The RCEM Lecture Notes E-Book
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- Herausgeber: John Wiley & Sons
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- Serie: Lecture Notes
- Sprache: Englisch
The RCEM Lecture Notes: Emergency Medicine 5th Edition Comprehensive introduction to the core specialty area of emergency medicine Presented in a user-friendly format, combining flowcharts and high-quality illustrations together for an easy-to-read experience, this fifth edition of The RCEM Lecture Notes: Emergency Medicine has been thoroughly revised to reflect recent advances in the field of emergency medicine and to give readers a comprehensive and highly accessible overview of the field. The RCEM Lecture Notes: Emergency Medicine, Fifth Edition presents important 'need to know' information for all those involved in treating patients in an emergency setting. The text serves as an excellent starting point to support initial teaching on the subject and reference or revision at the end of a module, rotation, or final exams. Contributions made by a variety of healthcare professionals with significant firsthand experience in the field, The RCEM Lecture Notes: Emergency Medicine contains information on: * Major trauma and injuries. * Burns, contamination, irradiation, and poisoning. * Acute medical, surgical and obstetric conditions relevant to emergency medicine. * Paediatric emergency medicine. * Mental health and medicolegal aspects of emergency medicine. For more information on the complete range of Wiley medical student and junior doctor publishing, please visit: www.wiley.com To receive automatic updates on Wiley books and journals, join our email list. Sign up today at www.wiley.com/email This new edition is also available as an e-book. For more details, please see http://www.wiley.com/buy/9781119325819 All content reviewed by students for students Wiley Medical Education books are designed exactly for their intended audience. All of our books are developed in collaboration with students. This means that our books are always published with you, the student, in mind. If you would like to be one of our student reviewers, go to www.reviewmedicalbooks.com to find out more.
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Table of Contents
Cover
Table of Contents
Title Page
Copyright Page
List of contributors
Preface to the fifth edition
Preface to the fourth edition
Preface to the second edition
Preface to the first edition
About the Companion Website
1 What every Emergency Physician needs to know
EMERGENCY ASSESSMENT OF THE UNDIFFERENTIATED PATIENT
FURTHER MANAGEMENT IN THE ED
SEDATION AND GENERAL ANAESTHESIA
2 Major trauma and multiple injuries
TRAUMA CARE
PRIMARY SURVEY AND RESUSCITATION
FURTHER CARE OF THE TRAUMA PATIENT
SPECIAL SITUATIONS
OTHER ASPECTS OF TRAUMA CARE
3 Head injuries
THE PATIENT WITH A DEPRESSED LEVEL OF CONSCIOUSNESS
THE AMBULANT PATIENT WITH A HEAD INJURY
SPECIFIC INJURIES
4 The neck and the back
INJURY TO THE SPINAL CORD
IMAGING AND CLEARANCE OF THE SPINE IN TRAUMA
NECK AND BACK INJURIES
WOUNDS TO THE NECK AND BODY
5 Facial injuries
FRACTURES OF THE FACIAL BONES
FACIAL WOUNDS
INJURIES INSIDE THE MOUTH
INJURIES TO THE EAR
INJURIES AROUND THE EYE
6 Injuries to the trunk
CHEST INJURIES
ABDOMINAL INJURIES
PELVIC INJURIES
7 The lower limb
GENERAL APPROACH TO LIMB PROBLEMS
THE HIP AND THIGH
THE KNEE
THE LOWER LEG
THE ANKLE
THE FOOT
VASCULAR CONDITIONS OF THE LOWER LIMB
8 The upper limb
THE SHOULDER AND UPPER ARM
THE ELBOW
THE FOREARM AND WRIST
FOREARM FRACTURES IN CHILDREN
VASCULAR PROBLEMS IN THE UPPER LIMB
9 The hand
IMMEDIATE ASSESSMENT AND MANAGEMENT
WOUNDS TO THE HAND
METACARPAL FRACTURES
BONE AND JOINT INJURIES OF THE FINGERS
THUMB INJURIES
HAND INFECTIONS
10 Burns, contamination and irradiation
LARGE BURNS
SMALL BURNS
SPECIAL BURNS
ELECTROCUTION
CONTAMINATION AND IRRADIATION
11 Cardiac arrest and cardiac dysrhythmias
CARDIAC DYSRHYTHMIAS
12 Chest pain
IMMEDIATE ASSESSMENT AND MANAGEMENT
MI AND THE ACUTE CORONARY SYNDROMES
OTHER SERIOUS CAUSES OF CHEST PAIN
13 Respiratory distress
THE UPPER AIRWAYS
THE LOWER AIRWAYS AND LUNGS
14 Collapse and sudden illness
COLLAPSE
NEUROLOGICAL PROBLEMS
CONDITIONS RELATED TO ENVIRONMENT AND EXPOSURE
CARDIOVASCULAR PROBLEMS
METABOLIC AND ENDOCRINE DISORDERS
ZOONOSES AND DISEASES RELATED TO TRAVEL
HAEMATOLOGICAL CONDITIONS
DERMATOLOGICAL CONDITIONS
15 Poisoning
GENERAL PRINCIPLES IN POISONING
POISONING WITH COMMON MEDICINES
POISONING WITH RECREATIONAL AND ILLEGAL DRUGS
POISONING WITH SUBSTANCES FOUND AT HOME AND AT WORK
POISONING WITH HARMFUL AGENTS THAT HAVE BEEN RELEASED INTO THE ENVIRONMENT
FURTHER CONSIDERATIONS IN POISONING
ATYPICAL REACTIONS TO DRUGS AND OTHER SUBSTANCES
16 Abdominal pain and GI problems
ELDERLY PATIENTS WITH ABDOMINAL PAIN
PAIN AND BLEEDING IN THE OESOPHAGUS AND UPPER ABDOMEN
PAIN AND BLEEDING IN THE CENTRAL AND LOWER ABDOMEN
PAIN FROM THE GENITOURINARY TRACT
PERINEAL PROBLEMS
17 Obstetric, gynaecological and genitourinary problems
OBSTETRIC PROBLEMS
GYNAECOLOGICAL PROBLEMS
GENITOURINARY PROBLEMS
18 Children's problems in the emergency department
IN THE UK IN 2021 (BASED ON MOST RECENT DATA)
IMMEDIATE ASSESSMENT AND MANAGEMENT
FURTHER ASSESSMENT OF THE CHILD
RESPIRATORY PROBLEMS
OTHER MAJOR ILLNESSES IN CHILDHOOD
COMMON PAEDIATRIC PRESENTATIONS
NEONATAL PRESENTATIONS
SAFEGUARDING ISSUES AND NON ACCIDENTAL INJURY
19 The disturbed patient
INITIAL ASSESSMENT AND MANAGEMENT OF THE DISTURBED OR DISTRESSED PATIENT
CONFUSION AND PSYCHOTIC BEHAVIOUR
ALCOHOL‐RELATED PROBLEMS
DEPRESSED MOOD AND SELF‐HARM
SPECIAL SITUATIONS
20 Medicolegal aspects of emergency medicine
CLINICAL FORENSIC MEDICINE
ALCOHOL AND OTHER DRUGS/FITNESS TO DRIVE
LEGAL ISSUES
RESPONSIBILITIES TO CHILDREN
DEATH
OTHER ED ISSUES
21 Small wounds and localised infections
SMALL WOUNDS
SPECIFIC TYPES OF WOUNDS
LOCALISED INFECTIONS AND INFLAMMATIONS
22 Ophthalmic, ENT and facial conditions
THE EYES
THE EARS
THE NOSE
THE MOUTH AND THE THROAT
THE FACE
23 Global health
GLOBAL HEALTH AND EMERGENCY MEDICINE
Index
End User License Agreement
List of Tables
Chapter 1
Table 1.1 American society of Anaesthesiologists classification of grades o...
