal arcus
• Xanthomata
Neck 4
• JVP – height, waveform
• Carotid bruits
6 Eyes
• Hypertensive retinopathy
• Diabetic retinopathy
Pulse and blood pressure 3 7 Precordium
• Inspect scars, pacemaker sites
• Palpation
apex beat, heaves, thrills
•Auscultation
heart sounds
added sounds
murmurs
8 Lung bases
• Crackles
• Pleural effusion
Hands 2
• Clubbing

• Splinter haemorrhages

• Skin temperature

• Tremor

9 Abdomen

• Hepatomegaly

• Ascites

• Aortic aneurysm/bruits

• Sacral oedema

• Urine output

General observation 1

• Cyanosis

• Breathlessness

• Distress, demeanour

• Sweating

• Body habitus

• Body mass (obesity, weight loss)

• Marfan’s and other syndromes

10 Legs

• Femoral pulses, bruits, radio-femoral delay

• Popliteal and foot pulses

• Ankle oedema

• Leg ulcers

THE HEART ANATOMY

The heart comprises two muscular pumps working in series, covered in a serous sac (pericardiu m) which allows free movement with

each heart beat and respiration. The heart delivers blood to both pulmonary and systemic circulations (Fig. 6.1). The right heart ( right

atrium and ventricle) pumps deoxygenated blood returning from the sy stemic veins into the pulmonary circulation at relatively low

pressures. The left heart (left atrium and ventricle) receives blood from the lungs and pumps it ro und the body to the tissues at higher

pressures (Fig. 6.2). The heart muscle (myocardium) is thicker in the ventricles than in the atria and in the left ventricle than the right

ventricle, to generate higher pressures.

Superior vena cava

Ascending aorta

Pulmonary trunk

Right atrium

Pulmonary valve

Tricuspid valve

Right ventricular wall

Papillary muscle

Inferior vena cava

Heart valves

Atrioventricular valves (tricuspid on the right side, mitral on the left) separate the atria from the ventricles. They are attached to papillary

muscles in the ventricular myocardium by chordae tendineae (Fig. 6.1) which prevent them fro m prolapsing into the atria when the

ventricle contracts. The pulmonary valve on the right side of the heart and the aortic valve on the left separate the ventricles from the

pulmonary and systemic arterial systems respectively. Each has three half-moo n-shaped 6

cusps called semilunar valves. Cardiac contraction is

coordinated by specialised groups of cells ( Fig. 6.3). The cells in the sinoatrial node normally act as the cardiac pacemaker. S ubsequent

spread of impulses through the heart ensures that atrial contraction is complet e before ventricular contraction (systole) begins. At the end

of systole the atrioventricular valves open, allowing blood to flow from the atria to refill the ventricles (diastole).

Left atrium

Left pulmonary veins Aortic valve

Mitral valve

Chordae tendineae

Left ventricular wall

Fig. 6.1 The heart chambers and valves.

Aorta

sys. 90-140 dias. 60-90 mean 70-105

sys. 15-30

dias. 8-15

mean 10-20

SYMPTOMS AND DEFINITIONS

See Box 6.1.

Chest pain and discomfort

Chest pain and discomfort are crucial symptoms because of their association with major pathology such as coronary artery disease and

aortic dissection. Use a systematic history to distinguish serious from benign causes. Patients often describe discomfort rather than pain,

and the severity of discomfort does not necessarily reflect the severity of the underlying problem . Coronary artery disease may produce

no symptoms in its early phases and in elderly or diabetic patients.

Angina pectoris

Angina pectoris is the most common cardiac pain. It is usually due to myocardial ischaemia from obstr ucted

0-8

4-12 Atrioventricular Bundle of His (AV) node

Sinoatrial (SA) node Left

atrium

sys. 15-30

end-dias. 0-5

sys. 90-140 end-dias. 4-12 Right

atrium

Right

bundle branch

Fig. 6.2 Normal resting pressures (mmHg) in the heart and great vessels. PA, pulmona ry artery; RA, right atrium; LA, left

atrium; RV, right ventricle; LV, left ventricle; sys., systolic; dias., diastolic .

Right ventricle Left

bundle branch

Left

ventricle Purkinje fibres

Fig. 6.3 Conducting system of the heart. 99

6 6.1 Common symptoms of heart disease Symptom

Chest

discomfort

Breathlessness

Palpitation

Cardiovascular causes

Myocardial

infarction

Angina

Pericarditis

Aortic dissection

Heart failure

Angina

Pulmonary

embolism

Pulmonary

hypertension

Tachyarrhythmias Ectopic beats

Syncope/ dizziness

Oedema Arrhythmias

Postural hypotension Aortic stenosis

Hypertrophic

cardiomyopathy

Atrial myxoma

Heart failure

Constrictive

pericarditis

Venous stasis

Lymphoedema

Other causes

Oesophageal spasm Pneumothorax

Musculoskeletal pain

Respiratory disease Anaemia

Obesity

Anxiety

Hyperthyroidism Drugs

Simple faints Epilepsy

Anxiety

Nephrotic syndrome Liver disease

Drugs

Immobility

flow in an epicardial coronary vessel, but can occur in conditions such as aortic stenosis or hypertrophic cardiomyopathy when there is

increased myocardial oxygen demand due to increased left ventricular afterload (Box 6.2). Charac teristically angina is an ache or dull

discomfort, felt diffusely in the centre of the anterior chest, lasting <10 minute s. Patients describe a tight or pressing ‘band-like’

sensation, similar to a heavy weight, which can be confused with indigestion. It may radiat e down one or both arms and into the throat,

jaw and teeth (Fig. 6.4). It is not affected by inspiration, twisting or turning. The severity of the discomfort is a poor guide to prognosis. It

may be precipitated by anything that increases the force of cardiac contracti on, heart rate or blood pressure (BP) and increases

myocardial oxygen demand. Triggers include:

• exercise

• cold or windy weather (causes peripheral

vasoconstriction)

• walking uphill or carrying a heavy load (increases

cardiac output and BP)

• exercise following a heavy meal (postprandial

angina) causing redistribution of myocardial

blood flow.

Angina is relieved by rest and glyceryl trinitrate (GTN), and is more likely to occur early durin g exercise. Some patients describe ‘walk-

through’ angina, as peripheral vasodilatation during exercise decreases myocardial workload. Use an objective assessment of the impact

100

angina on the patient’s activity (Box 6.3):

Fig. 6.4 Site and radiation of angina.

• Unstable angina is limiting angina of abrupt onset, or of increasing severity, duration or frequency. It may occur with minimal exertion

or at rest. It is a medical emergency, as it may herald myocardial infarction.

• Crescendo angina occurs at increasing frequency at lower workloads, but not at rest.

• Nocturnal or decubitus angina occurs at night or on lying flat. It is caused either by increas ed venous return or reducing efficacy of

antiangina drugs, which are often taken in the morning and may wear off overnight. It i ndicates severe coronary artery disease.

It may be difficult to distinguish between angina pectoris and non-car diac causes of chest pain, such as oesophageal pain (Box 6.2).

Myocardial infarction causes symptoms that are similar to, but more severe and prolo nged than, those of angina pectoris. Other features

include restlessness, breathlessness and a feeling of impending death (angor animi). Autonomic stimulation pr oduces sweating, pallor,

nausea, vomiting and diarrhoea, particularly in inferior wall infarction. Pain is absent in up to 30 % of patients with myocardial infarction,

especially the elderly and those with diabetes mellitus.

Pericardial pain is a sharp anterior central chest pain exacerbated by inspiration an d movement, particularly leaning forward. It may be

confused with angina but both may coexist. It is caused by inflammation of the pericardium secondary to myocardial infarction, viral

infection, or after surgery, catheter ablation, angioplasty or radiotherapy.

Aortic dissection is a tear in the intima of the aorta that allows blood to penetrate the media under high pressure, cleaving the aortic wall.

It is usually associated with abrupt onset of very severe, tearing chest pain which can radiate to the back (typically interscapular) and

may be associated with profound autonomic stimulation. If the tear involves the coronary, cranial or upper limb arteries, it may cause

myocardial infarction, syncope, stroke and upper limb pulse asymmetry. If the tear extends into the thoracoabdominal aorta it can affect

the intercostal, visceral, lumbar, renal and iliac arteries, leading to paraplegia, mes enteric infarction, renal failure and lower limb

ischaemia (often with an absent femoral

6.2 Cardiovascular causes of chest pain and their characteristics Angina

Site Retrosternal

Myocardial infarction Retrosternal

Onset Over 1–2 minutes Rapid over a few minutes

Aortic dissection Pericardial pain Oesophageal pain

Interscapular/ retrosternal Very sudden

Character Constricting, heavy Constricting, heavy Tearing or ripping

Radiation Sometimes arm(s), neck, epigastrium

Associated features

Breathlessness

Timing 2–10 minutes

Often to arm(s), neck, jaw,

sometimes

epigastrium

Sweating, nausea, vomiting,

breathlessness, feeling of

impending death (angor animi)

Prolonged

Back, between shoulders

Retrosternal or

left-sided

Gradual, postural

change may suddenly aggravate

Sharp, ‘stabbing’, pleuritic

Left shoulder or back

Sweating, syncope, focal neurological signs, signs of limb ischaemia,

mesenteric

ischaemia

Prolonged

E xacerbating/ relieving factors Triggered by

emotion, exertion, especially if cold, windy. Relieved by rest, nitrates

Severity Mild to moderate

‘Stress’ and

exercise rare

triggers, usually spontaneous.

Not relieved by rest or nitrates

Usually severe

Spontaneous

No manoeuvres relieve pain

Very severe Flu-like prodrome, breathlessness, fever Retrosternal or

epigastric

Over 1–2 minutes;

can be sudden

(spasm)

Gripping, tight or

burning

Often to back,

sometimes to arms 6

Heartburn, acid

reflux

Gradual onset,

variable duration

Pleuritic

Sitting up/lying down may affect intensity Non-steroidal

anti-inflammatory drugs (NSAIDs) help

Can be severe

Cause Coronary artery

disease, aortic stenosis,

hypertrophic cardiomyopathy Plaque rupture and coronary artery

occlusion

Thoracic aortic dissection rupture Pericarditis (usually viral, also post

myocardial infarction) Nighttime common, variable duration

Lying flat some

foods may trigger Not relieved by rest; nitrates sometimes relieve

Usually mild but oesophageal spasm can mimic

myocardial

infarction

Oesophageal

spasm, reflux,

hiatus hernia

6.3 Canadian Cardiovascular Society: functional classification of stable angina

Grade 1 Ordinary physical activity, such as walking and climbing stairs, does not cause angin a. Angina with strenuous or rapid or

prolonged exertion at work or recreation

Grade 2 Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphi ll, walking or stair climbing after meals, in

cold, in wind, or when under emotional stress, or only during the few hours after a wakening

Grade 3 Marked limitation of ordinary physical activity. Walking 1–2 blocks on the level and climbing less than one flight in normal

conditions

Grade 4 Inability to carry on any physical activity without discomfort; angina may be present at rest pulse on the affected side if the

dissection extends into the iliac artery). Predisposing factors include smoking, hypertension and connective tissue disorders such as

Marfan’s syndrome (Fig. 3.28).

Dyspnoea (breathlessness)

This is an awareness of increased drive to breathe and is normal on exercise. It is patho logical if it occurs at a significantly lower

threshold than expected. Breathlessness is a non-specific symptom and may be caused by cardiac, respiratory, neuromuscular and

metabolic conditions, or by toxins or anxiety (Ch. 7).

Dyspnoea may be caused by myocardial ischaemia and is k nown as ‘angina equivalent’. It may occur instead o f, or with, chest

discomfort, especially in elderly and diabetic patients. It has identical precipitan ts to angina and may be relieved by GTN. Dyspnoea in

heart

101

6.4 Some mechanisms and causes of heart failure

Mechanism

Reduced ventricular contractility (systolic dysfunction)

Impaired ventricular filling (diastolic

dysfunction)

Increased metabolic and cardiac demand

Arrhythmia

Valvular or structural cardiac lesions

Fluid overload

Other

6.5 New York Heart Association classification of heart failure symptom sever ity

Cause

Myocardial ischaemia

Myocardial infarction

Cardiomyopathy

Myocarditis

Drugs with negative inotropic

actions, e.g. beta-blockers

Left ventricular hypertrophy Constrictive pericarditis

Class III

Pregnancy *

Anaemia*

Fever*

Thyrotoxicosis

Arteriovenous fistulae

Paget’s disease

Tachycardia, especially atrial fibrillation

Bradycardia

Mitral and/or aortic valve disease Tricuspid and/or pulmonary valve disease (rare)

Ventricular septal defect

Hypertrophic cardiomyopathy

Excessive intravenous infusion Drugs, e.g. non-steroidal

anti-inflammatory drugs, steroids

Intercurrent non-cardiac illness in patients with cardiac disease

Class IV No limitations. Ordinary physical activity does not cause undue fatigue, dyspnoea or palpitation (asymptomatic left ventricular

dysfunction)

Slight limitation of physical activity. Such patients are comfortable at rest. Ordina ry physical activity results in fatigue, palpitation,

dyspnoea or angina pectoris (symptomatically ‘mild’ heart failure)

Marked limitation of physical activity. Less than ordinary physical activity will lead to symptom s (symptomatically ‘moderate’ heart

failure)

Symptoms of congestive heart failure are present, even at rest. With any physical activity increased discomfort is experienced

(symptomatically ‘severe’ heart failure)

but patients with heart failure may also produce frothy, blood-stained sputum.

Platypnoea is breathlessness on sitting upright. It is much rarer than orthopnoea and is usually associated with deoxygenation

(platypnoea–orthodeoxia syndrome). It requires both anatomical and functional abnorm alities. The anatomical component is usually an

intracardiac communication, e.g. atrial septal defect. Platypnoea then develops when a right-to- left shunt occurs because of the

functional component. This may be cardiac, e.g. pericardial effusion; pulmonary, e.g. pneumonectomy ; abdominal, e.g. liver cirrhosis; or

vascular, e.g. aortic aneurysm.

*Aggravating factors which rarely cause heart failure alone.

failure may be associated with fatigue. Pulmonary oedema (accumulation of fluid in the alveoli) oc curs with left heart failure because

increased left atrial enddiastolic pressure leads to elevated pressure in the pulmonary veins and capillaries (Box 6.4). Patients with acute

pulmonary oedema usually prefer to be upright. Those with pulmonary embolism are often more comfortable ly ing flat and may faint

(syncope) if made to sit upright. Use the New York Heart Association grading system to assess the degree of symptomatic limitation

caused by the exertional breathlessness of heart failure (Box 6.5). Other cardiovascular cause s of acute breathlessness include pulmonary

embolism and arrhythmias.

Orthopnoea is dyspnoea on lying flat and is a sign of advanced heart failure. L ying flat increases venous return and in patients with left

ventricular impairment may precipitate pulmonary oedema. The severity can be g raded by the number of pillows used at night, e.g.

‘three-pillow orthopnoea’.

Paroxysmal nocturnal dyspnoea is sudden breathlessness waking the patient from slee p (Fig. 6.5). It is caused by accumulation of

alveolar fluid. Patients may choke or gasp for air, sit on the edge of the bed and open w indows in an attempt to relieve their distress. It

may be confused with asthma, which can also cause

102

night-time dyspnoea, chest tightness, cough and wheeze, Class I

Class II

Palpitation

Palpitation is an unexpected awareness of the heart beating in the chest. It may be rapid, forceful or irregular, and described as thumping,

pounding, fluttering, jumping, racing or skipping. The patient may be able to mim ic the rhythm by tapping it out.

Palpitation may occur in sinus rhythm with anxiety, with in4termittent irregularity of the he art beat, e.g. extrasystoles, or with an

abnormal rhythm (arrhythmia). Not all patients with arrhythmia experience palpitation, e.g. atria l fibrillation often occurs in the elderly

but rarely causes palpitation. The history helps distinguish different types of palpitation ( Box 6.6).

Healthy people are occasionally aware of their heart beating with normal ( sinus) rhythm, e.g. after exercise, or when waiting for an

interview or examination. The sensation is more common in bed at night when external visual and au ditory inputs are minimal and

visceral sensations are more prominent. Slim people may notice it when lying on thei r left side.