Chapter 2
Table 2.1 Estimation of traumatic blood loss in an adult (closed injuries)...
Chapter 3
Table 3.1 The Glasgow Coma Scale (GCS)
Table 3.2 Risk of intracranial haematoma in adults with head injuries
Table 3.3 Risk of intracranial haematoma in children with head injuries
Chapter 4
Table 4.1 Nerve roots supplying tendon and superficial reflexes
Chapter 7
Table 7.1 Well's scoring system for clinical deep vein thrombosis (DVT)
Chapter 10
Table 10.1 Referral criteria for specialist burns services
Chapter 11
Table 11.1 CHA2DS2VASC Score for stroke risk in atrial fibrillation
Table 11.2 Pacemaker codes
Table 11.3 ECG diagnosis of bundle‐branch blocks (
also →
Figure 11.
...
Chapter 12
Table 12.1 Significance of T‐wave inversion on a 12‐lead ECG
Table 12.2 Aortic dissection detection risk score ADD‐RS
Table 12.3 Comparison of ECG changes seen in benign early repolarisation (B...
Chapter 14
Table 14.1 ECG Changes to consider in Syncope ‘WOBBLER’
Chapter 15
Table 15.1 Toxidromes and their associated drugs, signs and symptoms
Table 15.2 Biochemical abnormalities and their associated drugs
Table 15.3 Therapeutic and toxic levels of common drugs
Table 15.4 Comparison of benzodiazepines
Table 15.5 Toxicity of elemental iron.
Table 15.6 Common symptoms of carbon monoxide poisoning
Chapter 17
Table 17.1 Estimated risks of seroconversion after blood exposure
Chapter 18
Table 18.1 Normal respiratory rates and pulse rates in children
Table 18.2 Differences between epiglottitis and croup
Table 18.3 Westley croup score
Table 18.4 Doses of common antibiotics for children
Table 18.5 Rectal dose of diazepam
Table 18.6 Signs of dehydration
Table 18.7 UK immunisation schedule for children
Chapter 19
Table 19.1 AUDIT C
Chapter 20
Table 20.1 Personal and sensitive information
Chapter 21
Table 21.1 Tetanus prophylaxis
List of Illustrations
Chapter 1
Figure 1.1 The management of major haemorrhage.
Figure 1.2 Spikes model for breaking bad news.
Chapter 2
Figure 2.1 The site for cricothyroidotomy.
Figure 2.2 (a) Pelvic binder. Anterior view of a fractured pelvis with a pel...
Chapter 3
Figure 3.1 Comparison of (a) extradural.(b) Subdural haemorrhages.
Extra
...
Chapter 4
Figure 4.1 (a and b) Sensory dermatomes of the body.
Figure 4.2 Canadian C‐Spine Rule.
Figure 4.3 (a) Lateral view. (b) Upper AP (odontoid peg) view.(c) Antero...
Chapter 5
Figure 5.1 Le Fort classification of fractures of the middle third of the fa...
Figure 5.2 Types of dental injury in relation to the dental anatomy.
Chapter 6
Figure 6.1 Appearance on fluid on supine and erect chest radiographs.
Figure 6.2 The triangle of safety for insertion of a chest drain.
Figure 6.3 Battle score.
Figure 6.4 Traumatic cardiac arrest algorithm.
Figure 6.5 Thoracotomy incision.
Figure 6.6 ‘Clamshell’ thoracotomy incision follows the fourth or fifth inte...
Figure 6.7 Fluid within Morrison's pouch – red arrows.
Chapter 7
Figure 7.1 Pressure dressing application.
Figure 7.2 Intact Shenton line (green) and disrupted Shenton line (red) due ...
Figure 7.3 Perthes' disease, with incidental normal enlargement of the ischi...
Figure 7.4 Slipped left proximal femoral epiphysis (arrowed) (anteroposterio...
Figure 7.5 Fracture of the medial tibial plateau.
Figure 7.6 Osteochondritis dissecans (arrow).
Figure 7.7 Bipartite patella.
Figure 7.8 Osgood–Schlatter disease (arrowed).
Figure 7.9 Ligaments around the ankle joint.
Figure 7.10 The bones of the foot.
Figure 7.11 Loss of Böhler's angle.
Figure 7.12 Avascular necrosis of the navicular bone.
Chapter 8
Figure 8.1 Anterior dislocation of the shoulder joint.
Figure 8.2 The normal appearance of the shoulder joint (apical view).
Figure 8.3 The normal appearance of the shoulder joint (lateral view).
Figure 8.4 Posterior dislocation of the shoulder joint.
Figure 8.5 Secondary ossification centres around the elbow.
Figure 8.6 Gartland classification of supracondylar fractures.
Figure 8.7 Lateral radiograph of the elbow joint showing anterior and poster...
Figure 8.8 Aide memoire for testing motor nerve function in the hand.
Figure 8.9 Fracture dislocations of the radius and ulna.
G
a
leazzi fracture d
...
Figure 8.10 Posterior displacement of distal radial epiphysis (shaded) with ...
Figure 8.11 Buckle fracture of the distal radius (arrowed).
Figure 8.12 Metaphyseal (pronator quadratus) fracture of the distal radius a...
Figure 8.13 Comminuted Colles' fracture (with angle ABC identified).
Figure 8.14 The carpal bones (AP view).
Figure 8.15 Sites of fracture in the scaphoid bone.
Figure 8.16 Lateral views of the wrist: (a) normal left and (b) abnormal rig...
Chapter 9
Figure 9.1 Crush–flexion injury to the fingertip.
Figure 9.2 Position of sutures after removal of nail in crush–flexion injury...
Figure 9.3 Greenstick fracture of the base of the proximal phalanx of the li...
Figure 9.4 The extensor tendons of the finger. The central slip to the middl...
Chapter 10
Figure 10.1 The ‘rule of nines’.
Figure 10.2 The Lund–Browder chart.
Figure 10.3 Comparative doses of radiation.
Chapter 11
Figure 11.1 Adult basic life support algorithm.
Figure 11.2 Adult advanced life support algorithm.
Figure 11.3 ‘4 Hs and 4 Ts’.
Figure 11.4 Complete heart block.
Figure 11.5 Adult bradycardia algorithm.
Figure 11.6 Agonal ECG rhythm.
Figure 11.7 The AVNRT ECG is regular with no visible atrial activity.
Figure 11.8 Accelerated junctional rhythm. Note the retrograde P waves.
Figure 11.9 The adult tachycardia algorithm ALS 2021.
Figure 11.10 A suggested approach to the management of new AF in an acute se...
Figure 11.11 ECG trace of Torsades de pointes.
Figure 11.12 Differentiation of RBBB and LBBB using the morphology of V1.
Chapter 12
Figure 12.1 The ECG limb leads and the cardiac axis.
Figure 12.2 Two examples of hyperacute T waves in acute MI.
Figure 12.3 12‐lead ECG of Wellen's syndrome – demonstrating biphasic and de...
Figure 12.4 12‐lead ECG of De Winter's T waves, best seen in V3 and V4.
Figure 12.5 12‐lead ECG of a true posterior infarction.
Figure 12.6 How to record a 15‐lead ECG.
Figure 12.7 The release of the three main cardiac markers into the bloodstre...
Figure 12.8 Stanford and DeBakey classification of aortic dissection.
Figure 12.9 ECG showing classic ST and PR changes of pericarditis.
Figure 12.10 Plain radiograph of the chest demonstrating a large right pneum...
Figure 12.11 POCUS image in M‐mode showing pneumothorax (‘barcode sign’) on ...
Chapter 13
Figure 13.1 Treatment of a choking adult.
Figure 13.2 Treatment of a choking child.
Figure 13.3 Predicted peak expiratory flow rates in adults.
Figure 13.4 Chest radiography in pulmonary oedema – portable, erect AP film....
Figure 13.5 Appearance of lobar collapse on a chest X‐ray.
Figure 13.6 Radiological appearances of right middle lobe collapse on AP and...
Figure 13.7 Subtle chest X‐ray appearance of consolidation behind cardiac sh...
Figure 13.8 Appearance of Tuberculosis on a chest X‐ray with bilateral chang...
Figure 13.9 POCUS image of right sided pleural effusion using curvilinear pr...
Figure 13.10 Chest radiograph of a patient treated initially for infection b...
Figure 13.11 ECG of a patient with sub‐massive PE, demonstrating sinus tachy...
Chapter 14
Figure 14.1 J waves on the ECG in hypothermia.
Figure 14.2 The role of the kallikrein–kinin system in the pathogenesis and ...
Chapter 15
Figure 15.1 Paracetamol treatment nomogram.
Figure 15.2 Mechanism of action of antidotes in paracetamol toxicity.
Figure 15.3 The mechanism of action of antidotes in poisoning with methanol ...
Figure 15.4 Hunter serotonin toxicity criteria.
Chapter 16
Figure 16.1 POCUS measurement of aortic lumen diameter.
Figure 16.2 POCUS examination identifying aorta and other anatomical feature...
Figure 16.3 Radiographs in bowel obstruction.
Chapter 17
Figure 17.1 Examination of the abdomen during pregnancy.
Figure 17.2 Resuscitation Council (UK) algorithm for life support of the new...
Figure 17.3 Sites for ectopic pregnancies: (1) fallopian tube – isthmic; (2)...
Figure 17.4 Dorsal penile nerve block.
Chapter 18
Figure 18.1 Predicted peak expiratory flow rates in children.
Figure 18.2 The Salter–Harris classification of epiphyseal injuries.
Chapter 19
Figure 19.1 ECIWA‐Ar.
Figure 19.2 Timeline for alcohol withdrawal states.
Chapter 20
Figure 20.1 The involvement of alcohol in trauma and RTC (road traffic colli...
Chapter 21
Figure 21.1 The human bot fly and its larva.
Figure 21.2 Anatomy of the eponychium.
Figure 21.3 Drainage of paronychia.
Chapter 22
Figure 22.1 Hyphaema – blood in the anterior chamber of the eye.
Figure 22.2 Performing a lateral canthotomy.
Figure 22.3 Auricular ring block.
Figure 22.4 Anterior nasal packing.
Figure 22.5 Retropharyngeal abscess.
Chapter 23
Figure 23.1 Global DALYSs and age‐standardised DALY rates.
Figure 23.2 Income and lifespan. Each bubble is a country, and its size refl...
Figure 23.3 Emergency Care system framework.
Figure 23.4 Trauma Care checklist.
Figure 23.5 Training for Deployment. Camacho, N. A., Hughes, A., Burkle, F. ...
Figure 23.6 The cluster system and UN lead agency.
Figure 23.7 WHO classification of emergency medical teams.
Figure 23.8 WHO EMT verification process.
Figure 23.9 Frequency of disasters and associated deaths.
Figure 23.10 Short‐term effects of major disasters.
Figure 23.11 Healthcare needs after sudden onset disasters.
Figure 23.12 Healthcare needs during armed conflict.
Guide
Cover Page
Table of Contents
Title Page
Copyright Page
List of contributors
Preface to the fifth edition
Preface to the fourth edition
Preface to the second edition
Preface to the first edition
About the Companion Website
Begin Reading
Index
WILEY END USER LICENSE AGREEMENT
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The RCEM Lecture Notes:
Emergency Medicine
Edited by
Catherine Williams
Emergency Medicine Consultant, Royal Bolton Hospital, Bolton, UK
Health Education North West, Manchester, UK
Amy Nickson
Emergency Medicine Consultant, Royal Bolton Hospital, Bolton, UK
Sexual Offences Examiner, Lancashire SAFE Centre, Preston, UK
Fifth Edition
This Fifth Edition is edited by Catherine Williams and Amy Nickson, has been revised and updated by contributors, and is based on the Fourth Edition of Lecture Notes: Emergency Medicine which was authored by Chris Moulton and David Yates.
This edition first published 2024© 2024 John Wiley & Sons Ltd
Edition History(1e, 1984; 2e, 1999; 3e, 2006; 4e, 2012)
This Fifth Edition is edited by Catherine Williams and Amy Nickson, has been revised and updated by contributors, and is based on the Fourth Edition of Lecture Notes: Emergency Medicine which was authored by Chris Moulton and David Yates.
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by law. Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions.
The right of The RCEM to be identified as the authors of the editorial material in this work has been asserted in accordance with law.