Palpitation can be induced by excessive caffeine or nicotine intake. Prescription or ‘over-the-counter’ drugs can cause p alpitation, e.g.

decongestants, antihistamines, as can stimulant recreational drugs, e.g. amphetamines, ecstasy and cocai ne. Carotid artery disease may

cause an intermittent whooshing noise (bruit) heard in the affected sid e of the head during an arrhythmia.

Ectopic beats (extrasystoles) are a benign cause of palpitation at rest and are abolished by exercise. Patients

Fig. 6.5 Paroxysmal nocturnal dyspnoea.

6.6 Descriptions of arrhythmias Extrasystoles Sinus tachycardia

S ite

Onset

Character –

Sudden

‘Jump’, missed beat or flutter

–

Gradual

Regular, fast

Supraventricular tachycardia

–

Sudden, with ‘jump’ Regular, fast

Radiation Associated features

–

Nil –

Anxiety –

Polyuria,

lightheadedness, chest tightness

Timing

Exacerbating/ relieving factors Brief

Fatigue, caffeine, alcohol may trigger. Often

relieved by walking

(increases sinus rate) A few minutes

Exercise or anxiety may trigger

Severity Mild (usually)

Mild to moderate Minutes to hours

Usually at rest, trivial movements, e.g.

bending, may trigger. Vagal manoeuvres may relieve

Moderate to severe

Atrial fibrillation

–

Sudden

Irregular, usually fast; slower in

elderly

–

Polyuria,

breathlessness. Syncope

uncommon

Variable

Exercise or alcohol may trigger; often spontaneous

Ventricular tachycardia –

Sudden

Regular, fast

–

Presyncope, syncope, chest tightness

Variable

Exercise may trigger; often spontaneous

Very variable, may be asymptomatic Often severe

may describe ‘missed beats’, sometimes followed by a particularly strong heart beat. Th e ectopic beat produces a small stroke volume

and an impalpable impulse due to incomplete left ventricular filling. The subsequent compensatory pause lea ds to ventricular overfilling

and a forceful contraction with the next beat.

Supraventricular tachycardia produces sudden paroxysms of rapid, regular palpitation which can sometimes be terminated with breathing

manoeuvres or carotid sinus pressure. Supraventricular tachycardia often affects y oung patients with no other underlying cardiac disease.

Ventricular tachycardia can produce similar symptoms but is more often associated with presyncope or syncope, and tends to affect

patients with cardiomyopathy or previous myocardial infarction.

Urgently investigate palpitation with any high-risk features, including:

• Recent (<3 months) myocardial infarction, percutaneous coronary intervention or ca rdiac surgery

• Associated syncope or severe chest pain

• Family history of syncope or sudden death

• Wolff–Parkinson–White syndrome, or inherited channelopathy, e.g. long QT syndrom e

• Significant structural heart disease, e.g.

hypertrophic cardiomyopathy, aortic stenosis.

Syncope

Syncope is a loss of consciousness due to cerebral hypoperfusion. Dizziness may be due to vertigo or

103

6 6.7 Symptoms related to medication

Symptom Medication

Dyspnoea Beta-blockers in patients with asthma Exacerbation of heart failure by beta-b lockers, some calcium channel antagonists

(verapamil, diltiazem), NSAIDs

Dizziness Vasodilators, e.g. nitrates, alpha-blockers, angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor

antagonists

Angina Aggravated by thyroxine or drug-induced anaemia, e.g. aspirin or N SAIDs

Oedema Steroids, NSAIDs, some calcium channel antagonists, e.g. nifedipine, amlo dipine

Palpitation Tachycardia and/or arrhythmia from thyroxine, β

stimulants, e.g. salbutamol, digoxin toxicity, hypokalaemia from diuretics,

tricyclic antidepressants

NSAIDs, non-steroidal anti-inflammatory drugs.

6.8 Causes of unilateral and bilateral leg oedema Unilateral

• Deep vein thrombosis

• Soft-tissue infection

• Trauma

• Immobility, e.g. hemiplegia

• Lymphoedema

Bilateral

• Heart failure

• Chronic venous insufficiency

• Hypoproteinaemia, e.g. nephrotic syndrome, kwashiorkor, cirrhosis

• Lymphatic obstruction, e.g. pelvic tumour, filariasis

• Drugs, e.g. NSAIDs, nifedipine, amlodipine, fludrocortisone

• Inferior vena caval obstruction

• Thiamine (vitamin B

) deficiency (wet beriberi)

• Milroy’s disease (unexplained lymphoedema which appears at puberty; more c ommon in females)

• Immobility

lightheadedness ( p. 245). Vertigo is rarely caused by heart disease. Lightheadedness, sy ncope or a feeling of impending loss of

consciousness (presyncope) may be cardiovascular in origin. The main causes ar e:

• postural hypotension

• neurocardiogenic syncope

• arrhythmias

• mechanical obstruction to cardiac output. Patients with vascular disease affecting the ca rotid and/ or vertebral arteries may present with

non-focal cerebral symptoms due to hypoperfusion. Common precipitating factors are head turning, getting up quickly from sitting or

lying and starting or increasing antihypertensive drugs.

Postural hypotension is a fall of >20 mmHg in systolic BP on standing. It can be caused by hypovolaemia, antihypertensive dr ug therapy,

especially diuretics and vasodilators (Box 6.7), and autonomic neuropath y. Postural hypotension is common in the elderly, affecting up

to 30% of individuals aged >65 years.

Neurocardiogenic syncope is a group of conditions caused by abnormal autonomic re flexes. A simple faint occurs in healthy people

forced to stand for a long time in a warm environment or subject to painful or emotional stimuli, e.g. the sight of blood. It results from

sudden slow heart rate (bradycardia) and/or vasodilatation. There may be a prior history of fainting with a prodrome of lightheadedness,

tinnitus, nausea, sweating and facial pallor and a darkening of vision from th e periphery as the retinal blood supply (the most

oxygensensitive part of the nervous system) is reduced,. The person then slides to the floor, losing consciousness. Whe n laid flat to aid

cerebral circulation, the individual wakes up, often flushing from vasodilatation and nauseat ed or even vomiting due to vagal

overactivity. If held upright by misguided bystanders, continued cerebral hypoperfusion dela ys recovery and may lead to a seizure and a

mistaken diagnosis of epilepsy.

Frequent fainting caused by minor stimuli may be due

104

to malignant vasovagal syndrome or hypersensitive carotid sinus syndrome

(HCSS). In patients with HCSS, gentle pressure over the carotid sinus may reproduce the s ymptoms by triggering bradycardia.

Arrhythmias can cause syncope or presyncope. The most common cause is bradyarr hythmia, due to sinoatrial disease or to

atrioventricular block, i.e. Stokes–Adams attacks. Drugs, including digoxin, beta-blockers and rate-limiting calcium channel blockers,

e.g. verapamil, diltiazem are a common cause of bradyarrhythmia. Supraven tricular tachyarrhythmias, e.g. atrial fibrillation, rarely cause

syncope. Ventricular tachycardia often causes syncope or presyncope, especially in patients with impaired left ventricular function.

Mechanical obstruction to cardiac output, including severe aortic stenosis and hypertrophic cardiomyopathy, can obstruct left ventricular

outflow causing syncope or presyncope, especially on exertion when cardiac output canno t meet the increased metabolic demand.

Pulmonary embolism can obstruct outflow from the right ventricle, and is a frequently overlooked cause of recurrent syncope. Cardiac

tumours, e.g. atrial myxoma, and thrombosis or failure of prosthetic heart valves are rare ca uses of syncope.

Oedema

Excess fluid in the interstitial space causes oedema (tissue swelling). It is u sually gravity-dependent and so especially seen around the

ankles, or over the sacrum in patients lying in bed. The most common causes of lower limb swellin g are chronic venous disease and

lymphoedema. Other causes include heart failure and vasodilator medications (Box 6.8 and Box 3.16). In general, if the jugular venous

pressure (JVP) is not elevated, then oedema is not cardiogenic.

Infective endocarditis is microbial infection of the heart valves (natural or prosthetic), the lining of the cardiac chambers or blood vessels

or a congenital abnormality, e.g. septal defect. The causative organism is usually bacterial, but may be fungal, rickettsial or

The history

6.9 Cardiovascular disease presenting with ‘non-cardiac’ symptoms System Symptom

Central nervous Stroke

system

Gastrointestinal Jaundice Abdominal pain

Renal Oliguria

Cause

Cerebral embolism Endocarditis

Hypertension

Liver congestion

secondary to heart failure

Mesenteric embolism Heart failure

Chlamydia . The presentation may be acute or subacute. Many features of infective en docarditis are thought to result from circulating

immune complexes or emboli, e.g. petechial rash, haematuria, splinter haemorrhages, cerebral emboli. Features such as fever,

splenomegaly and clubbing may occur.

Other symptoms

Non-cardiac symptoms occur in heart disease ( Box 6.9). Infective endocarditis may present with non-specific symptoms, including

weight loss, tiredness, fever and night sweats, and atrial fibrillation with symptoms and signs of cerebral or systemic embolisation

(commonly legs, arms or viscera).

THE HISTORY

Heart disease commonly occurs without abnormal physical findings so the history is crit ical in making a diagnosis. Examination may

confirm a cardiac diagnosis, e.g. murmur or signs of heart failure but, even in serious disease, physical signs may be completely absent.

• Patients with severe carotid artery stenosis may

have no neck bruit due to low volume flow.

• Large abdominal aortic aneurysms (AAAs) can be

impalpable in the obese.

• Patients with extensive deep vein thrombosis (DVT)

often appear to have normal legs.

Presenting complaint

Establish the frequency, duration and severity of symptoms, exacerbating and relieving factors. Urgently attend to breathlessness, recent

chest or lower limb pain. As many cardiovascular diseases are slowly progr essive, the evolution of symptoms guides the timing of

investigations and treatment, e.g. surgery for carotid artery disease is most effective soon after a cere bral event; and heart valve surgery is

indicated for significantly limiting symptoms.

Functional impairment

How do symptoms affect your patient’s functional capacity? Establish the intensity of exercise re quired to induce symptoms.

• Are symptoms provoked by gentle walking or

strenuous exercise like climbing hills or stairs?

• Can patients keep up when walking with

their peers?

• Do patients feel frustrated or restricted by their

symptomatic limitation?

• How are domestic (cooking, cleaning, shopping),

social (hobbies, sport) and occupational

activities limited?

Lightheadedness and syncope may impair confidence, raise fear of physical injury and have s afety implications when driving.

Calf leg pain on walking (intermittent claudicat ion) from lower limb arterial disease is the most common 6

symptom of peripheral vascular

disease (p. 127):

• How far can the patient walk before the pain comes on? Is this on the flat or uphill?

Past history

Ask about rheumatic fever or heart murmurs during childhood and associated conditions, including:

• Hypertension

• Diabetes mellitus

• Kidney disease

• Thyrotoxicosis (atrial fibrillation)

• Marfan’s syndrome (aortic regurgitation or aortic

dissection).

In suspected infective endocarditis ask about potential causes of bacteraemia e.g. skin infection ; recent dental work; intravenous drug use

and penetrating trauma.

Consider possible links between other diseases and cardiovascular illness. Examples include patients wit h renal failure or cancer and

pericardial effusion; cytotoxic drugs and heart failure; radiotherapy and radiation arteritis. Patients with chronic lung disease may

develop right-sided heart failure (cor pulmonale; p. 115) or atrial fibrillation. Conn ective tissue diseases, e.g. rheumatoid arthritis, are

associated with Raynaud’s phenomenon (Fig. 6.38) and pericarditis.

Drug history

Drugs may cause or aggravate symptoms such as breathlessness, chest pain, oedem a, palpitation or syncope (Box 6.7). Starting thyroxine

for hypothyroidism may precipitate or exacerbate angina. ‘Recreational’ drugs such as cocaine and am phetamines can cause arrhythmias,

chest pain, occlusive and aneurysmal peripheral arterial disease (PAD) and even myocardial infarction. Ask about ‘over-the-counter’

purchases such as NSAIDs, alternative and herbal medicines, as these may have cardiovascular actions. Beta-blocker s and

antihypertensives may impair the peripheral circulation and aggravate symptoms of inte rmittent claudication.

Family history

Many cardiac disorders have a genetic component ( Box 6.10). Ask about premature c oronary artery disease in first-degree relatives (<60

years in a female or <55 years in a male) or sudden unexplained death at a young age, raising the possibility of a cardiomyopathy or

inherited arrhythmia disorder. Patients with venous thrombosis

105

6.10 Genetically determined cardiovascular disorders

Single-gene defects

Hypertrophic cardiomyopathy

Marfan’s syndrome

Familial

hypercholesterolaemia

Polygenic inheritance Ischaemic heart disease Hypertension

Type 2 diabetes mellitus Muscular dystrophies

Long Q–T syndrome

Arrhythmogenic right

ventricular cardiomyopathy (ARVC)

Hyperlipidaemia

Abdominal aortic aneurysm

may have inherited thrombophilia, e.g. factor V Leiden mutation. Familial hypercholesterolaemia is associated with premature arterial

disease.

Social history

Smoking is the strongest risk factor for coronary artery and PAD. Take a detailed smoking history (p. 16).

Alcohol can induce atrial fibrillation and, in excess, is associated with obesity, hype rtension and dilated cardiomyopathy. Excess alcohol

intake with poor nutrition also predisposes to PAD. Intravenous drug use can damage p eripheral arteries and veins, causing infected false

aneurysms, e.g. of the common femoral artery in the groin, which can act as a source fo r infective endocarditis.

Occupational history

Heart disease may impair physical activity and affect employment. This may b e a source of anxiety and an indication for treatment. The

diagnosis of heart disease and/or PAD has significant consequences in certain occupations, e.g. commercial drivers and pilots (Box 6.1 1).

Workers exposed to occupational vibration through the use of air-powered tools may dev elop hand–arm vibration syndrome, which

presents with vasospastic symptoms, e.g. Raynaud’s phenomenon, and neurosensory (numbness , tingling) symptoms.

6.11 Occupational aspects of cardiovascular disease

Occupational exposure associated with cardiovascular disease

• Organic solvents: arrhythmias, cardiomyopathy

• Vibrating machine tools: Raynaud’s phenomenon

• Publicans: alcohol-related cardiomyopathy

Occupational exposure exacerbating pre-existing

cardiac conditions

• Cold exposure: angina, Raynaud’s disease

• Deep-sea diving: embolism through foramen ovale

Occupational requirements for high standards

of cardiovascular fitness

• Pilots

• Public transport/heavy goods vehicle drivers

• Armed forces

• Police

Hands and skin

Examination sequence

■ Look for signs of tobacco staining (Fig. 7.8).

■ Look for peripheral cyanosis.

■ Feel the temperature.

■ Check for clubbing (p. 49).

■ Look at the nails for splinter haemorrhages (linear, reddishbrown marks a long the axis of the finger and toenails, thought

to be due to circulating immune complexes.

■ Look at the palmar aspect of the hands for:

■

Janeway lesions – painless red spots, which blanch on pressure, on the thena r/hypothenar eminences of the

palms, and soles of the feet.

■

Osler’s nodes – painful raised erythematous lesions which

are rare but found most often on the pads of the fingers

and toes.

■ Look at the palmar and extensor surfaces of the hands for xanthomata ( yellow skin or tendon nodules from lipid

deposits). ■ Look at the entire skin surface for petechiae.

THE PHYSICAL EXAMINATION

Tailor the sequence and extent of examination to the patient’s condition:

• Patients with cardiac or respiratory arrest or

requiring immediate emergency: manage first and leave more detailed examination for later ( Fig. 19.9).

• Stable patients: examine thoroughly first.