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Library of Congress Cataloging‐in‐Publication DataNames: Williams, Catherine (Consultant in emergency medicine), editor. | Nickson, Amy, editor. Lecture notes. Emergency medicine. | Royal College of Emergency Medicine (Great Britain), issuing body.Title: The RCEM lecture notes. Emergency medicine / edited by Catherine Williams, Amy Nickson.Other titles: Royal College of Emergency Medicine lecture notes. Emergency medicineDescription: Fifth edition. | Hoboken, NJ : Wiley‐Blackwell, 2024. | Preceded by Lecture notes. Emergency medicine / Chris Moulton, David Yates. 4th ed. 2012.Identifiers: LCCN 2023016562 (print) | LCCN 2023016563 (ebook) | ISBN 9781119325819 (paperback) | ISBN 9781119325840 (Adobe PDF) | ISBN 9781119325857 (epub)Subjects: MESH: Emergencies | Emergency Treatment–methods | Emergency Medicine–methodsClassification: LCC RC86.7 (print) | LCC RC86.7 (ebook) | NLM WB 105 | DDC 616.02/5–dc23/eng/20230912LC record available at https://lccn.loc.gov/2023016562LC ebook record available at https://lccn.loc.gov/2023016563
Cover Design: WileyCover Image: © Christine Müller/EyeEm; Tyler Olson
List of contributors
Vivek ChhabraYork and Scarborough Teaching, Hospitals NHS Foundation Trust, Calderdale and Huddersfield NHS Foundation Trust, UK
Kate ClaytonQueen Elizabeth Hospital Birmingham, Birmingham, UK
James ConroyLeeds Teaching Hospitals, Leeds, UK
Laura CotteyAcademic Department of Military Emergency Medicine, Royal Centre for Defence Medicine
Fiqry FadillahRoyal Free Hospital, London, UKMagpas Air Ambulance, Huntingdon, UK
Katie FulcherBradford Teaching Hospitals NHS Foundation Trust, Bradford, UK
Abu HassanSheffield Children’s Hospital and the Northern General Hospital, Sheffield, UK
Antonia HazleriggEmergency Department, Royal Infirmary of Edinburgh, Edinburgh, UKAcademic Department of Military Emergency Medicine, Royal Centre for Defence Medicine
Sophie JefferysSt Mary’s Hospital, Imperial College Healthcare NHS Trust, London, UK
Amy NicksonRoyal Bolton Hospital, Bolton, UKLancashire SAFE Centre, Preston, UK
Shah RahmanOxford Deanery, Oxford, UK
A.D. RedmondHumanitarian and Conflict Response Institute, University of Manchester, Manchester, UK
Rob SummerhayesUniversity Hospital Southampton, Southampton, UKHampshire and Isle of Wight Air Ambulance
Alan G A WeirUK Defence Medical Services, Lichfield, UKAcademic Department of Military Emergency Medicine, Royal Centre for Defence Medicine, Birmingham, UKMajor Trauma Centre, University Hospital Southampton, Southampton, UK
Jodie WilkinsonNorthern Care Alliance,Royal Oldham Hospital, Oldham, UK
Catherine WilliamsRoyal Bolton Hospital, Bolton, UKHealth Education North West, Manchester, UK
Preface to the fifth edition
Emergency medicine is facing some of the greatest challenges since the specialty first began. Departments are faced with crowding, exit block and higher attendances than ever before. Our bright and talented doctors want to provide the highest standards of care but are struggling to do so. Maintaining our compassion in the face of extremely challenging working conditions is clearly essential for the patients that we care for and has also been demonstrated to reduce physician burnout and emotional fatigue.
Despite its challenges, emergency medicine remains an innovative and forward‐thinking speciality, which is rising to meet these challenges and continually adapting to meet the needs of our patients. The joy and challenge of Emergency Medicine has always been the intellectual stimulus of providing high‐quality emergency care for the very sickest patients and managing the broad range of undifferentiated patients attending our departments, and this remains undimmed.
We hope this book provides you with a strong foundation to begin your journey into Emergency Medicine. Most of the important skills you will need cannot be learned from a book alone. Practical skills and pattern recognition only come with thousands of hours of deliberate practice under the supervision of experienced clinicians. Amongst those, we hope you find a role model for the type of doctor you would like to be – a leader, a pioneer, a teacher. We hope you find satisfaction in working in the most challenging of careers, where each of your actions can have such a profound impact on the lives of others.
Attempting to produce a textbook for a speciality as wide ranging and rapidly evolving as Emergency Medicine is a daunting task. In updating this text, we hope that we have represented the changes in both Emergency Medicine practice, and in society, in the years since previous editions. In doing so, we are highly cognisant that we are standing on the shoulders of giants. We would like to express sincere gratitude for the mentorship and support of the previous editor of this book, Dr Chris Moulton, and for the training, challenge and constructive criticism of all the colleagues, trainers and patients who have shaped our practice.
Catherine Williams and Amy Nickson, 2023
Preface to the fourth edition
The intervals between editions of this text are getting shorter, perhaps reflecting the increasing speed of change in medicine in general and emergency medicine in particular. We have introduced new material on emerging topics and updated information on established topics and now support this with a bank of multiple‐choice questions (MCQs) available online. The MCQs are supplemented by short explanations to reinforce your understanding.
The original layout has been retained – providing immediately accessible didactic advice supported by evidence‐based rationale. The latter is now firmly established in the practice of the specialty, vindicating the aspiration in our first preface that ‘future developments must ensure that the scientific method is woven into the fabric of the department’™.
There is an increasing tendency for more professionals to be exposed to the emergency department for shorter periods of time and, to many, the sometimes deceptive lure of the internet as a source of immediate knowledge seems to be all‐satisfying. We hope that you will agree that, although search engines can reinforce a book, they can never replace it. Using both, you will gain knowledge and understanding. Your patients will then be treated by the experienced rather than be used by you to gain experience.
We are very grateful to Anne Bassett whose help improved the quality of this book.
Chris Moulton and David Yates, 2012
Preface to the second edition
Emergency physicians work in an environment where measured interrogation is a luxury, where life‐saving skills can be required urgently and where the art of rapid and effective communication is essential. Add to this list the expectation that the doctor will have an encyclopaedic knowledge of the emergency aspects of every medical condition – and not a few social crises – and it is not surprising that most medical students and young doctors approach the emergency department with excitement that is tinged with anxiety.
This book is designed, in its approach, layout and content, to address these fears. Information is presented in an order that is relevant to the enquirer. It is demand led. Pathophysiology and relevant explanations follow. The reader learns how to deal with the emergency and then reads the background to the crisis and how, perhaps, it could have been avoided. This link with prevention is an increasingly emphasised part of emergency medicine, together with its concern to blur the boundaries between hospital and community care. Our primary aim has been to equip the reader with the knowledge to deal with crises, but we hope that we have shared, in these pages, our concern to ensure that doctors are also trained to try to avoid them.
Professor AD Redmond was the co‐author of the first edition of this work, with Professor Yates. Although the book has been completely rewritten, we have retained all the innovations that were so successfully introduced in Lecture Notes on Accident and Emergency Medicine in 1985. Professor Redmond has provided valuable advice on the development of this new edition, and it is a pleasure to record our appreciation of this support and encouragement.
The authors are very grateful for the support of their families, whose accidents and emergencies were neglected during the writing of this book.
Chris Moulton and David Yates Manchester, UK, 1999
Preface to the first edition
Our aim has been to cover all aspects of the work of a doctor in a busy accident and emergency department. Much of the text should be of interest to medical students during their clinical studies, but we hope that the book will be of special value to doctors studying for postgraduate diplomas.
Clearly, some restrictions must be placed on our definition of accident and emergency work unless we are to be overwhelmed, both here as authors and in our departments as casualty officers. These lecture notes have not been conceived as comprehensive treatises on the management of the many topics discussed – for only some aspects of most diseases and injuries are germane to the accident and emergency department. But it is precisely these aspects that are often inadequately covered in the standard texts. This book is based on our daily experience of the plethora of conditions presenting to what is inevitably an unstructured environment.
Sections devoted to ‘Urgent action’ are designed to facilitate the book’s use during emergencies. The remaining text continues this rather didactic format but is supported by background material, which attempts to justify our dogma. It is, however, not always enough to state that the advice given here has worked in practice (but it has!). Emergency medicine, like all other branches of medicine, must be based on sound scientific principles. A significant recent development has been the acceptance that emergencies are better treated by the experienced than used to gain experience. Future developments must ensure that the scientific method is woven into the fabric of the department.
The academic base for accident and emergency medicine in Manchester has been created by the foresight and hard work of three men. We wish to record our thanks to Professor MH Irving, Dr GS Laing and Professor HB Stoner who have given so much to the specialty in its early days and who have supported us during the preparation of this book. The doctors, nurses, clerical staff and patients of Salford and Stockport have also given us invaluable help. Their encouragement has been greatly appreciated. Jackie Fortin typed some of the preparatory work and Julie Rostron exercised great skill and patience in compiling the manuscript.
Veronica Yates responded to our vague requests for pictures with precise illustrations, and our publishers displayed remarkable tolerance during a long gestation.
DW Yates and AD Redmond, August 1984
About the Companion Website
This book is accompanied by a companion website:
www.wiley.com/go/LNEM5
This website includes:
Case studies
Best practices
Test questions
1What every Emergency Physician needs to know
Catherine Williams
Emergency Medicine Consultant, Royal Bolton Hospital, Bolton, UK
Health Education North West, Manchester, UK
People from many different backgrounds, of all ages and with an enormous variety of problems, present to an emergency department (ED) both by day and by night. The definition of ‘what constitutes an emergency’ is highly variable, and the ED often acts as a medical and societal safety net.
EMERGENCY ASSESSMENT OF THE UNDIFFERENTIATED PATIENT
All emergency physicians must be able to respond to, and manage an undifferentiated patient, presenting with a sudden emergency. A structured initial approach, following the ABCDE format discussed below, will ensure that immediately life‐threatening problems are addressed in order or priority. In many cases, where multiple clinicians are involved, these elements may be undertaken in parallel, but it remains important for a team leader to maintain a structured overview.
Cardiac arrest → Chapter 11, p. 157.
Children → p. 342.
The ABCDE assessment
A rapid initial ABCDE assessment should be possible in about 30 seconds. Immediate threats should be addressed at each stage before moving on.
Special considerations of the ABCDE assessment in traumaChapter 2,p → 22.
A – Airway
The airway may be:
patent, partially obstructed or completely obstructed (from physical obstruction or loss of muscle tone)
adequately protected or at risk (this depends on the protective reflexes of the airway).
Check for responsiveness
Is the patient alert and responsive to questions? A verbal reply confirms that there is:
a maintained and protected airway
temporarily adequate breathing and circulation
cerebral functioning.
If responsive, then the patient will usually be able to elaborate on the cause of the sudden deterioration that has brought him or her to an ED.
Failure to respond indicates a significantly lowered level of consciousness and therefore an airway that may be obstructed and is definitely at risk. There may be a need for airway‐opening manoeuvres and action to protect the airway.
Foreign body obstruction may initially present as a distressed, very agitated, cyanosed patient – ‘choking’.
Cardiorespiratory arrest → p. 157.
Choking → p. 205.
Respiratory arrest → p. 209.
Look for signs of partial upper airway obstruction
Complete upper airway obstruction will be silent.
Snoring
: the familiar sound of obstruction caused by the soft tissues of the mouth and pharynx. Often it accompanies the reduced muscle tone of a lowered level of consciousness.
Rattling or gurgling
: the sound of fluids in the upper airway.
Stridor
: a harsh, ‘crowing’ inspiratory (or occasionally biphasic) noise. Stridor suggests obstruction at the level of the larynx and upper trachea, which may be caused by foreign body or local infection. In cases of suspected supraglottic swelling, instrumentation of the throat (including the use of tongue depressor) should not be carried out, and examination should be undertaken very carefully as there is a risk of precipitating complete obstruction.
Drooling
: suggests obstruction at the posterior pharynx.
Hoarseness
: gross voice change suggests obstruction at the level of the larynx.
‘See‐saw’ respiration (abdominal expansion with thoracic wall indrawing)
: is indicative of airway obstruction with ongoing respiratory effort.
Cyanosis and reduced saturation readings on a pulse oximeter are very late signs of airway obstruction.
Allergic reactions → p. 306.
Laryngotracheal obstruction → p. 205.
Surgical airways → p. 23.
Assess the need for cervical spine protection before any airway intervention.
Clearance and maintenance of the airway
There are two main ways in which the airway becomes blocked.
Depressed level of consciousness:
the most common cause. When muscle tone is lost, the relaxation of soft tissues around the airway, in particular the tongue, may precipitate airway obstruction.
Physical obstruction:
from a variety of causes such as direct trauma, external or intramural mass or foreign body.
Airway obstruction may be immediately relieved by:
removing the cause of the obstruction (suction, manual removal or choking manoeuvre)
chin lift/head tilt manoeuvre
jaw thrust – pushing the jaw and the hyoid bone and their attached soft tissues forward
use of an oro‐pharyngeal/nasopharyngeal airway, supraglottic airway (i‐gel or laryngeal mask) or endotracheal intubation
reducing the swelling with vasoconstrictor drugs (adrenaline)
tracheal intubation
bypassing the cause of obstruction with a surgical airway.
Protection of the airway
Airway reflexes may be compromised by specific nerve palsies (e.g. stroke), the effect of drugs (including alcohol) and decreased conscious level. They may also be impaired at the extremes of age and in states of general debilitation. Vigilance is required in all such situations as there is a risk of aspiration of vomitus.
The recovery position should be used whenever possible if consciousness is decreased. This allows fluid and vomitus to drain from the airway under gravity, and the airway should be positioned to ensure patency. A high‐flow suction catheter must always be near the patient’s head.
The patient trolley must be capable of tilting ‘head down’ to drain vomitus out of the airway.
Obtunded patients require consideration of endotracheal intubation for airway protection.
Over 10% of normal individuals have no gag reflex, and thus presence or absence of a gag reflex is not a good predictor of need for intubation.
In a patient with a reduced level of consciousness, the airway must be assumed to be at risk until proved otherwise.