General examination
• Look at the patient’s general appearance. Does he look:
• unwell?
• breathless or cyanosed?
• frightened or distressed?
• Check the temperature (p. 61).
106
 • Perform urinalysis.
Normal findings
The hands usually feel dry at ambient temperature. Peripheral cyanosis (p. 45) is common  in healthy patients when the hands are cold.
One or two isolated splinter haemorrhages are common in healthy individuals fr om trauma.
Abnormal findings
Fever is a feature of infective endocarditis and pericar
ditis and may occur after myocardial infarction. With autonomic  stimulation the hands may feel warm and sweaty; with hypotension an d
shock they may be cold and clammy.
Splinter haemorrhages are found in infective endocarditis and some vasculitic disorders .
A petechial rash (caused by vasculitis), most often pr esent on the legs and conjunctivae (Fig. 6.6), is a transient finding in endocardit is
and can be confused with the rash of meningococcal disease (Fig. 17.2A ). Janeway lesions, Osler’s nodes, nail fold infarcts and finger
A
B
E
D
6
C
Fig. 6.6  Clinical features which may be present in infective endocarditis: (A) Janeway le sions on hypothenar eminence (arrows), 
(B) Splinter  haemorrhages, (C) Osler’s nodes, (D) Roth’s spot on fundoscopy , (E) Petechial haemorrhages on conjunctiva. 
clubbing are uncommon features of endocarditis (Ch. 3 and Fig. 6.6).
Urinalysis is necessary to check haematuria (endocarditis, vasculitis), glucose (diabetes)  and protein (hypertension and renal disease).
The face and eyes
Examination sequence
Look:
■  in the mouth for central cyanosis.
■  at the eyelids for xanthelasmata (soft yellowish plaques 
periorbitally and on the medial aspect of the eyelids associated  with hyperlipidae mia).
■  at the iris for a corneal arcus.
■  at the conjunctivae for petechiae.
■  Examine the fundi (p. 293) for features of hypertension  (F ig. 6.16), diabetes and Roth’s spots  (flame-shaped retinal 
haemorrhages with a ‘cotton-wool’ centre).
Abnormal findings
Central cyanosis may be due to heart failure or, rarely, congenital heart disease, where it is  associated with right-to-left shunting and
finger clubbing (p. 49).
Xanthelasmata are an important predictor of cardiovascular disease (Figs 6.7 and 6.8A ). If present, also check the patellar and Achilles
tendons for xanthomata (Fig. 6.8B).
Corneal arcus is a creamy yellow discoloration at the  boundary of the iris and cornea caused by cholesterol deposition. It  is more
common in men and black
Corneal arcus
Xanthelasma Malar flush
Central cyanosis Venous pulsation
Fig. 6.7  Facial clues to heart disease.  Carotid bruit
patients ( Fig. 6.8C). Both xanthelasmata and corneal arcus can, however, occur in normolipidaemic patients  (Box 6.12).
Roth’s spots ( Fig. 6.6) are caused by a similar mechanism to splinter haemorrhages a nd can also occur in anaemia or leukaemia.

Arterial pulses

Anatomy

Ejection of blood from the left ventricle into the systemic arterial circulation (Fig. 6.9) creates a pre ssure wave that can be felt as a ‘pulse’

where the arteries are superficial

107

Fig. 6.8 Features of hyperlipidaemia. (A) Xanthelasma. (B) Skin xanthomata over kn ees. (C) Corneal arcus (arrow).

6.12 Risk predictors of cardiovascular disease

The presence of xanthelasma predicts risk of myocardial infarction, coronary heart disease and death in the general population

independently of well-known cardiovascular risk factors such as plasma cho lesterol and triglyceride

concentrations. Corneal arcus, however, is not an independent risk factor.

Christofferson M, Frikke-Schmidt R, Schnohr P et al. Xanthelasmata, arcus corn ea and ischaemic vascular disease and death

in the general population: prospective cohort study. BMJ 2011;343:731.

Loose connective

tissue

Smooth

muscle

Endothelial

lining

Lumen of Elastic lamina

artery

(elastin fibres)

Basal lamina

100 µm

Fig. 6.9 Cross-section of an artery.

or they pass over bone. This pressure wave is not the same as, and travels faster than, the blood flow itself. It can be possible, therefore,

to feel a ‘pulse’ even if there is no flow in the artery being palpated. The pulse wav eform depends upon heart rate, stroke volume, left

ventricular outflow obstruction, arterial elasticity and peripheral resistance.

Use the larger (brachial, carotid or femoral) pulses to assess the pulse volume an d character (Box 6.13). When taking a pulse, assess:

• Rate

• Rhythm

• Volume

• Character.

Record individual pulses as:

• Normal +

• Reduced ±

• Absent –

• Aneurysmal + +

If you are in any doubt about whose pulse you are feeling, p alpate your own pulse at the same time. If it is not synchronous with yours, i t

is the patient’s.

Radial pulse

Examination sequence

■ Place the pads of your index and middle fingers over the right radial a rtery.

■ Assess rate, and rhythm (Fig. 6.10A).

■ Count the pulse rate over 30 seconds; multiply by 2 to obtain the beats p er minute (bpm).

■ To detect a collapsing pulse: first, check that the patient has no shoulder or arm pain or restriction on movement. Feel

the pulse with the base of your fingers, then raise the patient’s arm vertically above the patient’s head (Fig. 6.10B).

■ Palpate both radial pulses simultaneously, assessing any delay between the two, and any difference in pulse volume.

■ Palpate the radial and femoral pulses simultaneously, again noting any timin g and volume differences.

A B C D E

Fig. 6.10 The radial, brachial and carotid pulses. (A) Locating and palpating the radia l pulse. (B) Feeling for a collapsing

radial pulse. (C) Assessing the brachial pulse. (D) Locating the right carotid pu lse with the fingers. (E) Examining the

femoral artery, while simultaneously checking for radio-femoral delay.

6.13 Surface markings of the arterial pulses Artery Radial

Brachial

Carotid

Femoral

Popliteal

Posterior tibial

Dorsalis pedis

Surface marking

At the wrist, lateral to the flexor carpi radialis tendon

In the antecubital fossa, medial to the biceps tendon

At the angle of the jaw, anterior to the sternocleidomastoid muscle

Just below the inguinal ligament, midway between the anterior superior iliac spine and the pubic sym physis (the mid inguinal point). It

is immediately lateral to the femoral vein and medial to the femoral nerve

Lies posteriorly in relation to the knee joint, at the level of the knee crease, dee p in the popliteal fossa

Located 2 cm below and posterior to the medial malleolus, where it passes beneath the flexo r retinaculum between flexor digitorum

longus and flexor hallucis longus Passes lateral to the tendon of extensor hallucis longu s and is best felt at the proximal extent of the

groove between the first and second metatarsals. It may be absent or abnormally s ited in 10% of normal subjects, sometimes being

‘replaced’ by a palpable perforating peroneal artery

If you do examine the carotid pulse do this gently and never assess both carotid s simultaneously.

Examination sequence

■ Explain what you are going to do.

■ Lie the patient semirecumbent in case you induce

a reflex bradycardia.

■ Gently place the tips of your fingers between the larynx and the anterior border of the sternocleidomastoid muscle and

feel the pulse (Fig 6.10D).

■ Listen for bruits over both carotid arteries, using the diaphragm of your stethoscope during held inspiration.

Femoral pulse

Examination sequence

■ Lie the patient supine if possible and explain what you are going to do.

■ Place your index and middle fingers over the femoral artery, which is ju st inferior to the midpoint between the anterior

superior iliac spine and the pubis (Fig. 6.10E).

■ Check for radiofemoral delay (coarctation of the aorta, Fig. 6.11) by simultaneously feeling the radial pulse.

■ Listen for bruits over both femoral arteries, using the diaphragm of the s tethoscope.

Brachial pulse

Examination sequence

■ Use your index and middle fingers to palpate this over the lower end o f the humerus just above the elbow joint. Assess

the character and volume.

Carotid pulse

Some clinicians consider routine examination of the carotid pulse is inappropriate because it may cause distal vascular events, e.g.

transient ischaemic attack, or induce reflex, vagally mediated bradycardia. In assessing a patient who may have had a cardiac arrest,

however, it is the pulse of choice.

Normal findings

Rate Assess the pulse rate in the clinical context. A pulse r ate of 40 bpm can be normal in a fit young adult, whereas a pulse rate of 65

bpm may be abnormally low in acute heart failure. Resting heart rate is normally 60–90 bpm.

Bradycardia is a pulse rate <60 bpm; tachycardia is a rate of >100 bpm.

Rhythm Sinus rhythm originates from the sinoatrial node and produces a regular rhythm (Fig. 6.12A). It varies slightly with the

respiratory cycle, mediated by the vagus nerve, and is most pr onounced in children, young adults or athletes (sinus arrhythmia). During

inspiration, parasympathetic tone falls and the heart rate incre ases; on expiration, the heart rate decreases (Box 6.14).

Collaterals sometimes felt (and heard) around scapula May be prominent pulsation in su praclavicular notch

Bruit may be present over site of coarctation Upper limb hypertension Sinus rhythm

A Ventricular ectopic beat

Blood pressure in legs lower than in arms

Atrial fibrillation

Femoral pulses delayed relative to radial pulse

Atrial flutter

Fig. 6.11  Features of coarctation of the aorta. 
6.14 Haemodynamic effects of respiration
Pulse/heart rate
Systolic blood pressure
Jugular venous pressure Second heart sound
Inspiration Accelerates Falls (up to 10 mmHg) Falls
Splits
Expiration Slows
Rises
Rises Fuses
Volume Volume refers to the perceived degree of pulsation and reflects the p ulse pressure.
D
Ventricular tachycardia
E
Fig. 6.12  Electrocardiogram rhythm strip. (A) Sinus rhythm. 
(B)  Ventricular ectopic beat. (C) Atrial fibrillation with ‘controlled’  ventricular  response. (D) Atrial flutter: note the 
regular ‘saw-toothed’  atrial flutter waves at about 300/min. (E) Ventricular tach ycardia, with  ventricular rate of about 
150/min. 
Character Character refers to the waveform or shape of the arterial pulse.
Abnormal findings
Rate The most common causes of bradycardia are medication, athletic conditioning, and sin oatrial or atrioventricular node dysfunction.
The most common cause of tachycardia is sinus tachycardia (Box 6.15).
Rhythm The pulse may be regular or irregular (Box 6.16). If irregular, it may be  regularly irregular, due to an ectopic beat occurring at a
regular interval or to second-degree atrioventricular block (Fig. 6.12B). Atrial fibrillation is  the most common cause of an irregularly
irregular pulse (Box 6.17 and Fig. 6.12C). The rate in atrial fibrillation depends on the number o f beats conducted by the atrioventricular
node. Untreated, the ventricular rate may be very fast (up to 200 bpm). The variability o f the pulse rate (and therefore ventricular filling)
explains why the pulse volume varies and there
110
 may be a pulse deficit, with some cycles not felt at the radial artery. Calculate the pulse defic it by counting the radial pulse rate and
subtracting this from the apical heart rate assessed by auscultation (Fig. 6.12D  and E).
Volume The ventricles fill during diastole. Longer diastolic intervals  are associated with increased stroke volume, which is reflected by
increased pulse volume on examination. This is why pulse volume and BP  vary widely during atrial fibrillation, and why the
‘compensatory pause’ following a premature ectopic beat is sometimes fe lt by the patient.
A large pulse volume is a reflection of a large pulse pressure, which can be physiologi cal or pathological (Box 6.18). The most common
cause of a large pulse pressure is arteriosclerosis, which is seen in patients with widespre ad vascular disease, hypertension and advanced
age.
A low pulse volume may be due to reduced stroke volume and occur s in left ventricular failure, hypovolaemia or peripheral arterial
disease.
6.15 Causes of a fast or slow pulse
Heart rate
Fast
(tachycardia, >100 bpm)
Slow 
(bradycardia, <60 bpm)
Sinus rhythm
Exercise
Pain
Excitement/anxiety Fever
Hyperthyroidism
Medication:
Sympathomimetics, e.g salbutamol
Vasodilators
Sleep

Athletic training

Hypothyroidism

Medication:

Beta-blockers

Digoxin

Verapamil, diltiazem

Arrhythmia

Atrial fibrillation

Atrial flutter

Supraventricular

tachycardia

Ventricular tachycardia

200

150 Aortic regurgitation

Hypertrophic cardiomyopathy Normal carotid pulse

Aortic stenosis

Carotid sinus

hypersensitivity

Sick sinus syndrome Second-degree heart block

Complete heart block

100

6.16 Causes of an irregular pulse 0

• Sinus arrhythmia

• Atrial extrasystoles

• Ventricular extrasystoles

• Atrial fibrillation

• Atrial flutter with variable response

• Second-degree heart block with variable response

0 100 200 300 400 Milliseconds Fig. 6.13 Pulse waveforms.

6.17 Common causes of atrial fibrillation

• Hypertension

• Heart failure

• Myocardial infarction

• Thyrotoxicosis

• Alcohol-related heart disease

• Mitral valve disease

• Infection, e.g. respiratory, urinary

• Following surgery,

especially cardiothoracic surgery

6.18 Causes of increased pulse volume

Physiological

• Exercise

• Pregnancy

• Advanced age

Pathological

• Peripheral vascular disease

• Hypertension

• Fever

• Thyrotoxicosis

• Anaemia

• Increased environmental temperature

• Aortic regurgitation

• Paget’s disease of bone

• Peripheral atrioventricular shunt

Coarctation is a congenital narrowing of the aorta, usua lly distal to the left subclavian artery. The clinical signs depend on the location

and severity of the narrowing and the patient’s age. In children, the upper limb pulses are usually norm al with reduced volume lower

limb pulses, which are delayed relative to the upper limb pulses (radiofemoral delay) (Fig. 6.11). In adults, coarctation u sually presents

with hypertension and heart failure.

Character A collapsing pulse is when the peak of the pulse wave arrives early and is follow ed by a rapid descent. This rapid fall imparts

the ‘collapsing’ sensation. This is exaggerated by raising the p atient’s arm above the level of the heart (Fig. 6.10B). It occurs in severe

aortic regurgitation and is associated with wide pulse pressure (systolic BP – diasto lic BP >80 mmHg).

A slow-rising pulse has a gradual upstroke with a reduced peak occurring late in systole, an d is a feature of severe aortic stenosis.

Pulsus bisferiens is an increased pulse with a double systolic peak separated by a distinct mid-sy stolic dip. Causes include aortic

regurgitation, and concomitant aortic stenosis and regurgitation (Fig. 6.13).

Pulsus alternans is a beat-to-beat variation in pulse volume with a normal rhythm . It is rare and occurs in advanced heart failure.

Pulsus paradoxus is an exaggeration of the normal variability of p ulse volume with breathing. Pulse volume normally increases in

expiration and decreases during inspiration due to intrathoracic pressure changes affe cting venous return to the heart. This variability in

exaggerated diastolic filling of both ventricles is impeded by increased intrapericardial pressure. This occurs in cardiac tamponad e

because of accumulation of pericardial fluid and in constrictive pericarditis.

111

BP (mmHg)

Optimal <120

Normal <130 High normal 130–139 Hypertension

Grade 1 (mild) 140–159 Grade 2 (moderate) 160–179 Grade 3 (severe) >180 Is olated systolic hypertension

Grade 1 140–159 Grade 2 >160

Diastolic BP (mmHg)

<80

<85

85–89

90–99

100–109 >110

<90 <90

Fig. 6.14 Measuring the blood pressure. Cushingoid facies

Examination sequence

■ Place a BP cuff and inflate until no sounds are heard.

■ Decrease the cuff pressure until sounds are heard only on expiration. N ote the reading.

■ Decrease the cuff pressure again until sounds are heard throughout the respiratory cycle; again note the reading.

■ A difference >10 mmHg on inspiration is pulsus paradoxus.

Blood pressure

BP is a measure of the pressure that the circulating blood exerts against the arterial walls. Systolic BP is the maximal pressure that

occurs during ventricular contraction (systole). During ventricular filling (diastole), arterial pre ssure is maintained at a lower level by the

elasticity and compliance of the vessel wall. The lowest v alue (diastolic BP) occurs immediately before the next cycle.

BP is usually measured using a sphygmomanometer (Fig. 6.14). In certain situations, such as the intensive care unit, it is measure d

invasively using an indwelling intra-arterial catheter connected to a pressure sensor.

BP is measured in mmHg and recorded as systolic pressure/diastolic pressure, together with where, and how, the reading was taken, e.g.

BP: 146/92 mmHg, right arm, supine.

BP is an important guide to cardiovascular risk and provides vital information on th e haemodynamic condition of acutely ill or injured

patients. BP constantly varies and rises with stress, excitement and environment. ‘W hite-coat hypertension’ occurs in patients only when

a patient is seeing a healthcare worker. Ambulatory BP measurement, using a portable d evice at intervals during normal daytime activity

and at night, is better at determining cardiovascular risk.