Protection of the cervical spine
If the patient has an injury to the cervical spine, there is a risk of damage to the spinal cord during the procedures needed to maintain the airway. Because of the potentially devastating outcomes of cervical cord injury, care must be taken to protect the cervical spine in patients who are:
unresponsive with a history of trauma or no clear history
suffering from multiple trauma
difficult to assess
showing any symptoms or signs that might be attributable to the cervical spine.
Adequate protection of the potentially unstable cervical spine conventionally consists of a rigid collar and blocks secured with tape. Cervical immobilisation makes airway management more challenging and can be distressing for the patient and so in these circumstances, manual inline stabilisation may be preferable.
Exclusion of cervical spine injury → p. 54.
B – Breathing
Look for
Difficulty in talking
Abnormal respiratory rate
: usually fast, laboured breathing. Very slow respiratory rates may occur just before respiratory arrest or due to poisoning with respiratory depressant drugs (e.g. opiates)
Nasal flaring and use of shoulder and neck muscles
Paradoxical respiration
: a see‐sawing movement of the chest and abdomen, which indicates airway obstruction, fatigue of the diaphragm or occasionally cervical cord injury
Unequal, diminished or abnormal breath sounds
Hyperresonance or dullness to percussion
Displacement of the trachea or apex beat
A flail segment
In children, subcostal or intercostal recession and tracheal tug
: indrawing of the elastic tissues caused by increased respiratory effort.
All the above suggest that the patient is struggling to achieve normal respiration. Failure to oxygenate the blood adequately and hence the tissues are shown by:
Tachycardia:
the nervous system has detected hypoxia and is stimulating the heart
Pallor and sweating
: caused by sympathetic stimulation
Cyanosis
: a late sign
Irritability, confusion or reduced responsiveness
: the brain is short of oxygen. This is an extremely worrying sign
A low SaO
2
(<94%)
: pulse oximetry should be established as soon as possible
Allergic reactions → p. 306.
Chest decompression and drainage → p. 76.
Chest injuries → p. 74.
Respiratory distress → p. 205.
Oxygen therapy
The common denominator of most life‐threatening illness, irrespective of cause, is the failure to deliver adequate amounts of oxygen to the tissues.
In the initial phase of assessment of the critically ill patient, high‐flow oxygen (usually via a non‐rebreathing mask) is an appropriate temporising measure. It is increasingly recognised that administration of high‐flow oxygen carries its own risks, so once accurate oxygen saturation measurement has been obtained, the FiO2 should be reduced to target oxygen saturations at 94–98% in most patients and 88–92% in those with chronic obstructive pulmonary disease. It is important to recognise that oxygen is a treatment for hypoxia and not breathlessness.
Some patients present with apparent breathlessness due to a non‐respiratory cause (metabolic acidosis, DKA) – these patients will not generally benefit from oxygen in the absence of hypoxia. Conversely, pneumothoraces may reduce in size up to four times more rapidly in a patient breathing high‐flow supplemental oxygen.
Ventilatory support
This should always be considered when:
the patient cannot maintain a clear airway, often as a result of significantly reduced conscious level
high‐flow oxygen via facemask (or continuous positive pressure device if appropriate) is insufficient to maintain acceptable oxygen saturations
spontaneous ventilation is inadequate
there has been a return of spontaneous circulation following a prolonged cardiac arrest
the patient is multiply injured
the patient has a severe chest injury (particularly multiple rib fractures and/or flail segments)
the patient is to be transferred, and there is a risk of severe deterioration en route.
The emergency induction of anaesthesia for the purpose of intubation and ventilation in a hypoxic or unstable patient is a challenging task. It should be carried out by a clinician with appropriate anaesthetic training and well‐maintained skills.
A pneumothorax is more likely to tension in a positive‐pressure ventilated patient. Chest drains should be inserted before ventilating patients with chest injuries.
C – Circulation
Check for a central pulse (over 10 seconds)
The absence of a central pulse (or a rate of <60 beats/min in infants) indicates the need to follow procedures for cardiorespiratory arrest:
Asystole → p. 161.
Pulseless electrical activity (PEA) → p. 161.
Ventricular fibrillation (VF) → p. 158.
If a pulse is detected, ensure that continuous electrocardiography monitoring is applied, and arrangements are made for a 12‐lead ECG.
Look for
Pallor and coolness of the skin:
the body diverts blood away from the skin when there are circulatory problems, and these signs are thus very useful indicators of shock
Pallor and sweating
: signs of gross sympathetic disturbance
Active bleeding or melaena
A fast or slow heart rate
: fast heart rates usually mean that either there is a cardiac arrhythmia or more commonly the sympathetic nervous system is responding to another problem (such as hypoxia, hypoglycaemia, pain or fear) and is driving the heart to beat faster. A slow heart rate usually means that something is wrong with the heart itself. The worst cause of this is severe hypoxia (or hypovolaemia) and, in this case, it means that terminal bradycardia and asystole are only seconds away
Abnormal blood pressure
: be aware that automatic blood pressure cuffs can be inaccurate at the extremes of blood pressure and may give inaccurate results in atrial fibrillation (particularly diastolic measurement). If in doubt obtain manual readings
A prolonged capillary refill time
: it should be less than 2 seconds if the circulation is satisfactory. However, peripheral vasoconstriction in a cold, wet patient can easily produce a prolonged refill time
Absent or quiet heart sounds and raised jugular venous pulse (JVP)
: classically suggestive of tamponade if accompanied by hypotension and tachycardia; these signs can be difficult to detect in a busy resuscitation room, and their absence cannot be used to rule out tamponade. JVP will not be raised if there is also hypovolaemia
A precordial wound
An abnormal electrocardiogram (ECG) trace on the monitor
Signs of left ventricular failure
(dyspnoea, gallop rhythm and crepitations)
Signs of abdominal, pelvic or occult bleeding
(may need per rectum examination and a nasogastric tube or ultrasound scan)
Signs of dehydration
(especially in children)
Purpura
(e.g. meningococcal sepsis)
Inadequate circulation will reduce tissue oxygenation and thus may also cause:
a raised respiratory rate
altered mental status.
Initial bolus resuscitation fluid should comprise 500 mL crystalloid containing sodium of 130–154 mmol/L over 15 min. In elderly patients, those of low body weight or where there are concerns about fluid tolerance (cardiac or kidney disease), smaller boluses of 250 mL with frequent reassessment are appropriate.
Abdominal bleeding → pp. 82 312 and 316.
Allergic reactions and anaphylaxis → p. 306.
Blood transfusion → p. 25.
Cardiac arrhythmias → p. 172.
Cardiac failure → pp. 219 and 251.
Cardiac tamponade → pp. 80 and 253.
Resuscitative thoracotomy → p. 83.
Pelvic bleeding → p. 86.
Renal effects of shock → p. 258.
Shock → p. 25 and 250.
Cardiac function
The stroke volume is the amount of blood ejected from the heart with each beat. It is determined by the left ventricular filling pressure, myocardial contractility and systemic vascular resistance. The product of heart rate and stroke volume is the cardiac output – the most important parameter of cardiac function. (Cardiac index is cardiac output divided by body surface area.) An increase in heart rate will directly increase the cardiac output and is the earliest cardiac response to hypoxia. However, the faster the heart beats the less time there is for it to fill and, eventually, a rise in heart rate will no longer be matched by a rise in cardiac output.
Myocardial function is compromised at high pulse rates because coronary blood flow occurs chiefly in diastole. When the heart rate rises above about 130 in an adult, the filling time is so reduced that cardiac output will actually fall.
Pulse and blood pressure
The autonomic response to hypovolaemia is complex. Rapid blood loss can produce reflex bradycardia, but when associated with tissue damage, it produces the more familiar tachycardia. Systolic blood pressure is the product of cardiac output and systemic vascular resistance. A high catecholamine response to hypoxia and hypovolaemia will produce a high systemic vascular resistance. This will maintain a ‘normal’, or even high, blood pressure in the presence of a falling cardiac output.
Knowledge of systemic blood pressure provides only very limited information about cardiac function and is a very late indicator of haemodynamic instability.
Maintenance of systemic vascular resistance is a vital response to hypovolaemia and hypoxia. (Skin pallor reflects this early on but is an imprecise clinical sign.) Similar to other compensatory mechanisms to hypoxia, this vasomotor response consumes oxygen and will eventually fail.
Measurements of pulse and blood pressure are very poor indicators of haemodynamic function in critically ill patients. Central venous pressure may not reflect the functioning of the left side of the heart and is thus of limited use in the assessment of overall cardiac performance.
Point of care ultrasound (POCUS) and echocardiography can give valuable information in the assessment of cardiovascular and fluid status and should be used in parallel with clinical examination wherever the equipment and skills are available → p. 10.
Fluid replacement
Left ventricular filling pressure (and hence cardiac output) is a function of the circulating blood volume. Increases in heart rate, systemic vascular resistance and myocardial contractility can maintain cardiac output and blood pressure in the early stages of hypovolaemia. This will, however, be at the expense of increased oxygen demands by the cardiovascular system and reduced tissue perfusion in many other areas. The Bezold‐Jarisch reflex, comprising sudden bradycardia, hypotension and apnoea, can result from contraction of the empty ventricle triggering vagal efferent fibres.
Older patients with deteriorating physiological reserve, those with pre‐existing organ dysfunction and those on certain medications will be less able to mount and maintain the compensatory reflexes. Early restoration of circulating volume can mitigate against the harmful effects of hypovolaemia.
Early restoration of blood pressure by transfusion does not necessarily indicate the correction of the circulatory deficit, nor normalisation of oxygen delivery to tissues.
The delivery of oxygen to the tissues depends not only on the pumping mechanism of the heart but also on the red cells in the circulating blood. A modest fall in haematocrit can reduce viscosity and increase blood flow while maintaining oxygen delivery but will still require an increase in cardiac output to be effective. Maintenance of haemoglobin levels by blood transfusion may reduce the impact of hypoxia by increasing the effectiveness of each cardiac cycle and reducing the need for an increase in cardiac output. Transfused blood will also maintain the oncotic pressure of the circulating fluid, thereby increasing the filling pressure. However, adequate levels of 2,3‐diphosphoglycerate (2,3‐DPG) are also necessary for satisfactory oxygen delivery, and stored blood is deplete in 2,3‐DPG such that even with a restored haemoglobin concentration, oxygen delivery is likely to be substantially lower than normal → p. 25.
Maintenance of adequate tissue perfusion is not synonymous with the return of a normal blood pressure. Indeed, the latter may be contraindicated in the ED in an actively bleeding patient (e.g. with an aortic aneurysm). Resuscitation can be achieved while keeping the blood pressure relatively low. This has been shown to improve survival until definitive surgery can be undertaken (‘permissive hypotension’). A similar approach is recommended in the prehospital management of injured adults and older children with presumed blood loss, in which fluid resuscitation may be titrated against the presence of peripheral pulses (or central pulses in the case of penetrating trauma).
When rapid fluid replacement is required, warmed IV fluids (40°C) delivered through a rapid infuser should ideally be used. Many clinicians believe that a balanced solution such as Plasmalyte or Hartmann’s solution is preferable to 0.9% saline if large volumes are required; however, evidence of a difference in patient outcomes is lacking.
The management of massive blood loss is summarised in Figure 1.1.
D – Disability
After A, B and C (airway, breathing and circulation) have been assessed and management is in progress, it is necessary to look at the state of the brain. In this context, the term disability is now widely used to describe a brief assessment of neurological functioning.
Figure 1.1 The management of major haemorrhage.
Newcastle Hospitals NHS Foundation Trust, Dr Rachel Hawes, Consultant Anaesthetist, Alison Muir, Transfusion Lab Manager, Aimi Baird, Transfusion Practitioner.
Look for
A reduced level of consciousness
: this is the most important sign of any problem affecting the brain. AVPU scoring is useful initially:
A
–Alert
V
–Voice elicits a response
P
–Pain elicits a response. (Attending relatives are usually in a highly distressed state so be careful how you elicit this sign) Pain should be elicited in the cranial nerve territories, in case of spinal injury.
U
–Unresponsive
Later, the Glasgow Coma Scale (GCS) should be used (→ p. 35 for adults and → p. 345 for children).
Always consider hypoglycaemia as a cause for a reduced level of consciousness.
Abnormal pupils
: look for size, equalness and reactivity. These features can be affected by both drugs and brain disease.
Physiological anisocoria is present in up to 20% of the healthy population.
Abnormal posture and limb movements
Severe intracerebral problems may also cause:
airway obstruction
respiratory depression (respiration, unlike the heartbeat, requires an intact brain stem)
bradycardia and hypertension (Cushing’s response)
neurogenic pulmonary oedema (caused by massive sympathetic vasoconstriction).
Diagnosis of death using neurological criteria → p. 405.
Head injury → p. 34.
Hypoglycaemia → p. 254.
Intracranial pathology → p. 236.
Poisoning → p. 277.
Depression of consciousness
There is a continuum of consciousness that ranges from an alert and oriented patient to one with brainstem death. Causes of impaired consciousness →Box 1.1. To maintain consciousness requires at least one functioning cerebral hemisphere and a working reticular activating system (RAS) in the brainstem. The RAS may be affected by brainstem stroke or increased intracerebral pressure leading to movement of cerebellar tonsils through the foramen magnum (‘coning’). For both cerebral hemispheres to be impaired suggests systemic insult such as inadequate oxygen delivery, hypoglycaemia, or the effect of toxins.
Unconsciousness is an imprecise term usually describing a condition of an unaware patient with whom verbal communication is not possible; unresponsive is thus a better description. Such patients will usually be amnesic for the duration of the unresponsiveness.