Hypertension

Abnormal elevation of BP is defined by the British

112

Hypertension Society (Box 6.19). Normal BP is defined

6.19 British Hypertension Society classification of blood pressure (BP) levels Systolic BP

Buffalo ‘hump’

Signs of

alcohol-related disease

Renal disease ± bruit

Radio-femoral delay

Cerebrovascular disease

Retinopathy

Left ventricular hypertrophy 3rd/4th heart sound

Basal crackles Renal failure

Atrial fibrillation

Dependent oedema

Fig. 6.15 Physical signs which may be associated with hypertension.

as <130/85 mmHg. Hypertension is extremely common, affecting 20–30% of the UK adult population, with higher rates in black

Africans (Box 6.22).

Hypertension is asymptomatic although, rarely in severe hypertension, headaches and visua l disturbances occur (Fig. 6.15). It is

associated with significant morbidity and mortality from vascular disease (heart failure, coronary artery disease, cerebrovascular disease

and renal failure). The risk rises progressively with increasing systolic and diastolic pressu re; for example, isolated grade 1 systolic

hypertension has a two- to threefold increased risk of cardiac mortality. Lowering BP lowers vascula r risk regardless of the starting

value. In most hypertensive patients there is no identifiable cause

Fig. 6.16 Hypertensive retinopathy. (A) Grade 1: early changes: increased tortuosity of a retinal vessel and increased

reflectiveness (silver wiring) of a retinal artery are seen at 1 o’clock. (B) Gra de 2: increased tortuosity and silver wiring

(double arrow) with ‘nipping’ of the venules at arteriovenous crossings (single arrow). (C) Grade 3: similar to grade 2 plus

flame-shaped retinal haemorrhages and soft ‘cotton-wool’ exudates. (D) Grade 4: swelling of the optic disc (papilloedema),

retinal oedema and hard exudates around the fovea, producing a ‘macular star ’.

6.20 Causes of secondary hypertension Renal arterial disease,

including renal artery stenosis Phaeochromocytoma

Conn’s syndrome

Cushing’s syndrome

Coarctation of the aorta Adult polycystic kidney disease (p. 204)

Suspect if there is other

evidence of vascular disease Neuroendocrine tumour that

secretes catecholamines, causing hypertension,

headaches, sweating and palpitation

Tumour of the adrenal cortex that secretes aldosterone

Microadenoma of the pituitary that secretes

adrenocorticotrophic hormone (ACTH)

– so-called ‘essential hypertension’. Secondary hypertension is rare, occurring in <1% of the hypertensive population (Box 6. 20).

Assess the hypertensive patient for:

• Any underlying cause

• End-organ damage:

• cardiac: heart failure

• renal: chronic kidney disease

• eye: hypertensive retinopathy – four grades (Fig. 6.16)

• Overall risk of vascular disease, i.e. of stroke, myocardial infarction, heart failure.

Korotkoff sounds

These sounds are produced between systole and diastole because the ar tery collapses completely and reopens with each heart beat,

producing a snapping or knocking sound. The first appearance of sounds (p hase 1) during cuff deflation indicates systole. As pressure is

gradually reduced, the sounds muffle (phase 4) and then disappear (phase 5). Interobserver agre ement is better for phase 5 and this is the

diastolic BP. Occasionally, muffled sounds persist (phase 4) and do not disappear; in this case, record phase 4 as the diastolic pressure

(Fig. 6.17).

Examination sequence

■ Rest the patient for 5 minutes.

■ Always measure BP in both arms (brachial arteries); the higher of the tw o is closest to central aortic pressure and

should be

used to determine treatment.

■ With the patient seated or lying down, support the patient’s

arm comfortably at about heart level, with no tight clothing

constricting the upper arm. You can measure over thin

clothing, as it makes no difference to the result.

■ The usual sphygmomanometer cuff has a bladder width of

12.5 cm and length of 30–35 cm. Apply the cuff to the upper

arm, with the centre of the bladder over the brachial artery.

113

■ Palpate the brachial pulse.

■ Inflate the cuff until the pulse is impalpable. Note the pressure on the ma nometer; this is a rough estimate of systolic

pressure.

■ Inflate the cuff another 30 mmHg and listen through the diaphragm of t he stethoscope placed over the brachial artery.

■ Deflate the cuff slowly (2–3 mmHg/s) until you hear a regular tapping s ound (phase 1 Korotkoff sounds). Record the

reading to the nearest 2 mmHg. This is the systolic pressure.

■ Continue to deflate the cuff slowly until the sounds disappear.

■ Record the pressure at which the sounds completely disappear as the dias tolic pressure (phase 5). If muffled sounds

persist (phase 4) and do not disappear, use the point of muffling as the diasto lic pressure.

Common problems

in BP measurement

• BP is different in each arm: a difference >10 mmHg suggests the presence of subclavian artery disease. Unequal brachial BP is a

marker of increased cardiovascular morbidity and mortality (Box 6.21). Record the highest p ressure and use this to guide management

• Wrong cuff size: the bladder should be

approximately 80% of the length and 40% of the width of the upper arm circumfe rence. A standard adult cuff has a bladder

approximately 13 × 30 cm and suits an arm circumference 22–26 cm. In obese patien ts a standard adult cuff will overestimate BP,

Phase Korotkoff sounds

1 A thud

2 A blowing noise

3 A softer thud 120 mmHg systolic

110 mmHg

100 mmHg

90 mmHg diastolic (1st) 4 A disappearing blowing noise

80 mmHg diastolic (2nd) 5 Nothing

Fig. 6.17 Korotkoff sounds.

so use a large adult (bladder 16 × 38 cm) or thigh cuff (20 × 42 cm)

• Auscultatory gap: up to 20% of elderly hypertensive patients have Korotkoff soun ds which appear at systolic pressure and disappear for

an interval between systolic and diastolic pressure. If the first appearance of the sound is missed, the systolic pressure will be recorded at

a falsely low level. Avoid this by palpating the systolic pressure first

• Patient’s arm at the wrong level: the patient’s elbow should be level with the heart. Hydrostatic pr essure causes ~5 mmHg change in

recorded systolic and diastolic BP for a 7 cm change in arm elevation

• Terminal digit preference: record the true reading rather than rounding value s to the nearest 0 or 5

• Postural change: the pulse increases by about 11 bpm, systolic BP falls by 3–4 mmHg an d diastolic BP rises by 5–6 mmHg when a

healthy person stands. The BP stabilises after 1–2 minutes. Check the BP afte r a patient has been standing for 2 minutes; a drop of ≥20

mmHg on standing is postural hypotension

• Atrial fibrillation: makes BP assessment more difficult because of beat-to-beat variabilit y. Deflate the cuff at 2 mmHg per beat and

repeat

measurement if necessary.

Jugular venous pressure and waveform Anatomy

The internal jugular vein enters the neck behind the mas toid process. It runs deep to the sternocleidomastoid muscle before entering the

thorax between the sternal and clavicular heads and should be examined with the neck muscles relaxed. A pulsation is visible w hen the

pressure in the internal jugular vein is elevated.

The external jugular vein is more superficial, prominent and easier to see. It can be kinked or obstructed as it traverses the deep fascia of

the neck but, when visible, pulsatile and not obstructed, it can be used to estimate the JVP in difficult cases.

Estimate the JVP by observing the level of pulsation in the inte rnal jugular vein. The normal waveform has two main peaks per cycle,

which helps to distinguish it from the carotid arterial pulse (Box 6.23).

The JVP level reflects right atrial pressure (normally <7 mmHg/9 cmH

O). The sternal angle is approximately 5 cm above the righ t

atrium, so the JVP in health should be ≤4 cm above this angle when the patient li es at 45°. If right atrial pressure is low, the patient may

have to lie flat for the JVP to be seen; if high, the patient may need to sit upright (Fig. 6.18).

6.21 Aortic dissection

The presence of: (1) chest pain that is tearing or ripping; (2) a difference in blood pressure o f >20mmHg between arms; and (3)

mediastinal or aortic widening on chest X-ray is pathognomonic of aortic dissectio n.

Von Kodolitsch Y, Schwartz AG, Nienaber CA. Clinical prediction of acute ao rtic dissection. Arch Intern Med

2000;160:2977–2982. 114

6.22 Hypertension

If the clinic blood pressure is 140/90 mmHg or higher, offer ambulatory blood pressure m onitoring to confirm the diagnosis of

hypertension.

NICE. Hypertension. Clinical management of primary hypertension in adults. 20 11. Available online

at: www.nice.org.uk/guidance/CG127.

Jugular venous pressure

A B C

Fig. 6.18 Jugular venous pressure in a healthy subject. (A) Supine: jugular vein disten ded, pulsation not visible. (B) Reclining

at 45°: point of transition between distended and collapsed vein can usually be seen to pulsate just above the clavicle. (C)

Upright: upper part of vein collapsed and transition point obscured.

6.23 Differences between carotid artery and jugular venous pulsation

Carotid

Rapid outward movement

One peak per heart beat

Palpable

Pulsation unaffected by pressure at the root of the neck

Independent of respiration

Independent of position of patient

Independent of abdominal pressure

Jugular

Rapid inward movement

Two peaks per heart beat

(in sinus rhythm)

Impalpable

Pulsation diminished by pressure at the root of the neck

Height of pulsation varies with respiration

Varies with position of patient

Rises with abdominal pressure

• Abdomino-jugular test: firmly press over the abdomen. This increases venous return to the right side of the heart temporarily and the

JVP normally rises.

• Changes with respiration: the JVP normally falls with inspiration due to decreased intrathoraci c pressure.

• Waveform (Fig. 6.19C): the normal JVP waveform has two distinct peaks per cardiac cycle:

• ‘a’ wave corresponds to right atrial contraction and occurs just before the first h eart sound. In atrial fibrillation the ‘a’ wave is absent.

• ‘v’ wave is caused by atrial filling during ventricular systole when the tricuspid va lve is closed.

• Rarely, a third peak (‘c’ wave) may be seen due to closure of the tricuspid valve.

• Occlusion: the JVP waveform is obliterated by gently occluding the vein at the base of the neck with your finger.

Examination sequence

The JVP is best seen on the patient’s right side.

■ Position the patient supine, reclined at 45°, with the head on a pillow to relax the sternocleidomastoid muscles.

■ Look across the patient’s neck from the right side (Fig. 6.19A ). Use oblique lighting if the JVP is difficult to see.

■ Identify the jugular vein pulsation in the suprasternal notch or behind the sternocleidomastoid muscle.

■ Use the abdomino-jugular test or occlusion to confirm it is the JVP.

■ The JVP is the vertical height in centimetres between the upper limit of th e venous pulsation and the sternal angle

(junction of the manubrium and sternum at the level of the second costal cartil ages) (Fig. 6.19B).

■ Identify the timing and waveform of the pulsation and note any abnorma lity.

Normal findings

Aids to differentiate the jugular venous waveform from arterial pulsation:

Abnormal findings

The JVP is primarily a sign of right ventricular function. It is elevated in states of fluid overload, notably in heart failure and in

conditions with right heart dilatation, e.g. acute pulmonary embolism and chronic obstructive pulmonary disease (when it is called cor

pulmonale). Mechanical obstruction of the superior vena cava (most often caused by lung cancer) may cause extreme, nonpulsatile

elevation of the JVP. Here the JVP no longer refle cts right atrial pressure and the abdominojugular test will be negative (Box 6.24 ).

Kussmaul’s sign: a paradoxical rise of JVP on inspiration seen in pericardial constriction or tamponade, severe right ventricular failure

and restrictive cardiomyopathy.

Prominent ‘a’ wave: caused by delayed or restricted right ventricular filling, e. g. pulmonary hypertension or tricuspid stenosis.

Cannon waves: giant ‘a’ waves occur when the right atrium contracts against a cl osed tricuspid valve. Irregular cannon waves are seen in

complete heart block and are due to atrio-ventricular dissociation. Regular cannon

115

Clavicle Internal jugular vein Sternocleidomastoid muscle

6.24 Abnormalities of the jugular venous pulse

Condition

Heart failure

Pulmonary embolism Pericardial effusion Pericardial constriction

Superior vena caval obstruction

Atrial fibrillation

Tricuspid stenosis

Tricuspid regurgitation Complete heart block

Abnormalities

Elevation, sustained abdominojugular reflux >10 seconds

Elevation

Elevation, prominent ‘y’ descent Elevation, Kussmaul’s sign

Elevation, loss of pulsation

Absent ‘a’ waves Giant ‘a’ waves Giant ‘v’ waves ‘Cannon’ waves

Sternocleidomastoid muscle

Top of jugular venous pulsation

Clavicle Measure

vertical height in centimetres R1

Sternal angle R3

B R4 Patient lying at 45° R5

5 8 7

R6 Ventricular

Systole Diastole

Jugular

pulse

y = Aortic valve = Pulmonary valve = Tricuspid valve

1 Right atrium 5 Right ventricle

2 Right atrial appendage 6 Left ventricle

3 Left atrial appendage 7 Apex of the heart

4 Atrioventricular groove 8 Anterior interventricular groove C Time

Fig. 6.19 Jugular venous pressure. (A) Inspecting the jugular venous pressure from the side (the internal jugular vein lies

deep to the sternocleidomastoid muscle). (B) Measuring the height of the jugula r venous pressure. (C) Form of the venous

pulse wave tracing from the internal jugular vein: a, atrial systole; c, c losure of the tricuspid valve; v, peak pressure in

right atrium immediately prior to opening of tricuspid valve; a–x, descent, due t o downward displacement of the tricuspid

ring during systole; v–y, descent at commencement of ventricular filling.

waves occur during junctional rhythm and with some ventricular and supraven tricular tachycardias. ‘cv’ wave: a fusion of the ‘c’ and ‘v’

waves resulting in a large systolic wave and associated with a pulsatile

116

liver is seen in tricuspid regurgitation.

= Mitral valve

Fig. 6.20 Surface anatomy of the chambers and valves of the heart.

The precordium

The precordium is the anterior chest surface overlying the hea rt and great vessels (Fig. 6.20).

Learn the surface anatomy of the heart to understand how and where the sounds and murm urs radiate and basic cardiac physiology to

appreciate their timing (Figs 6.20 and 6.21). The auscultatory areas (aortic, pu lmonary, apex and left sternal border) do not correspond

with the location of cardiac structures, but are where transmitted sounds and murmurs a re best heard (Box 6.25).

A = Aortic MCL = Midclavicular line P = Pulmonary

M = Mitral

T = Tricuspid

MCL

impulse results from the left ventricle moving forward and striking the chest wall during systole. The apex beat is normally in the fifth

left intercostal space at, or medial to, the mid-clavicular line (halfway between the suprasternal notc h and the acromioclavicular joint).

A thrill is the tactile equivalent of a murmur and is a palpable vibration.

A heave is a palpable impulse that noticeably lifts your hand.

T M

Fig. 6.21 Sites for auscultation. Sites at which murmurs from the relevant valves are usually, but not preferentially, heard.

6.25 Cardiac auscultation: the best sites for hearing abnormality Site

Cardiac apex

Lower left sternal border

Upper left sternal border

Upper right sternal border

Left axilla

Below left clavicle

Sound

First heart sound

Third and fourth heart sounds Mid-diastolic murmur of mitral stenosis

Early diastolic murmurs of aortic and tricuspid

regurgitation

Second heart sound

Opening snap of mitral stenosis Pulmonary valve murmurs Pansystolic murmur of

ventricular septal defect

Systolic ejection (outflow)

murmurs, e.g. aortic stenosis, hypertrophic cardiomyopathy Radiation of the pansys tolic murmur of mitral regurgitation Continuous

‘machinery’ murmur of a persistent patent ductus arteriosus

Chest wall abnormalities

Pectus excavatum (funnel chest), a posterior displacement of the lower sternum, and pectus ca rinatum (pigeon chest) may displace the

heart and affect palpation and auscultation (Fig. 7.14).

A midline sternotomy scar usually indicates previous coronary artery bypass surgery or ao rtic valve replacement. A left submammary

scar is usually the result of mitral valvotomy. Infraclavicular scars are seen after pacemaker or defibrillator implantation, and the bulge of

the device may be obvious.

Apex beat

The apex beat is the most lateral and inferior position w here the cardiac impulse can be felt. The cardiac

Examination sequence

■ Explain that you wish to examine the chest and ask the patient to remove all clothing above the waist. Keep a female

patient’s 6

chest covered with a sheet as far as possible.

■ Inspect the precordium with the patient sitting at a 45° angle with shoulde rs horizontal. Look for surgical scars, visible

pulsations and chest deformity.

■ Place your right hand flat over the precordium to obtain a general impr ession of the cardiac impulse (Fig. 6.22A).

■ Locate the apex beat by lying your fingers on the chest parallel to the r ib spaces; if you cannot feel it, ask the patient

to roll on to his left side (Fig. 6.22B).

■ Assess the character of the apex beat and note its position.

■ Apply the heel of your right hand firmly to the left parasternal area and feel for a right ventricle heave. Ask the patient

to hold his breath in expiration (Fig. 6.22C).

■ Palpate for thrills at the apex and both sides of the sternum using the fla t of your fingers.

Normal findings

A normal apical impulse briefly lifts your fingers and is localised. There should be no parasternal heave or thrill. Abnormal findings

The apex beat may be impalpable in overweight or muscular people or in patients with a sthma or emphysema because the lungs are

hyperinflated. It may be diffusely displaced inferiorly and laterally in left ventricular dilatation, e.g . after myocardial infarction, with

aortic stenosis, severe hypertension and dilated cardiomyopathy or in chest deformity. In dex trocardia, with a prevalence of 1 : 10 000,

the cardiac apex is on the right side.

Left ventricular hypertrophy, e.g. with hypertension, aortic stenosis, produces a forcefu l, undisplaced apical impulse. This thrusting

apical ‘heave’ is quite different from the diffuse impulse of left ventricular dilatation. Pulsation over th e left parasternal area (right

ventricular heave) indicates right ventricular hypertrophy or dilatation, most often acco mpanying pulmonary hypertension. The ‘tapping’

apex beat in mitral stenosis represents a palpable first heart sound, and is not usually d isplaced. A double apical impulse is characteristic

of hypertrophic cardiomyopathy.

The most common thrill is that of aortic stenosis which may be palpable at the apex, at the lower sternum or in the neck. The thrill

caused by a ventricular septal defect is best felt at the left and right sternal edges. Diastolic thrills are very rare.

Heart sounds

Normal heart valves make a sound only when they close. The ‘lub-du b’ sounds are caused by closure of the

117

A B C

Fig. 6.22 Palpating the heart. (A) Use your hand to palpate the cardiac impulse. (B) Localise the apex beat with your finger

(roll the patient, if necessary, into the left lateral position). (C) Palpate from ape x to sternum for parasternal pulsations.

atrioventricular (mitral and tricuspid) valves followed by the outlet (a ortic and pulmonary) valves.

The bell of the stethoscope transmits all sounds well but in some patients with high-fr equency murmurs any additional low-frequency

sound masks the highfrequency murmur. The bell is particularly useful at the apex and left sternal edge to listen for the diastolic murmur

of mitral stenosis and third and fourth heart sounds.

The diaphragm attenuates all frequencies equally, therefore making some low-frequency sounds less audible. Use the diaphragm to

identify high-pitched sounds, e.g. early diastolic murmur of aortic regurgitation . Listen with it over the whole precordium for a

pericardial friction rub.

Examination sequence

Make sure the room is quiet when you auscultate. Your stethoscope should fit comfortably with the earpieces angled

slightly forward. The tubing should be ~25 cm long and thick enough to redu ce external sound.

■ Listen with your stethoscope diaphragm at the:

■

apex

■

lower left sternal border

■

upper right and left sternal borders.

■ Listen with your stethoscope bell at the:

■

apex

■

lower left sternal border.

■ Listen over the carotid arteries (ejection systolic murmur of aortic stenosis ) and in the left axilla (pansystolic murmur of

mitral regurgitation).

■ At each site identify the S

and S

sounds. Assess their character and intensity; note any splitting of the S

. Palpate

the carotid pulse to time any murmur. The S

barely precedes the upstroke of the carotid pulsation, while the S

is clearly

out of phase with it.

■ Concentrate in turn on systole (the interval between S

and S

) and diastole (the interval between S

and S

). Listen

for added sounds and then for murmurs. Soft diastolic murmurs are

118

sometimes described as the ‘absence of silence’. ■ Roll the patient on to his left side. Listen at the apex using light

pressure with the bell, to detect the mid-diastolic and presystolic murmur of mitr al stenosis (Fig. 6.23A).

■ Ask the patient to sit up and lean forwards, then to breathe out fully an d hold his breath (Fig. 6.23B). Listen over the

right second intercostal space and over the left sternal edge with the diaphragm for the murmur of aortic regurgitation.

■ Note the character and intensity of any murmur heard. ■ Develop a routine for auscultation so that you do not overlook

subtle abnormalities. Identify and describe the following:

■

the first and second heart sounds (S

and S

)

■

extra heart sounds (S

and S

)

■

additional sounds, e.g. clicks and snaps

■

pericardial rubs

■

murmurs in systole and/or diastole.

Normal findings

• First heart sound (S

), ‘lub’, is caused by closure of the mitral and tricuspid valves at the onset of ventric ular systole. It is best heard at

the apex.

• Second heart sound (S

), ‘dup’, is caused by closure of the pulmonary and aortic valves at the end of ventricular sy stole and is best

heard at the left sternal edge. It is louder and higher-pitched than the S

‘lup’, and the aortic component is normally louder than the

pulmonary one. Physiological splitting of S

occurs because left ventricular contraction slightly precedes that of the right ventr icle so that

the aortic valve closes before the pulmonary valve. This splitting increases at end-ins piration because increased venous filling of the right

ventricle further delays pulmonary valve closure. This separation disappears on expiration (Fig. 6.24). Splitting of S

is best heard at the

left sternal edge. On auscultation, you hear ‘lub d/dub’ (inspiration) ‘lub-dub’ (expir ation)

• Third heart sound (S

) is a low-pitched early diastolic sound best heard with the bell at the apex. It coincides w ith rapid ventricular

filling immediately after opening of the atrioventricular valves and is therefore heard after th e second as ‘lub-dub-dum’. It is a normal

finding in children, young adults and during pregnancy.

Expiration

Physiological S

splitting

Note: a single second sound S

in inspiration is normal in adults

Inspiration

Expiration

Fixed

splitting of

S1second

sound

Inspiration S

A2P2

True fixed

splitting is a

characteristic

of atrial

septal defect. 6

A2P2

Increased splitting

occurs in right

bundle branch

block and

pulmonary

hypertension.

It is not fixed.

Expiration

Reversed

splitting of

second S

sound

Inspiration Reversed

splitting

occurs in left

ventricular

outflow

obstruction and left bundle branch block

Fig. 6.23 Auscultating the heart. (A) Listen for the murmur of mitral stenosis with the lightly applied bell with the patient

in the left lateral position. (B) Listen for the murmur of aortic regurgitation with the diaphragm with the patient leaning

forward.

Fig. 6.24 Normal and pathological splitting of the second heart sound.

Abnormal findings

First heart sound: In mitral stenosis the intensity of S

is increased due to elevated left atrial pressure (Box 6.26).

Second heart sound: The aortic component of S

is sometimes quiet or absent in calcific aortic stenosis and reduced in aortic

regurgitation (Box 6.27). The aortic component is loud in systemic hypertension, a nd the pulmonary component increased in pulmonary

hypertension.

Wide splitting of S

, but with normal respiratory variation, occurs in conditions which delay right ventricula r emptying, e.g. right bundle

branch block. Fixed splitting, i.e. no variation with respiration of S

, is a feature of atrial septal defect (Fig. 6.25). In this condition the

right ventricular stroke volume is larger than the left, and the splitting is fixed because the defect equalises the pressure between the two

atria throughout the respiratory cycle.

In reversed splitting the two components of S

occur together on inspiration and separate on expiration. This occurs when left ventricular

emptying is delayed so that the aortic valve closes after the pulmonary valve. Examples include left bundle branch block and right

ventricular pacing.

6.26 Abnormalities of intensity of the first heart sound

Quiet

Low cardiac output

Poor left ventricular function

Rheumatic mitral regurgitation

Loud

Increased cardiac output

Large stroke volume

Mitral stenosis

Variable

Atrial fibrillation

Extrasystoles

Long P–R interval (firstdegree heart block)

Short P–R interval Atrial myxoma (rare)

Complete heart block

Third heart sound: This is usually pathological after the age of 40 years (Box 6.28 ). The most common causes are left ventricular failure,

when it is an early sign, and mitral regurgitation, due to volume loading of the ventricle. In heart failure S

occurs with a tachycardia,

referred to as a ‘gallop’ rhythm, and S

and S

are quiet (lub-da-dub; Box 6.29).

Fourth heart sound: This is less common. It is soft and low-pitched, best heard with the stethoscope bell at the apex. It occurs just before

(da-lub-dub). It is always pathological and is caused by forceful atrial contracti on against a non-compliant or stiff ventricle. An S

most often heard with left ventricular hypertrophy (due to

119

Pulmonary valve

Atrial septal defect

Tricuspid valve

Ejection systolic murmur (pulmonary flow murmur) with fixed splitting of seco nd sound

Diastolic murmur (tricuspid flow murmur) in children Fig. 6.25 Atrial septal defect. RA, right atriu m; LA, left atrium.

6.27 Abnormalities of the second heart sound

Quiet

Low cardiac output

Calcific aortic stenosis

Aortic regurgitation

Loud

Systemic hypertension (aortic component)

Pulmonary hypertension (pulmonary component) Split

Widens in inspiration (enhanced physiological splitting):

Right bundle branch block

Pulmonary stenosis

Pulmonary hypertension

Ventricular septal defect

Fixed splitting (unaffected by respiration):

Atrial septal defect

Widens in expiration (reversed splitting):

Aortic stenosis

Hypertrophic cardiomyopathy

Left bundle branch block

Ventricular pacing

6.28 Causes of a third heart sound

Physiological

• Healthy young adults

• Athletes

Pathological

• Large, poorly contracting

left ventricle

• Pregnancy

• Fever

• Mitral regurgitation

hypertension, aortic stenosis or hypertrophic cardiomyopathy). It cannot occur when there is atrial fibrillation.

Both an S

and an S

cause a ‘triple’ or ‘gallop’ rhythm.

Added sounds

An opening snap is commonly heard in mitral (rarely

120

tricuspid) stenosis. It results from sudden opening of a

6.29 Heart failure

In an adult with acute breathlessness a third heart sound is highly suggestive of heart failu re with depressed left ventricular ejection

fraction. Other useful signs, if present, are raised jugular venous pressure, perip heral oedema and basal lung crackles.

McGee S. Evidence based physical diagnosis. St Louis, MO: Saunders/ Elsevier, 2007, pp. 436–440.

stenosed valve and occurs early in diastole, just after the S

(Fig. 6.26A). It is best heard by the diaphragm at the apex.

Ejection clicks are high-pitched sounds best heard by the diaphragm. They occ ur early in systole just after the S

, in patients with

congenital pulmonary or aortic stenosis (Fig. 6.26B). The mechanism is similar to that of an opening snap. Ejection clicks do not occur in

calcific aortic stenosis because the cusps are rigid.

Mid-systolic clicks are high-pitched and best heard at the apex by the diaphragm. They occur in mitral valve prolapse (Fig. 6.26C) and

may be associated with a late systolic murmur.

Mechanical heart valves can make a sound when they close or open. The closure sou nd is normally louder, especially with modern

valves. The sounds are highpitched, ‘metallic’ and often palpable, and may be h eard even without a stethoscope. A mechanical mitral

valve replacement makes a metallic S

and a sound like a loud opening snap (Fig. 6.26D). Mechanical aortic valves have a loud, m etallic

and an opening sound like an ejection click (Fig. 6.26E). They are normally associated with a flow murmur.

Pericardial rub (friction rub) is a coarse scratching sound, often with systolic and dia stolic components. It is best heard using the

diaphragm with the patient holding his breath in expiration. It may be audible over any part of the precordium but is often localised. It is

most often heard in acute viral pericarditis and sometimes 24–72 hours after myocardial infarction. Pericardial rubs vary in intensity over

time, and with the position of the patient.

A pleuro-pericardial rub is a similar sound that occurs in time with the cardiac cycle but is also inf luenced by

A S

Opening snap

B S

Ejection S

2click

C Closing sound

Midsystolic S

2click

Opening sound

D Opening sound Prosthetic valve S

2sounds: mitral

Closing sound

E S

Prosthetic valve sounds: aortic Fig. 6.26 ‘Added sounds’ on auscultation.

6.30 Grades of intensity of murmur

Grade 1 Heard by an expert in optimum conditions Grade 2 Heard by a non-expert in optimum conditions Grade 3 Easily heard; no thrill

Grade 4 A loud murmur, with a thrill

Grade 5 Very loud, often heard over wide area, with thrill Grade 6 Extremely loud, he ard without stethoscope

respiration and is pleural in origin. Occasionally a ‘crunching’ noise can be heard caused by g as in the pericardium (pneumo-

pericardium).

Murmurs

Heart murmurs are produced by turbulent flow across an abnormal valve, septal defect or o utflow obstruction. ‘Innocent’ murmurs

caused by increased volume or velocity of flow through a normal valve occur when stroke volume is increased, e.g. during pregnancy, in

athletes with resting bradycardia or children with fever.

Examination sequence

Timing

Identify the S

and S

sounds. It may help to palpate the patient’s carotid pulse while listening to the precordium.

Determine whether the murmur is systolic or diastolic:

■ Systole begins with the S

(mitral and tricuspid valve closure).

This occurs when left and right ventricular pressures exceed

the corresponding atrial pressures. For a short period all four

heart valves are closed (pre-ejection period). Ventricular

pressures continue to rise until they exceed those of the aorta

and pulmonary artery, causing the aortic and pulmonary valves

to open. Systole ends with the closure of these valves,

producing the S

■ Diastole is the interval between S

and S

. Physiologically it is

divided into three phases:

■

early diastole (isovolumic relaxation): the time from the closure of the aortic a nd pulmonary valves until the opening of

the mitral and tricuspid valves 6

■

mid-diastole: the early period of ventricular filling when atrial pressures excee d ventricular pressures

■

pre-systole: coinciding with atrial systole.

Murmurs of aortic (and pulmonary) regurgitation start in early diastole and ex tend into mid-diastole. The murmurs of

mitral or tricuspid stenosis cannot start before mid-diastole. Likewise, S

occurs in mid-diastole and S

in pre-systole.

Duration

The murmurs of mitral and tricuspid regurgitation start with S

, sometimes muffling or obscuring it, and continue

throughout systole (pansystolic) (Fig. 6.27). The murmur produced by mitral valve prolapse does not begin until the mitral

valve leaflet has prolapsed during systole, producing a late systolic murmur. Th e ejection systolic murmur of aortic or

pulmonary stenosis begins after S

reaches maximal intensity in mid-systole, then fades, stopping before S

(Fig. 6.27).

Character and pitch

The quality of a murmur is subjective, but terms such as

harsh, blowing, musical, rumbling, high- or low-pitched can help. High-pitched murmurs often correspond with high-

pressure gradients, so the diastolic murmur of aortic

regurgitation is higher-pitched than that of mitral

stenosis.

Intensity

Describe any murmur according to its grade of intensity (Box 6.30). Diastolic murmurs are rarely louder than grade 3. The

intensity of a murmur does not correlate with severity of valve dysfunction; fo r instance, the murmur of critical aortic

stenosis can be quiet and occasionally inaudible. Changes in intensity with time are important, as they can denote

progression of a valve lesion. Rapidly changing murmurs can occur with infec tive endocarditis because of valve destruction.

Location

Record the site(s) where you hear the murmur best. This helps to differentiate diastolic murmurs (mitral stenosis at the

apex, aortic regurgitation at the left sternal edge), but is less helpful with systol ic murmurs, which are often loud over all

the precordium (Fig. 6.21).

Radiation

Murmurs radiate in the direction of the blood flow to specific sites outside the precordium. Differentiate this from

location. The pansystolic murmur of mitral regurgitation radiates towards the le ft axilla, the murmur of ventricular septal

defect towards the right sternal edge, and that of aortic stenosis to the aortic ar ea and the carotid arteries.

121

'Straight' left heart border on chest X-ray

Apical pansystolic murmur radiates to axilla

Variant: midsystolic click/ late systolic murmur (mitral valve prolapse)

MSC S

Fig. 6.27 Mitral regurgitation. The murmur begins at the moment of valve closure a nd may obscure the first

heart sound. It varies little in intensity throughout systole. In mitral valve prolaps e, the murmur begins in mid or late

systole and there is often a mid-systolic click (MSC).