The ability to protect the airway decreases as the level of consciousness falls, and finally, the ability to maintain an open airway is also lost. Breathing indicates a functioning brain stem; in a cardiac arrest patient, it often returns quickly after cerebral circulation is restored. Sudden cerebral trauma may cause transitory apnoea and all of the causes of impaired consciousness listed in → Box 1.1 may lead to terminal apnoea.
Box 1.1 Causes of impaired consciousness
Hypoxia, hypovolaemia or cerebral ischaemia
Hypoglycaemia
Hypothermia
Poisoning or gross metabolic disturbance (including CO
2
narcosis)
Injury to the brain
Intracranial pathology (bleeding, thrombosis, embolism, infection, swelling, tumour, fits, etc.)
If prolonged, many of the above problems (including hypoxia, ischaemia, hypoglycaemia and status epilepticus) will lead to a remarkably similar outcome – selective neuronal necrosis and permanent brain injury.
E – Environment and exposure
In cases of trauma, collapse and depressed conscious level, the whole body must be exposed – including the back – so that nothing important is missed. In major trauma, rolling the patient is best avoided prior to imaging, due to the risk of exacerbating spinal or pelvic injury →p. 49.
Control of body temperature is important for successful resuscitation. Remove wet clothes and, if high volumes of IV fluids are to be given, they should be warmed. Even at this early stage, avoid extrinsic factors that may harm the patient.
Look for
Medical alert bracelets/necklaces or drug patches
Cold extremities
Shivering
Wet clothing
Pyrexia and clamminess
The position in which the patient is most comfortable
Uncomfortable splints (including collars and spinal boards)
Loss of the protective reflexes of the eyes
Areas where pressure sores might form
The proximity of the next of kin.
Attention to these details early on can radically change the well‐being (and demeanour) of a patient.
If a patient cannot blink, then the eyes should be covered to protect them.
Hyperpyrexia and hyperthermia → p. 249.
Hypothermia → p. 247.
F – Fits
Fits or seizures deprive the brain of oxygen and make assessment almost impossible. Stopping them is as important as the ABCs.
Look for
Frank tonic or clonic activity
Spasmodic twitching
Post‐ictal drowsiness
Gurgling, rattling or other signs of post‐ictal airway obstruction
Cyanosis: there is increased demand for oxygen and ventilation may be inadequate
Signs of head injury
Signs of other injury caused by a convulsion (e.g. a bitten tongue and intraoral bleeding)
Hypoglycaemia
Pyrexia or other signs of infection (especially in children).
Convulsions must be terminated before any further action can be effective.
Convulsions in adults → p. 243 and in children → p. 356 Hypoglycaemia → pp. 254 and 346.
Fitting indicates that something is wrong with the brain or its fuel supply. The list of possibilities is almost the same as that for causes of reduced consciousness → Box 1.2. Convulsive activity causes a dramatic increase in cerebral and muscle oxygen demand; a post‐ictal acidosis is inevitable following all but the briefest of seizures. The uncoordinated muscle action that occurs during the tonic or clonic stages of a fit makes control of the airway extremely difficult; some regurgitation may also occur. Ventilation of the lungs is usually reduced for the same reason. Alveolar oxygenation is thus poor at a time of high oxygen demand. This combination explains why prolonged fitting can be associated with permanent neurological damage.
Box 1.2 Causes of fits
Hypoxia
Shock
Hypoglycaemia
Poisoning
Metabolic disturbance
Intracranial pathology:
bleeding
trauma
thrombosis
embolism
infection
swelling
tumour
epilepsy
G – Glucose
The human body can be compared to an engine that needs an oxygen supply (airway and breathing) delivered in the bloodstream (circulation). However, we should not forget that the oxygen is required to burn fuel (glucose). Fat and protein are, of course, also important, but the brain uses glucose almost exclusively.
Look for
Restlessness, agitation or other mental change (‘jitteriness’ in a neonate)
Inappropriate lack of cooperation or aggression
A reduced level of consciousness
Convulsions
Signs of insulin usage
A low blood sugar level on testing with a reagent strip.
A reagent‐strip measurement of blood glucose should be performed in all patients who have depression of consciousness. If hypoglycaemia is found, it should be immediately treated with IV/IO glucose solution (50 mL of 50% glucose for a normal adult, 0.2 g/kg for a child). If no venous access is immediately available or rapidly obtained, then glucagon 1 mg by intramuscular (IM) injection is a useful standby.
Hypoglycaemia → pp. 254 and 346.
Hypoglycaemia is always waiting to catch you out. A comatose, or bizarrely behaving, patient with profuse sweating should always make you think of low blood sugar.
H – History
At this juncture, a brief history becomes a necessity using the mnemonic ‘AMPLE’:
A
Allergies
M
Medication
P
Past and present illnesses of significance
L
Last food and drink
E
Events leading up to the patient’s presentation
The people who accompany the patient to the department are a vital source of this information, hence the need to collect facts before the paramedic team leaves the ED.
Adrenocortical suppression
Patients who are undergoing prolonged treatment with steroids (i.e. for >3 weeks) may develop adrenocortical suppression. This can also occur for up to a year after stopping long‐term steroid therapy. During a medical crisis, such patients should be given supplementary corticosteroids (e.g. IV hydrocortisone 100 mg) in the ED.
I – Immediate analgesia and investigations
This is the point (if you have not already done it) to call for help. There should be no hesitation in seeking another pair of hands or a more experienced opinion.
In many patients who are not in extremis, the above will take only a matter of seconds. Once life‐threatening problems have been identified and treated, it is necessary to perform the tasks that are at the very heart of emergency medicine – to ensure the immediate relief of suffering. This will include the following:
Administration of analgesia:
assessment of pain
→
Box 1.3
Provision of splintage and support for injuries:
lower limb
→
pp. 89 and 95; upper limb
→
p. 114
Further relief of dyspnoea
Reassurance.
Box 1.3 Assessment of pain
Pain is a subjective experience. Clinical assessment of a patient’s level of pain depends on:
the patient’s description of the pain
the patient’s behaviour
the known injuries or condition
any observed signs of pain (sweating, tachycardia, posture, etc.)
the use of visual pain scales – analogue or image type (pain ladders and faces, etc.)
This is not just a matter of humanity. The trust of the patient (and the relatives and friends) is more easily gained by staff who are seen to address the patient’s distressing symptoms. This trust leads to the provision of better information and more easily achieved concordance with treatment. Conversely, nothing distresses relatives or friends more than the sight of a doctor or nurse asking endless questions whilst the patient continues to suffer. It is always better to overestimate pain rather than to underestimate it.
Relevant imaging and other investigations can now be requested. Twelve lead ECG and blood gas analysis are helpful early on. In the vast majority of cases, venous blood gas analysis is adequate and obviates the need for the difficulty and discomfort often associated with arterial blood gases. A low or normal pCO2 on venous blood gas analysis rules out hypercapnia with a high degree of certainty.