6.31 Causes of systolic murmurs

Ejection systolic murmurs

Increased flow through normal valves

‘Innocent systolic murmur’: fever, athletes (bradycardia → large

stroke volume), pregnancy (cardiac output maximum at 15 weeks)

Atrial septal defect (pulmonary flow murmur)

Severe anaemia

Normal or reduced flow though a stenotic valve

Aortic stenosis

Pulmonary stenosis

Other causes of flow murmurs

Hypertrophic cardiomyopathy (obstruction at

subvalvular level)

Aortic regurgitation (aortic flow murmur)

Pansystolic murmurs

All caused by a systolic leak from a high- to a lower-pressure chamber:

• Mitral regurgitation

• Tricuspid regurgitation

• Ventricular septal defect

• Leaking mitral or tricuspid prosthesis

Abnormal findings

Systolic murmurs Ejection systolic murmurs are caused by incre ased stroke volume (flow murmur), or stenosis of the aortic or

pulmonary valve (Box 6.31). An ejection murmur is also a feature of hypertrophic cardiomyopathy and is accentuated by exercise. An

atrial septal defect is characterised by a pulmonary flow murmur during systole.

The murmur of aortic stenosis is often audible all over the precordium (F ig. 6.28). It is harsh, high-pitched and musical, and radiates to

the upper right sternal edge and carotid arteries. It is usually loud and there may be a thrill.

Pansystolic murmurs are usually caused by mitral regurgitation. Th e murmur is often loud and blowing in

122

character, best heard at the

apex and radiating to the axilla. With mitral valve prolapse, regurgitation begins in mid-systole, producing a late systolic murmur (Fig.

6.27). The murmur of tricuspid regurgitation is heard at the lower left sternal edge; if significa nt, it is associated with a ‘v’ wave in the

JVP and a pulsatile liver.

Ventricular septal defect also causes a pansystolic murmur. Small congenital defects produce a loud murmur audible at the left sternal

border, radiating to the right sternal border and often associated with a thrill. Rupture of the interventricular septum can complicate

myocardial infarction, producing a harsh pansystolic murmur. Other murmurs heard after myocardial infarction include acute mitral

regurgitation due to papillary muscle rupture, functional mitral regurgitation caused by left ventricular dilatation and a pericardial rub.

Diastolic murmurs

Early diastolic murmurs The term ‘early diastolic murmur’ is misleading; usua lly the murmur lasts throughout diastole, but is loudest in

early diastole. It is typically caused by aortic regurgitation (Fig. 6.29), and is best heard at the left sternal edge with the patient leanin g

forward holding the breath in expiration. In general the duration of the aortic regurgitation murmur is inversely proportional to lesion

severity. Since the regurgitant blood volume must be ejected during the subsequent systole, significant aortic regurgitation leads to

increased stroke volume and is almost always associated with a systolic flow murmur.

Pulmonary regurgitation is uncommon. It may be caused by pulmonary artery dilatation in pulmonary hypertension (Graham Steell

murmur) or a congenital defect of the pulmonary valve.

Mid-diastolic murmurs A mid-diastolic murmur is usually caused by mitral ste nosis. This is a low-pitched, rumbling sound which may

follow an opening snap (Fig. 6.30). It is best heard with the stethoscope bell at the apex with the patient rolled to the left side. T he

murmur is accentuated by exercise. The cadence sounds like ‘lup-ta-ta-rru’; ‘lup’ is the loud S

, ‘ta-ta’ the S

, and opening snap and ‘rru’

the mid-diastolic murmur. If the patient is in sinus rhythm, left atrial contraction i ncreases

Aortic dilatation

EC S

Lean patient forward with breath held in expiration to feel thrill and hear murmur best

Aortic valve 6

EC S

Fig. 6.28 Aortic stenosis. There is a systolic pressure gradient across the stenosed a ortic valve. The resultant high-velocity

jet (arrow) impinges on the wall of the aorta, and is best heard with the diaph ragm in the aortic area. Alternatively, the

bell may be placed in the suprasternal notch. The ejection systolic murmur prec edes an ejection click (EC). A fourth heart

sound may be heard at the apex.

Uncoiled

aorta

Aortic valve

Left ventricular apex

Lean patient forward with breath held

2in expiration to hear murmur best

Fig. 6.29 Aortic regurgitation. The pulse pressure is usually increased; the jet from the aortic valve is directed inferiorly

towards the left ventricular outflow tract (arrow) during diastole, producing a h igh-pitched early diastolic murmur, best heard

with the diaphragm. An associated systolic murmur is common because of the i ncreased flow through the aortic valve in

systole.

Left atrial

appendix may be seen on chest X-ray

Mitral valve

Left atrium

Roll patient towards left

Loud S2

Loud

to hear murmur best

S1 S1

Fig. 6.30 Mitral stenosis. There is a pressure gradient across the mitral valve; in this example it continues throughout

diastole. This causes a sharp movement of the tethered anterior cusp of the mit ral valve at the time when the flow

commences, and an opening snap (OS) results. The jet through

123the stenosed valve (arrow) strikes the endocardium at the cardiac apex.

Best heard 2nd left

intercostal space

Continuous S

murmur

Left to right shunt from

aorta to pulmonary artery

Pulmonary artery

shadow may be

enlarged on chest X-ray

Left ventricular

enlargement

Large-volume peripheral pulses

(including dorsalis pedis pulse in infants)

Fig. 6.31 Persistent patent ductus arteriosus. A continuous ‘machinery’ murmur is hea rd because aortic pressure always

exceeds pulmonary arterial pressure, resulting in continuous ductal flow. The pr essure difference is greatest in systole,

producing a louder systolic component to the murmur.

the blood flow across the stenosed valve, leading to presystolic accentuation of the mur mur. The murmur of tricuspid stenosis is similar

but rare.

An Austin Flint murmur is a mid-diastolic murmur that acc ompanies aortic regurgitation. It is caused by the regurgitant jet striking the

anterior leaflet of the mitral valve, restricting inflow to the left ventricle.

Continuous murmurs Continuous murmurs are rare in adults. The most common cause is a pate nt ductus arteriosus. In the fetus this

connects the upper descending aorta and pulmonary artery and normally closes just after birth. T he murmur is best heard at the upper left

sternal border and radiates over the left scapula. Its continuous character is ‘machinery -like’ (Fig. 6.31).

PUTTING IT ALL TOGETHER

Auscultation remains an important clinical skill despite the ready availability of echocardiography. You must be able to detect abnormal

signs to prompt appropriate investigation. Auscultatory signs, e.g. S

or S

and pericardial friction rubs, have no direct equivalent on

echocardiography but are diagnostically important. Some patients, especially those with rheumatic heart disease, have multiple heart

valve defects, and the interpretation of more subtle physical signs is important. For example, a patient with mixed mitral stenosis and

regurgitation will probably have dominant stenosis if the S

is loud, but dominant regurgitation if there is an S

INVESTIGATIONS

See Box 6.32.

Electrocardiography (ECG)

The standard 12-lead ECG ( Fig. 6.32) uses recordings

124

made from six precordial electrodes (V

–V

) and six different recordings

from the limb electrodes (left arm, right arm and left leg). The right leg electrode is used as a reference.

Ambulatory ECG monitoring

This is a continuous ECG recording that lasts 24–48 hours and is read by computer. Patient-activated recorders capture occasional

arrhythmias and are activated only when symptoms occur (Fig. 6.33).

Exercise ECG

An exercise ECG may unmask evidence of coronary artery disease. Severe ECG abnormalities, or changes that occur during minor

exertion, are of prognostic significance and may require invasive investigation with coronary angiography.

Ambulatory BP monitoring

A portable device is worn by the patient at home: this device takes at least two BP measurements per hour during the person’s usual

waking hours. The average value of at least 14 measurements is used to confirm a diagnosis of hypertension.

Chest X-ray

An enlarged heart, as judged by the cardiothoracic ratio (Fig. 7.22), is common in valvular heart disease and hear t failure. In heart failure

this is often accompanied by distension of the upper lobe pulmonary veins, diffu se shadowing within the lungs due to pulmonary oedema

and Kerley B lines (horizontal engorged lymphatics at the peripher y of the lower lobes) (Fig. 6.34A). A widened mediastinum may

indicate a thoracic aneurysm.

Echocardiography

Echocardiography uses high-frequency sound waves to evaluate valve abnormalities, left ventricular function

Investigations

Fig. 6.32 Electrocardiography. (A) Diagram to show the directions from which the 12 standard leads ‘look at the heart’.

The transverse section is viewed from below like a computed tomography scan . (B) Normal PQRST complex. (C) Acute

anterior myocardial infarction. Note ST elevation in leads V

–V

and aVL, and ‘reciprocal’ ST depression in leads II, III

and aVF.

* *

Fig. 6.33 Printout from 24-hour ambulatory electrocardiogram recording, showing comp lete heart block. Arrows indicate visible P

waves; at times these are masked by the QRS complex or T wave (*).

125

6 6.32 Investigations in cardiac disease

Investigation

Blood tests

Full blood count and erythrocyte sedimentation rate Urine and

electrolytes

Blood glucose

Lipids

Cardiac enzymes Serology

Blood culture

Electrophysiology

Electrocardiogram (ECG)

Exercise ECG

Ambulatory ECG monitoring

Radiology

Chest X-ray

Echocardiography (transoesophageal echocardiogram more sensitive)

Radionuclide

studies

Invasive tests

Cardiac

catheterisation

Indication/comment

Anaemia unmasking angina and connective tissue disease

Renal function

Hypertension more common in diabetes Hyperlipidaemia

Troponins rise after myocardial infarction

Connective tissue disease, streptococcal infection

Infective endocarditis

Cardiac rhythm, conduction, e.g. left bundle branch block

Myocardial infarction and ischaemia (usually normal in angina)

Assess left ventricular hypertrophy

Ischaemia, prognosis post myocardial infarction

Confirms if palpitation coincides with arrhythmia

Cardiothoracic ratio (maximum width of the cardiac silhouette/widest part of lung fiel ds) increased in heart failure and valve disease

Quantifies valvular defects; assesses left ventricular function (heart failure); valve vegetations in infective endocarditis

Left ventricular function; myocardial ischaemia; pulmonary embolism

Coronary angiography (angina)

determines therapy, prior to surgery in valve disease to assess coronary anatomy, and seve re heart failure for cardiac transplantation

and blood flow (Doppler echocardiography). Most scans are performed through the anterior chest wall (transthoracic) (Fig. 6.34B).

Transoesophageal echocardiography requires sedation, but gives high resolution of po sterior structures, e.g. left atrium, tricuspid valve

and descending aorta.

Radionuclide studies

Technetium-99 is injected intravenously and detected using a gamma camera to assess left ventricular

126

function. Thallium and sesta-

MIBI are taken up by

Infarct

LV AO

LAD

Fig. 6.34 Cardiovascular imaging. (A) Chest X-ray in heart failure. This shows ca rdiomegaly with patchy alveolar shadowing

of pulmonary oedema and Kerley B lines (engorged lymphatics) at the periphe ry of both lungs. (B) Transthoracic

echocardiogram in parasternal long-axis view. This shows thinning of the interv entricular septum, which has an irregular

shape and bright echoes indicating fibrous scarring. This is the site of an old infarct. LA, left atrium; LV, left ventricle;

AO, aortic root. (C) Coronary angiography. The arrow indicates a severe disc rete stenosis in the circumflex coronary artery.

LM, left main; LAD, left anterior descending; CX, circumflex.

myocardial cells and indicate myocardial perfusion at rest and exercise.

Cardiac catheterisation

A fine catheter is introduced under local anaesthetic via a peripheral artery (usually the b rachial or femoral) and advanced to the heart

under X-ray guidance. Although measurements of intracardiac pressures and therefore estima tes of valvular and cardiac function are

possible, the primary application of this technique is coronary arterial imaging, using co ntrast medium. This is performed to inform

revascularisation, either by coronary angioplasty or bypass grafting (Fig. 6.34C).

Computed tomography (CT)

and magnetic resonance

imaging (MRI)

CT, with its superior temporal resolution of the coronary arteries, is particular ly useful to investigate symptomatic patients at low-

intermediate risk of coronary artery disease. It can also reduce the need for invasive investigation in patients, with a low probability of

occlusive coronary disease, awaiting valve surgery. MRI provides superior tissue resolution and is the imaging modality of choice for

investigating heart muscle disease (cardiomyopathy).

PERIPHERAL VASCULAR SYSTEM PERIPHERAL ARTERIAL SYSTEM

See Figures 6.9 and 6.35.

Carotid artery Subclavian artery

Brachial artery Aorta

Radial artery Ulnar artery

Femoral artery

Popliteal artery

Posterior tibial artery

Dorsalis pedis artery

Identifying patients with PAD is important for the following reasons:

• PAD, even if asymptomatic, is a powerful marker

for premature vascular death

• The first manifestation of PAD may be a life- or

limb-threatening complication, e.g. stroke, acute

limb ischaemia or ruptured AAA

• Modifying vascular risk factors dramatically

improves outcomes

• PAD may affect medical and surgical treatment for

other conditions, e.g. prescription of a beta-blocker

may precipitate intermittent claudication.

PAD affects the legs eight times more commonly than the arms for the following reasons:

• The arterial supply to the legs is less well developed

in relation to the muscle mass

• The lower limb is more frequently affected by

atherosclerosis.

There are four stages of lower limb lack of blood supply (ischaemia) (Box 6 .33).

Asymptomatic ischaemia

Haemodynamically significant lower limb ischaemia is defined as an ankle to brachial pressure index ( ABPI) <0.9 at rest. Most of these

patients are asymptomatic, either because they choose not to walk very far, or because their exercise tolerance is limited by other

comorbidity. Although asymptomatic, these patients are at high risk of ‘vascular’ complications and should be assessed and treated

medically as if they have intermittent claudication.

Fig. 6.35 The arterial system.

CLINICAL PRESENTATION

Lower limb

Approximately 20% of people aged >60 years in developed countries have PAD but only a quarter of these are symptomatic. The

underlying pathology is usually atherosclerosis (hardening of the arteries) affecting large and medium-sized vessels.

III IV

6.33 Classification of lower limb ischaemia Asymptomatic

Intermittent claudication Night/rest pain

Tissue loss (ulceration/gangrene) 127

6 6.34 The clinical features of arterial, neurogenic and venous claudication

Pathology

Arterial

Stenosis or occlusion of major lower limb arteries

Neurogenic

Lumbar nerve root or cauda equina compression (spinal stenosis)

Site of pain Muscles, usually the calf but may involve thigh and buttocks

Laterality

Onset

Relieving features

Colour Unilateral if femoropopliteal, and bilateral if aortoiliac disease

Gradual after walking the

‘claudication distance’

On stopping walking, the pain disappears completely in 1–2 minutes

Normal or pale

Ill defined. Whole leg. May be associated with numbness and tingling

Often bilateral

Venous

Obstruction to the venous outflow of the leg due to iliofemoral venous occlu sion Whole leg. ‘Bursting’ in nature

Nearly always unilateral

Often immediate on walking or standing up

Bending forwards and stopping walking. May sit down for full relief Normal

Temperature Oedema

Pulses

Normal or cool

Absent

Reduced or absent Normal Absent Normal

Straight-leg raising Normal

May be limited Gradual, from the moment walking starts

Leg elevation

Cyanosed. Often visible

varicose veins

Normal or increased

Always present

Present but may be difficult to feel owing to oedema

Normal

Intermittent claudication

Intermittent claudication is pain felt in the legs on walking due to arterial insufficiency and is the most common symptom of PAD. The

pain typically occurs in the calf secondary to femoropopliteal disease but may be felt in the thigh and/or buttock in proximal (aorto-iliac)

obstruction. Patients describe tightness or ‘cramp-like’ pain which develops after a relat ively constant distance; the distance is often

shorter if walking uphill, in the cold and after meals. The pain disappears completely with in a few minutes of rest but recurs on walking.

The ‘claudication distance’ is how far patients say they can walk before the pain stops them from walking.

There are two other types of claudication

• Neurogenic claudication is due to neurological and musculoskeletal disorder s of the lumbar spine

• Venous claudication is due to venous outflow obstruction from the leg, following extensive DVT.

Neurogenic and venous claudication are much less

common than arterial claudication, and can be distinguished on history and examination (Box 6. 34).

Night/rest pain

The patient goes to bed, falls asleep, but is then woken 1–2 hours later with severe pa in in the foot, usually in the instep. The pain is due

to poor perfusion resulting from the loss of the beneficial effects of gravity on lying down and the reduction in heart rate, BP and cardiac

output that occurs when sleeping. Patients often obtain relief by hanging the leg out of bed or by getting up and walking around.

However, on return to bed, the pain recurs and patients often choose to sl eep in a chair. This

128

leads to dependent oedema, increased interstitial tissue pressure, a further reduction in tissue perfusion and ultimately a worseni ng of

the pain.

Rest (night) pain indicates severe, multilevel lower limb PAD and is a ‘red flag’ symptom that mandates urgent referral to a vascular

surgeon as failure to revascularise the leg usually leads to the development of critical lim b ischaemia with tissue loss (gangrene,

ulceration) and amputation.

In diabetic patients it may be difficult to differentiate between rest pain and diabetic neuropathy as both may be worse at night.

Neuropathic pain is not usually confined to the foot, is associated with burning and t ingling, is not relieved by dependency and is

associated with dysaesthesia (pain or uncomfortable sensations sometimes described as burn ing, tingling or numbness). Many patients

cannot even bear the pressure of bedclothes on their feet.

Tissue loss (ulceration

and/or gangrene)

In patients with severe lower limb PAD, even trivial injuries to the feet fail to heal. This allows bacteria to enter, leading to gangrene

and/or ulceration. This usually progresses rapidly and, without revascularisation, often lead s quickly to amputation and/or death.

Signs of lower limb PAD

Ischaemic signs include absence of hair, thin skin and brittle nails ( Box 6.34). The presence of foot pulses does not completely exclude

significant lower limb PAD but they are almost alway s diminished or absent. If the history is convincing but pulses are felt, ask the

patient to walk until the claudication pain stops him and then recheck the pulses; if they have disappeared then PAD is very likely.

6.35 Signs of acute limb ischaemia

Soft signs

• Pulseless • Perishing cold

• Pallor

Hard signs (indicating a threatened limb)

• Paraesthesia • Pain on squeezing muscle

• Paralysis

6.36 Acute limb ischaemia: embolus versus thrombosis in situ

Onset and severity

Embolic source

claudication

Pulses in

contralateral leg Diagnosis

Treatment

Embolus

Acute (seconds or minutes), ischaemia profound (no

pre-existing

collaterals)

Present (usually

atrial fibrillation)

Absent

Thrombosis

Insidious (hours or days), ischaemia less severe

(pre-existing

collaterals)

Absent

Present

Present Often absent

Clinical

Embolectomy and anticoagulation Angiography

Medical, bypass surgery,

thrombolysis

Patients with critical limb ischaemia (rest pain, tissue loss) typically have an ankle BP <50 mmHg and a positive Buerger’s test.

Acute limb ischaemia

The classical features of acute limb ischaemia are the ‘six Ps’ (Box 6.35). Paralysis (inability to wiggle the toes/ fingers) and

paraesthesia (loss of light touch sensation over the forefoot/dorsum of the hand) are the most important and indicate severe ischaemia

affecting nerve function. Muscle tenderness is a grave sign indicating impending muscle infarction. A limb with these features will

usually become irreversibly damaged unless the circulation is re stored within a few hours.

The commonest causes of acute limb ischaemia are:

• Thromboembolism: usually from the left atrium in association with atrial fibrillation

• Thrombosis in situ: thrombotic occlusion of an already narrowed atherosclerotic ar terial segment (Box 6.36).

Acute arterial occlusion produces intense spasm in the

arterial tree distal to the blockage. The limb appears

‘marble white’. Over a few hours, the spasm relaxes

and the skin microcirculation fills with deoxygenated

blood, leading to light blue or purple mottling, which

has a fine reticular pattern and blanches on pressure. As

ischaemia progresses, blood coalesces in the skin, producing a coarser pattern of mottling which is dark

Fig. 6.36 Gangrene of the foot.

purple, almost black, and does not blanch. Finally, large patches of fixed staining lea d to blistering and liquefaction. Fixed mottling of an

anaesthetic, paralysed limb, with muscle rigidity and turgor, indicates irreversible ischaemia; amputation or end-of-life care is the only

option (Fig. 6.36).

Compartment syndrome occurs where there is increased pressure within the fascial compartments of the limb, most commonly the calf,

which compromises perfusion and viability of muscle and nerves. The two commonest causes are lower trauma, e.g. fractured tibia, and

reperfusion following treatment of acute lower limb ischaemia. Failure to recognise a nd treat compartment syndrome may require limb

amputation. The key symptom is severe pain often unrelieved by opioids and exacerba ted by active or passive movement. Peripheral

pulses are usually present.

Stroke

Stroke is a focal central neurological deficit of vascular cause. Approximately 8 0% of strokes are ischaemic rather than haemorrhagic.

Transient ischaemic attack (TIA) describes a stroke in which symptoms resolve within 24 hours. The term ‘stroke’ is reserved for those

events in which symptoms last for more than 24 hours.

Carotid artery territory

(anterior circulation)

Up to half of all strokes and TIAs are due to embolism from an atheromatou s plaque at the origin of the internal

129

6.37 Imaging in suspected carotid territory transient ischaemic attack (TIA) or stroke All pat ients with suspected carotid territory

TIA or stroke should

undergo urgent duplex Doppler ultrasound imaging as the

finding of a carotid bruit is unreliable in detecting or excluding

significant carotid disease that may be an indication for

endarterectomy.

Sauve J-S, Laupacis A, Ostbye T et al. Does this patient have a clinically impor tant carotid bruit? In: Simel D, Rinne D

(eds) The rational clinical examination. New York: JAMA and Archives Journa ls/McGraw-Hill Professional, 2008, pp. 103–

110.

carotid artery. Clinical features vary according to the cerebral area involved but can include motor deficit, visual f ield defect, e.g.

homonymous hemianopia (Fig. 12.3), or difficulty with speech (dysphasia, p. 250) (Box 6.37).

Vertebrobasilar artery territory (posterior circulation)

TIAs and strokes in this territory cause giddiness, collapse with or without loss of consciousness, transient occipital blindness or

complete loss of vision in both eyes (Ch. 11). Subclavian artery stenosis or occlusion proximal to the origin of the vertebral artery may

cause vertebrobasilar symptoms as part of the ‘subclavian steal’ syndrome. This happens when the arm is exercised. The increased blood

supply requirement in the arm is met by blood travelling up the carotid arteries and then, via the circle of Willis (Fig. 11.29), down the

vertebral artery into the arm, so ‘stealing’ blood from the posterior cerebral circulation. Signs of this include asymmetry of the pulses and

BP in the arms, sometimes with a bruit over the subclavian artery in the supraclavicular fossa.

Abdominal symptoms

Mesenteric angina

Because of the rich collateral circulation, usually two of the three major visceral arte ries (coeliac axis, superior and inferior mesenteric

arteries) must be critically stenosed or occluded before symptoms and signs of chronic mesen teric arterial insufficiency occur. Severe

central abdominal pain typically develops 10–15 minutes after eating. The patient becomes sc ared of eating and significant weight loss is

a universal finding. Diarrhoea may occur and visceral ischaemia may mim ic a whole range of gastrointestinal pathologies. The patient

may have had numerous investigations, even laparotomy, before the diagnosis is made and confirmed by angiography. Any patie nt

suspected of visceral ischaemia should undergo urgent angiography.

Acute mesenteric ischaemia is a surgical emergency. The patient presents with sever e abdominal pain, shock, bloody diarrhoea and

profound metabolic acidosis. Rarely, renal angle pain occurs from ren al infarction or ischaemia, and is associated with microscopic or

macro

130

scopic haematuria.

Fig. 6.37 Abdominal aortic aneurysm. (A) Abdominal X-ray showing

calcification (arrow). (B) Computed tomography of the abdomen showing an abdominal aortic aneurysm (arrow). (C) At

laparotomy the aorta is seen to be grossly and irregularly dilated.

Abdominal aortic aneurysm

AAA is an abnormal dilatation of the aorta ( Fig. 6.37) and is present in 5% of men aged >65 years. The m ain risk factors are smoking

and hypertension; there is also a familial/genetic element to the disease. AAA i s three times more common in men than women. Most

patients are asymptomatic until the aneurysm ruptures, although they may present with abdominal and/or back pain or an awareness of

abdominal pulsation.

Clinical examination is unreliable in establishing the presence or size of an AAA ; if in any doubt, obtain an ultrasound scan of the aorta.

In the UK there is now an ultrasound-based AAA screening programme for men as they reach their 65th birthday.

Fig. 6.38 Raynaud’s syndrome. (A) The acute phase, showing severe blanching o f the tip of one finger. (B) Primary

Raynaud’s syndrome occasionally progresses to fingertip ulceration or even gan grene.

A ruptured AAA can be difficult to diagnose because many patients do not have the classical features of abdominal and/or back pain,

pulsatile abdominal mass and shock (hypotension). The most common misdiagno sis is renal colic (a man, >60 years, presenting with

‘renal colic’ has a ruptured AAA until proved otherwise). If there is any suspicion of a ruptured AAA speak to a vascular surgeon straight

away who will probably request an immediate contrast-enhanced CT of the abdomen (if the p atient is cardiovascularly stable).

Athero-embolism from an AAA can cause ‘blue toe syndro me’, characterised by purple discoloration of the toes and forefoot of both

feet. There is usually a full set of pedal pulses.

Vasospastic symptoms

Raynaud’s phenomenon is digital ischaemia induced by cold and em otion and has three phases (Fig. 6.38):

• Pallor: due to digital artery spasm and/or

obstruction

• Cyanosis: due to deoxygenation of static venous

blood (this phase may be absent)

• Redness: due to reactive hyperaemia.

Raynaud’s phenomenon may be primary (Raynaud’s disease) an d due to idiopathic digital artery vasospasm, or secondary (Raynaud’s

syndrome) (Box 6.38).

Patients >40 years old presenting with unilateral Raynaud’s phenomenon have underlying PAD unles s proven otherwise, especially if

they have risk factors (smoking, diabetes).

6.38 Diseases associated with secondary

Raynaud’s syndrome

• Connective tissue syndromes, e.g. systemic sclerosis,

CREST (calcinosis, Raynaud’s phenomenon, oesophageal dysfunction, sclerodactyly, telan giectasia) and systemic

lupus erythematosus

• Atherosclerosis/embolism from proximal source, e.g.

subclavian artery aneurysm

• Drug-related, e.g. nicotine, beta-blockers, ergot

• Thoracic outlet syndrome

• Malignancy

• Hyperviscosity syndromes, e.g. Waldenström’s

macroglobulinaemia, polycythaemia

• Vibration-induced disorders (power tools)

• Cold agglutinin disorders 6

THE HISTORY

Ask about risk factors for atheroma (smoking, hypercholesterolaemia, hypertension, diabetes mellitus) and any family history of

premature arterial disease. Specifically ask about diabetes because it is associated with the early development and rapid progression of

widespread atheroma.

The impact of intermittent claudication relates to the patient’s age and lifestyle. A postman/p ostwoman who can walk only 400 metres

has a serious problem, but an elderly person who simply wants to cross the ro ad to the shops may cope well. Rather than focusing upon

absolute distances, ask specific questions like:

• Can you walk to the clinic from the bus stop or car

park without stopping?

• Can you do your own shopping?

• What can’t you do because of the pain?

Ask about the patient’s other medical conditions. There is little point in subjecting patients with intermittent claudication to the risks of

vascular surgery, only to find that they are then equally limited by osteoarthritis of the hip, angina or severe breathlessness.

Male patients with buttock (gluteal) intermittent claudication due to internal iliac dis ease have erectile dysfunction. Ask about sexual

function as many men and their partners are extremely concerned by erectile dysfunction yet too embarrassed to mention it.

THE PHYSICAL EXAMINATION

Follow the routine described for the heart, looking for evidence of anaemia or cyanosis, signs of heart failure, and direct or indirect

evidence of PAD (Box 6.39). Then perform a detailed examination of the arterial pulses. Abnormally prominent pulsation in the neck of

an elderly person is rarely of clinical significance and is normally caused by tort uous arteries rather than a carotid aneurysm or carotid

body tumour. However, if in any doubt, arrange for a duplex ultrasound sca n.

131

6 6.39 Signs suggesting vascular disease

Sign

Hands and arms

Tobacco stains

Purple discoloration of the fingertips

Pits and healed scars in the finger pulps

Calcinosis and visible nailfold capillary loops

Wasting of the small muscles of the hand

Face and neck

Corneal arcus and

xanthelasma

Horner’s syndrome

Hoarseness of the voice and ‘bovine’ cough

Prominent veins in the neck, shoulder and anterior chest

Abdomen

Epigastric/umbilical pulsation Mottling of the abdomen

Evidence of weight loss Smoking

Atheroembolism from a

proximal subclavian aneurysm Secondary Raynaud’s

syndrome

Systemic sclerosis and CREST (calcinosis, Raynaud’s

phenomenon, oesophageal dysfunction, sclerodactyly, telangiectasia)

Thoracic outlet syndrome

Implication

Hypercholesterolaemia

Carotid artery dissection or aneurysm

Recurrent laryngeal nerve palsy from a thoracic aortic aneurysm

Axillary/subclavian vein occlusion

Aortoiliac aneurysm

Ruptured abdominal aortic aneurysm or saddle embolism occluding aortic bifurcation

Visceral ischaemia

Examination sequence

Start at the patient’s head and work down the body, using the sequence and p rinciples of inspection, palpation and

auscultation for each area.

The arms

■ Examine the radial and brachial pulses (p. 108 and

Fig. 6.10 ).

■ Measure the BP in both arms.

The abdomen

■ Look for obvious pulsation.

■ Palpate and listen over the abdominal aorta. The aortic

bifurcation is at the level of the umbilicus, so feel in the epigastrium for a palp able AAA. If the aorta is easily palpable,

consider the possibility of an AAA. In thin patients a tortuous but normal-diame ter aorta can feel aneurysmal. If in any

doubt, arrange a duplex ultrasound scan. A pulsatile mass below the umbilicus suggests an iliac aneurysm.

The legs

■ Inspect and feel the legs and feet for changes of ischaemia, including te mperature and colour changes.

■ Note scars from previous vascular or non-vascular surgery and

132

the position, margin, depth and colour of any

ulceration.

Femoral nerve Femoral artery Femoral vein

Fig. 6.39 Femoral triangle: vessels and nerves.

■ Look specifically between the toes for ulcers and at the heels for ischae mic changes (commonest site of ‘pressure sores’).

Femoral pulse

■ Ask the patient to lie down and explain what you are going to do.

■ Place the pads of your index and middle fingers over the femoral artery . It can be difficult to feel in the obese.

■ Listen for bruits over both femoral arteries, using the stethoscope diaphra gm (Figs 6.39 and 6.40A).

Popliteal pulse

■ Ask the patient to lie on a firm comfortable surface and relax.

■ Flex the patient’s knee to 30°.

■ With your thumbs in front of the knee and your fingers behind, press firmly in the midline over the popliteal artery.

■ Then slide your fingers 2–3 cm below the knee crease and try to comp ress the artery against the back of the tibia as it

passes under the soleal arch (Fig. 6.40B).

Posterior tibial pulse

■ Feel 2 cm below and 2 cm behind the medial malleolus, using the pads o f your middle three fingers (Fig. 6.40C).

Dorsalis pedis pulse

■ Using the pads of your middle three fingers, feel in the middle of the d orsum of the foot just lateral to the tendon of

extensor hallucis longus (Fig. 6.40D).

Buerger’s test

Examination sequence

■ With the patient lying supine, stand at the foot of the bed. Raise the pati ent’s feet and support the legs at 45° to the

horizontal for 2–3 minutes.

■ Watch for pallor with emptying or ‘guttering’ of the superficial veins.

■ Ask the patient to sit up and hang the legs over the edge of the bed.

■ Watch for reactive hyperaemia on dependency; the loss of pallor and sp reading redness is a positive test.

Ankle to brachial pressure index

Assessing pulse status can be unreliable in patients

with obesity or oedema. Routinely measure ABPI in all patients with difficulty palpating lower limb pulses or where PAD is suspected

on the basis of history.

6.40 Investigations in peripheral arterial disease

Investigation

Blood tests

Full blood count and erythrocyte sedimentation rate

Urine and electrolytes Blood glucose

Serology

Microbiology

Bacteriology

Radiology

Doppler ultrasound

B-mode ultrasound

Duplex ultrasound

Computed tomography

Magnetic resonance imaging

Angiography

Indication/comment

Anaemia unmasking symptoms and connective tissue disease

Renal function

Hypertension more common in diabetes

Connective tissue disease

Swab base of ulcer

Ankle pressure, ankle to brachial pressure index, pulse waveform analysis

Abdominal aortic aneurysm, popliteal artery aneurysm

Carotid artery stenosis, vein bypass graft surveillance

Abdominal aortic aneurysm, detection of cerebral infarct/ haemorrhage

Arteriovenous malformations, carotid artery stenosis

Acute and chronic limb ischaemia, carotid artery stenosis

Fig. 6.40 Examination of the femoral, popliteal, posterior tibial and dorsalis pedis arteries. (A) Examine the femoral artery, while

simultaneously checking for radiofemoral delay. (B) Feel the popliteal artery wit h the fingertips, having curled the fingers

into the popliteal fossa. (C) Examination of the posterior tibial artery. (D) Exa mination of the dorsalis pedis artery.

• Use a hand-held Doppler and a

sphygmomanometer

• Hold the probe over the posterior tibial artery

• Inflate a BP cuff round the ankle

• Note the pressure when Doppler signal disappears. This is the systolic pressure in that arte ry as it passes under the cuff

• Repeat holding the probe over dorsalis pedis, and then the perforating peroneal (Box 6.13 )

• Measure the brachial BP in both arms, holding the Doppler probe over the b rachial artery at the elbow of the radial artery at the wrist.

Normal findings The ratio of the highest pedal artery pressure to the highest brachial artery pressure is the ABPI. In health, the ABPI is

>1.0 when the patient is supine. The poplitea l artery is always hard to feel – if you feel it easily, consider an aneurysm.

Abnormal findings

Typical values in intermittent claudication and critical limb ischaemia are <0.9 and <0.4 respec tively. Absolute values may be less

informative than the trend over time.

Patients with lower limb PAD, particularly those with diabetes mellitus, often have incompressible, calcified crural arteries with falsely

elevated pedal pressures and ABPI. Use a Doppler ultrasound probe to detect the foot arteries while elevating the foot. The Doppler

signal disappears at a height (in cm) above the bed that approximates to the perfusi on pressure (in mmHg).

Choose further tests to provide the most information at the least risk to the patien t and at least expense. In most situations duplex

Doppler ultrasound has replaced angiography as the first-line investigation of choice (Box 6.40).

133

6 PERIPHERAL VENOUS SYSTEM

Whereas venous return from the head and neck is passive, that from the legs m ust be actively pumped back up to the heart against

gravity. Pressure on the sole of the foot on walking, together with contraction o f muscles in the calf (the ‘calf muscle pump’), and, to a

lesser extent in the thighs and buttocks, forces venous blood back up deep (90%) and superficial (10%) veins. Backward flow (reflux) is

prevented by valves which divide the long column of blood from the foot to the right atrium into a series of short low-pressure segments.

As a result, the ‘ambulatory venous pressure’ in the feet in health is usually <20 mmHg. The gre at majority of lower limb venous

symptoms and signs are due to failure of the muscle pump and/or valves and the r esulting ‘ambulatory venous hypertension’.

Deep veins follow the course of the main arteries; are often paired; and may be affected by primary or postthrombotic (following DVT)

valvular insufficiency. DVT often leads to deep venous obstruction as well as ref lux

Femoral vein

Profunda femoris vein

Popliteal vein

Short saphenous vein

Dorsal venous arch

134

Fig. 6.41 Veins of the lower limb. Great saphenous vein

Venae comitantes of posterior and anterior tibial

arteries

(leading to the symptoms and signs of the postthrombotic syndrome).

Superficial veins may also be affected by primary valvular failure and by refl ux following superficial thrombophlebitis.

The great (long) saphenous vein passes anterior to the medial malleo lus at the ankle, up the medial aspect o f the calf to behind the knee,

then up the medial aspect of the thigh to join the common femoral vein in the groin at the saphenofemoral junction (Fig. 6.41).

The lesser (short) saphenous vein passes behind the lateral malleolus at the ankle and up the posterior aspect of the calf. It commonly

joins the popliteal vein at the saphenopopliteal junction, which usua lly lies 2 cm above the posterior knee crease.

There are numerous intercommunications between the long and short saphenous, a nd between the deep and superficial venous (via

perforating or communicating veins) systems; and the venous anatomy of the leg is highly varia ble.

CLINICAL PRESENTATION

Lower limb venous disease presents in four ways:

• Varicose veins

• Superficial thrombophlebitis

• DVT

• Chronic venous insufficiency and ulceration. The severity of symptoms and signs ma y bear little relationship to the severity of the

underlying pathology and the physical signs. Life-threatening DVT may be asymptomatic, whil e apparently trivial varicose veins may be

associated with significant complaints.

Pain

Patients with uncomplicated varicose (dilated, tortuous, superficial) veins often co mplain of aching leg discomfort, itching and a feeling

of swelling. Symptoms are aggravated by prolonged standing and are often worse towards the end of the day. Once established, DVT

causes pain and tenderness in the affected part (usually the calf). Superficia l thrombophlebitis produces a red, painful area overlying the

vein involved. Varicose ulceration may be surprisingly painless; if it is painful , this may be relieved by limb elevation (but exclude

coexisting arterial disease) (Box 6.41). Bandaging for a leg ulcer is contr aindicated unless there is documented evidence of adequate

arterial circulation. Do this by feeling the pulses or by measuring the ABPI.

Great saphenous vein

Swelling

Swelling (or oedema), or a ‘feeling of swelling’, may be associated with lower limb venou s disease.

Discoloration

Chronic venous insufficiency is associated with lipodermatosclerosis, which results from the deposition of haemosiderin (from the

breakdown of extravasated blood) in the skin. Lipodermatosclerosis varies in colour

Clinical presentation

6.41 Clinical features of venous and arterial ulceration Clinical feature Age

Sex

Past medical history

Risk factors

Venous ulceration

Develops at age 40–45 but may not present for years; multiple recurrences common

More common in women

Deep vein thrombosis (DVT) or suggestive of occult DVT, i.e. leg swelling after childbir th, hip/knee replacement or long bone fracture

Thrombophilia, family history, previous DVT

Pain

Site

Margin

Base

Surrounding skin Veins

Swelling (oedema) Temperature

Pulses

One-third have pain (not usually severe) that improves with elevating the leg

Gaiter areas; usually medial to long saphenous vein; 20% are lateral to short saphenous vein Irr egular, often with neoepithelium (appears

whiter than mature skin)

Often pink and granulating under green slough

Arterial ulceration

First presents in over-60s

More common in men

Peripheral arterial disease, cardio- and cerebrovascular disease

Smoking, diabetes, hypercholesterolaemia and

hypertension

Severe pain, except in diabetics with neuropathy;

improves on dependency 6 Pressure areas (malleoli, heel, fifth metatarsal base,

metatarsal heads and toes)

Regular, indolent, ‘punched out’

Lipodermatosclerosis always present Full and usually varicose

Usually present

Warm

Present, but may be difficult to feel Sloughy (green) or necrotic (black), with no granu lation No venous skin changes

Empty with ‘guttering’ on elevation

Absent

Cold

Absent

from deep blue/black to purple or bright red and usually affects the medial aspect of the lower third of the leg, although it may be lateral

if superficial reflux predominates in the lesser saphenous vein.

Chronic venous ulceration

In developed countries about 70–80% of leg ulcers are due primarily to venous disease. Other causes include pyoderma gangrenosum,

syphilis, tuberculosis, leprosy, sickle cell disease and tropical conditions. Chronic venous ulceration usually affects the medial aspect, is

shallow; is pink (granulation tissue) or yellow/ green (slough); has an irregular margin; and is always associated with other skin changes

of chronic venous insufficiency (varicose eczema, lipodermatosclerosis) (Fig. 6.42).

Deep vein thrombosis

The leg

The clinical features of DVT depend upon its site, extent and whether it is occlusive or not (Box 6.42 ). The so-called ‘classical’ features

of DVT relate to well-established occlusive thrombus. Most patients who die from pulmonary embolism have non-occlusive thrombosis

and the leg is normal on clinical examination. Non-occlusive DVT poses the greatest threat of pulmonary embolism as the clot lies

within a flowing stream of venous blood, is more likely to propagate and has not yet induced an inflammatory response in the vein wall

to anchor it in place. Risk factors for DVT are listed in Box 6.43 . Perform an urgent duplex Doppler ultrasound scan of the leg in any

patient with a suspected DVT.

Fig. 6.42 Venous ulceration.

The arm

Axillary subclavian vein thrombosis can occur as a result of repetitive trauma at the thoracic out let due to vigorous, repetitive exercise.

Upper limb DVT may also complicate indwelling subclavian/jugular venous catheters. Symptoms include arm swelling and discomfort,

often exacerbated by activity, especially when holding the arm overhead.

135

6.42 Features of deep vein thrombosis of the lower limb

Clinical feature

Pain

Calf tenderness Swelling

Temperature

Superficial veins

Pulmonary embolism

Non-occlusive thrombus

Often absent

Absent

Normal or slightly increased

Normal

High risk

Occlusive

thrombus

Usually present

Usually present Present

Increased

Distended Low risk

The arm is swollen and the skin is cyanosed and mottled, especially when dependent. Look for superficial distended veins (acting as

collaterals) in the upper arm, over the shoulder region and on the anterior chest wall (Fig. 6 .43).

Superficial venous thrombophlebitis

This condition affects up to 10% of patients with severe varicose veins and is more common duri ng pregnancy. Recurrent superficial

venous thrombophlebitis, especially affecting different areas sequentially and nonvaricose veins, m ay be associated with underlying

malignancy. It may propagate into the deep system, leading to DV T and pulmonary embolism.

6.43 Risk factors for deep vein thrombosis

• Recent bed rest or operations (especially to the leg, pelvis or abdomen)

• Recent travel, especially long flights

• Previous trauma to the leg, especially long-bone fractures, plaster of Paris splintage and im mobilisation

• Pregnancy or features to suggest pelvic disease

• Malignant disease

• Previous deep vein thrombosis

• Family history of thrombosis

• Recent central venous catheterisation, injection of drugs, etc.

Fig. 6.43 Axillary vein thrombosis. (A) Angiogram. Single arrow

shows site of thrombosis. Double arrows show dilated collateral vessels.

136

(B) Clinical appearance with swollen left arm

and dilated superficial veins.

The physical examination

Examination sequence

Expose the patient’s legs and examine them with the patient standing and then l ying supine.

■ Inspect the skin for colour changes, swelling and superficial

venous dilatation and tortuosity.

■ Feel for any temperature difference.

■ Press with your fingertip above the ankle medially for a few

seconds (gently, as this can be painful; do not do this near an ulcer) and then see if your finger has left a pit (pitting

oedema). ■ If the leg is grossly swollen, press at a higher level to establish how far oedema extends.

■ If you find oedema, check the JVP (p. 114). If the JVP is raised, this suggests cardiac disease or pulmonary

hypertension as a cause.

■ Elevate the limb to about 15° above the horizontal and note the rate of venous emptying.

■ If appropriate, perform the Trendelenburg test to detect saphenofemoral j unction reflux.

The Trendelenburg test

Examination sequence

■ Ask the patient to sit on the edge of the examination couch. ■ Elevate the limb as far as is comfortable for the patient

and empty the superficial veins by ‘milking’ the leg towards

the groin.
■  With the patient’s leg still elevated, press with your thumb over 
the sapheno-femoral junction (2–3 cm below and 2–3 cm 
lateral to the pubic tubercle). A high thigh tourniquet can  
be used instead.
■  Ask the patient to stand while you maintain pressure over 
the saphenofemoral junction.
■  If saphenofemoral junction reflux is present, the patient’s 
varicose veins will not fill until your digital pressure, or the 
tourniquet, is removed.
Clinical examination is unreliable, and all patients being co nsidered for treatment should undergo a colour flow duplex, Doppler
ultrasound scan before intervention.
SECTION 2 SYSTEM EXAMINATION
Graham Devereux Graham Douglas
RESPIRATORY EXAMINATION 138 Anatomy 139
Symptoms and definitions 139
Cough 139
Dysphonia (hoarseness) 140 Wheeze 140
Stridor 140
Stertor 140
Sputum 140
Haemoptysis 141
Dyspnoea 142
Chest pain 143
Respiratory pattern 143
The respiratory system7
The history 144
The physical examination 146
Putting it all together 155
Investigations 155
RESPIRATORY EXAMINATION
Face 4
• Central cyanosis
• Ptosis/Horner’s syndrome
Neck 3
• Cervical/scalene lymphadenopathy
• JVP
• Accessory muscle use
5 Chest
• Inspect scars
deformity: scoliosis,
kyphoscoliosis,
pigeon chest
• Palpation
mediastinal shift: tracheal deviation, cardiac apex beat, expansion
• Percussion
resonant – normal
dull – collapse or consolidation ‘stony dull’ – effusion
hyper-resonant – pneumothorax
• Auscultation
breath sounds
vesicular – normal
bronchial – consolidation
added sounds
crackles – pulmonary oedema, fibrosis or infection
wheeze – asthma, COPD

6 Abdomen

• Hepatomegaly

• Sacral oedema

Hands 2

• Clubbing

• Peripheral cyanosis

• Tobacco staining

• CO

retention flap

General observation 1

• Respiratory rate

• Body mass (obesity, weight loss)

• Fever

• Confusion

• Distress, demeanour

7 Legs

• Bilateral oedema – cor pulmonale

• Unilateral oedema – deep vein

thrombosis

ANATOMY

The respiratory system comprises the upper airway; the nose, mouth, oropharynx and larynx, and the lower airway; the trachea and

lungs. The left lung only contains 45% of the total surface area available for gas exchange, because the heart lies principally within the

left side of the chest. The right lung has three lobes (upper, middle and lower) and the left, tw o (upper and lower) (Fig. 7.1).

The airways (bronchi) transport air to the alveoli o n inspiration and carry waste gases, e.g. carbon dioxide, away on expiration. The gas

exchange unit of the lung is the acinus, with branching bronchiol es leading to clusters of alveoli (Fig. 7.2). Alveoli are tiny air sacs lined

by flattened epithelial cells (type I pneumocytes) and covered in capillaries where gas exchange occurs. T he alveoli and capillaries have

extremely thin walls and come into very close contact (the alveolar–capillary membrane); carbon dioxide and oxygen readily diffuse

between them. There are approximately 300 million alveoli in each lung, with a total surface area for gas exchange of 40–80 m

The lung has two blood supplies: the bronchial arteries arise from the aorta and supply oxygenated blood to the bronchial walls. The

pulmonary arteries circulate deoxygenated blood to the capillaries surrounding the alveol i.

A 1 & 2 6 1 & 2

5 3 4 2

1 Pleural markings

2 Lung markings

3 Cardiac notch 4 Oblique fissure 5 Horizontal fissure 6 Trachea

Right upper lobe 4

Middle lobe Right lower lobe

Liver

B 5

SYMPTOMS AND DEFINITIONS

Cough

Cough is a characteristic sound caused by a forced expulsion against an initially closed glottis. Acute cough is one lasting less than 3

weeks; chronic cough lasts more than 8 weeks. The most common cause of acute cough is acute upper respiratory tract viral infection.

Acute cough is usually self-limiting and benign, but may occur in more serious conditions ( Box 7.1). Chronic cough in a non-smoker

with a normal chest X-ray is usually caused by gastro-oesophageal reflux disease, chronic sinus disease with postnasal drip or

angiotensin-converting enzyme inhibitors (Box 7.2).

Severe asthma or chronic obstructive pulmonary disease (COPD) causes prolonged wheezy cough and often a paroxysmal dry cough

after a viral infection that lasts several months (bronchial hyperreactivity).

A feeble non-explosive ‘bovine’ cough with hoarseness suggests lung cancer invading the left recurrent laryngeal nerve causing left

vocal cord paralysis, but may also occur with respiratory muscle weakness due to neuromuscula r disorders.

Laryngeal inflammation, infection or tumour causes harsh, barking or painful coughs a nd associated hoarseness and the rasping or

croaking inspiratory sound of stridor (p. 142). A moist cough suggests secretions in the upper a nd larger airways from bronchial infection

and bronchiectasis. A persistent moist ‘smoker’s cough’ first thing in the morning is typical of chronic bronchitis. Smokers often

consider this normal but any change in this cough may indicate lung cancer. Tracheitis and